Fundamentals of clinical cardiology

Clinical uses of His bundle electrocardiography. Part I

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

The advent of His bundle electrocardiography (HBE) has contributed significantly to our understanding of many aspects of cardiac electro- physiology. ~ In comparison to the surface ECG the technique allows a more precise localization of (1) the areas and degrees of conduction delay, ~-~ (2) the site of impulse formation and direction of impulse propagation, 5-7 (3) the mechanisms of initiation and termination of tachycardias, ~-1~ and (4) the site of action drugs. 1~ The procedure, which is relatively simple and safe, consists of positioning an electrode catheter in the region of the tricuspid valve to record the bundle of His activity. The catheter can be advanced to the desired position via a femoral or an arm vein under fluoroscopic guidance. The His bundle potential is a rapid bi- or triphasic deflection sandwiched between the atrial and ventricular deflections occurring within the P-R segment of the electrocardiographic (ECG) tracing. The use of additional electrode catheters for stimulating or recording from various areas within the atria and/or ventricles broadens, significantly, the scope of clinical application of the HBE.

The use of HBE is particularly fruitful under the following settings.

A-V blocks

P-R prolongation. Prolongation of the P-R interval (> 0.20 sec.) may be the result of conduc- tion delay at one or more sites within the A-V

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 Projects HE 12536-04.

Received for publication May 29, 1975.

Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Depart- ment, United States Public Health Service Hospital, Staten Island, N. Y. 10304.

conducting system (A-V node, His-Purkinje system, bundle of His itself, or a combination of sites). 3 By far, the most common cause of P-R prolongation is conduction delay within the A-V node which is reflected in an A-H interval which exceeds upper limits of normal values (normal values for our laboratory, 60 to 140 msec.). A normal A-H interval in association with a prolonged H-V interval (normal values for our laboratory, 30 to 55 msec.) localizes the conduc- tion delay to the His-Purkinje system (HPS). Conduction delay within the bundle of His itself is an uncommon cause of P-R prolongation and usually presents as either split His bundle poten- tials (H and H') or a single, low-amplitude, wide deflection.

Delay in the A-V node does not alter the QRS complex, whereas delay in the HPS usually does. Not all patients with wide QRS complexes or bundle branch block patterns have prolonged H-V intervals, especially when conduction in the contralateral bundle is normal. Prolonged H-V interval associated with normal QRS complex may represent either uniform de lay along the entire HPS or intra-His bundle delay, where H' cannot be recorded.

A-V nodal conduction, both normal and abnor- mal, is under the influence of the autonomic nervous system, whereas conduction within the HPS is little, if at all, is affected by changes in the autonomic tone. 14, 1~

Second-degree A-V block. Second-degree A-V block may be of two types. Type I, which is commonly referred to as Wenckebach phenome- non, is characterized by a progressive prolonga- tion in P-R interval preceding a nonconducted P wave (Fig. 1), 1~, 17 The greatest increment of delay frequently, though not invariably occurs with the second conducted beat of the cycle (Fig. 1, panels

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Clinical uses of His bundle electrocardiography. I

Fig. 1. Type I second-degree A-V block within the A-V node. Tracings from top to bottom are standard ECG Leads I, II, and VI, high right atrial electrogram (HRA), bundle of His electrogram (HBE), and time lines (10 and 100 msec.). Same abbreviations used in all subsequent tracings. Panel A shows 4:3 A-V conduction with progressive prolongation of the A-H interval ( l l0 to 290 msec.) preceding an atrial impulse which biocks proximal to the bundle of His. The H-V intervals remain constant at 40 msec. Even though the QRS shows a right bundle branch block pattern the degree of P-R prolongation and marked P-R shortening following the block atrial impulse should suggest that the A-V node is the probable site of delay and block. Panel A shows the so-called classical P-R increment which is maximum with the second conducted beat of the cycle. Panels B and C (which are continuous) demonstrate that the maximum P-R increment (A-H increment) may occur with the last conducted beat of the cycle.

B a n d C). T h e E C G p a t t e r n of t y p e I s e c o n d - degree A - V b l o c k m o s t f r e q u e n t l y r e s u l t s f r o m c o n d u c t i o n d e l a y a n d b l o c k o c c u r r i n g w i t h i n t h e A-V node b u t m a y a lso r e s u l t f r o m a b n o r m a l c o n d u c t i o n w i t h i n t h e H P S or t h e b u n d l e of H i s i t se l f (Fig. 2).

I n t h e p re sence of n o r m a l Q R S c o m p l e x e s , t h e s i te of t y p e I s e c o n d - d e g r e e A - V b l o c k is u s u a l l y t he A-V node and , r a r e l y , w i t h i n t h e b u n d l e of His . V e r y o f t e n t y p e I , A - V n o d a l b l o c k is r evers -

ib le b u t i t m a y p r o g r e s s on to h i g h - d e g r e e (2:1 o r 3:1) A-V n o d a l b lock .

T y p e I s e c o n d - d e g r e e A - V b l o c k w i t h i n t h e H P S is u s u a l l y a s s o c i a t e d w i t h a p r e - e x i s t i n g b u n d l e b r a n c h b l o c k ( B B B ) p a t t e r n . (Figs. 2 a n d 3). T h e i n c r e m e n t o f P - R p r o l o n g a t i o n is u s u a l l y , a l t h o u g h n o t a l w a y s (Fig. 2), s i g n i f i c a n t l y less t h a n t h a t o b s e r v e d in A-V n o d a l W e n c k e b a c h t y p e of b lock . A t t imes , t h e i n c r e a s e in H - V i n t e r v a l m a y be so s u b t l e (Fig. 3) t h a t t h e s t a n -

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Fig. 2. Type I second-degree A-V block within the HPS in a pat ient with RBBB and left anterior hemiblock. The figure demonstrates a 3:2 and a 4:3 Wenckebach periodicity in which the site of delay and block is below the bundle of His. The ECG registers measurable P-R prolongations from beat to beat and significant P-R shortening following the block beat (a shortening of 75 msec.). A-V nodal conduction time (i.e., A-H interval) is constant a t 85 msec. and the P-R prolongation is accounted for by delay in the HPS.

Fi 9. 3. Type I second-degree A-V block within the PIPS. The tracing displays two cycles of 3:2 A-V conduction. The QRS complexes of conducted beats show a fixed R B B B and increasing right axis deviation. The third atrial impulse blocks without prior discernible P-R prolongation. HBE demonstrates constant and normal A-H intervals and a subtle H-V prolongation prior to block of the third atrial impulse within the HPS.

Fig. 4. Type II second-degree A-V block within the HPS. During sinus r h y t h m the A-H and H-V intervals measure 85 and 60 msec.i respectively. The P-R intervals are within normal limits. The fifth atrial impulse unexpectedly blocks below the bundle of His without prior H-V prolongation. In this case, the block did not appear to be cycle length dependent since it is preceded by shorter H-H intervals and is followed by longer H-H intervals with 1:1 A-V response.

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Clinical uses o f His bundle electrocardiography. I

Fig. 5.2:1 A-V block within the HPS. A 2:1 A-V block in the HPS is present at an atrial cycle length of 700 msec. The P-R interval of conducted beats is at the upper limits of normal and the QRS complexes have a LBBB pattern. S represents stimulus artifact.

1 P , _t.,~ P P_

l = _ f i l l - -

HRA f:~. ?~' ~. . . . . . ~ ~. . . . . .

Fig. 6 .2:1 A-V nodal block in a patient with LBBB. At sinus rhythm the site of block during 2:1 A-V conduction is the A-V node: The P-R interval is slightly prolonged. The QRS morphology is very similar to that shown in Fig. 5. The site of block will be difficult to determine without HBE in this and similar situations.

dard ECG recordings taken at a paper speed of 25 mm. per second mimics classical type I I or Mobitz II block (see below).

Type II second-degree A-V block (Mobitz II), Sudden and unexpected block of a P wave without prolongation of the preceding P-R inter- vals has been termed Mobitz I I or type I I second- degree A-V block TM 19 (Fig. 4). In this form of block the QRS morphology usually shows a BBB pattern. The P-R interval of conducted beats is frequently within normal limits, which makes block of the P wave appear "unexpected." Elec- trophysiological studies have confirmed tha t the site of block is always within the HPS. Some cases of Mobitz type I I block, in all probabili ty, are examples of subtle Wenckebach type of conduc-

tion in the HPS (Fig. 3). Conversely, a subtle Wenckebach type of conduct ion within the A-V node may mimic a type I I second-degree A-V block. A significant shortening of the P-R interval following the blocked beat suggests tha t t h e A-V node is the site of block.

High-degree (2:1, 3:1) A-V block. In fixed high- degree A-V block, it is difficult by ECG tracings alone to precisely localize the site of block, espe- cially when the QRS complexes are abnormal . When the QRS complexes are normal, the site of block is most often within the A-V node bu t occasionally is within the bundle of His itself. High-degree A-V block in association with BBB patterns may be within the H P S or the A-V node {Figs, 5 and 6).

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R

Fig. 7. A-V block due to concealed bundle of His extrasystoles. Panel A shows 3:2 A-V block associated with narrow QRS complexes (Lead VI). The P-R intervals of conducted beats are normal and no P-R prolongation is observed prior to the block. Analysis of long rhythm strips (panel B) revealed perio(iic occurrence of premature QRS complexes with a RBBB pattern just preceding the blocked P waves (arrows). These premature QRS complexes most probably result from aberrant conduction of impulses originating in the region of the bundle of His. Retrograde penetration into the A-V node induces block of the oncoming (panel B) sinus beats (retrograde concealed conduction in the A-V node). When premature His bundle extrasystoles failed to propagate to the ventricles but did propagate retrogradely into the A-V node, the subsequent P waves were suddenly and unexpectedly blocked (panel A). After an initial lidocaine bolus (ling. per kilogram), bundle of His extrasystoles conducted to the ventricles with narrow QRS complexes (panel C) and finally were abolished and 1:1 A-V conduction was restored (panel D). The normalization Of the premature QRS complex which occurred from either shortening of the relative refractoriness of the HPS or slight shortening of the preceding ventricular cycle length (or both) further attests to the origin of premature impulse in the bundle of His.

Third-degree A-V block. T h i r d - d e g r e e A-V block refers to comple t e a b s e n c e of A-V conduc - t ion ( a l t hough V-A c o n d u c t i o n m a y be p resen t ) . ~~ Th i s si te of b lock can be r e a s o n a b l y p red ic t ed f rom the m o r p h o l o g y of t he Q R S complexes a n d the ra t e of the escape pacemaker . W h e n t he site of b lock is in the A-V node, t h e s u b s i d i a r y pace-

m a k e r is u s u a l l y loca ted w i t h i n t he b u n d l e of His a n d the Q R S m o r p h o l o g y is n o r m a l or the s a m e as prior to block. I n add i t ion , v e n t r i c u l a r r a t e is

f r equen t ly > 40 per m i n u t e w h e n the s u b s i d i a r y pacemake r is loca ted in the b u n d l e of His. W h e n the pa c e ma ke r is s u b j u n c t i o n a l ( id ioven t r i cu la r ) , the v e n t r i c u l a r r a t e is u s u a l l y < 40 per m i n u t e

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Clinical uses o f His bundle electrocardiography. I

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r l V I'~ ~ Z b U T L l H l l l T i i l i l l l l h l i . . . . . . . . . t . . . . . . . . . + . . . . . . . . . + . . . . . . . . . t . . . . . . . . . I . . . . . . . . . , . . . . . . . . . t . . . . . . . . . i . . . . . . . . . l . = ~ . . . + . l . . . . . . . . . i . . . . . . . . . . . . . . . . . . . t . . . . . . . . . I . . . . . . . . . = + . = . . . . . . t . . . . . . . . . ++ . . . . . . . . . I . . . . . . . . . .t . . . . . . . . . i . . . . . . . . . l . . . . . . . . . . . . . . . . . . i . . . . . . . . . | . . . . . . . . . r . . . . . . . . . + . . . . . . . . .

Fig. 8. Type I I second-degree A-V block experimentally induced by programmed bundle of His stimulation. Following the four th sinus beat the bundle of His is electrically s t imulated (S) at an H-S interval of 250 msec. There is no ventricular response because the distal bundle b ranch-Purk in je system is refractory. However, retrograde concealment in the A-V node results in unexpected block of the fifth sinus beat.

and the QRS complexes are wide. HBE recordings are required to substantiate the uncommon situa- tion of intra-His bundle block associated with a junctional pacemaker2

In all forms of A-V block, important clues as to the site of conduction delay or block may be uncovered from ECG recordings taken during exercise or following administration of drugs which affect autonomic balance. Delay or block within the A-V node usually improves with exer- cise, atropine, or isoproterenol administration, whereas delay and block within the HPS do not. However, failure to improve conduction with these maneuvers does not necessarily localize the conduction abnormality to the HPS. Subsidiary pacemakers located in the bundle of His usually show some degree of acceleration in response to exercise, atropine, or isoproterenol, whereas pace- makers more distally located are usually only responsive to isoproterenol administration.

Functional blocks

A-V node. In almost all patients incremental atrial pacing results in progressive prolongation of A-V nodal conduction time and at higher paced rates in A-V nodal Wenckebach periods and high- degree A-V nodal block (i.e., 2:1 or 3:1). This is an expected response of the A-V node when the atrial rate is increased without a concomitant increase in sympathetic tone. It represents a functional block because the atrial rate exceeds the capacity of the A-V node to transmit impulses to the ventricle. The A-V block commonly asso-

ciated with atrial flutter represents the clinical counterpart of this type of functional block. Occasionally relatively slow atrial rates, i.e., < 110 per minute, may result in A-V nodal Wenckebach phenomenon, which may or may not represent abnormality. The response of A-V node to exercise in these patients may demon- strate capacity of the A-V node to sustain 1:1 A-V response at even higher rates in the presence of " endogenous sympathetic stimulation which ac- companies exercise.

HPS. Block developing within the HPS during incremental atrial pacing with continuous reli- able atrial capture is an abnormal response, since conduction within the HPS normally remains constant at increasing heart rates. However, abrupt increases in atrial rates following a long cycle length (H-H interval) may result in a functional 2:1 A-V block in the HPS, if the first paced atrial beat reaches the HPS during its effective refractory period. 21 This type of block cannot be considered abnormal at the present time and therefore it is important that events preceding the occurrence of such a block be carefully analyzed for changes in the cycle length.

A-V blocks due to concealed His-bundle extra- systoles. Closely coupled extrasystolic impulses arising from the bundle of His and concealing antegradely within the HPS (no ventricular response) as well as retrogradely within the A-V node may cause conduction delay or block of subsequent sinus impulses. 22 Bundle of His

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recordings permit a precise diagnosis of this phenomenon. 23 Concealed bundle of His extrasys- toles can cause first-degree, both types of second- degree, and high-degree A-V blocks. The diagnosis can be suspected from long ECG rhythm strips which show, in addition to A-V blocks, junctional extrasystoles which do conduct to the ventricles with normal or aberrant QRS complexes (Fig. 7).

Fig. 8 illustrates the experimental production of this phenomenon. The spontaneous bundle of His extrasystole is simulated by electrically stimulating this structure at appropriate times in the cardiac cycle. ~-4

REFERENCES

1. Scherlag, B. J., Lau, S. H., Helfant, R. H., Berkowitz, W. D., Stein, E., and Damato, A. N.: Catheter technique for recording His bundle activity in man, Circulation 39:13, 1969.

2. Damato, A. N., Lau, S. H , Helfant, R. H., Stein, E., Patton, R. D., Scherlag, B. J., and Berkowitz, W. D.: A study of heart block in man using His bundle recordings, Circulation 39:297, 1969.

3. Narula, O. S., Cohen, L. S,, Scherlag, B. J., Samet, P., Lister, J. W., and Hildner, F. J.: Localization of A-V conduction defects in man by recording of the His bundle electrogram, Am. J. Cardiol. 25:228, 1970.

4. Narula, O. S.: Current concepts of atrioventricular block, in His bundle electrocardiography and clinical electro- physiology, Narula, O. S., ed., Philadelphia, 1975, F. A. Davis Company, Chap. 9, p. 139.

5. 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.

6. Puech, P., and Grolleau, R.: L'activit~ du faisceau de His, normale et pathologique, Paris, 1972, Sandoz Ed.

7. Touboul, P., Clement, C., Magrina, J., Tessier, Y., and Delahave, J. P.: Enregistrement de l'activit~ electrique du tissu de conduction auriculoventriculaire au cours de taycardies ventriculaires, Arch. Mal. Coeur 65:1409, 1972.

8. G01dreyer, B. N., and Bigger, J. T., Jr.: The site of reentry in paroxysmal supraventricular tachycardia, Circulation 42:673, 1970.

9. 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.

10. Varghese, P. J., Damato, A. N., Caracta, A. R., Gallagher, J. J., Josephson, M. E., and Lau, S. H.: Intraventricular conduction delay as a determinant of atrial echo beats, Circulation 49:805, 1974.

11. Weisfogel, G. M., Batsford, W. P., Paulay, K. L., Joseph- son, M. E., Ogunkelu, J. B., Akhtar, M., Seides, S. F., and Damato, A. N.: Sinus node re-entrant tachycardia in man, AM. HEART J. 90:295, 1975.

12. Wellens, H. J., Schuilenburg, R. M., and Durrer, D.: Electrical stimulation of the heart in patients with ventricular tachycardia, Circulation 46:216, 1972.

13. Damato, A. N., Caracta, A. R., Akhtar, M., and Lau, S. H.: The effects of commonly used cardiovascular drugs on AV conduction and refractoriness, in His bundle electrocardiography and clinical electrophysiology, Na- rula, 0. S., ed., Philadelphia, 1975, F. A. Davis Company, Chap. 7, p. 105.

14. Akhtar, M., Damato, A. N., Caracta, A. R., Batsford, W. P., Josephson, M. E., and Lau, S. H.: Electrophysio- logic effects of atropine on atrioventricular conduction studied by His bundle electrogram, Am. J. Cardiol. 33:333, 1974.

15. Vargas, G., Akhtar, M., and Damato, A. N.: Electrophys- iologic effects of isoproterenol on cardiac conduction system in man, AM. HEART J. 90:25, 1975.

16. Wenckebach, K. F.: Zur analyse des urregelmassigen Pulses, Z. Klin. Med. 37:475, 1899.

17. Katz, L. N., and Pick, A.: Clinical electrocardiography. Part I. The arrhythmias, Philadelphia, 1956, Lea & Febiger, Publishers, p. 540.

18. Mobitz, W.: Uber die unvollstandinge Storung der Erreg- ungsuberleitung zwischen Vorhofund Kammer des men- schichen Herzens, Z. Gesamte Exp. Med. 41:180, 1924.

19. Langendorf, R., Cohen, H., and Gozo, E. G.: Observa- tions on second degree atrioventricular block, including new criteria for the different diagnosis between type I and type II block, Am. J. Cardiol. 29:111, 1972.

20. Narula, O. S., Scherlag, B. J., Javier, R. P., Hildner, F. J., and Samet, P.: Analysis of the A-V conduction defect in complete heart block utilizing His bundle electrograms, Circulation 41:437, 1970.

21. Damato, A. N., Varghese, P. J., Caracta, A. R., M. Akhtar, and S. H. Lau.: Functional 2:1 A-V block within the His-Purkinje system: Similation of type II second degree A-V block, Circulation 47:534, 1973.

22. Langendorf, R., and Mehiman, J. S.: Blocked (noncon- ducted) A-V nodal premature systoles imitating first and second degree A-V block, AM. HEART J. 34:500, 1947.

23. Rosen, K. M., Rahimtoola, S. H., and Gunnar, R. M.: Pseudo A-V block secondary to premature non-propa- gated His bundle depolarizations: Documentation by His bundle electrocardiography, Circulation 42:367, 1970.

24. Damato, A. N., Lau, S. H., and Bobb, G. A.: Cardiac arrhythmias simulated by concealed bundle of His extra- systoles in the dog, Circ. Res. 28:316, 1971.

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