Mobitz type I (Wenckebach type): PR interval progressively prolongs until QRS drops, i.e., until a regularly occurring P wave is not followed by a QRS. This contrasts with SA block, where both P and QRS drop. To make the diagnosis, compare the PR that follows the blocked P wave (the shortest PR) with the PR that immediately precedes the blocked P wave (the longest PR).
Mobitz type II: QRS suddenly drops without a preceding PR change. The baseline QRS is usually wide. It may present as intermittently non-conducted P waves or as one non-conducted P wave that is not preceded by progressive PR prolongation and not followed by PR shortening. It is more ominous than Mobitz type I and is almost always a distal infranodal AV block. It progresses to a complete infranodal AV block commonly and suddenly.
2:1 AV block (alternative drop of one QRS) could be equivalent to Mobitz I or Mobitz II AV block. If QRS is wide, the block is likely a Mobitz II equivalent. If QRS is narrow, the block is likely a Mobitz I equivalent. Also, look for periods of 3:2 conduction on a rhythm strip, as this may elucidate the Mobitz type of block.
Third-degree or complete AV block (Figures 13.6, 13.7). No P wave is conducted.
A junctional or ventricular escape rhythm takes over. The ventricular rate is regular and unrelated to P waves (AV dissociation). The PR distance is variable yet the R–R interval is regular, providing evidence that none of these P waves is conducted. There are more P waves than there are QRS complexes.
High-grade or advanced second-degree AV block is a block in which the AV conduction ratio is 3:1 or worse. In one form, P waves and the escape QRS complexes are dissociated but P wave occasionally conducts: R–R intervals are mostly regular, with occasional R–R intervals that are shorter as they relate to the few conducted P waves.
In patients with AF, a slow and regular ventricular response implies complete AV block. A long AF pause, >3 seconds, generally implies high-grade AV block and is concerning when it occurs during wakefulness.
Figure 13.1 Wenckebach 3:2 AV block. P–P intervals are typically regular. P–, non-conducted P wave.
Figure 13.2 Wenckebach 5:4 AV block. P–P intervals are regular. PR progressively lengthens, whereas R–R progressively shortens. This is due to the fact that the absolute PR interval increases less with each cycle (e.g., PR 200 → 280 → 300), not compensating for the larger reduction of the preceding RP interval, P–P interval being stable.
Figure 13.3 High-grade AV block alternating with Mobitz II AV block.
Figure 13.4 Wenckebach AV block. Two groups of beats are seen, which raises the suspicion of a second-degree AV block. P2 is not conducted: this could be AV block or block of a very premature PAC. P2 is not premature as it marches out with the preceding P waves→the diagnosis is AV block. The clue to Wenckebach is the progressive PR prolongation, especially manifest when comparing P3R to P1R (P3R <P1R) and the progressive R–R shortening before the block.
Figure 13.5 ECG of a patient presenting with palpitations. Looking at parts 1 and 2 of this ECG, no P wave is seen and one might think the patient has a junctional rhythm. Whenever a junctional rhythm is initially presumed, consider the possibility of sinus rhythm with a very long PR interval. The pause between 1 and 2 unveils the diagnosis. P waves are seen: P1 is a blocked P wave, P2 and P3 are conducted with a progressively longer PR interval. Thus, the patient has a Mobitz type 1 AV block with a very long cycle. Outside P2 and P3, PR interval is very long with P waves falling onto T waves (fusion of P and T). Palpitations are due to simultaneous atrial and ventricular contractions.
Figure 13.6 Third-degree AV block with regular P rate and regular QRS rate, unrelated to each other. Many P waves fall onto the QRS–T complexes and appear as notches over QRS or T. PR interval is variable but R–R interval is regular, which implies AV dissociation and, in this case, complete AV block.
Figure 13.7 Regular, slow QRS rate of ~33 bpm. P rate is mostly regular at ~75 bpm. There is AV dissociation, with no evidence of any P-wave conduction (as also evidenced by the regular QRS escape rhythm). This is complete AV block. P’ could be a PAC or a retrogradely conducted P wave (patients with abnormal AV conduction may have a preserved VA retrograde conduction).
The escape is ventricular with a wide QRS complex if the block is infranodal (rate 20–40 bpm). The escape is junctional with a narrow QRS complex if the block is at the nodal level (rate 40–60 bpm); the junctional escape may be wide if a bundle branch block is present on the baseline ECG. Patients with complete AV block at the infranodal level may have preserved VA conduction, and retrograde P waves may be seen.
B. Causes of a pause on the rhythm strip
Outside the pause that follows an obvious PAC or PVC, a pause on a rhythm strip may be secondary to:
Sinus pause: no P wave is seen within the pause.
Second-degree AV block (Mobitz I or Mobitz II): a blocked P wave is seen within the pause. The blocked P wave marches out with the regularly occurring sinus P wave. Occasionally, however, if sinus arrhythmia is present, the blocked P wave of the AV block may not perfectly march out with the other P waves. A particular form of sinus arrhythmia seen with AV block (especially 2:1 AV block) is ventriculophasic sinus arrhythmia, in which the P–P interval containing a QRS is shorter than the P–P interval not containing a QRS (the QRS complex leads to a stroke volume which leads to reflex slowing of the P–P interval).
Blocked PAC (the most benign pause): the blocked P wave is a very premature P wave that falls in the AV nodal refractory period and does not get conducted. As opposed to AV block, the blocked P wave does not march out with the sinus P waves and often has a different morphology.
Concealed premature junctional complex (less common): a premature junctional complex (His complex) is rare, much less common than a PAC or a PVC. A blocked premature junctional complex prevents the conduction of the next sinus impulse through the His (still in refractory period), creating the impression of a Mobitz II AV block. The presence of conducted premature junctional complexes elsewhere on the rhythm monitor is a hint to this phenomenon.
In patients with intermittent AF, a long pause may occur at the junction between AF and sinus rhythm (the sinus node is “sleeping” during AF and needs time to wake up); this pause is a common cause of syncope in intermittent AF (Figure 13.10).
Figure 13.8 At first glance, the rhythm seems to be sinus bradycardia, ~40 bpm, and the waves that follow QRS complexes seem to be U waves. However, in any sinus bradycardia of 40–50 bpm, verify whether the true rhythm is, in fact, a sinus rhythm of 80–100 bpm with 2:1 AV block. The presumed U waves are actually P waves as they march out with P waves preceding the QRS complexes (arrows). Thus, the rhythm is sinus rhythm with 2:1 AV block. In 2:1 AV block, one cannot tell if the dropped QRS is preceded by progressive PR prolongation or not, i.e., Mobitz I or II. In order to say Mobitz I or II in 2:1 AV block, analyze the following:
QRS width. If QRS is wide, the block is usually an infranodal block, i.e., Mobitz II; if QRS is narrow, the block is usually Mobitz I. The 2:1 AV block on the current ECG is, therefore, a Mobitz II AV block.
PR interval of the conducted beats. PR interval is normal in this case (~200 ms), implying that the block is unlikely to be at the level of the AV node.
Figure 13.9 Outside the PVC, the rhythm seems regular. But on further analysis, there is some R–R irregularity.
Analyze the P–QRS relationship. Some QRS complexes seem to be preceded by P waves, with a consistent PR relationship (conducted P wave, noted as P’). On the other hand, some QRS complexes are not preceded by any P wave and are junctional QRS complexes. This suggests that a sinus rhythm and a junctional rhythm are competing at a rate of ~60 bpm. When the sinus rhythm slows a bit, the junctional rhythm takes over. This is isorhythmic AV dissociation. Note that, during the junctional rhythm, sinus P waves occur regularly, dissociated from QRS and falling around it (marked by*). This is not AV block, as P waves get conducted when the competing junctional rhythm does not kick in. Note also that QRS of the junctional rhythm is a bit wider, suggesting a low junctional or fascicular origin.
Figure 13.10 Long sinus pause at the point of transition from AF (top row) to sinus rhythm (bottom row). This pause is the most common cause of syncope in patients with tachy-brady syndrome: off and on AF, with pause at every AF conversion.
Figure 13.11 P blocks (arrow) without being premature and without progressive PR prolongation before the dropped beat, or PR shortening after the dropped beat. This implies Mobitz II AV block, further suggested by the wide QRS. The rate is ~80 bpm and the patient is asymptomatic, which may falsely suggest that the block is innocuous. In fact, this block is ominous because it is likely Mobitz II not Mobitz I, with a class I indication for pacemaker placement. That is why it is important to carefully analyze every small pause. A benign Mobitz I or a blocked PAC may simulate the malignant Mobitz II AV block.
In Mobitz II, the first PR interval that follows the pause may be shorter than the steady-state PR interval outside the pause, and may lead to a misdiagnosis of Mobitz I. Two explanations: (1) the first QRS after the pause may actually be an escape beat falling over the P wave, simulating a short PR interval; (2) the first QRS may be narrow, as the bundles are given time to recover from their refractory periods; PR may seem shorter if it includes less isoelectric QRS.
Figure 13.12 Note the block of a P wave (vertical arrow). This blocked P wave is not premature, and therefore the diagnosis is AV block. This blocked P wave is not preceded by any change in PR interval, even when PR intervals before and after the blocked P wave are compared (bars), which is concerning for a Mobitz II AV block. However, note that the P–P interval is progressively lengthening before and during the pause, a hint to an increase in vagal tone causing the AV block (line of arrows). Therefore, this is an AV nodal block, an equivalent of Mobitz I AV block. Also, the narrow QRS argues against Mobitz II AV block. Note that a junctional escape complex is seen after the pause (horizontal arrow), and coincides with the subsequent sinus P wave (arrowhead), preventing it from getting conducted: this is isorhythmic AV dissociation over one beat (rather than a conducted P with very short PR).
C. Location of the AV block
AV block may occur at the level of the AV node or at the infranodal level, i.e., at the His or the infra-His/Purkinje level (Figure 13.13). Infranodal AV block is ominous and leads to a slow ventricular escape rhythm, or no escape at all. Usually, in infranodal AV block, the baseline QRS is wide as the fascicles have abnormal baseline conduction. Occasionally, the block is at the His level and the baseline QRS may not be wide.
Nodal AV block is less ominous and leads to a faster, junctional, narrow escape rhythm. Location of the block in each type of AV block:
First-degree AV block is usually a nodal block, particularly if QRS is narrow. A PR interval >250 ms with a narrow QRS ~always implies a nodal block.
Mobitz I is often a nodal block, especially when QRS is narrow. When the QRS is wide, 75% of Mobitz I blocks are still nodal blocks, while 25% are infranodal blocks. A wide-QRS Mobitz I block with a maximal PR change of <50 ms is likely an infranodal Mobitz I block.
Mobitz II is an infranodal block, with a QRS that is often wide on the baseline ECG. If the baseline QRS is narrow, the block is likely infranodal at the level of the His bundle (~20% of Mobitz II block). Occasionally, what seems to be a narrow-QRS Mobitz II can be an overlooked Mobitz I with small overlooked increments in PR intervals, or can result from a sudden burst of vagal tone blocking one or several consecutive P waves.
2:1 AV block: analyze the QRS width and the PR interval to define the site of the block:
if QRS is wide, the block is likely infranodal; if QRS is narrow, the block is likely nodal.
PR interval has two components: nodal component (AH interval, normally <125 ms) and infranodal component (HV interval, nor- mally <55 ms and shorter than the AH component). A PR interval >250 ms more likely results from a delay of the nodal com- ponent, i.e., an increase in AH interval; infranodal HV interval rarely prolongs enough to cause such PR prolongation. On the other hand, a PR interval that is <200–250 ms argues against a block at the AV nodal level.
Two additional modalities help elucidate the type of 2:1 AV block: exercise testing (Table 13.1) or prolonged rhythm monitoring.
Third-degree AV block or high-grade AV block (e.g., 3:1, 4:1) may be nodal or infranodal. As such, it may be less ominous than Mobitz II AV block. Determine the location of the AV block by the width and the rate of the escape. An escape rhythm that is wide usually implies an infranodal block; the rate is usually, but not necessarily, <40 bpm (Figure 13.14). VA conduction (retrograde P waves) implies an infranodal block as well.
Figure 13.13 Mobitz I vs. Mobitz II AV block. (1) is the right bundle, (2) is the left bundle, (3) is the left anterior fascicle, (4) is the left posterior fascicle.
Table 13.1 Effect of atropine and exercise on AV block.
AV nodal block
Conduction ratio improves (AV node has rich autonomic innervations and is affected by cholinergic and sympathetic effects)
AV infranodal block
Conduction ratio remains unchanged or worsens His and Purkinje conduction is not substantially affected by the cholinergic system. On the other hand, the increase in sinus rate leads to more atrial depolarizations reaching the infranodal area. Many of these atrial depolarizations partially penetrate the infranodal area without getting conducted all the way; as such, they extend the refractory period and not only they do not conduct, they prevent subsequent beats from getting conducted. This is concealed conduction= blocked, partial conduction that does not show up on the ECG yet modifies the expected behavior of subsequent beats (blocked P waves prevent the conduction of subsequent P waves). A slower atrial rate is more likely to get conducted
Figure 13.14 Complete AV block, with underlying sinus tachycardia (arrows point to sinus P waves), and a wide QRS escape of ~25 bpm. The escape has the morphology of pseudo-RBBB + LAFB. It may be a junctional escape with RBBB + LAFB; however, short of a baseline ECG showing RBBB + LAFB, the escape should be considered ventricular. The RBBB morphology suggests a left ventricular origin, while the LAFB morphology suggests a posterior origin. Overall, the block is infranodal and the escape originates from the LV posterior wall close to the posterior fascicle. The underlying sinus tachycardia indicates that the complete AV block is due to an intrinsic conduction disease, rather than a high vagal tone or drugs.
D. Causes
Degenerative, fibrotic disease is the most common cause of AV block (Lenegre); it may extend to the cardiac skeleton, such as the mitral annulus and the aortic valve (Lev). It is related to aging and atherosclerotic risk factors but may have an inherited premature component.
AV block may result from acute anterior or inferior ischemia, or chronic ischemic cardiomyopathy with diffuse myocardial fibrosis.
Calcific valvular disease.
Any cardiomyopathy can affect the conduction system. Varying degrees of AV blocks are seen in up to 15% of dilated cardiomyopathies.
Drugs, electrolytes (hypo- or hyperkalemia, hypermagnesemia).
High vagal tone (sleep, vomiting, cough, athlete’s heart) may lead to AV block at the nodal level. Vasovagal syncope may lead to a vagally-mediated AV block, in which case AV block is part of the vagal reaction, not the sole cause of syncope (Figure 13.15).
AV block after cardiac surgery (~5–10% of valvular surgeries and congenital heart disease surgeries, in which AV block resolves in 2/3 of the cases). AV block usually resolves within 7 days, if at all.
Lyme disease leads to cardiac involvement in 1–5% of the cases, mostly high-degree AV block (80–90%), that is nodal and reversible. The degree of AV block can abruptly fluctuate. This AV block typically resolves within 1–2 weeks of antibiotic therapy but may persist for months; it is a nodal AV block that paradoxically worsens with exercise, leading to significant exercise limitation. Diagnosis is suggested by the context (outdoor exposure in endemic areas, tick bites, erythema migrans in the last 1–2 months) and established by serology.
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