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{{CMG}}; {{AE}}{{Akash}}
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{{SK}}  
{{SK}} [[idiopathic paroxysmal AV block]], [[extrinsic vagal paroxysmal AV block]], [[extrinsic idiopathic paroxysmal AV block]], [[Paroxysmal Atrio-Ventricular block]], [[Paroxysmal Atrioventricular block]], [[intrinsic paroxysmal AV block]], [[idiopathic paroxysmal Atrioventricular block]], [[idiopathic paroxysmal Atrio-Ventricular block]], [[extrinsic vagal paroxysmal Atrioventricular block]], [[extrinsic vagal paroxysmal Atrio-Ventricular block]], [[extrinsic idiopathic paroxysmal Atrio-Ventricular block]], [[extrinsic idiopathic paroxysmal Atrioventricular block]], [[Paroxysmal av block]], [[extrinsic vagal paroxysmal av block]], [[extrinsic idiopathic paroxysmal av block]], [[Paroxysmal atrio-ventricular block]], [[Paroxysmal atrioventricular block]], [[intrinsic paroxysmal av block]], [[idiopathic paroxysmal atrioventricular block]], [[idiopathic paroxysmal atrio-ventricular block]], [[extrinsic vagal paroxysmal etrioventricular block]], [[extrinsic vagal paroxysmal atrio-ventricular block]], [[extrinsic idiopathic paroxysmal atrio-ventricular block]], [[extrinsic idiopathic paroxysmal atrioventricular block]]


==[[Paroxysmal AV block overview|Overview]]==
==[[Paroxysmal AV block overview|Overview]]==


==[[Paroxysmal AV block historical perspective|Historical Perspective]]==
==[[Paroxysmal AV Block Historical Perspective|Historical Perspective]]==
 
*There is limited information about the historical perspective of paroxysmal AV block.
*In 1931, Adolph Sachs et al reported one of the first cases on paroxysmal AV block. The patient had presented with multiple spells of palpitations, hot flashes, dizziness, ringing in the ears, weakness and diaphoresis accompanied by convulsions. During an acute episode, he noticed an irregular ventricular rhythm, irregular complexes and given a time interval of 30 seconds, the ventricle would beat once in the first 15 second window and 4-5 times in the succeeding window.  It was noticed that the duration of the block progressively increased until it was present all the time. Mitral valvulitis was put down as the cause of the attack and the fact that a response to atropine does not rule out an intrinsic conduction defect was emphasized. <ref name="urlParoxysmal complete auriculo-ventricular heart-block: A case report - ScienceDirect">{{cite web |url=https://www.sciencedirect.com/science/article/abs/pii/S000287033390722X |title=Paroxysmal complete auriculo-ventricular heart-block: A case report - ScienceDirect |format= |work= |accessdate=}}</ref>
*In 1972, Philippe Coumel et al hypothesized that the cause of bradycardia/pause dependent AV block was the spontaneous depolarization of specialized conducting fibers in the late stages of diastole. It was during this ‘zone of opportunity’ that they noticed this ‘AV dissociation’. In this case, they found that the block occurred to be proximal to the division of the His bundle. <ref name="urlBradycardia-dependent atrio-ventricular block: Report of two cases of A-V block elicited by premature beats - ScienceDirect">{{cite web |url=https://www.sciencedirect.com/science/article/abs/pii/S0022073671800109 |title=Bradycardia-dependent atrio-ventricular block: Report of two cases of A-V block elicited by premature beats - ScienceDirect |format= |work= |accessdate=}}</ref>
*In 1997. Brignole et al first described EI AVB in a group of 15 syncope patients with an initial negative work up. They fortuitously stumbled upon ECG findings indicating a paroxysmal AV block and reconfirmed this by performing an adenosine triphosphate test in each patient. <ref name="pmid9403616">{{cite journal |vauthors=Brignole M, Gaggioli G, Menozzi C, Gianfranchi L, Bartoletti A, Bottoni N, Lolli G, Oddone D, Del Rosso A, Pellinghelli G |title=Adenosine-induced atrioventricular block in patients with unexplained syncope: the diagnostic value of ATP testing |journal=Circulation |volume=96 |issue=11 |pages=3921–7 |date=December 1997 |pmid=9403616 |doi=10.1161/01.cir.96.11.3921 |url=}}</ref>


==[[Paroxysmal AV block classification|Classification]]==
==[[Paroxysmal AV block classification|Classification]]==
*Paroxysmal AV Block may be classified according to the cause into three types :
#Intrinsic AV Block (I-AVB)
#Extrinsic Vagal AV Block (EV- AVB)
#Extrinsic Idiopathic AV Block (EI- AVB)<ref name="pmid29255501">{{cite journal |vauthors=Aste M, Brignole M |title=Syncope and paroxysmal atrioventricular block |journal=J Arrhythm |volume=33 |issue=6 |pages=562–567 |date=December 2017 |pmid=29255501 |doi=10.1016/j.joa.2017.03.008 |url=}}</ref>
{{familytree/start}}
{{familytree | | | | | | | |A01| | |A01='''Paroxysmal AV Block classification based on cause'''}}
{{familytree | | | |,|-|-|-|-|+|-|-|-|-|-|.|}}
{{familytree | | | |B10| | |B11| | | |B12|B10='''Intrinsic AV Block (I-AVB):'''
Due to innate structural/ conduction defect| B11='''Extrinsic Vagal AV Block (EV- AVB):'''
Due to vagal surge/reflex |B12='''Extrinsic Idiopathic AV Block (EI- AVB) :''' Due to innately low adenosine plasma levels |}}
{{familytree |,|-|-|-|^|-|-|.| | | | |}}
{{familytree |C10| | | C11| | | | | | |C10= '''Tachycardia Dependent AV Block (TD- AVB)'''|C11= '''Bradcardia/Pause Dependent AV Block (BD- AVB/PD-AVB)}}
{{familytree/end}} <ref name="pmid29255501">{{cite journal |vauthors=Aste M, Brignole M |title=Syncope and paroxysmal atrioventricular block |journal=J Arrhythm |volume=33 |issue=6 |pages=562–567 |date=December 2017 |pmid=29255501 |doi=10.1016/j.joa.2017.03.008 |url=}}</ref>


==[[Paroxysmal AV block pathophysiology|Pathophysiology]]==
==[[Paroxysmal AV block pathophysiology|Pathophysiology]]==
==Intrinsic AV Block==
*Intrinsic AV block (I-AVB) is an AV block secondary to an innate anatomical defect.
*It is hugely recognized on an ECG as an atrial premature beat (APB) or ventricular premature beat (VPB) before and after a variable period of complete AV block/asystole.
**Sinus rate increase/ decrease prior to the VPB/APB or during the period of asystole further divides it into '''Tachycardia Dependent AV block (TD-AVB) and Pause/Bradycardia dependent AV block (PD- AVB).'''
*Normal cardiac myocytes are associated with '''a more negative resting membrane potential, an increased amplitude of action potential and a fast depolarizing sodium current.'''
*An '''exact opposite''' is seen in diseased myocytes responsible for TD- PAVB. An '''imbalance''' between inward depolarizing sodium and calcium currents and outward repolarizing potassium currents causes an increase in recovery time and leads to a phenomenon called '''‘post-repolarization refractoriness’.'''
*Despite repolarization being complete, a stimulus would not be able to induce an action potential.
*A hypothetical line of thinking that could be attributed to both PD-AVB and TD-AVB is a '''‘concealed conduction’  in the intra His Bundle''' which serves as a source of a delayed escape rhythm, thereby disrupting  the refractoriness and recovery time of the surrounding myocytes. This predisposes the patient to fatal complications such as syncope, presyncope, sudden cardiac death and atrial fibrillation with a rapid ventricular repose rate. <ref name="pmid19968933">{{cite journal |vauthors=El-Sherif N, Jalife J |title=Paroxysmal atrioventricular block: are phase 3 and phase 4 block mechanisms or misnomers? |journal=Heart Rhythm |volume=6 |issue=10 |pages=1514–21 |date=October 2009 |pmid=19968933 |pmc=2877697 |doi=10.1016/j.hrthm.2009.06.025 |url=}}</ref>
*Certain studies hypothesize that ventricular or supraventricular impulses reach this ‘concealed conduction’ at a time when there is a local phase 4 block (when sodium channels are inactive.) This subsequent long pause is reflected by the '''increased H-H interval in EPS studies''' and confirms an intra His Bundle block (an entity commonly missed and mislabeled as an infra-His Bundle block or AV- block on electrophysiological studies)
*Much debate surrounds this as it has also been documented that TD- AV/ PD-AV blocks are not related to phase 3 or phase 4 conduction defects, as previously hypothesized. It is related to myocardial ischemia, Mobitz type II block, RBBB and Intra His bundle conduction defects, retrograde ventricular premature beats and anterograde atrial premature beats; all factors that are independent of local phase 4 blocks. <ref name="pmid19632639">{{cite journal |vauthors=Lee S, Wellens HJ, Josephson ME |title=Paroxysmal atrioventricular block |journal=Heart Rhythm |volume=6 |issue=8 |pages=1229–34 |date=August 2009 |pmid=19632639 |doi=10.1016/j.hrthm.2009.04.001 |url=}}</ref>
==Extrinsic Vagal AV Block==
*An extrinsic vagally mediated AV block (EV-AVB) may occur due to a '''vagal surge or a condition causing an increase in vagal tone''' such as during tilt table tesing, carotid sinus massage, coughing, micturition, defecation, swallowing, myocardial infarction, injection of dypramidole and cardiac transplant rejection.
*It causes SA and AV node slowing and is therefore reflected on the ECG as '''sinus rate slowing, increasing/irregular PP and PR intervals''' prior to a period of compete AV block. A heterogenous presentation in terms of Mobitz type I or II and complete heart block may also be noted. This is followed by a period of sinus acceleration. 
*Electrophysiological studies indicate a '''normal H-H interval''' and therefore it can be assumed that it does not have any effect on conduction in the bundle of His and is not associated with any anatomic involvement, as seen in intrinsic AV Block. <ref name="pmid">{{cite journal |vauthors=Alboni P, Holz A, Brignole M |title=Vagally mediated atrioventricular block: pathophysiology and diagnosis |journal=Heart |volume=99 |issue=13 |pages=904–8 |date=July 2013 |pmid= |doi=10.1136/heartjnl-2012-303220 |url=}}</ref>
*The pathophysiology of EV-AVB may even be related to the autonomic control of the sinus and AV nodes. A parasympathetic predominance over the SA node and sympathetic predominance over the AV node is exerted in a normal autonomic nervous system.
*A disruption in this regulation may cause '''parasympathetic bursts''' and therefore, an AV block. <ref name="url(PDF) Spontaneous paroxysmal atrioventricular block in patients with positive tilt tests and negative electrophysiologic studies | Ivan Mendoza - Academia.edu">{{cite web |url=https://www.academia.edu/6286513/Spontaneous_paroxysmal_atrioventricular_block_in_patients_with_positive_tilt_tests_and_negative_electrophysiologic_studies |title=(PDF) Spontaneous paroxysmal atrioventricular block in patients with positive tilt tests and negative electrophysiologic studies &#124; Ivan Mendoza - Academia.edu |format= |work= |accessdate=}}</ref>
*The effect of vagal stimulation depends on the method and intensity of stimulation and the resting sympathetic activity.
*Vasalva maneuver, carotid sinus massage,  water face immersion, tilt table testing may or may not induce an EV- AVB and in some cases a '''reversal may be seen on atropine administration'''. <ref name="urlParoxysmal vagally mediated av block with recurrent syncope - Talwar - 1985 - Clinical Cardiology - Wiley Online Library">{{cite web |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/clc.4960080606 |title=Paroxysmal vagally mediated av block with recurrent syncope - Talwar - 1985 - Clinical Cardiology - Wiley Online Library |format= |work= |accessdate=}}</ref>
==Extrinsic Idiopathic AV Block==
*The pathogenesis of extrinsic idiopathic paroxysmal AV block (EI-AVB) can be correlated to ''' adenosine plasma levels (APL) and increased affinity of adenosine A1 receptors'''.
*There is a recurrent history of unexplained syncope, absence of ECG and cardiac abnormalities and a good prognosis.
*Due to innately low APL values seen in these patients, there is '''an upregulation of A1 receptors''', such that even during a mild transient surge in endogenous adenosine levels, AV block occurs.
*A1 receptors, which are present more in the AV node than the SA node, impose an '''antiadrenergic action''' by antagonizing β1 receptors, the sympathetic nervous system, hyperpolarizing the SA and AV nodes through potassium channels and lowering intracellular cAMP levels.
*Therefore, in such patients an injection of adenosine or adenosine triphosphate (ATP) may reproduce the attack and adenosine antagonists such as theophylline may be an efficacious treatment option.
*On an ECG, there is an absence of signs of vagal stimulation, atrial/ventricular premature beats and there may be a presence of narrow QRS complexes prior to the period of complete AV Block/ asystole<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>
*Certain studies have also noticed '''genetic polymorphisms in A2A receptors''' in a population of people experiencing recurrent unexplained syncope.<ref name="pmid19386617">{{cite journal |vauthors=Saadjian AY, Gerolami V, Giorgi R, Mercier L, Berge-Lefranc JL, Paganelli F, Ibrahim Z, By Y, Guéant JL, Lévy S, Guieu RP |title=Head-up tilt induced syncope and adenosine A2A receptor gene polymorphism |journal=Eur. Heart J. |volume=30 |issue=12 |pages=1510–5 |date=June 2009 |pmid=19386617 |doi=10.1093/eurheartj/ehp126 |url=}}</ref>
==[[Paroxysmal AV block causes|Causes]]==
==[[Paroxysmal AV block differential diagnosis|Differentiating Paroxysmal AV block from other Diseases]]==
==[[Paroxysmal AV block epidemiology and demographics|Epidemiology and Demographics]]==
==[[Paroxysmal AV block risk factors|Risk Factors]]==


==[[Paroxysmal AV block screening|Screening]]==
==[[Paroxysmal AV block Causes|Causes]]==


==[[Paroxysmal AV block natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
==[[Paroxysmal AV block Differentiating Paroxysmal AV Block from other Diseases |Differentiating Paroxysmal AV Block from other Diseases]]==


===Initial Approach===
==[[Paroxysmal AV block epidemiology and Demographics |Epidemiology and Demographics]]==


*The pathway to conclusively diagnosing a patient with paroxysmal AV block is not straightforward.
==[[Paroxysmal AV block Risk Factors|Risk Factors]]==
*Since most patients present with a history of recurrent unexplained syncope and fortuitous timing would be required to document classical ECG findings during an acute episode, it *would be best to treat it as a diagnosis of exclusion.
*An initial evaluation strategy of taking a detailed history, physical examination, risk stratification, ECG recording and BP measurement should help decide what investigations should be ordered (based on whether the syncope is cardiac related, reflex/neutrally mediated, secondary to cerebrovascular disease or due to orthostatic hypotension).
IMAGE TO BE INSERTED


==[[Paroxysmal AV block Screening|Screening]]==


===History===
==[[Paroxysmal AV Block Natural History, Complications and Prognosis|Natural History, Complications and Prognosis]]==
*History of syncope, presyncope, duration of each episode, number of episodes, activities during the syncopal episode, aggravating or relieving factors, history of past medical illnesses, prodrome/ recovery phase description in terms of signs, symptoms and duration are important points to be addressed whilst taking a history of a syncope patient.
*A study of 341 syncope patients showed that the time between the first and last syncopal episode being less than 4 years, syncope during effort or supine position, a history of palpitations, convulsions or blurring of vision were important predictors of a cardiac syncope. <ref name="pmid11401133">{{cite journal |vauthors=Alboni P, Brignole M, Menozzi C, Raviele A, Del Rosso A, Dinelli M, Solano A, Bottoni N |title=Diagnostic value of history in patients with syncope with or without heart disease |journal=J. Am. Coll. Cardiol. |volume=37 |issue=7 |pages=1921–8 |date=June 2001 |pmid=11401133 |doi=10.1016/s0735-1097(01)01241-4 |url=}}</ref>
*Similarly, duration of prodrome > 10 seconds history of pallor, nausea, diaphoresis, dizziness, presyncope, abdominal discomfort and time between first and last syncopal episode being more than 4 years were important predictors of a neutrally mediated syncope. <ref name="pmid11401133">{{cite journal |vauthors=Alboni P, Brignole M, Menozzi C, Raviele A, Del Rosso A, Dinelli M, Solano A, Bottoni N |title=Diagnostic value of history in patients with syncope with or without heart disease |journal=J. Am. Coll. Cardiol. |volume=37 |issue=7 |pages=1921–8 |date=June 2001 |pmid=11401133 |doi=10.1016/s0735-1097(01)01241-4 |url=}}</ref>
*Based on a detailed history, one can decide whether a cardiac syncope was secondary to a rhythm dysfunction, structural cause or ischemia related and would warrant a work up of an ECG, Holter monitoring, echocardiography, electrophysiologic study, or an exercise stress test.
*Similarly, neutrally mediated syncope maybe vasovagal, situational, secondary to increased carotid sinus sensitivity or non classical and orthostatic hypotension may be due to a primary or secondary autonomic failure, secondary to drugs or hypovolemia. This may be further explored by a carotid sinus massage, tilt table testing, adenosine plasma levels or an adenosine triphosphate stimulation test. <ref name="urlESC Guidelines on Syncope (Diagnosis and Management of)">{{cite web |url=https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Syncope-Guidelines-on-Diagnosis-and-Management-of |title=ESC Guidelines on Syncope (Diagnosis and Management of) |format= |work= |accessdate=}}</ref>
*Lab investigations such as arterial blood gas analysis, hemoglobin, troponin or D- dimer may help with the diagnoses in appropriate clinical situations. <ref name="urlESC Guidelines on Syncope (Diagnosis and Management of)">{{cite web |url=https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Syncope-Guidelines-on-Diagnosis-and-Management-of |title=ESC Guidelines on Syncope (Diagnosis and Management of) |format= |work= |accessdate=}}</ref>


==Diagnosis==
==Diagnosis==
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[[Category:Cardiovascular diseases]]
[[Category:Cardiovascular diseases]]
[[Category:Arrythmia]]
[[Category:Arrhythmia]]
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[[Category:Emergency medicine]]
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Latest revision as of 19:51, 3 September 2020

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

Synonyms and keywords: idiopathic paroxysmal AV block, extrinsic vagal paroxysmal AV block, extrinsic idiopathic paroxysmal AV block, Paroxysmal Atrio-Ventricular block, Paroxysmal Atrioventricular block, intrinsic paroxysmal AV block, idiopathic paroxysmal Atrioventricular block, idiopathic paroxysmal Atrio-Ventricular block, extrinsic vagal paroxysmal Atrioventricular block, extrinsic vagal paroxysmal Atrio-Ventricular block, extrinsic idiopathic paroxysmal Atrio-Ventricular block, extrinsic idiopathic paroxysmal Atrioventricular block, Paroxysmal av block, extrinsic vagal paroxysmal av block, extrinsic idiopathic paroxysmal av block, Paroxysmal atrio-ventricular block, Paroxysmal atrioventricular block, intrinsic paroxysmal av block, idiopathic paroxysmal atrioventricular block, idiopathic paroxysmal atrio-ventricular block, extrinsic vagal paroxysmal etrioventricular block, extrinsic vagal paroxysmal atrio-ventricular block, extrinsic idiopathic paroxysmal atrio-ventricular block, extrinsic idiopathic paroxysmal atrioventricular block

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