Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 8. Atrioventricular Block

Types of AV Block

·         ▪ The atria and ventricles are contiguous structures separated by a dense mass of fibrous tissues that are electrically inert. This prevents the direct spread of electrical impulses between the atria and ventricles. The only pathway by which the sinus impulse can reach the ventricles is through the normal atrioventricular (AV) conduction system (Fig. 8.1).

·         ▪ The normal AV conduction system consists of the AV node, bundle of His, bundle branches, and fascicular branches of the left bundle branch. The sinus impulse can be delayed or interrupted anywhere along this conduction pathway, resulting in varying degrees of AV block.

·         ▪ There are three types of AV block based on the severity of the conduction abnormality:

o    ▪ First-degree AV block

o    ▪ Second-degree AV block

§  Mobitz type I or AV Wenckebach

§  Mobitz type II

§  Advanced or high grade

o    ▪ Third-degree or complete AV block

Figure 8.1: Diagrammatic Representation of the Atrioventricular (AV) Conduction System. The atria and ventricles are separated by a dense mass of fibrous tissues. This prevents the spread of atrial impulses directly to the ventricles. The only pathway by which the atrial impulse can propagate to the ventricles is through the AV conduction system.

First-Degree AV Block

·         ▪ Normal AV conduction: The normal PR interval measures 0.12 to 0.20 seconds in the adult (Fig. 8.2). It represents the time required for the sinus impulse to travel from atria to ventricles.

·         ▪ First-degree AV block: First-degree AV block simply means that the PR interval is prolonged and measures >0.20 seconds (Fig. 8.3). It indicates delay in the conduction of the sinus impulse from atria to ventricles with most of the delay occurring at the level of the AV node.

·         ▪ Although the PR interval is prolonged in first-degree AV block, all P waves are conducted to the ventricles and are always followed by QRS complexes (Fig. 8.4). First-degree AV block therefore is a conduction delay rather than actual block. This conduction delay can occur anywhere between the atria and the ventricles.

·         ▪ First-degree AV block is usually a conduction delay at the AV node. This can be due to a variety of causes including enhanced vagal tone; use of pharmacologic agents that prolong AV conduction such as beta blockers, calcium channel blockers, and digitalis; or it might indicate disease of the AV conduction system.

·         ▪ Once a sinus P wave is not conducted to the ventricles, the AV block has advanced to second degree (Fig. 8.5).

Figure 8.2: Normal Atrioventricular (AV) Conduction. Rhythm strip showing normal PR interval measuring 0.15 seconds. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex and normally varies from 0.12 to 0.20 seconds. If a Q wave is present, the PR interval is measured from the beginning of the P wave to the beginning of the Q wave (P-Q interval). The PR interval represents the time required for the sinus impulse to travel from atria to ventricles.

Common Mistakes in First-Degree AV Block

·         ▪ The diagnosis of first-degree AV block is usually straightforward but can be very confusing if the PR interval is unusually prolonged. The P wave may be hidden within the T wave or it can be mistaken for a T wave of the previous complex (Figs. 8.6C and 8.7).

·         ▪ First-degree AV block does not cause symptoms. However, when the P wave falls within the Q-T interval of the previous cardiac cycle, which corresponds to ventricular systole, simultaneous contraction of both atria and ventricles may cause symptoms of low cardiac output (Figs. 8.6C and 8.7).

Figure 8.3: First-Degree Atrioventricular (AV) Block. Rhythm strip showing PR interval of 0.34 seconds. Any PR interval measuring >0.20 seconds is first-degree AV block and indicates that there is a delay in the conduction of the sinus impulse from atria to ventricles.

First-Degree AV Block

Electrocardiogram Findings

·         The PR interval is prolonged and measures >0.20 seconds.

·         Every P wave is followed by a QRS complex.

Mechanism

·         ▪ The PR interval represents the time required for the sinus impulse to travel from atria to ventricles. There are several structures involved in the propagation of the sinus impulse to the ventricles. These include the atria, AV node, His bundle, bundle branches, and fascicles. The sinus impulse can be delayed anywhere between the atria and ventricles although the prolongation of the PR interval is almost always due to slowing of conduction within the AV node. Less commonly, first-degree AV block can occur in the His-Purkinje system or within the atria.

Figure 8.4: First-Degree Atrioventricular (AV) Block. The PR interval measures 0.42 seconds and is unusually prolonged. Regardless of the duration of the PR interval as long as every P wave is followed by a QRS complex, the conduction abnormality is first-degree AV block.

Figure 8.5: Second-Degree Atrioventricular (AV) Block. When a sinus P wave is not conducted to the ventricles and is not followed by a QRS complex (star), the conduction abnormality is no longer first-degree but has advanced to second-degree AV block.

Figure 8.6: First-Degree Atrioventricular (AV) Block. When the PR interval is unusually prolonged, the P wave may be mistaken for a T wave. Rhythm strips (A, B, C) are from the same patient taken on separate occasions. (A) Top normal PR interval of 0.20 seconds. Arrows identify the P waves. The PR interval is longer in (B) (0.36 seconds) and is even much longer in (C) (0.41 seconds). In (C), the PR interval is unusually prolonged such that the P waves can be mistaken for T waves of the previous complex.

Figure 8.7: First-Degree Atrioventricular (AV) Block with Unusually Prolonged PR Interval. The PR interval measures 0.46 seconds and is unusually prolonged. The P wave is difficult to recognize (arrows) because it is superimposed on the T wave of the previous complex. This can result in synchronous contraction of both atria and ventricles, which may cause symptoms of low cardiac output.

Clinical Significance

·         ▪ First-degree AV block is the mildest form of AV conduction abnormality characterized by delay in conduction of the sinus impulse from atria to ventricles. All P waves conduct to the ventricles, thus first-degree AV block is a misnomer because the impulse is only delayed. There is no actual block.

·         ▪ First-degree AV block may not be appreciated if the PR interval is markedly prolonged or the P wave is buried within the T wave of the previous complex. In both instances, the P wave may be difficult to identify.

·         ▪ First-degree AV block can be the result of enhanced vagal tone; administration of pharmacologic agents that can block the AV node such as beta blockers, calcium blockers, digitalis; and other antiarrhythmic agents. It can be caused by hypothyroidism, rheumatic fever, or intrinsic disease of the AV node and conducting system from ischemia, inflammation, infiltration, and fibrosis.

·         ▪ The first heart sound is usually diminished in intensity when there is first-degree AV block. If the PR interval is prolonged, the AV valves slowly drift back to a semiclosed position before the ventricles contract, resulting in a soft first heart sound. When the PR interval is unusually prolonged and the P wave is inscribed at the T wave or ST segment of the preceding complex, cannon A waves may be seen in the jugular neck veins because atrial contraction occurs simultaneously with ventricular systole, which may result in diminished cardiac output.

Treatment

·         ▪ First-degree AV block is benign and does not require any treatment. The etiology of the AV block should be recognized and corrected.

·         ▪ First-degree AV block may compromise left ventricular filling if the PR interval is >0.30 seconds because atrial contraction may occur during ventricular systole. This may elevate atrial and pulmonary venous pressures and reduce ventricular filling and cardiac output resulting in symptoms of congestion and low output very similar to the symptoms associated with the pacemaker syndrome (see Chapter 26, The ECG of Cardiac Pacemakers). If the long PR interval is not reversible and temporary AV pacing can improve the symptoms related to low cardiac output, the American College of Cardiology (ACC), American Heart Association (AHA), and Heart Rhythm Society (HRS) guidelines for permanent pacemaker implantation consider this type of first-degree AV block as a class IIa indication for permanent pacing (meaning that the weight of evidence is in favor of usefulness or efficacy of the procedure).

Figure 8.8: Type I Second-Degree Atrioventricular (AV) Block. The rhythm strip shows type I second-degree AV block. Three P waves are conducted with gradual prolongation of the PR interval. Only one P wave (marked by the arrows) is not followed by a QRS complex.

Prognosis

·         ▪ Prognosis is generally good and favorable especially if the cause is reversible. If the cause is due to structural cardiac abnormalities, first-degree AV block may progress to higher grades of AV block. The prognosis therefore depends on the associated cardiac abnormalities rather than the presence of first-degree AV block.

Second-Degree AV Block

·         ▪ Second-degree AV block: There are three types of second-degree AV block.

o    ▪ Mobitz type I also called AV Wenckebach

o    ▪ Mobitz type II

o    ▪ Advanced, also called high-grade second-degree AV block

·         ▪ Type I and type II second-degree AV block: In type I and type II second-degree AV block, two or more consecutive P waves are conducted to the ventricles and only single P waves are blocked (Fig. 8.8).

·         ▪ Advanced second-degree AV block: The AV block is advanced when the second-degree block cannot be classified as type I or type II. An example of advanced second-degree AV block is when two or more consecutive P waves are blocked as in 3:1, 4:1, or 5:1 AV block (Fig. 8.9). Another example is when only a single P wave is followed by a QRS complex as in 2:1 AV block (Fig. 8.10).

Type I Second-Degree AV Block

·         ▪ Type I second-degree AV block: Type I second-degree AV block is also called AV Wenckebach. The following features characterize type I second-degree AV block (Figs. 8.11 and8.12):

o    ▪ Two or more consecutive P waves are conducted.

o    ▪ Only single P waves are blocked.

o    ▪ There is gradual prolongation of the PR interval before a ventricular complex is dropped.

o    ▪ The PR interval always shortens immediately after the pause.

o    ▪ The QRS complexes may be narrow or wide but are typically narrow.

Figure 8.9: Advanced 3:1 Second-Degree Atrioventricular (AV) Block. The rhythm strip shows intermittent 3:1 AV block (brackets). The first two P waves are not conducted. When two or more consecutive P waves are not conducted, the rhythm is advanced second-degree block. Arrows point to the P waves.

Figure 8.10: Advanced 2:1 Second-Degree Atrioventricular (AV) Block. In 2:1 AV block, the first P wave is conducted and the next P wave is blocked (arrows). A common error is to classify 2:1 AV block as a type II second-degree AV block. Because only one P wave is followed by a QRS complex, the AV block cannot be classified as type I or II.

Figure 8.11: Type I Second-Degree Atrioventricular (AV) Block. The rhythm strip shows 4:3 AV Wenckebach with four P waves (labeled 1 to 4) conducting only three QRS complexes. The PR interval gradually prolongs before a ventricular complex is dropped (star). The long pause allows the conduction system to rest and recover so that the next P wave (5) is conducted more efficiently, resulting in a PR interval that measures the shortest. The QRS complexes are narrow and only a single P wave is not conducted (4).

Figure 8.12: Type I Second-Degree Atrioventricular (AV) Block. Instead of measuring for gradual prolongation of the PR interval, one can simply compare the PR interval before (1) and after (2) the pause. If the PR interval shortens after the pause, type I AV block is present. The stars identify single P waves that are not conducted.

Figure 8.13: Group Beating. Group beating simply means that if you “eyeball” the tracing from left to right, one gets the impression that the beats (the QRS complexes) are grouped together because of the spaces created by P waves without QRS complexes (stars). Four such groups can be identified in the above tracing (groups 1 to 4). Group beating is frequently seen in type I atrioventricular (AV) block because AV Wenckebach has a tendency to be repetitive. The above is an example of 4:3 AV Wenckebach meaning that there are four P waves for every three QRS complexes.

Type I Second-Degree AV Block

·         ▪ There are additional features commonly seen in classical type I second-degree AV block:

o    ▪ Group beating is present (Fig. 8.13)

o    ▪ The R-R intervals (distance between two R waves) are variable (Fig. 8.14). The R-R interval straddling a blocked P wave is less than the R-R interval straddling a conducted sinus impulse.

·         ▪ Conduction ratio: The conduction ratio refers to the total number of P waves to the total number of QRS complexes that are conducted. Thus, a 4:3 AV Wenckebach implies that of four consecutive P waves, only three are conducted; a 5:4 AV Wenckebach means that of five consecutive P waves, only four are conducted.

Figure 8.14: Varying R-R Interval in Type I Second-Degree Atrioventricular (AV) Block. Type I can be differentiated from type II second-degree AV block by the R-R intervals. In type I AV block, the R-R intervals are variable because the PR intervals are also variable. Note that the R-R interval straddling a blocked P wave (1.2 seconds) is less than the R-R interval straddling a conducted sinus impulse (1.52 seconds). This is in contrast to type II block, where the R-R intervals are fixed because the PR intervals are also fixed (see Fig. 8.20). The longest R-R interval occurs immediately after the pause (0.80 seconds) with gradual shortening of the next R-R interval (0.72 seconds). The stars mark the P waves that are not conducted.

·         ▪ Shortening of the PR interval after a pause is much easier to recognize than gradual prolongation of the PR interval, as shown in Figure 8.15. This always favors second-degree type I AV block.

·         ▪ Type I second-degree AV block may have narrow or wide QRS complexes.

·         ▪ Localizing the AV block: Type I second-degree AV block is almost always localized at the level of the AV node, although it can also occur below the AV node (infranodal) at the level of the His-Purkinje system. The presence of bundle branch block (Fig. 8.16) or myocardial infarction (Fig. 8.17) may be helpful in localizing whether the block is nodal or infranodal.

o    ▪ Narrow QRS complexes: When the QRS complexes are narrow, the block is almost always confined to the AV node (Fig. 8.18). A block occurring at the bundle of His (intra-His block) is possible, but is rare.

o    ▪ Wide QRS complexes: When the QRS complexes are wide because of the presence of bundle branch block, the block may be AV nodal although an infranodal block at the level of the bundle branches is more likely (Fig. 8.16).

o    ▪ Acute myocardial infarction (MI):

§  Acute inferior MI: When AV block occurs in the setting of an acute inferior MI, the location of the AV block is at the AV node (Fig. 8.17, see also Figs. 8.30 and 8.39). The QRS complexes are narrow.

§  Acute anterior MI: When AV block occurs in the setting of an acute anterior MI, the AV block is below the AV node (infranodal block). The QRS complexes are usually wide (See section on Complete AV Block).

Figure 8.15: Type I Second-Degree Atrioventricular (AV) Block. The PR interval looks fixed but suddenly shortens after the pause. The shortening of the PR interval is characteristic of type I second-degree AV block. The star identifies a P wave without a QRS complex. Note that gradual lengthening of the PR interval is not obvious before the pause.

Figure 8.16: Second-Degree Atrioventricular (AV) Block with Wide QRS Complexes. The QRS complexes in AV Wenckebach are usually narrow. In this example, the QRS complexes are wide because of the presence of right bundle branch block and left anterior fascicular block. The rhythm strip at the bottom of the tracing shows 3:2 AV Wenckebach. Note that the PR interval is longer before the pause (0.32 seconds) and shortens immediately after the pause (0.25 seconds). Shortening of the PR interval after the pause is consistent with type I second-degree AV block. The P waves that are not conducted are identified by the stars.

ECG Findings of Type I AV Block

·         Two or more consecutive P waves are conducted.

·         Only single P waves are blocked.

·         There is gradual prolongation of the PR interval before a ventricular complex is dropped.

·         The PR interval always shortens immediately after the pause.

·         The QRS complexes are usually narrow.

·         Group beating is present.

·         The R-R intervals are variable. The longest R-R interval is noted immediately after the pause and shortening of the R-R interval occurs successively thereafter.

Mechanism

·         ▪ Type I second-degree AV block or AV Wenckebach is usually a block at the level of the AV node although it can occur anywhere in the AV conduction system. When the QRS complexes are narrow, the block is almost always AV nodal. A block in the distal His-Purkinje system is suspected when there is bundle branch block (a sign of distal conduction system disease) or when the AV block occurs in the setting of an acute anterior MI.

·         ▪ Because the sinus impulses constantly bombard the AV node, conduction through the AV node becomes progressively delayed until a sinus impulse can no longer be conducted, resulting in a P wave without a QRS complex. The pause allows the AV node to rest and recover, allowing the next impulse to be conducted more efficiently resulting in a shorter PR interval.

Figure 8.17: Atrioventricular (AV) Block and Acute Inferior Myocardial Infarction (MI). When type I block occurs in the setting of acute inferior MI as shown, the block is AV nodal. The stars identify the blocked P waves.

Clinical Significance

·         ▪ Type I AV block may be a normal finding in healthy individuals, especially during sleep, because of enhanced vagal tone. It may be caused by intense vagal stimulation such as vomiting or coughing. The arrhythmia may be caused by agents that block the AV node, such as calcium blockers, beta blockers, or digitalis. These examples of AV block are the result of extrinsic causes and are reversible. AV block can also be due to structural cardiac disease such as degenerative and calcific disease of the conduction system, ischemia, infarction or inflammation of the AV node, or intraventricular conduction system including acute myocarditis, rheumatic fever, and Lyme disease. These examples of AV block are due to intrinsic disease of the AV node and conduction system and may not be reversible.

Figure 8.18: Two to One Atrioventricular (AV) Block. The initial portion of the tracing shows a classical 3:2 AV Wenckebach with gradual prolongation of the PR interval. This is followed by 2:1 AV block. The presence of 2:1 block associated with classical AV Wenckebach with narrow QRS complexes suggests that the 2:1 AV block is AV nodal. The stars identify the P waves.

·         ▪ Type I AV block is usually confined to the AV node. The QRS complexes are narrow. Type I AV block with wide QRS complexes may be AV nodal but is more frequently infranodal. When the block is infranodal, the cause of the AV block is usually due to structural cardiac disease.

o    ▪ AV nodal block: AV block at the level of the AV node is generally benign with a good prognosis. Even when type I block progresses to complete AV block, the AV block is usually reversible. Furthermore, the rhythm that comes to the rescue (escape rhythm), is from the AV junction.

AV junctional rhythm is more stable and more physiologic than a ventricular escape rhythm and has a relatively fast rate that can be further enhanced with atropine.

o    ▪ Infranodal block: Type I block with wide QRS complexes may be nodal or infranodal. Infranodal AV block may occur at the level of the bundle of His, bundle branches, or distal fascicles. Infranodal AV block is almost always associated with bundle branch block and the immediate prognosis is more ominous when compared with that occurring at the AV node (Fig. 8.19).

o    ▪ Type I AV block is a common complication of acute inferior MI and is usually reversible since the block is at the level of the AV node.

Figure 8.19: Complete Atrioventricular (AV) block and Junctional Escape Rhythm. Complete AV block can occur anywhere in the conduction system. In the upper column, complete AV block is at the AV node (A); in (B), at the bundle of His; in (C), both bundle branches; and in (D), right bundle branch and both fascicles of the left bundle. If the block is AV nodal (A), the escape rhythm will be AV junctional (star) and will have narrow QRS complexes (electrocardiogram A). However, if the block is infranodal (diagrams B, C, and D), AV junctional rhythm is not possible and the escape rhythm will be ventricular with wide QRS complex (electrocardiogram B).

Treatment

·         ▪ Symptomatic patients:

o    ▪ For symptomatic patients with type I second-degree AV block that does not resolve, especially in patients with left ventricular systolic dysfunction, the ACC/AHA/HRS guidelines recommend the insertion of a permanent pacemaker as a Class I indication regardless of the location of the AV block. (Class I means there is evidence or general agreement that the procedure is beneficial, useful, and effective.)

o    ▪ Patients with second-degree AV block with symptoms similar to those of the pacemaker syndrome; insertion of a permanent pacemaker is a Class IIa recommendation.

o    ▪ Patients with neuromuscular disease with second-degree AV block with or without symptoms; insertion of a permanent pacemaker is a Class IIb recommendation.

·         ▪ Asymptomatic patients: Type I second-degree AV nodal block is usually reversible and generally does not require any therapy. The cause of the AV block should be identified and corrected. The following are the ACC/AHA/HRS recommendations regarding insertion of permanent pacemakers in completely asymptomatic patients with type I second-degree AV block.

o    ▪ AV nodal block:

§  If the block is AV nodal and the patient is hemodynamically stable and asymptomatic, with a heart rate >50 beats per minute (bpm), insertion of a permanent pacemaker is a Class III recommendation. Class III means that there is evidence or general agreement that the procedure is not useful and in some cases may be harmful.

§  If the block is AV nodal and is expected to resolve and unlikely to recur (such as effect of drugs, Lyme disease, hypoxia from sleep apnea), permanent pacing is also a Class III recommendation.

o    ▪ Infranodal block:

§  If the AV block is infranodal, at the level of the bundle of His (intra-His) or bundle branches (infra-His), insertion of a permanent pacemaker is a Class IIa indication. This includes asymptomatic patients with infranodal block diagnosed during an electrophysiologic study for other indications.

o    ▪ Any level: Some patients with second-degree AV block at any level may be completely asymptomatic, but may need permanent pacing for the following conditions:

§  Patients who develop second of third-degree AV block during exercise in the absence of myocardial ischemia. This is a Class I recommendation.

§  Myotonic muscular dystrophy, Erb dystrophy, and peroneal muscular dystrophy with any degree of AV block (including first-degree AV block) with or without symptoms because of unpredictable progression of AV conduction disease. This is a class IIb recommendation.

o    ▪ Emergency treatment of symptomatic patients with bradycardia includes atropine (see Treatment of Complete AV Block in this Chapter) and if not effective, a temporary transvenous or transcutaneous pacemaker may be necessary before a permanent pacemaker can be implanted.

o    ▪ Other pharmacologic agents that can be tried for treatment of the bradycardia before a pacemaker can be inserted include adrenergic agents such as isoproterenol, epinephrine, or dobutamine. These are further discussed under treatment of complete heart block in this chapter.

Figure 8.20: Type II Second-Degree Atrioventricular (AV) Block. In Mobitz type II AV block, the PR intervals are fixed and measure the same throughout. It does not lengthen before nor shorten after a QRS complex is dropped. Note that only single P waves are blocked (stars) and that the QRS complexes are wide because of the presence of a bundle branch block.

Prognosis

·         ▪ Type I AV block most often occurs at the level of the AV node and is usually reversible with a good prognosis. The AV block is often seen in normal healthy athletic individuals, especially during sleep.

·         ▪ If the AV block occurs more distally at the level of the His-Purkinje system, structural cardiac disease is usually present. The overall prognosis in these patients will depend on the underlying cardiac abnormality. If the underlying cause is degenerative disease confined to the conduction system, the prognosis is similar to a patient without the conduction abnormality after a permanent pacemaker is implanted.

Type II Second-Degree AV Block

·         ▪ Mobitz type II second-degree AV block: Mobitz type II second-degree AV block is characterized by the following features:

o    ▪ Two or more consecutive P waves are conducted.

o    ▪ Only single P waves are blocked.

o    ▪ All PR intervals measure the same throughout. The PR interval is fixed and does not prolong before or shorten after a pause (Figs. 8.20 and 8.21).

o    ▪ The QRS complexes are usually wide (Figs. 8.20 and 8.21) because of the presence of bundle branch block.

o    ▪ The R-R intervals (distance between R waves) are constant and measure the same throughout as long as the sinus rhythm is stable—that is, the heart rate or P-P intervals are regular (Fig. 8.22).

·         ▪ Type II block with wide QRS complexes: Mobitz type II second-degree AV block is always an infranodal block and occurs exclusively at the level of the His-Purkinje system (Fig. 8.23). Type II block is unlikely unless there is evidence of infranodal disease such as bundle branch block or anterior MI.

·         ▪ Type II block with narrow QRS complexes: Type II block with narrow QRS complexes is possible, although rare. The block involves the His bundle (intra-His block) rather than the bundle branches. If the PR interval looks fixed, but the QRS complexes are narrow and no evidence of anterior MI is present, the block may be AV nodal rather than infranodal. More often, the PR interval looks fixed because there is only minimal prolongation in the surface electrocardiogram (ECG), which is difficult to demonstrate unless the PR interval is measured carefully (Fig. 8.24).

·         ▪ Treatment: Even in completely asymptomatic patients, a permanent pacemaker should be considered when the diagnosis is type II second-degree AV block.

o    ▪ Type II AV block with wide QRS complexes: Insertion of a permanent pacemaker is a Class I indication for patients with type II second-degree AV block associated with wide QRS complexes.

o    ▪ Type II AV block with narrow QRS complexes: If the QRS complexes are narrow and type II second-degree AV block is present, insertion of a permanent pacemaker is a Class IIa indication. If the level of the AV block is uncertain, an electrophysiologic study should be performed before a permanent pacemaker is implanted.

·         ▪ Prognosis: Because type II second-degree AV block is an infranodal disease, the immediate prognosis is more ominous than type I AV block, where the block is usually AV nodal (Fig. 8.25). Infranodal disease is associated with structural heart disease and is progressive and usually not reversible. When complete AV block occurs, it is usually sudden without warning.

Figure 8.21: Type II Second-Degree Atrioventricular (AV) Block. The PR intervals are fixed (distances between paired arrows measure 0.20 seconds throughout). The QRS complexes are wide and only single P waves are not conducted (stars).

Figure 8.22: Constant R-R Intervals. In type II second-degree atrioventricular (AV) block, the R-R intervals are constant because the PR intervals are also constant. Distance A and C with three consecutive complexes measure the same as distance B with a dropped QRS complex. Thus, the RR interval straddling a pause (distance B) measures the same as the R-R interval straddling a conducted sinus impulse (A or C). The P waves are marked by the arrows.

ECG Findings of Type II Second-degree AV Block

·         Two or more consecutive P waves are conducted.

·         Only single P waves are blocked.

·         The PR intervals are fixed and do not vary. The PR interval does not prolong before or shorten after the pause.

·         The QRS complexes are wide due to the presence of bundle branch block.

·         If the sinus rate is stable, the R-R intervals are fixed. The R-R interval between three successively conducted sinus complexes is equal to the R-R interval straddling the pause.

Mechanism

·         ▪ In Mobitz type II second-degree AV block, one bundle branch has a fixed block and the other bundle branch is intermittently blocked, resulting in P waves that are not conducted. The PR interval remains constant throughout. The PR interval immediately after the pause should not shorten and should measure the same as the PR interval before the pause.

·         ▪ Mobitz type II second-degree AV block occurs exclusively at the His-Purkinje system, usually at the level of the bundle branches. Although the block can occur within the His bundle, an intra-His block is rare. Before the diagnosis of type II block is secured, there should be evidence of infranodal disease in the form of left bundle branch block or right bundle branch block with or without fascicular block. When one bundle branch is blocked, intermittent block of the other bundle causes the QRS complex to be dropped intermittently. If the QRS complex is narrow and the PR interval looks fixed, the possibility of a block at the level of the bundle of His is likely (intra-His block), although this is rare and, more commonly, may be due to AV nodal block with minimal prolongation of the PR interval that may be difficult to appreciate in the surface ECG unless the PR interval is measured carefully.

Figure 8.23: Mobitz Type II Second-Degree Atrioventricular (AV) Block. The 12-lead electrocardiogram shows all the findings of type II second-degree AV block. The PR interval is fixed, only single P waves are blocked (stars), two consecutive P waves are conducted, and there is left bundle branch block.

Figure 8.24: Fixed PR Interval with Narrow QRS Complexes. The PR interval looks fixed and the QRS complexes are narrow. However, if the PR interval is measured carefully, there is subtle shortening immediately after the pause. Shortening of the PR interval after a pause suggests type I second-degree atrioventricular block. The stars identify the nonconducted P waves.

Figure 8.25: Location of Atrioventricular (AV) Block. In type I second-degree AV block or AV Wenckebach (A), the AV block is almost always at the AV node although it can also occur anywhere in the His-Purkinje system. In type II second-degree AV block (B), the AV block occurs exclusively at the bundle of His, bundle branches, and distal conduction system. The lines transecting the AV conduction system indicate the potential sites of AV block.

Clinical Significance

·         ▪ Type II block is an infranodal disease involving the bundle of His, and, more commonly, the bundle branches and fascicles. Type II block does not occur at the level of the AV node.

·         ▪ It is a common mistake to include 2:1 AV block as Mobitz type II block. It is not possible to distinguish type I from type II block when there is 2:1 AV block because prolongation of the PR interval cannot be observed when only one P wave is conducted. In 2:1 AV block, the PR interval looks fixed because only a single P wave is conducted.

·         ▪ When an acute infarct is complicated by type II second-degree AV block, the location of the infarct is anterior. Even with insertion of a pacemaker, mortality remains high because an anterior infarct with second-degree AV block is usually an extensive infarct.

·         ▪ If there is difficulty in differentiating type I (usually AV nodal) from type II (always infranodal) block, sympathetic and parasympathetic manipulation may be tried. Both sinus node and AV node are influenced by sympathetic and parasympathetic stimulation, whereas the intraventricular conduction system below the AV node is affected mainly by sympathetic but not by parasympathetic stimuli. Sympathetic stimulation such as exercise increases the rate of the sinus node and enhances conduction across the AV node. Atropine and adrenergic agents can cause the same effect. Thus, exercise, atropine, or adrenergic agents will increase the sinus rate and will also improve AV nodal block, but will not improve and may even worsen type II or infranodal block. On the other hand, parasympathetic stimulation such as carotid sinus compression can improve infranodal block by slowing the sinus rate and prolonging AV conduction, thus allowing the distal conduction system and infranodal block more time to recover.

·         ▪ Type II block is usually caused by structural cardiac disease such as sclerosis or calcification of the conducting system resulting from aging. It can also be due to ischemia, infarction, and infiltrative diseases including sarcoid, amyloid, and neuromuscular dystrophy. It can occur postoperatively after cardiac surgery or ablation procedures.

Treatment

·         ▪ Because type II block is an infranodal disease, a permanent pacemaker should be inserted even in asymptomatic patients. If type II AV block is associated with wide QRS complexes, this is a Class I indication for permanent pacing, according to the ACC/AHA/HRS guidelines. If the QRS complexes are narrow, the recommendation becomes Class IIa.

·         ▪ Patients with type II block can develop complete heart block suddenly without warning. Thus, a transcutaneous pacemaker or a temporary pacemaker should be available even if the patient is not bradycardic. If the patient suddenly develops complete AV block before a pacemaker can be inserted, adrenergic agents such as isoproterenol or epinephrine may be given to increase the intrinsic rate of the escape rhythm. Infranodal block will not respond to atropine (see Treatment of Complete AV Block in this Chapter).

·         ▪ When the QRS complexes are narrow and the PR intervals look fixed, the diagnosis of Mobitz type II block may be questionable. If the diagnosis of type II block is uncertain, an electrophysiologic study may be necessary to ascertain that the block is infranodal before a permanent pacemaker is implanted, especially in asymptomatic patients with second-degree AV block.

Prognosis

·         ▪ Because type II block is an infranodal disease, the immediate prognosis is more ominous than type I second-degree AV block. When complete AV block occurs, the escape rhythm has to originate below the level of the block. Thus, only a ventricular escape rhythm can come to the rescue. Unlike type I block, type II block is commonly associated with structural heart disease; therefore, the conduction abnormality is usually not reversible and progression to complete AV block may be sudden without warning (see complete AV block).

·         ▪ The overall prognosis of type II block depends on the presence or absence of associated cardiac abnormalities.

o    ▪ If the AV block is confined to the conduction system and no evidence of structural cardiac disease is present, insertion of a permanent pacemaker to correct the conduction abnormality will result in the same natural history as a patient without the conduction abnormality.

o    ▪ If the conduction abnormality is associated with structural cardiac disease, such as ischemic heart disease or cardiomyopathy, the prognosis will depend on the etiology of the cardiac abnormality.

Advanced 2:1 Second-Degree AV Block

·         ▪ Advanced second-degree AV block: 2:1 AV block is an example of advanced second-degree AV block.

o    ▪ In 2:1 block, every other P wave is conducted alternating with every other P wave that is blocked (Figs. 8.26 and 8.27).

o    ▪ The QRS complexes may be narrow or wide (Figs. 8.26 and 8.27).

o    ▪ A common error is to include 2:1 AV block as a type II block because the PR interval is fixed. Two to one AV block is neither type I nor type II second-degree block. The PR interval looks fixed because only a single P wave is conducted, thus only one PR interval can be measured. To differentiate type I from type II block, at least two consecutive P waves should be conducted so that the lengthening of the PR interval can be observed.

·         ▪ Ventriculophasic sinus arrhythmia: During 2:1 AV block, sinus arrhythmia may be present. The sinus arrhythmia is ventriculophasic if the P-P interval with a QRS complex is shorter than the P-P interval without a QRS complex (Fig. 8.26).

·         ▪ 2:1 AV block may be nodal or infranodal. To differentiate one from the other, continuous monitoring should be performed until conduction improves and more than one consecutive P wave is conducted (3:2 or better). When this occurs, the level of the AV block may be localized.

o    ▪ When conduction improves and 2:1 block is seen in association with type I block, the block is AV nodal (Fig. 8.28).

o    ▪ When conduction improves and 2:1 block is seen in association with type II block (fixed PR intervals and wide QRS complexes), the block is infranodal (Fig. 8.29).

·         ▪ Acute MI and AV block: When 2:1 block complicates acute MI, the location of the infarct is helpful in identifying the level of the AV block. If the infarct is inferior and the QRS complexes are narrow, the AV block is at the level of the AV node (Fig. 8.30).

Figure 8.26: 2:1 Second-Degree Atrioventricular (AV) Block with Narrow QRS Complexes. Every other P wave is conducted alternating with every other P wave that is blocked (arrows) consistent with 2:1 AV block. Two to one AV block is not a type II block because only a single P wave is conducted. Note that the QRS complexes are narrow, thus an infranodal block is unlikely. Because there is no evidence of distal conduction system disease, the 2:1 AV block is most likely at the level of the AV node. Note also that the P-P interval with a QRS complex is shorter (820 milliseconds) than the P-P interval without a QRS complex (870 milliseconds) because of ventriculophasic sinus arrhythmia.

Figure 8.27: 2:1 Second-Degree Atrioventricular (AV) Block with Wide QRS Complexes. The rhythm is 2:1 AV block similar to Figure 8.26. In this example, the QRS complexes are wide because of right bundle branch block, a sign of distal conduction system disease. This type of 2:1 block can be infranodal occurring at the level of the bundle branches although AV nodal block is also possible. The stars point to the nonconducted P waves.

Advanced Second-Degree AV Block: 3:1 and Higher

·         ▪ Advanced second-degree AV block: When the AV block is 2:1, 3:1, 4:1, or higher, the AV block cannot be classified as type I or type II because only a single P wave is conducted (2:1 block) or two or more consecutive P waves are blocked (3:1 AV block or higher). These are examples of advanced second-degree AV block (Figs. 8.31,8.32,8.33).

·         ▪ The conduction ratio refers to the number of P waves that are blocked before a P wave is conducted. Thus, a 3:1 conduction ratio implies that of three consecutive P waves, only one is conducted.

·         ▪ Advanced AV block with narrow QRS complexes may be nodal or infranodal (Figs. 8.31 and 8.32). When the QRS complexes are wide, the block is almost always infranodal (Fig. 8.33).

ECG Findings of Advanced Second-Degree

Figure 8.28: 2:1 Second-Degree Atrioventricular (AV) Block Occurring with AV Wenckebach. Rhythm strip 1 shows 2:1 AV block. Rhythm strip 2 is from the same patient taken several minutes later showing 3:2 AV Wenckebach. Because 2:1 AV block is seen in association with classical AV Wenckebach with narrow complexes, the 2:1 block is at the level of the AV node. The stars identify the blocked P waves.

AV Block

·         Advanced or high-grade AV block is a form of second-degree block where two or more consecutive P waves are not conducted as in 3:1, 4:1, or 5:1 AV block. A 2:1 AV block is also included as a form of advanced second-degree AV block because only a single P wave is conducted.

·         The QRS complexes may be narrow or wide.

·         The long pauses are often terminated by escape beats.

Mechanism

·         ▪ Advanced second-degree AV block can occur at the level of the AV node (AV nodal block). It can also occur more distally at the level of the His-Purkinje system (infranodal block).

o    ▪ AV nodal block: Advanced second-degree AV block occurring at the AV node may have narrow or wide QRS complexes, although typically the QRS complexes are narrow.

Figure 8.29: 2:1 Second-Degree Atrioventricular (AV) Block with Wide QRS Complexes. The rhythm strips labeled 1, 2, and 3 are continuous. Rhythm strip1 shows 2:1 AV block; rhythm strip 2 shows three consecutively conducted P waves with a classical Mobitz type II pattern. The PR interval is fixed and the R-R interval is also fixed. In rhythm strip 3, 2:1 AV block is again present. The transient occurrence of Mobitz type II AV block, which is an infranodal block, suggests that the 2:1 block is infranodal, occurring at the level of the bundle branches. The stars identify the blocked P waves.

o    ▪ Infranodal block: Advanced second-degree AV block can occur at the level of the bundle of His or more distally at the level of the bundle branches. The QRS complexes may be narrow or wide, although typically the QRS complexes are wide.

§  Bundle of His: Advanced second-degree block can occur at the level of the bundle of His, but this type of AV block (intra-His block) is uncommon. The QRS complexes are narrow.

§  Bundle branches: When the block is at the level of the bundle branches, the baseline ECG will show wide QRS complexes because of right or left bundle branch block.

·         ▪ Ventriculophasic sinus arrhythmia may occur when there is 2:1 AV block. The P-P interval with a QRS complex is shorter than the P-P interval without a QRS complex. The P-P interval with a QRS complex has stroke volume that can stretch the carotid baroreceptors, causing vagal inhibition that is most pronounced in the next cardiac cycle. This results in a longer P-P interval in the cardiac cycle without a QRS complex.

Figure 8.30: Two to One Atrioventricular (AV) Block and Acute Inferior Myocardial Infarction (MI). Twelve-lead electrocardiogram showing 2:1 AV block with narrow QRS complexes occurring as a complication of acute inferior MI. The stars identify the P waves that are not conducted. The presence of acute inferior MI with narrow QRS complexes localizes the AV block at the level of the AV node.

Figure 8.31: Advanced Second-Degree Atrioventricular (AV) Block. The rhythm is normal sinus with 3:1 AV block (bracket). The QRS complexes are narrow. When the QRS complexes are narrow, the block may be nodal or infranodal, but is usually nodal. The P waves are marked by the arrows.

Figure 8.32: Advanced Second-Degree Atrioventricular (AV) Block. There are five consecutive P waves (labeled 4 to 8) that are not conducted. The pause is terminated by a junctional escape complex (arrow). Beats 1 to 4 and 10 to 12 show classical AV Wenckebach with gradual lengthening of the PR interval followed by a P wave that is not conducted (beats 4 and 12). The PR interval shortens immediately after the pause (beat 13). The presence of classical AV Wenckebach with narrow complexes indicates that the advanced AV block is at the level of the AV node. The presence of an AV junctional escape complex also indicates that the block is AV nodal.

 

Figure 8.33: Advanced (3:1) Second-Degree Atrioventricular (AV) Block. When advanced second-degree AV block has wide QRS complexes, the block is almost always infranodal. In this example, one bundle branch has a fixed blocked and the other bundle branch is intermittently blocked, resulting in nonconducted P waves. The arrows identify the P waves.

Clinical Significance

·         ▪ It is a common mistake to classify 2:1 AV block always as a type II block because the PR interval is fixed. Because there is only a single conducted P wave and the next P wave is blocked, there is only one PR interval that can be measured. Thus, it is not possible to classify 2:1 block as type I or type II. At least two consecutive P waves should be conducted to differentiate type I from type II block. A 2:1 AV block is an example of advanced AV block. It is preferable to leave the diagnosis of 2:1 block simply as 2:1 second-degree AV block without specifying that the AV block is type I or type II.

·         ▪ Infranodal block implies a more serious conduction abnormality than AV nodal block. The location of the conduction abnormality can be identified as nodal or infranodal by the following features.

o    ▪ When 2:1 AV block or a higher conduction ratio, such as 3:1 or 4:1 AV block is associated with AV Wenckebach with narrow QRS complexes, the block is at the level of the AV node.

o    ▪ When 2:1 AV block or a higher conduction ratio is associated with type II block with a fixed PR interval and wide QRS complexes, the block is below the AV node.

o    ▪ When advanced AV block is associated with the use of pharmacologic agents that can block the AV node (beta blockers, calcium blockers, or digitalis), the block is AV nodal.

o    ▪ When advanced AV block occurs in the setting of an acute infarction:

§  If the infarct is inferior, the block is AV nodal. The QRS complexes are narrow.

§  If the infarct is anterior, the block is infranodal. This is usually associated with wide QRS complexes.

o    ▪ If the AV block is infranodal, evidence of infranodal disease, such as right or left bundle branch block, should be present. In general, advanced AV block with wide QRS complexes with a conduction ratio of 3:1 or higher commonly involves the His-Purkinje system.

o    ▪ If an escape beat is present, the origin of the escape complex may be helpful in localizing the level of the AV block.

§  If the escape beat has a narrow QRS complex, the block is AV nodal. A block within the bundle of His (intra-His) is possible but uncommon.

§  If the escape complex is wide, the AV block is usually infranodal.

§  The causes of advanced second-degree AV block are identical to those of types I and II AV block.

Treatment

·         ▪ Advanced AV block, including 2:1 AV block at the level of the AV node, is usually transient with a good prognosis. Therapy is not required if the patient is asymptomatic and the heart rate exceeds 50 bpm. However, if symptoms related to bradycardia occur, atropine is the drug of choice (see Treatment of Complete AV Block in this Chapter). Atropine is not effective if the AV block is infranodal. An intravenous adrenergic agent such as isoproterenol, 2 to 10 mcg/minute or epinephrine 2 to 20 mcg/minute, may be given emergently as a continuous infusion until a transvenous (or transcutaneous) pacemaker becomes available. The dose is titrated according to the desired heart rate (see Treatment of Complete AV Block in this Chapter).

·         ▪ In patients where the AV block is not reversible, a permanent pacemaker is indicated. The following are indications for insertion of permanent pacemaker in advanced second-degree AV block according to the ACC/AHA/HRS guidelines.

o    ▪ Symptomatic patients: For patients with advanced second-degree AV block who have symptoms or ventricular arrhythmias related to the bradycardia, insertion of a permanent pacemaker is a Class I recommendation regardless of the anatomic level of the AV block.

o    ▪ Asymptomatic patients: In asymptomatic patients with advanced second-degree AV block, permanent pacing is a Class I indication in the following conditions regardless of the site of the AV block.

§  Patients with arrhythmias and other medical conditions that require drugs that can cause symptomatic bradycardia.

§  Documented asystole ≥3.0 seconds or any escape rate <40 bpm in patients with sinus rhythm who are awake and asymptomatic.

§  In patients with atrial fibrillation with ≥1 pauses of ≥5 seconds.

§  After catheter ablation of the AV junction.

§  Postcardiac surgery AV block that is not expected to resolve.

§  Neuromuscular diseases including myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy with or without symptoms.

§  During exercise in the absence of myocardial ischemia.

§  Asymptomatic patients with advanced AV block at the infranodal level diagnosed during electrophysiologic study for other indications. This is a Class IIa recommendation.

§  AV block that is expected to resolve or unlikely to recur such as those resulting from drug toxicity, Lyme disease, or during hypoxia related to sleep apnea in the absence of symptoms is a Class III recommendation.

Figure 8.34: Third-Degree or Complete Atrioventricular (AV) Block. In complete AV block, it is not possible for any atrial impulse to propagate to the ventricles, therefore only P waves (and no QRS complexes) will be present. Unless the ventricles are activated by another impulse originating below the level of the block, the ventricles will remain asystolic, resulting in syncope or sudden death.

Prognosis

·         ▪ The prognosis of high-grade AV block depends on the etiology of the AV block. Patients with isolated advanced AV block resulting from degenerative disease of the conduction system may have the same prognosis as those without advanced AV block after a permanent pacemaker is implanted.

Third-Degree or Complete AV Block

·         ▪ Complete or third-degree AV block: In complete or third-degree AV block, there is complete failure of all atrial impulses to conduct to the ventricles; therefore, only P waves will be present (Fig. 8.34). These P waves are unable to reach the ventricles because they are blocked or interrupted somewhere in the AV conduction system (Fig. 8.35). Unless an escape rhythm comes to the rescue, the ventricles will remain asystolic and the patient will develop syncope or die suddenly.

·         ▪ The origin of the escape rhythm will depend on the location of the AV block. These escape complexes are completely independent from the sinus P waves, resulting in complete dissociation between the P waves and the QRS complexes.

Figure 8.35: Complete Atrioventricular (AV) Block. Complete AV block can occur anywhere along the AV conduction system. It can occur at the AV node or bundle of His. It can involve both bundle branches simultaneously or the right bundle plus both fascicles of the left bundle branch. When complete AV block is present, the location of the conduction abnormality should always be identified because prognosis will depend on the location of the AV block.

Localizing the AV Block

·         ▪ Complete AV block may occur at the level of the AV node or it may be infranodal, occurring below the AV node anywhere in the His bundle, bundle branches, and more distal conduction system.

Figure 8.36: Complete Atrioventricular (AV) block with Narrow QRS Complexes. If complete AV block occurs at the level of the AV node, a junctional escape rhythm (star) comes to the rescue. The QRS complexes are narrow because the impulse originates above the bifurcation of the bundle of His and can activate both ventricles simultaneously. Arrows point to sinus P waves, which are completely dissociated from the QRS complexes.

·         ▪ AV nodal block: If complete AV block occurs at the level of the AV node, a junctional escape rhythm usually comes to the rescue.

o    ▪ AV junctional escape rhythm: The AV junction includes the AV node all the way down to the bifurcation of the bundle of His. The escape rhythm usually originates below the AV node at its junction with the bundle of His. Any impulse originating above the bifurcation of the bundle of His such as a junctional rhythm can activate both ventricles simultaneously, resulting in a narrow QRS complex (Fig. 8.36). The presence of AV junctional rhythm indicates that the block is at the level of the AV node. If the AV junction is suppressed or inhibited or is structurally abnormal, a ventricular escape rhythm may come to the rescue.

o    ▪ Ventricular escape rhythm: A ventricular escape rhythm has wide QRS complexes because it originates below the bifurcation of the bundle of His (Fig. 8.37). The presence of a ventricular escape rhythm usually indicates that the block is infranodal, although the AV block may occasionally occur at the level of the AV node.

·         ▪ Infranodal block: When the block is infranodal, it usually occurs at the level of the bundle branches or fascicles. It can also occur at the level of the bundle of His, although a block at the level of the bundle of His (intra-His block) is rare. When the block is infranodal, only a ventricular escape rhythm with wide QRS complexes can come to the rescue. The QRS complexes are wide because the impulse originates below the bifurcation of the bundle of His; thus, the ventricles are not activated simultaneously. Conduction of the impulse is delayed and is transmitted from one ventricle to the other by muscle cell to muscle cell conduction. A junctional escape rhythm cannot come to the rescue because it will not be able to continue down the conducting system and will not be able to reach the ventricles.

·         ▪ The origin of the escape rhythm is helpful in localizing the level of the AV block as shown in Figure 8.19.

·         ▪ The presence of an acute MI is useful in localizing the AV block.

o    ▪ Acute anterior MI: When complete AV block occurs in the setting of an acute anterior MI, the AV block is infranodal. The AV block is frequently preceded by left or right bundle branch block and the escape rhythm is ventricular (Fig. 8.38).

o    ▪ Acute inferior MI: When complete AV block occurs in the setting of an acute inferior MI, the AV block is at the AV node (Fig. 8.39).

·         ▪ Figure 8.39 shows acute inferior MI with complete AV dissociation. The presence of acute inferior MI with junctional rhythm (narrow QRS complexes) suggests that the AV block is at the level of the AV node.

·         ▪ Although a junctional escape rhythm points to the AV node as the site of the AV block, a ventricular escape rhythm does not indicate that the AV block is always infranodal. InFigure 8.40, the first three escape complexes are ventricular, suggesting an infranodal location of the AV block. The last three escape complexes, however, are narrow and are junctional in origin. This makes an infranodal block highly unlikely. The presence of junctional escape complexes therefore suggests that the AV block is AV nodal.

·         ▪ The surface ECG is an excellent diagnostic tool in localizing the level of AV block, making electrophysiologic testing rarely necessary. However, when the level of AV block remains uncertain, intracardiac ECG may be used to verify the exact location of the AV conduction abnormality.

·         ▪ Intracardiac ECG can be obtained by inserting an electrode catheter into a vein and advancing it to the right ventricle at the area of the bundle of His.

o    ▪ Surface ECG: When the atria and ventricles are activated by the sinus impulse, the surface ECG records a P wave, which corresponds to atrial activation and a QRS complex, which corresponds to ventricular activation (Fig. 8.41A).

o    ▪ Intracardiac ECG: The intracardiac ECG will be able to record not only atrial (A) and ventricular (V) activation, which corresponds to the P wave and QRS complex in the surface ECG, but can also record activation of the His bundle (H), which is represented as a deflection between the P wave and the QRS complex (Fig. 8.41B).

Figure 8.37: Complete Atrioventricular (AV) Block with Wide QRS Complexes. The atrial impulses, identified by the arrows, cannot conduct to the ventricles because of complete AV block, which can occur at the level of the bundle of His (A) or bundle branches and fascicles (B). A block at the level of the bundle of His is possible but is rare. When there is infranodal block, the QRS complexes are wide because the escape rhythm originates from the ventricles (star). It is not possible for a junctional escape rhythm (asterisk) to come to the rescue because the origin of the impulse is proximal to the block and will not be able to propagate to the ventricles.

Figure 8.38: Atrioventricular (AV) Block Complicating Acute Anterior Myocardial Infarction (MI). Electrocardiogram (ECG) A shows acute anteroseptal MI complicated by first-degree AV block, right bundle branch block, and left anterior fascicular block. ECG B shows complete AV dissociation. The P waves are marked by the arrows.

 

Figure 8.39: Acute Inferior Myocardial Infarction (MI) with Complete Atrioventricular (AV) Dissociation. When acute inferior MI is accompanied by AV dissociation, the AV block is at the level of the AV node. The arrows identify the P waves. Note also that the escape rhythm is AV junctional with narrow QRS complexes.

Intracardiac ECG or His Bundle Recording

·         ▪ The His deflection allows the PR or A-V interval to be divided into two components:

o    ▪ A-H interval: This represents conduction between atria and His bundle corresponding to the transmission of the impulse across the AV node.

o    ▪ H-V interval: This represents conduction between the His bundle and ventricles corresponding to the transmission of impulse in the bundle branches and distal conduction system.

·         ▪ When an atrial impulse is blocked and is not followed by a QRS complex, the intracardiac recording can localize the AV block.

o    ▪ AV nodal: If the atrial impulse is not followed by His deflection (and ventricular complex), the AV block is AV nodal (Fig. 8.42A).

o    ▪ Infranodal: If the atrial impulse is followed by His spike but not a ventricular complex, the AV block is infranodal (Fig. 8.42B).

Figure 8.40: Complete Atrioventricular (AV) Block. The presence of ventricular escape rhythm does not indicate that the block is always infranodal. The rhythm strip shows complete AV block. The QRS complexes are marked by the stars. The first three complexes are wide and represent ventricular escape complexes suggesting that the AV block is infranodal. The last three complexes, however, are narrow, representing junctional rhythm that makes an infranodal block unlikely.

 

o    ▪ Intra-His: The atrial impulse can be blocked at the level of the bundle of His (intra-His block), although this is rare.

·         ▪ In complete AV block, the ventricular rate should always be slower than the atrial rate and not the other way around. The ventricles and AV conduction system should be given enough time to recover so that the atrial impulse will not find the ventricles refractory. Thus, the ventricular rate should not only be slower than the atrial rate but should be <50 bpm, usually in the low to mid-40s before the AV block is considered complete.

·         ▪ Complete AV block can occur regardless of the atrial rhythm, which could be normal sinus (Fig. 8.43), atrial flutter (Fig. 8.44), or atrial fibrillation (Fig. 8.45).

Figure 8.41: The Surface Electrocardiogram (ECG) and Intracardiac Recording. The surface ECG is capable of recording only the P wave and the QRS complex, whereas an intracardiac study is capable of recording not only atrial (A) and ventricular (V) activation but also that of the His (H) bundle. The presence of the His deflection allows the PR interval to be divided into two main components: the A-H interval (atrium to His interval), which represents conduction through the AV node (normal 60 to 125 milliseconds) and H-V interval, which represents conduction through the distal conduction system between the His bundle and ventricles (normal, 35 to 55 milliseconds).

Figure 8.42: Intracardiac Electrocardiogram (ECG). (A) Atrioventricular (AV) block at the level of the AV node. The surface ECG shows a P wave that is not conducted (arrow). The intracardiac ECG shows an atrial deflection (A) that is not followed by a His deflection thus the AV block is AV nodal. (B) AV block involving the distal conduction system. The surface ECG shows a P wave that is not conducted (arrow). Intracardiac ECG shows an atrial deflection followed by a His deflection but not a ventricular deflection suggesting that the AV block is distal to the His bundle at the bundle branches and distal conduction system. A, atrial complex; H, His spike; V, ventricular complex.

Common Mistakes in AV Block

·         ▪ Sinus arrest: When only QRS complexes are present and atrial activity is absent (no P waves), the rhythm is sinus arrest and not complete AV block (Figs. 8.46 and 8.47).

·         ▪ Complete AV block versus advanced second-degree AV block: In complete AV block, there should be complete dissociation between the P waves and the QRS complexes. If a single P wave captures a QRS complex, the AV block is no longer complete (Fig. 8.48).

·         ▪ Blocked Premature Atrial Complexes (PACs): Blocked premature atrial complexes may be mistaken for nonconducted sinus P waves and mistaken for second-degree AV block (Fig. 8.49).

·         ▪ Concealed conduction: Concealed conduction is commonly mistaken for AV block. Concealed conduction indicates that a previous impulse had infiltrated the conduction system. This will have an effect on the next impulse. Figure 8.50 shows a sinus P wave (star) that is not followed by a QRS complex. This can be mistaken for second-degree AV block. Although a nonconducted sinus P wave is obvious, there is a premature ventricular impulse preceding the P wave. This premature impulse depolarized not only the ventricles, but also the AV conduction system ret-rogradely, rendering the AV node refractory. The effect of the premature impulse on the conduction system is not apparent until the arrival of the next sinus impulse, which is unable to conduct to the ventricles because the AV node is still refractory. This is an example of concealed conduction and not second-degree AV block.Figure 8.51 is a similar example of concealed conduction showing sinus P waves that are not conducted (arrows). The blocked P waves are preceded by premature ventricular complexes.

·         ▪ Figure 8.52 summarizes diagrammatically the different types of AV block.

Figure 8.43: Complete Atrioventricular (AV) Block. The rhythm is normal sinus with a rate of 96 beats per minute. The ventricular rate is 26 beats per minute (arrows). Note that the P waves are completely dissociated and have no relation to the QRS complexes because complete AV block. Note also that the atrial rate is faster than the ventricular rate.

Figure 8.44: Complete Atrioventricular (AV) Block. The rhythm is atrial flutter. The ventricular rate is slow and regular and is <30 beats per minute because of complete AV block. The presence of wide QRS complexes indicates that the escape rhythm is ventricular in origin and suggests that the block is infranodal.

Figure 8.45: Complete Atrioventricular (AV) Block. The rhythm is atrial fibrillation with complete AV block with a slow ventricular rate of approximately 33 beats per minute. The QRS complexes are wide and regular, suggesting that the escape rhythm is ventricular in origin. This favors an infranodal block. In atrial fibrillation, the R-R intervals are irregularly irregular. When the R-R intervals suddenly become regular, complete AV block should always be considered.

Figure 8.46: This is Not Complete Atrioventricular (AV) Block. Because there is no atrial activity, atrioventricular block is not present. The underlying mechanism is due to complete absence of sinus node activity (sinus arrest) because of sick sinus syndrome. The sinus arrest is terminated by a ventricular escape complex.

Figure 8.47: Sinus Node Dysfunction Mistaken for Complete Atrioventricular Block. Again, there is no evidence of atrial activity; therefore, atrioventricular (AV) block is not present. The rhythm is AV junctional with a slow ventricular rate of 39 beats per minute because of sick sinus syndrome.

 

Figure 8.48: Advanced Atrioventricular Block (AV) Mistaken for Complete AV Block. The P wave with a circle captures a QRS complex resulting in sudden shortening of the R-R interval to 1.04 seconds. If one P wave is able to capture the ventricles as shown, the atrioventricular (AV) block is not complete. This is an example of advanced but not complete AV block.

Figure 8.49: Blocked Premature Atrial Complexes (PACs) Resembling Second-Degree Atrioventricular (AV) Block. The blocked PACs are marked by the arrows. Note that the P waves are premature and are followed by pauses. These nonconducted premature atrial complexes may be mistaken for sinus P waves and the rhythm can be mistaken for second-degree AV block.

Figure 8.50: Concealed Conduction. The rhythm strip shows a sinus P wave without a QRS complex (star), which can be mistaken for second-degree atrioventricular (AV) block. Preceding the sinus P wave is a premature ventricular complex (arrow) that retrogradely penetrated the AV conduction system, making the AV node refractory. Thus, the next sinus impulse was not conducted. This is an example of concealed conduction and not second-degree AV block.

Figure 8.51: Concealed Conduction. Sinus P waves without QRS complexes (arrows) are noted only after every ventricular ectopic impulse. This is an example of concealed conduction and not second-degree atrioventricular block.

 

TABLE 8.1 Indications for Insertion of Permanent Cardiac Pacemakers in Patients with Acquired AV Block in Adults

 Third-degree and advanced  second-degree AV block at any  anatomic level

Symptomatic individuals: Bradycardia causes symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block.

Asymptomatic individuals:

·         Arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia.

·         Documented asystole of ≥3.0 seconds or escape rate is <40 beats per minute in awake or asymptomatic patients in sinus rhythm.

·         Atrial fibrillation and bradycardia of ≥1 or more episodes of ≥5 seconds duration.

·         Heart rate >40 beats per minute when awake but with persistent third-degree AV block with cardiomegaly or left ventricular dysfunction.

·         Second or third-degree AV block during exercise in the absence of myocardial ischemia.

After cardiac procedures:

·         Postablation of the AV junction

·         AV block occurring after cardiac surgery that is not expected to resolve

AV block Associated with neuromuscular diseases:a

·         The patient may be symptomatic or asymptomatic

 Type II second-degree AV block

Symptomatic patients:

·         Symptomatic patients because of bradycardia.

Asymptomatic patients:

·         Type II second-degree AV block with wide QRS complexes.

·         Type II second-degree AV block with narrow QRS complexes (Class IIa).

 Type I second-degree AV block

Symptomatic individuals:

·         Symptoms of low output and hypotension because of bradycardia regardless of     the level of AV block.

·         Patient may not be bradycardic but symptoms are similar to pacemaker syndrome (Class IIa).

Asymptomatic individuals:

·         AV block at or below the level of the bundle of His usually diagnosed during electrophysiological study performed for other indications (Class IIa).

Patients with neuromuscular disease:a

·         Patients may be symptomatic or asymptomatic (Class IIb).

 Marked first-degree AV block

Symptomatic individuals:

·         Symptoms of low output and hypotension similar to pacemaker syndrome in     patients with left ventricular dysfunction or congestive heart failure. The symptoms should be improved by temporary AV pacing (Class IIa).

Patients with neuromuscular disease:a

·         Patients may be symptomatic or asymptomatic (Class IIb).

 From the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. All the above recommendations  for permanent pacemaker insertion are Class I indications unless specified.

 a Neuromuscular diseases include myotonic muscular dystrophy, Erb dystrophy (limb-girdle), peroneal muscular atrophy, and  Kearns-Sayre syndrome. AV, atrioventricular.

Indications for Permanent Pacing in AV Block

·         ▪ Unless specified, the following are Class I indications for implantation of permanent pacemakers in adult patients with acquired AV block according to the ACC/AHA/HRS guidelines (see Table 8.1).

                               

Figure 8.52: Atrioventricular (AV) Block. The figure summarizes the different types of AV block.                 

ECG Findings of Complete AV Block

·         In complete AV block, there is complete failure of the atrial impulses to capture the ventricles.

·         Only P waves will be present. Unless an escape rhythm comes to the rescue, ventricular asystole will occur.

·         The escape rhythm (the QRS complexes) can be narrow or wide.

·         The P waves and QRS complexes are completely dissociated.

·         The ventricular rate should be slower than the atrial rate and should be <50 bpm, usually in the mid- to low 40s.

Mechanism

·         ▪ The intraventricular conduction system contains special cells with automatic properties that are capable of becoming pacemakers. These cells are called latent pacemakersbecause their rate of discharge is slower than the sinus node and do not become manifest because they are depolarized by the propagated sinus impulse. When the sinus impulse is blocked or when there is significant slowing of the sinus node, these latent pacemakers can become the dominant pacemaker of the heart. Cells in the middle portion of the AV node called the N region do not have automatic properties and cannot become pacemakers. Cells at the upper portion of the AV node at its junction with the atria (AN region), lower portion of the AV node at its junction with the bundle of His (NH region) and His-Purkinje system have pacemaking properties. Cells with automatic properties that are located higher in the conduction system (closer to the AV node) have higher rates than cells that are located more distally. Thus, the intrinsic rate of the AV junction is 40 to 60 bpm and cells that are located more distally in the His-Purkinje system have slower rates of 20 to 40 bpm.

·         ▪ Complete AV block can occur anywhere in the AV conduction system. It can occur at the level of the AV node, bundle of His, both bundle branches, or the right bundle branch in combination with block involving both fascicular branches of the left bundle branch. If complete AV block is present, the sinus impulse will not be able to reach the ventricles because the AV conduction system is the only pathway by which the sinus impulse can reach the ventricles. This will result in syncope or sudden death unless an ectopic impulse comes to the rescue and initiates a ventricular rhythm. The escape rhythm has to originate below the level of the AV block. Thus, if the AV block is at the AV node, a junctional escape rhythm with narrow QRS complex usually comes to the rescue, and if the AV block is at the level of the His-Purkinje system, a ventricular escape rhythm with wide QRS complex is usually the escape mechanism. The presence of complete AV block is not certain unless the ventricles and AV conduction system are given enough time to recover from the previous impulse. For this to occur, the ventricular rate should be slower than the atrial rate and should be <50 bpm, usually in the mid- to low 40s.

Clinical Implications

·         ▪ Complete AV block can occur suddenly and can cause syncope or sudden death. The location of the AV block has prognostic significance and should be localized in all patients with AV block. The origin of the escape rhythm as well as the clinical setting in which the AV block occur are useful in localizing the AV block.

o    ▪ If the escape rhythm is AV junctional, the block is at the level of the AV node. In infranodal block, the escape rhythm is always ventricular.

o    ▪ The presence of bundle branch block before the onset of complete AV block suggests that there is distal conduction disease and favors an infranodal block.

o    ▪ If the patient is taking pharmacologic agents that block the AV node, such as digitalis, calcium channel blockers, or beta blockers, the block is AV nodal.

o    ▪ When complete AV block occurs in the setting of an acute inferior MI and the QRS complexes are narrow, the AV block is AV nodal.

o    ▪ When complete AV block occurs in the setting of acute anterior MI, the AV block is infranodal. When the AV block is infranodal, bundle branch block is usually present.

·         ▪ There are multiple causes of complete AV block. Complete AV block may be congenital, occurring at birth, or advanced age resulting from calcification of the aortic ring and mitral annulus (also called Lev disease) and fibrosis or sclerodegenerative changes involving the conduction system (also called Lenègre disease). It could also be due to acute MI, inflammation of the conduction system as in Lyme disease, diphtheria, or Chagas disease, or from infiltrative diseases such as sarcoid or amyloid, hypothyroidism, and neuromuscular diseases. It could also be due to drugs that block the AV node or distal conducting system or during intracardiac surgery or ablation procedures.

·         ▪ Physical examination of a patient with complete AV block will show cannon A waves in the jugular neck veins, variable intensity of the first heart sound, and variable pulse volume. This is similar to the physical findings of ventricular tachycardia (see Chapter 22, Wide Complex Tachycardia). These physical findings are due to the presence of complete AV dissociation.

o    ▪ Cannon A waves in the neck: When there is complete AV dissociation, there is no relationship between atrial and ventricular contraction; thus, atrial contraction often occurs during systole when the tricuspid and mitral valves are closed, resulting in prominent jugular neck vein pulsations called cannon A waves. These cannon A waves occur intermittently, only when atrial and ventricular contractions are simultaneous.

o    ▪ Varying intensity of the first heart sound: The intensity of the first heart sound depends on the position of the mitral and tricuspid valves at the onset of systole. When the valves are wide open, the first heart sound is markedly accentuated because of the wide distance the leaflets have to travel to their closure points. On the other hand, when the valves are near their coaptation points, the first heart sound will be very soft and hardly audible because the leaflets are almost in a semiclosed position at the onset of systole. During atrial contraction corresponding to the P wave in the ECG, the mitral and tricuspid leaflets are pushed wide open toward the ventricles away from their closure points. If this is immediately followed by ventricular contraction (as when the PR interval is short), closure of the mitral and tricuspid leaflets will be loud and often booming. On the other hand, if atrial contraction is not immediately followed by ventricular contraction (as when the PR interval is unduly prolonged), the closure of the leaflets will be soft or inaudible because the leaflets are allowed to drift back to a semiclosed position at the onset of ventricular contraction. Because the PR interval is variable when there is complete AV dissociation, the intensity of the first heart sound will also be variable.

o    ▪ Varying pulse volume: When the P waves and the QRS complexes are completely dissociated, some ventricular beats will be preceded by atrial contraction, whereas other beats are not. When a P wave precedes a QRS complex, ventricular filling is augmented, resulting in a larger stroke volume, whereas QRS complexes without preceding P waves will have a lower stroke volume.

·         ▪ Jugular venous pulsations: The jugular venous pulsations may be useful in the diagnosis of cardiac arrhythmias. In 1899, Wenckebach described the second-degree AV block that bears his name without using an ECG by examining jugular pulse tracings. The jugular pulse consists of three positive waves (a, c, and v waves) and two negative waves (x and y descents). To identify these waves and descents at bedside, the patient should be positioned properly and lighting should be adequate. The internal jugular veins lie deep behind the sternocleidomastoid muscle; thus, the venous column is not normally visible unless there is increased venous pressure because of right heart failure. The internal jugular pulsations, however, can be identified because they are transmitted superficially to the skin. Simultaneous auscultation of the heart or palpation of the radial pulse or opposite carotid artery is useful in timing the pulsations.

o    ▪ Jugular versus carotid pulsations: If there is difficulty in differentiating jugular venous from carotid arterial pulsations, the patient should be positioned more vertically upright because the venous pulse may disappear, whereas the arterial pulse does not disappear with any position. The venous pulse has two waves, with an inward motion corresponding to the x and y descents, whereas the arterial pulse has a single wave with an outward motion. If there is still doubt whether the pulse is venous or arterial, the base of the neck above the clavicle should be compressed. If the pulsation is venous, the pulse will disappear. Deep inspiration may enhance the venous pulsations, whereas the carotid pulse is not altered by pressure or by inspiration.

§  The “a” wave: The “a” wave corresponds to the P wave in the ECG and is due to the rise in jugular venous pressure during atrial contraction. There is slight mechanical delay in the transmission of the atrial pulse to the neck; thus, the peak of the “a” wave usually coincides with the onset of the first heart sound. The “a” wave is prominent when there is increased resistance to the flow of blood to the right ventricle, as when there is tricuspid stenosis, right ventricular hypertrophy, pulmonic stenosis, or pulmonary hypertension. It is also prominent when there is left ventricular hypertrophy because the septum is shared by both ventricles. The “a” wave is absent if there is atrial fibrillation or the rhythm is AV junctional.

§  The x descent: The x descent is the most conspicuous jugular motion occurring immediately after the “a” wave and is due to atrial relaxation and downward motion of the tricuspid annulus during systole. Because timing is systolic, it is easy to identify using the heart sounds or radial pulse. The x descent is prominent when the “a” wave is prominent. It is also prominent in constrictive pericarditis and in cardiac tamponade. The x descent is absent when there is no “a” wave, such as when there is AV junctional rhythm or atrial fibrillation.

§  The “c” wave: The x descent in the jugular pulse is often interrupted by the “c” wave, which is due to transmitted pulsation from the carotid artery. Additionally, during right ventricular contraction, there is bulging of the tricuspid leaflets into the right atrium. The x descent continues as the x′ descent after the c wave. The “c” wave is prominent when there is tricuspid regurgitation, often combining with the “v” wave to form a prominent “cv” wave. In some normal individuals, the “c” wave may not be demonstrable.

§  The “v” wave: The “v” wave is due to the rise in right atrial pressure as blood accumulates in the atrium when the tricuspid valve is closed during systole. The peak of the “v” wave occurs with the onset of the second heart sound. The “v” wave becomes a large “cv” wave when there is tricuspid regurgitation. It is also prominent when there is increased right atrial pressure resulting from cardiomyopathy or increased volume due to atrial septal defect.

§  The y descent: The y descent follows the downslope of the “v” wave and is due to the fall in right atrial pressure when the tricuspid valve opens during diastole. The y descent occurs after the second heart sound or after the radial pulse and is prominent in restrictive cardiomyopathy, constrictive pericarditis, right ventricular infarction, and tricuspid regurgitation. The y descent becomes diminished when there is tricuspid stenosis.

o    ▪ The jugular neck vein pulsations may be helpful in the diagnosis of certain arrhythmias:

§  First-degree AV block: When the PR interval is prolonged, the “a” to “c” interval is wide.

§  Type I second-degree AV block or AV Wenckebach: In AV Wenckebach, the interval between the “a” wave and “c” wave gradually widens until the “a” wave is not followed by a “v” wave. Additionally, as the PR interval becomes longer, the intensity of the first heart sound becomes softer until a dropped beat occurs.

§  Type II block: When there is type II block, the interval between the “a” and “c” waves do not vary. The intensity of the first heart sound will not vary because the PR interval is fixed.

§  Other arrhythmias: Cannon A waves are intermittently present when there is complete AV dissociation resulting from complete AV block or ventricular tachycardia. Cannon A waves are constantly present when the PR interval is markedly prolonged (see First-Degree AV Block in this chapter) when there is AV junctional rhythm, supraventricular tachycardia from AV nodal reentry, or AV reentry (see Chapter 16, Supraventricular Tachycardia.) or when there is ventricular tachycardia with retrograde conduction to the atria.

Treatment

·         ▪ If complete AV block occurs at the level of the AV node and the patient is asymptomatic with narrow QRS complexes and a heart rate of at least 50 bpm, no treatment is necessary, other than further monitoring and observation. Any agent that can cause AV block should be discontinued.

·         ▪ Patients with AV block may become symptomatic because of bradycardia, which includes hypotension, altered mental status, ischemic chest pain, or signs of heart failure and low cardiac output. Treatment of the bradycardia includes airway and blood pressure support and identification of immediately reversible causes of AV block, including respiratory causes and blood gas and electrolyte abnormalities, hypovolemia, hypothermia, hypoglycemia, and acute coronary vasospasm.

·         ▪ The following intravenous agents may be useful in increasing the ventricular rate or improving AV conduction. These agents can enhance myocardial oxygen consumption and therefore should be used cautiously in the setting of acute MI because this may result in further extension of the myocardial infarct.

o    ▪ Atropine: The drug of choice for the treatment of bradycardia is atropine. If there are no immediately reversible causes of AV block, this agent remains the drug of choice for symptomatic bradycardia and receives a Class IIa recommendation according to the AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care.

§  Atropine 0.5 mg should be given intravenously every 3 to 5 minutes until a desired heart rate is achieved. Complete vagal blockade is expected when a total dose of 0.04 mg/kg or 3.0 mg is given intravenously over 2 hours.

§  Atropine should not be given in doses smaller than 0.5 mg because small doses stimulate the vagal nuclei and may enhance parasympathetic activity, resulting in paradoxical slowing and worsening of the AV block.

§  The drug can be given intratracheally during resuscitation, although subcutaneous or intramuscular administration should be avoided because these routes of administration can also result in paradoxical slowing.

§  Atropine is not effective in patients with AV block at the infranodal level. If the AV block is infranodal or the bradycardia does not respond to atropine, transcutaneous pacing should be instituted immediately in patients who are symptomatic.

o    ▪ Alternative medications: There are other medications that can be tried for the treatment of bradycardia if atropine is not effective. These drugs are given only as alternative agents and receive a Class IIb recommendation according to the AHA guidelines.

§  Epinephrine: This can be given as an alternate to atropine if atropine is not effective or the AV block is infranodal and transcutaneous pacing is not available or has failed. This will serve as a temporizing measure before a transvenous pacemaker can be inserted. For the treatment of bradycardia and or hypotension, the infusion is prepared by adding 1 mg to 500 mL saline or D5W and started at an initial infusion of 1 µg/minute. The recommended dose is 1 to 10 µg/minute titrated according to the desired heart rate.

§  Dopamine: Dopamine may be given instead of atropine or epinephrine. It can be given as monotherapy or in combination with epinephrine. The dose is 2 to 10 µg/kg/minute titrated according to the desired heart rate.

§  Glucagon: If atropine is not effective, glucagon has been shown to improve symptomatic bradycardia induced by drugs such as beta blockers and calcium channel blockers. The dose is 3 mg given intravenously followed by infusion of 3 mg/hour if needed.

§  Digibind: If complete AV block is due to digitalis excess, digitalis should be discontinued and Digibind given as an antidote.

o    ▪ Transcutaneous pacing: This intervention receives a Class I recommendation in patients who do not respond to atropine. Transcutaneous pacing is easier to perform than transvenous pacing and can be provided by most hospital personnel because the procedure is noninvasive.

o    ▪ Transvenous pacing: Transvenous pacing should be performed if transcutaneous pacing is ineffective or unsuccessful or if the patient cannot tolerate transcutaneous pacing. This procedure is invasive and takes longer to accomplish, but provides more stable pacing.

·         ▪ Permanent pacing: The following are indications for insertion of permanent pacemaker in complete AV block according to the ACC/AHA/HRS guidelines. In patients in whom the AV block is not reversible, a permanent pacemaker is indicated.

o    ▪ Symptomatic patients: Patients with complete AV block at any anatomic level with symptoms related to the bradycardia, insertion of a permanent pacemaker is a Class I recommendation.

o    ▪ Asymptomatic patients: Asymptomatic patients with complete AV block, permanent pacing is a Class I indication in the following conditions.

§  Patients with arrhythmias and other medical conditions that require drugs that can cause symptomatic bradycardia.

§  Documented asystole ≥3.0 seconds or any escape rate <40 bpm in patients with sinus rhythm who are awake and asymptomatic.

§  After catheter ablation of the AV junction.

§  Postcardiac surgery AV block that is not expected to resolve.

§  Neuromuscular diseases including myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy with or without symptoms.

§  The recommendation is Class IIa in asymptomatic patients with complete AV block at any level with average awake ventricular rates of ≥40 bpm if cardiomegaly or left ventricular dysfunction is present.

·         ▪ A permanent pacemaker should not be inserted if the AV block is expected to resolve or is unlikely to recur, such as those resulting from drug toxicity, Lyme disease, or during hypoxia related to sleep apnea in the absence of symptoms. These are Class III recommendations.

Prognosis

·         ▪ In patients with congenital complete AV block, the block is almost always at the level of the AV node. The escape rhythm is AV junctional and most patients remain stable and minimally symptomatic without therapy. These patients will eventually have permanent pacemakers implanted.

·         ▪ When complete AV block is due to an acute inferior infarct, the block is AV nodal and is usually the result of enhanced parasympathetic activity when it occurs within 24 to 48 hours after the acute infarct. It is usually reversible and responds to atropine. If the onset of the AV block is after the second or third day, it is usually the result of continuing ischemia or structural damage to the AV node. Although the prognosis is good because the level of the block is AV nodal, inferior infarction with complete AV block generally indicates a larger infarct than one without AV block and therefore has a higher mortality.

·         ▪ When complete AV block occurs in the setting of an acute anterior MI, the block is almost always infranodal and is very often preceded by bundle branch block. The mortality remains high even if a pacemaker is inserted because anterior infarct associated with AV block is usually extensive.

·         ▪ The prognosis will also depend on the level of the AV block.

o    ▪ AV nodal block: AV nodal block has a better prognosis than an infranodal block because AV nodal block is usually reversible and a permanent pacemaker is often not needed. The AV junction can come to the rescue and has the highest firing rate among all potential pacemakers below the AV node. AV junctional rhythm has an intrinsic rate of 40 to 60 bpm and can be enhanced with atropine. It has narrow QRS complexes because the impulse originates above the bifurcation of the bundle of His. An AV junctional impulse is more effective than a ventricular impulse because it is able to activate both ventricles simultaneously. Finally, AV junctional rhythm is more stable than a ventricular escape rhythm. A pacemaker may be indicated if the AV block remains persistent and the patient becomes symptomatic. A permanent pacemaker is not needed and is a Class III indication if the AV block is transient and is not expected to recur.

o    ▪ Infranodal: When the block is infranodal, a ventricular escape rhythm usually comes to the rescue. The rhythm has inherently slower rate of 20 to 40 bpm. Unlike AV junctional rhythm, it cannot be enhanced with atropine. Additionally, the QRS complexes are wide because both ventricles are not activated synchronously. Thus, the ventricles do not contract simultaneously, the beat is ineffective, and a lower cardiac output than a junctional escape complex is generated. A ventricular rhythm, compared with AV junctional rhythm, is not a stable rhythm. Finally, an infranodal block is usually progressive and permanent and is frequently associated with structural abnormalities not only of the conduction system, but also of the ventricles. Before the era of pacemaker therapy, complete AV block involving the distal conduction system was invariably fatal. Insertion of a permanent pacemaker is currently the only effective therapy available.

o    ▪ The overall prognosis depends on the underlying cause of the AV block. If the AV block is isolated and no structural cardiac disease is present, the prognosis is similar to patients without AV block after a permanent pacemaker is implanted.

Figure 8.53: Complete Atrioventricular (AV) Dissociation from Ventricular Tachycardia. The rhythm is ventricular tachycardia with complete AV dissociation. Note that the ventricular rate is faster than the atrial rate (arrows), which should be the other way around in complete AV block.

Complete AV Dissociation

·         Complete AV dissociation: Complete AV dissociation and complete AV block are not necessarily the same. Complete AV dissociation is a much broader term than complete AV block and includes any arrhythmia in which the atria and ventricles are completely independent from each other. Complete AV dissociation includes complete AV block as well as other arrhythmias not resulting from AV block such as ventricular tachycardia (Fig. 8.53), junctional tachycardia (Fig. 8.54), accelerated junctional rhythm (Fig. 8.55), and accelerated ventricular rhythm (Fig. 8.56). In junctional and ventricular tachycardia, the ventricular rate is faster than the atrial rate. Thus, the atrial impulse cannot conduct to the ventricles because the ventricles do not have ample time to recover before the arrival of the atrial impulse. In these examples, the dissociation between atria and ventricles is not the result of AV block.

Figure 8.54: Complete Atrioventricular (AV) Dissociation from Junctional Tachycardia. The rhythm is junctional tachycardia with a rate of 101 beats per minute. Both P waves and QRS complexes are regular but are completely dissociated. Although the P waves have no relation to the QRS complexes, complete AV block is not present because the ventricular rate is not slow enough to be captured by the atrial impulse. The arrows identify the P waves, which have no relation to the QRS complexes.

Figure 8.55: Complete Atrioventricular (AV) Dissociation from Accelerated Junctional Rhythm. Lead II rhythm strip showing complete AV dissociation with an atrial rate of 100 beats per minute and a ventricular rate at 80 beats per minute. The dissociation between the atria and ventricles may not be due to AV block. In complete AV block, the ventricular rate should be in the 40s to allow enough time for the conduction system and the ventricles to recover completely before the arrival of the next impulse. The P waves are marked by the arrows.

Figure 8.56: Complete Atrioventricular (AV) Dissociation from Accelerated Idioventricular Rhythm. There is complete AV dissociation with an atrial rate of almost 100 beats per minute and ventricular rate of 56 beats per minute. The QRS complexes are wide because of accelerated idioventricular rhythm. Although the dissociation between the P waves and QRS complex may be due to complete AV block, this cannot be certain because the ventricular rate is not slow enough. Thus, the rhythm is more appropriately complete AV dissociation rather than complete AV block. The arrows identify the sinus P waves.

Figure 8.57: Complete Atrioventricular (AV) Dissociation. Complete AV block is an example of complete AV dissociation. The other arrhythmias in which complete AV dissociation may occur are shown.

·         ▪ Complete AV block: In complete AV block, the ventricular rate is slower than the atrial rate. The ventricular rate is not only slower, but should be slow enough to allow sufficient time for the ventricles to recover so that it can be captured by the atrial impulse. Thus, the rate of the ventricles should be <50 bpm, usually in the low 40s before AV block is considered complete.

·         ▪ Accelerated rhythms: In accelerated junctional or idioventricular rhythm, the atria and ventricles may be completely dissociated. The rate of the ventricles may not be slow enough and may not be able to recover on time before the arrival of the atrial impulse. This may result in complete AV dissociation, not necessarily AV block. Figure 8.57 shows the different arrhythmias that can result in AV dissociation.

ECG Findings in Complete AV Dissociation

·         P waves and QRS complexes are completely dissociated and have no relation to each other.

·         In complete AV dissociation, the underlying rhythm may be ventricular tachycardia, junctional tachycardia, accelerated junctional rhythm, accelerated ventricular rhythm, or complete AV block.

Mechanism

·         ▪ Complete AV dissociation occurs when two completely independent pacemakers, one controlling the atria and the other controlling the ventricles, are present.

o    ▪ When there is ventricular tachycardia, junctional tachycardia or accelerated junctional, or ventricular rhythms, the sinus impulse may not be able to propagate to the ventricles because the ventricular rate is faster than the atrial rate. Absence of ventricular capture when the ventricular rate is faster than the atrial rate is not necessarily because of complete AV block, but may be from the ventricles being completely refractory every time atrial impulses arrive at the ventricles. This is a form of electrical interference resulting in AV dissociation. In these examples, complete AV block is not present.

o    ▪ In complete AV block, there is complete absence of AV conduction. The atrial impulse is unable to conduct through the ventricles because of an abnormality in the conduction system. The atrial impulse is given the opportunity to conduct to the ventricles, but is unable to do so when complete AV block is present.

Clinical Implications

·         ▪ Complete AV dissociation is a broader term that includes any rhythm where the atria and ventricles are completely independent from each other and includes complete AV block as well as other arrhythmias not resulting from complete AV block such as ventricular tachycardia, junctional tachycardia, AV junctional, or ventricular rhythm.

·         ▪ Complete AV block is just one of the many examples of complete AV dissociation. For complete AV block to occur, the ventricular rate should be slower than the atrial rate and should be <50 bpm, usually in the low to mid-40s. This will allow enough time for the ventricles to recover before the next atrial impulse arrives. If the atrial impulse cannot capture the ventricles even when the ventricular rate is slow, then complete AV block is the cause of the AV dissociation.

Treatment and Prognosis

·         Because there are other causes of complete AV dissociation other than complete AV block, treatment and prognosis will depend on the specific arrhythmia causing the AV dissociation.

Suggested Readings

2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.3: management of symptomatic bradycardia and tachycardia.Circulation. 2005;112:67-77.

2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.4: monitoring and medications. Circulation. 2005; 112:78-83.

Barold SS, Hayes DL. Second-degree atrioventricular block: a reappraisal. Mayo Clin Proc. 2001;76:44-57.

Chatterjee K. Physical examination. In: Topol EJ, ed. Textbook of Cardiovascular Medicine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2002:280-284.

Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to update the 1998 pacemaker guidelines). Circulation.2002;106:2145-2161.

Epstein AE, DiMarco JP, Ellenbogen KA, et. al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation 2008;117:e350-e408.

Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342:703-709.

Marriot HJL. Intra-atrial, sino-atrial and atrio-ventricular block. In: Practical Electrocardiography. 5th ed. Baltimore: Williams & Wilkins; 1972:194-211.