Paroxysmal AV Block Intrinsic AV Block: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
*Intrinsic [[AV block]] (I-AVB) is an AV block secondary to an innate anatomical defect. | *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. | *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).''' | **[[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 depolarizing sodium current.''' | *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’.''' | *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. | *Despite [[repolarization]] being complete, a [[Stimulus (physiology)|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 | *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 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 | *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]]) | ||
*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. | *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. | ||
==References== | ==References== | ||
<references /> | <references /> | ||
Revision as of 14:07, 27 June 2020
Intrinsic AV Block
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.
Pathophysiology
- 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 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)
- 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.