Second-degree heart block, type i, is likely to occur with which type of myocardial infarction?

Type I Second-Degree Atrioventricular Block

Second-degree AV block is divided into type I and type II on the basis of the ECG pattern. In type I, the P-R interval lengthens before the nonconducted beat and shortens on the first beat after the nonconducted beat (Wenckebach conduction); in type II, the P-R interval is fixed. In general, type I second-degree AV block suggests a supra-His level of block and is associated with a more benign prognosis, while type II occurs with intra-His or infra-His conduction system disease and has a higher rate of progression to complete heart block.5 It should be remembered that in pathologic conditions, it is possible for any component of the conduction system, even the structures below the AV node, to exhibit Wenckebach conduction. Thus, type I second-degree AV block has a benign prognosis only when it is caused by supra-His block, which is usually the case when the QRS is narrow.

Regardless of the level of block, patients with symptomatic bradycardia resulting from second-degree AV block from irreversible causes or essential drug therapy should undergo permanent pacemaker implantation (class I). In the setting of high vagal tone such as sleep or in highly conditioned athletes at rest, type I second-degree AV block is frequently observed and is a normal finding.9 For asymptomatic patients, pacemaker implantation is therefore not recommended (class III). However, as with first-degree AV block, patients with type I second-degree AV block can have symptoms caused by loss of AV synchrony, and pacemaker implantation should be considered for this indication (class IIa) as well as for symptomatic bradycardia. Indications for pacing in type I second-degree AV block are summarized in Appendix Table 33-4.

DIFFERENTIAL DIAGNOSIS OF SECOND-DEGREE AV BLOCK

Second-degree AV block may be simulated by blocked premature atrial impulses (see Chapter 14). This occurs especially when the coupling interval of the premature atrial impulse is relatively long. Careful measurement of the PP cycle length and examination of the P wave morphology can clarify the diagnosis. Conversely, ventriculophasic sinus arrhythmias are present with some second-degree AV blocks. The PP intervals that contain the QRS complexes are shorter than those that do not. The blocked P waves may be mistaken for blocked premature atrial complexes.

An AV conduction ratio of 2:1 may simulate sinus bradycardia when the nonconducted P waves fall on the preceding T waves and escape recognition (see Figure 19-13) or are mistaken for U waves. Conversely, the U waves in patients with sinus bradycardia may be mistaken for blocked P waves, causing an erroneous diagnosis of second-degree AV block.

Mortality

High-degree AV block is associated with increased mortality in patients with inferior or anterior MI. Most of the increased risk is within the first 30 days.12 High-degree AV block in patients with an anterior wall MI is associated with a greater increase in in-hospital and 30-day mortality than seen with an inferior wall MI, probably because of more extensive myocardial involvement and a higher incidence of hemodynamic complications.13

The presence of a fascicular or bundle branch block during an acute MI is associated with an increased in-hospital and long-term mortality. The 30-day mortality is significantly increased only in patients with a RBBB at baseline and an anterior MI and in patients with a new LBBB or new RBBB with an anterior MI. Piotrowicz and colleagues14 noted that patients with LBBB, RBBB, or indeterminate ventricular conduction disturbances show longer repolarization duration than patients without these conduction disturbances. Q–T and J–T intervals (as measured by Rautaharju Q–T and J–T (R–R) formulas) significantly and independently predict mortality in patients after MI with conduction disturbances. The authors have noted no evidence of LBBB among 200 consecutive cases of left anterior descending artery percutaneous coronary intervention in the setting of anterior acute MI (personal observation).

His-Purkinje System

Type 2 second-degree AV block is almost always below the AVN, occurring in the HB in approximately 30% of cases and in the bundle branches in the remainder. Infrequently, type 2 second-degree AV block is found with a narrow QRS complex and is caused by intra-Hisian block (Fig. 9-11; see Fig. 9-9).

Atrioventricular Node

Type 2 second-degree AV block has not yet been convincingly demonstrated in the body of the AVN or the N zone. Although multiple reports have described the occurrence of type 2 second-degree AV block in the AVN, in each case either the block could have been localized to the HPS, rather than the AVN, or the block probably was atypical Wenckebach block.

2. Type 2 Second-Degree Atrioventricular Block

Type 2 second-degree (Mobitz type II) AV block is characterized on the surface ECG by a constant (normal or prolonged) PR interval of all conducted P waves, followed by sudden failure of a P wave to be conducted to the ventricles (Fig. 6-9). The RP-PR reciprocity, the hallmark of type 1 block, is absent in type 2 block. Consequently, the PR interval following a long RP interval (immediately following the pause) is identical to that following a short RP interval (immediately preceding the nonconducted P wave). Type 2 block cannot be diagnosed if the first P wave after a blocked beat is absent or if the PR interval following the pause is shorter than all the other PR intervals of the conducted P waves, regardless of the number of constant PR intervals before the block. The P-P intervals remain constant, and the pause encompassing the nonconducted P wave equals twice the P-P interval.24

A true Mobitz type II block in conjunction with a narrow QRS complex is relatively rare and occurs without sinus slowing and without associated type 1 sequences. Atypical forms of Wenckebach block with only minimal PR interval variation should be excluded (see Fig. 6-5). Apparent Mobitz type II AV block can be observed under the influence of increased vagal tone during sleep, in which case, a type 1 block without discernible or measurable increments in the PR intervals is the actual diagnosis; sinus slowing with AV block essentially rules out type 2 block.26 When a narrow QRS type 2-like pattern occurs with intermittent type 1 sequences (as in Holter recordings), a true type 2 block can be safely excluded because narrow QRS type 1 and type 2 blocks almost never coexist within the HB. Sustained advanced second-degree AV block is far more common in association with true type 2 block than with type 1 block or its variant.24

Apparent Mobitz type II AV block can also be caused by concealed junctional extrasystoles (confined to the specialized conduction system and not propagated to the myocardium) and junctional parasystole. Exercise-induced second-degree AV block is most commonly infranodal and rarely is secondary to AVN disease or cardiac ischemia.24

Second-Degree Atrioventricular Block

Symptomatic second-degree AV block is a class I indication for pacing regardless of type of block. The use of pacing therapy for asymptomatic patients with second-degree AV block is controversial and depends on the type (site) of AV block.

In general, type 1 second-degree AV block associated with a narrow QRS complex (<0.12 seconds) is due to block in the AV node, and the current published guidelines do not recommend pacemaker implantation in the asymptomatic patient. In a study of 56 patients with documented chronic second-degree AV block caused by AV nodal conduction delay, those without associated cardiac disease had a benign course, whereas those with associated cardiac disease had a poor prognosis because of progression of underlying cardiac disease rather than the development of sudden bradycardia.86 However, in another retrospective study of 214 patients with second-degree AV block, survival and requirement for pacing were not different among patients with type 1 and type 2 heart block, and the presence or absence of bundle branch block did not appear to aid in the prediction of survival.87 In view of these conflicting data, it is prudent to closely monitor patients with type 1 second-degree AV block and a narrow QRS complex for symptoms and for progression of conduction tissue disease (e.g., development of fascicular block or QRS widening). If type 1 second-degree AV block is associated with a wide QRS complex (>0.12 seconds) AV block will be located in the AV node in 30% to 40% of patients and in the His-Purkinje system in 60% to 70% of cases.88,89 In these cases, an invasive electrophysiological study is often required to identify the site of block. If intra-Hisian or infra-Hisian block is identified, a pacemaker should be implanted, as these conditions usually progress to complete heart block within 5 years.90

Type 2 second-degree AV block generally occurs in His-Purkinje tissue. Asymptomatic patients with type 2 AV block usually do develop symptoms and will require permanent pacing.79

In 2 : 1 second-degree AV block, every other P wave conducts, preventing comparison of consecutive P-R intervals. The QRS complex provides a clue as to the site of block: A narrow QRS complex is associated with His-Purkinje block 30% of the time, and a wide QRS complex is associated with His-Purkinje block approximately 80% of the time.17,91 In the asymptomatic patient with 2 : 1 block, maneuvers (such as exercise, atropine, or continuous ECG monitoring) to alter the conduction ratio between the atria and the ventricles may allow localization of the site of block. However, in some cases, electrophysiological evaluation to determine the site of block will be required.

Mortality

High-degree AV block is associated with increased mortality in patients with inferior or anterior MI. Most of the increased risk is within the first 30 days.27 High-degree AV block in patients with an anterior wall MI is associated with a greater increase in in-hospital and 30-day mortality than seen with an inferior wall MI, probably because of more extensive myocardial involvement and a higher incidence of hemodynamic complications.9

The presence of a fascicular or bundle branch block during an acute MI is associated with increased in-hospital and long-term mortality. However, since it is usually impossible to know if these findings are chronic or acute, the increased mortality may represent increased comorbidity in the former and a larger infarct in the latter. Among 26,000 patients treated with thrombolytic therapy in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-1 trial, in-hospital mortality was higher in patients with a BBB on initial ECG (18% vs. 11%). In addition, patients with a BBB were more likely to develop cardiogenic shock (19% vs. 11%), AV block or asystole (30% vs. 9%), and to require a pacemaker (18% vs. 11%). In the primary PCI era, RBBB or LBBB on baseline ECG remains associated with increased in-hospital and long-term mortality.28–30 A post-hoc analysis of over 17,000 patients demonstrated that after adjustment for baseline characteristics, 30-day mortality was significantly increased only in patients with an RBBB at baseline and an anterior MI and in patients with a new LBBB or new RBBB with an anterior MI.8

Review

Clinicians should address three major issues related to apparent abnormalities in AV conduction: (1) What is the degree of AV block: first, second or third degree? (2) What is the likely level of the AV block: nodal or infranodal? (3) What is the likely cause of the AV block? The answers will help determine what, if any, further evaluation or therapy is required, and especially whether a temporary or permanent pacemaker (Chapter 22) is indicated.

First-degree AV block is characterized by a P wave (usually sinus in origin) followed by a QRS complex with a uniformly prolonged PR interval >200 msec. Some clinicians prefer the descriptive term PR interval prolongation because the signal is not really blocked; rather it is delayed.

Second-degree AV block is characterized by intermittently “dropped” QRS complexes. There are two major subtypes of second-degree AV block: Mobitz type I (AV Wenckebach) and Mobitz type II.

With Mobitz type I, the classic AV Wenckebach pattern, each stimulus from the atria has progressive “difficulty” traversing the AV node to the ventricles (i.e., the node becomes increasingly refractory). Finally, the atrial stimulus is not conducted at all, such that the expected QRS complex is blocked (“dropped QRS”). This cycle is followed by relative recovery of the AV junction; then the cycle starts again. The characteristic ECG signature of AV Wenckebach block, therefore, is progressive lengthening of the PR interval from beat to beat until a QRS complex is not conducted. The PR interval following the nonconducted P wave (the first PR interval of the new cycle) is always shorter than the PR interval of the beat just before the nonconducted P wave.

Mobitz type II AV block is a rarer and more serious form of second-degree heart block. Its characteristic feature is the sudden appearance of a single, nonconducted sinus P wave without (1) the progressive prolongation of PR intervals seen in classic Mobitz type I (Wenckebach) AV block and (2) without substantial (≤40 msec) shortening of the PR interval in the beat following the nonconducted P wave as seen with type I block. A subset of second-degree heart block occurs when there are multiple consecutive nonconducted P waves present (P–QRS ratios of 3 : 1, 4 : 1, etc.). This finding is referred to as high degree (or advanced) AV block. It can occur at any level of the conduction system. A common mistake is to call this pattern Mobitz type II block.

First- and second-degree heart blocks are examples of incomplete blocks because the AV junction conducts some stimuli to the ventricles. With complete (third-degree) AV heart block, no stimuli are transmitted from the atria to the ventricles. Instead, the atria and ventricles are paced independently. The atria often continue to be paced by the sinoatrial (SA) node. The ventricles, however, are paced by a nodal or infranodal escape pacemaker located somewhere below the point of block. The resting ventricular rate with complete heart block may as slow as 30 beats/min or less or as high as 50–60 beats/min.

Complete heart block may also occur in patients whose basic atrial rhythm is flutter or fibrillation. In these cases, the ventricular rate is very slow and almost completely regular.

Interruption of electrical conduction can occur at any level starting from the AV node itself (nodal block) down to the His bundle and its branches (infranodal block).

In general, block at the level of the AV node (1) is often caused by reversible factors, (2) progresses more slowly, if at all, and (3) in the case of complete heart block, is associated with a relatively stable escape rhythm. In contrast, infranodal block (1) is usually irreversible and (2) may progress rapidly and unexpectedly to complete heart block with a slow, unstable escape mechanism. Therefore, infranodal block (even second degree) generally requires pacemaker implantation.

Sinus rhythm with 2 : 1 AV block is usually considered as a “special” category of second-degree block and may be due to nodal or infranodal conduction abnormalities.

Be aware that cardiologists use the term AV dissociation in two related, though not identical, ways, which may cause confusion: (1) As a general term, it is used to describe any arrhythmia in which the atria and ventricles are controlled by independent pacemakers. This definition includes complete heart block (usually requiring an electronic pacemaker) as well as some instances of ventricular tachycardia or accelerated idioventricular rhythm in which the atria remain in sinus rhythm (see Chapter 16). (2) As a more specific term, it is used to describe a particular family of arrhythmias in which the SA node and AV junction appear to be “out of sync;” thus, the SA node loses its normal control of the ventricular rate. As a result the atria and ventricles are paced independently—the atria from the SA node, the ventricles from the AV junction. This situation is similar to that which occurs with complete heart block. However, in this instance, the ventricular rate is the same as or slightly faster than the atrial rate. When the atrial and ventricular rates are almost the same, the term isorhythmic AV dissociation is used and a pacemaker is not indicated.

Clinicians should recognize the difference between AV dissociation resulting from “desynchronization” of the SA node and AV junction and actual complete heart block, which results from true AV conduction failure. With AV dissociation (e.g., isorhythmic) a properly timed P wave can be conducted through the AV junction; in contrast, with complete (third-degree) heart block, no P wave can stimulate the ventricles because of severed electrical signaling between upper and lower cardiac chambers.

22 Which type of second-degree heart block is worrisome and why?

Second-degree AV block is rarely symptomatic and by itself is not dangerous. The question is whether second-degree block indicates increased risk for complete AV block, and if so whether asystole is likely to occur. AV node block rarely progresses to third-degree block and often has a reliable escape rhythm if it does. HP block is more likely to progress to complete block and is more likely to result in asystole. AV node suppression typically results in Mobitz I block, whereas HP block leads to Mobitz II block. Therefore Mobitz II block is an indication for permanent pacemaker placement. In the presence of 2:1 AV block Mobitz I and II cannot be distinguished; widened QRS and normal PR interval suggest that block is at the HP level. Atropine improves AV node conduction. It has no direct effect on HP conduction but by causing increased sinus rate can paradoxically increase HP block and therefore should be avoided in this setting.

Associated Conditions

High-degree AVB can be benign (e.g., when due to an increase in vagal tone as may occur with vomiting, intubation, and suctioning, when it is referred to as “vagotonic” AVB), or it can be associated with serious and potentially life-threatening bradycardia-asystolic pauses. Causes include idiopathic degeneration of the conduction system, MI, surgery, trauma, myocarditis, infiltrative processes (e.g., amyloidosis), sarcoidosis, Lyme disease, neuromuscular diseases (e.g., myotonic muscular dystrophy, Erb limb-girdle muscular dystrophy, Kearns-Sayre syndrome, peroneal muscular atrophy), collagen vascular disease, or metastatic disease. When high-grade AVB is present due to block in the His-Purkinje system, the sinus rate tends to be normal to rapid, whereas if reduced, vagal tone is often the cause of the problem because the sinus rate will slow concomitantly. Sometimes, EP testing is needed to clarify the level of the block.