DIAGNOSTIC SHELF
Atrioventricular
Block After Reciprocating
Atrioventricular
Junctional Tachycardia
JUAN
M. ARANDA,
FEDERICO AGUSTIN
MOLEIRO,
MD MD
CASTELLANOS,
MD,
FACC
BENJAMIN BEFELER, MD, FACC Miami, Florida
Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 set) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the “upper” His bundle, above the site from which the H deflection was recorded.
It is well known that abnormal rhythms, including multifocal ectopic beats, asystole and even short runs of ventricular tachycardia, frequently appear in the transition period after the termination of supraventricular tachycardia.i Although some prolongation of atrioventricular (A-V) conduction time also occurs, blockage of several consecutive P waves seems to be a rare event.] To provide some insight into the possible genesis of symptomatic A-V block occurring after supraventricular tachycardia, we discuss the clinical findings in a patient with this unusual disorder. Case Report
From the Cardiovascular Laboratory, Veterans Administration Hospital and the Division of Cardiology, University of Miami School of Medicine, Miami, Fla. Manuscript accepted October 30, 1974. Address for reprints: Benjamin Befeler, MD. Cardiovascular Laboratory, Veterans Administration Hospital, 1201 N.W. 16th St., Miami, Fla. 33125.
A 61 year old man with sinus bradycardia and right bundle branch block was referred to our laboratory because of intermittent dizzy spells for which no extracardiac cause had been found. Before this admission he had undergone cardiac monitoring on three separate occasions with the Holter equipment. The 10 hour recordings showed only sinus bradycardia (rate 50 to 571 min) and short runs of “supraventricular” tachycardia. Informed consent was obtained and intracardiac electrophysiologic studies were performed as previously described.‘,” During sinus rhythm at a rate of 56/min (Fig. 1) the A-H interval (120 msec) was at the upper limit of normal values for our laboratory (50 to 120 msec). Atria1 pacing with the extrastimulus method resulted in three episodes of reciprocating A-V tachycardia that occurred only at AI-AS intervals of 320 to 340 msec. Figure 2 shows the onset of one of these paroxysms. The Az impulse triggering the tachycardia reached the His bundle with considerable delay (300 msec). G The low right atria1 deflection was lost within the ventricular deflections of the His bundle electrogram. Since a high right atria1 electrogram was not obtained during this episode, the position of the retrograde P waves could not be conclusively identified: the site indicated in the diagram was obtained by extrapolating information obtained from Figure 3. The ventricular rate was 17Olmin. Spontaneous termination of another paroxysm can be seen in Figure 3. At this moment the recording of a high right atria1 electrogram permitted adequate identification of retrograde atria1 activation. The arrhythmia ended when a P wave was not followed by an H deflection. Immediately after the end of the tachycardia there was a period of A-V block during which the atrial deflections apparently failed to activate the His bundle. The correspond-
November 1975
The American Journal of CARDIOLOGY
Volume 36
807
A-V BLOCK AFTER JUNCTIONAL TACHYCARDIA-ARANDA
I
ET AL
1000 MSEC.
tachycardia. The patient was given digoxin, in an attempt to prevent the tachyarrhythmias.
0.25 mg daily,
Discussion In this patient with right bundle branch block and a normal H-V interval, the symptoms could have been due to sinus nodal dysfunction or A-V block, or
both. Abnormal function of the sinus node was manifested by persistent sinoatrial slowing (Fig. 1) and by t,he prolonged (posttachycardia) sinus nodal recovery time (Fig. 3). Mechanisms of Posttachycardia A-V Block HBE+
*/id'
Concealed conduction. A-V block was seen only after spontaneous termination of the reciprocating tachycardia. Since the latter was not abolished by vagal maneuvers, the presence of A-V nodal block related (iatrogenically) to enhanced vagal tone appeared an unlikely explanation. Concealed conduction could explain the genesis of this conduction disturbance if one assumes that the reciprocating A-V tachycardia caused enough (abnormal) prolongation of A-V nodal refractoriness to prevent propagation of subsequent P waves (Fig. 3). But this occurrence would have required that the duration of the refractory period thus created be at least 2,627 msec, which was the duration of the interval between the last retrograde atria1 impulse (A-) and the last blocked P wave. “Pseudo” A-V block: Another explanation appears attractive. The tachycardia might not have stopped after the third QRS complex in Figure 3. As postulated by Pick,fi continued reciprocation (not detected in surface leads) is possible when there is bidirectional (coexisting retrograde and antegrade) exit block. If the latter had been manifested by failure to activate the atria and ventricles, respectively, persis-
~lr~rmcs* t
P-A: 35 A-H:120 H-V: 40 ---P-R:195 FIGURE 1. Sinus rhythm showing right bundle branch block and a normal P-R interval. The duration of the A-H interval is at the upper limit of normal. Other conduction intervals are normal. In this and other figures intervals are expressed in milliseconds. HBE = His bundle electrogram; HRA = high right atrium.
ing P-P intervals preceding the first conducted beat measured 1,027, 1,600 and 1,640 msec, respectively. The prolonged duration of the last two intervals suggested the coexistence of sinus nodal dysfunction. In all three posttachycardia intervals that occurred in the laboratory the patient had symptoms similar to those he had experienced before admission to the hospital. Although the electrogenesis of the A-V block was not clear, pacemaker implantation was recommended because this intermittent conduction disturbance occurred in a symptomatic patient who also had sinus nodal dysfunction, right bundle branch block and reciprocating A-V junctional
H
808
November 1975
H
H
The American Journal of CARDIOLOGY
H
Volume 36
H
FIGURE 2. Reciprocating A-V tachycardia occurring at an AT-A2 interval of 340 msec. Low right atrial deflections are buried within the ventricular deflections of the His bundle electrogram. A2 = atrial deflection produced by St2; H = His bundle electrograms; St, = driving stimuIus artifact: St2 = testing stimulus artifact: Intervals between the vertical lines are 975 msec.
A-V BLOCK AFTER JUNCTIONAL TACHYCARDIA-ARANDA
ET AL.
1027
FIGURE 3. Spontaneous termination of an episode of reciprocating A-V junctional tachycardia followed by block of two consecutive P waves during which the A deflections are not followed by detectable His bundle activation. The intervals between P waves are abnormally long. A- = retrograde high right atrial electrograms. The low right atrial deflections recorded by His bundle electrograms are lost within the corresponding ventricular electrograms. Therefore the sequence of atrial depolarization is from the low to high right atrium. By contrast, the sequence of the last P wave is from the high to the low right atrium.
reciprocation within the more central portions of the A-V node would have prevented subsequent P waves from reaching the His bundle until cessation of the tachycardia (Fig. 2). The resulting arrhythmia might be termed “pseudo” A-V block produced by concealed reciprocating A-V junctional tachycardia. However, this assumption could not be proved on the basis of the information obtained from the catheter recordings. Bradycardia-dependent A-V block: A third explanation has to be considered. Several investigators7-l3 have recently discussed the mechanisms of bradycardia-dependent A-V block. This conduction disturbance occurs when A-V block is seen after a critical slowing of the rate or an increase in cycle length. It is believed that delayed appearance of a P wave allows the supraventricular impulse to reach a group of cells located in an area that is the only connection between the atria and the ventricles. These cells must have an enhanced or slightly rising slope of phase 4 depolarization. 7,8 Conduction failure occurs because the supraventricular impulse reaches the affected zone when membrane potential is abnormally close to 0. Bradycardia-dependent A-V block is an infra A-V nodal phenomenon because the His-Purtent
kinje system is the one possessing the property of phase 4 depolarization.7-12 At first glance Figure 3 suggests that this mechanism cannot be applied to explain the genesis of the blocked P waves since the conduction disturbance occurred at the A-H level, an area usually identified with the A-V node. Besides, disappearance of HisPurkinje bradycardia-dependent A-V block requires the presence of ventricular escape beats for the reinitiation of A-V conduction.8 Figure 3 shows the reappearance of 1:l A-V conduction without the presence of an escape beat. However, in two recent reports1 ‘,12 bradycardiadependent A-V block was postulated even when the low right atria1 electrogram was not followed by H deflections. The authors considered that this A-H block did not reflect an A-V nodal disturbance but resulted from a conduction defect located in the “upper” or “proximal” His bundle, above the site from which the His bundle electrogram was recorded. More studies are necessary to elucidate the mechanism of the type of A-V block following runs of reciprocating A-V junctional tachycardia. We hope that this preliminary study stimulat.es further interest in this unusual arrhythmia.
References 1. Bellet S: Clinical Disorders of the Heart Beat, third edition. Philadelphia, Lea 8 Febiger, 1971, p 319 2. Castillo CA, Castellanos A Jr: Retrograde activation of the His bundle during intermittent paired stimulation in the human heart. Circulation 42:1079-1092, 1970 3. Castillo CA, Castellanos A Jr: His bundle recordings in patients with reciprocating tachycardia and Wolff-Parkinson-White syndrome. Circulation 42:271-285, 1970 4. Goldreyer BN, Damato AN: Essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43:679-687. 1971 5. Goldreyer BN, Bigger JT Jr: The site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43:15-26, 1971 6. Pick A: Mechanisms of cardiac arrhythmias: from hypothesis to physiological fact. Am Heart J 86:249-269. 1973 7. El Sherif N, Scherlag BJ, Lazzara R, et al: Pathophysiology of tachycardia- and bradycardiadependent block in the canine proximal His-Purkinje system after acute myocardial ischemia.
Am J Cardiol 33:529-540, 1974 8. Rosenbaum MB, Elizari MV, Levi RJ, et al: Paroxysmal atrioventricular block related to hypopolarization and spontaneous diastolic depolarization. Chest 53:678-688, 1973 9. Corrado G, Levi RJ, Nau GJ, et al: Paroxysmal atrioventricular block related to phase 4 bilateral bundle branch block. Am J Cardiol 33:553-556, 1974 IO. Coumel P, Fablato A, Waynberger W, et al: Bradycardiadependent atrioventricular block. Report of two cases elicited by premature beats. J Electrocardiol 4:168-177, 1971 11. Castellanos A, Sung RJ, Cunha D, et al: His bundle recordings in paroxysmal A-V block produced by carotid sinus massage. Br Heart J 36:467-491, 1974 12. Goodfriend MA, Barold SS: Tachycardiadependent and bradycardiadependent Mobitz type II atrioventricular block within the bundle of His. Am J Cardiol 33:908-913, 1974 13. Jonas EA, Kosowsky BD, Ramaswamy K: Complete His-Purkinje block produced by carotid sinus message. Circulation 50: 192-197. 1974
November 1975
The American Journal of CARDIOLOGY
Volume 36
809
Atrioventricular
Block After Reciprocating
Atrioventricular
Junctional Tachycardia
JUAN
M. ARANDA,
FEDERICO AGUSTIN
MOLEIRO,
MD MD
CASTELLANOS,
MD,
FACC
BENJAMIN BEFELER, MD, FACC Miami, Florida
Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 set) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the “upper” His bundle, above the site from which the H deflection was recorded.
It is well known that abnormal rhythms, including multifocal ectopic beats, asystole and even short runs of ventricular tachycardia, frequently appear in the transition period after the termination of supraventricular tachycardia.i Although some prolongation of atrioventricular (A-V) conduction time also occurs, blockage of several consecutive P waves seems to be a rare event.] To provide some insight into the possible genesis of symptomatic A-V block occurring after supraventricular tachycardia, we discuss the clinical findings in a patient with this unusual disorder. Case Report
From the Cardiovascular Laboratory, Veterans Administration Hospital and the Division of Cardiology, University of Miami School of Medicine, Miami, Fla. Manuscript accepted October 30, 1974. Address for reprints: Benjamin Befeler, MD. Cardiovascular Laboratory, Veterans Administration Hospital, 1201 N.W. 16th St., Miami, Fla. 33125.
A 61 year old man with sinus bradycardia and right bundle branch block was referred to our laboratory because of intermittent dizzy spells for which no extracardiac cause had been found. Before this admission he had undergone cardiac monitoring on three separate occasions with the Holter equipment. The 10 hour recordings showed only sinus bradycardia (rate 50 to 571 min) and short runs of “supraventricular” tachycardia. Informed consent was obtained and intracardiac electrophysiologic studies were performed as previously described.‘,” During sinus rhythm at a rate of 56/min (Fig. 1) the A-H interval (120 msec) was at the upper limit of normal values for our laboratory (50 to 120 msec). Atria1 pacing with the extrastimulus method resulted in three episodes of reciprocating A-V tachycardia that occurred only at AI-AS intervals of 320 to 340 msec. Figure 2 shows the onset of one of these paroxysms. The Az impulse triggering the tachycardia reached the His bundle with considerable delay (300 msec). G The low right atria1 deflection was lost within the ventricular deflections of the His bundle electrogram. Since a high right atria1 electrogram was not obtained during this episode, the position of the retrograde P waves could not be conclusively identified: the site indicated in the diagram was obtained by extrapolating information obtained from Figure 3. The ventricular rate was 17Olmin. Spontaneous termination of another paroxysm can be seen in Figure 3. At this moment the recording of a high right atria1 electrogram permitted adequate identification of retrograde atria1 activation. The arrhythmia ended when a P wave was not followed by an H deflection. Immediately after the end of the tachycardia there was a period of A-V block during which the atrial deflections apparently failed to activate the His bundle. The correspond-
November 1975
The American Journal of CARDIOLOGY
Volume 36
807
A-V BLOCK AFTER JUNCTIONAL TACHYCARDIA-ARANDA
I
ET AL
1000 MSEC.
tachycardia. The patient was given digoxin, in an attempt to prevent the tachyarrhythmias.
0.25 mg daily,
Discussion In this patient with right bundle branch block and a normal H-V interval, the symptoms could have been due to sinus nodal dysfunction or A-V block, or
both. Abnormal function of the sinus node was manifested by persistent sinoatrial slowing (Fig. 1) and by t,he prolonged (posttachycardia) sinus nodal recovery time (Fig. 3). Mechanisms of Posttachycardia A-V Block HBE+
*/id'
Concealed conduction. A-V block was seen only after spontaneous termination of the reciprocating tachycardia. Since the latter was not abolished by vagal maneuvers, the presence of A-V nodal block related (iatrogenically) to enhanced vagal tone appeared an unlikely explanation. Concealed conduction could explain the genesis of this conduction disturbance if one assumes that the reciprocating A-V tachycardia caused enough (abnormal) prolongation of A-V nodal refractoriness to prevent propagation of subsequent P waves (Fig. 3). But this occurrence would have required that the duration of the refractory period thus created be at least 2,627 msec, which was the duration of the interval between the last retrograde atria1 impulse (A-) and the last blocked P wave. “Pseudo” A-V block: Another explanation appears attractive. The tachycardia might not have stopped after the third QRS complex in Figure 3. As postulated by Pick,fi continued reciprocation (not detected in surface leads) is possible when there is bidirectional (coexisting retrograde and antegrade) exit block. If the latter had been manifested by failure to activate the atria and ventricles, respectively, persis-
~lr~rmcs* t
P-A: 35 A-H:120 H-V: 40 ---P-R:195 FIGURE 1. Sinus rhythm showing right bundle branch block and a normal P-R interval. The duration of the A-H interval is at the upper limit of normal. Other conduction intervals are normal. In this and other figures intervals are expressed in milliseconds. HBE = His bundle electrogram; HRA = high right atrium.
ing P-P intervals preceding the first conducted beat measured 1,027, 1,600 and 1,640 msec, respectively. The prolonged duration of the last two intervals suggested the coexistence of sinus nodal dysfunction. In all three posttachycardia intervals that occurred in the laboratory the patient had symptoms similar to those he had experienced before admission to the hospital. Although the electrogenesis of the A-V block was not clear, pacemaker implantation was recommended because this intermittent conduction disturbance occurred in a symptomatic patient who also had sinus nodal dysfunction, right bundle branch block and reciprocating A-V junctional
H
808
November 1975
H
H
The American Journal of CARDIOLOGY
H
Volume 36
H
FIGURE 2. Reciprocating A-V tachycardia occurring at an AT-A2 interval of 340 msec. Low right atrial deflections are buried within the ventricular deflections of the His bundle electrogram. A2 = atrial deflection produced by St2; H = His bundle electrograms; St, = driving stimuIus artifact: St2 = testing stimulus artifact: Intervals between the vertical lines are 975 msec.
A-V BLOCK AFTER JUNCTIONAL TACHYCARDIA-ARANDA
ET AL.
1027
FIGURE 3. Spontaneous termination of an episode of reciprocating A-V junctional tachycardia followed by block of two consecutive P waves during which the A deflections are not followed by detectable His bundle activation. The intervals between P waves are abnormally long. A- = retrograde high right atrial electrograms. The low right atrial deflections recorded by His bundle electrograms are lost within the corresponding ventricular electrograms. Therefore the sequence of atrial depolarization is from the low to high right atrium. By contrast, the sequence of the last P wave is from the high to the low right atrium.
reciprocation within the more central portions of the A-V node would have prevented subsequent P waves from reaching the His bundle until cessation of the tachycardia (Fig. 2). The resulting arrhythmia might be termed “pseudo” A-V block produced by concealed reciprocating A-V junctional tachycardia. However, this assumption could not be proved on the basis of the information obtained from the catheter recordings. Bradycardia-dependent A-V block: A third explanation has to be considered. Several investigators7-l3 have recently discussed the mechanisms of bradycardia-dependent A-V block. This conduction disturbance occurs when A-V block is seen after a critical slowing of the rate or an increase in cycle length. It is believed that delayed appearance of a P wave allows the supraventricular impulse to reach a group of cells located in an area that is the only connection between the atria and the ventricles. These cells must have an enhanced or slightly rising slope of phase 4 depolarization. 7,8 Conduction failure occurs because the supraventricular impulse reaches the affected zone when membrane potential is abnormally close to 0. Bradycardia-dependent A-V block is an infra A-V nodal phenomenon because the His-Purtent
kinje system is the one possessing the property of phase 4 depolarization.7-12 At first glance Figure 3 suggests that this mechanism cannot be applied to explain the genesis of the blocked P waves since the conduction disturbance occurred at the A-H level, an area usually identified with the A-V node. Besides, disappearance of HisPurkinje bradycardia-dependent A-V block requires the presence of ventricular escape beats for the reinitiation of A-V conduction.8 Figure 3 shows the reappearance of 1:l A-V conduction without the presence of an escape beat. However, in two recent reports1 ‘,12 bradycardiadependent A-V block was postulated even when the low right atria1 electrogram was not followed by H deflections. The authors considered that this A-H block did not reflect an A-V nodal disturbance but resulted from a conduction defect located in the “upper” or “proximal” His bundle, above the site from which the His bundle electrogram was recorded. More studies are necessary to elucidate the mechanism of the type of A-V block following runs of reciprocating A-V junctional tachycardia. We hope that this preliminary study stimulat.es further interest in this unusual arrhythmia.
References 1. Bellet S: Clinical Disorders of the Heart Beat, third edition. Philadelphia, Lea 8 Febiger, 1971, p 319 2. Castillo CA, Castellanos A Jr: Retrograde activation of the His bundle during intermittent paired stimulation in the human heart. Circulation 42:1079-1092, 1970 3. Castillo CA, Castellanos A Jr: His bundle recordings in patients with reciprocating tachycardia and Wolff-Parkinson-White syndrome. Circulation 42:271-285, 1970 4. Goldreyer BN, Damato AN: Essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43:679-687. 1971 5. Goldreyer BN, Bigger JT Jr: The site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43:15-26, 1971 6. Pick A: Mechanisms of cardiac arrhythmias: from hypothesis to physiological fact. Am Heart J 86:249-269. 1973 7. El Sherif N, Scherlag BJ, Lazzara R, et al: Pathophysiology of tachycardia- and bradycardiadependent block in the canine proximal His-Purkinje system after acute myocardial ischemia.
Am J Cardiol 33:529-540, 1974 8. Rosenbaum MB, Elizari MV, Levi RJ, et al: Paroxysmal atrioventricular block related to hypopolarization and spontaneous diastolic depolarization. Chest 53:678-688, 1973 9. Corrado G, Levi RJ, Nau GJ, et al: Paroxysmal atrioventricular block related to phase 4 bilateral bundle branch block. Am J Cardiol 33:553-556, 1974 IO. Coumel P, Fablato A, Waynberger W, et al: Bradycardiadependent atrioventricular block. Report of two cases elicited by premature beats. J Electrocardiol 4:168-177, 1971 11. Castellanos A, Sung RJ, Cunha D, et al: His bundle recordings in paroxysmal A-V block produced by carotid sinus massage. Br Heart J 36:467-491, 1974 12. Goodfriend MA, Barold SS: Tachycardiadependent and bradycardiadependent Mobitz type II atrioventricular block within the bundle of His. Am J Cardiol 33:908-913, 1974 13. Jonas EA, Kosowsky BD, Ramaswamy K: Complete His-Purkinje block produced by carotid sinus message. Circulation 50: 192-197. 1974
November 1975
The American Journal of CARDIOLOGY
Volume 36
809
