Paroxysmal AV block: Difference between revisions

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==[[Paroxysmal AV block classification|Classification]]==
==[[Paroxysmal AV block classification|Classification]]==
[[Paroxysmal AV Block Classification Based on Cause| Classification Based on Cause]]
*Paroxysmal AV Block may be classified according to the cause into three types :  
*Paroxysmal AV Block may be classified according to the cause into three types :  
#Intrinsic AV Block (I-AVB)
#Intrinsic AV Block (I-AVB)

Revision as of 07:12, 15 June 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]

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Overview

Historical Perspective

Historical Perspective | Famous cases

Classification

Classification Based on Cause

  • Paroxysmal AV Block may be classified according to the cause into three types :
  1. Intrinsic AV Block (I-AVB)
  2. Extrinsic Vagal AV Block (EV- AVB)
  3. Extrinsic Idiopathic AV Block (EI- AVB) "Syncope and paroxysmal atrioventricular block - Aste - 2017 - Journal of Arrhythmia - Wiley Online Library".


 
 
 
 
 
 
 
Paroxysmal AV Block classification based on cause
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intrinsic AV Block (I-AVB): Due to innate structural/ conduction defect
 
 
Extrinsic Vagal AV Block (EV- AVB): Due to vagal surge/reflex
 
 
 
Extrinsic Idiopathic AV Block (EI- AVB) : Due to innately low adenosine plasma levels
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Tachycardia Dependent AV Block (TD- AVB)
 
 
Bradcardia/Pause Dependent AV Block (BD- AVB/PD-AVB)
 
 
 
 
 
 

[1]

Pathophysiology

Intrinsic AV Block | Extrinsic Vagal AV Block | Extrinsic Idiopathic AV Block

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. [2]
  • 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. [3]
  • 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 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. [4]
  • 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.[5]

Causes

Differentiating Paroxysmal AV block from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Diagnosis

Initial Approach | History and Symptoms | Electrocardiogram, Holter Monitoring, External Loop Recorder | Implantable Loop Recorder | Electrophysiologic studies | Vagal Maneuvers,Carotid Sinus Massage and Tilt Table testing | Laboratory Findings and Stimulation tests | Diagnostic Summary Table |


Treatment

Cardiac Pacing |Treatment for Reflex Syncope|Theopylline |

Case Studies

Case #1


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  1. Aste M, Brignole M (December 2017). "Syncope and paroxysmal atrioventricular block". J Arrhythm. 33 (6): 562–567. doi:10.1016/j.joa.2017.03.008. PMID 29255501.
  2. 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.
  3. 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.
  4. 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.
  5. 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.