Pulseless ventricular tachycardia overview: Difference between revisions

Jump to navigation Jump to search
 
(13 intermediate revisions by the same user not shown)
Line 12: Line 12:
{{CMG}}; {{AE}}{{Aisha}}
{{CMG}}; {{AE}}{{Aisha}}
==Overview==
==Overview==
Pulseless ventricular tachycardia is an often fatal cardiac [[dysrhythmia]] where the regular rhythmic [[contraction]] of the [[heart]] is replaced by non-rhythmic, faster, yet inadequate contractions. In 1906 Gallavardin discovered the reasons behind the [[cardiac]] [[instability]] which leads to ventricular tachycardia, and put forth the idea that VT could convert into [[ventricular fibrillation]], pulselessness and sudden death. In 1909,Thomas Lewis gave the first [[electrocardiographic]] description of ventricular tachycardia. It was also first implied in 1921 that [[coronary]] occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia do not appropriately perfuse the organ, leading to [[ischemia]] as well as [[heart failure]]. This condition requires immediate medical attention as it is an emergency and can lead to [[ventricular fibrillation]] and [[sudden death]].<ref name="pmid32119354">{{cite journal |vauthors=Foglesong A, Mathew D |title= |journal= |volume= |issue= |pages= |date= |pmid=32119354 |doi= |url=}}</ref>
Pulseless ventricular tachycardia is an often fatal cardiac [[dysrhythmia]] where the regular rhythmic [[contraction]] of the [[heart]] is replaced by non-rhythmic, faster, yet inadequate contractions. In 1906 Gallavardin discovered the reasons behind the [[cardiac]] [[instability]] which leads to ventricular tachycardia, and put forth the idea that VT could convert into [[ventricular fibrillation]], pulselessness and sudden death. In 1909,Thomas Lewis gave the first [[electrocardiographic]] description of ventricular tachycardia. It was also first implied in 1921 that [[coronary]] occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia do not appropriately perfuse the organ, leading to [[ischemia]] as well as [[heart failure]]. This condition requires immediate medical attention as it is an emergency and can lead to [[ventricular fibrillation]] and [[sudden death]].
As a result of markedly rapid ventricular contractions, [[diastole]] is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in [[cardiac output]], and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, [[wide complex tachycardia|wide QRS complexes]] above 120 milliseconds, the [[dissociation]] between the [[atria]] and [[ventricles]], presence of fusion beats, and an electrical axis between -90 to -180.<ref name="pmid32119354">{{cite journal |vauthors=Foglesong A, Mathew D |title= |journal= |volume= |issue= |pages= |date= |pmid=32119354 |doi= |url=}}</ref> Because majority of wide complex tachycardia cases will be ventricular tachycardia, any [[wide complex tachycardia]] should always be assumed to be due to ventricular tachycardia until proven otherwise.
As a result of markedly rapid ventricular contractions, [[diastole]] is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in [[cardiac output]], and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, [[wide complex tachycardia|wide QRS complexes]] above 120 milliseconds, the [[dissociation]] between the [[atria]] and [[ventricles]], presence of fusion beats, and an electrical axis between -90 to -180. Because the majority of wide complex tachycardia cases will be ventricular tachycardia, any [[wide complex tachycardia]] should always be assumed to be due to ventricular tachycardia until proven otherwise.


==Historical Perspective==
==Historical Perspective==
* There is limited information about the historical perspective of Pulseless ventricular tachycardia.
There is limited information about the historical perspective of Pulseless ventricular tachycardia.
 
* Gallavardin in 1906 was responsible for the discovery of the rationale behind cardiac instability leading to ventricular tachycardia. He further put forth the idea that ventricular tachycardia could convert to ventricular fibrillation and lead to cardiac arrest and death.
 
*The first electrographic description of ventricular tachycardia was given by Thomas Lewis in 1909.
 
*Coronary occlusion was suggested to be the main cause of ventricular tachycardia in 1921.
 
*Several advancements have since been made in the diagnosis and management protocols on Ventricular tachycardia.
<ref name="urlVentricular tachycardia historical perspective - wikidoc">{{cite web |url=https://www.wikidoc.org/index.php/Ventricular_tachycardia_historical_perspective |title=Ventricular tachycardia historical perspective - wikidoc |format= |work= |accessdate=}}</ref>


==Classification==
==Classification==
Line 31: Line 22:


==Pathophysiology==
==Pathophysiology==
Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]]. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal [[resting membrane potential]]. The higher the reduction in [[membrane potential]], the faster and more rapid the already abnormal [[automaticity]].<ref name="pmid4237287">{{cite journal |vauthors=Armendares S, Pérez Treviño C |title=[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)] |language=Spanish; Castilian |journal=Arch Inst Cardiol Mex |volume=38 |issue=6 |pages=779–91 |date=1968 |pmid=4237287 |doi= |url=}}</ref> Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on [[afterdepolarizations]] (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: [[Early afterdepolarizations]](EAD) and [[Delayed afterdepolarizations]] (DAD). When either of these afterdepolarizations become high enough to reach the [[membrane threshold]], they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.<ref name="pmid1855225">{{cite journal |vauthors=Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A |title=Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7 |journal=Cancer Res. |volume=51 |issue=15 |pages=4097–101 |date=August 1991 |pmid=1855225 |doi= |url=}}</ref>
Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]].
 
In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.<ref name="pmid32119354">{{cite journal |vauthors=Foglesong A, Mathew D |title= |journal= |volume= |issue= |pages= |date= |pmid=32119354 |doi= |url=}}</ref>


==Causes==
==Causes==
[[Structural heart disease]] is the most common cause of [[pulseless ventricular tachycardia]]. Other causes include but are not limited to,  drugs/medications, [[congenital heart diseases]], not to mention congenital and inherited [[channelopathies]]. It is important to note that [[QT interval]] lengthening medications, as well as [[electrolyte]] disturbances, can also result in pulseless ventricular tachycardia.<ref name="pmid27484660">{{cite journal |vauthors=Baldzizhar A, Manuylova E, Marchenko R, Kryvalap Y, Carey MG |title=Ventricular Tachycardias: Characteristics and Management |journal=Crit Care Nurs Clin North Am |volume=28 |issue=3 |pages=317–29 |date=September 2016 |pmid=27484660 |doi=10.1016/j.cnc.2016.04.004 |url=}}</ref>
[[Structural heart disease]] is the most common cause of [[pulseless ventricular tachycardia]]. Other causes include but are not limited to,  drugs/medications, [[congenital heart diseases]], not to mention congenital and inherited [[channelopathies]]. It is important to note that [[QT interval]] lengthening medications, as well as [[electrolyte]] disturbances, can also result in pulseless ventricular tachycardia.
 
===Life-threatening Causes===
*Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. They are mainly due to acute conditions that promote rapid dysfunction of automaticity and include. but are not limited to;<ref name="AjijolaTung2014">{{cite journal|last1=Ajijola|first1=Olujimi A.|last2=Tung|first2=Roderick|last3=Shivkumar|first3=Kalyanam|title=Ventricular tachycardia in ischemic heart disease substrates|journal=Indian Heart Journal|volume=66|year=2014|pages=S24–S34|issn=00194832|doi=10.1016/j.ihj.2013.12.039}}</ref><ref name="Meja LopezMalhotra2019">{{cite journal|last1=Meja Lopez|first1=Eliany|last2=Malhotra|first2=Rohit|title=Ventricular Tachycardia in Structural Heart Disease|journal=Journal of Innovations in Cardiac Rhythm Management|volume=10|issue=8|year=2019|pages=3762–3773|issn=21563977|doi=10.19102/icrm.2019.100801}}</ref><ref name="CoughtrieBehr2017">{{cite journal|last1=Coughtrie|first1=Abigail L|last2=Behr|first2=Elijah R|last3=Layton|first3=Deborah|last4=Marshall|first4=Vanessa|last5=Camm|first5=A John|last6=Shakir|first6=Saad A W|title=Drugs and life-threatening ventricular arrhythmia risk: results from the DARE study cohort|journal=BMJ Open|volume=7|issue=10|year=2017|pages=e016627|issn=2044-6055|doi=10.1136/bmjopen-2017-016627}}</ref><ref name="El-Sherif2001">{{cite journal|last1=El-Sherif|first1=Nabil|title=Mechanism of Ventricular Arrhythmias in the Long QT Syndrome: On Hermeneutics|journal=Journal of Cardiovascular Electrophysiology|volume=12|issue=8|year=2001|pages=973–976|issn=1045-3873|doi=10.1046/j.1540-8167.2001.00973.x}}</ref><ref name="urlVentricular tachycardia causes - wikidoc">{{cite web |url=https://www.wikidoc.org/index.php/Ventricular_tachycardia_causes |title=Ventricular tachycardia causes - wikidoc |format= |work= |accessdate=}}</ref>


*[[Acute coronary syndrome]]
==Differentiating pulseless ventricular tachycardia from Other Diseases==
*[[Congestive heart failure]]
Pulseless ventricular tachycardia must be differentiated from other diseases that cause [[wide complex tachycardia]], such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia
*[[NSTEMI]]
*[[STEMI]]
*[[Unstable angina]]
 
===Common Causes===  
*[[Acid-base disturbances]]
*[[Antiarrhythmics]]
*[[Azithromycin]]
*[[Cardioversion]]
*[[Clarithromycin]]
*[[Claritin]]
*[[Cocaine]]
*[[Congestive heart failure]]
*[[Dilated cardiomyopathy]]
*[[Erythromycin]]
*[[Hypokalemia]]
*[[Hypomagnesemia]]
*[[Myocarditis]]
*[[Obstructive sleep apnea]]
*[[Pulmonary artery catheter]]
*[[STEMI]]
*[[Tricyclic antidepressants]]
 
==Differentiating Xyz from Other Diseases==


==Epidemiology and Demographics==
==Epidemiology and Demographics==
*Ventricular tachycardia and ventricular fibrillation<ref name="pmid29173411">{{cite journal |vauthors=Tang PT, Shenasa M, Boyle NG |title=Ventricular Arrhythmias and Sudden Cardiac Death |journal=Card Electrophysiol Clin |volume=9 |issue=4 |pages=693–708 |date=December 2017 |pmid=29173411 |doi=10.1016/j.ccep.2017.08.004 |url=}}</ref> are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn't account for deaths due to unwitnessed dysrhythmias.<ref name="pmid21796098">{{cite journal |vauthors=McNally B, Robb R, Mehta M, Vellano K, Valderrama AL, Yoon PW, Sasson C, Crouch A, Perez AB, Merritt R, Kellermann A |title=Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010 |journal=MMWR Surveill Summ |volume=60 |issue=8 |pages=1–19 |date=July 2011 |pmid=21796098 |doi= |url=}}</ref>
Ventricular tachycardia and ventricular fibrillation are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn't account for deaths due to unwitnessed dysrhythmias. The majority of deaths due to ventricular arrhythmias occur In adults over 35 years of age.
*The majority of deaths due to ventricular arrhythmias occur In adults over 35 years of afe.


==Risk Factors==
==Risk Factors==
Risk factors for [[pulseless ventricular tachycardia]] as a cause of [[wide complex tachycardia]] includes any disease or condition that stresses or damages [[myocardial]] tissue. A family history of [[ventricular tachycardia]] or other [[rhythm]] disturbances may increase risk, while some lifestyle changes or medications may decrease risk.


==Screening==
==Screening==
According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms such as
According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms or has a positive family history of conditions like [[Long QT syndrome|QT syndrome]], [[Hypertrophic cardiomyopathy|hypertrophic]], [[dilated cardiomyopathy]] and right ventricular dysplasia.
*[[Long QT syndrome|QT syndrome]],  
*[[Hypertrophic cardiomyopathy|hypertrophic]] or [[dilated cardiomyopathy]] and  
*right ventricular dysplasia.<ref name="pmid5731530">{{cite journal |vauthors=Shoubkhova TS |title=[Determination of the particle size of suspensions of dried bacteria by the method of turbidimetric analysis] |language=Russian |journal=Zh. Mikrobiol. Epidemiol. Immunobiol. |volume=45 |issue=7 |pages=108–10 |date=July 1968 |pmid=5731530 |doi= |url=}}</ref><ref name="pmid30554599">{{cite journal |vauthors=Flannery MD, La Gerche A |title=Sudden Death and Ventricular Arrhythmias in Athletes: Screening, De-Training and the Role of Catheter Ablation |journal=Heart Lung Circ |volume=28 |issue=1 |pages=155–163 |date=January 2019 |pmid=30554599 |doi=10.1016/j.hlc.2018.10.004 |url=}}</ref>


==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
*On initial presentation, patients with impending [[pulseless ventricular tachycardia]] may present with signs of inadequate [[cardiac perfusion]] such as [[chest pain]], [[shortness of breath]], [[diaphoresis]], [[palpitations]], and [[syncope]].
On initial presentation, patients with impending [[pulseless ventricular tachycardia]] may show signs of inadequate [[cardiac perfusion]] such as [[chest pain]], [[shortness of breath]], [[diaphoresis]], [[palpitations]], and [[syncope]]. Physical examination may be positive for [[hypotension]], [[tachycardia]], [[tachypnea]], [[increased JVD]], and an [[S1]]. Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse. If [[defibrillation]] is not begun as soon as possible patients may progress to cardiac arrest and death.
*Physical examination may be positive for [[hypotension]], [[tachycardia]], [[tachypnea]], [[increased JVD]], and an [[S1]].
*Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse.  
*If [[defibrillation]] is not begun as soon as possible patients may progress to cardiac arrest and death.  
*Common complications include but are not limited to anoxic brain injury, ischemic-reperfusion injury, infections, cardiac arrest, and death.
*Prognosis is best if the tachycardia is treated almost immediately after onset. <ref name="pmid32119354">{{cite journal |vauthors=Foglesong A, Mathew D |title= |journal= |volume= |issue= |pages= |date= |pmid=32119354 |doi= |url=}}</ref><ref name="pmid31723926">{{cite journal |vauthors=Kang Y |title=Management of post-cardiac arrest syndrome |journal=Acute Crit Care |volume=34 |issue=3 |pages=173–178 |date=August 2019 |pmid=31723926 |pmc=6849015 |doi=10.4266/acc.2019.00654 |url=}}</ref><ref name="pmid31200920">{{cite journal |vauthors=Kang JY, Kim YJ, Shin YJ, Huh JW, Hong SB, Kim WY |title=Association Between Time to Defibrillation and Neurologic Outcome in Patients With In-Hospital Cardiac Arrest |journal=Am. J. Med. Sci. |volume=358 |issue=2 |pages=143–148 |date=August 2019 |pmid=31200920 |doi=10.1016/j.amjms.2019.05.003 |url=}}</ref>


==Diagnosis==
==Diagnosis==
===Diagnostic Study of Choice===
===Diagnostic Study of Choice===
The diagnosis of pulseless ventricular tachycardia is based on ECG and physical examination findings. An ECG should be the initial study, and other investigations may be carried out afterward to determine the underlying etiology.


===History and Symptoms===
===History and Symptoms===
Pulseless ventricular tachycardia may be symptomatic or asymptomatic. In a young patient with a family history of sudden death, immediate evaluation for an inherited ventricular syndrome is recommended. If symptomatic, the ventricular rate, duration of tachycardia, and the presence of underlying disease determine the kind of symptoms that present.


===Physical Examination===
===Physical Examination===
Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Physical examination may be positive for [[hypotension]], [[tachycardia]], [[tachypnea]], [[increased JVD]], and an [[S1]].


===Laboratory Findings===
===Laboratory Findings===
There aren't any specific findings associated with pulseless ventricular tachycardia. However, investigations such as serial [[cardiac enzymes]], serum [[electrolytes]], and [[toxicology]] screen should be conducted to find the underlying etiology of the arrhythmia.


===Electrocardiogram===
===Electrocardiogram===
An ECG is very helpful in the diagnosis of [[Pulseless ventricular tachycardia]]. Findings on an ECG suggestive or diagnostic of [[Pulseless ventricular tachycardia]] include regular R-R intervals, rapid ventricular rate with an indistinguishable atrial rate (absence of p-waves), Av dissociation, and a wide QRS complex (more 0.12 sec).


===X-ray===
===X-ray===
There are no x-ray findings associated with Pulseless ventricular tachycardia.


===Echocardiography and Ultrasound===
===Echocardiography===
 
There are no specific echocardiography/ultrasound findings associated with pulseless ventricular tachycardia. However, echocardiography/ultrasound may be helpful in the evaluation of underlying etiologies in patients as well as complications due to the arrhythmia.
===CT scan===
 
===MRI===


===Other Imaging Findings===
===Cardiac MRI===
There are no specific [[MRI]] findings associated with [[pulseless ventricular tachycardia]]. However, a cardiac MRI may be helpful when [[structural heart disease]] is implicated as an etiology and the assessment provided by echocardiography is not satisfactory. A [[cardiac MRI]] is particularly helpful in the evaluation of structural heart disease i.e [[arrhythmogenic right ventricular cardiomyopathy]] as well it's infiltrative diseases such as [[sarcoidosis]].


===Other Diagnostic Studies===
===Other Diagnostic Studies===
2017 guidelines from the AHA/ACC/HRS state that [[MRI]], [[cardiac computed tomography]] (CT), or [[radionuclide angiography]] can be useful in detecting and characterizing underlying [[heart disease]] when [[echocardiography]] fails to provide an accurate evaluation of LV or RV function and/or assessment of structural changes. [[Electrophysiologic (EP) testing]] can be useful when an uncertain diagnosis of [[sustained monomorphic ventricular tachycardia]]. An [[electrophysiological study]] is especially useful for assessing the risk of [[ventricular tachycardia]] in patients with [[ischemic cardiomyopathy]], [[non-ischemic cardiomyopathy]], or adult [[congenital heart disease]] who have [[syncope]] or other [[ventricular arrhythmia]] symptoms and who do not meet indications for a primary prevention [[implantable cardioverter-defibrillator]].


==Treatment==
==Treatment==
===Medical Therapy===
===Medical Therapy===
Medical therapy with IV [[vasopressors]] and [[antiarrhythmic medications]] i.e amiodarone, is usually simultaneous with [[defibrillation]]. 1mg 1V of [[epinephrine]] administered every 3-5 minutes or, a single dose of 40 units IV of vasopressin can be used as vasopressors.


=== Interventions ===
=== Interventions ===
Immediate defibrillation is the main intervention for pulseless ventricular tachycardia.


===Surgery===
===Surgery===
Surgery is not a mainstay or a preferred method of treatment for pulseless ventricular tachycardia.


===Primary Prevention===
===Primary Prevention===
Implantable cardiac defibrillators are recommended in high-risk patients i.e, patients with dilated cardiomyopathy for the primary prevention of pulseless ventricular tachycardia.


===Secondary Prevention===
===Secondary Prevention===

Latest revision as of 01:21, 10 July 2020


Pulseless ventricular tachycardia overview
Rythm; Pulseless ventricular tachycardia

Pulseless ventricular tachycardia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Pulseless ventricular tachycardia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography

Cardiac MRI

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Pulseless ventricular tachycardia overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Pulseless ventricular tachycardia overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Pulseless ventricular tachycardia overview

CDC on Pulseless ventricular tachycardia overview

Pulseless ventricular tachycardia overview in the news

Blogs on Pulseless ventricular tachycardia overview

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Pulseless ventricular tachycardia overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

Overview

Pulseless ventricular tachycardia is an often fatal cardiac dysrhythmia where the regular rhythmic contraction of the heart is replaced by non-rhythmic, faster, yet inadequate contractions. In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation, pulselessness and sudden death. In 1909,Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia. It was also first implied in 1921 that coronary occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia do not appropriately perfuse the organ, leading to ischemia as well as heart failure. This condition requires immediate medical attention as it is an emergency and can lead to ventricular fibrillation and sudden death. As a result of markedly rapid ventricular contractions, diastole is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in cardiac output, and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, wide QRS complexes above 120 milliseconds, the dissociation between the atria and ventricles, presence of fusion beats, and an electrical axis between -90 to -180. Because the majority of wide complex tachycardia cases will be ventricular tachycardia, any wide complex tachycardia should always be assumed to be due to ventricular tachycardia until proven otherwise.

Historical Perspective

There is limited information about the historical perspective of Pulseless ventricular tachycardia.

Classification

Pulseless ventricular tachycardia as a ventricular tachycardia may be classified based on the morphology of the QRS complexes into two subtypes/groups: monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia.

Pathophysiology

Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia.

Causes

Structural heart disease is the most common cause of pulseless ventricular tachycardia. Other causes include but are not limited to, drugs/medications, congenital heart diseases, not to mention congenital and inherited channelopathies. It is important to note that QT interval lengthening medications, as well as electrolyte disturbances, can also result in pulseless ventricular tachycardia.

Differentiating pulseless ventricular tachycardia from Other Diseases

Pulseless ventricular tachycardia must be differentiated from other diseases that cause wide complex tachycardia, such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia

Epidemiology and Demographics

Ventricular tachycardia and ventricular fibrillation are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn't account for deaths due to unwitnessed dysrhythmias. The majority of deaths due to ventricular arrhythmias occur In adults over 35 years of age.

Risk Factors

Risk factors for pulseless ventricular tachycardia as a cause of wide complex tachycardia includes any disease or condition that stresses or damages myocardial tissue. A family history of ventricular tachycardia or other rhythm disturbances may increase risk, while some lifestyle changes or medications may decrease risk.

Screening

According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms or has a positive family history of conditions like QT syndrome, hypertrophic, dilated cardiomyopathy and right ventricular dysplasia.

Natural History, Complications, and Prognosis

On initial presentation, patients with impending pulseless ventricular tachycardia may show signs of inadequate cardiac perfusion such as chest pain, shortness of breath, diaphoresis, palpitations, and syncope. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1. Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse. If defibrillation is not begun as soon as possible patients may progress to cardiac arrest and death.

Diagnosis

Diagnostic Study of Choice

The diagnosis of pulseless ventricular tachycardia is based on ECG and physical examination findings. An ECG should be the initial study, and other investigations may be carried out afterward to determine the underlying etiology.

History and Symptoms

Pulseless ventricular tachycardia may be symptomatic or asymptomatic. In a young patient with a family history of sudden death, immediate evaluation for an inherited ventricular syndrome is recommended. If symptomatic, the ventricular rate, duration of tachycardia, and the presence of underlying disease determine the kind of symptoms that present.

Physical Examination

Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1.

Laboratory Findings

There aren't any specific findings associated with pulseless ventricular tachycardia. However, investigations such as serial cardiac enzymes, serum electrolytes, and toxicology screen should be conducted to find the underlying etiology of the arrhythmia.

Electrocardiogram

An ECG is very helpful in the diagnosis of Pulseless ventricular tachycardia. Findings on an ECG suggestive or diagnostic of Pulseless ventricular tachycardia include regular R-R intervals, rapid ventricular rate with an indistinguishable atrial rate (absence of p-waves), Av dissociation, and a wide QRS complex (more 0.12 sec).

X-ray

There are no x-ray findings associated with Pulseless ventricular tachycardia.

Echocardiography

There are no specific echocardiography/ultrasound findings associated with pulseless ventricular tachycardia. However, echocardiography/ultrasound may be helpful in the evaluation of underlying etiologies in patients as well as complications due to the arrhythmia.

Cardiac MRI

There are no specific MRI findings associated with pulseless ventricular tachycardia. However, a cardiac MRI may be helpful when structural heart disease is implicated as an etiology and the assessment provided by echocardiography is not satisfactory. A cardiac MRI is particularly helpful in the evaluation of structural heart disease i.e arrhythmogenic right ventricular cardiomyopathy as well it's infiltrative diseases such as sarcoidosis.

Other Diagnostic Studies

2017 guidelines from the AHA/ACC/HRS state that MRI, cardiac computed tomography (CT), or radionuclide angiography can be useful in detecting and characterizing underlying heart disease when echocardiography fails to provide an accurate evaluation of LV or RV function and/or assessment of structural changes. Electrophysiologic (EP) testing can be useful when an uncertain diagnosis of sustained monomorphic ventricular tachycardia. An electrophysiological study is especially useful for assessing the risk of ventricular tachycardia in patients with ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who have syncope or other ventricular arrhythmia symptoms and who do not meet indications for a primary prevention implantable cardioverter-defibrillator.

Treatment

Medical Therapy

Medical therapy with IV vasopressors and antiarrhythmic medications i.e amiodarone, is usually simultaneous with defibrillation. 1mg 1V of epinephrine administered every 3-5 minutes or, a single dose of 40 units IV of vasopressin can be used as vasopressors.

Interventions

Immediate defibrillation is the main intervention for pulseless ventricular tachycardia.

Surgery

Surgery is not a mainstay or a preferred method of treatment for pulseless ventricular tachycardia.

Primary Prevention

Implantable cardiac defibrillators are recommended in high-risk patients i.e, patients with dilated cardiomyopathy for the primary prevention of pulseless ventricular tachycardia.

Secondary Prevention

References


Template:WH Template:WS