wikidoc - User contributions [en]

Jugular venous pressure

2020-12-10T18:56:04Z

Mandana Chitsazan: /* JVP waveform */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''[[jugular venous pressure]]''' ([[JVP]], sometimes referred to as ''[[jugular venous pulse]]'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of various forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections (waves) and two downward deflections (toughs) have been described. The upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v" (atrial venous filling) waves, and the downward deflections are the "x"(when tricuspid opens and ventricular filling occurs) and the "y" descents (filling of ventricle after tricuspid opening).

The interpretation of [[JVP]] findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the [[JVP]] can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated [[JVP]] is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the [[JVP]] with [[inspiration]] (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of [[Kussmaul's sign]] includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the [[JVP]]===
The [[JVP]] is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva manuver]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The [[CVP]] vs the JVP===
The [[central venous pressure]] ([[CVP]]) lies approximately 5 cm above the middle of the [[right atrium]]. The [[CVP]] is therefore estimated to be the [[JVP]] in cm plus 5 cm. Normally, the [[CVP]] is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the [[JVP]] from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained [[cardiologist]]s do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the [[JVP]] "beats" twice (in quick succession) in each[[cardiac cycle]]. In other words, there are two waves in the [[JVP]] for each contraction-relaxation cycle by the heart. The first beat represents the [[atrial contraction]] (termed ''a'' wave) and the second beat represents venous filling against a closed [[tricuspid valve]] (termed ''v''wave) and not the commonly mistaken '[[ventricular contraction]]'. The [[carotid artery]] has only one beat in the [[cardiac cycle]].
*'''Non-palpable''' - the [[JVP]] cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be obliterated by occluding the [[internal jugular vein]] by lightly pressing the base of the neck.
*''' Varies with head-up-tilt (HUT)''' - the [[JVP]] varies with the angle of the neck. If a person is standing their [[JVP]] appears to be lower on the [[neck]] (or may not be seen at all because it below the [[sternal angle]]). The location of [[carotid pulse]] location does not vary with HUT.
*''' Varies with [[respiration]]''' - the [[JVP]] usually decreases with deep [[inspiration]]. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as [[inspiration]] decreases the thoracic pressure and increases blood movement into the heart ([[venous return]]), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the [[JVP]] changes with abdominal pressure. If the [[JVP]] is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the [[JVP]] remains elevated for a longer period of time it suggests [[heart failure]].

{| class="wikitable"
|+
| colspan="3" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Diffenetiating the jugular venous pulse from the carotid pulse'''
|+
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF" |'''Feature'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Internal Jugular vein'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Carotid artery'''
|+
| colspan="1" rowspan="1" |'''Appearance of [[pulse]]'''
| colspan="1" rowspan="1" |
* Biphasic: Two peaks and two troughs in each [[cardiac cycle]]
| colspan="1" rowspan="1" |
* Monophasic: A single brisk upstroke in [[cardiac systole]]
|-
| colspan="1" rowspan="1" |'''Palpability'''
| colspan="1" rowspan="1" |
* Not palpable (except in severe [[TR]])
| colspan="1" rowspan="1" |
* Palpable
|-
| colspan="1" rowspan="1" |'''Changes during [[inspiration]]'''
| colspan="1" rowspan="1" |
*Height of column falls
*Troughs become more prominent
| colspan="1" rowspan="1" |
* No [[respiratory]] change
|-
| colspan="1" rowspan="1" |'''Effects of pressure'''
| colspan="1" rowspan="1" |
*A gentle pressure at the base of the vein (clavicle) can obliterate the [[jugular venous pulsation]]
| colspan="1" rowspan="1" |
* Pressure cannot obliterate the [[carotid pulse]]
|-
|}

===[[Hepatojugular reflux]]===
{{main|Abdominojugular test}}
''[[Hepatojugular reflux]]'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the [[JVP]] measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The [[JVP]] increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the [[JVP]] after checking for [[hepatojugular reflux]] can indicate [[right ventricular failure]].

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting various [[JVP]] waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal [[jugular venous pressure]] changes during different stages of [[cardiac cycles]] as a result of phasic pressure changes in the [[right atrium]].
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right atrial contraction. During [[inspiration]], increased [[venous return]] to the [[right atrium]] may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a distinctive positive waveform. During early [[systole]], right ventricular [[isovolumetric contraction]] bulges the [[tricuspid valve]] into the [[right atrium]], leading to the appearance of the "c" wave. In addition, the increased [[carotid artery]] pressure during early [[systole]] may impact the adjacent [[jugular vein]].
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the [[tricuspid valve]] into the [[right ventricle]].
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the [[right atrium]] during the ventricular [[systole]] while the [[tricuspid valve]] is closed.
*''' "Y" descend:''' The Y descend results from the opening of the [[tricuspid valve]] and rapid inflow of blood into the [[right ventricle]].

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various [[JVP]] waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal [[JVP]] waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Conditions'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large "a" wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon "a" wave'''
(caused by contraction of the [[right atrium]] against the closed [[tricuspid valve]])
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x" descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent "v" wave'''
(caused by the backflow of blood to the [[right atrium]] during ventricular [[systole]])
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by slow emptying of the [[right atrium]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "Y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "Y" descent with a deep "Y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by obstruction to right [[ventricular filling]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "Y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T17:55:13Z

Mandana Chitsazan: /* A few things to remember: */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''[[jugular venous pressure]]''' ([[JVP]], sometimes referred to as ''[[jugular venous pulse]]'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of various forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections (waves) and two downward deflections (toughs) have been described. The upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v" (atrial venous filling) waves, and the downward deflections are the "x"(when tricuspid opens and ventricular filling occurs) and the "y" descents (filling of ventricle after tricuspid opening).

The interpretation of [[JVP]] findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the [[JVP]] can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated [[JVP]] is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the [[JVP]] with [[inspiration]] (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of [[Kussmaul's sign]] includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the [[JVP]]===
The [[JVP]] is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva manuver]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The [[CVP]] vs the JVP===
The [[central venous pressure]] ([[CVP]]) lies approximately 5 cm above the middle of the [[right atrium]]. The [[CVP]] is therefore estimated to be the [[JVP]] in cm plus 5 cm. Normally, the [[CVP]] is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the [[JVP]] from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained [[cardiologist]]s do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the [[JVP]] "beats" twice (in quick succession) in each[[cardiac cycle]]. In other words, there are two waves in the [[JVP]] for each contraction-relaxation cycle by the heart. The first beat represents the [[atrial contraction]] (termed ''a'' wave) and the second beat represents venous filling against a closed [[tricuspid valve]] (termed ''v''wave) and not the commonly mistaken '[[ventricular contraction]]'. The [[carotid artery]] has only one beat in the [[cardiac cycle]].
*'''Non-palpable''' - the [[JVP]] cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be obliterated by occluding the [[internal jugular vein]] by lightly pressing the base of the neck.
*''' Varies with head-up-tilt (HUT)''' - the [[JVP]] varies with the angle of the neck. If a person is standing their [[JVP]] appears to be lower on the [[neck]] (or may not be seen at all because it below the [[sternal angle]]). The location of [[carotid pulse]] location does not vary with HUT.
*''' Varies with [[respiration]]''' - the [[JVP]] usually decreases with deep [[inspiration]]. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as [[inspiration]] decreases the thoracic pressure and increases blood movement into the heart ([[venous return]]), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the [[JVP]] changes with abdominal pressure. If the [[JVP]] is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the [[JVP]] remains elevated for a longer period of time it suggests [[heart failure]].

{| class="wikitable"
|+
| colspan="3" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Diffenetiating the jugular venous pulse from the carotid pulse'''
|+
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF" |'''Feature'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Internal Jugular vein'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Carotid artery'''
|+
| colspan="1" rowspan="1" |'''Appearance of [[pulse]]'''
| colspan="1" rowspan="1" |
* Biphasic: Two peaks and two troughs in each [[cardiac cycle]]
| colspan="1" rowspan="1" |
* Monophasic: A single brisk upstroke in [[cardiac systole]]
|-
| colspan="1" rowspan="1" |'''Palpability'''
| colspan="1" rowspan="1" |
* Not palpable (except in severe [[TR]])
| colspan="1" rowspan="1" |
* Palpable
|-
| colspan="1" rowspan="1" |'''Changes during [[inspiration]]'''
| colspan="1" rowspan="1" |
*Height of column falls
*Troughs become more prominent
| colspan="1" rowspan="1" |
* No [[respiratory]] change
|-
| colspan="1" rowspan="1" |'''Effects of pressure'''
| colspan="1" rowspan="1" |
*A gentle pressure at the base of the vein (clavicle) can obliterate the [[jugular venous pulsation]]
| colspan="1" rowspan="1" |
* Pressure cannot obliterate the [[carotid pulse]]
|-
|}

===[[Hepatojugular reflux]]===
{{main|Abdominojugular test}}
''[[Hepatojugular reflux]]'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the [[JVP]] measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The [[JVP]] increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the [[JVP]] after checking for [[hepatojugular reflux]] can indicate [[right ventricular failure]].

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting various [[JVP]] waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== [[JVP]] waveform ==

The normal [[jugular venous pressure]] changes during different stages of [[cardiac cycles]] as a result of phasic pressure changes in the [[right atrium]].
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right atrial contraction. During [[inspiration]], increased [[venous return]] to the [[right atrium]] may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a distinctive positive waveform. During early [[systole]], right ventricular [[isovolumetric contraction]] bulges the [[tricuspid valve]] into the [[right atrium]], leading to the appearance of the "c" wave. In addition, the increased [[carotid artery]] pressure during early [[systole]] may impact the adjacent [[jugular vein]].
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the [[tricuspid valve]] into the [[right ventricle]].
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the [[right atrium]] during the ventricular [[systole]] while the [[tricuspid valve]] is closed.
*''' "Y" descend:''' The Y descend results from the opening of the [[tricuspid valve]] and rapid inflow of blood into the [[right ventricle]].

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various [[JVP]] waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal [[JVP]] waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Conditions'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large "a" wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon "a" wave'''
(caused by contraction of the [[right atrium]] against the closed [[tricuspid valve]])
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x" descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent "v" wave'''
(caused by the backflow of blood to the [[right atrium]] during ventricular [[systole]])
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by slow emptying of the [[right atrium]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "Y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "Y" descent with a deep "Y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by obstruction to right [[ventricular filling]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "Y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T17:54:37Z

Mandana Chitsazan:

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''[[jugular venous pressure]]''' ([[JVP]], sometimes referred to as ''[[jugular venous pulse]]'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of various forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections (waves) and two downward deflections (toughs) have been described. The upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v" (atrial venous filling) waves, and the downward deflections are the "x"(when tricuspid opens and ventricular filling occurs) and the "y" descents (filling of ventricle after tricuspid opening).

The interpretation of [[JVP]] findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the [[JVP]] can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated [[JVP]] is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the [[JVP]] with [[inspiration]] (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of [[Kussmaul's sign]] includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the [[JVP]]===
The [[JVP]] is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva manuver]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The [[CVP]] vs the JVP===
The [[central venous pressure]] ([[CVP]]) lies approximately 5 cm above the middle of the [[right atrium]]. The [[CVP]] is therefore estimated to be the [[JVP]] in cm plus 5 cm. Normally, the [[CVP]] is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the [[JVP]] from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained [[cardiologist]]s do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the [[JVP]] "beats" twice (in quick succession) in each[[cardiac cycle]]. In other words, there are two waves in the [[JVP]] for each contraction-relaxation cycle by the heart. The first beat represents the [[atrial contraction]] (termed ''a'' wave) and the second beat represents venous filling against a closed [[tricuspid valve]] (termed ''v''wave) and not the commonly mistaken '[[ventricular contraction]]'. The [[carotid artery]] has only one beat in the [[cardiac cycle]].
*'''Non-palpable''' - the [[JVP]] cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be obliterated by occluding the [[internal jugular vein]] by lightly pressing the base of the neck.
*''' Varies with head-up-tilt (HUT)''' - the [[JVP]] varies with the angle of the neck. If a person is standing their [[JVP]] appears to be lower on the [[neck]] (or may not be seen at all because it below the [[sternal angle]]). The location of [[carotid pulse]] location does not vary with HUT.
*''' Varies with [[respiration]]''' - the [[JVP]] usually decreases with deep [[inspiration]]. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as [[inspiration]] decreases the thoracic pressure and increases blood movement into the heart ([[venous return]]), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the [[JVP]] changes with abdominal pressure. If the [[JVP]] is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the [[JVP]] remains elevated for a longer period of time it suggests [[heart failure]].

{| class="wikitable"
|+
| colspan="3" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Diffenetiating the jugular venous pulse from the carotid pulse'''
|+
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF" |'''Feature'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Internal Jugular vein'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Carotid artery'''
|+
| colspan="1" rowspan="1" |'''Appearance of [[pulse]]'''
| colspan="1" rowspan="1" |
* Biphasic: Two peaks and two troughs in each [[cardiac cycle]]
| colspan="1" rowspan="1" |
* Monophasic: A single brisk upstroke in [[cardiac systole]]
|-
| colspan="1" rowspan="1" |'''Palpability'''
| colspan="1" rowspan="1" |
* Not palpable (except in severe [[TR]])
| colspan="1" rowspan="1" |
* Palpable
|-
| colspan="1" rowspan="1" |'''Changes during [[inspiration]]'''
| colspan="1" rowspan="1" |
*Height of column falls
*Troughs become more prominent
| colspan="1" rowspan="1" |
* No [[respiratory]] change
|-
| colspan="1" rowspan="1" |'''Effects of pressure'''
| colspan="1" rowspan="1" |
*A gentle pressure at the base of the vein (clavicle) can obliterate the [[jugular venous pulsation]]
| colspan="1" rowspan="1" |
* Pressure cannot obliterate the [[carotid pulse]]
|-
|}

===[[Hepatojugular reflux]]===
{{main|Abdominojugular test}}
''[[Hepatojugular reflux]]'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the [[JVP]] measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The [[JVP]] increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the [[JVP]] after checking for [[hepatojugular reflux]] can indicate [[right ventricular failure]].

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting various [[JVP]] waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== [[JVP]] waveform ==

The normal [[jugular venous pressure]] changes during different stages of [[cardiac cycles]] as a result of phasic pressure changes in the [[right atrium]].
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right atrial contraction. During [[inspiration]], increased [[venous return]] to the [[right atrium]] may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a distinctive positive waveform. During early [[systole]], right ventricular [[isovolumetric contraction]] bulges the [[tricuspid valve]] into the [[right atrium]], leading to the appearance of the "c" wave. In addition, the increased [[carotid artery]] pressure during early [[systole]] may impact the adjacent [[jugular vein]].
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the [[tricuspid valve]] into the [[right ventricle]].
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the [[right atrium]] during the ventricular [[systole]] while the [[tricuspid valve]] is closed.
*''' "Y" descend:''' The Y descend results from the opening of the [[tricuspid valve]] and rapid inflow of blood into the [[right ventricle]].

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various [[JVP]] waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal [[JVP]] waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Conditions'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large "a" wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon "a" wave'''
(caused by contraction of the [[right atrium]] against the closed [[tricuspid valve]])
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x" descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent "v" wave'''
(caused by the backflow of blood to the [[right atrium]] during ventricular [[systole]])
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by slow emptying of the [[right atrium]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "Y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "Y" descent with a deep "Y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "Y" descent'''
(caused by obstruction to right [[ventricular filling]])
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "Y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T17:19:55Z

Mandana Chitsazan: /* Differentiation of the JVP from the carotid pulse */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the [[JVP]] "beats" twice (in quick succession) in each[[cardiac cycle]]. In other words, there are two waves in the [[JVP]] for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second beat represents VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The [[carotid artery]] has only one beat in the cardiac cycle.
*'''Non-palpable''' - the [[JVP]] cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the [[JVP]] varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The location of [[carotid pulse]] location does not vary with HUT.
*''' Varies with respiration''' - the [[JVP]] usually decreases with deep [[inspiration]]. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as [[inspiration]] decreases the thoracic pressure and increases blood movement into the heart ([[venous return]]), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the [[JVP]] changes with abdominal pressure. If the [[JVP]] is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the [[JVP]] remains elevated for a longer period of time it suggests [[heart failure]].

{| class="wikitable"
|+
| colspan="3" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Diffenetiating the jugular venous pulse from the carotid pulse'''
|+
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF" |'''Feature'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Internal Jugular vein'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Carotid artery'''
|+
| colspan="1" rowspan="1" |'''Appearance of pulse'''
| colspan="1" rowspan="1" |
* Biphasic: Two peaks and two troughsin very cardiac cycle
| colspan="1" rowspan="1" |
* Monophasic: A single brisk upstroke in cardiac systole
|-
| colspan="1" rowspan="1" |'''Palpability'''
| colspan="1" rowspan="1" |
* Not palpable (except in severe [[TR]])
| colspan="1" rowspan="1" |
* Palpable
|-
| colspan="1" rowspan="1" |'''Changes during inspiration'''
| colspan="1" rowspan="1" |
*Height of column falls
*Troughs become more prominent
| colspan="1" rowspan="1" |
* No respiratory change
|-
| colspan="1" rowspan="1" |'''Effects of pressure'''
| colspan="1" rowspan="1" |
*A gentle pressure at the base of the vein (clavicle) can obliterate the [[jugular venous pulsation]]
| colspan="1" rowspan="1" |
* Pressure cannot obliterate the [[carotid pulse]]
|-
|}

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T17:16:37Z

Mandana Chitsazan: /* Differentiation of the JVP from the carotid pulse */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the JVP "beats" twice (in quick succession) in the [[cardiac cycle]]. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second, beat the VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The [[carotid artery]] has only one beat in the cardiac cycle.
*'''Non-palpable''' - the JVP cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the [[JVP]] varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The location of [[carotid pulse]] location does not vary with HUT.
*''' varies with respiration''' - the JVP usually decreases with deep inspiration. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the [[JVP]] changes with abdominal pressure. If the [[JVP]] is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the [[JVP]] remains elevated for a longer period of time it suggests [[heart failure]].

{| class="wikitable"
|+
| colspan="3" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Diffenetiating the jugular venous pulse from the carotid pulse'''
|+
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF" |'''Feature'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Internal Jugular vein'''
| colspan="1" rowspan="1" align="center" style="background: #87CEEB; color: #FFFFFF " |'''Carotid artery'''
|+
| colspan="1" rowspan="1" |'''Appearance of pulse'''
| colspan="1" rowspan="1" |
* Biphasic: Two peaks and two troughsin very cardiac cycle
| colspan="1" rowspan="1" |
* Monophasic: A single brisk upstroke in cardiac systole
|-
| colspan="1" rowspan="1" |'''Palpability'''
| colspan="1" rowspan="1" |
* Not palpable (except in severe [[TR]])
| colspan="1" rowspan="1" |
* Palpable
|-
| colspan="1" rowspan="1" |'''Changes during inspiration''
| colspan="1" rowspan="1" |
*Height of column falls
*Troughs become more prominent
| colspan="1" rowspan="1" |
* No respiratory change
|-
| colspan="1" rowspan="1" |'''Effects of pressure'''
| colspan="1" rowspan="1" |
*A gentle pressure at the base of the vein (clavicle) can obliterate the [[jugular venous pulsation]]
| colspan="1" rowspan="1" |
* Pressure cannot obliterate the [[carotid pulse]]
|-
|}

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T16:56:58Z

Mandana Chitsazan: /* Differentiation of the JVP from the carotid pulse */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the [[JVP]] are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The [[JVP]] and [[carotid pulse]] can be differentiated in several ways:
*'''Multiphasic''' - the JVP "beats" twice (in quick succession) in the [[cardiac cycle]]. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second, beat the VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The [[carotid artery]] has only one beat in the cardiac cycle.
*'''Non-palpable''' - the JVP cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the JVP varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The carotid pulse's location does not vary with HUT.
*''' varies with respiration''' - the JVP usually decreases with deep inspiration. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the JVP changes with abdominal pressure. If the JVP is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the JVP remains elevated for a longer period of time it suggests [[heart failure]].

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T16:48:57Z

Mandana Chitsazan: /* Anatomy */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the [[jugular foramen]], then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial [[scalp]] and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the [[right atrium]] or [[superior vena cava]]; therefore, are less preferred for estimation of [[JVP]] compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the JVP are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The JVP and carotid pulse can be differentiated in several ways:
*'''Multiphasic''' - the JVP "beats" twice (in quick succession) in the [[cardiac cycle]]. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second, beat the VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The carotid artery only has one beat in the cardiac cycle.
*'''Non-palpable''' - the JVP cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the JVP varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The carotid pulse's location does not vary with HUT.
*''' varies with respiration''' - the JVP usually decreases with deep inspiration. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the JVP changes with abdominal pressure. If the JVP is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the JVP remains elevated for a longer period of time it suggests [[heart failure]].

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T16:43:24Z

Mandana Chitsazan: /* Abnormal JVP waveforms */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the jugular foramen, then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery[]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial scalp and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the right atrium or [[superior vena cava]]; therefore, are less preferred for estimation of JVP compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the JVP are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The JVP and carotid pulse can be differentiated in several ways:
*'''Multiphasic''' - the JVP "beats" twice (in quick succession) in the [[cardiac cycle]]. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second, beat the VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The carotid artery only has one beat in the cardiac cycle.
*'''Non-palpable''' - the JVP cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the JVP varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The carotid pulse's location does not vary with HUT.
*''' varies with respiration''' - the JVP usually decreases with deep inspiration. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the JVP changes with abdominal pressure. If the JVP is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the JVP remains elevated for a longer period of time it suggests [[heart failure]].

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows:
{{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous pressure

2020-12-10T16:42:35Z

Mandana Chitsazan: /* Abnormal JVP waveforms */

__NOTOC__
{{SI}}

{{CMG}} {{AE}} {{Mitra}} {{MC}}

{{SK}} Jugular venous distention; elevated JVP; JVD; elevated neck veins; distended neck veins

==Overview==
The '''jugular venous pressure''' (JVP, sometimes referred to as ''jugular venous pulse'') is the indirectly observed pressure over the [[vein|venous system]]. It can be useful in the differentiation of different forms of [[heart disease|heart]] and [[lung disease]].

Classically three upward deflections and two downward deflections have been described. the upward deflections are the "a" (atrial filling), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumic systole), and "v"= atrial venous filling. and the downward deflections of the wave are the "x"(tricuspid opens and ventricular filling occurs) and the "y" descent reflects filling of ventricle after tricuspid opening.

The interpretation of JVP findings can be challenging and is becoming a lost art, as much of the subtle information previously obtained by careful observation of the JVP can now be gained easily with [[echocardiography]] and/or [[Electrocardiogram|EKG]]. Certain waveform abnormalities include "''[[Cannon a-waves]]''", which result when the atrium contracts against a closed tricuspid valve, due to [[complete heart block]] (3rd-degree heart block), or even in [[ventricular tachycardia]]. Another abnormality, "''c-v waves''", can be a sign of [[tricuspid regurgitation]].

An elevated JVP is the classic sign of venous hypertension (e.g. right-sided [[heart failure]]). The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the [[Kussmaul sign]] and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes [[constrictive pericarditis]], [[restrictive cardiomyopathy]], [[pericardial effusion]], and severe right-sided [[heart failure]].

==Anatomy==
*'''Right and left [[internal jugular vein]]s ([[IJV]]s):'''
** Paired neck [[veins]] draining the head and neck.
** Originate from the [[dural venous sinuses]] and leave the [[skull]] via the jugular foramen, then descend through the neck alongside and lateral to the [[internal carotid arterie]]s.
** Then join the [[subclavian vein]]s (at the base of the neck) to form the [[brachiocephalic vein]].
** The [[IJV]]s lies deep to the skin and soft tissues; therefore, they are not directly visible and identification only is possible via visualization of pulsations transmitted to the surface of the neck.
** Additionally, these blood vessels are under much lower pressure than the adjacent, pulsating [[carotid artery[]]. It, therefore, takes a sharp eye to identify the relatively weak, transmitted venous impulses.

*'''Right [[internal jugular vein]]'''
**It directly Communicates with the [[right atrium]] via the [[superior vena cava]]
**The right [[IJV]] can therefore function as a manometer, with distention indicating an elevation of [[Central venous pressure]] ([[CVP]]).
**This in turn is an important marker of intravascular volume status and related cardiac function.

*'''Right and left [[external jugular vein]]s ([[EJV]]):'''
**These veins drain superficial scalp and face structures
**They descend the lateral neck, pass diagonally over the top of the [[sternocleidomastoid muscle]]s and empty into the [[subclavian veins]]
**The [[EJV]]s are valved, and not directly in the line with the right atrium or [[superior vena cava]]; therefore, are less preferred for estimation of JVP compared to the left [[IJV]].

==Technique==

[[Image:Jvp-examination.jpg|left|thumb|Method to examine the JVP]]
*A classical method for quantifying the [[JVP]] was described by Borst & Molhuysen in 1952.<ref>{{cite journal | author = Borst J, Molhuysen J | title = Exact determination of the central venous pressure by a simple clinical method. | journal = Lancet | volume = 2 | issue = 7 | pages = 304-9 | year = 1952 | id = PMID 14955978}}</ref> It has since been modified in various ways.
*The patient is positioned under 45°, and the filling level of the [[jugular vein]] is determined. In healthy people, it is a maximum of several (3-4) centimeters above the [[sternum|sternal]] angle. Some physicians employ a ''venous arc'', an instrument to measure the [[JVP]] more accurately. A pen-light can aid in discerning the jugular filling level.

===Visualization of the JVP===
The JVP is easiest to observe if one looks ''along'' the surface of the [[sternocleidomastoid muscle]], as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90-degree angle). Like judging the movement of an automobile from a distance, it is easier to see the movement of an automobile when it is crossing one's path at 90 degrees (i.e. moving left to right or right to left), as opposed to coming toward one. Remember, tangential light is critical.

===A few things to remember:===

*'''Think anatomically'''
**The right [[internal jugular vein]] (IJV) runs between the two heads (sternal and clavicular) of the [[sternocleidomastoid muscle]] ([[SCM]]) and up in front of the ear.
**This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement.
**The two heads form the sides of a small triangle, with the [[clavicle]] making up the bottom edge. You should be able to feel a shallow defect formed by the borders of these landmarks.
**Note, you are trying to identify impulses originating from the [[IJV]] and transmitted to the overlying skin in this area. You can't actually see the [[IJV]].
**The [[external jugular vein]] ([[EJV]]) runs in an oblique direction across the [[sternocleidomastoid muscle]] and, in contrast to the [[IJV]], can usually be directly visualized.
**If the [[EJV] is not readily apparent, have the patient look to the left and do a [[Valsalva]]. This usually makes it quite obvious.
**[[EJV]] distention is not always a reliable indicator of elevated [[CVP]] as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when [[CVP]] is normal. It also makes several turns before connecting with the central venous system and is thus not in a direct line with the [[right atrium]].
*'''Take your time.'''
**Look at the area in question for several minutes while the patient's head is turned to the left.
**The [[carotid artery]] is adjacent to the IJV, lying just medial to it.
**If you are unsure whether a pulsation is caused by the [[carotid artery]] or the [[IJV]], place your hand on the patient's [[radial artery]] and use this as a reference.
**The [[carotid impulse]] coincides with the palpated [[radial artery]] pulsation and is characterized by a single upstroke timed with [[systole]].
**The venous impulse (at least when the patient is in [[sinus rhythm]] and there is no [[tricuspid regurgitation]]) has three components, each associated with a, c, and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin.
**In contrast, the [[carotid artery]] causes a single up and down pulsation.
**Furthermore, the [[carotid artery]] is palpable, while the [[IJV]] is not palpable and can, in fact, be obliterated by applying pressure in the area where it emerges above the [[clavicle]].
*'''Search along the entire projected course of the [[IJV]] as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking'''.
**In fact, if the patient's [[CVP]] is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45 degrees or more (else there will be no identifiable "top" of the column as the entire [[IJV]] will be engorged).
**After you have found the top of the wave, see what effect sitting straight up and lying down flat has on the height of the column. Sitting should cause it to appear at a lower point in the neck while lying has the opposite effect. Realize that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position of the top of the pulsations in relation to other structures in the neck and chest.
*'''Shine a penlight tangentially across the neck'''. This sometimes helps to accentuate the pulsations.
*'''If you are still uncertain, apply gentle pressure to the [[right upper quadrant]] of the abdomen for 5 to 10 seconds.'''
**This elicits [[Hepatojugular reflux]] which, in pathological states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the [[IJV]], making the transmitted pulsations more apparent.
**Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.
*'''Once you identify [[JVD]], try to estimate how high in cm the top of the column is above the [[Angle of Louis]]'''.
**The angle is the site of the joint that connects the [[manubrium]] with the body of the [[sternum]]. First identify the [[suprasternal notch]], a concavity at the top of the manubrium.
**Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch.
**This is roughly at the level of the 2nd [[intercostal space]].
**The vertical distance from the top of the column to this angle is added to 5cm, the rough vertical distance from the angle to the [[right atrium]] with the patient lying at a 45-degree angle.
**The sum is an estimate of the [[CVP]]. Normal [[CVP]] is 7-9 cm.

===The CVP vs the JVP===
The central venous pressure (CVP) lies approximately 5 cm above the middle of the [[right atrium]]. The CVP is therefore estimated to be the JVP in cm plus 5 cm. Normally the CVP is 5-9 cm of H2O.

<div align="left">
<gallery heights="225" widths="225">
Image:angle_louis1.jpg|The wooden Q-tips highlight the different slopes of the [[sternum]] and [[manubrium]].
Image:angle_louis2.jpg|The point at which the Q-tips cross is the [[Angle of Louis]]
Image:cardiac_jvp_estimate.jpg|Determining the CVP
Image:Elevated JVP.JPG|Elevated JVP</gallery>
</div>
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California)

===Differentiation of the JVP from the [[carotid pulse]]===
[[Image:Jvp-vs-carotid.jpg|left|300px]]

[[Pulse]]s in the JVP are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the [[right atrium]].

The JVP and carotid pulse can be differentiated in several ways:
*'''Multiphasic''' - the JVP "beats" twice (in quick succession) in the [[cardiac cycle]]. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart. The first beat represents that atrial contraction (termed ''a'') and the second, beat the VENOUS FILLING against a closed tricuspid valve (termed ''v'') and not the commonly mistaken 'ventricular contraction'. The carotid artery only has one beat in the cardiac cycle.
*'''Non-palpable''' - the JVP cannot be palpated. If one feels a pulse in the neck, it is generally the [[common carotid artery]].
*'''Occlude''' - the [[JVP]] can be stopped by occluding the [[internal jugular vein]] by lightly pressing against the neck.
*''' Varies with head-up-tilt (HUT)''' - the JVP varies with the angle of the neck. If a person is standing their JVP appears to be lower on the neck (or may not be seen at all because it below the [[sternal angle]]). The carotid pulse's location does not vary with HUT.
*''' varies with respiration''' - the JVP usually decreases with deep inspiration. Physiologically, this is a consequence of the [[Frank-Starling mechanism]] as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the [[pulmonary circulation]].
*'''Abdominal jugular reflux (AJR)''' (also hepatojugular reflux) - the JVP changes with abdominal pressure. If the JVP is elevated 4 cm, it usually returns to its baseline level within 10 seconds. If the JVP remains elevated for a longer period of time it suggests [[heart failure]].

===Hepatojugular reflux===
{{main|Abdominojugular test}}
''Hepatojugular reflux'', sometimes incorrectly referenced as a "reflex",<ref>{{cite journal | author = Aronson J | title = Hepatojugular reflux | journal = BMJ | volume = 318 | issue = 7192 | pages = 1172 | year = 1999 | id = PMID 10221938}} [http://bmj.bmjjournals.com/cgi/content/full/318/7192/1172 Free Full Text].</ref> is an expanded form of the JVP measurement. By pressing on the [[liver]] (''hepato-'') for 15-30 seconds, venous blood is advanced into the circulation. The JVP increases in a normal person, and distention should appear more pronounced. However, a slow decrease of the JVP after checking for hepatojugular reflux can indicate right ventricular failure.

==Video Instruction==
This video contains a detailed explanation of what the [[JVP]] is, how it is measured, and what are the diagnostic considerations of [[JVP]], in terms of interpreting JVP waveforms.

{{#ev:youtube|https://https://www.youtube.com/watch?v=O1MfBEmNj2s}}

==Causes of Elevated Jugular Venous Pressure==

*The most common causes of elevated [[JVP]] are:
**[[Heart failure]]
**[[Constrictive pericarditis]] ([[JVP]] increases on [[inspiration]]- called [[Kussmaul's sign]])
**[[Cardiac tamponade]]
**[[Right ventricular myocardial infarction]]
**[[Fluid overload]] (eg, renal disease)
**[[Superior vena cava obstruction]] (no [[JVP]] pulsation)

*'''To view a complete list of causes of elevated [[jugular venous pressure]], [[Jugular venous distention resident survival guide|click here]].'

== JVP waveform ==

The normal jugular venous pressure changes during different stages of cardiac cycles as a result of phasic pressure changes in the right atrium.
It consists of two (and sometimes three) positive waves and two negative troughs.

*''' "a" wave:''' This presystolic wave is caused by venous distension due to the right trial contraction. During inspiration, increased venous return to the right atrium may accentuate this wave.
*''' "c" wave:''' This wave may sometimes be noted as a district positive waveform. During early systole, right ventricular isovolumetric contraction bulges the tricuspid valve into the right atrium, leading to the appearance of the "c" wave. In addition, the increased carotid artery pressure during early systole may impact the adjacent jugular vein.
*''' "X" descend:''' The X descend is caused by atrial relaxation and downward displacement of the tricuspid valve.
*''' "v" wave:''' This late-systolic wave is caused by the increasing volume of blood accumulating in the right atrium during the ventricular systole while the tricuspid valve is closed.
*''' "Y" descend:''' The Y descend results from the opening of the tricuspid valve and rapid inflow of blood into the right ventricle.

===Components of the JVP Waveform===

[[Image:Jvp-waveform.jpg|left|frame|
'''a''' = atrial contraction, occurs just before 1st heart sound and carotid pulse
'''x''' = atrial relaxation
'''c''' = bulging of tricuspid valve during isovolumetric contraction; x 1 = occurs during ventricular contraction pulling down the tricuspid valve “descent of the base”; v = occurs during venous filling of the atrium with a closed tricuspid valve\; y = opening of tricuspid valve and right atrium emptying]]
<br clear="left"/>

===Abnormal JVP waveforms===

*Various JVP waveform abnormalities are summarized as it follows: {{cite book | last = Bickley | first = Lynn | title = Bates' guide to physical examination and history taking | publisher = Wolters Kluwer | location = Philadelphia | year = 2017 | isbn = 9781469893419 }} {{cite book | last = Perloff | first = Joseph | title = Physical examination of the heart and circulation | publisher = People's Medical Pub. House | location = Shelton, CT | year = 2009 | isbn = 9781607950233 }}

{| class="wikitable"
|+
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Abnormal JVP waveform'''
| colspan="1" rowspan="1" align="center" style="background: #4479BA; color: #FFFFFF " |'''Associated Condition'''
|+
| colspan="1" rowspan="1" |'''Absent "a" wave'''
| colspan="1" rowspan="1" |
*[[Atrial fibrillation]]
|-
| colspan="1" rowspan="1" |'''Large “a” wave'''
(caused by increased atrial contraction pressure)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Pulmonary hypertension]]
*[[Pulmonic stenosis]]
*[[Right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Cannon “a” wave'''
(caused by contraction of the right atrium against the closed tricuspid valve)
| colspan="1" rowspan="1" |
*[[Complete heart block]] [[(Third-degree atrioventricular block)]]
*[[Premature atrial contractions]]
*[[Junctional rhythm]]
*[[Ventricular tachycardia]]
|-
| colspan="1" rowspan="1" |'''Decreased nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Right ventricular dilation]]
|-
| colspan="1" rowspan="1" |'''Obliteration or reversed nadir of "x" descent'''
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Accentuated "x' descent'''
| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
|-
| colspan="1" rowspan="1" |'''Prominent “v” wave'''
(caused by the backflow of blood to the right atrium during ventricular systole)
| colspan="1" rowspan="1" |
*[[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Slow “y” descent'''
(caused by slow emptying of right atrium)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Rapid, deep "y" descent'''
| colspan="1" rowspan="1" |
*Severe [[Tricuspid regurgitation]]
|-
| colspan="1" rowspan="1" |'''Sharp "y" descent with a deep "y" trough and a rapid ascent to the baseline''' (referred to as [[Friedreich's sign]])

| colspan="1" rowspan="1" |
*[[Constrictive pericarditis]]
*Severe [[right-sided heart failure]]
|-
| colspan="1" rowspan="1" |'''Slow "y" descent'''
(caused by obstruction to right ventricular filling)
| colspan="1" rowspan="1" |
*[[Tricuspid stenosis]]
*[[Right atrial myxoma]]
|-
| colspan="1" rowspan="1" |'''Absent "y" descent'''
| colspan="1" rowspan="1" |
*[[Cardiac tamponade]]
|-
|}<br />

==References==
{{reflist|2}}

{{Physical exam}}
[[Category:Medical signs]]
[[Category:Signs and symptoms]]
[[Category:Cardiology]]
[[Category:Physical examination]]

Jugular venous distention resident survival guide

2020-09-10T15:13:07Z

Mandana Chitsazan: /* Life Threatening Causes */

__NOTOC__

{{WikiDoc CMG}}; {{AE}} {{Mitra}} {{MC}}

==Overview==
Jugular venous distension (JVD), or an elevated jugular venous pressure (JVP), is considered a useful physical finding for assessing ventricular filling pressures and central venous pressure (CVP). JVD is defined as an estimated JVP ≥10 cm H2O.

==Causes==
===Life Threatening Causes===
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
*[[Acute heart failure]]
*[[Cardiac Tamponade]]
*[[Massive pulmonary emboli]]
*[[Right ventricular myocardial infarction]]
*[[Tension Pneumothorax]]

===Common Causes===
*[[Congestive heart failure]]
*[[Cardiomyopathy]]
*[[Cor pulmonale]]
*[[Constrictive pericarditis]]
*[[Chronic obstructive pulmonary disease|Chronic obstructive pulmonary disease (copd)]]
*[[Fluid overload]]
*[[Pulmonary embolism]]
*[[Pulmonary hypertension]]
*[[Pulmonary valve stenosis]]
*[[Restrictive cardiomyopathy]]
*[[Right atrial myxoma]]
*[[Right heart failure]]
*[[Right ventricular myocardial infarction]]
*[[Tension pneumothorax]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of jugular venous distension. <ref name="pmid8409071">{{cite journal| author=Butman SM, Ewy GA, Standen JR, Kern KB, Hahn E| title=Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 4 | pages= 968-74 | pmid=8409071 | doi=10.1016/0735-1097(93)90405-p | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8409071 }} </ref> <ref name="pmid17943049">{{cite journal| author=Devine PJ, Sullenberger LE, Bellin DA, Atwood JE| title=Jugular venous pulse: window into the right heart. | journal=South Med J | year= 2007 | volume= 100 | issue= 10 | pages= 1022-7; quiz 1004 | pmid=17943049 | doi=10.1097/SMJ.0b013e318073c89c | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17943049 }} </ref> <ref name="pmid9665212">{{cite journal| author=McGee SR| title=Physical examination of venous pressure: a critical review. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 1 | pages= 10-8 | pmid=9665212 | doi=10.1016/s0002-8703(98)70175-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9665212 }} </ref> <ref name="pmid6638720">{{cite journal| author=Dell'Italia LJ, Starling MR, O'Rourke RA| title=Physical examination for exclusion of hemodynamically important right ventricular infarction. | journal=Ann Intern Med | year= 1983 | volume= 99 | issue= 5 | pages= 608-11 | pmid=6638720 | doi=10.7326/0003-4819-99-5-608 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6638720 }} </ref>

{{familytree/start |summary=JVD diagnosis Algorithm.}}
{{familytree | | | | | A01 | | | | | | |A01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> [[Jugular Venous Distension]]}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | |,|-|-|^|-|-|-|.| | | | | |}}
{{familytree | | B01 | | | | | B02 | | | | |B01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> With [[pulmonary edema]]|B02=Without [[pulmonary edema]]}}
{{familytree | | |!| | | |,|-|-|^|-|-|-|-|.|}}
{{familytree | | C01 | | C02 | | C03 | | C04 |C01=<div style="float: Center; text-align: Center; width:12em; padding:1em;">
[[Congestive heart failure]]
|C02=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased right atrial pressure'''
|C03=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Venous obstruction'''
|C04=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased intrathoracic pressure'''}}
{{familytree | | | | | | |!| | | |!| | | |!|}}
{{familytree | | | | | | D01 | | D02 | | D03|D01=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''Restriction of right atrial and right ventricular filling:'''
:❑ [[Cor pulmonale]] (Massive [[pulmonary emboli]], [[COPD]])
:❑ [[Pulmonary Hypertension]]
:❑ [[Constrictive pericarditis]]
:❑ [[Cardiac Tamponade]]

❑'''RV Failure:'''
:❑ [[Cardiomyopathy]]
:❑ [[RV myocardial infarction]]

❑ '''Fluid overload due to renal diseases'''

❑ '''Tricuspid valve incompetence'''

❑ '''Tricuspid valve stenosis or obstruction'''|D02=<div style="float: Center; text-align: Center; width:20em; padding:1em;">

❑ '''Superior vena cava obstrcution'''|D03=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''[[Positive pressure ventilation]]'''

❑ '''A large [[pleural effusion]]'''

❑'''[[Tension Pneumothorax]]'''}}

{{familytree/end}}

==Treatment==
*The management of jugular venous distension should be directed towards the underlying causes.
*Treatment of [[congestive heart failure]] usually includes [[diuretics]] (for symptom relief), [[beta blockers]], [[angiotensin converting enzyme inhibitors]] ([[ACE-I]]) /[[aldosterone receptor blockers]] ([[ARB]]).
**For a complete guide on the treatment of congestive heart failure, [[Heart failure resident survival guide|click here]].<br />
*Treatment of [[right ventricular myocardial infarction]] includes [[reperfusion]], maintenance of right ventricular [[preload]], decreasing right ventricular [[afterload]], restoring cardiac rate/rhythm and [[atrioventricular synchrony]], and inotropic support.
**For a complete guide on the treatment of right ventricular myocardial infarction, [[Right ventricular myocardial infarction resident survival guide|click here]].<br />
*Treatment of massive [[pulmonary embolism]] usually includes [[fibrinolytic therapy]].
**For a complete guide on the treatment of pulmonary embolism, [[Pulmonary embolism resident survival guide|click here]].<br />
*Treatment of [[pericardial tamponade]] usually includes [[pericardiocentesis]].
**For a complete guide on the treatment of cardiac tamponade, [[Cardiac tamponade resident survival guide|click here]].<br />
*Treatment of [[tension pneumothorax]] includes immediate [[needle decompression]] followed by [[chest tube]] insertion.
**For a complete guide on the treatment of tension pnemuothorax, [[Tension pneumothorax resident survival guide|click here]].<br />

==Do's==
* If the [[JVP]] does not seem elevated when the patient is supine, a provocative test, i.e., [[abdominojugular test]], should be performed.

==Don'ts==
* [[JVD]] only provides clues to the presence of an elevated [[central venous pressure]] ([[CVP]]). Clinicians should avoid making decisions about the degrees of [[CVP]] elevation based on the [[JVP]] measurement.

==References==
{{Reflist|2}}

[[Category:Help]]
[[Category:Projects]]
[[Category:Resident survival guide]]
[[Category:Templates]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Jugular venous distention resident survival guide

2020-09-10T15:12:24Z

Mandana Chitsazan: /* Common Causes */

__NOTOC__

{{WikiDoc CMG}}; {{AE}} {{Mitra}} {{MC}}

==Overview==
Jugular venous distension (JVD), or an elevated jugular venous pressure (JVP), is considered a useful physical finding for assessing ventricular filling pressures and central venous pressure (CVP). JVD is defined as an estimated JVP ≥10 cm H2O.

==Causes==
===Life Threatening Causes===
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
* [[Acute heart failure]]
* [[Massive pulmonary emboli]]
* [[Right ventricular myocardial infarction]]
* [[Cardiac Tamponade]]
* [[Tension Pneumothorax]]

===Common Causes===
*[[Congestive heart failure]]
*[[Cardiomyopathy]]
*[[Cor pulmonale]]
*[[Constrictive pericarditis]]
*[[Chronic obstructive pulmonary disease|Chronic obstructive pulmonary disease (copd)]]
*[[Fluid overload]]
*[[Pulmonary embolism]]
*[[Pulmonary hypertension]]
*[[Pulmonary valve stenosis]]
*[[Restrictive cardiomyopathy]]
*[[Right atrial myxoma]]
*[[Right heart failure]]
*[[Right ventricular myocardial infarction]]
*[[Tension pneumothorax]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of jugular venous distension. <ref name="pmid8409071">{{cite journal| author=Butman SM, Ewy GA, Standen JR, Kern KB, Hahn E| title=Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 4 | pages= 968-74 | pmid=8409071 | doi=10.1016/0735-1097(93)90405-p | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8409071 }} </ref> <ref name="pmid17943049">{{cite journal| author=Devine PJ, Sullenberger LE, Bellin DA, Atwood JE| title=Jugular venous pulse: window into the right heart. | journal=South Med J | year= 2007 | volume= 100 | issue= 10 | pages= 1022-7; quiz 1004 | pmid=17943049 | doi=10.1097/SMJ.0b013e318073c89c | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17943049 }} </ref> <ref name="pmid9665212">{{cite journal| author=McGee SR| title=Physical examination of venous pressure: a critical review. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 1 | pages= 10-8 | pmid=9665212 | doi=10.1016/s0002-8703(98)70175-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9665212 }} </ref> <ref name="pmid6638720">{{cite journal| author=Dell'Italia LJ, Starling MR, O'Rourke RA| title=Physical examination for exclusion of hemodynamically important right ventricular infarction. | journal=Ann Intern Med | year= 1983 | volume= 99 | issue= 5 | pages= 608-11 | pmid=6638720 | doi=10.7326/0003-4819-99-5-608 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6638720 }} </ref>

{{familytree/start |summary=JVD diagnosis Algorithm.}}
{{familytree | | | | | A01 | | | | | | |A01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> [[Jugular Venous Distension]]}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | |,|-|-|^|-|-|-|.| | | | | |}}
{{familytree | | B01 | | | | | B02 | | | | |B01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> With [[pulmonary edema]]|B02=Without [[pulmonary edema]]}}
{{familytree | | |!| | | |,|-|-|^|-|-|-|-|.|}}
{{familytree | | C01 | | C02 | | C03 | | C04 |C01=<div style="float: Center; text-align: Center; width:12em; padding:1em;">
[[Congestive heart failure]]
|C02=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased right atrial pressure'''
|C03=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Venous obstruction'''
|C04=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased intrathoracic pressure'''}}
{{familytree | | | | | | |!| | | |!| | | |!|}}
{{familytree | | | | | | D01 | | D02 | | D03|D01=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''Restriction of right atrial and right ventricular filling:'''
:❑ [[Cor pulmonale]] (Massive [[pulmonary emboli]], [[COPD]])
:❑ [[Pulmonary Hypertension]]
:❑ [[Constrictive pericarditis]]
:❑ [[Cardiac Tamponade]]

❑'''RV Failure:'''
:❑ [[Cardiomyopathy]]
:❑ [[RV myocardial infarction]]

❑ '''Fluid overload due to renal diseases'''

❑ '''Tricuspid valve incompetence'''

❑ '''Tricuspid valve stenosis or obstruction'''|D02=<div style="float: Center; text-align: Center; width:20em; padding:1em;">

❑ '''Superior vena cava obstrcution'''|D03=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''[[Positive pressure ventilation]]'''

❑ '''A large [[pleural effusion]]'''

❑'''[[Tension Pneumothorax]]'''}}

{{familytree/end}}

==Treatment==
*The management of jugular venous distension should be directed towards the underlying causes.
*Treatment of [[congestive heart failure]] usually includes [[diuretics]] (for symptom relief), [[beta blockers]], [[angiotensin converting enzyme inhibitors]] ([[ACE-I]]) /[[aldosterone receptor blockers]] ([[ARB]]).
**For a complete guide on the treatment of congestive heart failure, [[Heart failure resident survival guide|click here]].<br />
*Treatment of [[right ventricular myocardial infarction]] includes [[reperfusion]], maintenance of right ventricular [[preload]], decreasing right ventricular [[afterload]], restoring cardiac rate/rhythm and [[atrioventricular synchrony]], and inotropic support.
**For a complete guide on the treatment of right ventricular myocardial infarction, [[Right ventricular myocardial infarction resident survival guide|click here]].<br />
*Treatment of massive [[pulmonary embolism]] usually includes [[fibrinolytic therapy]].
**For a complete guide on the treatment of pulmonary embolism, [[Pulmonary embolism resident survival guide|click here]].<br />
*Treatment of [[pericardial tamponade]] usually includes [[pericardiocentesis]].
**For a complete guide on the treatment of cardiac tamponade, [[Cardiac tamponade resident survival guide|click here]].<br />
*Treatment of [[tension pneumothorax]] includes immediate [[needle decompression]] followed by [[chest tube]] insertion.
**For a complete guide on the treatment of tension pnemuothorax, [[Tension pneumothorax resident survival guide|click here]].<br />

==Do's==
* If the [[JVP]] does not seem elevated when the patient is supine, a provocative test, i.e., [[abdominojugular test]], should be performed.

==Don'ts==
* [[JVD]] only provides clues to the presence of an elevated [[central venous pressure]] ([[CVP]]). Clinicians should avoid making decisions about the degrees of [[CVP]] elevation based on the [[JVP]] measurement.

==References==
{{Reflist|2}}

[[Category:Help]]
[[Category:Projects]]
[[Category:Resident survival guide]]
[[Category:Templates]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Jugular venous distention resident survival guide

2020-09-10T15:12:10Z

Mandana Chitsazan: /* Common Causes */

__NOTOC__

{{WikiDoc CMG}}; {{AE}} {{Mitra}} {{MC}}

==Overview==
Jugular venous distension (JVD), or an elevated jugular venous pressure (JVP), is considered a useful physical finding for assessing ventricular filling pressures and central venous pressure (CVP). JVD is defined as an estimated JVP ≥10 cm H2O.

==Causes==
===Life Threatening Causes===
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
* [[Acute heart failure]]
* [[Massive pulmonary emboli]]
* [[Right ventricular myocardial infarction]]
* [[Cardiac Tamponade]]
* [[Tension Pneumothorax]]

===Common Causes===
*[[Congestive heart failure]]
*[[Cardiomyopathy]]
*[Cor pulmonale]]
*[[Constrictive pericarditis]]
*[[Chronic obstructive pulmonary disease|Chronic obstructive pulmonary disease (copd)]]
*[[Fluid overload]]
*[[Pulmonary embolism]]
*[[Pulmonary hypertension]]
*[[Pulmonary valve stenosis]]
*[[Restrictive cardiomyopathy]]
*[[Right atrial myxoma]]
*[[Right heart failure]]
*[[Right ventricular myocardial infarction]]
*[[Tension pneumothorax]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of jugular venous distension. <ref name="pmid8409071">{{cite journal| author=Butman SM, Ewy GA, Standen JR, Kern KB, Hahn E| title=Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. | journal=J Am Coll Cardiol | year= 1993 | volume= 22 | issue= 4 | pages= 968-74 | pmid=8409071 | doi=10.1016/0735-1097(93)90405-p | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8409071 }} </ref> <ref name="pmid17943049">{{cite journal| author=Devine PJ, Sullenberger LE, Bellin DA, Atwood JE| title=Jugular venous pulse: window into the right heart. | journal=South Med J | year= 2007 | volume= 100 | issue= 10 | pages= 1022-7; quiz 1004 | pmid=17943049 | doi=10.1097/SMJ.0b013e318073c89c | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17943049 }} </ref> <ref name="pmid9665212">{{cite journal| author=McGee SR| title=Physical examination of venous pressure: a critical review. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 1 | pages= 10-8 | pmid=9665212 | doi=10.1016/s0002-8703(98)70175-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9665212 }} </ref> <ref name="pmid6638720">{{cite journal| author=Dell'Italia LJ, Starling MR, O'Rourke RA| title=Physical examination for exclusion of hemodynamically important right ventricular infarction. | journal=Ann Intern Med | year= 1983 | volume= 99 | issue= 5 | pages= 608-11 | pmid=6638720 | doi=10.7326/0003-4819-99-5-608 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6638720 }} </ref>

{{familytree/start |summary=JVD diagnosis Algorithm.}}
{{familytree | | | | | A01 | | | | | | |A01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> [[Jugular Venous Distension]]}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | |,|-|-|^|-|-|-|.| | | | | |}}
{{familytree | | B01 | | | | | B02 | | | | |B01=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> With [[pulmonary edema]]|B02=Without [[pulmonary edema]]}}
{{familytree | | |!| | | |,|-|-|^|-|-|-|-|.|}}
{{familytree | | C01 | | C02 | | C03 | | C04 |C01=<div style="float: Center; text-align: Center; width:12em; padding:1em;">
[[Congestive heart failure]]
|C02=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased right atrial pressure'''
|C03=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Venous obstruction'''
|C04=<div style="float: Center; text-align: Center; width:12em; padding:1em;"> '''Increased intrathoracic pressure'''}}
{{familytree | | | | | | |!| | | |!| | | |!|}}
{{familytree | | | | | | D01 | | D02 | | D03|D01=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''Restriction of right atrial and right ventricular filling:'''
:❑ [[Cor pulmonale]] (Massive [[pulmonary emboli]], [[COPD]])
:❑ [[Pulmonary Hypertension]]
:❑ [[Constrictive pericarditis]]
:❑ [[Cardiac Tamponade]]

❑'''RV Failure:'''
:❑ [[Cardiomyopathy]]
:❑ [[RV myocardial infarction]]

❑ '''Fluid overload due to renal diseases'''

❑ '''Tricuspid valve incompetence'''

❑ '''Tricuspid valve stenosis or obstruction'''|D02=<div style="float: Center; text-align: Center; width:20em; padding:1em;">

❑ '''Superior vena cava obstrcution'''|D03=<div style="float: Center; text-align: Center; width:20em; padding:1em;">
❑ '''[[Positive pressure ventilation]]'''

❑ '''A large [[pleural effusion]]'''

❑'''[[Tension Pneumothorax]]'''}}

{{familytree/end}}

==Treatment==
*The management of jugular venous distension should be directed towards the underlying causes.
*Treatment of [[congestive heart failure]] usually includes [[diuretics]] (for symptom relief), [[beta blockers]], [[angiotensin converting enzyme inhibitors]] ([[ACE-I]]) /[[aldosterone receptor blockers]] ([[ARB]]).
**For a complete guide on the treatment of congestive heart failure, [[Heart failure resident survival guide|click here]].<br />
*Treatment of [[right ventricular myocardial infarction]] includes [[reperfusion]], maintenance of right ventricular [[preload]], decreasing right ventricular [[afterload]], restoring cardiac rate/rhythm and [[atrioventricular synchrony]], and inotropic support.
**For a complete guide on the treatment of right ventricular myocardial infarction, [[Right ventricular myocardial infarction resident survival guide|click here]].<br />
*Treatment of massive [[pulmonary embolism]] usually includes [[fibrinolytic therapy]].
**For a complete guide on the treatment of pulmonary embolism, [[Pulmonary embolism resident survival guide|click here]].<br />
*Treatment of [[pericardial tamponade]] usually includes [[pericardiocentesis]].
**For a complete guide on the treatment of cardiac tamponade, [[Cardiac tamponade resident survival guide|click here]].<br />
*Treatment of [[tension pneumothorax]] includes immediate [[needle decompression]] followed by [[chest tube]] insertion.
**For a complete guide on the treatment of tension pnemuothorax, [[Tension pneumothorax resident survival guide|click here]].<br />

==Do's==
* If the [[JVP]] does not seem elevated when the patient is supine, a provocative test, i.e., [[abdominojugular test]], should be performed.

==Don'ts==
* [[JVD]] only provides clues to the presence of an elevated [[central venous pressure]] ([[CVP]]). Clinicians should avoid making decisions about the degrees of [[CVP]] elevation based on the [[JVP]] measurement.

==References==
{{Reflist|2}}

[[Category:Help]]
[[Category:Projects]]
[[Category:Resident survival guide]]
[[Category:Templates]]

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Right ventricular myocardial infarction resident survival guide

2020-08-11T18:49:58Z

Mandana Chitsazan: /* Treatment */

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right-sided lead V4 (V4R), and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated jugular venous pressure]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of [[Right ventricular myocardial infarction]]([[RVMI]]) according to the American College of Cardiology and European Society of Cardiology guidelines.

{{familytree/start |summary=Sample 6}}
{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] (RV MI)'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to RV MI''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Right ventricular myocardial infarction resident survival guide

2020-08-11T18:44:07Z

Mandana Chitsazan: /* Overview */

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right-sided lead V4 (V4R), and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated jugular venous pressure]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of [[Right ventricular myocardial infarction]]([[RVMI]]) according to the American College of Cardiology and European Society of Cardiology guidelines.

{{familytree/start |summary=Sample 6}}
{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] ([[RVMI]])'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to [[RVMI]]''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Right ventricular myocardial infarction resident survival guide

2020-08-11T18:41:42Z

Mandana Chitsazan: /* Diagnosis */

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right sided lead V4, and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated neck veins]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of [[Right ventricular myocardial infarction]]([[RVMI]]) according to the American College of Cardiology and European Society of Cardiology guidelines.

{{familytree/start |summary=Sample 6}}
{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] ([[RVMI]])'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to [[RVMI]]''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Right ventricular myocardial infarction resident survival guide

2020-08-11T18:39:59Z

Mandana Chitsazan: Undo revision 1649981 by Mandana Chitsazan (talk)

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right sided lead V4, and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated neck veins]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of <nowiki>[[disease name]]</nowiki> according the the [...] guidelines.

{{familytree/start |summary=Sample 6}}
{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] ([[RVMI]])'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to [[RVMI]]''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Right ventricular myocardial infarction resident survival guide

2020-08-11T18:39:15Z

Mandana Chitsazan: /* Diagnosis */

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right sided lead V4, and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated neck veins]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of <nowiki>[[Right ventricular myocardial infarction]] ([[RVMI]]) according to the ACC and ESC guidelines.

{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] ([[RVMI]])'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to [[RVMI]]''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Right ventricular myocardial infarction resident survival guide

2020-08-11T18:38:07Z

Mandana Chitsazan: /* Diagnosis */

__NOTOC__
{{CMG}} {{Mitra}} {{MC}}

==Overview==
RV infarction is a form of [[ST elevation myocardial infarction]] ([[STEMI]]) and is characterized by the presence of symptoms of [[myocardial ischemia]] associated with persistent [[ST elevation]] on [[electrocardiogram]] in right sided lead V4, and elevated [[cardiac enzymes]], [[hypotension]], signs of elevated right heart filling pressures ([[elevated neck veins]]) in the absence of signs of elevated left heart filling pressures (clear lung fields). [[Nitrates]], [[diuretics]] and [[beta-blockers]] should not be administered to the patient with an RV MI.

==Causes==
===Life Threatening Causes===
[[STEMI]] is a life-threatening condition and must be treated as such irrespective of the underlying cause.

===Common Causes===
* [[Plaque rupture]]
* [[Aortic dissection]] with propagation to the [[right coronary artery]]
* [[Cocaine]]

==Diagnosis==
Shown below is an algorithm summarizing the diagnosis of <nowiki>[[disease name]]</nowiki> according the the [...] guidelines.

{{familytree/start |summary=Sample 6}}
{{familytree | | | | | A01 | | | | | | | | |A01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' All patients with acute [[inferior wall myocardial infarction]] ([[ST elevation]] in leads II, III, aVF)'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | |B01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Obtain right-sided precordial leads'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | C01 | | | | | | | | |C01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' >= 1mm [[ST elevation]] in lead V4R'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | D01 | | | | | | | | |D01=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Highly suggestive of RVMI'''}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|v|-|-|-|.| |}}
{{familytree | F01 | | F02 | | F03 | | F04 |F01=<div style="float: left; text-align: Center; width: 14em; padding:1em;"> ''' Physical examination'''|F02=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Echocardiography'''|F03=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> '''Coronary Angiography'''|F04=<div style="float: Center; text-align: Center; width: 28em; padding:1em;"> ''' Hemodynamic study'''|}}
{{familytree | |!| | | |!| | | |!| | | |!| |}}
{{familytree | G01 | | G02 | | G03 | | G04 |G01=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Classic triad of: <br>
:❑ [[Hypotension]] <br>
:❑ Elevated [[JVP]] <br>
:❑ Clear Lungs <br>
❑ [[Kussmaul sign]] <br>
❑ [[Pulsus paradoxus]] <br>
❑ [[Tricuspid regurgitation]] murmur <br>
❑ [[Atrioventrcicular dissociation]] <br>
❑ Vagal symptoms: <br>
:Bradycardia <br>
:❑ Nausea
:❑ Vomiting
:❑ Diaphoresis
:❑ Pallor
|G02=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ RV dilatation <br>
❑ Depressed RV systolic function <br>
❑ RV wall akinesia or dyskinesia <br>
❑ RA enlargement <br>
❑ Elevated pulmonary pressures <br>
❑ [[Pulmonary regurgitation]] <br>
❑ [[Tricuspid regurgitation]] <br>
❑ Increased right atrial pressure <br>
|G03=<div style="float: Center; text-align: left; width: 28em; padding:1em;"> '''Gold standard diagnostic modality'''
❑ In the majority of RVMI:<br>
:❑ The culprit artery: Proximal [[Right Coronary Artery]] <br>
❑ Occasionally:<br>
:❑ The culprit artery: [[Left circumflex artery]] or [[left anterior descending artery]] <br>
|G04=<div style="float: Center; text-align: left; width: 28em; padding:1em;">
❑ Hemodynamically significant RVMI:<br>
:❑ Increased RAP>10 mmHg <br>
:❑ RAP to PCWP ratio >0.8 (normal<0.6) <br>
:❑ RAP within 5 mmHg of the PCWP <br>
:❑ Reduced [[cardiac index]] <br>
:❑ Disproportionate elevation of right-sided filling pressures: Hallmark of RVMI <br>
❑ In concomitant LV dysfunction: <br>
:❑ RAP to PCWP ratio can change <br>
❑ Additional hemodynamic changes: <br>
:❑ Prominent [[Y-descend]] of the RAP <br>
:❑ Drop of the systemic arterial pressure >10 mmHg with inspiration <br>
:❑ "Dip and plateau" morphology and equalization of the diastolic filling pressures<br>|}}

{{familytree/end}}

{{familytree/end}}

==Treatment==
Shown below is an algorithm summarizing the treatment of [[Right ventricular myocardial infarction]] according to the ACC and ESC guidelines.

{{familytree/start}}
{{familytree | | | | | | | | | | | | | A01 | | | | | | | | | | |A01= <div style="float: Center; text-align: Center; width: 20em; padding:1em;"> '''Therapuetic Considerations in [[Right Ventriculay Myocardial Infarction]] ([[RVMI]])'''| | | |}}
{{familytree | | | | | | | | | | | | | |!| | | | | | | | | | | | | |}}
{{familytree | | | |,|-|-|-|-|v|-|-|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|.| |}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| |}}
{{familytree | | | B01 | | | B02 | | | B03 | | B04 | | B05 | | | B06 |B01=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Reperfusion]]'''|B02=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Maintenance of [[RV]] [[preload]]'''|B03=<div style="float: center; text-align: center; width: 5em; padding:1em;">'''Decreasing [[RV]] [[afterload]]'''|B04=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Restoring [[Rate]]/[[Rhythm]] and [[AV synchrony]]'''|B05=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''Inotropic support'''|B06=<div style="float: Center; text-align: Center; width: 5em; padding:1em;">'''[[Mechanical Circulatory Support]]'''}}
{{familytree | | | |!| | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | |}}
{{familytree | | | C01 | | | C02 | | | C03 | | C04 | | C05 | | | C06 |C01=<div style="float: Center; text-align: Center; width: 5em; padding:2em;"> •'''[[Thrmobolytics]]''' <br> •'''[[Percutaneous coronary intervention]] ([[PCI]])'''
|C02= <div style="float: Center; text-align: left;"> • '''Avoidance of preload-reducing agents''', such as:
:❑ [[Nitrates]]
:❑ [[Diuretics]]
:❑ [[Morphin]]
• '''In patients with [[hypotension]] (without [[pulmonary congestion]]):
:❑ Intravenous administration of Fluids ([[N/S]] 0.9% at 40mL/min for up to 2L, to maintain [[CVP]] <15 mmHg and [[PCWP]] between 18-24 mmHg)
|C03=<div style="float: Center; text-align: left;"> • '''Systemic or pulmonary [[vasodilators]]:'''
:❑ [[Nitrosrusside]]
:❑ Inhaled [[nitric oxide]]
|C04=<div style="float: Center; text-align: left;"> • '''In patients with [[bradyarrhthmias]]:'''
:❑ [[Atropine]]
:❑ [[Pacemaker]]
• '''In patients with atrioventricular block:'''
:❑ Temporary dual-chamber [[pacemaker]]
|C05=<div style="float: Center; text-align: left;"> '''In patients with refractory [[hypotension]]:'''
:❑ [[Dobutamine]] (along with fluids)
:❑ Other [[inotropes]]:
* [[Milrinone]]
* [[Norepinephrine]]
|C06= <div style="float: Center; text-align: left;"> • '''May be needed in patients with [[cardiogenic shock]] secondary to [[RVMI]]''':
:❑ Direct RV support
:❑ Indirect RV support
:❑ Biventricular support}}

{{familytree/end}}

==Do's==

* [[Right ventricular myocardial infarction]] [[(RVMI)]] should be ruled out in all patients presenting with acute [[inferior wall myocardial infarction]], in particular in patients with [[hypotension]].

*In patients presenting with [[chest pain]] and clinical findings of [[hypotension]], elevated [[JVP]] and clear lung fields, consider the differential diagnoses of [[RVMI]]. These include:
**[[Pulmonary embolism]]
**[[Pericarditis]] with [[pericardial tamponade]]

*Systemic or pulmonary [[vasodilators]] may be considered in selected patients to reduce [[RV afterload]], thereby improving [[cardiac output]].

*In patients with severe [[tricuspid regurgitation]] due to [[RVMI]], replacement of [[tricuspid valve]] or repair of the valve with annuloplasty rings may be considered.

*In patients with [[RVMI]] who have unexplained [[hypoxemia]] despite administration of 100% oxygen, [[right-to-left shunting]] -through a [[patent foramen ovale]] or [[atrial septal defect]]-, caused by the disproportionate elevation in right-sided filling pressures compared to the normal or slightly increased left-sided filling pressures should be considered.

*Patients with extensive [[necrosis]] due to [[RVMI]] may be at higher risk of [[right ventricular]] perforation during interventional procedures. [[Right ventricular catheterization]] or [[pacemaker]] insertion should be performed with great care in these patients.

==Don'ts==
* In patients with [[RVMI]], avoid preload-reducing agents such as [[nitrates]], [[diuretics]], [[morphine]], [[beta-blockers]], and [[calcium channel blockers]].

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Resident survival guide]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

The WikiDoc Living Textbook of Cardiology

2020-07-01T16:34:40Z

Mandana Chitsazan: /* List of Chapters Requiring Content */

__NOTOC__

== List of Chapters Requiring Content ==
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Category}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Chapters that need content}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Assignment Status}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Scholar's name}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Coach name}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Completion Status}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Review status}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 | {{fontcolor|#FFFFFF|Reviewer name}}
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" rowspan="35" |Cardiovascular system
|-
| style="padding: 5px 5px; background: #F5F5F5;" |AV block (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Qasim Khurshid
| style="padding: 5px 5px; background: #F5F5F5;" |Maneesha
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Blalock-Taussig procedure
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Usman Ali Akbar
| style="padding: 5px 5px; background: #F5F5F5;" |Sara
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Bridge to transplant (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Cardiac transplant (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |Ifrah Fatima
| style="padding: 5px 5px; background: #F5F5F5;" |Sogand
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Cardiopulmonary resuscitation (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Amir Bagheri
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Paradoxical embolism
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Hira Rehman
| style="padding: 5px 5px; background: #F5F5F5;" |Roukoz
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Paroxysmal supraventricular tachycardia (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Noha Elzeiny
| style="padding: 5px 5px; background: #F5F5F5;" |Homa
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Palpitation(assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Debduti Mukhopadhyay ( starting on July 1st)
| style="padding: 5px 5px; background: #F5F5F5;" |Homa
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Paroxysmal AV block (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Akash Daswaney
| style="padding: 5px 5px; background: #F5F5F5;" |Homa
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Pre-excitation syndrome (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Shivam Single
| style="padding: 5px 5px; background: #F5F5F5;" |Sara
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Pulseless ventricular tachycardia(assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Aisha Adigun
| style="padding: 5px 5px; background: #F5F5F5;" |Homa
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Premature ventricular contraction
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Homa Najafi
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Post-cardiac injury syndrome (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Sara
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Maxomatous degeneration of mitral valve
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Sheikh Ashia Sultana
| style="padding: 5px 5px; background: #F5F5F5;" |Ali
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Ventricular Assist device
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Tayebah Choudhary
| style="padding: 5px 5px; background: #F5F5F5;" |Ali
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Short QT syndrome
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Sumanth
| style="padding: 5px 5px; background: #F5F5F5;" |Huda
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Coronary artery bypass grafting
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Tayyaba Ali
| style="padding: 5px 5px; background: #F5F5F5;" |Huda
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Post infarction conduction abnormalities
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Hamid Parsa
| style="padding: 5px 5px; background: #F5F5F5;" |Ramyar
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Transesophageal echocardiography (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Shakiba
| style="padding: 5px 5px; background: #F5F5F5;" |Elsaiey,Ahmed
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Collateral circulation (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Mydah
| style="padding: 5px 5px; background: #F5F5F5;" |Elsaiey,Ahmed
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
|-
|-
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Holter monitor (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Hypokalemia (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Paget-Schroetter disease (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Paradoxical septal motion (assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Mitra
| style="padding: 5px 5px; background: #F5F5F5;" |Sogand
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Persistent juvenile T-wave pattern
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Zaida
| style="padding: 5px 5px; background: #F5F5F5;" |Farima
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
| style="padding: 5px 5px; background: #F5F5F5;" |
|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Post-infarction conduction abnormalities
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Hassan
| style="padding: 5px 5px; background: #F5F5F5;" |Ramyar
| style="padding: 5px 5px; background: #F5F5F5;" |
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| style="padding: 5px 5px; background: #F5F5F5;" |
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|-
| style="padding: 5px 5px; background: #F5F5F5;" |PR interval alternans (Assigned)
| style="padding: 5px 5px; background: #F5F5F5;" |
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|-
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| style="padding: 5px 5px; background: #F5F5F5;" |Postural orthostatic tachycardia syndrome
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Saud Khan
| style="padding: 5px 5px; background: #F5F5F5;" |Mahshid, Sahar
| style="padding: 5px 5px; background: #F5F5F5;" |
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|-
|-
| style="padding: 5px 5px; background: #F5F5F5;" |Pentalogy of Fallot
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Abdulkareem
| style="padding: 5px 5px; background: #F5F5F5;" |Sahar
| style="padding: 5px 5px; background: #F5F5F5;" |
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| style="padding: 5px 5px; background: #F5F5F5;" |
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| style="padding: 5px 5px; background: #F5F5F5;" |Pacemaker syndrome
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Tayyaba
| style="padding: 5px 5px; background: #F5F5F5;" |Ali
| style="padding: 5px 5px; background: #F5F5F5;" |
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|-
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| style="padding: 5px 5px; background: #F5F5F5;" |Aortic regurgitation
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Mohammed Salih
| style="padding: 5px 5px; background: #F5F5F5;" |Ali
| style="padding: 5px 5px; background: #F5F5F5;" |
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|-
|}

==In progress chapters==

{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Category}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Chapters that need content}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Assignment Status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Scholar's name}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Coach name}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Completion Status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Review status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Reviewer name}}
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| rowspan="22" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |CVS
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|}

==Completed chapters==

{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Category}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Chapters that need content}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Assignment Status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Scholar's name}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Coach name}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Completion Status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Review status}}
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Reviewer name}}
|-
| rowspan="22" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |CVS
| style="padding: 5px 5px; background: #F5F5F5;" |Bifascicular block
| style="padding: 5px 5px; background: #F5F5F5;" |Assigned
| style="padding: 5px 5px; background: #F5F5F5;" |Shadi Ebr
| style="padding: 5px 5px; background: #F5F5F5;" |Sahar
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==[[:Category:Cardiology|Alphabetical Index of all Pages in the Cardiology Textbook]]==

=ANATOMY=
==[[Cardiovascular Anatomy]]==
<small> '''Arteries''' | [[Coronary arteries]] | [[Arteries of the head and neck|Head and Neck]] | [[Arteries of the upper limbs|Upper Limbs]] | [[Arteries of the torso-chest|Torso-Chest]] | [[Arteries of the torso-abdomen|Torso-Abdomen]] | [[Arteries of the lower limbs|Lower Limbs]] | [[Artery|All]] </small>

<small> '''Veins''' | [[Veins of the head and neck|Head and Neck]] | [[Veins of the upper extremity |Upper Extremity]] | [[Veins of the torso|Torso]] | [[Veins of the lower extremity|Lower Extremity]]</small>

<small> '''Atria''' | [[Atrium (heart)|Atria]] | [[Left atrium]] | [[Right atrium]] | [[Interatrial septum]] | [[Musculi pectinati]]</small>

<small>'''Ventricles''' | [[Ventricle (heart)|Ventricles]] | [[Left ventricle]] | [[Right ventricle]] | [[Interventricular septum]] | [[Trabeculae carneae]] | [[Chordae tendinae]] | [[Papillary muscle]]</small>

<small>'''Valves''' | [[Heart valve|Valves]] | [[Aortic valve]] | [[Mitral valve]] | [[Pulmonic valve]] | [[Tricuspid valve]] | [[Cusps of heart valves|Cusps]]</small>

<small>'''Regions''' | [[Base of the heart|Base]] | [[Apex of the heart|Apex]]</small>

<small> '''Grooves''' | [[Coronary sulcus|Coronary/atrioventricular]] | [[Interatrial groove|Interatrial]] | [[Anterior interventricular sulcus|Anterior interventricular]] | [[Posterior interventricular sulcus|Posterior interventricular]] </small>

<small> '''Surfaces''' | [[Sternocostal surface|Sternocostal]] | [[Diaphragmatic surface of heart|Diaphragmatic]] </small>

<small>'''Borders''' | [[Right border of heart|Right]] | [[Left margin of heart|Left]]</small>

<small>'''Right heart''' | [[Vena cavae]] | [[Coronary sinus]] | [[Right atrium]] | [[Right auricular appendix|Right auricle]] | [[Fossa ovalis (heart)|Fossa ovalis]] | [[Limbus of fossa ovalis]] | [[Crista terminalis]] | [[Valve of the inferior vena cava]] | [[Valve of the coronary sinus]] | [[Tricuspid valve]] | [[Right ventricle]] | [[Conus arteriosus]] | [[Septomarginal trabecula|Moderator band/septomarginal trabecula]] | [[Pulmonary valve]] | [[Pulmonary artery]] | [[Pulmonary circulation]]</small>

<small> '''Left heart''' | [[Pulmonary veins]] | [[Left atrium]] | [[Left auricular appendix|Left Auricle]] | [[Mitral valve]] | [[Left ventricle]] | [[Aortic valve]] | [[Aortic sinus]] | [[Aorta]] | [[Systemic circulation]]</small>

<small> '''Pericardium''' | [[Pericardium]] | [[Fibrous pericardium]] | [[Serous pericardium]] | [[Pericardial cavity]] | [[Epicardium|Epicardium/visceral layer]] | [[Pericardial sinus]]</small>

<small> '''Myocardium''' | [[Myocardium]] | [[Endocardium]] | [[Cardiac skeleton]] | [[Fibrous trigone]] | [[Fibrous rings of heart|Fibrous rings]]</small>

<small>'''Conduction system''' | [[Electrical conduction system of the heart|Conduction system]] | [[Cardiac pacemaker]] | [[SA node]] | [[AV node]] | [[Bundle of His]] | [[Purkinje fibers]]</small>
<br>

=PHYSIOLOGY=
==[[Cardiovascular Physiology]]==
<small>'''Volumes''' | [[Preload]] | [[Afterload]] | [[End-systolic volume]] | [[End-diastolic volume]] | [[Frank-Starling law of the heart]] | [[Cardiac output]]</small>

<small> '''Interactions''' | [[Wiggers diagram]] | [[Pressure volume diagram]]</small>

<small> '''Tropism''' | [[Chronotropic|Chronotropy]] | [[Dromotropic|Dromotropy]] | [[Inotropic|Inotropy]]</small>

<small> '''Hemodynamics''' | [[Hemodynamics]] | [[Baroreflex|Baroreflexes]] | [[Kinin-kallikrein system]] | [[Renin-angiotensin system]] | [[Vasoconstrictors]] | [[Vasodilator|Vasodilators]] | [[Compliance (physiology)|Compliance]] | [[Vascular resistance]]</small>

<small>'''Conduction''' | [[Electrical conduction system of the heart ]]| [[Cardiac action potential]] </small>

<small> '''Cardiopulmonary''' | [[Respiratory physiology]] | [[Blood]] | [[Pulmonary circulation]] | [[Perfusion|Perfusion (Q)]] | [[Hypoxic pulmonary vasoconstriction]] | [[Pulmonary shunt]] | [[Ventilation/perfusion scan]] | [[ventilation/perfusion ratio]] (V/Q) | [[Zones of the lung]] | [[Gas exchange]] | [[Pulmonary gas pressures]] | [[Alveolar gas equation]] | [[Hemoglobin]] | [[Oxygen-haemoglobin dissociation curve]] | [[2,3-Bisphosphoglycerate|2,3-DPG]] | [[Bohr effect]] | [[Haldane effect]] | [[Carbonic anhydrase]] | [[Chloride shift]] | [[Oxyhemoglobin]] | [[Respiratory quotient]] | [[Arterial blood gas]] | [[Diffusion capacity]] | [[Dlco]] </small>

=DEVELOPMENTAL BIOLOGY=
==[[Cardiovascular Development]]==
<small>'''Arteries''' | [[Dorsal aorta]] | [[Aortic arches]] | [[Vitelline arteries]] | [[Ductus arteriosus]] | [[Umbilical artery]]</small>

<small>'''Veins''' | [[Cardinal veins]] | [[Ducts of Cuvier]] | [[Vitelline veins]] | [[Ductus venosus]] | [[Umbilical vein]]</small>

<small>'''Heart Development''' | [[Primitive heart tube]] | [[Truncus arteriosus]] | [[Bulbus cordis]] | [[Primitive ventricle]] | [[Primitive atrium]] | [[Sinus venosus]] | [[Septum primum]] | [[Ostium primum]] | [[Ostium secundum]] | [[Septum secundum]] | [[Foramen ovale]] | [[Endocardial cushions]] | [[Septum intermedium]] | [[Aorticopulmonary septum]] | [[Atrial canal]]</small>

=BASIC SCIENCE=
==[[Cardiovascular Biochemistry]]==
<small>[[:Category:Molecular biology|Molecular Biology]] | [[:Category:Biochemistry|Biochemistry]] | [[:Category:Organic chemistry|Organic Chemistry]] | [[Enzymes]] | [[:Category:Immunology|Immunology]]</small>

=DIAGNOSTIC MODALITIES IN CARDIOLOGY=

==[[The Patient History in Cardiovascular Disease]]==
<small>[[Chest Pain]] | [[Claudication]] | [[Cough]] | [[Dyspnea]] | [[Orthopnea]] | [[Palpitation|Palpitations]] | [[Paroxysmal Nocturnal Dyspnea]] | [[Pedal Edema]]</small>

==[[The Physical Examination in Cardiovascular Disease]]==
<small>[[The Physical Examination in Cardiovascular Disease: The Pulse|The Pulse]] | [[The Physical Examination in Cardiovascular Disease:The Neck|The Neck]] | [[The Physical Examination in Cardiovascular Disease:The Heart|The Heart]] | [[The Physical Examination in Cardiovascular Disease:The Lungs|Lungs]] |
[[The Physical Examination in Cardiovascular Disease: The Extremities|The Extremities]]</small>

==[[The Electrocardiogram]]==
<small>'''Intervals''' | [[PR Interval]] | [[QRS Interval]] | [[QT Interval]] | [[T Wave]] | [[The U Wave|U Wave]]</Small>

<small>'''Hypertrophy''' | [[Electrocardiographic Findings in LVH]] | [[Electrocardiographic Findings in Right Ventricular Hypertrophy (RVH)]] | [[Electrocardiographic Findings in Biventricular Hypertrophy|Biventricular Hypertrophy]]</small>

<small>'''Bundle Branch Block''' | [[Left Bundle Branch Block|LBBB]] | [[Left anterior hemiblock|LAHB]] | [[Right Bundle Branch Block|RBBB]] | [[Trifascicular block]]</small>

<small>'''Atrial Arrhythmias''' | [[Premature Atrial Contractions (PACs)]] | [[Ectopic Atrial Rhythm]] | [[Paroxysmal Atrial Tachycardia (PAT)]] | [[Paroxysmal Atrial Tachycardia (PAT) with Block]] | [[Multifocal Atrial Tachycardia (MAT)]] | [[Atrial flutter|Atrial Flutter]] | [[Atrial fibrillation|Atrial Fibrillation]]</small>

<small>'''Ventricular Arrhythmias''' | [[Differential Diagnosis of Tachycardia with a Wide QRS Complex]]
| [[Accelerated Idioventricular Rhythm]] | [[Ventricular Parasystole]] | [[Ventricular Tachycardia Including Torsades De Pointes and Polymorphic Ventricular Tachycardia|Premature Ventricular Contractions]] | [[Ventricular Tachycardia Including Torsades De Pointes and Polymorphic Ventricular Tachycardia]]</small>

<small>'''Conduction Abnormalities''' | [[First Degree AV Block]] | [[Second Degree AV Block]] | [[Complete or Third-Degree AV Block]] | [[Concealed conduction]] | [[AV Junctional Rhythms]] | [[Wolff-Parkinson-White Syndrome]]</small>

<small>'''Electrocardiographic Abnormalities in Different Disease States''' | [[The EKG in the Patient with an Atrial Septal Defect (ASD)]] | [[EKG Changes of Hypothermia]] | [[EKG Abnormalities in CNS Disease]] | [[The EKG of Cardiac Transplantation]] | [[The EKG in a Patient with a Pacemaker]] | [[Electrocardiography of Traumatic Heart Disease]]</small>

<small>'''Drug Effects on the EKG''' | [[The EKG in the Patient Treated with Digitalis|Digitalis]] | [[The EKG in the Patient Treated with Quinidine|Quinidine]] | [[The EKG in the Patient Treated with Procainamide|Procainamide]] | [[The EKG in the Patient Treated with Disopyramide|Disopyramide]] | [[The EKG in the Patient Treated with Lidocaine|Lidocaine]] | [[The EKG in the Patient Treated with Tocainide|Tocainide and Mexiletine]] | [[The EKG in the Patient Treated with Phenytoin|Phenytoin]] | [[The EKG in the Patient Treated with Encainide, Flecainide and Propafenone|Encainide, Flecainide and Propafenone]] | [[The EKG in the Patient Treated with Beta Blockers|β-blockers]] | [[The EKG in the Patient Treated with Amiodarone|Amiodarone]] | [[The EKG in the Patient Treated with Bretylium|Bretylium]] | [[The EKG in the Patient Treated with Ca Channel Blockers|Ca Channel Blockers]] | [[The EKG in the Patient Treated with Adenosine|Adenosine]] | [[The EKG in the Patient Treated with Phenothiazines|Phenothiazines]] | [[The EKG in the Patient Treated with Tricyclic Antidepressants|Tricyclic Antidepressants]] | [[The EKG in the Patient Treated with Lithium|Lithium]]</small>

<small>'''EKG in Electrolyte Disturbances''' | [[The EKG in Hyperkalemia]] | [[The EKG in Hypokalemia]] | [[The EKG in Hypercalcemia]] | [[The EKG in Hypocalcemia]] | [[Nonspecific ST-Segment and T-Wave Changes]]</small>

==[[Exercise Stress Testing]]==

==[[Cardiac Electrophysiology]]==

==[[The WikiDoc Living Textbook of Biomarkers|Cardiac Biomarkers]]==
<small>[[Creatine Kinase]] | [[Cytokines and their receptors]] | [[Lipoprotein-associated phospholipase A2 (Lp-PLA2)]] | [[Metalloproteinases (MMPs)]] | [[Natriuretic peptides‎]] | [[Prothrombin fragment 1.2 (F1.2)]] | [[Prothrombin time (PT)]] | [[Soluble CD40 ligand (sCD40L)]] | [[Thrombus precursor protein (TpP)]] | [[Von Willebrand factor (vWF)]] | [[White blood cell (WBC) count]]</small>

==[[Cardiac Imaging|An Overview of Cardiac Imaging]]==

==[[The Chest X Ray in Cardiovascular Disease]]==

==[[Echocardiography]]==

==[[Nuclear Cardiology]]==

==[[Coronary Angiography]]==

==[[Cardiovascular Magnetic Resonance Imaging (CMR)]]==

==[[CT Angiography]]==

==[[Positron Emission Tomography]]==
<br>

=CARDIAC DISEASE STATES=

==[[The Genetic Basis of Heart Disease]]==

==[[Congenital Heart Disease]]==
Click on Show on the right to expand:
{{Congenital malformations and deformations of circulatory system}}

==[[Cardiac Disease in Pregnancy]]==

==[[Cardiac Diseases in AIDS]]==

==[[Diseases of the Pericardium]]==

==[[Trauma and the Heart]]==
<small>[[Commotio cordis]] </small>

==[[Diseases of the Valvular Structures]]==

<small> [[Aortic Stenosis]] | [[Aortic Regurgitation]] | [[Mitral Stenosis]] | [[Mitral Regurgitation]] | [[Mitral Valve Prolapse]] | [[Pulmonic Regurgitation]] | [[Pulmonic Stenosis]] | [[Tricuspid Prolapse|Tricuspid Valve Prolapse]] | [[Tricuspid Regurgitation]] | [[Tricuspid Stenosis]] | [[Infective Endocarditis]]</small>

==[[Diseases of the Myocardium]]==
<small>[[Cardiomegaly]] | [[Cardiomyopathy]] | [[Congestive Heart Failure]] | [[Left Ventricular Hypertrophy]] | [[Myocarditis]]</small>

==[[Cardiac Electrophysiology|Cardiac Arrhythmias]]==
<br>

=VASCULAR MEDICINE=
==[[Vascular Medicine]]==

==[[Diseases of the Aorta]]==

==[[Peripheral Arterial Disease]]==

==[[Sytemic Arterial Hypertension]]==

==[[Hypotension]]==

==[[Primary Cardiac Tumors]]==

==[[The Heart in Oncologic Disease]]==

==[[Endocrine Disease and the Heart]]==
<small>[[Endocrine Disease and the Heart#Hyperthyroidism|Hyperthyroidism]] | [[Endocrine Disease and the Heart#Hypothyroidism|Hypothyroidism]] | [[Endocrine Disease and the Heart#Hypoparathyroidism and the heart|Hypoparathyroidism]] | [[Endocrine Disease and the Heart#Acromegalic cardiomyopathy|Acromegaly]]</small>

==[[Renal Disease and the Heart]]==

==[[Infectious Disease and the Heart]]==
<small>[[Cardiac Diseases in AIDS|AIDS]] | [[The Heart in Chagas' disease|Chagas']]</small>

==[[Autoimmune Disease and the Heart|Autoimmune/Rheumatologic Disease and the Heart]]==
<small>[[The Heart in Ankylosing Spondylitis|Ankylosing Spondylitis]] | [[The Heart in Antiphospholipid Syndrome|Antiphospholipid Syndrome]] | [[The Heart in Behçet's disease|Behçet]] | [[The Heart in Chagas' disease|Chagas]] | [[The Heart in Crohn's Disease|Crohn]] | [[The Heart in Essential Mixed Cryoglobulinemia|Essential Mixed Cryoglobulinemia]] | [[The Heart in Juvenile Rheumatoid Arthritis|Juvenile Idiopathic Arthritis]] | [[The Heart in Kawasaki Disease|Kawasaki]] | [[The Heart in Systemic Lupus Erythematosus (SLE)|Lupus]] | [[The Heart in Mixed Connective Tissue Disorder|Mixed Connective Tissue Disorder]] | [[The Heart in Polyarteritis Nodosa|Polyarteritis Nodosa]] | [[The Heart in Polychondritis|Polychondritis]] | [[The Heart in Polymyositis and Dermatomyositis|Polymyositis & Dermatomyositis]] | [[The Heart in Psoriasis|Psoriasis]] | [[The Heart in Rheumatoid Arthritis|Rheumatoid Arthritis]] | [[The Heart in Progressive Systemic Sclerosis (Scleroderma)|Scleroderma]] | [[The Heart in Sarcoidosis|Sarcoidosis]] | [[The Heart in Takayasu Arteritis|Takayasu]] | [[The Heart in Temporal Arteritis / Giant Cell Arteritis|Temporal Arteritis]] | [[The Heart in Ulcerative colitis|Ulcerative Colitis]] | [[The Heart in Wegener's Granulomatosis| Wegener's Granulomatosis]] | [[The Heart in Wilson's Disease|Wilson]]</small>

==[[Pulmonary Embolism]]==

==[[Pulmonary Hypertension]]==

==[[Cor Pulmonale]]==

==[[Pre-Operative Clearance]]==
<br>

=HEMOCARDIOLOGY=

==[[The Role of the Coagulation System in Heart Disease]]==
<br>

=CORONARY ARTERY DISEASE=

==[[Atherosclerosis Prevention and Risk Factor Modification]]==

==[[Chronic Stable Angina]]==
<small>[[Chronic Stable Angina Introduction|Introduction]] | [[Chronic Stable Angina Definition|Definition]] | [[Chronic Stable Angina Historical Perspective|Historical Perspective]] | [[Chronic Stable Angina Epidemiology|Epidemiology]] | [[Chronic Stable Angina Pathophysiology|Pathophysiology]] | [[Chronic Stable Angina Clinical Presentation|Presentation]] | [[Chronic Stable Angina Recognition of Clinical Subsets|Recognition of Clinical Subsets]] | [[Chronic Stable Angina Recognition and Evaluation of Risk Factors|Risk Factors]] | [[Chronic Stable Angina Diagnosis|Diagnosis]] | [[Chest Pain|Differential Diagnosis of Chest Pain]] | [[Chronic Stable Angina Treatment|Treatment]] | [[Chronic Stable Angina Prognosis|Prognosis]] | [[Chronic Stable Angina Rehabilitation|Rehabilitation]] | [[Chronic Stable Angina Secondary Prevention|Prevention]]</small>

==[[Unstable Angina]]==

==[[Non ST Elevation Myocardial Infarction]]==

==[[ST Elevation Myocardial Infarction]]==

<small>[[ST Elevation Myocardial Infarction Overview|Overview]] | [[ST Elevation Myocardial Infarction: Epidemiology and Demographics | Epidemiology and Demographics]] | [[ST Elevation Myocardial Infarction: Pathophysiology of Reperfusion |Pathophysiology of Reperfusion]] | [[ST Elevation Myocardial Infarction Risk Factors|Risk Factors]] | [[ST Elevation Myocardial Infarction Pathophysiology|Pathophysiology]] | [[ST Elevation Myocardial Infarction Triggers|Triggers]] | [[ST Elevation Myocardial Infarction Classification|Classification]]</small>

<small>[[ST Elevation Myocardial Infarction Diagnosis|Diagnosis]] | [[ST Elevation Myocardial Infarction Symptoms|Symptoms]] | [[ST Elevation Myocardial Infarction Physical Examination|Physical Examination]] | [[ST Elevation Myocardial Infarction Electrocardiogram|Electrocardiogram]] | [[ST Elevation Myocardial Infarction Cardiac Markers|Cardiac Markers]] | [[ST Elevation Myocardial Infarction Coronary Angiography|Coronary Angiography]] | [[ST Elevation Myocardial Infarction Histopathology|Histopathology]] </small>

<small>[[Treatment]] | [[ST Elevation Myocardial Infarction Pre-Hospital Care|Pre-Hospital Care]] | [[ST Elevation Myocardial Infarction Initial Care|Initial Care]] | [[ST Elevation Myocardial Infarction Thrombolytic Therapy|Thrombolytic Therapy]] | [[ST Elevation Myocardial Infarction Primary Percutaneous Coronary Intervention|Primary Percutaneous Coronary Intervention]] | [[ST Elevation Myocardial Infarction Rescue Percutaneous Coronary Intervention|Rescue Percutaneous Coronary Intervention]] | [[ST Elevation Myocardial Infarction Facilitated Percutaneous Coronary Intervention|Facilitated Percutaneous Coronary Intervention]] | [[ST Elevation Myocardial Infarction Coronary Artery Bypass Graft Surgery|Coronary Artery Bypass Graft Surgery]] | [[Barriers to Implementing Clinical Guidelines]]</small>

<small>[[ST Elevation Myocardial Infarction Arrhythmia Monitoring]] | [[ST Elevation Myocardial Infarction Secondary Prevention|Secondary Prevention]] | [[ST Elevation Myocardial Infarction Complications|Complications]] | [[ST Elevation Myocardial Infarction Prognosis|Prognosis]] |
[[ST Elevation Myocardial Infarction]] | [[Cardiac Rehabilitation]]</small>

==[[The Living Guidelines]]==
<br>

=PHARMACOTHERAPY=
==[[:Category:Cardiovascular_Drugs|Cardiovascular Pharmacotherapy]]==
===Adrenergic Agonists===
<Small>'''Adrenergic Agonists [[Adrenergic agonist|Overview]]'''</small>

<small>'''Direct Acting''' | [[Dobutamine]] | [[Dopamine]] | [[Epinephrine]] | [[Formoterol]] | [[Isoproterenol]] | [[Metaproterenol]] | [[Methoxamine]] | [[Norepinephrine]] | [[Phenylephrine]] | [[Salmeterol]] | [[Tamsulosin]] | [[Terbutaline]]</small>

<small>'''Indirect Acting''' | [[Amphetamine]] | [[Tyramine]] </small>

<small>'''Mixed Action''' | [[Ephedrine]]</small>
----
===Angiotensin-Renin Inhibitors ([[ATC code C09|C09]])===

<small>'''ACE Inhibitor [[ACE inhibitor|Overview]]''' | [[Benazepril]] | [[Captopril]] | [[Enalapril]] | [[Fosinopril]] | [[Lisinopril]] | [[Perindopril]] | [[Quinapril]] | [[Ramipril]] | [[Spirapril]] | [[Trandolapril]]</small>

<small>'''Angiotensin II receptor antagonist [[Angiotensin II receptor antagonist|Overview]]''' | [[Candesartan]] | [[Eprosartan]] | [[Irbesartan]] | [[Losartan]] | [[Olmesartan]] | [[Tasosartan]] | [[Telmisartan]] | [[Valsartan]]</small>

<small>'''Renin Inhibitors [[Renin inhibitor|Overview]]''' | [[Aliskiren]] | [[Remikiren]]</small>
----
===Antiarrhythmic agents===
<small>'''Antiarrhythmic Agents [[Antiarrhythmic agent|Overview]]''' ([[ATC code C01#C01B Antiarrhythmics, class I and III|C01B]])</small>

<small>'''Class Ia''' | [[Ajmaline]] | [[Disopyramide]] | [[Prajmaline]] | [[Procainamide]] | [[Quinidine]] | [[Sparteine]]</small>

<small>'''Class Ib''' | [[Aprindine]] | [[Lidocaine]] | [[Mexiletine]] | [[Tocainide]]</small>

<small>'''Class Ic''' | [[Encainide]] | [[Flecainide]] | [[Lorcainide]] | [[Moricizine]] | [[Propafenone]] </small>

<small>'''Class II''' | [[Propranolol]] | [[Metoprolol]] | [[Nadolol]] | [[Atenolol]] | [[Acebutolol]] | [[Pindolol]] see [[Beta blockers]] ([[ATC code C07|C07]])</small>

<small>'''Class III''' | [[Amiodarone]] | [[Bretylium|Bretylium tosylate]] | [[Bunaftine]] | [[Dofetilide]] | [[Ibutilide]] | [[Sotalol]]</small>

<small>'''Class IV''' | [[Verapamil]] | [[Diltiazem]] see [[Calcium channel blocker]]s ([[ATC code C08|C08]])</small>

<small>'''Class V''' | [[Adenosine]] | [[Atropine]] | [[Digoxin]]</small>
----
===Anticoagulants===
<small>'''Anticoagulants [[Anticoagulant|Overview]]'''</small>

<small>'''Vitamin K Antagonists [[Vitamin K|Overview]]''' | [[Acenocoumarol]] | [[Clorindione]] | [[Coumatetralyl]] | [[Dicumarol]] (Dicoumarol) | [[Diphenadione]] | [[Ethyl biscoumacetate]] | [[Phenprocoumon]] | [[Phenindione]] | [[Tioclomarol]] | [[Warfarin]]</small>
----
=== Antihypertensives and Diuretics===
<small>'''Antihypertensive [[Antihypertensive|Overview]]''' ([[ATC code C02|C02]]) and '''Diuretic [[Diuretic|Overview]]''' ([[ATC code C03|C03]])</small>

<small>'''Sympatholytic Agents [[Sympatholytic|Overview]] (including Alpha Blockers [[Alpha blocker|Overview]])'''</small>

:<small>'''Centrally Acting Antiadrenergics [[antiadrenergic|Overview]]''' | [[Clonidine]] | [[Guanfacine]] | [[Methyldopa]] | [[Moxonidine]] | [[Rescinnamine]] | [[Reserpine]] | [[Rilmenidine]] </small>

:<small>'''Ganglionic Blocker [[Ganglionic blocker|Overview]] / Nicotinic Antagonist [[Nicotinic antagonist|Overview]]''' | [[Mecamylamine]] | [[Trimethaphan]]</small>

:<small>'''Peripherally acting/Antiadrenergics''' | [[Prazosin]] | [[Guanethidine]] | [[Indoramin]] | [[Doxazosin]]</small>

<small>'''Vasodilators [[Vasodilator|Overview]]''' | [[Diazoxide]] | [[Hydralazine]] | [[Minoxidil]] | [[Sodium nitroprusside|Nitroprusside]] | [[Phentolamine]]</small>

<small>'''Other antihypertensives''' </small>

:<small>'''Serotonin Antagonist [[Serotonin antagonist|Overview]]''' |[[Ketanserin]] </small>

:<small>'''Endothelin Receptor Antagonist [[Endothelin receptor antagonist|Overview]]''' | [[Bosentan]] | [[Ambrisentan]] | [[Sitaxsentan]] </small>

<small>'''Low ceiling diuretics''' </small>

:<small>'''Thiazide [[Thiazide|Overview]]''' | [[Bendroflumethiazide]] | [[Chlorothiazide]] | [[Hydrochlorothiazide]] </small>

:<small>'''Non-thiazides''' | [[Chlortalidone]] | [[Indapamide]] | [[Quinethazone]] | [[Mersalyl]] | [[Metolazone]] | [[Theobromine]] | [[Cicletanine]]</small>

<small>'''High ceiling diuretics'''</small>

:<small>'''Loop Diuretic [[Loop diuretic|Overview]]''' | [[Bumetanide]] | [[Furosemide]] | [[Torasemide]])</small>

:<small>'''Potassium-Sparing Diuretics [[Potassium-sparing diuretic|Overview]]'''</small>

:<small>'''Epithelial Sodium Channel [[Epithelial sodium channel|Overview]]''' |[[Amiloride]] | [[Triamterene]])</small>

:<small>'''Aldosterone Antagonist [[Aldosterone antagonist|Overview]]''' |[[Spironolactone]] | [[Eplerenone]] | [[Potassium canrenoate]] | [[Canrenone]]</small>
----
===Antiplatelet Agents===
<small>'''Glycoprotein IIb/IIIa Inhibitors [[Glycoprotein IIb/IIIa inhibitors|Overview]]''' | [[Abciximab]] | [[Eptifibatide]] | [[Tirofiban]]</small>

<small>'''ADP Receptor Antagonists''' | [[Clopidogrel]] | [[Ticlopidine]] | [[Prasugrel]] </small>

<small>'''Prostaglandin Analogues [[prostaglandin analogue|Overview]]''' | [[Beraprost]] | [[Prostacyclin]] | [[Iloprost]] | [[Treprostinil]]</small>

<small>'''Other Antiplatelet Agents''' [[Acetylsalicylic acid|Acetylsalicylic acid/Aspirin]] | [[Aloxiprin]] | [[Ditazole]] | [[Carbasalate calcium]] | [[Cloricromen]] | [[Dipyridamole]] | [[Indobufen]] | [[Picotamide]] | [[Triflusal]] </small>

----
===Antithrombins===
<small>'''Direct Thrombin Inhibitors [[Direct thrombin inhibitor|Overview]]''' | [[Argatroban]] | [[Bivalirudin]] | [[Dabigatran]] | [[Desirudin]] | [[Hirudin]] | [[Lepirudin]] | [[Melagatran]] | [[Ximelagatran]]</small>

<small>'''Indirect Thrombin Inhibitors '''</small>
:<small>'''Heparins''' | [[Danaparoid]] | [[Heparin]] | [[Sulodexide]]</small>
:<small>'''Low Molecular Weight Heparins''' | [[Bemiparin]] | [[Dalteparin]] | [[Enoxaparin]] | [[Nadroparin]] | [[Parnaparin]] | [[Reviparin]] | [[Tinzaparin]]</small>

<small>'''Other Antithrombotics''' | [[Defibrotide]] | [[Dermatan sulfate]] | [[Fondaparinux]] | [[Rivaroxaban]]</small>

<small>'''Non-Medicinal Antithrombins [[Anticoagulant#Anticoagulants outside the body|Overview]]''' | [[Citrate]] | [[EDTA]] | [[Oxalate]]</small>
----
===Beta Blockers===
<small>'''Beta Blockers [[Beta blocker|Overview]]''' [[ATC code C07|(C07)]]</small>

<small>'''Non-selective β antagonists''' | [[Metipranolol]] | [[Nadolol]] | [[Oxprenolol]] | [[Penbutolol]] | [[Pindolol]] | [[Propranolol]] | [[Timolol]] | [[Sotalol]]</small>

<small>'''β<sub>1</sub> antagonists (cardioselective)''' | [[Atenolol]] | [[Acebutolol]] | [[Betaxolol]] | [[Bisoprolol]] | [[Esmolol]] | [[Metoprolol]] | [[Nebivolol]]</small>

<small>'''Mixed α<sub>1</sub>/β antagonists''' | [[Carvedilol]] | [[Labetalol]]</small>
----
===Calcium Channel Blockers===
<small>'''Calcium Channel Blocker [[Calcium channel blocker|Overview]]'''</small>

<small>'''Class I''' Phenylalkylamines ([[ATC code C08#C08DA_Phenylalkylamine_derivatives|C08DA]]) | [[Verapamil]]</small>

<small>'''Class II''' Dihydropyridines ([[ATC code C08#C08CA_Dihydropyridine_derivatives|C08CA]])
| [[Amlodipine]] | [[Felodipine]] | [[Isradipine]] | [[Lacidipine]] | [[Lercanidipine]] | [[Nicardipine]] | [[Nifedipine]] | [[Nimodipine]] | [[Nisoldipine]]</small>

<small>'''Class III''' Benzothiazepines ([[ATC code C08#C08DB_Benzothiazepine_derivatives|C08DB]])
| [[Diltiazem]]</small>
----

===Cardiac Glycosides===
<small>'''Cardiac Glycoside [[Cardiac glycoside|Overview]]''' ([[ATC_code_C01#C01A_Cardiac_glycosides|C01A]])</small>

<small>'''Digitalis Glycosides [[Digitalis|Overview]]''' | [[Acetyldigitoxin]] | [[Acetyldigoxin]] | [[Digitalis]] leaves | [[Digitoxin]] | [[Digoxin]] | [[Lanatoside C]] | [[Deslanoside]] | [[Medigoxin|Metildigoxin]] | [[Gitoformate]]</small>

<small>'''Scilla Glycosides [[Scilla|Overview]]''' | [[Proscillaridin]]</small>

<small>'''Strophantus Glycosides [[Strophantus|Overview]]''' | [[Ouabain|G-strophanthin]] | [[Cymarin]]</small>

<small>'''Other Cardiac Glycosides''' | [[Peruvoside]]</small>
----
=== Cardiac Stimulants Excluding Cardiac Glycosides===
'''Cardiac stimulants excluding cardiac glycosides''' ([[ATC_code_C01#C01C_Cardiac_stimulants_excluding_cardiac_glycosides|C01C]])

'''Adrenergic [[adrenalin|Overview]] and Dopaminergic [[dopaminergic|Overview]] agents''' |
[[Etilefrine]] | [[Isoproterenol|Isoprenaline]] | [[Norepinephrine]] | [[Dopamine]] | [[Norfenefrine]] | [[Phenylephrine]] | [[Dobutamine]] | [[Synephrine|Oxedrine]] | [[Metaraminol]] | [[Methoxamine]] | [[Mephentermine]] | [[Dimetofrine]] | [[Prenalterol]] | [[Dopexamine]] | [[Gepefrine]] | [[Ibopamine]] | [[Midodrine]] | [[Octopamine]] | [[Fenoldopam]] | [[Cafedrine]] | [[Arbutamine]] | [[Theodrenaline]] | [[Epinephrine]]

'''Phosphodiesterase Inhibitors [[Phosphodiesterase inhibitor|Overview]] ([[PDE3 inhibitor|PDE3I]])''' | [[Amrinone]] | [[Milrinone]] | [[Enoximone]] | [[Bucladesine]]

'''Other cardiac stimulants''' | [[Angiotensinamide]] | [[Xamoterol]] | [[Levosimendan]]

----
===Fibrinolytics===
<small>[[Tissue plasminogen activator|Alteplase]] | [[Reteplase]] | [[Tenecteplase]] | [[Streptokinase]], [[Urokinase]] | [[Saruplase]] | [[Anistreplase]]</small>
----
===Hypolipidemic Agents===

<small>'''Statins [[Statins|Overview]]''' | [[Atorvastatin]] | [[Cerivastatin]] | [[Fluvastatin]] | [[Lovastatin]] | [[Mevastatin]] | [[Pitavastatin]] | [[Pravastatin]] | [[Rosuvastatin]] | [[Simvastatin]] </small>

<small>'''Fibrates [[Fibrate|Overview]]''' | [[Clofibrate]] | [[Bezafibrate]] | [[Aluminium clofibrate]] | [[Gemfibrozil]] | [[Fenofibrate]] | [[Simfibrate]] | [[Ronifibrate]] | [[Ciprofibrate]] | [[Etofibrate]] | [[Clofibride]]</small>

<small>'''Bile Acid Sequestrant [[Bile acid sequestrant|Overview]]''' | [[Cholestyramine|Colestyramine]] | [[Colestipol]] | [[Colextran]] | [[Colesevelam]]</small>

<small>'''Niacin and Derivatives''' | [[Niceritrol]] | [[Niacin]] | [[Nicofuranose]] | [[Aluminium nicotinate]] | [[Nicotinyl alcohol]] | [[Acipimox]]</small>

<small>'''Other''' | [[Dextrothyroxine]] | [[Probucol]] | [[Tiadenol]] | [[Benfluorex]] | [[Meglutol]] | [[Omega-3-triglycerides]] | [[Magnesium pyridoxal 5-phosphate glutamate]] | [[Policosanol]] | [[Ezetimibe]]</small>
----
===Nitrates===
<small>'''Nitrates [[Nitrate|Overview]]''' | [[Glyceryl trinitrate (pharmacology)|Glyceryl trinitrate]] | [[Isosorbide dinitrate]] | [[Isosorbide mononitrate]] | [[Molsidomine]] | [[PETN|Pentaerythritol tetranitrate]]</small>
----
===Pulmonary Artery Hypertension===
<small>Medications used in the management of pulmonary arterial hypertension [[pulmonary hypertension|Overview]] ([[ATC code B01|B01]], [[ATC code C02|C02]])</small>

<small>'''Prostacyclin [[Prostacyclin|Overview]]''' | [[Beraprost]] | [[Epoprostenol]] | [[Iloprost]] | [[Treprostinil]]</small>

<small>'''Endothelin Receptor Antagonists [[Endothelin receptor antagonist|Overview]]''' | [[Ambrisentan]] | [[Bosentan]] | [[Sitaxsentan]]</small>

<small>'''PDE5 Inhibitors [[PDE5 inhibitor|Overview]]''' | [[Sildenafil]] | [[Tadalafil]] | [[Vardenafil]]</small>

<small>'''Adjunctive therapy''' | [[Calcium channel blocker]]s | [[Diuretic]]s | [[Digoxin]] | [[Oxygen therapy]] | [[Warfarin]]</small>
----
===Vasodilators===

<small>'''Vasodilators [[Vasodilator|Overview]] ([[ATC_code_C01#C01D_Vasodilators_used_in_cardiac_diseases|C01D]]) </small>

<small>'''Quinolone Vasodilators [[Quinolone|Overview]]''' | [[Flosequinan]]</small>

<small>'''Other Vasodilators''' | [[Heptaminol]] | [[Molsidomine]] | [[Nicorandil]] | [[Nesiritide]]</small>
----
<br>

=INTERVENTIONAL CARDIOLOGY=
==[[Interventional Cardiology]]==
<small>'''Diagnostic Catheterization''' | [[Risk Stratification and the Benefits of PCI vs Medical Therapy]] | [[Conscious Sedation]] | [[Preparation of the Patient for Diagnostic Catheterization]] | [[Technical Aspects of the Cardiac Catheterization Laboratory]] | [[Obtaining Venous and Arterial Access]] | [[Equipment Used in Diagnostic Cardiac Catheterizaiton]] | [[Hemodynamic Assessment in the Cardiac Catheterization Laboratory]] | [[Radiation Safety]]</small>

<small>'''Assesement of coronary lesions''' | [[Coronary Fractional Flow Reserve (FFR)]]) | [[Coronary flow reserve]]([[CFR]]) | [[Intravascular ultrasound]] ([[IVUS]])</small>

<small>'''PCI''' | [[Preparation of the Patient for Percutaneous Coronary Intervention (PCI)]] | [[Percutaneous Coronary Intervention (PCI): Basic Principles and Guidelines]] | [[Equipment Used in Percutaneous Coronary Intervention]] | [[Pharmacotherapy to Support PCI]] | [[Antiplatelet therapy]] | [[Antithrombotic therapy]] | [[Angiography and PCI in Special Patient Populations]] | [[Management Of Specific Lesion Types]] | [[High Risk Percutaneous Coronary Intervention (PCI)]] | [[Vascular Closure Devices]] | [[Post PCI Medical Management of the Interventional Patient]] | [[Complications During and Following Cardiac Catheterization and Percutaneous Coronary Intervention]] | [[Coronary stent thrombosis]]

'''PCI in Specific Populations and Lesion Types'''
*[[Assessment of Lesion Complexity and Morphology Using Coronary Lesion Classification Systems]]
*[[PCI in the Patient with Angiographically Visible Thrombus|Angiographically Visible Thrombus]]
*[[PCI in the Calcified Lesion|The Calcified Leison]]
*[[PCI in the Ostial Lesion|The Ostial Lesion]]
*[[PCI in the Angulated or Tortuous Lesion|The Angulated or Tortuous Lesion]]
*[[PCI in the Bifurcation Lesion|Management of the Bifurcation Lesion]]
*[[PCI in the Long Lesion|The Long Lesion]]
*[[Myocardial bridge|Management of a Coronary Bridge Lesion and Kinks]]
*[[PCI in the Patient with Coronary Vasospasm|Management of Coronary Vasospasm]]
*[[PCI in the Patient with a Chronic Total Occlusion|The Chronic Total Occlusion (CTO)]]
*[[PCI in Small Vessels|Intervention in Small Vessels]]
*[[PCI in Diffusely Diseased Vessels|Intervention in Diffusely Diseased Vessels]]
*[[Intervention in Saphenous Vein Grafts (SVG)|Intervention in Saphenous Vein Grafts (SVG)]]
*[[PCI in the Left Internal Mammary Artery|Intervention in the LIMA]]
*[[PCI in the Right Internal Mammary Artery|Intervention in the RIMA]]
*[[PCI in a Free Radial Artery or Other Conduit|Intervention in a Free Radial and other Conduits]]
*[[Multivessel PCI|Multivessel Intervention]]
*[[PCI in the Patient with Restenosis|PCI in the Patient with Restenosis]]
*[[Stent Thrombosis|Management of the Patient with Stent Thrombosis]]
*[[Treatment of Distal Anastomotic Lesions|Treatment of Distal Anastomotic Lesions]]
*[[Coronary Artery Perforation|Coronary Artery Perforation]]
*[[Left Main Intervention|Left Main Intervention]]
*[[Management of the Thrombotic Lesion|Management of the Thrombotic Lesion]]

</small>

<small>'''High Risk PCI''' | [[PCI in the Patient in Cardiogenic Shock|PCI in the Patient in Cardiogenic Shock]] | [[PCI in the Patient Requiring CPR and Refractory Ventricular Arrhythmias|PCI in the Patient Requiring CPR and Refractory Ventricular Arrhythmias]] | [[PCI in the Patient with Severely Depressed Ventricular Function|PCI in the Patient with Severely Depressed Ventricular Function]] | [[PCI in the Patient with Critical Valve Stenosis|PCI in the Patient with Critical Valve Stenosis]] | [[PCI in the Sole Remaining Conduit|PCI in the Sole Remaining Conduit]] | [[PCI in the Unprotected Left Main Patient|PCI in the Unprotected Left Main Patient]] | [[Adjuncts for High Risk Percuatenous Coronary Intervention|Adjuncts for High Risk Percuatenous Coronary Intervention]]</small>

<small>'''Mechanical circulatory support''' | [[Mechanical circulatory support]] | [[Intra-aortic balloon pump]] | [[Ventricular assist device|Ventricular assist devices]]

[[Artificial heart]]

<small>'''Other Topics'''[[Non Coronary Interventions in the Cardiac Catheterization Laboratory]] | [[Transfusion in ACS management]] | [[Revascularization in the "No Option" Patient]]</small>
<br>

=Cardiac Surgery=
{{Cardiac surgery}}

=Vascular Surgery=
{{Vascular surgery}}
=BIOSTATISTICS=
==[[Biostatistics Home Page|Biostatistics]]==
<br>

=COST EFFECTIVENESS AND QUALITY OF LIFE=
==[[Cost Effectiveness in Cardiovascular Disease]]==

{{WH}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T22:25:54Z

Mandana Chitsazan:

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} Novel coronavirus, COVID-19, Wuhan coronavirus, coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, covid-19, 2019-nCoV, 2019 novel coronavirus, heart failure, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*[[Heart Failure]] ([[(HF)]] in [[COVID-19]] may be classified similarly to [[heart failure]] from other causes.
* In general, [[heart failure]] can be classified based on:
**'''The pathophysiology of heart failure''':
***[[systolic HF]] vs [[diastolic HF]]
***[[left-sided HF]] vs [[right-sided HF]]
**'''The duration of symptoms''':
***acute HF [[(AHF)]] vs chronic HF [[(CHF)]]
**'''The underlying physiology based on [[left ventricular ejection fraction (LVEF)]]:'''
***[[Heart failure with reduced ejection fraction]] [[(HFrEF)]] vs [[heart failure with mid-range ejection fraction]] [[(HFmrEF)]] and [[heart failure with preserved ejection fraction]] [[(HFpEF)]]
**'''The severity of [[heart failure]]''' (i.e., the [[New York Heart Association Class]] I-IV)
**'''The stage of congestive heart failure''' (i.e., [[AHA Class A, B, C, D]])

*[[Acute heart failure]] has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea]]
**Cool extremities
**[[Cyanosis ]]
**[[Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:57:45Z

Mandana Chitsazan: /* Differentiating ((COVID-19 associated heart failure)) from other Diseases */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{cite journal| author=Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D | display-authors=etal| title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219357 | doi=10.1001/jamacardio.2020.1096 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219357 }} </ref> <ref name="pmid32360242">{{cite journal| author=Mehra MR, Ruschitzka F| title=COVID-19 Illness and Heart Failure: A Missing Link? | journal=JACC Heart Fail | year= 2020 | volume= 8 | issue= 6 | pages= 512-514 | pmid=32360242 | doi=10.1016/j.jchf.2020.03.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32360242 }} </ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade
*Iatrogenic

==Differentiating COVID-19 associated heart failure from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
*COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
*Acute heart failure in COVID-19 may progress to cardiogenic shock.

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:57:11Z

Mandana Chitsazan: /* Pathophysiology */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{cite journal| author=Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D | display-authors=etal| title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219357 | doi=10.1001/jamacardio.2020.1096 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219357 }} </ref> <ref name="pmid32360242">{{cite journal| author=Mehra MR, Ruschitzka F| title=COVID-19 Illness and Heart Failure: A Missing Link? | journal=JACC Heart Fail | year= 2020 | volume= 8 | issue= 6 | pages= 512-514 | pmid=32360242 | doi=10.1016/j.jchf.2020.03.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32360242 }} </ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
*COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
*Acute heart failure in COVID-19 may progress to cardiogenic shock.

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:56:16Z

Mandana Chitsazan: /* Pathophysiology */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*[[Heart Failure]] ([[(HF)]] in [[COVID-19]] may be classified similarly to [[heart failure]] from other causes.
* In general, [[heart failure]] can be classified based on:
**'''The pathophysiology of heart failure''':
***[[systolic HF]] vs [[diastolic HF]]
***[[left-sided HF]] vs [[right-sided HF]]
**'''The duration of symptoms''':
***acute HF [[(AHF)]] vs chronic HF [[(CHF)]]
**'''The underlying physiology based on [[left ventricular ejection fraction (LVEF)]]:'''
***[[Heart failure with reduced ejection fraction]] [[(HFrEF)]] vs [[heart failure with mid-range ejection fraction]] [[(HFmrEF)]] and [[heart failure with preserved ejection fraction]] [[(HFpEF)]]
**'''The severity of [[heart failure]]''' (i.e., the [[New York Heart Association Class]] I-IV)
**'''The stage of congestive heart failure''' (i.e., [[AHA Class A, B, C, D]])

*[[Acute heart failure]] has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea]]
**Cool extremities
**[[Cyanosis ]]
**[[Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

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COVID-19-associated heart failure

2020-06-29T21:55:44Z

Mandana Chitsazan: /* Pathophysiology */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{cite journal| author=Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D | display-authors=etal| title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219357 | doi=10.1001/jamacardio.2020.1096 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219357 }} </ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
*COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
*Acute heart failure in COVID-19 may progress to cardiogenic shock.

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

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COVID-19-associated heart failure

2020-06-29T21:52:55Z

Mandana Chitsazan: /* History and Symptoms */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*[[Heart Failure]] ([[(HF)]] in [[COVID-19]] may be classified similarly to [[heart failure]] from other causes.
* In general, [[heart failure]] can be classified based on:
**'''The pathophysiology of heart failure''':
***[[systolic HF]] vs [[diastolic HF]]
***[[left-sided HF]] vs [[right-sided HF]]
**'''The duration of symptoms''':
***acute HF [[(AHF)]] vs chronic HF [[(CHF)]]
**'''The underlying physiology based on [[left ventricular ejection fraction (LVEF)]]:'''
***[[Heart failure with reduced ejection fraction]] [[(HFrEF)]] vs [[heart failure with mid-range ejection fraction]] [[(HFmrEF)]] and [[heart failure with preserved ejection fraction]] [[(HFpEF)]]
**'''The severity of [[heart failure]]''' (i.e., the [[New York Heart Association Class]] I-IV)
**'''The stage of congestive heart failure''' (i.e., [[AHA Class A, B, C, D]])

*[[Acute heart failure]] has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea]]
**Cool extremities
**[[Cyanosis ]]
**[[Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:52:13Z

Mandana Chitsazan: /* History and Symptoms */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*[[Heart Failure]] ([[(HF)]] in [[COVID-19]] may be classified similarly to [[heart failure]] from other causes.
* In general, [[heart failure]] can be classified based on:
**'''The pathophysiology of heart failure''':
***[[systolic HF]] vs [[diastolic HF]]
***[[left-sided HF]] vs [[right-sided HF]]
**'''The duration of symptoms''':
***acute HF [[(AHF)]] vs chronic HF [[(CHF)]]
**'''The underlying physiology based on [[left ventricular ejection fraction (LVEF)]]:'''
***[[Heart failure with reduced ejection fraction]] [[(HFrEF)]] vs [[heart failure with mid-range ejection fraction]] [[(HFmrEF)]] and [[heart failure with preserved ejection fraction]] [[(HFpEF)]]
**'''The severity of [[heart failure]]''' (i.e., the [[New York Heart Association Class]] I-IV)
**'''The stage of congestive heart failure''' (i.e., [[AHA Class A, B, C, D]])

*[[Acute heart failure]] has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea]]
**Cool extremities
**[[Cyanosis ]]
*[[Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:50:49Z

Mandana Chitsazan: /* Classification */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*[[Heart Failure]] ([[(HF)]] in [[COVID-19]] may be classified similarly to [[heart failure]] from other causes.
* In general, [[heart failure]] can be classified based on:
**'''The pathophysiology of heart failure''':
***[[systolic HF]] vs [[diastolic HF]]
***[[left-sided HF]] vs [[right-sided HF]]
**'''The duration of symptoms''':
***acute HF [[(AHF)]] vs chronic HF [[(CHF)]]
**'''The underlying physiology based on [[left ventricular ejection fraction (LVEF)]]:'''
***[[Heart failure with reduced ejection fraction]] [[(HFrEF)]] vs [[heart failure with mid-range ejection fraction]] [[(HFmrEF)]] and [[heart failure with preserved ejection fraction]] [[(HFpEF)]]
**'''The severity of [[heart failure]]''' (i.e., the [[New York Heart Association Class]] I-IV)
**'''The stage of congestive heart failure''' (i.e., [[AHA Class A, B, C, D]])

*[[Acute heart failure]] has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea ]]
**Cool extremities
**[[Cyanosis ]]
*[[*Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:46:34Z

Mandana Chitsazan:

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**'''The pathophysiology of heart failure''':
***systolic vs diastolic
***left-sided vs right-sided
**'''The duration of symptoms''':
***acute vs chronic
**'''The underlying physiology based on left ventricular ejection fraction (LVEF):'''
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**'''The severity of heart failure''' (i.e., the New York Heart Association Class I-IV)
**'''The stage of congestive heart failure''' (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with [[COVID-19]] include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*[[Acute myocardial injury]]
*[[Acute coronary syndromes]]
*[[Myocarditis]]
*[[Hypertensive crisis]]
*[[Arrhythmias]]: Tachycardia or severe bradycardia
*[[Stress-induced cardiomyopathy]]
*Circulatory failure:
**[[Acute pulmonary embolism]]
**[[Pericardial tamponade]]
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with [[COVID-19]] infection, [[acute heart failure]] should be differentiated from other diseases presenting with [[dyspnea]] and/or [[tachypnea]].
The differentials include the following:
*[[Pneumonia]]
*[[ARDS]]
*[[Myocarditis]]/[[pericarditis]]
*[[Acute pulmonary embolism]]

==Epidemiology and Demographics==
*Data on incidence on acute heart failure in COVID-19 patients is limited.
*In one study, [[acute heart failure]] was seen in 4.1% of patients with [[acute cardiac injury]].
*In a retrospective study on 191 [[COVID-19]] patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*[[COVID-19]] patients with [[chronic heart failure]] are more likely to develop severe forms of the disease.
*[[COVID-19]] patients who develop [[acute heart failure]] (either de novo AHF or ADHF) have worse outcomes.
*[[Acute heart failure]] in [[COVID-19]] may progress to [[cardiogenic shock]].

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of [[acute heart failure]] in [[COVID-19]] patients are:
**New or worsening [[dyspnea]]: may overlap with dyspnea caused by concomitant respiratory involvement and [[ARDS]] due to [[COVID-19]]
**[[Peripheral edema]]
**Confusion and altered mentation
**[[Orthopnea]]
**[[Palpitations]]
*Less common symptoms include:
**[[Paroxysmal nocturnal dyspnea ]]
**Cool extremities
**[[Cyanosis ]]
*[[*Dizziness]]
**[[Syncope]]
**Fatigue
**[[Hemoptysis]]

===Physical Examination===

*Physical examination of patients with [[acute heart failure]] is usually remarkable for:
**[[Crackles]] on auscultation
**[[Distended jugular veins]]
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated [[cardiac troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated heart failure.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased [[myocardial stress]] and are quantitative markers of increased [[intracardiac filling pressure]].<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with [[heart failure]].
**Increased [[BNP]] or [[NT-proBNP]] levels have been demonstrated in COVID-19 patients.
**Increased [[NT-proBNP]] level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased [[natriuretic peptide]] levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of [[BNP]]/[[NT-proBNP]] has not been recommended in [[COVID-19 patients]], unless there is a high suspicion of [[heart failure]] based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in [[COVID-19 patients]].
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*A [[Chest x-ray]] may be helpful in the diagnosis of [[heart failure]]. Findings on [[chest X-ray]] suggestive of [[heart failure]] include:
**[[Cardiomegaly]]
**[[Pulmonary congestion]]
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and [[ARDS]] due to [[COVID-19]].

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] [[(TTE)]] has not been recommended in [[COVID-19]] patients considering the limited [[personal protective equipment (PPE)]] and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] [[(POCUS)]]
**[[Focused cardiac ultrasound study]] [[(FoCUS)]]
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**[[Left ventricular systolic function]] [[(left ventricular ejection fraction, LVEF)]] to distinguish [[systolic dysfunction]] with a [[reduced ejection fraction]] (LVEF<40%) from [[diastolic dysfunction]] with a preserved ejection fraction (LVEF>40%)
**Left ventricular [[diastolic function]]
**Left ventricular structural abnormalities, including [[left ventricular size]] and [[left ventricular wall thickness]]
**Left atrial size
**Right ventricular size and function
**Detection and quantification of [[valvular abnormalities]]
**Measurement of [[systolic pulmonary artery pressure]]
**Detection and quantification of [[pericardial effusion]]
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*[[Acute heart failure]] in the setting of [[COVID-19]] is generally treated similarly to [[acute heart failure]] in other settings. These may include:
**[[Fluid restriction]]
**[[Diuretic]] therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their [[negative inotropic effects]].<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with [[acute heart failure]] due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with [[chronic heart failure]] are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACE inhibitors]] or [[Angiotensin II receptor blockers]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:38:23Z

Mandana Chitsazan:

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both [[de novo acute heart failure]] and [[acute decompensation of chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
*COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
*Acute heart failure in COVID-19 may progress to cardiogenic shock.

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:29:41Z

Mandana Chitsazan: /* Overview */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}} coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, 2019-nCoV, 2019 novel coronavirus, acute heart failure, de novo acute heart failure, chronic heart failure, acute decompensated heart failure, HFrEF, HFpEF, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction

==Overview==

*Both de novo [[acute heart failure]] and acute decompensation of [[chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A, B, C, D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade
*Iatrogenic

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==
*
*

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==
*COVID-19 patients with chronic heart failure are more likely to develop severe forms of the disease.
*COVID-19 patients who develop acute heart failure (either de novo AHF or ADHF) have worse outcomes.
*Acute heart failure in COVID-19 may progress to cardiogenic shock.

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**[[ST-T changes]]

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:21:50Z

Mandana Chitsazan: /* Physical Examination */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}}

==Overview==

*Both [[de novo acute heart failure]] and [[acute decompensation of chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A,B,C,D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

*Physical examination of patients with acute heart failure is usually remarkable for:
**Crackles on auscultation
**Distended jugular veins
**Lower extremity edema

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**ST-T changes

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:17:58Z

Mandana Chitsazan: /* History and Symptoms */

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}}

==Overview==

*Both [[de novo acute heart failure]] and [[acute decompensation of chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A,B,C,D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
**Peripheral edema
**Confusion and altered mentation
**Orthopnea
**Palpitations
**Paroxysmal nocturnal dyspnea
**Cool extremities
**Cyanosis
**Dizziness
**Syncope
**Fatigue
**Hemoptysis

===Physical Examination===

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**ST-T changes

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-29T21:13:47Z

Mandana Chitsazan:

__NOTOC__
'''For COVID-19 frequently asked inpatient questions, click [[COVID-19 frequently asked inpatient questions|here]]'''<br>
'''For COVID-19 frequently asked outpatient questions, click [[COVID-19 frequently asked outpatient questions|here]]'''<br>

{{SI}}

{{CMG}}; {{AE}}{{Mitra}}{{MC}}

{{SK}}

==Overview==

*Both [[de novo acute heart failure]] and [[acute decompensation of chronic heart failure]] can occur in patients with [[COVID-19]].
*Patients with [[chronic heart failure]] may be at higher risk of developing severe [[COVID-19]] infection due to the advanced age and the presence of multiple comorbidities.

==Historical perspective==

==Classification==

*Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
* In general, HF can be classified based on:
**The pathophysiology of heart failure:
***systolic vs diastolic
***left-sided vs right-sided
**The duration of symptoms:
***acute vs chronic
**The underlying physiology based on left ventricular ejection fraction (LVEF):
***Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
**The severity of heart failure (i.e., the New York Heart Association Class I-IV)
**The stage of congestive heart failure (i.e., AHA Class A,B,C,D)

*Acute heart failure has two forms:
**Newly-arisen (“de novo”) acute heart failure
**Acutely decompensated chronic heart failure (ADCHF)

==Pathophysiology==

*Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>

**Acute exacerbation of [[chronic heart failure]] caused by precipitating factors
**[[Acute myocardial injury]] (which in turn can be caused by several mechanisms)
**[[Stress cardiomyopathy]] (i.e., [[Takotsubo cardiomyopathy]])
**Impaired myocardial relaxation resulting in [[diastolic dysfunction]] [i.e., [[Heart failure with preserved ejection fraction (HFpEF)]] ]
**Right-sided heart failure, secondary to [[pulmonary hypertension]] caused by hypoxia and [[acute respiratory distress syndrome]] (ARDS)

==Causes==

*Acute myocardial injury
*Acute coronary syndromes
*Myocarditis
*Hypertensive crisis
*Arrhythmias: Tachycardia or severe bradycardia
*Stress-induced cardiomyopathy
*Circulatory failure:
**Acute pulmonary embolism
**Pericardial tamponade

==Differentiating ((COVID-19 associated heart failure)) from other Diseases==

In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea.
The differentials include the following:
*Pneumonia
*ARDS
*Myocarditis/pericarditis
*Acute pulmonary embolism

==Epidemiology and Demographics==
*In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
*In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).

==Risk Factors==

==Screening==
*There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
*Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.

==Natural History, Complications, and Prognosis==

==Diagnosis==
===Diagnostic Study of Choice===

===History and Symptoms===

*The most common symptoms of acute heart failure in COVID-19 patients are:
**New or worsening dyspnea
***Dyspnea may be due to concomitant respiratory involvement and ARDS due to COVID-19
Lower limb edema
Confusion and altered mentation
Cool extremities
Cyanosis
Dizziness
Syncope
Fatigue
Hemoptysis
Orthopnea
Palpitations
Paroxysmal nocturnal dyspnea
Shortness of breath
Syncope
Weakness

===Physical Examination===

===Laboratory Findings===

*Cardiac Troponins:
**Elevated cardiac [[troponin]] levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>

*Natriuretic Peptides:
**[[Natriuretic peptides]] (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated [[BNP]] and [[NT-proBNP]] are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

===Electrocardiogram===

*There is no specific electrocardiographic finding for [[acute heart failure]] in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as [[ischemia]], [[myocarditis]], and [[arrhythmias]].
*These ECG findings may include:
**Low QRS Voltage
**[[Left ventricular hypertrophy]]
**Left atrial enlargement
**[[Left bundle branch block]]
**[[Poor R progression]]
**ST-T changes

===X-ray===

*An x-ray may be helpful in the diagnosis of [[heart failure]]. Findings on an x-ray suggestive of heart failure include:
**[[Cardiomegaly]]
**Pulmonary congestion
**Increased pulmonary vascular markings.

*However, signs of [[pulmonary edema]] may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

===Echocardiography or Ultrasound===

*A complete standard [[transthoracicechocardiography]] (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**[[Cardiac point-of-care ultrasound]] (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography

*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of [[regional wall motion abnormalities]]/reduced [[strain]] that would suggest underlying [[ischemia]].

===CT scan===

===MRI===

===Other Imaging Findings===

===Other Diagnostic Studies===

==Treatment==
===Medical Therapy===

*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**[[Vasopressors]] and/or [[inotropes]]
**[[Ventricular assisted devices]] and [[extracorporeal membrane oxygenation (ECMO)]]
*[[Beta-blockers]] should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*[[Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)]] should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including [[beta-blockers]], [[ACEI]] or [[ARB]], and [[mineralocorticoid receptor antagonists]]. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

COVID-19-associated heart failure

2020-06-25T12:39:19Z

Mandana Chitsazan:

__NOTOC__
{{COVID-19-associated heart failure}}
'''For patient information, click [[COVID-19-associated heart failure (patient information)|here]]'''

{{CMG}}; {{AE}}{{MC}}{{Mitra}}

{{SK}}

==[[Xyz overview|Overview]]==

==[[Xyz historical perspective|Historical Perspective]]==

==[[Xyz classification|Classification]]==

==[[Xyz pathophysiology|Pathophysiology]]==

==[[Xyz causes|Causes]]==

==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]==

==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]==

==[[Xyz risk factors|Risk Factors]]==

==[[Xyz screening|Screening]]==

==[[Xyz natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Xyz medical therapy|Medical Therapy]] | [[Xyz interventions|Interventions]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Xyz case study one|Case #1]]

[[Category: (name of the system)]]

COVID-19-associated heart failure

2020-06-25T12:38:04Z

Mandana Chitsazan:

__NOTOC__
{{COVID-19-associated heart failure}}
'''For patient information, click [[COVID-19-associated heart failure (patient information)|here]]'''

{{CMG}}; {{AE}}{{MC}}{{Mitra}}

==[[Xyz overview|Overview]]==

==[[Xyz historical perspective|Historical Perspective]]==

==[[Xyz classification|Classification]]==

==[[Xyz pathophysiology|Pathophysiology]]==

==[[Xyz causes|Causes]]==

==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]==

==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]==

==[[Xyz risk factors|Risk Factors]]==

==[[Xyz screening|Screening]]==

==[[Xyz natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Xyz medical therapy|Medical Therapy]] | [[Xyz interventions|Interventions]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Xyz case study one|Case #1]]

[[Category: (name of the system)]]

COVID-19-associated heart failure

2020-06-25T12:37:26Z

Mandana Chitsazan:

__NOTOC__
{{COVID-19-associated heart failure}}
'''For patient information, click [[COVID-19-associated heart failure (patient information)|here]]'''

{{CMG}}; {{AE}}

{{MC}}{{Mitra}}

==[[Xyz overview|Overview]]==

==[[Xyz historical perspective|Historical Perspective]]==

==[[Xyz classification|Classification]]==

==[[Xyz pathophysiology|Pathophysiology]]==

==[[Xyz causes|Causes]]==

==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]==

==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]==

==[[Xyz risk factors|Risk Factors]]==

==[[Xyz screening|Screening]]==

==[[Xyz natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Xyz medical therapy|Medical Therapy]] | [[Xyz interventions|Interventions]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Xyz case study one|Case #1]]

[[Category: (name of the system)]]

COVID-19-associated heart failure

2020-06-25T11:53:14Z

Mandana Chitsazan:

__NOTOC__
{{COVID-19-associated heart failure}}
'''For patient information, click [[Xyz (patient information)|here]]'''

{{CMG}}; {{AE}}

{{SK}}

==[[Xyz overview|Overview]]==

==[[Xyz historical perspective|Historical Perspective]]==

==[[Xyz classification|Classification]]==

==[[Xyz pathophysiology|Pathophysiology]]==

==[[Xyz causes|Causes]]==

==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]==

==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]==

==[[Xyz risk factors|Risk Factors]]==

==[[Xyz screening|Screening]]==

==[[Xyz natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Xyz medical therapy|Medical Therapy]] | [[Xyz interventions|Interventions]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Xyz case study one|Case #1]]

[[Category: (name of the system)]]

COVID-19-associated heart failure

2020-06-25T11:52:16Z

Mandana Chitsazan: Blanked the page

Cardiovascular Disorders and COVID-19

2020-06-17T20:19:56Z

Mandana Chitsazan: /* Complications */

[[[[Link title]]]]__NOTOC__

{{CMG}} {{AE}} {{mitra}}{{MC}}

==Overview==

==Complications==

===Myocardial injury===

===Acute Coronary Syndromes===

===Heart Failure===

====Pathophysiology====
*Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
*Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
*Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include: <ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>
**Acute exacerbation of chronic heart failure
**Acute myocardial injury (which in turn can be caused by several mechanisms)
**Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
**Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
**Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)

====Symptoms and signs====
*Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
*Lower limb edema
*Orthopnea
*Paroxysmal nocturnal dyspnea
*Confusion and altered mentation
*Cool extremities
*Cyanosis
*Syncope
*Fatigue
*Hemoptysis
*Palpitations
*Weakness
*Wheezing or cardiac asthma
*Distended jugular veins
*Crackles on auscultation

====Electrocardiography (ECG)====
*There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
*These ECG findings may include:
**Low QRS Voltage
**Left ventricular hypertrophy
**Left atrial enlargement
**Left bundle branch block
**Poor R progression
**ST-T changes

====Chest x-ray (CXR)====
*The Chest x-ray may show evidence of:
**Cardiomegaly
**Pulmonary congestion
**Increased pulmonary vascular markings.
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

====Echocardiography====
*A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel. <ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**Cardiac point-of-care ultrasound (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography
*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia

====Cardiac biomarkers====
*Cardiac Troponins:
**Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF. <ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
*Natriuretic Peptides:
**Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure. <ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19. <ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases. <ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

====Treatment====
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include: <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
**Fluid restriction
**Diuretic therapy
**Vasopressors and/or inotropes
**Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
*Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects. <ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention. <ref name="pmid12656651">{{Cite pmid|12656651}}</ref>

===Cardiogenic Shock===

===Myocarditis===

===Pericarditis===

===Arrhythmias ===

==== Pathophysiology: ====
Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias.<ref name="WangHu2020">{{cite journal|last1=Wang|first1=Dawei|last2=Hu|first2=Bo|last3=Hu|first3=Chang|last4=Zhu|first4=Fangfang|last5=Liu|first5=Xing|last6=Zhang|first6=Jing|last7=Wang|first7=Binbin|last8=Xiang|first8=Hui|last9=Cheng|first9=Zhenshun|last10=Xiong|first10=Yong|last11=Zhao|first11=Yan|last12=Li|first12=Yirong|last13=Wang|first13=Xinghuan|last14=Peng|first14=Zhiyong|title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China|journal=JAMA|volume=323|issue=11|year=2020|pages=1061|issn=0098-7484|doi=10.1001/jama.2020.1585}}</ref> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]].<ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref> The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]].<ref name="ChenPrendergast2020">{{cite journal|last1=Chen|first1=Mao|last2=Prendergast|first2=Bernard|last3=Redwood|first3=Simon|last4=Xiong|first4=Tian-Yuan|title=Coronaviruses and the cardiovascular system: acute and long-term implications|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1798–1800|issn=0195-668X|doi=10.1093/eurheartj/ehaa231}}</ref> According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.<ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>

==== Signs and Symptoms: ====
Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).

*'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent of patients.<ref name="pmid32044814">{{cite journal| author=Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP | display-authors=etal| title=Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province. | journal=Chin Med J (Engl) | year= 2020 | volume= 133 | issue= 9 | pages= 1025-1031 | pmid=32044814 | doi=10.1097/CM9.0000000000000744 | pmc=7147277 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32044814 }} </ref><ref name="pmid32201335">{{cite journal| author=Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G | display-authors=etal| title=Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic. | journal=J Am Coll Cardiol | year= 2020 | volume= 75 | issue= 18 | pages= 2352-2371 | pmid=32201335 | doi=10.1016/j.jacc.2020.03.031 | pmc=7198856 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32201335 }} </ref>
*'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|corrected QT interval]] (QTc) >500 milliseconds at the time of admittance.<ref name="pmid32320003">{{cite journal| author=Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW | display-authors=etal| title=Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. | journal=JAMA | year= 2020 | volume= | issue= | pages= | pmid=32320003 | doi=10.1001/jama.2020.6775 | pmc=7177629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32320003 }} </ref> However, in another study that involved 84 patients who got [[hydroxychloroquine]] and [[azithromycin]], the baseline QTc interval was 435 milliseconds before receiving these medications.<ref name="GiudicessiNoseworthy2020">{{cite journal|last1=Giudicessi|first1=John R.|last2=Noseworthy|first2=Peter A.|last3=Friedman|first3=Paul A.|last4=Ackerman|first4=Michael J.|title=Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19)|journal=Mayo Clinic Proceedings|volume=95|issue=6|year=2020|pages=1213–1221|issn=00256196|doi=10.1016/j.mayocp.2020.03.024}}</ref>
*'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent)<ref name="GoyalChoi2020">{{cite journal|last1=Goyal|first1=Parag|last2=Choi|first2=Justin J.|last3=Pinheiro|first3=Laura C.|last4=Schenck|first4=Edward J.|last5=Chen|first5=Ruijun|last6=Jabri|first6=Assem|last7=Satlin|first7=Michael J.|last8=Campion|first8=Thomas R.|last9=Nahid|first9=Musarrat|last10=Ringel|first10=Joanna B.|last11=Hoffman|first11=Katherine L.|last12=Alshak|first12=Mark N.|last13=Li|first13=Han A.|last14=Wehmeyer|first14=Graham T.|last15=Rajan|first15=Mangala|last16=Reshetnyak|first16=Evgeniya|last17=Hupert|first17=Nathaniel|last18=Horn|first18=Evelyn M.|last19=Martinez|first19=Fernando J.|last20=Gulick|first20=Roy M.|last21=Safford|first21=Monika M.|title=Clinical Characteristics of Covid-19 in New York City|journal=New England Journal of Medicine|volume=382|issue=24|year=2020|pages=2372–2374|issn=0028-4793|doi=10.1056/NEJMc2010419}}</ref>

*'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].<ref name="pmid32219356">{{cite journal| author=Guo T, Fan Y, Chen M, Wu X, Zhang L, He T | display-authors=etal| title=Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219356 | doi=10.1001/jamacardio.2020.1017 | pmc=7101506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219356 }} </ref>
*'''Cardiac Arrest:''' According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of [[COVID-19]], 362 cases of out-of-hospital [[cardiac arrest]] were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital [[cardiac arrest]] were reported, which means an increment of 58% was observed in 2020 among [[COVID-19]] patients.<ref name="BaldiSechi2020">{{cite journal|last1=Baldi|first1=Enrico|last2=Sechi|first2=Giuseppe M.|last3=Mare|first3=Claudio|last4=Canevari|first4=Fabrizio|last5=Brancaglione|first5=Antonella|last6=Primi|first6=Roberto|last7=Klersy|first7=Catherine|last8=Palo|first8=Alessandra|last9=Contri|first9=Enrico|last10=Ronchi|first10=Vincenza|last11=Beretta|first11=Giorgio|last12=Reali|first12=Francesca|last13=Parogni|first13=Pierpaolo|last14=Facchin|first14=Fabio|last15=Bua|first15=Davide|last16=Rizzi|first16=Ugo|last17=Bussi|first17=Daniele|last18=Ruggeri|first18=Simone|last19=Oltrona Visconti|first19=Luigi|last20=Savastano|first20=Simone|title=Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMc2010418}}</ref> According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe [[COVID-19]], 151 patients developed in-hospital [[cardiac arrest]]. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), [[Pulseless electrical activity]] in 6 patients (4.4%), and [[asystole]] in 122 [[COVID-19]] patients (89.7%).<ref name="ShaoXu2020">{{cite journal|last1=Shao|first1=Fei|last2=Xu|first2=Shuang|last3=Ma|first3=Xuedi|last4=Xu|first4=Zhouming|last5=Lyu|first5=Jiayou|last6=Ng|first6=Michael|last7=Cui|first7=Hao|last8=Yu|first8=Changxiao|last9=Zhang|first9=Qing|last10=Sun|first10=Peng|last11=Tang|first11=Ziren|title=In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China|journal=Resuscitation|volume=151|year=2020|pages=18–23|issn=03009572|doi=10.1016/j.resuscitation.2020.04.005}}</ref>

==== Diagnostic Testing: ====

*'''ECG:''' Most patients with the severe COVID-19, and especially patients who receive QT-prolonging medications, should have a baseline electrocardiogram (ECG) performed at the time of admission to the hospital.<ref name="GandhiSolomon2020">{{cite journal|last1=Gandhi|first1=Rajesh T.|last2=Solomon|first2=Caren G.|last3=Lynch|first3=John B.|last4=del Rio|first4=Carlos|title=Mild or Moderate Covid-19|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMcp2009249}}</ref>The best technique to get the QT interval is with a 12-lead electrocardiogram (ECG). However, to scale back exposure to hospital workers, this could not perpetually be possible. A single-lead ECG might underestimate the QT interval, and there ought to be an effort to use a multiple-lead telemetry system to observe the QT interval.<ref name="ChangSaleh2020">{{cite journal|last1=Chang|first1=David|last2=Saleh|first2=Moussa|last3=Gabriels|first3=James|last4=Ismail|first4=Haisam|last5=Goldner|first5=Bruce|last6=Willner|first6=Jonathan|last7=Beldner|first7=Stuart|last8=Mitra|first8=Raman|last9=John|first9=Roy|last10=Epstein|first10=Laurence M.|title=Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated With Hydroxychloroquine and/or Azithromycin|journal=Journal of the American College of Cardiology|volume=75|issue=23|year=2020|pages=2992–2993|issn=07351097|doi=10.1016/j.jacc.2020.04.032}}</ref>
*'''Transthoracic echocardiography:''' Transthoracic echocardiography is recommended for an inpatient with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest x-ray or CT-chest.<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref>

==== Treatment:====

*'''Polymorphic Ventricular Tachycardia (torsades de pointes):''' All patients with torsades de pointes (TdP) should be determined if they are hemodynamically stable or unstable through immediate evaluation of the symptoms, vital signs, and level of consciousness.<ref name="PanchalBerg2018">{{cite journal|last1=Panchal|first1=Ashish R.|last2=Berg|first2=Katherine M.|last3=Kudenchuk|first3=Peter J.|last4=Del Rios|first4=Marina|last5=Hirsch|first5=Karen G.|last6=Link|first6=Mark S.|last7=Kurz|first7=Michael C.|last8=Chan|first8=Paul S.|last9=Cabañas|first9=José G.|last10=Morley|first10=Peter T.|last11=Hazinski|first11=Mary Fran|last12=Donnino|first12=Michael W.|title=2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care|journal=Circulation|volume=138|issue=23|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000613}}</ref>
**'''Unstable patients:''' Patients with COVID-19 with sustained torsades de pointes (TdP) usually become hemodynamically unstable, severely symptomatic because of perfusion failure, or pulseless and should be treated according to standard resuscitation algorithms, including cardioversion/defibrillation. Initial treatment with antiarrhythmic medications is not indicated for hemodynamically unstable or pulseless patients except intravenous (IV) magnesium.<ref name="PanchalBerg2018">{{cite journal|last1=Panchal|first1=Ashish R.|last2=Berg|first2=Katherine M.|last3=Kudenchuk|first3=Peter J.|last4=Del Rios|first4=Marina|last5=Hirsch|first5=Karen G.|last6=Link|first6=Mark S.|last7=Kurz|first7=Michael C.|last8=Chan|first8=Paul S.|last9=Cabañas|first9=José G.|last10=Morley|first10=Peter T.|last11=Hazinski|first11=Mary Fran|last12=Donnino|first12=Michael W.|title=2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care|journal=Circulation|volume=138|issue=23|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000613}}</ref>
**'''Stable patients:''' In a patient with a single episode of TdP, treatment with IV magnesium along with correction of metabolic/electrolyte disturbances or removal of any inciting medications may be sufficient. The patient should be kept under observation until the electrolytes, and the QT interval nearly normalizes.

===Out-of-hospital cardiac arrest and Sudden Cardiac Death===

===Spontaneous Coronary Artery Dissection===

==References ==
<references />

Cardiovascular Disorders and COVID-19

2020-06-17T20:19:01Z

Mandana Chitsazan: /* Cardiac biomarkers */

[[[[Link title]]]]__NOTOC__

{{CMG}} {{AE}} {{mitra}}{{MC}}

==Overview==

==Complications==

===Myocardial injury===

===Acute Coronary Syndromes===

===Heart Failure===

====Pathophysiology====
*Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
*Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
*Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include: <ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>
**Acute exacerbation of chronic heart failure
**Acute myocardial injury (which in turn can be caused by several mechanisms)
**Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
**Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
**Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)

====Symptoms and signs====
*Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
*Lower limb edema
*Orthopnea
*Paroxysmal nocturnal dyspnea
*Confusion and altered mentation
*Cool extremities
*Cyanosis
*Syncope
*Fatigue
*Hemoptysis
*Palpitations
*Weakness
*Wheezing or cardiac asthma
*Distended jugular veins
*Crackles on auscultation

====Electrocardiography (ECG)====
*There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
*These ECG findings may include:
**Low QRS Voltage
**Left ventricular hypertrophy
**Left atrial enlargement
**Left bundle branch block
**Poor R progression
**ST-T changes

====Chest x-ray (CXR)====
*The Chest x-ray may show evidence of:
**Cardiomegaly
**Pulmonary congestion
**Increased pulmonary vascular markings.
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

====Echocardiography====
*A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel. <ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**Cardiac point-of-care ultrasound (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography
*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia

====Treatment====
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include: <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
**Fluid restriction
**Diuretic therapy
**Vasopressors and/or inotropes
**Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
*Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects. <ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention. <ref name="pmid12656651">{{Cite pmid|12656651}}</ref>

===Cardiogenic Shock===

===Myocarditis===

===Pericarditis===

===Arrhythmias ===

==== Pathophysiology: ====
Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias.<ref name="WangHu2020">{{cite journal|last1=Wang|first1=Dawei|last2=Hu|first2=Bo|last3=Hu|first3=Chang|last4=Zhu|first4=Fangfang|last5=Liu|first5=Xing|last6=Zhang|first6=Jing|last7=Wang|first7=Binbin|last8=Xiang|first8=Hui|last9=Cheng|first9=Zhenshun|last10=Xiong|first10=Yong|last11=Zhao|first11=Yan|last12=Li|first12=Yirong|last13=Wang|first13=Xinghuan|last14=Peng|first14=Zhiyong|title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China|journal=JAMA|volume=323|issue=11|year=2020|pages=1061|issn=0098-7484|doi=10.1001/jama.2020.1585}}</ref> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]].<ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref> The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]].<ref name="ChenPrendergast2020">{{cite journal|last1=Chen|first1=Mao|last2=Prendergast|first2=Bernard|last3=Redwood|first3=Simon|last4=Xiong|first4=Tian-Yuan|title=Coronaviruses and the cardiovascular system: acute and long-term implications|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1798–1800|issn=0195-668X|doi=10.1093/eurheartj/ehaa231}}</ref> According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.<ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>

==== Signs and Symptoms: ====
Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).

*'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent of patients.<ref name="pmid32044814">{{cite journal| author=Liu K, Fang YY, Deng Y, Liu W, Wang MF, Ma JP | display-authors=etal| title=Clinical characteristics of novel coronavirus cases in tertiary hospitals in Hubei Province. | journal=Chin Med J (Engl) | year= 2020 | volume= 133 | issue= 9 | pages= 1025-1031 | pmid=32044814 | doi=10.1097/CM9.0000000000000744 | pmc=7147277 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32044814 }} </ref><ref name="pmid32201335">{{cite journal| author=Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G | display-authors=etal| title=Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic. | journal=J Am Coll Cardiol | year= 2020 | volume= 75 | issue= 18 | pages= 2352-2371 | pmid=32201335 | doi=10.1016/j.jacc.2020.03.031 | pmc=7198856 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32201335 }} </ref>
*'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|corrected QT interval]] (QTc) >500 milliseconds at the time of admittance.<ref name="pmid32320003">{{cite journal| author=Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW | display-authors=etal| title=Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. | journal=JAMA | year= 2020 | volume= | issue= | pages= | pmid=32320003 | doi=10.1001/jama.2020.6775 | pmc=7177629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32320003 }} </ref> However, in another study that involved 84 patients who got [[hydroxychloroquine]] and [[azithromycin]], the baseline QTc interval was 435 milliseconds before receiving these medications.<ref name="GiudicessiNoseworthy2020">{{cite journal|last1=Giudicessi|first1=John R.|last2=Noseworthy|first2=Peter A.|last3=Friedman|first3=Paul A.|last4=Ackerman|first4=Michael J.|title=Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19)|journal=Mayo Clinic Proceedings|volume=95|issue=6|year=2020|pages=1213–1221|issn=00256196|doi=10.1016/j.mayocp.2020.03.024}}</ref>
*'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent)<ref name="GoyalChoi2020">{{cite journal|last1=Goyal|first1=Parag|last2=Choi|first2=Justin J.|last3=Pinheiro|first3=Laura C.|last4=Schenck|first4=Edward J.|last5=Chen|first5=Ruijun|last6=Jabri|first6=Assem|last7=Satlin|first7=Michael J.|last8=Campion|first8=Thomas R.|last9=Nahid|first9=Musarrat|last10=Ringel|first10=Joanna B.|last11=Hoffman|first11=Katherine L.|last12=Alshak|first12=Mark N.|last13=Li|first13=Han A.|last14=Wehmeyer|first14=Graham T.|last15=Rajan|first15=Mangala|last16=Reshetnyak|first16=Evgeniya|last17=Hupert|first17=Nathaniel|last18=Horn|first18=Evelyn M.|last19=Martinez|first19=Fernando J.|last20=Gulick|first20=Roy M.|last21=Safford|first21=Monika M.|title=Clinical Characteristics of Covid-19 in New York City|journal=New England Journal of Medicine|volume=382|issue=24|year=2020|pages=2372–2374|issn=0028-4793|doi=10.1056/NEJMc2010419}}</ref>

*'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].<ref name="pmid32219356">{{cite journal| author=Guo T, Fan Y, Chen M, Wu X, Zhang L, He T | display-authors=etal| title=Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). | journal=JAMA Cardiol | year= 2020 | volume= | issue= | pages= | pmid=32219356 | doi=10.1001/jamacardio.2020.1017 | pmc=7101506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32219356 }} </ref>
*'''Cardiac Arrest:''' According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of [[COVID-19]], 362 cases of out-of-hospital [[cardiac arrest]] were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital [[cardiac arrest]] were reported, which means an increment of 58% was observed in 2020 among [[COVID-19]] patients.<ref name="BaldiSechi2020">{{cite journal|last1=Baldi|first1=Enrico|last2=Sechi|first2=Giuseppe M.|last3=Mare|first3=Claudio|last4=Canevari|first4=Fabrizio|last5=Brancaglione|first5=Antonella|last6=Primi|first6=Roberto|last7=Klersy|first7=Catherine|last8=Palo|first8=Alessandra|last9=Contri|first9=Enrico|last10=Ronchi|first10=Vincenza|last11=Beretta|first11=Giorgio|last12=Reali|first12=Francesca|last13=Parogni|first13=Pierpaolo|last14=Facchin|first14=Fabio|last15=Bua|first15=Davide|last16=Rizzi|first16=Ugo|last17=Bussi|first17=Daniele|last18=Ruggeri|first18=Simone|last19=Oltrona Visconti|first19=Luigi|last20=Savastano|first20=Simone|title=Out-of-Hospital Cardiac Arrest during the Covid-19 Outbreak in Italy|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMc2010418}}</ref> According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe [[COVID-19]], 151 patients developed in-hospital [[cardiac arrest]]. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), [[Pulseless electrical activity]] in 6 patients (4.4%), and [[asystole]] in 122 [[COVID-19]] patients (89.7%).<ref name="ShaoXu2020">{{cite journal|last1=Shao|first1=Fei|last2=Xu|first2=Shuang|last3=Ma|first3=Xuedi|last4=Xu|first4=Zhouming|last5=Lyu|first5=Jiayou|last6=Ng|first6=Michael|last7=Cui|first7=Hao|last8=Yu|first8=Changxiao|last9=Zhang|first9=Qing|last10=Sun|first10=Peng|last11=Tang|first11=Ziren|title=In-hospital cardiac arrest outcomes among patients with COVID-19 pneumonia in Wuhan, China|journal=Resuscitation|volume=151|year=2020|pages=18–23|issn=03009572|doi=10.1016/j.resuscitation.2020.04.005}}</ref>

==== Diagnostic Testing: ====

*'''ECG:''' Most patients with the severe COVID-19, and especially patients who receive QT-prolonging medications, should have a baseline electrocardiogram (ECG) performed at the time of admission to the hospital.<ref name="GandhiSolomon2020">{{cite journal|last1=Gandhi|first1=Rajesh T.|last2=Solomon|first2=Caren G.|last3=Lynch|first3=John B.|last4=del Rio|first4=Carlos|title=Mild or Moderate Covid-19|journal=New England Journal of Medicine|year=2020|issn=0028-4793|doi=10.1056/NEJMcp2009249}}</ref>The best technique to get the QT interval is with a 12-lead electrocardiogram (ECG). However, to scale back exposure to hospital workers, this could not perpetually be possible. A single-lead ECG might underestimate the QT interval, and there ought to be an effort to use a multiple-lead telemetry system to observe the QT interval.<ref name="ChangSaleh2020">{{cite journal|last1=Chang|first1=David|last2=Saleh|first2=Moussa|last3=Gabriels|first3=James|last4=Ismail|first4=Haisam|last5=Goldner|first5=Bruce|last6=Willner|first6=Jonathan|last7=Beldner|first7=Stuart|last8=Mitra|first8=Raman|last9=John|first9=Roy|last10=Epstein|first10=Laurence M.|title=Inpatient Use of Ambulatory Telemetry Monitors for COVID-19 Patients Treated With Hydroxychloroquine and/or Azithromycin|journal=Journal of the American College of Cardiology|volume=75|issue=23|year=2020|pages=2992–2993|issn=07351097|doi=10.1016/j.jacc.2020.04.032}}</ref>
*'''Transthoracic echocardiography:''' Transthoracic echocardiography is recommended for an inpatient with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest x-ray or CT-chest.<ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref>

==== Treatment:====

*'''Polymorphic Ventricular Tachycardia (torsades de pointes):''' All patients with torsades de pointes (TdP) should be determined if they are hemodynamically stable or unstable through immediate evaluation of the symptoms, vital signs, and level of consciousness.<ref name="PanchalBerg2018">{{cite journal|last1=Panchal|first1=Ashish R.|last2=Berg|first2=Katherine M.|last3=Kudenchuk|first3=Peter J.|last4=Del Rios|first4=Marina|last5=Hirsch|first5=Karen G.|last6=Link|first6=Mark S.|last7=Kurz|first7=Michael C.|last8=Chan|first8=Paul S.|last9=Cabañas|first9=José G.|last10=Morley|first10=Peter T.|last11=Hazinski|first11=Mary Fran|last12=Donnino|first12=Michael W.|title=2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care|journal=Circulation|volume=138|issue=23|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000613}}</ref>
**'''Unstable patients:''' Patients with COVID-19 with sustained torsades de pointes (TdP) usually become hemodynamically unstable, severely symptomatic because of perfusion failure, or pulseless and should be treated according to standard resuscitation algorithms, including cardioversion/defibrillation. Initial treatment with antiarrhythmic medications is not indicated for hemodynamically unstable or pulseless patients except intravenous (IV) magnesium.<ref name="PanchalBerg2018">{{cite journal|last1=Panchal|first1=Ashish R.|last2=Berg|first2=Katherine M.|last3=Kudenchuk|first3=Peter J.|last4=Del Rios|first4=Marina|last5=Hirsch|first5=Karen G.|last6=Link|first6=Mark S.|last7=Kurz|first7=Michael C.|last8=Chan|first8=Paul S.|last9=Cabañas|first9=José G.|last10=Morley|first10=Peter T.|last11=Hazinski|first11=Mary Fran|last12=Donnino|first12=Michael W.|title=2018 American Heart Association Focused Update on Advanced Cardiovascular Life Support Use of Antiarrhythmic Drugs During and Immediately After Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care|journal=Circulation|volume=138|issue=23|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000613}}</ref>
**'''Stable patients:''' In a patient with a single episode of TdP, treatment with IV magnesium along with correction of metabolic/electrolyte disturbances or removal of any inciting medications may be sufficient. The patient should be kept under observation until the electrolytes, and the QT interval nearly normalizes.

===Out-of-hospital cardiac arrest and Sudden Cardiac Death===

===Spontaneous Coronary Artery Dissection===

==References ==
<references />

File:Normalcxr.jpg

2020-06-11T21:14:18Z

Mandana Chitsazan:

Sandbox:Mitra

2020-06-11T20:53:36Z

Mandana Chitsazan:

__NOTOC__
{{Xyz}}

{{CMG}}; {{AE}}
==Overview==
There is no '''established''' system for the classification of [disease name].

<br />

==Classification==

There is no established system for the classification of [disease name].

OR

[Disease name] may be classified according to [classification method] into [number] subtypes/groups:
*[Group1]
*[Group2]
*[Group3]
*[Group4]

OR

[Disease name] may be classified into [large number > 6] subtypes based on:
*[Classification method 1]
*[Classification method 2]
*[Classification method 3]

[Disease name] may be classified into several subtypes based on:
*[Classification method 1]
*[Classification method 2]
*[Classification method 3]

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

'''If the staging system involves specific and characteristic findings and features:'''

According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

Cardiovascular Disorders and COVID-19

2020-06-11T20:50:16Z

Mandana Chitsazan: /* Complications */

__NOTOC__

{{CMG}} {{AE}} {{mitra}}{{MC}}

==Overview==

==Complications==

===Acute Coronary Syndromes===

===Heart Failure===

===Cardiogenic Shock===

===Myocarditis===

===Pericarditis===

===Arrhythmias===

==References==

Cardiovascular Disorders and COVID-19

2020-06-11T20:49:30Z

Mandana Chitsazan:

__NOTOC__

{{CMG}} {{AE}} {{mitra}}{{MC}}

==Overview==

==Complications==

===Acute Coronary Syndromes===
*
===Heart Failure===
===Cardiogenic Shock===
===Myocarditis===
===Pericarditis===
===Arrythmias===

==References==

Sandbox:Mitra

2020-06-11T20:07:47Z

Mandana Chitsazan:

__NOTOC__
{{Xyz}}

{{CMG}}; {{AE}}
==Overview==
There is no established system for the classification of [disease name].

OR

[Disease name] may be classified according to [classification method] into [number] subtypes/groups: [group1], [group2], [group3], and [group4].

OR

[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3].
[Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

If the staging system involves specific and characteristic findings and features:
According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

==Classification==

There is no established system for the classification of [disease name].

OR

[Disease name] may be classified according to [classification method] into [number] subtypes/groups:
*[Group1]
*[Group2]
*[Group3]
*[Group4]

OR

[Disease name] may be classified into [large number > 6] subtypes based on:
*[Classification method 1]
*[Classification method 2]
*[Classification method 3]

[Disease name] may be classified into several subtypes based on:
*[Classification method 1]
*[Classification method 2]
*[Classification method 3]

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

'''If the staging system involves specific and characteristic findings and features:'''

According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

Sandbox MC

2020-06-11T15:51:51Z

Mandana Chitsazan: /* Overview */

==Overview==

{{aliah}}{{mitra}}{{allahyar}}

{{mitra chitsazan}}

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

File:Snowman-sign-1.jpg

==Physical Examination==
Physical examination of patients with [disease name] is usually normal.

OR

Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

===Appearance of the Patient===
*Patients with PE usually appear normal/toxic.

===Vital Signs===

*High-grade
*Tachypnea / bradypnea
*Weak/bounding pulse / pulsus alternans / paradoxical pulse / asymmetric pulse

===Skin===
*[[Cyanosis]]

===HEENT===
*dilated pupils
*icteus

===Neck===
* Neck examination of patients with [disease name] is usually normal.
OR
*[[Jugular venous distension]]
*[[Carotid bruits]] may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope
*[[Lymphadenopathy]] (describe location, size, tenderness, mobility, and symmetry)
*[[Thyromegaly]] / thyroid nodules
*[[Hepatojugular reflux]]

===Lungs===
* Pulmonary examination of patients with [disease name] is usually normal.
OR
* Asymmetric chest expansion OR decreased chest expansion
*Lungs are hyporesonant OR hyperresonant
*Fine/coarse [[crackles]] upon auscultation of the lung bases/apices unilaterally/bilaterally
*Rhonchi
*Vesicular breath sounds OR distant breath sounds
*Expiratory wheezing OR inspiratory wheezing with normal OR delayed expiratory phase
*[[Wheezing]] may be present
*[[Egophony]] present/absent
*[[Bronchophony]] present/absent
*Normal/reduced [[tactile fremitus]]

===Heart===
*a low grade late systolic murmur

===Abdomen===
* Abdominal examination of patients with PE is usually normal.

===Back==

===Genitourinary===
* Genitourinary examination of patients with [disease name] is usually normal.
OR
*A pelvic/adnexal mass may be palpated
*Inflamed mucosa
*Clear/(color), foul-smelling/odorless penile/vaginal discharge

===Neuromuscular===
* Neuromuscular examination of patients with [disease name] is usually normal.
OR
*Patient is usually oriented to persons, place, and time
* Altered mental status
* Glasgow coma scale is ___ / 15
* Clonus may be present
* Hyperreflexia / hyporeflexia / areflexia
* Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
* Muscle rigidity
* Proximal/distal muscle weakness unilaterally/bilaterally
* ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
*Unilateral/bilateral upper/lower extremity weakness
*Unilateral/bilateral sensory loss in the upper/lower extremity
*Positive straight leg raise test
*Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
*Positive/negative Trendelenburg sign
*Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
*Normal finger-to-nose test / Dysmetria
*Absent/present dysdiadochokinesia (palm tapping test)

===Extremities===
* Extremities examination of patients with [disease name] is usually normal.
OR
*[[Clubbing]]
*[[Cyanosis]]
*Pitting/non-pitting [[edema]] of the upper/lower extremities
*Muscle atrophy
*Fasciculations in the upper/lower extremity

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

==Overview==
Patients with pulmonary emboli(PE) usually appear toxic. Physical examination of patients with PE is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

==Physical Examination==
Physical examination of patients with [disease name] is usually normal.

OR

Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

===Appearance of the Patient===
*Patients with pE usually appear toxic/normal.

===Vital Signs===

*Low-grade fever
*[[Hyperthermia]] / hyperthermia may be present
*[[Tachycardia]] with regular pulse or (ir)regularly irregular pulse
*[[Bradycardia]] with regular pulse or (ir)regularly irregular pulse
*Tachypnea / bradypnea

===Skin===
* Skin examination of patients with PE is usually normal.
OR
*[[Cyanosis]]
*[[Jaundice]]
* [[Pallor]]
* Bruises

<gallery widths="150px">

UploadedImage-01.jpg | Description {{dermref}}
UploadedImage-02.jpg | Description {{dermref}}

</gallery>

===HEENT===
* HEENT examination of patients with [disease name] is usually normal.
OR
* Abnormalities of the head/hair may include ___
* Evidence of trauma
* Icteric sclera
* [[Nystagmus]]
* Extra-ocular movements may be abnormal
*Pupils non-reactive to light / non-reactive to accommodation / non-reactive to neither light nor accommodation
*Ophthalmoscopic exam may be abnormal with findings of ___
* Hearing acuity may be reduced
*[[Weber test]] may be abnormal (Note: A positive Weber test is considered a normal finding / A negative Weber test is considered an abnormal finding. To avoid confusion, you may write "abnormal Weber test".)
*[[Rinne test]] may be positive (Note: A positive Rinne test is considered a normal finding / A negative Rinne test is considered an abnormal finding. To avoid confusion, you may write "abnormal Rinne test".)
* [[Exudate]] from the ear canal
* Tenderness upon palpation of the ear pinnae/tragus (anterior to ear canal)
*Inflamed nares / congested nares
* [[Purulent]] exudate from the nares
* Facial tenderness
* Erythematous throat with/without tonsillar swelling, exudates, and/or petechiae

===Neck===
* Neck examination of patients with [disease name] is usually normal.
OR
*[[Jugular venous distension]]
*[[Carotid bruits]] may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope
*[[Lymphadenopathy]] (describe location, size, tenderness, mobility, and symmetry)
*[[Thyromegaly]] / thyroid nodules
*[[Hepatojugular reflux]]

===Lungs===
* Pulmonary examination of patients with [disease name] is usually normal.
OR
* Asymmetric chest expansion OR decreased chest expansion
*Lungs are hyporesonant OR hyperresonant
*Fine/coarse [[crackles]] upon auscultation of the lung bases/apices unilaterally/bilaterally
*Rhonchi
*Vesicular breath sounds OR distant breath sounds
*Expiratory wheezing OR inspiratory wheezing with normal OR delayed expiratory phase
*[[Wheezing]] may be present
*[[Egophony]] present/absent
*[[Bronchophony]] present/absent
*Normal/reduced [[tactile fremitus]]

===Heart===
* Cardiovascular examination of patients with [disease name] is usually normal.
OR
*Chest tenderness upon palpation
*PMI within 2 cm of the sternum (PMI) / Displaced point of maximal impulse (PMI) suggestive of ____
*[[Heave]] / [[thrill]]
*[[Friction rub]]
*[[Heart sounds#First heart tone S1, the "lub"(components M1 and T1)|S1]]
*[[Heart sounds#Second heart tone S2 the "dub"(components A2 and P2)|S2]]
*[[Heart sounds#Third heart sound S3|S3]]
*[[Heart sounds#Fourth heart sound S4|S4]]
*[[Heart sounds#Summation Gallop|Gallops]]
*A high/low grade early/late [[systolic murmur]] / [[diastolic murmur]] best heard at the base/apex/(specific valve region) may be heard using the bell/diaphgram of the stethoscope

===Abdomen===
* Abdominal examination of patients with [disease name] is usually normal.
OR
*[[Abdominal distension]]
*[[Abdominal tenderness]] in the right/left upper/lower abdominal quadrant
*[[Rebound tenderness]] (positive Blumberg sign)
*A palpable abdominal mass in the right/left upper/lower abdominal quadrant
*Guarding may be present
*[[Hepatomegaly]] / [[splenomegaly]] / [[hepatosplenomegaly]]
*Additional findings, such as obturator test, psoas test, McBurney point test, Murphy test

===Back===
* Back examination of patients with [disease name] is usually normal.
OR
*Point tenderness over __ vertebrae (e.g. L3-L4)
*Sacral edema
*Costovertebral angle tenderness bilaterally/unilaterally
*Buffalo hump

===Genitourinary===
* Genitourinary examination of patients with [disease name] is usually normal.
OR
*A pelvic/adnexal mass may be palpated
*Inflamed mucosa
*Clear/(color), foul-smelling/odorless penile/vaginal discharge

===Neuromuscular===
* Neuromuscular examination of patients with [disease name] is usually normal.
OR
*Patient is usually oriented to persons, place, and time
* Altered mental status
* Glasgow coma scale is ___ / 15
* Clonus may be present
* Hyperreflexia / hyporeflexia / areflexia
* Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
* Muscle rigidity
* Proximal/distal muscle weakness unilaterally/bilaterally
* ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
*Unilateral/bilateral upper/lower extremity weakness
*Unilateral/bilateral sensory loss in the upper/lower extremity
*Positive straight leg raise test
*Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
*Positive/negative Trendelenburg sign
*Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
*Normal finger-to-nose test / Dysmetria
*Absent/present dysdiadochokinesia (palm tapping test)

===Extremities===
* Extremities examination of patients with [disease name] is usually normal.
OR
*[[Clubbing]]
*[[Cyanosis]]
*Pitting/non-pitting [[edema]] of the upper/lower extremities
*Muscle atrophy
*Fasciculations in the upper/lower extremity

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

This is my sandbox <ref name="urlBiomedical citation maker">{{cite web |url=http://sumsearch.org/cite/ |title=Biomedical citation maker |format= |work= |accessdate=}}</ref><ref name="pmid25387321">{{cite journal| author=Jokinen E| title=Obesity and cardiovascular disease. | journal=Minerva Pediatr | year= 2015 | volume= 67 | issue= 1 | pages= 25-32 | pmid=25387321 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25387321 }} </ref>.

Hello <ref name="pmid22874472">{{cite journal| author=Maron BJ, Maron MS| title=Hypertrophic cardiomyopathy. | journal=Lancet | year= 2013 | volume= 381 | issue= 9862 | pages= 242-55 | pmid=22874472 | doi=10.1016/S0140-6736(12)60397-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22874472 }} </ref>.

[[File:Cardiomyopathy.jpg|left|200px]]

{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Physical examination
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Cardiac murmur
! align="center" style="background:#4479BA; color: #FFFFFF;" + |ECG
! align="center" style="background:#4479BA; color: #FFFFFF;" + |CXR
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Echocardiography
|-
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Aortic valve stenosis]]'''
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
*Exertional chest pain
*Dyspnea on exertion
*Decreased exercise tolerance
*Exertional syncope/pre-syncope
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
*Narrow pulse pressure
*Normal to anacrotic carotid pulse (parvus et tardus)
*S1 usually normal
*A systolic ejection click may be audible afer S1
*Single S2
*If severe: paradoxical splitting of S2
*S4 may be audible
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
*Mid-to-late peaking systolic ejection murmur
*Best heard at right intercostal space
*Radiates equally to the carotid arteries
*Decseases with Valsalva maneuver
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
*Left ventricular hypertrophy
*Left ventricular strain pattern
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
*Left ventricualar hypertrophy
*If heart failure is present: pulmonary congestion
*Aortic valve calcification may be visible
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
* '''Mild AS''': Aortic Vmax 2.0-2.9 m/s or mean ΔP <20 mmHg
* '''Moderate AS''': Aortic Vmax 3.0-3.9 m/s or mean ΔP 20-39 mmHg
* '''Severe AS''': Aortic Vmax ≥ 4 m/s or mean ΔP ≥40 mmHg; AVA typically ≤ 1.0 cm<sup>2</sup> (or AVAi ≤ 0.6 cm<sup>2</sup>/m<sup>2)
* '''Very severe AS''': Aortic Vmax ≥ 5 m/s or mean ΔP ≥60 mmHg
*Ejection fraction (EF) may be normal or reduced
|-
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Aortic valve sclerosis without stenosis]]'''
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Supvalvular stenosis]]'''
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Supravalvular stenosis]]'''
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Hypertrophic cardiomyopathy]]'''
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" |
|-

|}

constrictive cardiomyopathy should be differentiated from restrictive cardiomyopathy<ref name="pmid29270320">{{cite journal |vauthors=Rammos A, Meladinis V, Vovas G, Patsouras D |title=Restrictive Cardiomyopathies: The Importance of Noninvasive Cardiac Imaging Modalities in Diagnosis and Treatment-A Systematic Review |journal=Radiol Res Pract |volume=2017 |issue= |pages=2874902 |date=2017 |pmid=29270320 |pmc=5705874 |doi=10.1155/2017/2874902 |url=}}</ref>,<ref name="pmid28885342">{{cite journal |vauthors=Hong JA, Kim MS, Cho MS, Choi HI, Kang DH, Lee SE, Lee GY, Jeon ES, Cho JY, Kim KH, Yoo BS, Lee JY, Kim WJ, Kim KH, Chung WJ, Lee JH, Cho MC, Kim JJ |title=Clinical features of idiopathic restrictive cardiomyopathy: A retrospective multicenter cohort study over 2 decades |journal=Medicine (Baltimore) |volume=96 |issue=36 |pages=e7886 |date=September 2017 |pmid=28885342 |pmc=6393124 |doi=10.1097/MD.0000000000007886 |url=}}</ref>

{| class="wikitable"
|+Differentiating restrictive cardiomyopathy from Other Diseases
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Type of disease'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''History'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Physical examination'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Chest X-ray'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''ECG'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''2D echo'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Doppler echo'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''CT'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''MRI'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Catheterization hemodynamics'''}}
| align="center" style="background: #4479BA;" | {{fontcolor|#FFF|'''Biopsy'''}}

|-
|'''Restrictive cardiomyopathy'''<ref name="pmid29270320">{{cite journal |vauthors=Rammos A, Meladinis V, Vovas G, Patsouras D |title=Restrictive Cardiomyopathies: The Importance of Noninvasive Cardiac Imaging Modalities in Diagnosis and Treatment-A Systematic Review |journal=Radiol Res Pract |volume=2017 |issue= |pages=2874902 |date=2017 |pmid=29270320 |pmc=5705874 |doi=10.1155/2017/2874902 |url=}}</ref><ref name="pmid12531876">{{cite journal |vauthors=Mogensen J, Kubo T, Duque M, Uribe W, Shaw A, Murphy R, Gimeno JR, Elliott P, McKenna WJ |title=Idiopathic restrictive cardiomyopathy is part of the clinical expression of cardiac troponin I mutations |journal=J. Clin. Invest. |volume=111 |issue=2 |pages=209–16 |date=January 2003 |pmid=12531876 |pmc=151864 |doi=10.1172/JCI16336 |url=}}</ref><ref name="pmid28885342">{{cite journal |vauthors=Hong JA, Kim MS, Cho MS, Choi HI, Kang DH, Lee SE, Lee GY, Jeon ES, Cho JY, Kim KH, Yoo BS, Lee JY, Kim WJ, Kim KH, Chung WJ, Lee JH, Cho MC, Kim JJ |title=Clinical features of idiopathic restrictive cardiomyopathy: A retrospective multicenter cohort study over 2 decades |journal=Medicine (Baltimore) |volume=96 |issue=36 |pages=e7886 |date=September 2017 |pmid=28885342 |pmc=6393124 |doi=10.1097/MD.0000000000007886 |url=}}</ref>
|Systemic disease (e.g., [[sarcoidosis]], [[hemochromatosis]]).
|
* ± [[Kussmaul sign]] [[S3 gallop|S3]] and [[S4]] [[Gallop rhythm|gallop]], [[murmurs]] of [[Mitral regurgitation|mitral]] and [[tricuspid regurgitation]]
|[[Atrial|Atrial dilatation]]
|[[Low QRS voltage|Low QRS voltages]] (mainly [[amyloidosis]]), [[Conduction disorders|conduction disturbances]], [[Nonspecific ST-Segment and T-Wave Changes|nonspecific ST abnormalities]]
|± Wall and valvular thickening, sparkling [[myocardium]]
|Decreased variation in [[mitral]] and/or [[tricuspid]] inflow ''E'' velocity, increased [[hepatic vein]] [[Inspiration|inspiratory]] [[diastolic]] flow reversal, presence of [[Mitral regurgitation|mitral]] and [[tricuspid regurgitation]]
|Normal [[pericardium]]
|Measurement of [[iron overload]], various types of LGE (late [[gadolinium]] enhancement)
|LVEDP – RVEDP ≥ 5 mmHg

RVSP ≥ 55 mmHg

RVEDP/RVSP ≤ 0.33
|May reveal underlying cause.
|-
|'''Constrictive pericarditis'''<ref name="pmid30344956">{{cite journal |vauthors=Ramasamy V, Mayosi BM, Sturrock ED, Ntsekhe M |title=Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis |journal=World J Cardiol |volume=10 |issue=9 |pages=87–96 |date=September 2018 |pmid=30344956 |pmc=6189073 |doi=10.4330/wjc.v10.i9.87 |url=}}</ref><ref name="pmid26613929">{{cite journal |vauthors=Biçer M, Özdemir B, Kan İ, Yüksel A, Tok M, Şenkaya I |title=Long-term outcomes of pericardiectomy for constrictive pericarditis |journal=J Cardiothorac Surg |volume=10 |issue= |pages=177 |date=November 2015 |pmid=26613929 |pmc=4662820 |doi=10.1186/s13019-015-0385-8 |url=}}</ref><ref name="pmid26613929">{{cite journal |vauthors=Biçer M, Özdemir B, Kan İ, Yüksel A, Tok M, Şenkaya I |title=Long-term outcomes of pericardiectomy for constrictive pericarditis |journal=J Cardiothorac Surg |volume=10 |issue= |pages=177 |date=November 2015 |pmid=26613929 |pmc=4662820 |doi=10.1186/s13019-015-0385-8 |url=}}</ref>
|
* Prior history of [[pericarditis]] or conditions affecting the [[pericardium]], such as uremia, HIV, TB, or radiation
|
*[[Pericardium|Pericardial]] knock
|
*[[Pericardial calcification]]
|
*[[Nonspecific ST-Segment and T-Wave Changes|Nonspecific ST and T abnormalities]], [[low QRS voltage]] (<50%)
|
* ± [[Pericardial]] thickening, [[respiratory]] [[ventricular]] septal shift.
|
* Increased variation in [[mitral]] and/or [[tricuspid]] inflow ''E'' velocity, [[hepatic vein]] [[Expiration|expiratory]] [[diastolic]] reversal ratio ≥ 0.79 medial ''e''′/lateral ''e''′ ≥ 0.91 (Annulus Reversus)
|
* Thickened/calcified [[pericardium]]
|
* Thickened pericardium
|
* LVEDP – RVEDP < 5 mmHg

* RVSP < 55 mmHg

* RVEDP/RVSP > 0.33

* Inspiratory decrease in RAP < 5 mmHg

* Systolic area index > 1.1 (Ref CP in the modern era)

* Left ventricular height of rapid filling wave > 7 mmHg
|
* Normal myocardium
|}

Template:Allahyar

2020-06-11T15:50:49Z

Mandana Chitsazan:

[[User:Allahyar|Allahyar]]
[mailto:allahyar2329@gmail.com]

Template:Allahyar

2020-06-11T15:48:01Z

Mandana Chitsazan: Created page with "Allahyar [mailto: allahyar2329@gmail.com]"

[[User:Allahyar|Allahyar]]
[mailto: allahyar2329@gmail.com]

Template:Aliah

2020-06-11T15:44:16Z

Mandana Chitsazan: Created page with "Alieh Bahjat,M.D. [mailto:aliabahjatmd@gmail.com]"

[[User:Alieh Bahjat|Alieh Bahjat,M.D.]]
[mailto:aliabahjatmd@gmail.com]

Sandbox: GDS

2020-06-11T14:32:49Z

Mandana Chitsazan:

__NOTOC__
{{Frequently Asked Inpatient Questions}}
{{CMG}}{{AE}}{{GDS}}{{Aisha}}{{HAR}}{{RAB}}{{Nuha}}{{IF}}{{MC}}
==Treatment Based Questions==
====I read about the retraction of the two articles that halted the use of hydroxychloroquine in COVID-19 patients, can I currently receive this medication if infected?====
====Does every patient with a positive COVID-19 test need to be admitted to the hospital?====
====What are the chances of recovery in a hospital admitted COVID-19 patient?====
====Are antibiotics effective in preventing or treating COVID-19?====
====What anti-viral medications are available to treat COVID-19?====
====Should I take ivermectin to prevent or treat COVID-19?====
==Complications Based Questions==
====What population is most at risk for severe disease from COVID-19?====
====What risk factors result in severe complications from COVID-19?====
====Will I be placed on a ventilator?====
====What systems other than the Respiratory system can be involved?====
====Does prolonged ventilation in hospitalized patients worsen the outcome of COVID-19?====
====Am I at risk for serious complications from COVID-19 if I smoke cigarettes?====
====If I vape tobacco or nicotine am I at risk for complications from COVID-19?====

==Co-Morbidity Based Questions==

=== <u>Patients with Hypertension</u> ===

====Should I stop my ACE Inhibitors and ARBs while on admission for COVID-19?====

=== <u>Patients with Asthma</u> ===

====If I experience an Asthma exacerbation, should that exacerbation be treated any differently to reduce the risk of COVID-19?====

==== Are any changes recommended to my treatment plan if a paitent with asthma has COVID 19? ====

=== <u>Patients currently Undergoing Hemodialysis</u> ===

===Can I continue receiving Hemodialysis in a hospital where other COVID-19 patients are treated?===

=== <u>Cancer Patients</u> ===

==== Can/Should Cancer surgery be delayed? What about radiation therapy? ====

==== Should treatment that suppresses my immune system be stopped or delayed? ====

==== Are the support groups or activites still available in the hospital? ====

==== Should I be taking an antiviral medication such as Tami flu for protection? ====

==Hospital Discharge Related Questions==
====I no longer have symptoms but my tests still came back positive for COVID-19, can I be discharged?====
====If after discharge I show new symptoms of COVID-19, should I be isolated and tested again?====
====If after discharge, a close contact test positive, should I self-isolate again?====
====After I have been discharged, should I continue to wear a face mask?====
====After discharge, how soon can I get back to my job?====
====After discharge can I use public places and transportation?====
====What can I expect after I leave the hospital?====

==Re-Infection Related Questions==
====Do I become immune after I have recovered from COVID-19?====
====Is re-infection worse than the initial infection?====
====Will a re-infected person show the same symptoms as the initial infection?====
====Are clinically recovered persons infectious to others if they test persistently or recurrently positive for SARS-COV-2 RNA?====

==Pregnancy Related Questions==
====If I deliver in the hospital will that increase my chances or my baby's chances of contracting COVID-19?====
====Should intrapartum fever be considered as a possible sign of COVID-19 infection?====
====I am currently pregnant and hospitalized due to COVID-19, is my unborn child infected?====
====What is the guidance available for labor and delivery Health Care Personnel with potential exposure in a healthcare setting to patients with COVID-19 infection?====
====Are Pregnant healthcare personnel at increased risk for adverse outcomes if they care for patients with COVID-19 infection?====
====Can I proceed with a scheduled cesarean delivery if hospitalized with COVID-19?====
====Are glucocorticoids contraindicated in pregnant patients with COVID-19?====
====Are pregnant women more susceptible to infection or at increased risk for severe illness, morbidity, or mortality with COVID-19?====
====I have heard that some hospitals are testing all women for COVID-19 who arrive at the hospital for labor—even women without any symptoms. Will I be tested?====
====If I contract COVID-19, will I still be able to breastfeed?====
====How many people can be present in the room during my birth?====
====If I have COVID-19 at the time of my birth, will my baby be able to stay with me?====
====Can COVID-19 be transmitted via breastmilk?====

==Pediatrics Related Questions==
====My child has congenital heart disease, is he at increased risk of COVID-19?====
====Are children with underlying conditions at increased risk of hospitalization?====
====I am currently hospitalized due to COVID-19, can I breastfeed my infant child?====
====What is KAWASAKI disease? What is the association with COVID-19?====
====What is a multisystem inflammatory syndrome? What is the association with COVID-19?====

==== Should routinely recommended Hepatitis A and B vaccines continue to be administered to the children? ====

==== Should vaccinations for HBV exposed infants be continued during the COVID 19 pandemic? ====

==Visitors Related Questions==
====Can I have visitors while I’m in the hospital?====
====Is there anything I can to do to help others who have COVID-19?====

==== I would like to accompany my family member or friend for their procedure or appointments I am concerned they will need my support to cope or understand the information being shared with them by the healthcare team ====

==General In-Patient Questions==
====Does being hospitalized with other COVID-19 patients worsen my outcome?====
====What are the diet recommendations if I get hospitalized?====
====What can I expect while I’m in the hospital?====
====When can I leave the hospital?====
====Is blood been tested for COVID-19 before blood transfusion?====
====Do wastewater & sewage workers need additional protection when handling untreated waste from hospitals with COVID-19 patients?====

==Management of Dead Bodies from COVID-19?==
====Do any special procedures exist for the management of bodies of persons who died from COVID-19?====

==Health Care Practitioner (HCP) questions==
====I have underlying health conditions, are there work restrictions in place for me?====
====Is post-exposure prophylaxis currently available, and when can it be used?====
====Can routine vaccinations still be administered to patients?====
====Should I use face mask/respirator while taking care of pregnant patients with known/suspected COVID-19 infection?====
====I am a Health Care Practitioner living with someone who is at a higher risk of severe illness from COVID-19 infection. What precautions should I take?====
====I am pregnant and a health care worker. Can I work with patients who are potentially infected with COVID-19?====
====Whom should healthcare providers notify if they suspect a patient has COVID-19?====
====Is remdesivir approved by the FDA to treat COVID-19?====
====Are there data showing remdesivir might benefit patients with COVID-19?====
====Are chloroquine phosphate or hydroxychloroquine sulfate approved by the FDA to treat COVID-19?====
====Are there data showing that chloroquine phosphate or hydroxychloroquine sulfate might benefit patients with COVID-19?====