Vagally Mediated Atrioventricular Block
A differential diagnosis must be made between a vagally mediated AV block and an AV block secondary to anatomical involvement of AV conduction—that is, an intrinsic AV block. A simultaneous depression of sinus node function and AV nodal conduction suggests that the mechanism of the block does not lie within, but above, the two nodes, and, the parasympathetic system is probably involved. Therefore, the simultaneous appearance of a second- or third-degree AV block and sinus slowing essentially rules out an intrinsic AV block. The differential diagnosis between vagally mediated and intrinsic AV block may be difficult when there is only a slight increase in PP intervals, which is consistent with sinus arrhythmia. In the opinion of some authors, an increase in this interval of as little as 40 ms, associated with paroxysmal AV block, suggests that the block is of vagal origin. As this value is arbitrary, we feel that a clearly evident slowing of the sinus rate should be documented.
Some intrinsic AV blocks may be tachycardia-dependent or bradycardia-dependent. The differential diagnosis between vagally mediated and tachycardia-dependent AV block is easy because in the latter there is an increase, not a decrease, in sinus rate simultaneously with the second- or third-degree AV block. The differential diagnosis between intrinsic AV block and vagally mediated AV block, which is bradycardia-associated, is more difficult. As bradycardia-dependent AV block is precipitated by a slowing of the heart rate, the ECG overlaps with that of vagally mediated AV block. Although a clear distinction may not always be possible, evidence of bradycardia-dependent AV block, as opposed to vagally mediated AV block, includes the following observations: a bundle branch or bifascicular block is present in about 90% of patients with bradycardia-dependent AV block, whereas it appears to be uncommon in patients with vagally mediated AV block; bradycardia-dependent AV block is almost always triggered by a premature supraventricular or ventricular beat, which initiates the pause; rather infrequently it is initiated by a ventricular tachycardia, via the suppression of anterograde AV conduction; prolongation of the PR interval in one or more beats is not present; sinus acceleration or an unchanged sinus rate has been seen during ventricular asystole; after a series of blocked P waves, 1:1 AV conduction is resumed by a premature ventricular beat in almost all patients.
The ECG criteria useful in the differential diagnosis between the two forms of AV block are reported in Table 1. It is important to distinguish between these two blocks because bradycardia-dependent AV block is always localised in the His-Purkinje system. Although no prospective studies have dealt with bradycardia-dependent AV block, it is probably life threatening. When a clear diagnosis is not possible, an electrophysiological study appears to be indicated in order to evaluate the conduction in the His-Purkinje system.
The differential diagnosis between true Mobitz II and pseudo-Mobitz II block is particularly challenging. It is important from the clinical point of view because Mobitz II block is also always localised within the His-Purkinje system. When a second-degree AV block with constant PR interval is seen on an ECG strip, the sinus rhythm must be carefully observed; simultaneous slowing of the sinus rate essentially rules out a true Mobitz II block. Moreover, in 50–100% of patients with pseudo-Mobitz II block, a Mobitz I block is also found in the same Holter recording; when these two blocks coexist, a true Mobitz II block should be excluded, since Mobitz type I and type II blocks do not seem to coexist within the His-Purkinje system, at least in the presence of narrow QRS complex. The diagnosis of a true Mobitz II block can only be made with confidence if the same pattern occurs repeatedly, without sinus slowing and in the absence of any sequence of Mobitz I block. If there is doubt, an electrophysiological study may be indicated.
Recently, a new form of paroxysmal AV block was described by Brignole et al. This occurs abruptly in subjects with normal AV conduction and without heart disease, and is characterised on the ECG by a complete AV block with unchanged sinus rate. It is probably secondary to an increased susceptibility to adenosine. The differential diagnosis with vagally mediated AV block appears to be easy to make by observing the behaviour of the sinus rate before and during the AV block.
It is well known that a bolus of adenosine can induce a transient second- or third-degree AV associated with slowing of the sinus rhythm. Adenosine has similar effects to those of the neurotransmitter acetylcholine, although the receptors are different. A major role of acetylcholine and adenosine, in addition to their direct effects, is to function in parallel to oppose the cardiac stimulatory effect of the sympathetic neurotransmitters adrenaline and noradrenaline on adenylcyclase. Thus, adrenergic, cholinergic and purinergic outflows are integrated at the level of the receptor–effector coupling system, and the final cardiac effect results from the sum of these excitatory and inhibitory effects. However, the adenosine test, which has been investigated in patients with syncope of unknown origin, does not appear to be specific; indeed, the appearance of AV block after bolus administration does not predict the same ECG finding during spontaneous syncope. A possible role of adenosine, in parallel with vagal overactivity or a high AV nodal susceptibility to adenosine, has not yet been investigated in subjects with vagally mediated AV block.
Differential Diagnosis Between Vagally Mediated and Intrinsic AV Block
A differential diagnosis must be made between a vagally mediated AV block and an AV block secondary to anatomical involvement of AV conduction—that is, an intrinsic AV block. A simultaneous depression of sinus node function and AV nodal conduction suggests that the mechanism of the block does not lie within, but above, the two nodes, and, the parasympathetic system is probably involved. Therefore, the simultaneous appearance of a second- or third-degree AV block and sinus slowing essentially rules out an intrinsic AV block. The differential diagnosis between vagally mediated and intrinsic AV block may be difficult when there is only a slight increase in PP intervals, which is consistent with sinus arrhythmia. In the opinion of some authors, an increase in this interval of as little as 40 ms, associated with paroxysmal AV block, suggests that the block is of vagal origin. As this value is arbitrary, we feel that a clearly evident slowing of the sinus rate should be documented.
Some intrinsic AV blocks may be tachycardia-dependent or bradycardia-dependent. The differential diagnosis between vagally mediated and tachycardia-dependent AV block is easy because in the latter there is an increase, not a decrease, in sinus rate simultaneously with the second- or third-degree AV block. The differential diagnosis between intrinsic AV block and vagally mediated AV block, which is bradycardia-associated, is more difficult. As bradycardia-dependent AV block is precipitated by a slowing of the heart rate, the ECG overlaps with that of vagally mediated AV block. Although a clear distinction may not always be possible, evidence of bradycardia-dependent AV block, as opposed to vagally mediated AV block, includes the following observations: a bundle branch or bifascicular block is present in about 90% of patients with bradycardia-dependent AV block, whereas it appears to be uncommon in patients with vagally mediated AV block; bradycardia-dependent AV block is almost always triggered by a premature supraventricular or ventricular beat, which initiates the pause; rather infrequently it is initiated by a ventricular tachycardia, via the suppression of anterograde AV conduction; prolongation of the PR interval in one or more beats is not present; sinus acceleration or an unchanged sinus rate has been seen during ventricular asystole; after a series of blocked P waves, 1:1 AV conduction is resumed by a premature ventricular beat in almost all patients.
The ECG criteria useful in the differential diagnosis between the two forms of AV block are reported in Table 1. It is important to distinguish between these two blocks because bradycardia-dependent AV block is always localised in the His-Purkinje system. Although no prospective studies have dealt with bradycardia-dependent AV block, it is probably life threatening. When a clear diagnosis is not possible, an electrophysiological study appears to be indicated in order to evaluate the conduction in the His-Purkinje system.
The differential diagnosis between true Mobitz II and pseudo-Mobitz II block is particularly challenging. It is important from the clinical point of view because Mobitz II block is also always localised within the His-Purkinje system. When a second-degree AV block with constant PR interval is seen on an ECG strip, the sinus rhythm must be carefully observed; simultaneous slowing of the sinus rate essentially rules out a true Mobitz II block. Moreover, in 50–100% of patients with pseudo-Mobitz II block, a Mobitz I block is also found in the same Holter recording; when these two blocks coexist, a true Mobitz II block should be excluded, since Mobitz type I and type II blocks do not seem to coexist within the His-Purkinje system, at least in the presence of narrow QRS complex. The diagnosis of a true Mobitz II block can only be made with confidence if the same pattern occurs repeatedly, without sinus slowing and in the absence of any sequence of Mobitz I block. If there is doubt, an electrophysiological study may be indicated.
Does Adenosine Have a Role?
Recently, a new form of paroxysmal AV block was described by Brignole et al. This occurs abruptly in subjects with normal AV conduction and without heart disease, and is characterised on the ECG by a complete AV block with unchanged sinus rate. It is probably secondary to an increased susceptibility to adenosine. The differential diagnosis with vagally mediated AV block appears to be easy to make by observing the behaviour of the sinus rate before and during the AV block.
It is well known that a bolus of adenosine can induce a transient second- or third-degree AV associated with slowing of the sinus rhythm. Adenosine has similar effects to those of the neurotransmitter acetylcholine, although the receptors are different. A major role of acetylcholine and adenosine, in addition to their direct effects, is to function in parallel to oppose the cardiac stimulatory effect of the sympathetic neurotransmitters adrenaline and noradrenaline on adenylcyclase. Thus, adrenergic, cholinergic and purinergic outflows are integrated at the level of the receptor–effector coupling system, and the final cardiac effect results from the sum of these excitatory and inhibitory effects. However, the adenosine test, which has been investigated in patients with syncope of unknown origin, does not appear to be specific; indeed, the appearance of AV block after bolus administration does not predict the same ECG finding during spontaneous syncope. A possible role of adenosine, in parallel with vagal overactivity or a high AV nodal susceptibility to adenosine, has not yet been investigated in subjects with vagally mediated AV block.