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His Bundle Recordings in Atrioventricular Nodal Alternating Wenckebach Periods Ending in 5:1 Atrioventricular Block Coexisting with Paroxysmal Atrioventricular Nodal Block
His Bundle Recordings in Atrioventricular Nodal Alternating
Wenckebach
Ending in 5:1 Atrioventricular
Periods Block
Coexisting with Paroxysmal Atrioventricular Nodal Block* Agustin Castellanos, M.D., F.C.C.P.;*" Ruey J. Sung, M.D.;f Barouh V. Berkovits, E.E.% Victor M. Alatriste, M.D.;§and Robert }. Myerburg, A/.D.II
Atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block occurring during rapid atrial rhythms were explained by postulating the presence of block in three levels of the atrioventricular node. This pattern of conduction occurred in ten of 11 patients who either had received ouabain or veraparnil (nine patients) or who had organic atrioventricular nodal disease (two patients). In contrast, this pattern of con duction occurred in only one of eight nonmedicated patients without organic atrioventricular nodal disease. The frequent association of this pattern with paroxysmal,
tachycardia-dependent atrioventricular nodal block sug gested a similar, but not necessarily identical, mechanism. In conclusion, atrioventricular nodal alternating Wencke bach periods ending in 5:1 atrioventricular block, as well as paroxysmal atrioventricular nodal block, were only rarely the result of rapid atrial rates per se their occur rence indicating organic or pharmacologic effects on the atrioventricular node. Since both can be produced by carotid sinus pressure, further studies appear to be neces sary to determine the role that vagal effects can have in their genesis.
\ previous article published in Chest emphasized •¿ ^^ the electrocardiographic manifestations and clinical significance of atrioventricular nodal alter nating Wenckebach periods ending in 3:1 and 4:1 atrioventricular block.1 On the other hand, this com munication deals with atrioventricular nodal alter nating Wenckebach periods terminating in 5:1 atrioventricular block. As far as we know, this is the first report discussing the electrogenesis of this pat tern of conduction, as well as its relationship with paroxysmal atrioventricular nodal block.
outlined1'2 in 19 patients who, among other problems, had recurrent supraventricular tachyarrhythmias. The procedure was explained to the patients and their relatives, and wit nessed informed consent was obtained. As in other labora tories, part of our work-up on patients with recurrent supraventricular tachyarrhythmias includes attempts to reinduce these arrhythmias in the cardiovascular laboratory under controlled conditions, as well as the evaluation of the re sponse to intravenously administered drugs.2-4
MATERIALS ANDMETHODS Methods Electrophysiologic
studies were performed
as previously
"From the Division of Cardiology, Department of Med icine, University of Miami School of Medicine, Miami, Fla, and the Institute Nacional de Cardiologia, Mexico City. "Professor of Medicine and Director, Section of Clinical Electrophysiology. fAssociate Professor of Medicine and Director, Clinical Electrophysiology Laboratory. ^Associate in Electrophysiology. §AssistantProfessor of Medicine, Institute Nacional de Car diologia. I[Professor of Medicine and Director, Division of Cardiology. Manuscript received February 3; revision accepted May 3. Reprint requests: Dr. Castellanos, University of Miami School of Medicine, PO Box 520875, Miami 33152
274
CASTELLANOS ET AL
Definitions and Intervals of Conduction Unless otherwise specifically stated, the terminology used in reference to the various deflections, intervals of conduc tion, and disturbances in conduction, as well as in the ladder diagrams that incorporate His bundle electrograms, has been discussed previously.1 Normal values for the P-R, atrio-His (A-H), and His-ventricle (H-V) intervals in our laboratory range from 120 to 210 msec, from 55 to 120 msec, and from 35 to 55 msec, respectively. Normal values of atrioventric ular nodal refractory periods during pacing with extrastimulus technique were those given by Denes et al.5
Patients The patients (none of whom had coronary arterial dis ease) were divided into four groups. Group 1 consisted of eight nonmedicated patients without atrioventricular nodal disease (normal P-R intervals, A-H intervals, and atrio ventricular nodal refractory periods) in whom rapid atrial pacing was performed at gradually increasing rates until the
CHEST,
74:
3, SEPTEMBE
Table 1—Disturbances in Atrioventricular Nodal Conduction Coexisting with Alternating Wenckebach Periods Ending in 5:1 Atriovenlricular Block * Group Data No. of patients in group Atrioventricular block ending alternating Wenckebach periods 5:1 block 3:1 or 4:1 block Paroxysmal
block
"Table values are numbers of patients. occurrence of intra-atrial Wenckebach periods. Data con cerning this pattern of conduction in these cases has been presented elsewhere.- Group 2 included four patients with pacing-induced sustained episodes of atrial flutter with 2:1 atrioventricular conduction in whom intracardiac electrograms were recorded 30 minutes after the intravenous ad ministration of ouabain (0.01 mg/kg of body weight). Group 3 consisted of four patients in whom rapid atrial pacing was performed either 30 minutes after the administra tion of ouabain as outlined previously (three patients) or ten minutes after having received 10 mg of verapamil intravenously (one patient).0 These drugs had been given (successfully) to abolish previously present reciprocating atrioventricular nodal tachycardias. Group 4 included three patients with narrow QRS complexes who had the sick sinus syndrome, recurrent atrial tachyarrhythmias, and atrioven-
St
240A-H1MrL A !•VH240 PL
St
QRS St St
^^^^
tricular nodal disease manifested by prolonged P-R and A-H intervals and atrioventricular nodal refractory periods. In these cases, atrial pacing at increasing rates was performed only at cycle lengths between 600 and 350 msec.
RESULTS Atrioventricular nodal (A-H) alternating Wenckebach periods ending in 5:1 atrioventricular block occurred in one of the eight patients in group 1, in all four patients in group 2, in all four patients in group 3, and in two of the three patients in group 4 (Table 1). This pattern of conduction had not been observed in the four patients in group 2 and the four patients in group 3 prior to the administra tion of ouabain or verapamil. In addition, six of the eight patients in group 1 and all of the patients in groups 2, 3, and 4 also had atrioventricular nodal alternating Wenckebach periods ending in 3:1 and 4:1 block. Figure 1 was recorded from the only patient in group 1 who had atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block during rapid atrial stimulation. Recordings obtained immediately before had shown alternating Wenckebach periods terminating in 4:1 atrioven tricular block. The latter has been attributed (with penetration of all atrial impulses into, at least, the uppermost parts of the atrioventricular node) to the
QRS St St St
St
St
QRS St
230230EH230205^, 245V-\_\
7:6 \1,1\3: 2
FIGURE 1. Atrioventricular nodal alternating Wenckebach period ending in 5:1 atrioventricular block during rapid atrial stimulation in nonmedicated patient without atrioventricular nodal disease. Diagram depicts 7:6 block in "more proximal" level (MPL), 2:1 block in "proximal" level (PL), and 3:2 Wenckebach period in "distal" level (DL). Exact location of various atrioventricular nodal levels and type of disturbance in conduction in each level can only be surmised. Nevertheless, block at least in three levels of atrioventricular node has to be postulated to explain 5:1 atrioventricular block.16'20 Values are expressed in milliseconds. St, artifact from pacemaker's stimulus; HBE, His bundle electrogram; A, atrial deflections from vicinity of (presumably inscribed at entrance to) atrioventricular node; H, His bundle; A-H, atrio-His (atrioventricular nodal) region.
CHEST,74: 3, SEPTEMBER, 1978
HISBUNDLERECORDINGS275
A-H
\(190)\(205)(110)1:
H
1
FIGURE2. Atrioventricular nodal alternating Wenckebach period terminating in 5:1 atrioventricular block in medicated patient with atrial flutter (group 2). Diagram depicts 7:6 Wenckebach period in "more proximal" level (MPL), 2:1 block in "proximal" level (PL), and 3:2 block in "distal" level (DL). Numbers within parentheses indicate duration of corresponding A-H in tervals in milliseconds. HRA, bipolar electrogram from high right atrium; and HBE, His bundle electrogram.
coexistence of 2:1 block in a "proximal" atrioventricular nodal level and Wenckebach periods in a "distal" level.1'2'7'11 Partial penetration excludes true atrioventricular nodal entrance block and im plies the existence of a third atrioventricular nodal level, located "more proximally" to the previously mentioned "proximal" level (represented diagrammatically immediately below the horizontal level separating A from A-H) with a shorter effective refractory period. The diagram depicts the basic sequence postu lated to explain alternating Wenckebach periods ending in 4:1 atrioventricular block as influenced by erratic variations in the A-A intervals. As a conse quence of these fluctuations, one atrial impulse (A7 in Fig 1) appeared so soon (205 msec) after another SINUS
SINUS P
(930)
P
,
Sti
(A6) that it arrived at the atrioventricular node early enough either to have been unable to penetrate the "more proximal level" (true atrioventricular nodal entrance block) or to have decremented within it. In any case, this occurred during inscription of an atrial impulse (A7) which would (had the alternat ing Wenckebach sequence persisted) otherwise have been able to reach the His bundle. Therefore, the alternating Wenckebach period ended in 5:1 atrioventricular block. It is postulated that the events in Figure 1, as well as those in Figure 2 (group 2) were due to the coexistence of 7.6 block in the "more proximal level" with 2:1 block in the "proximal" level and a 3:2 Wenckebach period in the "distal" level. All four patients in group 3 and two of the three
s»2
(450)
1
HBE FIGURE 3. Paroxysmal, tachycardia-dependent atrioventricular nodal block initiated during sinus rhythm at 65 beats per minute (cycle length of 930 msec) by atrial pacing at 133 im pulses per minute (cycle length of 450 msec) in patient with organic disease of atrioventricular node. Values are expressed in milliseconds. St, artifact from pacemaker's stimulus; HRA, bipolar electrogram
276 CASTELLANOS ETAL
from high right atrium; and HBE, His bundle electrogram.
CHEST, 74:3,SEPTEMBER, 1978
patients in group 4 had episodes of pacing-induced paroxysmal atrioventricular block12 occurring at the atrioventricular node.13'14 The block was tachy cardia-dependent and emerged either directly from sinus rhythm with 1:1 atrioventricular conduction (Fig 3) or from brief episodes of 2:1 atrioventricu lar nodal block showing alternating Wenckebach sequences.14-15 DISCUSSION Value of His Bundle Recordings As in previous reports discussing alternating Wenckebach periods ending in 3:1 and 4:1 atrio ventricular block, His bundle recordings were im portant in the evaluation of 5:1 atrioventricular block only because they permitted the localization of the disturbances in conduction to the atrioven tricular node (A-H region ).1-2'9'11The exact loca tion of the atrioventricular nodal levels and the type of disturbances in conduction occurring in each level were impossible to determine, since only the input into the atrioventricular node (given by the atrial deflection) and its output (given by the His deflec tion ) could be recorded with the conventional tech nique using a catheter-electrode.1'2i9"n The 5:1 atrioventricular block need not have oc curred as depicted diagrammatically in Figures 1 and 2; however, several authors have postulated that block of more than three consecutive atrial impulses can indeed result from three levels of block in the atrioventricular node.1-9'16'19 These assumptions have been validated by a study in which a threelevel disturbance in conduction occurred in three different anatomic structures.2 Specifically, it was observed that high right atrial pacing at very fast
rates could produce a type of 5:1 stimulus-His (StH) block resulting from the association of Wencke bach periods in the atria with second-degree block in both the atrioventricular node and the His-Purkinje system.2 These findings can be extrapolated to the atrioventricular node by considering the atria equivalent to the "more proximal level," considering the atrioventricular node itself equivalent to the "proximal level," and considering the His-Purkinje system equivalent to the "distal" level.2 Periods Ending in 4:1 and 5:1 Atrioventricular Block In Figure 1, the 5:1 atrioventricular block ap peared because the impulse that was blocked at the "more proximal" level was one which had reached the His bundle during the previously present alter nating Wenckebach sequence. On the contrary, had this block at the "more proximal level" occurred during inscription of an impulse otherwise blocked in a lower atrioventricular nodal level (such as the atrial impulse labelled A6 in Fig 1), then the alter nating Wenckebach period would have terminated in 4:1 (not 5:1) atrioventricular block as a conse quence of a three-level disturbance in conduction, rather than as a result of the classic two-level block usually postulated to explain alternating Wencke bach periods ending in 4:1 atrioventricular block. That some types of 4:1 atrioventricular block can be due to more than two levels of block has been postulated before9'10"18and is supported by the previously mentioned study in which some episodes of 4:1 St-V block resulted from the association of intra-atrial Wenckebach periods with atrioventricu lar nodal and His-Purkinje block.2
DIGITALIS-INDUCED "PAT WITH 2:1 A-V BLOCK"
CAROTIDSINUSMASSAGE
•¿ v
FIGURE 4. Paroxysmal atrioventricular block produced (presumably at atrioventricular node) by massage of carotid sinuses in patient with digitalis-induced "paroxysmal" atrial tachycardia (PAT) with 2:1 atrioventricular block. Bottom strip (enlargement of first part of middle strip) shows, that paroxysmal atrioventricular block emerged from alternating Wenckebach sequence. Values are expressed in milliseconds (Other strips from this patient have been published elsewhere26).
CHEST,74: 3, SEPTEMBER, 1978
HIS BUNDLERECORDINGS277
Paroxysmal Atrioventricular Nodal Block Although both clinical reports16'20 and electrophysiologic studies utilizing the microelectrodes.21'23 have demonstrated repetitive concealed conduction in the atrioventricular node, paroxysmal atrioventricular nodal block is a less well known entity, in spite of occasional reports of its occurrence in man.13 VVatanabe and Dreifus23 showed an exam ple (their Fig 5-3) of paroxysmal block in the rab bit's atrioventricular node, which they attributed to "incomplete repolarization of the N region." Recent ly, El-Sherif and associates24 documented the exis tence of tachycardia-dependent block in the ischemic atrioventricular node of the dog. The genesis of paroxysmal atrioventricular nodal block in man is unclear. That there are mechanisms other than those operating in Figure 1 is sug gested by the fact that the enhancement of vagal tone produced by massage of the carotid sinuses can produce this disturbance in conduction in some pa tients (Fig 4).8-25-26AS in the His-Purkinje system, some of the episodes of paroxysmal atrioventricular nodal block emerged from alternating Wenckebach periods occurring during 2:1 atrioventricular con duction.15p27'31This suggests (but does not prove) a related electrogenetic mechanism, which could very well be repetitive concealed conduction. Ac cording to Elizari et al,31 the fact that the action potentials within the injured His-Purkinje system resembled those of the atrioventricular node and that refractoriness outlasted repolarization, with excitability and conduction not being completely reversed after the end of the preceding action poten tials, suggested repetitive concealed conduction in the affected portions of the His-Purkinje system (or the atrioventricular node); however, less and less penetration of each succeeding beat is unlikely, since this requires the levels of block to equal the number of consecutively blocked impulses. On the other hand, the 8:1 paroxysmal atrioven tricular nodal block in Figure 3 can be explained by assuming only block at three levels, the same num ber of levels postulated to explain the alternating Wenckebach periods ending in 5:1 atrioventricular block in Figures 1 and 2. Yet, for this to occur, the block at each level should be of the 2:1 type. When ever the ratio of atrioventricular conduction doubles, with 2:1 block in each additional level, the number of consecutive beats is simply one less than the ratio. With 2:1 block in only one level, the ratio of atrio ventricular conduction is obviously 2:1, and the number of consecutively blocked beats is one. With 2:1 block in two levels, the ratio is 4:1, and the number of consecutively blocked beats is three. With 2:1 block in three levels, the ratio of atrioven
278 CASTELLANOS ETAL
tricular conduction is 8:1, and the number of con secutively blocked beats is seven. Clinical Implications In this study, atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block and paroxysmal atrioventricular nodal block were only rarely due to rapid atrial rates per se. On the contrary, most episodes occurred in patients who had received ouabain or verapamil or who had organic atrioventricular nodal disease. Therefore, pharmacologic effects or organic disease can be suspected from clinical tracings alone (with out concomitant recording of the activity of the His bundle) wherever these patterns of conduction ap pear during atrial tachyarrhythmias or rapid atrial stimulation in patients with narrow QRS complexes. Although the mechanisms of paroxysmal atrioven tricular nodal block following administration of ouabain most probably resulted from the direct ef fects of this drug on the atrioventricular node, the role of vagal stimulation requires further studies (Fig 4); for example, both paroxysmal atrioven tricular nodal block and alternating Wenckebach periods can be produced by massage of the carotid sinuses in some patients with sinus rhythm (Fig 5-29 of Watanabe and Dreifus23), atrial flutter with 2:1 atrioventricular conduction (Fig 228 of Kosowsky et al9 and Fig 56-4 of Bellet25), and digitalis-induced "paroxysmal" atrial tachycardia with atrioventricu lar block26 (Fig 4). REFERENCES 1 Castellanos A, Sung RJ, Aldrich JL, et al: Electrocardiographic manifestations and clinical significance of atrioventricular nodal alternating Wenckebach periods. Chest 73:69-74, 1978 2 Castellanos A, Sung RJ, Mallon SM, et al: Effects of paroxysmal intra-atrial Wenckebach on distal atrioven tricular nodal and His Purkinje block with special refer ence to the theory of alternating Wenckebach periods. Am Heart J 95:228-234, 1978 3 Sellers TD Jr, Cambell RWP, Bashore TM, et al: Effects of procaine amide and quinidine supplement in the Wolff-Parkinson-White syndrome. Circulation 55:15-22, 1977 4 Wellens HJJ: The electrophysiological properties of the accessory pathway in Wolff-Parkinson-White syndrome. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduc tion System of the Heart: Structure, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 567-587 5 Denes P, Wu D, Dhingra R, et al: The effects of cycle length on cardiac refractory periods in man. Circulation 49:32-41, 1974 6 Rizzon P, DiBiase M, Calabrese P, et al: Electrophysio logical evaluation of intravenous verapamil in man. Eur J Cardiol 6:179-194, 1977 7 Besoain-Santander M, Pick A, Langendorf R: A-V con duction in auricular flutter. Circulation 2:604-616, 1950
CHEST, 74:3,SEPTEMBER, 1978
8 Katz LN, Pick A: Clinical Electrocardiography: The Arrhythmias (part 1). Philadelphia, Lea and Febiger, 1956, pp 413-418, 421 9 Kosowsky BD, Latif P, Radoff AM: Multilevel atrioventricular block. Circulation 54:914-921, 1976 10 Amat-y-Leon F, Chuquimia A, Wu D, et al: Alternating Wenckebach periods: A common electrophysiological re sponse. Am J Cardiol 36:757-764, 1957 11 Hartzler GO, Maloney HD: Supra-His alternate beat Wenckebach dysrhythmia. Mayo Clin Proc 50:475-481, 1975 12 Sachs A, Traynor RL: Paroxysmal complete auriculoventricular block. Am Heart J 9:267-271, 1933 13 Rosen KM, Loeb HS, Rahimtoola SH: Mobitz type II block with narrow QRS complex and Stakes-Adams attacks. Arch Intern Med 132:595-596, 1973 14 El-Sherif N, Scherlag BJ, Lazzara R: An appraisal of second degree and paroxysmal atrio-ventricular block. Eur J Cardiol 4:117-130, 1976 15 El-Sherif N, Scherlag BJ, Lazzara R: The pathophysiology of tachycardia dependent paroxysmal atrioventricular block after myocardial ischemia: Experimental and clinical observations. Circulation 50:515-528, 1974 16 Langendorf R, Pick A: Concealed conduction: Further evaluation of a fundamental aspect of propagation of the cardiac impulse. Circulation 13:381-399, 1956 17 Langendorf R: New aspects of concealed conduction of the cardiac impulse. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduction System of the Heart: Struc ture, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 410-423 18 Schindler S, Albers W: A-V block (letter to editor). Circulation 56:689, 1977 19 Langendorf R, Pick A, Edelist A, et al: Experimental conduction of concealed A-V conduction in the human heart. Circulation 32:386-393, 1965 20 Pick A: Mechanisms of cardiac arrhythmias: From hypo
CHEST,74: 3, SEPTEMBER, 1978
thesis to physiologic fact. Am Heart J 86:249-269, 1973 21 Moe GK, Abilskov JA, Mendez C: An experimental study of concealed conduction. Am Heart ] 67:338-356, 1964 22 Moore EN: Microelectrode studies on concealment of multiple premature atrial responses. Circ Res 18:660-672, 1966 23 Watanabe Y, Dreifus LS: Cardiac Arrhythmias: Electrophysiologic Basis for Clinical Interpretation. New York, Grune and Stratton, Inc, 1971, pp 187-188 24 El-Sherif N, Scherlag BJ, Lazzara R: Experimental pro duction of "Mobitz II" and paroxysmal block in the A-V node (abstract). Clin Res 23:181A, 1975 25 Bellet S: Clinical Disorders of the Heart Beat (3rd ed). Philadelphia, Lea and Febiger, 1971, p 1160 26 Calvino JM, Azan Cano L, Castellanos A Jr: Valor de las derivaciones esofagicas en las arritmias complejas. Rev Cubana Cardiol 16:293-316, 1955 27 Rosenbaum MB, Elizari MV, Levi RJ, et al: Paroxysmal atrioventricular block related to hypopolarization and spontaneous diastolic depolarization. Chest 63:678-688, 1973 28 Halpern MS, Nau GJ, Levi RJ: Wenckebach periods of alternate beats: Clinical and experimental observations. Circulation 48:41-49, 1973 29 Cohen HC, D'Cruz I, Pick A: Concealed intraventricular conduction in the His bundle electrogram. Circulation 53:776-783,1976 30 Castellanos A, Sung RJ, Aldrich JL, et al: Alternating Wenckebach periods occurring in the atria, His-Purkinje system, ventricles and Kent bundle. Am J Cardiol 40: 853-859, 1977 31 Elizari MV, Novakosky A, Quintero RA, et al: The exper imental evidence for the role of phase 3 and phase 4 block in the genesis of A-V conduction disturbances. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduction System of the Heart: Structure, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 360-377
HIS BUNDLERECORDINGS279
Wenckebach
Ending in 5:1 Atrioventricular
Periods Block
Coexisting with Paroxysmal Atrioventricular Nodal Block* Agustin Castellanos, M.D., F.C.C.P.;*" Ruey J. Sung, M.D.;f Barouh V. Berkovits, E.E.% Victor M. Alatriste, M.D.;§and Robert }. Myerburg, A/.D.II
Atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block occurring during rapid atrial rhythms were explained by postulating the presence of block in three levels of the atrioventricular node. This pattern of conduction occurred in ten of 11 patients who either had received ouabain or veraparnil (nine patients) or who had organic atrioventricular nodal disease (two patients). In contrast, this pattern of con duction occurred in only one of eight nonmedicated patients without organic atrioventricular nodal disease. The frequent association of this pattern with paroxysmal,
tachycardia-dependent atrioventricular nodal block sug gested a similar, but not necessarily identical, mechanism. In conclusion, atrioventricular nodal alternating Wencke bach periods ending in 5:1 atrioventricular block, as well as paroxysmal atrioventricular nodal block, were only rarely the result of rapid atrial rates per se their occur rence indicating organic or pharmacologic effects on the atrioventricular node. Since both can be produced by carotid sinus pressure, further studies appear to be neces sary to determine the role that vagal effects can have in their genesis.
\ previous article published in Chest emphasized •¿ ^^ the electrocardiographic manifestations and clinical significance of atrioventricular nodal alter nating Wenckebach periods ending in 3:1 and 4:1 atrioventricular block.1 On the other hand, this com munication deals with atrioventricular nodal alter nating Wenckebach periods terminating in 5:1 atrioventricular block. As far as we know, this is the first report discussing the electrogenesis of this pat tern of conduction, as well as its relationship with paroxysmal atrioventricular nodal block.
outlined1'2 in 19 patients who, among other problems, had recurrent supraventricular tachyarrhythmias. The procedure was explained to the patients and their relatives, and wit nessed informed consent was obtained. As in other labora tories, part of our work-up on patients with recurrent supraventricular tachyarrhythmias includes attempts to reinduce these arrhythmias in the cardiovascular laboratory under controlled conditions, as well as the evaluation of the re sponse to intravenously administered drugs.2-4
MATERIALS ANDMETHODS Methods Electrophysiologic
studies were performed
as previously
"From the Division of Cardiology, Department of Med icine, University of Miami School of Medicine, Miami, Fla, and the Institute Nacional de Cardiologia, Mexico City. "Professor of Medicine and Director, Section of Clinical Electrophysiology. fAssociate Professor of Medicine and Director, Clinical Electrophysiology Laboratory. ^Associate in Electrophysiology. §AssistantProfessor of Medicine, Institute Nacional de Car diologia. I[Professor of Medicine and Director, Division of Cardiology. Manuscript received February 3; revision accepted May 3. Reprint requests: Dr. Castellanos, University of Miami School of Medicine, PO Box 520875, Miami 33152
274
CASTELLANOS ET AL
Definitions and Intervals of Conduction Unless otherwise specifically stated, the terminology used in reference to the various deflections, intervals of conduc tion, and disturbances in conduction, as well as in the ladder diagrams that incorporate His bundle electrograms, has been discussed previously.1 Normal values for the P-R, atrio-His (A-H), and His-ventricle (H-V) intervals in our laboratory range from 120 to 210 msec, from 55 to 120 msec, and from 35 to 55 msec, respectively. Normal values of atrioventric ular nodal refractory periods during pacing with extrastimulus technique were those given by Denes et al.5
Patients The patients (none of whom had coronary arterial dis ease) were divided into four groups. Group 1 consisted of eight nonmedicated patients without atrioventricular nodal disease (normal P-R intervals, A-H intervals, and atrio ventricular nodal refractory periods) in whom rapid atrial pacing was performed at gradually increasing rates until the
CHEST,
74:
3, SEPTEMBE
Table 1—Disturbances in Atrioventricular Nodal Conduction Coexisting with Alternating Wenckebach Periods Ending in 5:1 Atriovenlricular Block * Group Data No. of patients in group Atrioventricular block ending alternating Wenckebach periods 5:1 block 3:1 or 4:1 block Paroxysmal
block
"Table values are numbers of patients. occurrence of intra-atrial Wenckebach periods. Data con cerning this pattern of conduction in these cases has been presented elsewhere.- Group 2 included four patients with pacing-induced sustained episodes of atrial flutter with 2:1 atrioventricular conduction in whom intracardiac electrograms were recorded 30 minutes after the intravenous ad ministration of ouabain (0.01 mg/kg of body weight). Group 3 consisted of four patients in whom rapid atrial pacing was performed either 30 minutes after the administra tion of ouabain as outlined previously (three patients) or ten minutes after having received 10 mg of verapamil intravenously (one patient).0 These drugs had been given (successfully) to abolish previously present reciprocating atrioventricular nodal tachycardias. Group 4 included three patients with narrow QRS complexes who had the sick sinus syndrome, recurrent atrial tachyarrhythmias, and atrioven-
St
240A-H1MrL A !•VH240 PL
St
QRS St St
^^^^
tricular nodal disease manifested by prolonged P-R and A-H intervals and atrioventricular nodal refractory periods. In these cases, atrial pacing at increasing rates was performed only at cycle lengths between 600 and 350 msec.
RESULTS Atrioventricular nodal (A-H) alternating Wenckebach periods ending in 5:1 atrioventricular block occurred in one of the eight patients in group 1, in all four patients in group 2, in all four patients in group 3, and in two of the three patients in group 4 (Table 1). This pattern of conduction had not been observed in the four patients in group 2 and the four patients in group 3 prior to the administra tion of ouabain or verapamil. In addition, six of the eight patients in group 1 and all of the patients in groups 2, 3, and 4 also had atrioventricular nodal alternating Wenckebach periods ending in 3:1 and 4:1 block. Figure 1 was recorded from the only patient in group 1 who had atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block during rapid atrial stimulation. Recordings obtained immediately before had shown alternating Wenckebach periods terminating in 4:1 atrioven tricular block. The latter has been attributed (with penetration of all atrial impulses into, at least, the uppermost parts of the atrioventricular node) to the
QRS St St St
St
St
QRS St
230230EH230205^, 245V-\_\
7:6 \1,1\3: 2
FIGURE 1. Atrioventricular nodal alternating Wenckebach period ending in 5:1 atrioventricular block during rapid atrial stimulation in nonmedicated patient without atrioventricular nodal disease. Diagram depicts 7:6 block in "more proximal" level (MPL), 2:1 block in "proximal" level (PL), and 3:2 Wenckebach period in "distal" level (DL). Exact location of various atrioventricular nodal levels and type of disturbance in conduction in each level can only be surmised. Nevertheless, block at least in three levels of atrioventricular node has to be postulated to explain 5:1 atrioventricular block.16'20 Values are expressed in milliseconds. St, artifact from pacemaker's stimulus; HBE, His bundle electrogram; A, atrial deflections from vicinity of (presumably inscribed at entrance to) atrioventricular node; H, His bundle; A-H, atrio-His (atrioventricular nodal) region.
CHEST,74: 3, SEPTEMBER, 1978
HISBUNDLERECORDINGS275
A-H
\(190)\(205)(110)1:
H
1
FIGURE2. Atrioventricular nodal alternating Wenckebach period terminating in 5:1 atrioventricular block in medicated patient with atrial flutter (group 2). Diagram depicts 7:6 Wenckebach period in "more proximal" level (MPL), 2:1 block in "proximal" level (PL), and 3:2 block in "distal" level (DL). Numbers within parentheses indicate duration of corresponding A-H in tervals in milliseconds. HRA, bipolar electrogram from high right atrium; and HBE, His bundle electrogram.
coexistence of 2:1 block in a "proximal" atrioventricular nodal level and Wenckebach periods in a "distal" level.1'2'7'11 Partial penetration excludes true atrioventricular nodal entrance block and im plies the existence of a third atrioventricular nodal level, located "more proximally" to the previously mentioned "proximal" level (represented diagrammatically immediately below the horizontal level separating A from A-H) with a shorter effective refractory period. The diagram depicts the basic sequence postu lated to explain alternating Wenckebach periods ending in 4:1 atrioventricular block as influenced by erratic variations in the A-A intervals. As a conse quence of these fluctuations, one atrial impulse (A7 in Fig 1) appeared so soon (205 msec) after another SINUS
SINUS P
(930)
P
,
Sti
(A6) that it arrived at the atrioventricular node early enough either to have been unable to penetrate the "more proximal level" (true atrioventricular nodal entrance block) or to have decremented within it. In any case, this occurred during inscription of an atrial impulse (A7) which would (had the alternat ing Wenckebach sequence persisted) otherwise have been able to reach the His bundle. Therefore, the alternating Wenckebach period ended in 5:1 atrioventricular block. It is postulated that the events in Figure 1, as well as those in Figure 2 (group 2) were due to the coexistence of 7.6 block in the "more proximal level" with 2:1 block in the "proximal" level and a 3:2 Wenckebach period in the "distal" level. All four patients in group 3 and two of the three
s»2
(450)
1
HBE FIGURE 3. Paroxysmal, tachycardia-dependent atrioventricular nodal block initiated during sinus rhythm at 65 beats per minute (cycle length of 930 msec) by atrial pacing at 133 im pulses per minute (cycle length of 450 msec) in patient with organic disease of atrioventricular node. Values are expressed in milliseconds. St, artifact from pacemaker's stimulus; HRA, bipolar electrogram
276 CASTELLANOS ETAL
from high right atrium; and HBE, His bundle electrogram.
CHEST, 74:3,SEPTEMBER, 1978
patients in group 4 had episodes of pacing-induced paroxysmal atrioventricular block12 occurring at the atrioventricular node.13'14 The block was tachy cardia-dependent and emerged either directly from sinus rhythm with 1:1 atrioventricular conduction (Fig 3) or from brief episodes of 2:1 atrioventricu lar nodal block showing alternating Wenckebach sequences.14-15 DISCUSSION Value of His Bundle Recordings As in previous reports discussing alternating Wenckebach periods ending in 3:1 and 4:1 atrio ventricular block, His bundle recordings were im portant in the evaluation of 5:1 atrioventricular block only because they permitted the localization of the disturbances in conduction to the atrioven tricular node (A-H region ).1-2'9'11The exact loca tion of the atrioventricular nodal levels and the type of disturbances in conduction occurring in each level were impossible to determine, since only the input into the atrioventricular node (given by the atrial deflection) and its output (given by the His deflec tion ) could be recorded with the conventional tech nique using a catheter-electrode.1'2i9"n The 5:1 atrioventricular block need not have oc curred as depicted diagrammatically in Figures 1 and 2; however, several authors have postulated that block of more than three consecutive atrial impulses can indeed result from three levels of block in the atrioventricular node.1-9'16'19 These assumptions have been validated by a study in which a threelevel disturbance in conduction occurred in three different anatomic structures.2 Specifically, it was observed that high right atrial pacing at very fast
rates could produce a type of 5:1 stimulus-His (StH) block resulting from the association of Wencke bach periods in the atria with second-degree block in both the atrioventricular node and the His-Purkinje system.2 These findings can be extrapolated to the atrioventricular node by considering the atria equivalent to the "more proximal level," considering the atrioventricular node itself equivalent to the "proximal level," and considering the His-Purkinje system equivalent to the "distal" level.2 Periods Ending in 4:1 and 5:1 Atrioventricular Block In Figure 1, the 5:1 atrioventricular block ap peared because the impulse that was blocked at the "more proximal" level was one which had reached the His bundle during the previously present alter nating Wenckebach sequence. On the contrary, had this block at the "more proximal level" occurred during inscription of an impulse otherwise blocked in a lower atrioventricular nodal level (such as the atrial impulse labelled A6 in Fig 1), then the alter nating Wenckebach period would have terminated in 4:1 (not 5:1) atrioventricular block as a conse quence of a three-level disturbance in conduction, rather than as a result of the classic two-level block usually postulated to explain alternating Wencke bach periods ending in 4:1 atrioventricular block. That some types of 4:1 atrioventricular block can be due to more than two levels of block has been postulated before9'10"18and is supported by the previously mentioned study in which some episodes of 4:1 St-V block resulted from the association of intra-atrial Wenckebach periods with atrioventricu lar nodal and His-Purkinje block.2
DIGITALIS-INDUCED "PAT WITH 2:1 A-V BLOCK"
CAROTIDSINUSMASSAGE
•¿ v
FIGURE 4. Paroxysmal atrioventricular block produced (presumably at atrioventricular node) by massage of carotid sinuses in patient with digitalis-induced "paroxysmal" atrial tachycardia (PAT) with 2:1 atrioventricular block. Bottom strip (enlargement of first part of middle strip) shows, that paroxysmal atrioventricular block emerged from alternating Wenckebach sequence. Values are expressed in milliseconds (Other strips from this patient have been published elsewhere26).
CHEST,74: 3, SEPTEMBER, 1978
HIS BUNDLERECORDINGS277
Paroxysmal Atrioventricular Nodal Block Although both clinical reports16'20 and electrophysiologic studies utilizing the microelectrodes.21'23 have demonstrated repetitive concealed conduction in the atrioventricular node, paroxysmal atrioventricular nodal block is a less well known entity, in spite of occasional reports of its occurrence in man.13 VVatanabe and Dreifus23 showed an exam ple (their Fig 5-3) of paroxysmal block in the rab bit's atrioventricular node, which they attributed to "incomplete repolarization of the N region." Recent ly, El-Sherif and associates24 documented the exis tence of tachycardia-dependent block in the ischemic atrioventricular node of the dog. The genesis of paroxysmal atrioventricular nodal block in man is unclear. That there are mechanisms other than those operating in Figure 1 is sug gested by the fact that the enhancement of vagal tone produced by massage of the carotid sinuses can produce this disturbance in conduction in some pa tients (Fig 4).8-25-26AS in the His-Purkinje system, some of the episodes of paroxysmal atrioventricular nodal block emerged from alternating Wenckebach periods occurring during 2:1 atrioventricular con duction.15p27'31This suggests (but does not prove) a related electrogenetic mechanism, which could very well be repetitive concealed conduction. Ac cording to Elizari et al,31 the fact that the action potentials within the injured His-Purkinje system resembled those of the atrioventricular node and that refractoriness outlasted repolarization, with excitability and conduction not being completely reversed after the end of the preceding action poten tials, suggested repetitive concealed conduction in the affected portions of the His-Purkinje system (or the atrioventricular node); however, less and less penetration of each succeeding beat is unlikely, since this requires the levels of block to equal the number of consecutively blocked impulses. On the other hand, the 8:1 paroxysmal atrioven tricular nodal block in Figure 3 can be explained by assuming only block at three levels, the same num ber of levels postulated to explain the alternating Wenckebach periods ending in 5:1 atrioventricular block in Figures 1 and 2. Yet, for this to occur, the block at each level should be of the 2:1 type. When ever the ratio of atrioventricular conduction doubles, with 2:1 block in each additional level, the number of consecutive beats is simply one less than the ratio. With 2:1 block in only one level, the ratio of atrio ventricular conduction is obviously 2:1, and the number of consecutively blocked beats is one. With 2:1 block in two levels, the ratio is 4:1, and the number of consecutively blocked beats is three. With 2:1 block in three levels, the ratio of atrioven
278 CASTELLANOS ETAL
tricular conduction is 8:1, and the number of con secutively blocked beats is seven. Clinical Implications In this study, atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block and paroxysmal atrioventricular nodal block were only rarely due to rapid atrial rates per se. On the contrary, most episodes occurred in patients who had received ouabain or verapamil or who had organic atrioventricular nodal disease. Therefore, pharmacologic effects or organic disease can be suspected from clinical tracings alone (with out concomitant recording of the activity of the His bundle) wherever these patterns of conduction ap pear during atrial tachyarrhythmias or rapid atrial stimulation in patients with narrow QRS complexes. Although the mechanisms of paroxysmal atrioven tricular nodal block following administration of ouabain most probably resulted from the direct ef fects of this drug on the atrioventricular node, the role of vagal stimulation requires further studies (Fig 4); for example, both paroxysmal atrioven tricular nodal block and alternating Wenckebach periods can be produced by massage of the carotid sinuses in some patients with sinus rhythm (Fig 5-29 of Watanabe and Dreifus23), atrial flutter with 2:1 atrioventricular conduction (Fig 228 of Kosowsky et al9 and Fig 56-4 of Bellet25), and digitalis-induced "paroxysmal" atrial tachycardia with atrioventricu lar block26 (Fig 4). REFERENCES 1 Castellanos A, Sung RJ, Aldrich JL, et al: Electrocardiographic manifestations and clinical significance of atrioventricular nodal alternating Wenckebach periods. Chest 73:69-74, 1978 2 Castellanos A, Sung RJ, Mallon SM, et al: Effects of paroxysmal intra-atrial Wenckebach on distal atrioven tricular nodal and His Purkinje block with special refer ence to the theory of alternating Wenckebach periods. Am Heart J 95:228-234, 1978 3 Sellers TD Jr, Cambell RWP, Bashore TM, et al: Effects of procaine amide and quinidine supplement in the Wolff-Parkinson-White syndrome. Circulation 55:15-22, 1977 4 Wellens HJJ: The electrophysiological properties of the accessory pathway in Wolff-Parkinson-White syndrome. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduc tion System of the Heart: Structure, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 567-587 5 Denes P, Wu D, Dhingra R, et al: The effects of cycle length on cardiac refractory periods in man. Circulation 49:32-41, 1974 6 Rizzon P, DiBiase M, Calabrese P, et al: Electrophysio logical evaluation of intravenous verapamil in man. Eur J Cardiol 6:179-194, 1977 7 Besoain-Santander M, Pick A, Langendorf R: A-V con duction in auricular flutter. Circulation 2:604-616, 1950
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8 Katz LN, Pick A: Clinical Electrocardiography: The Arrhythmias (part 1). Philadelphia, Lea and Febiger, 1956, pp 413-418, 421 9 Kosowsky BD, Latif P, Radoff AM: Multilevel atrioventricular block. Circulation 54:914-921, 1976 10 Amat-y-Leon F, Chuquimia A, Wu D, et al: Alternating Wenckebach periods: A common electrophysiological re sponse. Am J Cardiol 36:757-764, 1957 11 Hartzler GO, Maloney HD: Supra-His alternate beat Wenckebach dysrhythmia. Mayo Clin Proc 50:475-481, 1975 12 Sachs A, Traynor RL: Paroxysmal complete auriculoventricular block. Am Heart J 9:267-271, 1933 13 Rosen KM, Loeb HS, Rahimtoola SH: Mobitz type II block with narrow QRS complex and Stakes-Adams attacks. Arch Intern Med 132:595-596, 1973 14 El-Sherif N, Scherlag BJ, Lazzara R: An appraisal of second degree and paroxysmal atrio-ventricular block. Eur J Cardiol 4:117-130, 1976 15 El-Sherif N, Scherlag BJ, Lazzara R: The pathophysiology of tachycardia dependent paroxysmal atrioventricular block after myocardial ischemia: Experimental and clinical observations. Circulation 50:515-528, 1974 16 Langendorf R, Pick A: Concealed conduction: Further evaluation of a fundamental aspect of propagation of the cardiac impulse. Circulation 13:381-399, 1956 17 Langendorf R: New aspects of concealed conduction of the cardiac impulse. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduction System of the Heart: Struc ture, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 410-423 18 Schindler S, Albers W: A-V block (letter to editor). Circulation 56:689, 1977 19 Langendorf R, Pick A, Edelist A, et al: Experimental conduction of concealed A-V conduction in the human heart. Circulation 32:386-393, 1965 20 Pick A: Mechanisms of cardiac arrhythmias: From hypo
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thesis to physiologic fact. Am Heart J 86:249-269, 1973 21 Moe GK, Abilskov JA, Mendez C: An experimental study of concealed conduction. Am Heart ] 67:338-356, 1964 22 Moore EN: Microelectrode studies on concealment of multiple premature atrial responses. Circ Res 18:660-672, 1966 23 Watanabe Y, Dreifus LS: Cardiac Arrhythmias: Electrophysiologic Basis for Clinical Interpretation. New York, Grune and Stratton, Inc, 1971, pp 187-188 24 El-Sherif N, Scherlag BJ, Lazzara R: Experimental pro duction of "Mobitz II" and paroxysmal block in the A-V node (abstract). Clin Res 23:181A, 1975 25 Bellet S: Clinical Disorders of the Heart Beat (3rd ed). Philadelphia, Lea and Febiger, 1971, p 1160 26 Calvino JM, Azan Cano L, Castellanos A Jr: Valor de las derivaciones esofagicas en las arritmias complejas. Rev Cubana Cardiol 16:293-316, 1955 27 Rosenbaum MB, Elizari MV, Levi RJ, et al: Paroxysmal atrioventricular block related to hypopolarization and spontaneous diastolic depolarization. Chest 63:678-688, 1973 28 Halpern MS, Nau GJ, Levi RJ: Wenckebach periods of alternate beats: Clinical and experimental observations. Circulation 48:41-49, 1973 29 Cohen HC, D'Cruz I, Pick A: Concealed intraventricular conduction in the His bundle electrogram. Circulation 53:776-783,1976 30 Castellanos A, Sung RJ, Aldrich JL, et al: Alternating Wenckebach periods occurring in the atria, His-Purkinje system, ventricles and Kent bundle. Am J Cardiol 40: 853-859, 1977 31 Elizari MV, Novakosky A, Quintero RA, et al: The exper imental evidence for the role of phase 3 and phase 4 block in the genesis of A-V conduction disturbances. In Wellens HJJ, Lie KI, Janse MJ (eds): The Conduction System of the Heart: Structure, Function, and Clinical Implications. Leiden, the Netherlands, HE Stenfert Kroese NV, 1976, pp 360-377
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