Infra-Hisian Block: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(85 intermediate revisions by the same user not shown)
Line 40: Line 40:


==Pathophysiology==
==Pathophysiology==
===Normal Cardiac Conduction===
# The [[normal]] [[cardiac]] [[Conduction System|conduction]] proceeds in a way so as to allow [[Time constant|time]] for the [[atrium]] to [[Relaxation|relax]] during [[atrial]] [[diastole]].
# The [[electrical]] [[Impulse (psychology)|impulse]] [[Generation|generated]] in the [[SA node]] travels through the [[Internodal segment|internodal]] pathways towards the [[AV node]].
# The [[Conduction System|conduction]] through the [[Atrioventricular node|AV node]] is [[Slow|slowed]] down as it travels through it. This decrease in [[velocity]] of [[Conduction System|conduction]] allows [[Time constant|time]] for the [[atrium]] to [[Contraction|contract]] ahead of the [[ventricle]] so that the [[blood]] from the [[atria]] can fill up the [[ventricles]] through the [[atrioventricular valves]].
# As the [[Impulse (psychology)|impulse]] [[Flow|flows]] through the [[Compact tissue|compact]] [[Atrioventricular node|AV node]], it rapidly [[Conductance|conducts]] through the [[ventricular]] [[myocardial]] [[Cells (biology)|cells]]. Once the [[depolarization]] is complete, the [[ventricle]] [[Relaxation|relaxes]] during [[diastole]] in [[Preparation (dental)|preparation]] for the next [[Impulse (psychology)|impulse]].


* [[Mobitz type II]] [[second degree AV block]] is [[Characterization (mathematics)|characterized]] by a [[PR interval]] that remains unchanged prior to a [[P wave]] that [[Failure|fails]] to [[conduct]] to the [[ventricles]].
===Anatomy===
* The [[Conduction System|conduction system]] of [[heart]] consists of [[Specialize|specialized]] [[Cells (biology)|cells]] designed to [[Conductance|conduct]] [[electrical]] [[Impulse (psychology)|impulse]] faster than the surrounding [[myocardial]] [[Cells (biology)|cells]].
*[[Anatomical|Anatomically]], the [[Atrioventricular node|AV node]] is [[Division (biology)|divided]] into three [[Region of interest|regions]] as follows:
**'''[[Transitional cell]] zone''': This is the [[Region of interest|region]] where the [[Internodal segment|internodal]] [[atrial]] pathways merge with the [[Compact tissue|compact]] [[Atrioventricular node|AV node]].
**'''[[Compact tissue|Compact]] [[Atrioventricular node|AV node]]''': This [[Region of interest|region]] is [[Location parameter|located]] at the [[apex]] of the [[triangle of Koch]], which is formed by the [[ostium]] of [[coronary sinus]], [[tricuspid]] [[Annulus (mycology)|annulus]] and the [[tendon of Todaro]].
**'''[[Penetration|Penetrating]] portion of the [[Atrioventricular|AV]] [[Bundle branch|bundle]]''': This [[Region of interest|region]] enters the [[tendon of Todaro]] and runs within the [[fibrous]] [[body]] of the [[interventricular septum|membranous interventricular septum]] and eventually [[Division (biology)|divides]] at the crest of the [[interventricular septum|muscular interventricular septum]] into right and left branches.
* The [[Left bundle branch block|left bundle branch]] [[Penetrance|penetrates]] the [[Membrane|membranous]] portion of the [[interventricular septum]] and [[Division (biology)|divides]] into several smaller branches. Parts of the [[Left bundle branch block|left bundle branch]] include a pre-[[Division (biology)|divisional]] [[Segment (linguistics)|segment]], [[anterior]] [[fascicle]]/hemibundle and [[posterior]] [[fascicle]]/hemibundle. Rarely a [[median]] [[fascicle]] is [[Presenting symptom|present]] in some [[Heart|hearts]].
** The [[anterior]] [[fascicle]] supplies the [[anterior]] [[papillary muscle]] and the [[Purkinje System|Purkinje network]] of the [[Anterior|antero]]-[[lateral]] [[Surface anatomy|surface]] of the [[left ventricle]].
** The [[posterior]] [[fascicle]] supplies the [[posterior]] [[papillary muscle]] and the [[Purkinje System|Purkinje network]] of the [[Posterior|postero]]-inferior [[Surface anatomy|surface]] of the [[left ventricle]].
**[[Left bundle branch block|Left bundle branch]] receives its [[blood]] supply from [[left anterior descending artery]].
{|
|
[[Image:Conduction system of the heart.png|thumb|200px|none|Conduction system of the heart]]
|
[[Image:AV node.png|thumb|500px|none|Structure of the heart's conduction system]]
|
|}
 
===Pathophysiology of Mobitz type II second degree AV block===
* [[Mobitz type II]] [[second degree AV block]] is [[Characterization (mathematics)|characterized]] by a [[PR interval]] that remains unchanged with occasional [[Drop (liquid)|dropped]] [[Beats per minute|beats]] prior to a [[P wave]] that [[Failure|fails]] to [[conduct]] to the [[ventricles]] as [[Comparability|compared]] to the gradually [[Prolonged PR-interval|prolonging PR interval]] in [[Mobitz type I]].
*[[ECG]] findings include intermittently non-[[Conduct|conducted]] [[P wave]]s not preceded by [[PR prolongation]] and not followed by [[PR interval|PR]] [[shortening]].
*It almost always [[Result|results]] from a [[Conduction system disease|disease of the conduction system]] below the [[Level of measurement|level]] of [[Atrioventricular node|AV node]], occurring in the [[bundle of His]] in approximately 20% of the [[Case-based reasoning|cases]] and in the [[Bundle branch|bundle branches]] in the remainder.
*It almost always [[Result|results]] from a [[Conduction system disease|disease of the conduction system]] below the [[Level of measurement|level]] of [[Atrioventricular node|AV node]], occurring in the [[bundle of His]] in approximately 20% of the [[Case-based reasoning|cases]] and in the [[Bundle branch|bundle branches]] in the remainder.
*[[Dependent variable|Depending]] upon the [[Location parameter|location]] of the [[Heart block|block]], [[patients]] having [[bundle branch]] involvement also have [[axis]] shifts and [[QRS]] widening.
*[[Dependent variable|Depending]] upon the [[Location parameter|location]] of the [[Heart block|block]], [[patients]] having [[bundle branch]] involvement also have [[axis]] shifts and [[QRS]] widening.
*In addition, at least two-thirds of the [[patients]] with this [[disorder]] also have [[Bifascicular block|bifascicular]] or even [[Trifascicular heart block|trifascicular]] [[disease]].
*At least two-thirds of the [[patients]] with [[Mobitz type II]] [[second degree AV block]] have [[Bifascicular block|bifascicular]] or even [[Trifascicular heart block|trifascicular]] [[disease]].<ref name="pmid6544636">{{cite journal| author=Puech P, Wainwright RJ| title=Clinical electrophysiology of atrioventricular block. | journal=Cardiol Clin | year= 1983 | volume= 1 | issue= 2 | pages= 209-24 | pmid=6544636 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6544636  }}</ref><ref name="pmid8445186">{{cite journal |vauthors=Wogan JM, Lowenstein SR, Gordon GS |title=Second-degree atrioventricular block: Mobitz type II |journal=J Emerg Med |volume=11 |issue=1 |pages=47–54 |date=1993 |pmid=8445186 |doi=10.1016/0736-4679(93)90009-v |url=}}</ref>
*[[Mobitz type I]] and [[Mobitz type II AV block|Mobitz type II]] [[second degree AV block]] cannot be [[Differentiate|differentiated]] from the [[ECG]] when 2:1 [[Atrioventricular block|AV block]] is [[Presenting symptom|present]].
*In the presence of 2:1 [[Atrioventricular block|AV block]], [[Mobitz type I]] and [[Mobitz type II AV block|Mobitz type II]] [[second degree AV block]] cannot be [[Differentiate|differentiated]] on the basis of [[electrocardiographic]] findings. In such cases, every other [[P wave]] is non-[[Conduct|conducted]] without a chance to [[Observation|observe]] the [[constant]] [[PR interval]] that is [[Characteristic impedance|characteristic]] of [[Mobitz type II AV block|Mobitz type II]] [[second degree AV block]].
*In this situation, every other [[P wave]] is non-[[Conduct|conducted]] and there is no opportunity to [[Observation|observe]] for the [[constant]] [[PR interval]] that is [[Characteristic impedance|characteristic]] of [[Mobitz type II AV block|Mobitz type II]] [[second degree AV block]].
*The [[Conduction System|conduction]] delay seen in [[Mobitz type II AV block|Mobitz type II]] [[second degree block]] is almost always at the infra-[[Nodal (protein)|nodal]] level involving the [[distal]] [[Conduction system disease|conduction system]] ([[His bundle]] (20%), [[Bundle branch|bundle branches]] or/and [[fascicles]]).


*[[Conduction System|Conduction]] delay in [[Mobitz type II AV block|Mobitz type II]] [[second degree block]] is almost always infra-[[Nodal (protein)|nodal]] ([[His bundle]] [20%], [[Bundle branch|bundle branches]] or [[fascicles]]).
*Although often both the [[Term logic|terms]], [[Infranodal Wenkebach-type block|infranodal block]] or infrahisian [[Heart block|block]] are applied to [[Mobitz type II]] [[second degree AV block]], they are not [[Synonymous substitution|synonymous]] with it.
* Usually the [[morphology]] of the [[QRS complex]] is wide, except when the site of [[Heart block|block]] is the [[His bundle]].
* In this [[Variance|variant]] of [[second degree heart block]] the [[PR interval]] is [[constant]] with occasional [[Drop (liquid)|dropped]] [[Beats per minute|beats]] as [[Comparability|compared]] to the gradually [[Prolonged PR-interval|prolonging PR interval]] in [[Mobitz type I]].
*[[Bifascicular block|Bifascicular]] or [[Trifascicular heart block|trifascicular]] [[disease]] is seen in two thirds of the [[patients]] with [[Mobitz type II AV block|Mobitz type II]].<ref name="pmid6544636">{{cite journal| author=Puech P, Wainwright RJ| title=Clinical electrophysiology of atrioventricular block. | journal=Cardiol Clin | year= 1983 | volume= 1 | issue= 2 | pages= 209-24 | pmid=6544636 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6544636  }}</ref><ref name="pmid8445186">{{cite journal |vauthors=Wogan JM, Lowenstein SR, Gordon GS |title=Second-degree atrioventricular block: Mobitz type II |journal=J Emerg Med |volume=11 |issue=1 |pages=47–54 |date=1993 |pmid=8445186 |doi=10.1016/0736-4679(93)90009-v |url=}}</ref>
*Type 2 [[second degree AV block]], also known as [[Mobitz II]] is almost always a [[disease]] of the [[distal]] [[Conduction system disease|conduction system]] ([[electrical conduction system of the heart|His-Purkinje System]]).
 
*Although the [[Term logic|terms]] [[Infranodal Wenkebach-type block|infranodal block]] or infrahisian [[Heart block|block]] are often applied to this [[Disorder (medicine)|disorder]], they are not [[Synonymous substitution|synonymous]] with it.


:*[[Infranodal Wenkebach-type block|Infranodal]] [[Heart block|block]] and [[infra-Hisian block]] are [[Term logic|terms]] which [[Reference|refer]] to the [[anatomic]] [[Location parameter|location]] of the [[Heart block|block]], whereas
:*[[Infranodal Wenkebach-type block|Infranodal]] [[Heart block|block]] and [[infra-Hisian block]] are [[Term logic|terms]] which [[Reference|refer]] to the [[anatomic]] [[Location parameter|location]] of the [[Heart block|block]], whereas
:*[[Mobitz II]] [[Reference|refers]] to an [[electrocardiographic]] [[pattern]] [[Association (statistics)|associated]] with [[Heart block|block]] at these [[Leveling effect|levels]].<ref name="pmid29850368">{{cite journal |vauthors=Li X, Xue Y, Wu H |title=A Case of Atrioventricular Block Potentially Associated with Right Coronary Artery Lesion and Ticagrelor Therapy Mediated by the Increasing Adenosine Plasma Concentration |journal=Case Rep Vasc Med |volume=2018 |issue= |pages=9385017 |date=2018 |pmid=29850368 |pmc=5933017 |doi=10.1155/2018/9385017 |url=}}</ref>
:*[[Mobitz II]] [[Reference|refers]] to an [[electrocardiographic]] [[pattern]] [[Association (statistics)|associated]] with [[Heart block|block]] at these [[Leveling effect|levels]].<ref name="pmid29850368">{{cite journal |vauthors=Li X, Xue Y, Wu H |title=A Case of Atrioventricular Block Potentially Associated with Right Coronary Artery Lesion and Ticagrelor Therapy Mediated by the Increasing Adenosine Plasma Concentration |journal=Case Rep Vasc Med |volume=2018 |issue= |pages=9385017 |date=2018 |pmid=29850368 |pmc=5933017 |doi=10.1155/2018/9385017 |url=}}</ref>


*[[Mobitz II]] [[heart block]] is characterized on a surface [[ECG]] by intermittently non-conducted [[P wave]]s not preceded by [[PR prolongation]] and not followed by PR shortening.
===Pathophysiology of LBBB===
*The medical significance of this type of [[AV block]] is that it may progress rapidly to [[complete heart block]], in which no escape rhythm may emerge.  
* Unlike [[right bundle branch block]] ([[RBBB]]), [[left bundle branch block]] completely modifies the way of [[depolarization]] of the [[Electrical conduction system of the heart|conduction system of the heart]].  
*In this case, the person may experience a [[Stokes-Adams attack]], [[cardiac arrest]], or [[sudden cardiac death]].
*In [[Left bundle branch block|LBBB]] the [[Activation energy|activation]] of [[interventricular septum]] is from right to left due to uninterrupted [[Conductance|conduction]] in the [[Right bundle branch block|RBB]].
*The definitive [[Treatments|treatment]] for this form of AV Block is an [[implanted pacemaker]].<ref name="pmid29275956">{{cite journal |vauthors=Fu Md J, Bhatta L |title=Lyme carditis: Early occurrence and prolonged recovery |journal=J Electrocardiol |volume=51 |issue=3 |pages=516–518 |date=2018 |pmid=29275956 |doi=10.1016/j.jelectrocard.2017.12.035 |url=}}</ref><ref name="pmid28823599">{{cite journal |vauthors=Tuohy S, Saliba W, Pai M, Tchou P |title=Catheter ablation as a treatment of atrioventricular block |journal=Heart Rhythm |volume=15 |issue=1 |pages=90–96 |date=January 2018 |pmid=28823599 |doi=10.1016/j.hrthm.2017.08.015 |url=}}</ref>
* Then the [[electrical]] [[Impulse (psychology)|impulse]] propagates [[inferiorly]] to the left [[Result|resulting]] in delayed [[depolarization]] and [[Activation energy|activation]] of the [[left ventricle]] especially the left [[lateral]] wall.<ref name="pmid17385703">{{cite journal |author=Francia P, Balla C, Paneni F, Volpe M |title=Left bundle-branch block--pathophysiology, prognosis, and clinical management |journal=Clinical Cardiology |volume=30 |issue=3 |pages=110–5 |year=2007 |month=March |pmid=17385703 |doi=10.1002/clc.20034 |url=}}</ref>
* In [[Left bundle branch block|LBBB]], the right to left [[Activation energy|activation]] of the [[septum]] [[causes]] a small negative deflection ([[Q wave]]) in [[lead]] [[V1-morph|V<sub>1</sub>]] and a [[positive]] deflection ([[R wave]]) in [[lead]] V<sub>6</sub>.
*The [[right ventricle]] [[Depolarization|depolarizes]] earlier than the [[left ventricle]] giving an [[R wave]] in [[lead]] [[V1-morph|V<sub>1</sub>]] and an [[S wave]] in [[lead]] V<sub>6</sub>.
*Subsequent delayed [[depolarization]] of the [[left ventricle]] [[Result|results]] in an [[S wave]] in [[lead]] [[V1-morph|V<sub>1</sub>]] and another [[R wave]] in [[lead]] V<sub>6</sub>.
 
===Pathophysiology of RBBB===
*[[Right bundle branch block]] occurs when the [[electrical]] [[Impulse (psychology)|impulse]] is not [[Conductance|conducted]] along the [[Right bundle branch block|right bundle branch]].
* As the [[Conduction System|conduction]] along the [[Left bundle branch block|left bundle branch]] remains unaffected, the [[electrical]] [[Impulse (psychology)|impulse]] [[Travel medicine|travels]] [[Normal|normally]] within the [[septum]] from left to right.
* However, the [[right ventricular]] [[contraction]] occurs [[Comparability|comparatively]] [[Slow|slowly]] giving the [[Characteristic impedance|characteristic]] 'M' [[pattern]] on the [[electrocardiogram]].
 
====Genetics====
*[[Familial]] [[Case-based reasoning|cases]] of [[right bundle branch block]] have been [[Observation|observed]] in 4 Lebanese [[Family|families]] and the [[Abnormality (behavior)|abnormality]] was mapped to [[chromosome 19]].
* There is a [[subset]] of [[patients]] with [[Brugada syndrome]] who have [[mutations]] in [[SCN5A]], the [[gene]] [[Encoding (memory)|encoding]] for the [[Voltage-gated sodium channel|voltage-gated cardiac sodium channel]].


==Causes==
====Associated Syndromes====
*[[Duchenne muscular dystrophy]]
*[[Myotonic dystrophy]]: Other [[EKG]] findings include:
**[[First-degree AV block]]
**[[Left anterior fascicular block]]
**[[Intraventricular conduction delay]]
**[[Arrhythmias]]
*[[Stokes-Adams attacks]]
*[[Kearns-Sayre Syndrome]]
*[[Brugada syndrome]]
 
====Pseudo Right Bundle Branch Block====
'''[[Brugada syndrome]]:'''


The potential etiologies of Mobitz type II second degree AV block include reversible (both pathologic and iatrogenic) and idiopathic causes that are similar to other degrees of AV block (table 1). Common potentially reversible causes include:
*[[Brugada syndrome]] is due to a [[channelopathy]] [[Mediated transport|mediated]] by the [[SCN5A]] [[gene]].
* The [[Right bundle branch block|RBBB]] [[pattern]] seen in [[patients]] of [[Brugada syndrome]] is not actually [[Right bundle branch block|RBBB]] but instead it is due to a [[repolarization]] [[Abnormality (behavior)|abnormality]]. Therefore, the [[Right bundle branch block|RBBB]] like [[pattern]] seen in [[Brugada syndrome]] is [[Reference|referred]] to as a 'pseudo [[right bundle branch block]]'.
*[[EKG]] findings include [[ST-segment elevation]] in [[Lead|leads]] [[V1-morph|V1]]-[[V3 loop|V3]].
*[[Cocaine]] [[Consumer/Survivor/Ex-Patient Movement|consumption]] and/or the [[Usage analysis|use]] of the [[antiarrhythmic]] [[propafenone]] may unmask the [[EKG]] findings seen in [[Brugada syndrome]].<ref name="pmid23613002">{{cite journal |author=Yildiz BS, Gungor H, Gul I, Bilgin M, Zoghi M, Akilli A |title=Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome? |journal=Cardiovascular Journal of Africa |volume=24 |issue=2 |pages=e4–6 |year=2013 |pmid=23613002 |doi=10.5830/CVJA-2012-068 |url=}}</ref>


●Pathologic – Myocardial ischemia (acute or chronic) involving the conduction system, cardiomyopathy (eg, amyloidosis, sarcoidosis), myocarditis (eg, Lyme disease), endocarditis with abscess formation, hyperkalemia, and hypervagotonia.
==Causes==
===Mobitz type II second degree AV block causes===


●Iatrogenic – Medication-related (AV nodal blocking medications), post-cardiac surgery, post-catheter ablation, post-transcatheter aortic valve implantation.
*[[Mobitz type II AV block|Mobitz type II]] [[second degree AV block]] is [[Rare|rarely]] seen in the [[patients]] without any [[Underlying representation|underlying]] [[heart disease]].
*The most common [[causes]] of [[Mobitz type II]] [[second degree AV block]] include:
** Reversible [[causes]] (both [[Pathological|pathologic]] and [[iatrogenic]])
**[[Idiopathic]] [[causes]] similar to other [[Degree (angle)|degrees]] of [[Atrioventricular block|AV block]] such as [[idiopathic]] progressive [[Cardiac conduction disorder|cardiac conduction disease]] with [[myocardial]] [[fibrosis]] and/or [[sclerosis]] [[Affect|affecting]] the [[Conduction system disease|conduction system]].


Mobitz type II second degree AV block is rarely seen in patients without underlying heart disease. When identifiable, the reversible causes most commonly associated with Mobitz type II second degree AV block are myocardial infarction with ischemia of the AV node and medications that alter conduction through the AV node (eg, digoxin, beta blockers, calcium channel blockers). When no specific reversible cause is identified, the block is often felt to be related to idiopathic progressive cardiac conduction disease with myocardial fibrosis and/or sclerosis that affects the conduction system.
* Details of all the possible [[etiologies]] are given in the table below:


{| class="wikitable"
{| class="wikitable"
|+Major causes of atrioventricular (AV) block
|+Major reversible causes of atrioventricular (AV) block
!'''Physiologic and pathophysiologic'''
! colspan="2" style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|'''Physiologic and pathophysiologic'''}}
!
|-
|-
|Increased vagal tone
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Increased [[vagal]] [[Tone (linguistics)|tone]]
|
|
* Also known as hypervagotonia
|-
|-
|Ischemic heart disease, including acute myocardial infarction
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Ischemic heart disease]]
|
|
*[[Acute]] or [[chronic]] [[myocardial infarction]]/[[ischemia]] involving the [[Conduction system disease|conduction system.]]
|-
|-
| rowspan="2" |Progressive cardiac conduction system disease
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Progressive [[Cardiac conduction disorder|cardiac conduction system disease]]
|With fibrosis and/or sclerosis (Lenegre disease)
|[[Association (statistics)|Associated]] with:
|-
 
|With calcification (Lev disease)
*[[Calcification]] in [[Lev's disease]]
*[[Fibrosis]] and/or [[sclerosis]] in [[Lenegre's Disease|Lenegre's disease]]
|-
|-
|Infections (eg, viral myocarditis, Lyme carditis)
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Infections]]
|
|
*[[Viral myocarditis]]
*[[Lyme carditis]]
*[[Endocarditis]] with [[abscess]] [[Formation matrix|formation]]
|-
|-
| rowspan="2" |Cardiomyopathy
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Cardiomyopathy]]
|Infiltrative processes (eg, sarcoidosis, amyloidosis, hemochromatosis, malignancy, etc)
|[[Infiltration (medical)|Infiltrative]] [[Process (anatomy)|processes]] such as:
 
*[[Sarcoidosis]]
*[[Hemochromatosis]]
*[[Amyloidosis]]
*[[Malignancy]]
 
Other non-[[Ischemic cardiomyopathy|ischemic cardiomyopathies]] include:
 
*[[Idiopathic]]
*[[Infectious]]
|-
|-
|Other non-ischemic cardiomyopathies (eg, idiopathic, infectious, etc)
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Congenital]] [[Atrioventricular block|AV block]]
|
* It is [[Related changes|related]] to [[Structural biology|structural]] [[congenital heart disease]]
*It occurs as a part of [[neonatal lupus syndrome]]
|-
|-
| rowspan="2" |Congenital AV block
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Other [[Reversible cell|reversible]] [[causes]]
|Related to structural congenital heart disease
|
*[[Hyperkalemia]]
* Severe [[Hypothyroidism|hypo]]- or [[hyperthyroidism]]
*[[Degenerative]] [[Neuromuscular disease|neuromuscular diseases]]
*[[Trauma]]
|-
|-
|As part of neonatal lupus syndrome
| colspan="2" style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|'''Iatrogenic'''}}
|-
|-
| rowspan="4" |Other
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Drugs]] (altering [[Conduction System|conduction]] through [[Atrioventricular node|AV node]])
|Hyperkalemia
|
*[[Beta-blockers]]
*[[Digoxin]]
*[[Calcium channel blockers]]
*[[Adenosine]]
*[[Antiarrhythmic drugs]]
|-
|-
|severe hypo- or hyperthyroidism
|style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Cardiac surgery]]
|
* Post [[valvular]] [[surgery]]
* Post-[[Surgery|surgical]] [[Correction (newspaper)|correction]] of [[congenital heart disease]]
|-
|-
|trauma
| colspan="2" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Catheter ablation]] of [[arrhythmias]]
|-
|-
|degenerative neuromuscular diseases
| colspan="2" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Alcohol septal ablation]] for [[hypertrophic cardiomyopathy]]
|-
|-
| colspan="2" |'''Iatrogenic'''
| colspan="2" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Transcatheter [[Closure (psychology)|closure]] of [[ventricular septal defect]]
|-
|-
| rowspan="5" |Drugs
| colspan="2" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Post-[[transcatheter aortic valve implantation]]
|Beta blockers
|-
|calcium channel blockers
|-
|digoxin
|-
|antiarrhythmic drugs
|-
|adenosine
|-
| colspan="2" |Transcatheter aortic valve implantation
|-
| rowspan="2" |Cardiac surgery
|Post valvular surgery
|-
|post surgical correction of congenital heart disease
|-
|Catheter ablation of arrhythmias
|
|-
|Alcohol septal ablation for hypertrophic cardiomyopathy
|
|-
|Transcatheter closure of ventricular septal defect
|
|}
|}


Line 378: Line 433:
* [[sex linkage|X-linked inherited  conditions]]
* [[sex linkage|X-linked inherited  conditions]]
{{col-end}}
{{col-end}}
*'''For causes of [[Left bundle branch block]], click [[Left bundle branch block causes|here]].'''
*'''For causes of [[Right bundle branch block]], click [[Right bundle branch block causes|here]].'''


==Epidemiology and Demographics==
==Epidemiology and Demographics==
Line 410: Line 468:
==Natural History, Complications and Prognosis==
==Natural History, Complications and Prognosis==
===Natural History===
===Natural History===
*[[Mobitz II]] [[second degree AV block]] is due to the [[Blocking (statistics)|block]] [[Inferior angle|inferior]] to the [[Atrioventricular node|AV node]] (infra-Hisian [[Structure factor|structures]]) and it progresses to a [[complete heart block]].<ref name="pmid463945">{{cite journal |vauthors=Rodstein M, Wolloch L, Iuster Z |title=The natural history intraventricular conduction disturbances in the aged: an analysis of the developing second and third degree heart block with clinical pathological correlations |journal=Am. J. Med. Sci. |volume=277 |issue=2 |pages=179–88 |date=1979 |pmid=463945 |doi=10.1097/00000441-197903000-00006 |url=}}</ref>
*[[Mobitz II]] [[second degree AV block]] is due to the [[Blocking (statistics)|block]] [[Inferior angle|inferior]] to the [[Atrioventricular node|AV node]] (infra-Hisian [[Structure factor|structures]]) and it rapidly progresses to a [[complete heart block]] in which no escape [[rhythm]] may emerge.<ref name="pmid463945">{{cite journal |vauthors=Rodstein M, Wolloch L, Iuster Z |title=The natural history intraventricular conduction disturbances in the aged: an analysis of the developing second and third degree heart block with clinical pathological correlations |journal=Am. J. Med. Sci. |volume=277 |issue=2 |pages=179–88 |date=1979 |pmid=463945 |doi=10.1097/00000441-197903000-00006 |url=}}</ref>


===Complications===
===Complications===
Line 503: Line 561:
|MedCond = Second degree AV block(except in patients with a functioning artificial pacemaker)<ref name="pmid26115830">{{cite journal |vauthors=Brignole M, Deharo JC, Guieu R |title=Syncope and Idiopathic (Paroxysmal) AV Block |journal=Cardiol Clin |volume=33 |issue=3 |pages=441–7 |date=August 2015 |pmid=26115830 |doi=10.1016/j.ccl.2015.04.012 |url=}}</ref><ref name="pmid11229299">{{cite journal |vauthors=Kelkar PN |title=Atenolol induced high grade AV block |journal=J Assoc Physicians India |volume=46 |issue=8 |pages=748, 751 |date=August 1998 |pmid=11229299 |doi= |url=}}</ref>|Adenosine|Atenolol|Betaxolol|Bisoprolol|Brimonidine tartrate and Timolol maleate|Carteolol|Diltiazem|Disopyramide|Dronedarone|Fingolimod|Flecainide|Metoprolol|Mexiletine|Nadolol|Nebivolol|Penbutolol|Pindolol|Propranolol|Sotalol|Timolol|Labetalol}}<ref name="pmid15234417">{{cite journal |vauthors=Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S |title=Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug |journal=J. Am. Coll. Cardiol. |volume=44 |issue=1 |pages=105–8 |date=July 2004 |pmid=15234417 |doi=10.1016/j.jacc.2004.03.057 |url=}}</ref>
|MedCond = Second degree AV block(except in patients with a functioning artificial pacemaker)<ref name="pmid26115830">{{cite journal |vauthors=Brignole M, Deharo JC, Guieu R |title=Syncope and Idiopathic (Paroxysmal) AV Block |journal=Cardiol Clin |volume=33 |issue=3 |pages=441–7 |date=August 2015 |pmid=26115830 |doi=10.1016/j.ccl.2015.04.012 |url=}}</ref><ref name="pmid11229299">{{cite journal |vauthors=Kelkar PN |title=Atenolol induced high grade AV block |journal=J Assoc Physicians India |volume=46 |issue=8 |pages=748, 751 |date=August 1998 |pmid=11229299 |doi= |url=}}</ref>|Adenosine|Atenolol|Betaxolol|Bisoprolol|Brimonidine tartrate and Timolol maleate|Carteolol|Diltiazem|Disopyramide|Dronedarone|Fingolimod|Flecainide|Metoprolol|Mexiletine|Nadolol|Nebivolol|Penbutolol|Pindolol|Propranolol|Sotalol|Timolol|Labetalol}}<ref name="pmid15234417">{{cite journal |vauthors=Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S |title=Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug |journal=J. Am. Coll. Cardiol. |volume=44 |issue=1 |pages=105–8 |date=July 2004 |pmid=15234417 |doi=10.1016/j.jacc.2004.03.057 |url=}}</ref>
===Surgery for Mobitz II===
===Surgery for Mobitz II===
*[[Mobitz type II AV block|Type II Mobitz]] ([[symptomatic]] or [[asymptomatic]]) is by itself an [[Indication (medicine)|indication]] for [[insertion]] of a [[pacemaker]]. Other [[Indication (medicine)|indications]] include<ref name="pmid30412709">{{cite journal |vauthors=Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD |title=2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society |journal=J. Am. Coll. Cardiol. |volume=74 |issue=7 |pages=e51–e156 |date=August 2019 |pmid=30412709 |doi=10.1016/j.jacc.2018.10.044 |url=}}</ref><ref name="pmid7471363">{{cite journal |vauthors=Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM |title=Natural history of chronic second-degree atrioventricular nodal block |journal=Circulation |volume=63 |issue=5 |pages=1043–9 |date=May 1981 |pmid=7471363 |doi=10.1161/01.cir.63.5.1043 |url=}}</ref>:
====Definitive treatment-Pacemaker insertion====
*[[Mobitz type II AV block|Type II Mobitz]] ([[symptomatic]] or [[asymptomatic]]) is by itself an [[Indication (medicine)|indication]] for [[insertion]] of a [[pacemaker]] (definitive [[Treatments|treatment]]). Other [[Indication (medicine)|indications]] include:<ref name="pmid29275956">{{cite journal |vauthors=Fu Md J, Bhatta L |title=Lyme carditis: Early occurrence and prolonged recovery |journal=J Electrocardiol |volume=51 |issue=3 |pages=516–518 |date=2018 |pmid=29275956 |doi=10.1016/j.jelectrocard.2017.12.035 |url=}}</ref><ref name="pmid28823599">{{cite journal |vauthors=Tuohy S, Saliba W, Pai M, Tchou P |title=Catheter ablation as a treatment of atrioventricular block |journal=Heart Rhythm |volume=15 |issue=1 |pages=90–96 |date=January 2018 |pmid=28823599 |doi=10.1016/j.hrthm.2017.08.015 |url=}}</ref><ref name="pmid30412709">{{cite journal |vauthors=Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD |title=2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society |journal=J. Am. Coll. Cardiol. |volume=74 |issue=7 |pages=e51–e156 |date=August 2019 |pmid=30412709 |doi=10.1016/j.jacc.2018.10.044 |url=}}</ref><ref name="pmid7471363">{{cite journal |vauthors=Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM |title=Natural history of chronic second-degree atrioventricular nodal block |journal=Circulation |volume=63 |issue=5 |pages=1043–9 |date=May 1981 |pmid=7471363 |doi=10.1161/01.cir.63.5.1043 |url=}}</ref>:
**[[Myotonic dystrophy]]
**[[Myotonic dystrophy]]
** [[Kearns-Sayre syndrome]]
** [[Kearns-Sayre syndrome]]

Latest revision as of 20:59, 19 August 2020

Infra-Hisian Block Microchapters

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Treatment

Prevention

Differentiating Infra-Hisian Block from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Mohsin, M.D.[2]

Overview

Infra-Hisian block is defined as an impaired conduction in the electrical system of the heart that occurs below the atrioventricular node.

Historical Perspective

Classification

Classification of Infra-Hisian Block
Types of Infra-Hisian Block Sub-type
Type 2 second degree heart block (Mobitz II) _
Left bundle branch block Left anterior fascicular block
Left posterior fascicular block
Right bundle branch block _

Pathophysiology

Normal Cardiac Conduction

  1. The normal cardiac conduction proceeds in a way so as to allow time for the atrium to relax during atrial diastole.
  2. The electrical impulse generated in the SA node travels through the internodal pathways towards the AV node.
  3. The conduction through the AV node is slowed down as it travels through it. This decrease in velocity of conduction allows time for the atrium to contract ahead of the ventricle so that the blood from the atria can fill up the ventricles through the atrioventricular valves.
  4. As the impulse flows through the compact AV node, it rapidly conducts through the ventricular myocardial cells. Once the depolarization is complete, the ventricle relaxes during diastole in preparation for the next impulse.

Anatomy

Conduction system of the heart
Structure of the heart's conduction system

Pathophysiology of Mobitz type II second degree AV block

Pathophysiology of LBBB

Pathophysiology of RBBB

Genetics

Associated Syndromes

Pseudo Right Bundle Branch Block

Brugada syndrome:

Causes

Mobitz type II second degree AV block causes

  • Details of all the possible etiologies are given in the table below:
Major reversible causes of atrioventricular (AV) block
Physiologic and pathophysiologic
Increased vagal tone
  • Also known as hypervagotonia
Ischemic heart disease
Progressive cardiac conduction system disease Associated with:
Infections
Cardiomyopathy Infiltrative processes such as:

Other non-ischemic cardiomyopathies include:

Congenital AV block
Other reversible causes
Iatrogenic
Drugs (altering conduction through AV node)
Cardiac surgery
Catheter ablation of arrhythmias
Alcohol septal ablation for hypertrophic cardiomyopathy
Transcatheter closure of ventricular septal defect
Post-transcatheter aortic valve implantation

Life Threatening Causes

Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.[7]

Common Causes

Causes by Organ System

Cardiovascular Acute myocardial infarction, acute rheumatic fever, ASD, dilated cardiomyopathy, Ebstein's anomaly, hypersensitive carotid sinus syndrome, hypertension, hypertrophic cardiomyopathy, Lev's disease, myocardial bridging, myocarditis, normal variants, post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement, tetralogy of Fallot, endocardial cushion defect, transposition of the great vessels, valvular heart disease, VSD
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Amiodarone, beta-blockers, digitalis, calcium channel blockers, cholinesterase inhibitors, disopyramide, dofetilide, dolasetron, donepezil, eslicarbazepine acetate, fesoterodine, fingolimod, flecainide, ibutilide, lacosamide, magnesium, paliperidone, pramipexole, procainamide, propafenone, propoxyphene, quinidine, sotalol, terodiline
Ear Nose Throat No underlying causes
Endocrine Hyperthyroidism, myxedema, thyrotoxic periodic paralysis
Environmental Hypothermia
Gastroenterologic Hemochromatosis
Genetic Emery-Dreifuss muscular dystrophy, Fabry disease, glycogenosis type 2b, hereditary neuromuscular disease, Kearns-Sayre syndrome
Hematologic Multiple myeloma Lymphoma[11]
Iatrogenic Post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement
Infectious Disease Acute rheumatic fever, Chagas disease, diphtheria, Lyme disease, myocarditis, neonatal lupus erythematosus, protozoal infection, sarcoidosis, SLE, tuberculosis
Musculoskeletal / Ortho Ankylosing spondylitis, hereditary neuromuscular disease, Kearns-Sayre syndrome, mitochondrial genome inherited conditions, muscular dystrophy
Neurologic Enhanced vagal tone
Nutritional / Metabolic Fabry disease, glycogenosis type 2b
Obstetric/Gynecologic No underlying causes
Oncologic Multiple myeloma
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Sarcoidosis
Renal / Electrolyte Hyperkalemia, hypokalemia
Rheum / Immune / Allergy Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, SLE
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Amyloidosis, degenerative diseases

Causes in Alphabetical Order

Epidemiology and Demographics

Prevalence

Gender

Risk Factors

Natural History, Complications and Prognosis

Natural History

Complications

Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Patients with second degree AV block should be checked for the following laboratory tests:[27]

Electrocardiogram


Shown below is an electrocardiogram of a 12 lead EKG with a 2:1 AV block.

Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page


Shown below is an electrocardiogram of a type II second degree AV block (Mobitz type II).

Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page


Treatment

Medical therapy for Mobitz II

Contraindicated medications

Second degree AV block(except in patients with a functioning artificial pacemaker)[30][31] is considered an absolute contraindication to the use of the following medications:

Surgery for Mobitz II

Definitive treatment-Pacemaker insertion

Prevention

Primary Prevention

Differentiating Infra-Hisian Block from other Diseases


Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrioventricular block[36] First degree [37][38]
  • Regular



Second degree[12][39] QRS is normal but dropped as the following:
Third degree[40][41]
  • Regular
Atrial Fibrillation (AFib)[42][43]
  • Absent
Atrial Flutter[44]
Atrioventricular nodal reentry tachycardia (AVNRT)[45][46][47][48]
  • Regular
Multifocal Atrial Tachycardia[49][50]
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
Premature Atrial Contractrions (PAC)[51][52]
  • Upright
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[53][54]
  • Regular
Ventricular Fibrillation (VF)[55][56][57]
  • Absent
  • Absent
Ventricular Tachycardia[58][59]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent

References

  1. Upshaw CB, Silverman ME (2000). "John Hay: discoverer of type II atrioventricular block". Clin Cardiol. 23 (11): 869–71. doi:10.1002/clc.4960231118. PMC 6655013 Check |pmc= value (help). PMID 11097138.
  2. Puech P, Wainwright RJ (1983). "Clinical electrophysiology of atrioventricular block". Cardiol Clin. 1 (2): 209–24. PMID 6544636.
  3. 3.0 3.1 3.2 3.3 Wogan JM, Lowenstein SR, Gordon GS (1993). "Second-degree atrioventricular block: Mobitz type II". J Emerg Med. 11 (1): 47–54. doi:10.1016/0736-4679(93)90009-v. PMID 8445186.
  4. 4.0 4.1 4.2 Li X, Xue Y, Wu H (2018). "A Case of Atrioventricular Block Potentially Associated with Right Coronary Artery Lesion and Ticagrelor Therapy Mediated by the Increasing Adenosine Plasma Concentration". Case Rep Vasc Med. 2018: 9385017. doi:10.1155/2018/9385017. PMC 5933017. PMID 29850368.
  5. Francia P, Balla C, Paneni F, Volpe M (2007). "Left bundle-branch block--pathophysiology, prognosis, and clinical management". Clinical Cardiology. 30 (3): 110–5. doi:10.1002/clc.20034. PMID 17385703. Unknown parameter |month= ignored (help)
  6. Yildiz BS, Gungor H, Gul I, Bilgin M, Zoghi M, Akilli A (2013). "Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome?". Cardiovascular Journal of Africa. 24 (2): e4–6. doi:10.5830/CVJA-2012-068. PMID 23613002.
  7. 7.0 7.1 7.2 7.3 Mangi MA, Jones WM, Napier L. PMID 29493981. Missing or empty |title= (help)
  8. Misumida N, Ogunbayo GO, Kim SM, Abdel-Latif A, Ziada KM, Elayi CS (November 2018). "Frequency and Significance of High-Degree Atrioventricular Block and Sinoatrial Node Dysfunction in Patients With Non-ST-Elevation Myocardial Infarction". Am. J. Cardiol. 122 (10): 1598–1603. doi:10.1016/j.amjcard.2018.08.001. PMID 30227965.
  9. 9.0 9.1 9.2 Barold SS, Herweg B (December 2012). "Second-degree atrioventricular block revisited". Herzschrittmacherther Elektrophysiol. 23 (4): 296–304. doi:10.1007/s00399-012-0240-8. PMID 23224264.
  10. Kamatani T, Akizuki A, Kondo S, Shirota T (Fall 2016). "Second-Degree Atrioventricular Block Occurring After Tooth Extraction". Anesth Prog. 63 (3): 156–9. doi:10.2344/15-00042.1. PMC 5011958. PMID 27585419.
  11. Menicagli F, Lanza A, Sbrocca F, Baldi A, Spugnini EP (2016). "A case of advanced second-degree atrioventricular block in a ferret secondary to lymphoma". Open Vet J. 6 (1): 68–70. doi:10.4314/ovj.v6i1.10. PMC 4833871. PMID 27200273.
  12. 12.0 12.1 Zehender M, Meinertz T, Keul J, Just H (1990). "ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance". Am Heart J. 119 (6): 1378–91. doi:10.1016/s0002-8703(05)80189-9. PMID 2191578.
  13. 13.0 13.1 13.2 Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
  14. Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
  15. Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ, Kenttä TV, Rissanen H, Vittinghoff E, Knekt P, Heliövaara M, Huikuri HV, Marcus GM (May 2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check |pmc= value (help). PMID 31125096.
  16. Schoeller R, Andresen D, Büttner P, Oezcelik K, Vey G, Schröder R (March 1993). "First- or second-degree atrioventricular block as a risk factor in idiopathic dilated cardiomyopathy". Am. J. Cardiol. 71 (8): 720–6. doi:10.1016/0002-9149(93)91017-c. PMID 8447272.
  17. Rodstein M, Wolloch L, Iuster Z (1979). "The natural history intraventricular conduction disturbances in the aged: an analysis of the developing second and third degree heart block with clinical pathological correlations". Am. J. Med. Sci. 277 (2): 179–88. doi:10.1097/00000441-197903000-00006. PMID 463945.
  18. 18.0 18.1 Bexton RS, Camm AJ (March 1984). "Second degree atrioventricular block". Eur. Heart J. 5 Suppl A: 111–4. doi:10.1093/eurheartj/5.suppl_a.111. PMID 6373268.
  19. Thiruganasambandamoorthy V, Hess EP, Turko E, Tran ML, Wells GA, Stiell IG (July 2012). "Defining abnormal electrocardiography in adult emergency department syncope patients: the Ottawa Electrocardiographic Criteria". CJEM. 14 (4): 248–58. PMID 22813399.
  20. Barold SS, Van Heuverswyn FE, Timmers L, Stroobandt RX (August 2014). "Mobitz type II second-degree atrioventricular block during dobutamine stress echocardiography. True or false?". Echocardiography. 31 (7): 799–801. doi:10.1111/echo.12577. PMID 25080840.
  21. 21.0 21.1 Fu Md J, Bhatta L (2018). "Lyme carditis: Early occurrence and prolonged recovery". J Electrocardiol. 51 (3): 516–518. doi:10.1016/j.jelectrocard.2017.12.035. PMID 29275956.
  22. 22.0 22.1 Kashou AH, Goyal A, Nguyen T, Chhabra L. PMID 29083636. Missing or empty |title= (help)
  23. Zeppilli P, Fenici R, Sassara M, Pirrami MM, Caselli G (September 1980). "Wenckebach second-degree A-V block in top-ranking athletes: an old problem revisited". Am. Heart J. 100 (3): 281–94. doi:10.1016/0002-8703(80)90140-4. PMID 7405798.
  24. Rosen KM, Dhingra RC, Loeb HS, Rahimtoola SH (1973). "Chronic heart block in adults. Clinical and electrophysiological observations". Arch Intern Med. 131 (5): 663–72. PMID 4701376.
  25. Schneider MD, Roller DH, Morganroth J, Josephson ME (July 1978). "The syndromes of familial atrioventricular block with sinus bradycardia: prognostic indices, electrophysiologic and histopathologic correlates". Eur J Cardiol. 7 (5–6): 337–51. PMID 699934.
  26. Trappe HJ (September 2016). "[Consciousness disorders from cardiological view]". Dtsch. Med. Wochenschr. (in German). 141 (19): 1361–9. doi:10.1055/s-0042-103177. PMID 27642736.
  27. Gupta PK, Lichstein E, Chadda KD (1976). "Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients". Br Heart J. 38 (12): 1343–9. doi:10.1136/hrt.38.12.1343. PMC 483178. PMID 1008977.
  28. Steere AC, McHugh G, Damle N, Sikand VK (2008). "Prospective study of serologic tests for lyme disease". Clin Infect Dis. 47 (2): 188–95. doi:10.1086/589242. PMC 5538270. PMID 18532885.
  29. Schernthaner C, Kraus J, Danmayr F, Hammerer M, Schneider J, Hoppe UC, Strohmer B (March 2016). "Short-term pacemaker dependency after transcatheter aortic valve implantation". Wien. Klin. Wochenschr. 128 (5–6): 198–203. doi:10.1007/s00508-015-0906-4. PMID 26745972.
  30. Brignole M, Deharo JC, Guieu R (August 2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.
  31. Kelkar PN (August 1998). "Atenolol induced high grade AV block". J Assoc Physicians India. 46 (8): 748, 751. PMID 11229299.
  32. Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S (July 2004). "Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug". J. Am. Coll. Cardiol. 44 (1): 105–8. doi:10.1016/j.jacc.2004.03.057. PMID 15234417.
  33. Tuohy S, Saliba W, Pai M, Tchou P (January 2018). "Catheter ablation as a treatment of atrioventricular block". Heart Rhythm. 15 (1): 90–96. doi:10.1016/j.hrthm.2017.08.015. PMID 28823599.
  34. Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD (August 2019). "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 74 (7): e51–e156. doi:10.1016/j.jacc.2018.10.044. PMID 30412709.
  35. Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM (May 1981). "Natural history of chronic second-degree atrioventricular nodal block". Circulation. 63 (5): 1043–9. doi:10.1161/01.cir.63.5.1043. PMID 7471363.
  36. Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ; et al. (2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check |pmc= value (help). PMID 31125096.
  37. Barold SS (1996). "Indications for permanent cardiac pacing in first-degree AV block: class I, II, or III?". Pacing Clin Electrophysiol. 19 (5): 747–51. doi:10.1111/j.1540-8159.1996.tb03355.x. PMID 8734740.
  38. Upshaw CB (2004). "Comparison of the prevalence of first-degree atrioventricular block in African-American and in Caucasian patients: an electrocardiographic study III". J Natl Med Assoc. 96 (6): 756–60. PMC 2568382. PMID 15233485.
  39. Friedman HS, Gomes JA, Haft JI (1975). "An analysis of Wenckebach periodicity". J Electrocardiol. 8 (4): 307–15. doi:10.1016/s0022-0736(75)80003-3. PMID 1176840.
  40. OSTRANDER LD, BRANDT RL, KJELSBERG MO, EPSTEIN FH (June 1965). "ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN". Circulation. 31: 888–98. doi:10.1161/01.cir.31.6.888. PMID 14297523.
  41. Movahed MR, Hashemzadeh M, Jamal MM (October 2005). "Increased prevalence of third-degree atrioventricular block in patients with type II diabetes mellitus". Chest. 128 (4): 2611–4. doi:10.1378/chest.128.4.2611. PMID 16236932.
  42. Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  43. Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  44. Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  45. Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  46. Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  47. "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  48. Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  49. Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  50. Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  51. Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  52. Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  53. Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  54. Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  55. Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  56. Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  57. Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  58. Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  59. Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.


Template:WikiDoc Sources