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The Gouaux-Ashman Phenomenon: His Bundle Recordings*

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The Gouaux-Ashman Phenomenon: His Bundle Recordings* The Gouaux-Ashman Phenomenon: His Bundle Recordings* BENJAMIN J. SCHERLAG, Ph.D. From the Division of Cardiovascular Disease, Department of Internal Medicine, Mount Sinai Medical Center, Miami Beach, Florida, and the Department of Medicine, University of Miami School of Medicine, Coral Gables, Florida The differentiation of ventricular premature logical behavior of A-V nodal and His bundle con­ beats from supraventricular beats with aberrant duction under these two circumstances. ventricular conduction is often difficult on the basis Figure I, taken from a study by Damato et al. of the surface electrocardiogram. The diagnosis of (1), shows the response of the His-Purkinje system aberrant conduction has been based largely on the to atrial premat~re beats delivered at varying in­ presence of a right bundle branch block pattern ap­ tervals after the previous cardiac cycle. A slight pearing in a short cycle subsequent to a longer cycle degree of aberration can be seen even with no pro­ (2). Several other criteria for diagnosing aberrant longation of the H-V or H-Q time. However, more conduction of a supraventricular beat such as vari­ marked aberration occurs with the prolongation of able coupling time have been used to differentiate His-Purkinje conduction time from 45 to 65 msec. these abnormal ventricular complexes from ventric­ Finally, block is shown distal to the recorded His ular premature beats which are most commonly fol­ bundle deflection, and these properties of the His­ lowed by a full compensatory pause. This differenti­ Purkinje system during premature activation have ation is often inexact and under some critical clinical been confirmed in other clinical laboratories. There­ circumstances cannot be accomplished with any fore, the normal response to atrial premature or His degree of reliability. In 1947, Gouaux and Ashman premature beats which result in aberrant ventricular wrote a report entitled: "Auricular Fibrillation with condui;:tion is either an unchanged or prolonged Aberration Simulating Ventricular Paroxysmal H-V time. Tachycardia" (2). It is thus in the clinical context In contrast to the constancy or prolongation of of atrial fibrillation that the diagnosis of aberrant the H-V interval during supraventricular beats conduction of supraventricular beats as opposed to conducted with aberration, ventricular ectopic beats ventricular tachycardia becomes particularly difficult. or fusion beats show either no His potential pre­ Recent reports in the literature have emphasized ceding the aberrant QRS complex or a shortened the use of the His bundle-electrocardiographic H-V time. In figure 2, the His bundle-ECG technique as a means of differentiating between tracings reveal an H-V time of 50 msec with a aberrant conduction and ventricular ectopic com­ wide QRS complex. Note that the P-R interval is plexes (3, 4, and 6). In order to evaluate this method 190 msec during sinus rhythm. In the second beat in of differentiation, it is important to note the physio- panel A, a shortening of the P-R interval from 190 to 175 msec with a narrowing of the QRS complex is observed. Also, a shortening of the H-V time to 35 * Presented by Dr. Scherlag at the Symposium on msec occurred. That this beat represents in fact a Cardiac Arrhythmias, June 8, 1972, at Virginia Beach, Virginia. Please send reprint requests to: Dr. B. Scherlag, fusion of a normally conducted atrial impulse and a Mount Sinai Medical Center, 4300 Alton Road, Miami ventricular ectopic peat is indicated in panels B and Beach, Florida 33140. C. Here the :P-R shortens to 135 msec in the sec- 34 MCV QUARTERLY 9(1): 34-38, 1973 SCHERLAG: GOUAUX-ASHMAN PHENOMENON 35 ond beat of each panel with a negative H-V time, DAMATO ET A that is, ventricular activity precedes His bundle ac­ tivity by 5 msec and 20 msec, respectively. It can A P-H 95 MSEC 132 P-f>'380 --H--Q"\ 4;.5__ _,, __ 4_5'"' be seen that the change in H-V time from normal Vl - is appropriately matched by the change in the P-R Q S P.1. QRS interval. Unfortunately, these quantitative aspects of the HBE__,.....phi:'"'J, ·-----"~·- · · l ' ·.·.-- ------- His bundle recording in regard to ventricular ectopic ! \ ,0.2 SEC• beats and supraventricular beats conducted with ab­ p-p' 370 erration have been essentially ignored in several B P-H recent publications. In a report by Lau et al. ( 3), t+Q the authors were the first to note that the recording Vl---..... of His bundle activity represents a valid method for p H . '" ~,' .::,_ .. ___ diagnosing aberrant conduction, particularly in dif­ HBE-{i.-\', ~~. \ IV~ - I ferentiating supraventricular beats and ventricular RBBB premature contractions of ventricular tachycardia. However, in illustrating this point, a case of atrial c P-H 132 fibrillation was examined with simultaneous record­ HQ 65 ings of His bundle electrogram and a standard ECG v1---..... lead (fig. 3). The authors state that the second com­ plex in this figure is a supraventricular beat con­ --'~. ducted from above with aberrant ventricular activa­ LBBB tion. However, the H-V time is clearly shorter in p..p'355 this beat than in the normally conducted beats, l, O P·H 95 MSEC P H 132 t+Q 4!S 4, and 6. Note that the H-V time is measured from the H deflection to the earliest ventricular activation V1 --v------'~~---------------- which in this case is the standard ECG lead. In the HBE_!:._~. l.,.._P._.1_,~"-- ------ normally conducted beats, the earliest ventricular . '1 ~0.2 SEC~ activation occurs in the His bundle electrogram. ~ ·. In another recent report by Massumi, a case was presented (fig. 4) in which the first two beats Fig. I-In panels A through D, the top tracing is a lead shown are sinus beats showing atrial, His bundle, V1 and the bottom tracing a His bundle electro gram (HBE) . and ventricular activity. The third beat shows a When the atrium was prematurely stimulated at a coupling QRS complex which the author describes as a pat­ interval of 380 msec (panel A), a delay in A-V conduction tern of "incomplete right bundle branch block and occurred as manifested by an increase in the P-H interval to 132 msec. The H-Q interval remained constant, and left axis deviation suggesting impaired conduction ventricular depolarization was only slightly altered. Shorten­ through the right bundle branch and superior di­ ing the coupling interval to 370 msec (panel B) and 365 vision of the left bundle branch." Massumi localizes msec (panel C) resulted in aberrant ventricular depolariza­ the extrasystolic focus as occurring within the His tion (RBBB and LBBB) with an associated prolongation of bundle and bases this conclusion on the observation the H-Q interval. At a coupling interval of 355 msec (panel that this extrasystole is preceded by a His bundle D), complete block below the His bundle resulted. (Repro­ duced by permission of the American Heart Association, potential. However, it should be noted that the H­ Inc. from Damato, A. N . et al. "A Study of Atrioventricular y time of this third beat is markedly shortened com­ Conduction in Man Using Premature Atrial Stimul ation and pared to the H-V time seen during sinus beats. Both His Bundle Recordings." Circulation 40:64, 1969) . of the previous records can be interpreted as ven­ tricular beats arising in the proximal portion of the tial would appear before the QRS with a shortened right or left bundle branch which are simultaneously H-V time. conducted antegrade to the ventricular myocardium Just such recordings have been made in our and retrograde to the His bundle. Under these clinical laboratory by N arula et al. (5). Figure 5 circumstances the QRS would be aberrant and if one shows a simultaneous recording of His bundle and were only recording His bundle activity, this poten- left bundle activity during sinus rhythm in a patient 36 SCHERLAG: GOUAUX-ASHMAN PHENOMENON A B i ' ·:'I •" ,\ AH Ii A j v A i :v ~ H:/i:v :, ~ii_____ w~!,..v----1!.J ·:,r BE1Hb)-~r----~'v.----~.)l ' i~ { : ::( :i I P-R = 190 msec P-Rl= 175 msec ' i P-R = 135 msoc l,.il1; P-A = I 50 m1ec P-A = 50 m1ec . , ! : I P-A = 50 m ..c , A-H = 90 msec A-H = 90 msec ' i i I ..:.:, . == 9~ .:::~ , ~ H-V = 50 msec H-V = 35 msec · F : . F , ! i L-1 -------/\..... - t-~t=-ls I I """i'""""'""""""""'""""I~: i _,,,.--...__ __..... ..._J aVF v c L-1 : I : aVF i , 107 IJS Fig. 2- The effect of fusion beats on the H-V interval in a patient with intermittent ventricular ectopic beats. Traces from above: Bipolar His bundle electrogram (BE, Hb) and 3 simultaneously recorded ECG leads I, A VF, and Y1. A. During sinus beats, the P-R of 190 msec was composed of intra-atrial conduction time (P-A = 50 msec). A-V nodal conduction (A-H) = 90 msec and His-Purkinje conduction (H-V) = 50 msec. A fusion beat (F) caused a shortening of the "P-R" to 175 msec entirely due to H-V diminution of 15 msec (50-35 msec). The vertical dotted line indicates the earliest ventricular activation in all leads. B. Another fusion beat (2nd complex marked F) causes a further shortening of the P-R to 135 msec and a reversal of the H-V with the onset of ventricular activa­ tion preceding His bundle activation by 5 msec. C. Another fusion beat (F) produced "normalization" of the QRS complex as com­ pared to other beats. Note that the shortening of the P-R in each case is matched exactly by the alteration in H-V or V-H time; the P-A and A-H interval remain constant throughout.
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