Paroxysmal AV block
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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:
Overview
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. "Paroxysmal complete auriculo-ventricular heart-block: A case report - ScienceDirect".
- 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. [1]
- 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. [2]
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) "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) | ||||||||||||||||||||||||||||||||||
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. [4]
- 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.
- 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) [5]
- 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 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. [6]
- 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. [7]
- 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. [8]
- 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.[9]
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 | Summary Table |
Vagal Maneuvers : Carotid Sinus massage and Tilt Table testing
- Though not specific,tilt table testing (TT) and other vagal maneuvers such as the vasalva maneuver, eye ball pressure and immersing one's face in cold water can be used in the diagnosis of EV-AVB.
- The Syncope Unit Project-2 study found an increase recurrence rate in patients who did not undergo tilt table testing. This highlights the utility of TT as a screening test for reflex syncope.
- A positive response is indicated as a marker of hypotensive susceptibility which involves a decrease in both preload and afterload. Brignole M, Arabia F, Ammirati F, Tomaino M, Quartieri F, Rafanelli M, Del Rosso A, Rita Vecchi M, Russo V, Gaggioli G (September 2016). "Standardized algorithm for cardiac pacing in older patients affected by severe unpredictable reflex syncope: 3-year insights from the Syncope Unit Project 2 (SUP 2) study". Europace. 18 (9): 1427–33. doi:10.1093/europace/euv343. PMID 26612880.
- Having said that, a negative test does not rule out the possibility of an extrinsic vagal paroxysmal AV block.
- A carotid sinus massage is indicated in patients more than 40 years of age with syncope of unknown origin compatible with reflex mechanism.
- Carotid sinus sensitivity is confirmed if carotid sinus massage causes bradycardia (asystole) and/or hypotension that reproduce spontaneous symptoms and patients have clinical features compatible with reflex mechanism of syncope. "ESC Guidelines on Syncope (Diagnosis and Management of)".
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Laboratory Investigations and stimulation tests
- Adenosine plasma levels and Adneosine Triphosphate (ATP)stimulation tests are tests of value in extrinsic idiopathic AV Block.
- As previously discussed, APL levels are innately low in patients with EI AVB and therefore, on injection of ATP, AV blocks maybe reproduced.
- Other lab investigations such as arterial blood gas analysis, hemoglobin, troponin or D- dimer may help with the diagnoses in appropriate clinical situations. "ESC Guidelines on Syncope (Diagnosis and Management of)".
Treatment
Cardiac Pacing |Treatment for Reflex Syncope|Theopylline |
Case Studies
- ↑ Coumel P, Fabiato A, Waynberger M, Motte G, Slama R, Bouvrain Y (1971). "Bradycardia-dependent atrio-ventricular block. Report of two cases of A-V block elicited by premature beats". J Electrocardiol. 4 (2): 168–77. doi:10.1016/s0022-0736(71)80010-9. PMID 5113605.
- ↑ Brignole M, Gaggioli G, Menozzi C, Gianfranchi L, Bartoletti A, Bottoni N; et al. (1997). "Adenosine-induced atrioventricular block in patients with unexplained syncope: the diagnostic value of ATP testing". Circulation. 96 (11): 3921–7. doi:10.1161/01.cir.96.11.3921. PMID 9403616.
- ↑ 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.
- ↑ 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.