Clinical uses of His bundle electrocardiography. Part II

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Fundamentals of clinical cardiology Clinical uses of His bundle electrocardiography. Part II Masood Akhtar, M.D. Anthony N. Damato, M.D. Antonio R. Caracta, M.D. Staten Island, N.Y. Supraventricular vs. ventricular arrhythmias. The origin of single or multiple beats with wide and bizarre QRS complexes may at times be difficult to determine from the surface ECG alone (Fig. 1). This is especially true in atrial fibrilla- tion, where there is absence of discrete P waves (Fig. 2). HBE recordings have proved useful in making the distinction between beats of supra- ventricular and ventricular origin. 1, ~ In the former (i.e., arising from the bundle of His or above), bundle of His deflections precede the QRS complex by a normal or longer than normal H-V interval (Figs. 1 and 2). For beats arising more distally (i.e., bundle branches or the Purkinje network) the inscription of the His bundle poten- tial either occurs within the ventricular electro- gram (Fig. 1) or precedes it by a value signifi- cantly less than normal. The ECG distinction between ventricular tachycardia (VT) and supraventricular tachy- cardia (SVT) with aberration depends primarily on analysis of: (1) the rate and regularity of the arrhythmia, (2) the QRS morphology, (3) presence or absence of P waves, (4) the relation- ship of P waves to QRS complexes, and (5) the presence of fusion beats. The occurrence of normal or fusion QRS complexes during a tachy- cardia with wide QRS complexes is considered the hallmark for the ECG diagnosis of VT. There are at least three mechanisms responsible for normal From the Cardiopulmonary Laboratory, United States Public Health Service Hospital, Staten Island, N. Y. This work was supported in part by the Bureau of Medical Services, United States Public Health Service Project Py 75-1, and National Heart and Lung Institute Project HE 12536-04. Received for publication May 29, 1975. Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Labora- tory, United States Public Health Service Hospital, Staten Island, N. Y. 10304. or fusion beats occurring during a VT: (1) disso- ciated sinus capture beats, (2) retrograde A-V nodal re-entry with ventricular echo beats, and (3) premature ventricular beats originating from the contralateral ventricle. Even though fusion or normal QRS complexes occurring during an episode of tachycardia with wide QRS suggests a ventricular origin of the arrhythmia, such beats are occasionally seen in SVT with aberrant conduction to the ventricles. Intermittent nor- malization of the QRS complex during an SVT with aberrant ventricular conduction may occur under the following settings. (1) When Wencke- bach phenomenon occurs in a bundle branch displaying the block pattern on the surface E C G 3: The successive supraventricular impulses may block more proximally and finally the impulse does not penetrate the bundle branch, The nonpenetration of the bundle branch results in a longer recovery time and the next supraventric- ular impulse may have normal intraventricular conduction, following which the cycle is repeated. It should be pointed out that partial penetration with ineffective propagation or non- penetration of the bundle branch will result in similar QRS complexes, and the latter is reflected on the ECG as periodic QRS normalization, during a tachycardia with wide QRS complexes. (2) When during an SVT with aberrant ventric- ular conduction ectopic impulse formation occurs in the refractory bundle branch distal to the site of block. If ipsilateral ventricular activation from the ectopic impulse coincides with activation of the contralateral ventricle from the supraventric- ular impulse complete normalization of the QRS complex may be observed. Asynchronous activa- tion of the two ventricles by the two impulses may result in different degrees and types of fusion activation. 660 May, 1976, Vol. 91, No. 5, pp. 660=664

Transcript of Clinical uses of His bundle electrocardiography. Part II

Fundamentals of clinical cardiology

Clinical uses of His bundle electrocardiography. Part II

Masood Akhtar, M.D. Anthony N. Damato, M.D. Antonio R. Caracta, M.D. Staten Island, N.Y.

Supraventricular vs. ventricular arrhythmias.

The origin of single or multiple beats with wide and bizarre QRS complexes may at times be difficult to determine from the surface ECG alone (Fig. 1). This is especially true in atrial fibrilla- tion, where there is absence of discrete P waves (Fig. 2). HBE recordings have proved useful in making the distinction between beats of supra- ventricular and ventricular origin. 1, ~ In the former (i.e., arising from the bundle of His or above), bundle of His deflections precede the QRS complex by a normal or longer than normal H-V interval (Figs. 1 and 2). For beats arising more distally (i.e., bundle branches or the Purkinje network) the inscription of the His bundle poten- tial either occurs within the ventricular electro- gram (Fig. 1) or precedes it by a value signifi- cantly less than normal.

The ECG distinction between ventricular tachycardia (VT) and supraventricular tachy- cardia (SVT) with aberration depends primarily on analysis of: (1) the rate and regularity of the arrhythmia, (2) the QRS morphology, (3) presence or absence of P waves, (4) the relation- ship of P waves to QRS complexes, and (5) the presence of fusion beats. The occurrence of normal or fusion QRS complexes during a tachy- cardia with wide QRS complexes is considered the hallmark for the ECG diagnosis of VT. There are at least three mechanisms responsible for normal

From the Cardiopulmonary Laboratory, United States Public Health Service Hospital, Staten Island, N. Y.

This work was supported in part by the Bureau of Medical Services, United States Public Health Service Project Py 75-1, and National Heart and Lung Institute Project HE 12536-04.

Received for publication May 29, 1975. Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Labora- tory, United States Public Health Service Hospital, Staten Island, N. Y. 10304.

or fusion beats occurring during a VT: (1) disso- ciated sinus capture beats, (2) retrograde A-V nodal re-entry with ventricular echo beats, and (3) premature ventricular beats originating from the contralateral ventricle. Even though fusion or normal QRS complexes occurring during an episode of tachycardia with wide QRS suggests a ventricular origin of the arrhythmia, such beats are occasionally seen in SVT with aberrant conduction to the ventricles. Intermit tent nor- malization of the QRS complex during an SVT with aberrant ventricular conduction may occur under the following settings. (1) When Wencke- bach phenomenon occurs in a bundle branch displaying the block pattern on the surface E C G 3: The successive supraventricular impulses may block more proximally and finally the impulse does not penetrate the bundle branch, The nonpenetration of the bundle branch results in a longer recovery time and the next supraventric- ular impulse may have normal intraventricular conduction, following which the cycle is repeated. It should be pointed out that partial penetration with ineffective propagation or non- penetration of the bundle branch will result in similar QRS complexes, and the latter is reflected on the ECG as periodic QRS normalization, during a tachycardia with wide QRS complexes. (2) When during an SVT with aberrant ventric- ular conduction ectopic impulse formation occurs in the refractory bundle branch distal to the site of block. If ipsilateral ventricular activation from the ectopic impulse coincides with activation of the contralateral ventricle from the supraventric- ular impulse complete normalization of the QRS complex may be observed. Asynchronous activa- tion of the two ventricles by the two impulses may result in different degrees and types of fusion activation.

660 May, 1976, Vol. 91, No. 5, pp. 660=664

Clinical uses of His bundle electrocardiography. H

Fig. 1. Ventricular and supraventricular beats. Illustrated are two premature beats, Vp and Ab, the first of which (Vp) represents a beat ofventricular origin; the His bundle electrogram is obscured by the ventricular electrogram. The beat of supraventricular origin (Ab) is preceded by a His bundle deflection with H-V interval which is greater than normal.

Fig. 2. Atrial fibrillation with aberrant conduction of LBBB (last four QRS complexes) which could be misinterpretated as a ventricular tachycardia since, according to the general rule of aberration, the third QRS complex (short cycle following a long cycle) would be expected to be aberrant. Since aberration occurs at cycle lengths < 500 msec. this probably represents a rate-related phenomenon.

General ly the bundle of His dur ing ven t r i cu la r tachycard ia is ac t iva ted re t rograde ly and its inscription is obscured by the ven t r i cu la r electro- gram. Occasionally, however, the re t rograde His bundle deflection m a y precede the Q R S complex during a ventr icular t achycard ia , t he reby giving the erroneous impression t h a t the a r r h y t h m i a is of supravent r icu lar origin. In these ins tances the H-V intervals are significantly shor te r t h a n those recorded during ven t r i cu la r ac t iva t ion by supra- ventr icular impulses. ~

I t is impor t an t t h a t the His bundle po ten t i a l is carefully looked for dur ing n o r m a l or fusion

ventr icular bea ts when s tudy ing a suspected ventr icular tachycardia . I f spon taneous supra- ventr icular bea ts are not observed, t e rmina t ion of the a r r h y t h m i a m a y be a t t e m p t e d with a t r ia l pacing or wi th therapeut ic agents like p roca inam- ide.

The clinical usefulness of H B E in mak ing a more definitive diagnosis of V T is exemplified by the recent demons t ra t ion t h a t bidirect ional tachycardia m a y be of ven t r i cu la r or supravent r i - cular origin, the former being more c o m m o n in cases documented by H B E . 4-7 Dur ing bidirec- t ional t achycard ia the Q R S complexes usua l ly

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T 70

B 1

700

Fig. 3. Supraventricular tachycardia tA-V nodal re-entry). In panel A a premature atrial beat (A~) is coupled to the preceding basic drive beat (A1) at a coupling interval of 390 msec. A: conducts with an A2H2 of 110 msec. after which sinus rhythm follows. At a closer A~A2 interval of 350 msec. (panel B), As conducts with a longer A2H~ interval of 250 msec. and a sustained SVT is initiated. Note the low-to-high sequence of atrial activation during the SVT as compared to the high-to-low sequence during sinus rhythm (panel A). Note also that the low atrial activation precedes ventricular activation {H-Ae < H-V) and the P wave polarity is difficult to determine from the surface ECG.

display fixed r i gh t bundle b ranch block pa t t e rn and al ternating left and right axis deviation. ~

Paroxysmal atrial tachycardia

I t has been demons t ra ted tha t paroxysmal atrial tachycardia may result from re-ent ry occurring in either the sinus 9 or A-V nodes. 1~ Both types of tachycard ia may be abrup t ly initiated by a single, properly t imed p remature atrial beat occurring within the relative refrac- tory period (RRP) of either node (Figs. 3 and 4). A-V nodal re-entry is seen more f requent ly t h a n sinus nodal re-entry. In the former the sequence of atrial act ivat ion is from the low-to-high a t r ium and the P waves, a l though inverted i n Leads II ,

III , and aVF, are frequently obscured by the QRS complex or S-T segment (Fig. 3). In sinus nodal re-entry, the sequence of atrial act ivat ion is from the high-to-low right a t r ium and the P waves, which precede the QRS complexes, are very similar to those of sinus rhy thm. Both types of re- ent rant nodal t achycard ias may be abrupt ly terminated by (1) carotid sinus pressure (as well as other vagal maneuvers) or (2) a properly t imed premature atrial depolarization.

Sinus nodal re-entry can be initiated by prema- ture atrial beats which block in the A-V node whereas A-V nodal re-ent rant paroxysmal supraventricular tachycardias rarely, if ever, result from premature atrial beats which fail to

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Clinical uses of His bundle electrocardiography. H

Fig. 4. Supraventricular tachycardia (sinus node re-entry). During sinus rhythm (A~) a premature beat (As) initiates a SVT (sinus node re-entry) with a high-to-low atrial activation sequence similar to sinus beats. It is to be noted that the first beat of SVT (Ae) blocks proximal to the bundle of His, which also argues against A-V nodal re- entry being the mechanism of this type of tachycardia.

Fig. 5. Functional block in the HPS during a complex SVT. The tracing (taken from the same patient as shown in Fig. 3) shows an episode of SVT during which a functional 2:1 block within the HPS developed following a long- short cycle sequence (not shown}. Note the low-to-high atrial activation sequence (Ae) during the SVT and that the H-Ae interval remains constant during the block, indicating that ventricular muscle was not an essential link in the re-entrant circuit. The tracing also shows the mode of termination of the 2:1 block below the bundle of His. The fifth QRS complex shows a RBBB aberration with an H-V interval of 165 msec. during 3:2 Wenckebach type of conduction within the HPS, after which 1:1 A-V conduction resumes with ventricular aberration. The usefulness of His bundle electrogram recordings in this complex arrhythmia is obvious.

p r o p a g a t e t o t h e b u n d l e of His. R e - e n t r a n t t a c h y -

ca rd :as (wi th a l o w - t o - h i g h s e q u e n c e of a t r i a l

a c t i v a t i o n ) w h i c h are i n i t i a t e d by a p r e m a t u r e

a t r i a l b e a t wh ich a n t e g r a d e l y b locks w i t h i n t h e

H P S {i.e., no v e n t r i c u l a r r e sponse ) f a v o r s A-V

n o d a l r e - e n t r y {Fig. 5) a n d e x c l u d e s r e - e n t r y v i a a

m u s c l e - t o - m u s c l e bypas s t r a c t o f t h e K e n t type .

E v e n t h o u g h r e - e n t r y in t h e A - V a n d s i n o a t r i a l

nodes are r e l a t i v e l y w e l l - d o c u m e n t e d en t i t i e s

t h e r e is no d o u b t t h a t a s ign i f i can t n u m b e r of

a t r i a l t a c h y c a r d i a s are due to a t r i a l e c t o p y or

i n t r a - a t r i a l r e e n t r y , l~

REFERENCES

1. Damato, A. N., Gallagher, J. J., Caracta, A. R., and Lau, S. H.: Subjunctional conduction, in Dreifus, L. S., and

Likoff, W., editors: Cardiac arrhythmias, New York, 1973, Grune & Stratton, Inc., p. 363.

2. Puech, P.: Ectopic ventricular rhythms: Ventricular tachycardia and His bundle recordings, in His bundle electrocardiography and clinical electrophysiol0gy, Na- rula, 0. S., ed.. Philadelphia, 1975, F. A. Davis Company, Chap. 12.

3. Gallagher, J. J., Damato, A. N., Varghese, P. J., Caracta, A. R,~ Josephson, M. E., and Lau, S. H.: Alternative mechanisms of apparent supernormal atrioventricular conduction, Am. J. Cardiol. 31:362, 1973.

4. Kastor, J. A., and Goldreyer, B. N.: Ventricular origin of bidirectional tachycardia: A case report of a patient not toxic from digitalis, Circulation 48:897, 1973.

5. Morris, S. N., and Zipes, D. P.: His bundle electrocardiog- raphy during bidirectional tachycardia, Circulation 48:321, 19'73.

6. Puech, P., Grolleau, R., Basissus, C., Cabasson, J., and Latour, H.: Tachycardia bidirectionnelle d'origine m- frashi_sienne, Arch: Mal. Coeur 67:39, 1974.

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7. Cohen, S. I., and Voukydis, P.: Supraventricular origin of bidilu~tional tachycardia. Report of a case, Circulation 50:634, 1974.

8. Rosenbaum, M. B., Elizari, M. V., and Lazzari, J. 0.: The mechanism of bidirectional tachycardia, AM. HEART J. 78:4, 1969.

9. Weisfogel, G. M., Batsford, W. P., Paulay, K. L., Joseph- son, M. E., Ogunkelu, B. J., Akhtar, M., Seides, S. F , and Damato, A. N.: Sinus node re-entrant tachycardia in man, AM. HEART J. (in press).

10. Bigger, J. T., Jr., and Goldreyer, B. N.: The mechanism of

paroxysmal supraventricu!ar tachycardia, Circulation 42:673, 1970.

11. Goldreyer, B. N., and Bigger, J. T~, Jr.: The site of reentry in paroxysmal supraventricular tachycardia, Circulation 43:15, 1971.

12. Goldreyer, B. N., and Damato, A. N.: The essential role of A-V conduction delay in the initiation of paroxysmal supraventricular tachycardia, Circulation 43:679, 1971.

13. Goldreyer, B. N., Gallagher, J. J., and Damato, A. N.: The electrophysiological demonstrat ion of atrial ectopic tachycardia in man, AM. HEART J. 88:205, 1973.

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