Paroxysmal AV block pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Intrinsic paroxysmal AV block]] (I-AVB) is an AV block secondary to an [[innate]] [[anatomical]] [[defect]]. Given the presence of such a [[defect]] it's [[prognosis]], compared to [[extrinsic paroxysmal vagal AV block]] and [[extrinsic paroxysmal idiopathic AV block]] is poor. It may have a [[bradycardia]] or [[tachycardia]] component associated with it and is characterized by [[atrial]]/[[ventricular premature beats]] prior to the period of [[asystole]]. [[Extrinsic vagal paroxysmal AV Block]] occurs secondary to an increase in [[vagal tone]]. [[ECG]] findings reflecting this include [[sinus rate]] slowing and increasing [[PP interval|PP interva]]<nowiki/>l/ [[PR interval]] prior to the period of [[asystole]]. Individuals with low levels of [[adenosine]] are susceptible to sudden surges in [[adenosine]] levels which act on the [[AV node]] and cause episodes of [[presyncope]] or [[syncope]]. This would be seen on an [[ECG]] as a sudden increase in [[sinus rate]] with narrow [[QRS complexes]] just prior to the period of [[asystole]]. | |||
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==Intrinsic Paroxysmal AV Block== | |||
*Intrinsic [[AV block]] (I-AVB) is an [[AV block]] [[secondary]] to an [[Innate immune system|innate]] [[Anatomy|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 [[Atrioventricular block|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 [[Depolarization|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 (physiology)|stimulus]] would not be able to induce an [[action potential]]. <ref name="pmid19968933">{{cite journal| author=El-Sherif N, Jalife J| title=Paroxysmal atrioventricular block: are phase 3 and phase 4 block mechanisms or misnomers? | journal=Heart Rhythm | year= 2009 | volume= 6 | issue= 10 | pages= 1514-21 | pmid=19968933 | doi=10.1016/j.hrthm.2009.06.025 | pmc=2877697 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19968933 }} </ref> | |||
*A [[hypothetical]] line of thinking that could be attributed to both PD-AVB and TD-AVB is a '''‘concealed [[Conduction System|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 response rate]]. | |||
*Certain studies hypothesize that [[ventricular]] or [[Supraventricular arrhythmia|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 [[Electrophysiologic study|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]]) <ref name="pmid19632639">{{cite journal| author=Lee S, Wellens HJ, Josephson ME| title=Paroxysmal atrioventricular block. | journal=Heart Rhythm | year= 2009 | volume= 6 | issue= 8 | pages= 1229-34 | pmid=19632639 | doi=10.1016/j.hrthm.2009.04.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19632639 }} </ref> | |||
*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]], [[Right bundle branch 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. | |||
==Extrinsic Vagal Paroxysmal 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 test|tilt table testing]], [[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|sinus rate slowing]], increasing/irregular PP and [[PR interval]]<nowiki/>s''' 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 System|conduction]] in the [[bundle of His]] and is not associated with any [[anatomic]] involvement, as seen in intrinsic AV Block. <ref name="pmid23286970">{{cite journal| author=Alboni P, Holz A, Brignole M| title=Vagally mediated atrioventricular block: pathophysiology and diagnosis. | journal=Heart | year= 2013 | volume= 99 | issue= 13 | pages= 904-8 | pmid=23286970 | doi=10.1136/heartjnl-2012-303220 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23286970 }} </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="pmid10758936">{{cite journal| author=Mendoza IJ, Castellanos A, Lopera G, Moleiro F, Mitrani RD, Myerburg RJ| title=Spontaneous paroxysmal atrioventricular block in patients with positive tilt tests and negative electrophysiologic studies. | journal=Am J Cardiol | year= 2000 | volume= 85 | issue= 7 | pages= 893-6, A9 | pmid=10758936 | doi=10.1016/s0002-9149(99)00890-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10758936 }} </ref> | |||
*The effect of [[Vagus nerve|vagal]] stimulation depends on the method and [[intensity]] of stimulation and the resting [[Sympathetic nervous system|sympathetic]] activity. | |||
*[[Vasalva maneuver]], [[carotid sinus massage]], water face immersion, [[Tilt table test|tilt table testing]] may or may not induce an EV- AVB and in some cases a '''reversal may be seen on [[atropine]] [[administration]]'''. {{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=}} | |||
==Extrinsic Idiopathic Paroxysmal AV Block== | |||
*The [[pathogenesis]] of [[extrinsic idiopathic paroxysmal AV block]] (EI-AVB) can be correlated to ''' [[adenosine]] [[Blood plasma|plasma]] levels (APL) and increased [[affinity]] of [[Adenosine A1 receptor|adenosine]] A1 receptors'''. | |||
== | *There is a recurrent history of unexplained [[syncope]], absence of [[ECG]] and [[cardiac]] abnormalities and a good [[prognosis]]. | ||
*Due to [[innate]]<nowiki/>ly 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. | |||
The | *[[A1 receptors]], which are present more in the [[AV node]] than the [[SA node]], impose an '''[[antiadrenergic]] action''' by antagonizing [[Βeta receptors|β1 receptors]], the [[sympathetic nervous system]], [[hyperpolarizing]] the SA and [[AV nodes]] through [[potassium channels]] and lowering [[intracellular]] [[Cyclic adenosine monophosphate|cAMP]] levels. <ref name="pmid26115830">{{cite journal| author=Brignole M, Deharo JC, Guieu R| title=Syncope and Idiopathic (Paroxysmal) AV Block. | journal=Cardiol Clin | year= 2015 | volume= 33 | issue= 3 | pages= 441-7 | pmid=26115830 | doi=10.1016/j.ccl.2015.04.012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26115830 }} </ref> | ||
*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]] | |||
*Certain studies have also noticed '''[[genetic]] [[polymorphisms]] in [[Adenosine A2A receptor|A2A receptor]]<nowiki/>s''' in a population of people experiencing recurrent unexplained [[syncope]]. .<ref name="pmid19386617">{{cite journal| author=Saadjian AY, Gerolami V, Giorgi R, Mercier L, Berge-Lefranc JL, Paganelli F | display-authors=etal| title=Head-up tilt induced syncope and adenosine A2A receptor gene polymorphism. | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 12 | pages= 1510-5 | pmid=19386617 | doi=10.1093/eurheartj/ehp126 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19386617 }} </ref> | |||
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==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Cardiovascular diseases]] | [[Category:Cardiovascular diseases]] | ||
Latest revision as of 08:15, 11 July 2020
Overview
Intrinsic paroxysmal AV block (I-AVB) is an AV block secondary to an innate anatomical defect. Given the presence of such a defect it's prognosis, compared to extrinsic paroxysmal vagal AV block and extrinsic paroxysmal idiopathic AV block is poor. It may have a bradycardia or tachycardia component associated with it and is characterized by atrial/ventricular premature beats prior to the period of asystole. Extrinsic vagal paroxysmal AV Block occurs secondary to an increase in vagal tone. ECG findings reflecting this include sinus rate slowing and increasing PP interval/ PR interval prior to the period of asystole. Individuals with low levels of adenosine are susceptible to sudden surges in adenosine levels which act on the AV node and cause episodes of presyncope or syncope. This would be seen on an ECG as a sudden increase in sinus rate with narrow QRS complexes just prior to the period of asystole.
Intrinsic Paroxysmal 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. [1]
- 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 response rate.
- 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) [2]
- 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.
Extrinsic Vagal Paroxysmal 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 testing, 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. [3]
- 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. [4]
- 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. "Paroxysmal vagally mediated av block with recurrent syncope - Talwar - 1985 - Clinical Cardiology - Wiley Online Library".
Extrinsic Idiopathic Paroxysmal 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. [5]
- 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
- Certain studies have also noticed genetic polymorphisms in A2A receptors in a population of people experiencing recurrent unexplained syncope. .[6]
References
- ↑ El-Sherif N, Jalife J (2009). "Paroxysmal atrioventricular block: are phase 3 and phase 4 block mechanisms or misnomers?". Heart Rhythm. 6 (10): 1514–21. doi:10.1016/j.hrthm.2009.06.025. PMC 2877697. PMID 19968933.
- ↑ Lee S, Wellens HJ, Josephson ME (2009). "Paroxysmal atrioventricular block". Heart Rhythm. 6 (8): 1229–34. doi:10.1016/j.hrthm.2009.04.001. PMID 19632639.
- ↑ Alboni P, Holz A, Brignole M (2013). "Vagally mediated atrioventricular block: pathophysiology and diagnosis". Heart. 99 (13): 904–8. doi:10.1136/heartjnl-2012-303220. PMID 23286970.
- ↑ Mendoza IJ, Castellanos A, Lopera G, Moleiro F, Mitrani RD, Myerburg RJ (2000). "Spontaneous paroxysmal atrioventricular block in patients with positive tilt tests and negative electrophysiologic studies". Am J Cardiol. 85 (7): 893–6, A9. doi:10.1016/s0002-9149(99)00890-5. PMID 10758936.
- ↑ Brignole M, Deharo JC, Guieu R (2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.
- ↑ Saadjian AY, Gerolami V, Giorgi R, Mercier L, Berge-Lefranc JL, Paganelli F; et al. (2009). "Head-up tilt induced syncope and adenosine A2A receptor gene polymorphism". Eur Heart J. 30 (12): 1510–5. doi:10.1093/eurheartj/ehp126. PMID 19386617.