sign in sign up
<<
Home , Atrioventricular block, Heart block

Br J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

British Heart journal, I973, 35, I154-1I60. Cardiac pacing in incomplete with atrial

D. S. Reid, S. J. Jachuck, and C. B. Henderson From the Department of , Newcastle General Hospital, Newcastle upon Tyne

Three cases with a slow irregular ventricular response to atrialfibrillation, who benefitedfrom cardiac pacing, are described; two had ischaemic heart disease, and one had . In thefirst case the slow ventricu- lar response to atrialfibrillation was a result of incomplete atrioventricular nodal block, and in the other two His bundle electrograms demonstrated that the slow ventricular response was due to bilateral bundle-branch block. The association of and conduction delays in the and bundle- branches is discussed. The value of His bundle recordings in the investigation of these cases is shown and the importance of cardiac pacing in treatment is stressed.

Cardiac pacing is now a generally accepted method . Intravenous given before transfer of treatment in patients with complete or had resulted in a paroxysm of ventricular . bilateral bundle-branch block who have Adam- On admission there was no evidence of cardiac failure Stokes attacks or a low output to and the blood pressure was I05/50 mmHg. An electro- syndrome leading cardiogram showed atrial fibrillation with an irregular or cardiac failure. cardiac is However, pacing ventricular response of 40 to 44 beats a minute and acute now also becoming more widely used in the treat- inferolateral myocardial (Fig. i). ment of patients with disease ('sick Over the subsequent three days the ventricular rate sinus syndrome') who have disabling symptoms fell to 30 beats a minute and he developed cardiac fail- to or non-responsive atropine the sympathomimetic ure, hypotension, and oliguria. A slow infusion of iso- http://heart.bmj.com/ drugs (Bayley, I97I; Easley and Goldstein, I97I; prenaline resulted in which re- Cheng, I968). In some patients with sinus node verted to atrial fibrillation with a single DC shock. disease the sinus or is Transvenous demand cardiac pacing was started and associated with rapid supraventricular over the next 5 days he gradually improved. The pacemaker was removed on the ioth day at including atrial fibrillation with a rapid ventricular which time he was in atrial fibrillation with a ventricular response - the bradycardia-tachycardia syndrome rate of go beats a minute (Fig. 2), and there was no evi- (Schulman et al., I970). Atrial fibrillation with a dence of cardiac failure. On discharge 5 weeks after slow ventricular rate is not a generally accepted

admission and when seen 3 months later, he was well on October 1, 2021 by guest. Protected copyright. feature of this syndrome, though Ferrer (I968) but in atrial fibrillation with a ventricular rate of 8o to go included this in her definition, unless drugs affecting beats/minute. atrioventricular nodal conduction have been given as in one of the cases described by Bayley (I97I). Case 2 To our knowledge there has been no report of who have for atrial fibrilla- A 7i-year-old man was admitted with a one-year history patients requlired pacing of exertional chest pain and occasional . In the tion with a slow irregular ventricular response and week before admission syncope had occurred daily and it is the purpose of this paper to report 3 such he had become breathless on effort. patients. Examination revealed mild cardiac failure, left ven- tricular hypertrophy, a blood pressure of I50/80 mmHg, Case reports and a slow irregular pulse. An electrocardiogram showed atrial fibrillation with an Case I irregular ventricular response of 50 beats a minute, com- A 69-year-old man who had sustained an acute myo- plete right bundle-branch block, a mean frontal QRS cardial infarction 24 hours previously was transferred to axis to the left with an initial vector directed inferiorly this hospital because of a slow associated with suggesting left anterior hemiblock (Fig. 3). A chest x-ray Received I4 May I973. showed a cardiothoracic ratio of 6o per cent and promi- Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

Cardiac pacing in incomplete atrioventricular block with atrial fibrillation 155

aVR

*...... 'n aVL

M.' aVF

......

VI......

V4

.....^...... l,l

V7 http://heart.bmj.com/ FIG...... ~~~~~~~~~~~~~~~~~~~~~~.I Case i. Electrocardiogram 24 hours after .

I n II oVaR aVL aVF on October 1, 2021 by guest. Protected copyright.

VI V2 V3 V4 VS V6 V7

V3 ; days a m infart

FIG. 2 Case I. Electrocardiogram I4 days after myocardial infarction. Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

II56 Reid, Jachuck, and Henderson

I II HI aVR oV L oVF

V4R VA VS V6 V7 V2

V4 V3

I

FIG . 2. 3 Case Electrocardiogram showing atrial fibrillation, complete right bundle-branch http://heart.bmj.com/ block, and left anterior hemiblock. nence of the upper lobe veins. Shortly after admission (Fig. 4b). Sudden cessation of ventricular pacing was the heart rate fell to between 6 and 20 beats/minute and followed by a period of ventricular during which he became pale and confused, but recovered spon- His potentials were present in the His bundle electro- taneously. An infusion was started but this cardiogram. As the standard electrocardiogram showed resulted in frequent ventricular extrasystoles without right bundle-branch block and left anterior hemiblock any increase in heart rate. A temporary pacemaker was these findings indicate second-degree block Mobitz II on October 1, 2021 by guest. Protected copyright. inserted and in the subsequent 2 days the heart rate and 2: i block in the posterior division of the left bundle, increased and remained at 6o to go beats/minute. The these findings being concealed in the standard electro- pacemaker was therefore removed after I2 days and the cardiogram by the presence of atrial fibrillation. patient was discharged. However, one month later he A permanent demand pacemaker was implanted and had a recurrence of syncope and he was readmitted. in the 12 months follow-up he has had no further Electrophysiological studies were carried out on this syncopal episodes and there has been no evidence of admission at the time of insertion of the permanent cardiac failure. transvenous pacing electrode. The technique for record- ing His bundle electrograms was essentially the same as that described by Scherlag et al. (I969). All recordings Case 3 were made with the frequency response set at 40-500 A 68-year-old woman was first admitted to another cycles/second and a paper speed of Ioo mmsec. The HV hospital in January i969 after a syncopal episode. She time was measured from the onset of the His bundle had a short history of chest tightness on effort but no deflection to the earliest ventricular deflection (normal other symptoms of heart disease. On examination the 35-55 msec). blood pressure was i60/go mmHg, pulse was irregular The HV time was normal in the conducted beats (40 at 46 beats a minute, and there was no evidence of heart msec) but there was intermittent block distal to the failure. Electrocardiograms showed 2:i and 3:I sino- (Fig. 4a) and at times 2: i post H block atrial block with a junctional escape rhythm, at times Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

Cardiac pacing in incomplete atrioventricular block with atrial fibrillation 13157

Lead II

I N.1 H V .j

1.. Lead r- ____j .:

Load II ~

HB8E-? NIV HVNN

LeadI ______

FIG. 4 Case 2. His bundle electrogram recorded at ioo mm/sec with simultaneous leads I and II (a) Irregular His response to atrial fibrillation and Mobitz II post H block. HV normal in conducted beats (40 msec). (b) 2:i block distal to bundle of His. HBE=His bundle recording; = V = ventricular H His bundle electrogram; electrogram. http://heart.bmj.com/ with retrogijade P waves (Fig. 5a). Chest x-ray showed A His bundle electrogram (Fig. 6) demonstrated a cardiac enlargement. She had no further syncopal epi- prolonged HV time (6o msec) in the conducted beats and sodes and within 2 days the was resumed variable post H block; at times 2: post H block at other with a normal PR interval (o1i8 sec) and complete left times post H block without prolongation of the HV timne bundle-branch block (Fig. 5b). in the preceding beats as is usual in Mobitz type II In July 1971 she was admitted to the same hospital second-degree block (Narula and Samet, 1970). with .cardiac failure. Electrocardiograms on this admis- A Devices permanent demand pacemaker was inserted, sion showed atrial fibrillation with an irregular ventricu- and in the 6 months after this there has been no clinical on October 1, 2021 by guest. Protected copyright. lar response of ioo beats/min and complete left bundle- evidence of . branch block. She was treated with and diuretics and improved to some extent. Discussion She was initially seen at this hospital in November I972 because of breathlessness on minimal effort that The drug resistant which require had persisted since July 197i. The digoxin had been cardiac pacing usually fall into two groups. In the stopped several months before this admission because of first group the bradycardia is due to atrioventricular a slow ventricular rate and isoprenaline had been given node, His bundie, or bilateral bundle-branch disease in a dose of 6o mg 8-hourly without any improvement mn resulting in a slow but regular idioventricular or the symptoms or heart rate. Examination showed that even in the presence of atrial there was cardiac failure and the heart rhythm was fibrillation. In the other group, the bradycardia is irregular with a rate Of 43 beats a minute. There was left due to sinoatrial node disease sinus and an mur- causing brady- ventricu.lar hypertrophy apical pansystolic or of This mur. An electrocardiogram showed atrial fibrillation cardia varying degrees sinoatrial block. with a slow irregular ventricular response and complete second group may be associated with atrial fibrilla- left bundle-branch block (Fig. 5c). X-ray showed a tion in which the ventricular response is rapid and cardiothoracic ratio Of 75 per cent. irregular. The 3 cases reported do not fall clearly Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from nI58 Reid, Jachuck, and Henderson

(a)

VI

VI

aVF pi Pi

(b) I lI III aVoVR oV L aVF

vI V2 V3 V4 VY5 Vb

(ci http://heart.bmj.com/

V2 on October 1, 2021 by guest. Protected copyright.

Vb

FIG. 5 Case 3. (a) I7-I8January I969. V1 2:I to 3:I SA block, AVdissociation. aVF-A V dissociation due to slow atrial rate with retrograde P waves (P1) and a capture beat (arrows indicate P waves). (b) x9 January I969. Sinus rhythm and complete left bundle-branch block. (c) November I972. Atrial fibrillation with a slow ventricular rate. Left bundle-branch block. Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

Cardiac pacing in incomplete atrioventricular block with atrial fibrillation 1159

(a)

IH Yv H H: v H H v HBE _w~ ?.i.

Lead I _

Lead II

(b) H V H V H H V

- --J- I -.L %p ,. HBE -Y-- VWT

Lead I *- _ e-

Lead II

FIG. 6 Case 3. His bundle electrogram. (a) 2:I post H block. (b) HV prolonged in con- ducted beats (6o msec) Mobitz II second-degree block. into either group, as the atrial fibrillation was ventricular nodal ischaemia leading to incomplete associated with a slow but irregular ventricular atrioventricular nodal block and thus a slow irregu- http://heart.bmj.com/ response. This suggests that there may be a third lar ventricular response to atrial fibrillation. group of patients that may require cardiac pacing in In the second patient ischaemic heart disease was which the mechanism of production of the brady- also the probable basic aetiology of the . cardia is different from the above groups. The atrial fibrillation in this case could, therefore, be In the first case the bradycardia followed an a manifestation of sinoatrial node disease though this acute inferior transmural myocardial infarction. The is difficult to prove in established atrial fibrillation artery to the sinoatrial node arises from the proximal by electrophysiological studies such as atrial pacing part of the right coronary artery in 55 to 65 per cent (Mandel et al., 197I; Narula, Samet, and Javier, on October 1, 2021 by guest. Protected copyright. of the population (James, I96I; Kennel and Titus, I972). The cause of the slow irregular ventricular I972a). It, therefore, seems likely that the mechan- response to the atrial fibrillation, however, was ism of production of the atrial fibrillation was clearly demonstrated as bilateral bundle-branch proximal right coronary artery occlusion resulting block. Thus the arrhythmia in this case was due to a in sinoatrial node ischaemia or infarction. However, combination of atrial disease and bilateral bundle- it has also been suggested that atrial fibrillation in branch block. myocardial infarction may be due to raised left The underlying cause of the arrhythmia in the atrial pressure secondary to left ventricular failure third patient has not been established. The brief (Lown, Kosowsky, and Klein, I969). It seems un- history of chest tightness on effort may indicate that likely that this was the cause in this patient as the was the underlying cause atrial fibrillation preceded the onset of left ventricu- though anginal-type pain can occur in patients with lar failure. It has also been shown that the right slow heart rates without ischaemic heart disease coronary artery supplies the artery to the atrio- (Harris et al., I969). ventricular node in 83 to go per cent of the popula- Cardiomyopathy, therefore, seems a more likely tion (James, I96I; Kennel and Titus, I972b). Thus explanation of the cardiac failure and arrhythmia in right coronary occlusion could result in atrio- the absence of any clear evidence of ischaemic, Br Heart J: first published as 10.1136/hrt.35.11.1154 on 1 November 1973. Downloaded from

II6o Reid, Jachuck, and Henderson rheumatic, or hypertensive heart disease. The References initial electrocardiograms demonstrated the pre- Bayley, T. J. (197I). Long-term ventricular pacing in the sence of sinoatrial block suggesting that the atrial treatment of sino-atrial block. British Medical Journal, 3, 456. fibrillation was the result of sinus node disease. The Berkowitz, W. D., Lau, S. H., Patton, R. D., Rosen, K. M., His electrogram showed prolongation ofthe HV time and Damato, A. N. (I97I). The use of His bundle record- in the conducted beats and though this has been ings in the analysis of unilateral and bilateral bundle described in patients with left bundle-branch block branch block. American Heart Journal, 81, 340. Cheng, T. 0. (I968). Transvenous ventricular pacing in the (Berkowitz et al., I97I; Haft et al., 197I), the pre- treatment of paroxysmal atrial tachyarrhythmias alterna- sence of Mobitz type II second-degree block and ting with and standstill. American 2: I post H block confirmed the presence of a con- J'ournal of Cardiology, 22, 874. duction defect in the bundle-branch. Easley, R. M., and Goldstein, S. (I97I). Sino-atrial syncope. right Thus the AmericanJournal of Medicine, 50, I66. bradycardia in this patient, as in the second patient, Ferrer, M. I. (I968). The sick sinus syndrome in atrial disease. was due to the combination of sinoatrial node Journal of the American Medical Association, 2o6, 645. disease and bilateral bundle-branch block, the bi- Haft, J. I., Weinstock, M., DeGuia, R., Gupta, P. K., and lateral bundle-branch block in both these Fano, A. (197i). Assessment of atrio-ventricular conduc- patients tion in left and right using His being concealed in the standard electrocardiogram bundle electrograms and atrial pacing. American Journal by the presence of atrial fibrillation. of Cardiology, 27, 474. The combination of sinoatrial node disease Harris, A., Davies, M., Redwood, D., Leatham, A., and and Siddons, H. (i969). Aetiology of chronic heart block. A disease in the atrioventricular node and bundle- clinico-pathological correlation in 65 cases. British Heart branches has been recorded previously. That it may 'ournal, 31, 206. be more common than is realized was shown by James, T. N. (i96i). Anatomy of the Coronary Arteries. Paul Rosen and his colleagues (1971) who demonstrated, Hoeber, New York. Kennel, A. J., and Titus, J. L. (I972a). The vasculature of the by His bundle electrograms, conduction defects in 8 human sinus node. Mayo Clinic Proceedings, 47, 556. of I5 patients with symptomatic sinus node disease. Kennel, A. J., and Titus, J. L. (1972b). The vasculature of the They concluded, however, that in their experience human atrioventricular conduction system. Mayo Clinic conduction defects in patients with sinoatrial node Proceedings, 47, 562. Lown, B., Kosowsky, B. D., and Klein, M. D. (I969). Patho- disease did not appear to be serious. More recently, genesis, prevention and treatment of arrhythmias in myo- Rubenstein et al. (I972) showed that 33 of their 56 cardial infarction. Circulation, 39, Suppl. IV, 26I. patients with sick sinus syndrome had evidence of a Mandel, W., Hayakawa, H., Danzig, R., and Marcus, H. S. conduction disturbance in the atrioventricular node (I97i). Evaluation of sino-atrial node function in man by overdrive suppression. Circulation, 44, 59. or in the bundle-branches though none of their Narula, 0. S., and Samet, P. (I970). Wenckebach and Mobitz http://heart.bmj.com/ patients had second or third-degree block. Our three type II A-V block due to block within the His bundle and patients show that sinus node disease may be . Circulation, 41, 947. associated with serious conduction disturbances in Narula, 0. S., Samet, P., and Javier, R. P. (I972). Significance of the sinus-node recovery time. Circulation, 45, 140. the atrioventricular node or bundle-branches, and Rosen, K. M., Loeb, H. S., Sinno, M. Z., Rahimtoola, S. H., that His bundle electrograms may be necessary to and Gunner, R. W. (I97I). Cardiac conduction in patients demonstrate the severity of the conduction disturb- with symptomatic sinus node disease. Circulation, 43, 836. ance in the presence of slow atrial fibrillation. The Rubenstein, J. L., Schulman, C. L., Yurchak, P. M., and importance of demonstrating this association is DeSanctis, R. W. (I972). Clinical spectrum of the sick sinus syndrome. Circulation, 46, 5. on October 1, 2021 by guest. Protected copyright. shown by the fact that these patients did not im- Scherlag, B. J., Lau, S. H., Helfant, R. H., Berkowitz, W. D., prove when treated with digoxin, isoprenaline, and Stein, E., and Damato, A. N. (i969). Catheter technique for atropine, but responded dramatically to ventricular recording His bundle activity in man. Circulation, 39, I3. Schulman, C. L., Rubenstein, J. J., Yurchak, P. M., and pacing. Thus patients who have a slow ventricular DeSanctis, R. W. (1970). The sick sinus syndrome clinical response to atrial fibrillation and who have dizzi- spectrum. Circulation, 4I and 42, Suppl. III, 42. ness, syncope, cardiac failure, or angina may not Requests for reprints to Dr. D. S. Reid, Department of respond to drug therapy but improve if permanent Cardiology, Newcastle General Hospital, Westgate ventricular pacing is instituted. Road, Newcastle upon Tyne NE4 6BE.