editorial his bundle electrograms - hearteditorial british heartjournal, i971, 33, 633-638. his...

Editorial

British HeartJournal, I971, 33, 633-638.

His bundle electrograms

Charles S. Smithen' and Edgar Sowton

Since the recording of the first human electro-cardiogram by Wailer in I889 the science ofelectrocardiography has developed and ad-vanced rapidly, but has been limited by theinability to record electrical activity fromspecialized areas of the heart. A significantcontribution was made by Alanis, Gonzailez,and L6pez in 1958 when they recorded Hisbundle potentials in the isolated perfuseddog heart using fine needle electrodes placedalong the atrioventricular groove. The firstHis potentials to be recorded in humanswere described by Giraud, Puech, andLatour (i960), and later by Watson, Emslie-Smith, and Lowe (I967). However, it was leftto Scherlag and associates (I969) to develop asimple and safe electrode catheter techniquefor the consistent recording of electrical po-tentials from the His bundle site in man. Thistechnique was later extended to the recordingof atrioventricular nodal and right bundle-branch potentials (Damato et al., i969a) andhas resulted in an extensive investigation ofthe specialized conduction tissue in normaland abnormal circumstances. As a result cer-tain age-old concepts have now been provedcorrect or have had to be modified, and in par-ticular the traditional criteria for interpreta-tion of many dysrhythmias have been shownto be inadequate.

Catheter techniqueIn order to record the His bundle potential a bi-polar or multipolar electrode catheter is intro-duced percutaneously into the femoral vein andunder fluoroscopic control positioned across thetricuspid valve into the right ventricle. Theproximal terminals of the electrode catheter areattached to an electrocardiograph amplifier andused either as a unipolar or bipolar system. Hisbundle activity is best recorded at high frequencysettings of 4O to 5OO cps at a paper speed of ioo or200 mm/second. The position of the recordingelectrode is then adjusted until it is stable at the

1 Address: Department of Cardiology, Guy's Hospital,London.

1

base of the atrial septum in the middle of the tri-cuspid valve area where a sharp rapid biphasicor triphasic deflection should appear between theP and QRS complexes of a standard electrocardio-gram recorded simultaneously. The recording ofthis His potential is safe and is usually obtainedabout 5 minutes after the catheter is placed in thefemoral vein. The P-His interval, measured fromthe beginning of the P wave to the beginning ofthe His potential, represents conduction throughthe atrium and atrioventricular node; and theHis-Q interval, measured from the beginning ofthe His potential to the beginning of the QRScomplex, represents intraventricular conduction(Fig. i). The generally recognized normal valuesfor P-His interval are 80 to 140 msec and forHis-Q interval are 35 to 55 msec.

Validity of measurementAs there are several possible sites for recordingelectrical activity during the PR interval, proofthat this rapid deflection represents Hisbundle activity is imperative. By performingseveral interventions in isolated perfused doghearts, Alanis et al. (1958) were able to validatetheir measurements. Crushing of the SA noderesulted in His bundle activity followed byventricular activity without any correspond-ing atrial potential. Production of completeheart block resulted in atrial activity followedby a constantly related His potential with anindependent ventricular potential. Man-oeuvres such as atrial stimulation, vagalstimulation, acetylcholine and epinephrineinjection, or the production of asphyxiaappropriately modified the P-His intervalwithout affecting the His-Q interval.

In man validation of the His bundle poten-tial is more difficult. The position of the re-cording electrode is at the established ana-tomical position of the bundle of His. Duringseveral successive cardiac cycles the configura-tion of the potential should not vary signifi-cantly, and the distance from the P waveshould not vary by more than 5 msec. Thisconfiguration and relation to the P wave hasbeen validated by direct placement of the

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634 Smithen and Sowton

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H. B. E. *I*$# I

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'HF"<H I S-Q (45m sec)P-H I S (120m sec)

F I G. i A recording of His bundle activityin a normal subject. H.B.E. = His bundleelectrogram. Sinus rhythm at 8o beats/min ispresent. The P-His interval is 120 msec andthe His-Q interval is 45 msec. Paper speed isIOO mm/sec.

electrode on the His bundle during cardi-otomy under experimental conditions (Hoff-man et al., I960). However, in this catheterposition both atrioventricular nodal and rightbundle-branch activity may also be recorded.Atrioventricular nodal activity can be easilyidentified and differentiated from either thebundle of His or right bundle-branch poten-tials. It is of longer duration (up tO 50 msec),of lower amplitude, inscribed slowly, andoften with notching on the upstroke. Increas-ing the heart rate by atrial pacing results inprogressive prolongation of the P-His inter-val, the His-Q interval remaining constant(Damato and Lau, 1970). Though the P-atrio-ventricular nodal interval also increases withatrial pacing, the increase is only a fraction ofthe prolongation in the P-His interval. Thedistinction between right bundle-branch andHis bundle activity is more difficult. The

P-right bundle-branch interval is also pro-longed with atrial pacing. The right bundlepotential is normally about I0 msec in dura-tion and appears closer to the QRS complex,whereas the His potential is I5 to 20 msecin duration and appears closer to the P wave.However, if only one potential is recorded itis difficult to say for certain where it is re-corded from. Narula, Scherlag, and Samet(I97od), by pacing at the site of the electri-cal activity, were able to distinguish thesetwo potentials. Pacing the right bundle-branch resulted in left bundle-branch block,whereas pacing the bundle of His caused nochange in the QRS configuration. The pacingstimulus to QRS interval was the same as theHis-Q interval recorded during sinus rhythm.Thus, for absolute separation of the Hisbundle and right bundle-branch potentials,pacing at the recording site appears necessary.

Atrioventricular blockDuring the past few years it has becomeapparent largely from histological studies thatthe aetiology of complete atrioventricularblock is usually due to pathology in the mainbundle-branches rather than in the atrio-ventricular node (Lenegre, I964; Lepeschkin,I964). The electrocardiographic criteria forprecise location of the site of the lesion incomplete heart block have hitherto been un-reliable, but the recording of His bundleelectrograms now allows the cardiologist tomake an accurate assessment of the site ofthe block. In 86 per cent of one series (Narulaet al., I970c) the block was demonstrated tobe distal to the bundle of His, the P-Hisinterval being normal in all patients. In all I0patients studied by Damato and Lau (1970),the block was found to be in His-Purkinjesystem, atrioventricular nodal conductionbeing normal. In our own experience acquiredheart block appears to be almost uniformlydue to bundle-branch disease though onepatient with Ehlers-Danlos syndrome andcongenital heart block was found to have blockproximal to the bundle of His (Smithen andSowton, I971). It appears likely that congeni-tal heart block is frequently due to a defect inthe atrioventricular node.

His bundle recordings have been particu-larly useful in identifying mechanisms in thetwo types of second degree heart block.Mobitz Type I block (Wenckebach) is charac-terized by a progressive prolongation in thePR interval until there is a non-conducted Pwave. His bundle records show that thisdysrhythmia, either spontaneous or producedexperimentally by atrial pacing, is usually dueto block in the atrioventricular node and that



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His bundle electrograms 635

intraventricular conduction is normal (Da-matoetal., I969c; Narulaetal., I970a). MobitzType II block is characterized by a constantPR interval with periodic non-conducted Pwaves. It usually occurs with bundle-branchblock but sometimes with a narrow QRS com-plex. The clinical observations of Langendorfand Pick (I968), and the experimental obser-vations of Watanabe and Dreifus (I967), sug-gest that Type II block represents bilateralbundle-branch disease. His bundle electro-grams have confirmed that in cases of MobitzType II with bundle-branch block, the siteof block is distal to the His bundle, the atrio-ventricular nodal conduction being entirelynormal (Narula and Samet, I970). In Mo-bitz Type II block with narrow QRS thesite of block may be either in the atrio-ventricular node, bundle of His, or thebundle-branches.Not all cases fit this simple concept, and

Narula and Samet (I970) described two casesof Mobitz Type I block with normal atrio-ventricular nodal conduction and block in theHis-Purkinje system. They suggested that thedistinction in the second degree blocks shouldbe made on the basis of the site of block suchas nodal or His-Purkinje system rather thanMobitz Type I or Type II. From a clinicalpoint of view, this is extremely important forit is the blocks in the His-Purkinje systemthat seem to advance to complete heart blockand not those in the atrioventricular node.The site ofheart block in patients with acute

myocardial infarction was recently studied byRosen and associates (197ob). In patients withdiaphragmatic myocardial infarctions, theblock was found to be proximal to the Hispotential, while in anterior myocardial infarc-tions the block was distal. Since go per centof the time the right coronary artery suppliesthe atrioventricular node, it is not surprisingto find that the block occurring with diaphrag-matic infarcts, usually due to right coronary

artery occlusion, is in the atrioventricular node.Rosen's findings confirm the view that heartblock following acute anterior infarction isdue to bundle-branch disease. The differencein clinical behaviour between heart block inanterior and diaphragmatic infarctions canthus be explained by the different anatomicalsite of the lesion.A very fascinating case of what appears to

be second degree atrioventricular block on astandard electrocardiogram was reported byRosen, Rahimtoola, and Gunnar (1970c).His bundle electrograms revealed that theapparent block was due to multiple non-propagated premature His bundle depolariza-tions with concealed conduction in the atrio-ventricular junction. The authors called thisdysrhythmia pseudo-atrioventricular blockbecause there was no evidence of an intrinsicconduction abnormality.

DysrhythmiasThe interpretation of certain dysrhythmiasmay be considerably aided by the use ofbundle of His electrograms. The zone of con-cealment in both atrial fibrillation and flutterhas been found to be proximal to the bundleof His (Lau et al., I969). Of more importancefrom a therapeutic point of view is the dis-tinction between aberrantly conducted andventricular ectopic beats. The electrocardio-graphic criteria suggested by Marriott andSandler (I966) may be extremely misleadingparticularly in the absence of P waves asoccurs in atrial fibrillation. A His bundlerecording will conveniently allow this distinc-tion because ventricular ectopics will not bepreceded by a His deflection whereas aberrantbeats will, the His-Q interval being the sameas for the normal complexes. Recently apatient presented to us with atrial fibrillation,on large doses of digitalis. The standard elec-trocardiogram (Fig. 2) revealed several wideQRS complexes which were felt to be ven-

FIG. 2 Rhythm strip (lead VI) of a patient with coronary artery disease taking digitalis(see text). Atrial fibrillation is present. The wide QRS complexes were interpreted as ven-tricular ectopic beats, but aberrantly conducted supraventricular complexes could not be excluded.



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tricular ectopics, and the clinical impressionwas that of digitalis toxicity. However, a Hisbundle electrogram revealed that each wideQRS complex was preceded by a His poten-tial and the His-Q interval was the same in allcomplexes (Fig. 3). Because of this, digitaliswas continued rather than stopped, diureticswere introduced, and shortly thereafter theaberrant beats disappeared.The distinction between supraventricular

tachycardia with aberration and ventriculartachycardia can also be different. His bundlerecording can be of value in this situation byrecording His potentials in front of QRScomplexes in supraventricular dysrhythmiasand not in ventricular dysrhythmias.By recording from the specialized conduc-

tion system, Damato and Lau (I969) havebeen able to show that middle and low 'nodal'rhythms usually arise from the bundle of His.During these 'His bundle rhythms', a singleHis deflection and no nodal deflection pre-cedes each QRS complex. The His-Q intervalduring tachycardia is the same as that duringsinus rhythm. Retrograde conduction fromthe His bundle through the atrioventricularnode to the atrium has been shown, and insome cases nodal and His activity are inde-pendent of each other, while His and ventricu-lar deflections have a constant relation.

Paroxysmal supraventricular tachycardiahas been shown recently to be usually causedby re-entry in the atrioventricular conductionsystem (Bigger and Goldreyer, I970; Gettesand Yoshonis, 1970). The site of re-entry was

studied by Goldreyer and Bigger (I97I) in 5patients with episodes of paroxysmal supra-ventricular tachycardia. In all 5 patients Hisbundle potentials were recorded during tachy-cardia. Every episode of tachycardia wasinitiated by an atrial premature depolarizationwith prolonged conduction from atrium toHis bundle. However, in 2 patients a pre-mature depolarization induced supraventricu-lar tachycardia but failed to propagate acrossthe entire atrioventricular node to stimulatethe bundle of His. Since His bundle depolar-ization was not required for supraventriculartachycardia initiation, it can be inferred thatthe site of re-entry in these patients waswithin the atrioventricular node.

His bundle electrograms have proved usefulin the study of the genesis of Wolff-Parkinson-White syndrome. In 2 cases, Castellanos andco-workers (1970) were able to show ventricu-lar activation which preceded a His potential,suggesting that ventricular pre-excitation wasdue to a bypass of the His bundle. The samegroup also demonstrated that during supra-ventricular tachycardia in Wolff-Parkinson-White syndrome antegrade conduction con-sistently occurred through the His bundlewhereas retrograde conduction did not (Cas-tillo and Castellanos, I970). They concludedthat the reciprocating tachycardias in thissyndrome were probably a result of two separ-ate anatomical communications, but re-entrywithin the atrioventricular node was notexcluded.

FIG. 3 His bundle recording during the rhythm seen in Fig. 2. A His bundle potentialprecedes each QRS complex regardless of configuration. The His-Q interval is 50 msec. Thesecond andfourth complexes are normally conducted and the first and third complexes areabnormal. Paper speed is IOO mm/sec (see text).

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His bundle electrograms 637

Drug studiesOne of the more important applications ofHis bundle electrograms has been the study ofthe effect of certain cardiac drugs on atrio-ventricular conduction in man. With thistechnique it has been possible to show thatisoprenaline and atropine shorten atrioventri-cular nodal conduction (Damato et al., I969b)and digitalis prolongs it (Damato and Lau,I970). None of these drugs affect intraven-tricular conduction. We studied the effect ofcertain beta-adrenergic blocking agents onatrioventricular conduction using bundle ofHis recordings (Smithen, Balcon, and Sowton,I97I). Propranolol, in doses within the knowntherapeutic range, produced a significantincrease in atrioventricular nodal conductionof up tO I7 per cent without affecting intra-ventricular conduction. Dextropropranololproduced a much smaller but still statisticallysignificant change in the P-His interval with-out affecting the His-Q interval and practololproduced no significant effect on either inter-val in the doses used.The effects of lignocaine and procainamide

on atrioventricular conduction have beenstudied by Rosen et al. (I97oa). In the usualclinical doses lignocaine had no effect onatrioventricular and intraventricular conduc-tion whereas procainamide usually prolongedboth these intervals.

Future developmentsThough a great deal of information hasalready been obtained, application of thistechnique will help solve new problems in thefuture. The recording of left bundle-branchpotentials (Narula et al., 197ob; Lau, Bobb,and Damato, 1970) along with His bundle,atrioventricular node, and right bundle-branch potentials will provide better under-standing of the normal and abnormal activa-tion process. The problems of ventricular pre-

F excitation and re-entry mechanisms, and theeffect of new pharmacological agents on atrio-ventricular conduction can be studied. Inaddition to this type of information relatingto tachydysrhythmias, there are several ques-tions concerning slow rhythms under activeinvestigation. Do patients with sinus nodedisease have abnormalities of atrioventricularor intraventricular conduction? Do patientswith bundle-branch block have conductiondefects in the other bundle-branch ? Will it bepossible to predict which patients with bi-lateral bundle-branch disease will developcomplete heart block and when?The answers to these and other questions

will undoubtedly make the recording of His

bundle electrograms in man one of the mostuseful tools to become available to cardio-logical investigators and clinicians in recentyears.

ReferencesAlanis, J., Gonzilez, H., and L6pez, E. (I958). The

electrical activity of the bundle of His. J7ournal ofPhysiology, 142, 127.

Bigger, J. T., Jr., and Goldreyer, B. N. (I970). Themechanism of supraventricular tachycardia. Circu-lation, 42, 673.

Castellanos, A., Jr., Chapunoff, E., Castillo, C., May-tin, 0., and Lemberg, L. (I970). His bundle elec-trograms in two cases of Wolff-Parkinson-White(pre-excitation) syndrome. Circulation, 41, 399.

Castillo, C. A., and Castellanos, A., Jr. (I970). Hisbundle recordings in patients with reciprocatingtachycardias and Wolff-Parkinson-White syndrome.Circulation, 42, 27I.

Damato, A. N., and Lau, S. H. (I969). His bundlerhythm. Circulation, 40, 527.

Damato, A. N., and Lau, S. H. (1970). Clinical valueof the electrogram of the conduction system. Pro-gress in Cardiovascular Disease, 13, II9.

Damato, A. N., Lau, S. H., Berkowitz, W. D., Rosen,K. M., and Lisi, K. R. (I969a). Recording ofspecialized conducting fibers (A-V nodal, Hisbundle, and right bundle branch) in man using anelectrode catheter technic. Circulation, 39, 435.

Damato, A. N., Lau, S. H., Helfant, R. H., Stein, E.,Berkowitz, W. D., and Cohen, S. I. (I969b). Studyof atrioventricular conduction in man using elec-trode catheter recordings of His bundle activity.Circulation, 39, 287.

Damato, A. N., Lau, S. H., Helfant, R., Stein, E.,Patton, R. D., Scherlag, B. J., and Berkowitz, W.D. (I969c). A study of heart block in man usingHis bundle recordings. Circulation, 39, 297.

Gettes, L. S., and Yoshonis, K. F. (I970). Rapidlyrecurring supraventricular tachycardia: a manifes-tation of reciprocating tachycardia and an indica-tion for propranolol therapy. Circulation, 41, 689.

Giraud, G., Puech, P., and Latour, H. (I960).L'activite electrique physiologique du noeud deTawara et du faisceau de His chez l'homme.Bulletin de l'Acadbmie Nationale de Midecine, I44,363.

Goldreyer, B. N., and Bigger, J. T., Jr. (I971). Siteof reentry in paroxysmal supraventricular tachy-cardia in man. Circulation, 43, I5.

Hoffman, B. F., Cranefield, P. F., Stuckey, J. H., andBagdonas, A. A. (I960). Electrical activity duringthe P-R interval. Circulation Research, 8, I200.

Langendorf, R., and Pick, A. (I968). Atrioventricularblock, type II (Mobitz) - Its nature and clinicalsignificance. Circulation, 38, 8I9.

Lau, S. H., Bobb, G. A., and Damato, A. N. (1970).Catheter recording and validation of left bundle-branch potentials in intact dogs. Circulation, 42,375.

Lau, S. H., Damato, A. N., Berkowitz, W. D., andPatton, R. D. (I969). A study of atrioventricularconduction in atrial fibrillation and flutter in manusing His bundle recordings. Circulation, 40, 7I.

Lenegre, J. (1964). Etiology and pathology of bilateralbundle-branch block in relation to complete heartblock. Progress in Cardiovascular Disease, 6, 409.

Lepeschkin, E. (I964). The electrocardiographic diag-nosis of bilateral bundle-branch block in relation toheart block. Progress in Cardiovascular Disease, 6,445.



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Marriott, H. J. L., and Sandler, I. A. (I966). Criteria,old and new, for differentiating between ectopicventricular beats and aberrant ventricular conduc-tion in the presence of atrial fibrillation. Progress inCardiovascular Disease, 9, i8.

Narula, 0. S., Cohen, L. S., Samet, P., Lister, J. W.,Scherlag, B., and Hildner, F. J. (197oa). Localiza-tion ofA-V conduction defects in man by recordingof the His bundle electrogram. American Journalof Cardiology, 25, 228.

Narula, 0. S., Javier, R. P., Samet, P., and Maramba,L. C. (I97ob). Significance of His and left bundlerecordings from the left heart in man. Circulation,42, 385.

Narula, 0. S., and Samet, P. (1970). Wenckebach andMobitz type II A-V block due to block within theHis bundle and bundle branches. Circulation, 41,947.

Narula, 0. S., Scherlag, B. J., Javier, R. P., Hildner,F. J., and Samet, P. (I970c). Analysis of the A-Vconduction defect in complete heart block utilizingHis bundle electrograms. Circulation, 41, 437.

Narula, 0. S., Scherlag, B. J., and Samet, P. (I97od).Pervenous pacing of the specialized conductingsystem in man: His bundle and A-V nodal stimu-lation. Circulation, 41, 77.

Rosen, K. M., Lau, S. H., Weiss, M. B., and Damato,A. N. (I97oa). The effect of lidocaine on atrioven-tricular and intraventricular conduction in man.American Journal of Cardiology, 25, I.

Rosen, K. M., Loeb, H. S., Chuquimia, R., Sinno,M. Z., Rahimtoola, S. H., and Gunnar, R. M.(I97ob). Site of heart block in acute myocardialinfarction. Circulation, 42, 925.

Rosen, K. M. Rahimtoola, S. H., and Gunnar, R. M.(I970c). Pseudo A-V block secondary to prematurenonpropagated His bundle depolarizations: docu-mentation by His bundle electrocardiography.Circulation, 42, 367.

Scherlag, B. J., Lau, S. H., Helfant, R. H., Berkowitz,W. D., Stein, E., and Damato, A. N. (I969).Catheter technique for recording His bundleactivity in man. Circulation, 39, 13.

Smithen, C. S., Balcon, R., and Sowton, E. (I97I).Use of bundle of His potentials to assess changes inatrioventricular conduction produced by a seriesof beta-adrenergic blocking agents. British HeartJournal. In the press.

Smithen, C., and Sowton, E. (I97I). Analysis ofheart block and arrhythmias by bundle of Hiselectrograms. In Proceedings ofthe British CardiacSociety. British Heart Journal, 33, 607.

Watanabe, Y., and Dreifus, L. S. (1967). Seconddegree atrioventricular block. Cardiovascular Re-search, I, I50.

Watson, H., Emslie-Smith, D., and Lowe, K. G.(I967). The intracardiac electrocardiogram ofhuman atrioventricular conducting tissue. AmericanHeart Journal, 74, 66.



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