Syncope and cerebral dysfunction caused by bradycardia without atrioventricular block

Syncope and cerebral bradycardia without

dysfunction atrioventricular

caused by block

Noble 0. Fowler, M.D.” John C. Fenton, M.D.“” Gene F. Conway, M.D.““* Cincinnati, Ohio

S

yncope associated with a disorder of the heartbeat may result from a number of mechanisms. Although complete A-V block with excessive ventricular slowing, ventricular tachycardia, or ventricular fibrillation is regarded as the most common variety of cardiac syncope,l several other possibilities must be considered. Syncope may result from paroxysmal ventricular fibrillation, ventricular tachycardia, or supraventricular tachycardia in the absence of associated A-V block.2 Syncope may also occur when there is a supraventricular mechanism responsible for ventricular slowing, such as sinus bradycardia, S-A block, or sinus arrest. Shillingford and Thomas3 described sinus bradycardia in 20 per cent of patients with acute cardiac infarction. When the heart rate was 50 to 60 per minute, the bradycardia was of little clinical significance. When the heart rate was 25 to 40 per minute, the patient might have a fall in cardiac

output and blood pressure, with associated weakness, nausea, and syncope. In the surviving patients, the arrhythmia lasted only a few days. On the other hand, there have been relatively few reports of patients with chronic atria1 bradycardia and syncope. Persistent chronic sinoatrial bradycardia, unrelated to drugs or metabolic disorders, may be a cause of weakness, fatigue, synincapacity. In this cope, and relative setting, syncope may result from cardiac slowing or standstill or from a complicating paroxysmal tachyarrhythmia. Electronic cardiac pacing is a satisfactory form of treatment. It is the purpose of this paper to describe six patients who had symptomatic chronic sinoatrial bradycardia, five of whom had recurrent attacks of syncope. Second- or third-degree A-V block was not documented in any of these patients. Five of these patients were treated satisfactorily with cardiac electronic pacing.

From

the Cardiac Research Laboratory, Department of Internal Medicine, University of Cincinnati College of Medicine, and Cardiology Section, Veterans Administration Hospital, Cincinnati, Ohio. Supported in part by United States Public Health Service Grants HE-06307. HE-5445, and HE-5776. Received for publication Sept. 15, 1969. Reprint requests to: Dr. Noble 0. Fowler. Cardiac Research Laboralory; Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229. “Professor of Medicine, University of Cincinnati Medical School, and Director of Cardiac Research Laboratory, Cincinnati General Hospital, Cincinnati, Ohio. **Assistant Professor of Medicine, University of Cincinnati Medical School, and Director of Cardiology, Christ Hospital, Cincinnati, Ohio. **Associate Professor of Medicine. University of Cincinnati Medical School, and Chief of Cardiology. Veterans Administration Hospital, Cincinnati, Ohio.

Vol.

80, No. 3, pa. 303-312

Septenaber,

1970

Amerisan

Heart

Journal

303

Fig. 1. Patient sinus arrhythmia.

1, P. S. Electrocardiographic

Lead

l L made

Case reports Patient 1. P. S., a 77-year-old woman, w~as admitted to Memorial Hospital, Sarasota, Fla., on Oct. 28, 1966, because of syncopal attacks for the preceding four years. There was no history of previous heart disease. Hypertension had been present for five years. Her only medication was reserpine. On examination, there were no cardiac murmurs. A chest roentgenogram was normal. The serum protein-bound iodine (PBI) was 5 fig per 100 ml. An electrocardiogram showed sinus arrhythmia with occasional sinus pauses and a P-R interval of 0.28 sec. (Fig. 1). The P wave was broad and notched. On October 30, the patient collapsed while using the bedpan; the cardiac monitor showed the heart rate as slow as 20 per minute with sinus arrest and nodal or ventricular escape rhythm. Reserpine was discontinued. Two weeks later she developed atria1 fibrillation, followed by a return to sinus rhythm with long atria1 pauses. Reserpine was thought not responsible for her sinus pauses and slow atria1 mechanism. On November 23, an Atricor cardiac pacemaker was inserted. A day later she developed atria1 fibrillation with a ventricular rate of 120 per minute. She was given digitalis and quinidine, and sinus rhythm was restored. She was discharged from the hospital on Dec. 13, 1966. No electrocardiogram showed more than firstdegree A-V block and none suggested myocardial ischemia or infarction. In February, 1968, the patient remained free of syncope, and the electronic pacemaker was functioning satisfactorily. Patied 2. H. N., an 84.year-old man, was first examined on Jan. 3, 1969, when he was admitted to the Cincinnati Jewish Hospital because of chest pain. His personal physician had seen H. N. repeatedly since 1947. In 1951 he first complained of angina pectoris. An electrocardiogram of May 12, 1953, was normal. Syncope first occurred on July 24, 1954. On March 17, 195.5, an electrocardiogram showed sinus arrhythmia with periods of sinus bradycardia. The second attack of syncope occurred Aug. 27, 1957. Syncope occurred frequently between 1957 and 1964. The electrocardiogram continued to show sinus arrhythmia and bradycardia, and was otherwise normal. On July 31, 1964, he was hospitalized ‘oecause of syncope. Periods of atria1 and ventricular asystole of 2.5 seconds were observed on an elecfrocardiogram. A cardiac pacemaker was advised but

on Oct.

29, 1966,

showing

singes bradycardia

aml

refused by the patient. The patient tirst received digitalis in October, 1965, but did not receive digitalis later than 1966. An electrocardiogram of Feb. 3, 1966, demonstrated periods of sinus standstill and A-V nodal escape rhythm, with S-T segment and T-wave changes consistent with digitalis effects. On January 3, 1969, he was readmitted to the hospital with a diagnosis of coronary insufficiency. The electrocardiogram on January 6, 1969, showed evidence of anterolateral myocardial ischemia and a junctional pacemaker with a ventricular rate of 40 per minute. There was dissociated atria1 rhythm with an atria1 rate of 43 per minute. At no time did the patient’s electrocardiogram show evidence of atrioventricular block. The serum potassium was 4.5 mEq. per liter. The patient signed out of the hospital on Jan 7, 1969. Patient 3. M. J., a 6%year-old widow, was admitted to Christ Hospital, Cincinnati, Ohio, on Jan. 11, 1969. She was apparently well until 5 days before admission; during this period she had approximately 15 bouts of syncope. On the day of admission, Cardiac an episode was observed by her physician. arrest was present for approximately 10 seconds. Cardiac activity returned spontaneously with a ventricular rate of 50 per minute. The patient had been treated for hypertension since July, 1966, with chlorothiazide, 0.5 Gm., and reserpine, 0.25 mg. daily. She did not receive other drugs. Serum PBI was normal. An electrocardiogram in July, 1967, revea!ed interference A-V dissociation. In August, 1968, an electrocardiogram showed atria1 flutter with varying (2:i to 4:l) atrioventricular block. Physical examination on hospital admission was essentially normal. Reserpine was discontinued. Blood urea nitrogen (BUN) was normal; serum potassium was 3.1 mEq. per liter. She fainted 8 hours after admission; atria1 arrest and cardiac asystole of 10 seconds’ duration were observed on the cardiac monitoring oscilloscope. Isoproterenol, 0.5 to 1.0 pg per minute, was infused intravenously. During this period an A-V junctional pacemaker activated the ventricles at a rate of 52 per minute (Fig. 2). Syncope did not recur. On Jan. 14, 1969, because of repeated atria? arrest, a permanent pervenous demand right ventricular pacemaker was implanted (Fig. 3). Isoproterenol was

Volume Number

so 3

Fig. 2, Patient 3, M. J., a 68-year-old woman. The electrocardiogram (Lead II) Jan. 12, 1969, bradycardia; the heart rate is 43 per minute. The electrocardiogram of Jan. 14, 1969, demonstrates tional rhythm, Type III; the first cardiac cycle demonstrates A-V dissociation by interference.

shows A-V

sinus junc-

I

-1-15-69

I-20-69

l-23-69

Fig. 3. Patient 3. The electrocardiogram (Lead II) made on Jan. 15, 1969, after implantation of a pervenous demand right ventricular pacemaker. The first two cardiac cycles represent normal A-V conduction; the remaining four QRS complexes are activated by the demand pacemaker as the atria1 rate falls below 60 per minute. The record of Jan. 20, 1969, reveals no evidence of normal atria1 activity; the ventricles are activated by the demand pacemaker (broad QRS complexes), with retrograde atria1 activation and the negative P waves which fall on the end of the T waves are followed by ventricular echo beats (narrow QRS complexes). The record of Jan. 23, 1969, shows the development of atria1 flutter; the demand pacemaker is not activating the ventricles because the ventricular rate exceeds 60 per minute.

discontinued and syncope did not recur. On Jan. 23, 1969, atria1 flutter with a varying but predominately 4:1 A-V block developed (Fig. 3). The ventricular rate was 80 per minute. On Feb. 28, 1969, the atria! flutter was no longer present and the demand pacemaker unit seemed to be functioning normally, Patient 4. 6. B., a 6.5year-old man, was first examined in 1964 because of dizzy spells for the past few months. There was no history of angina or myocardial infarction. The patient was taking no drugs. Blood pressure was 150/70 mm. Hg. His heart rate

was 44 per minute with sinus arrhythmia (Fig. 4). The electrocardiogram was otherwise normai. In December, 1964, his response to exercise was evaluated. Cardiac output measurements were determined by the indicator-dilution method with the use of indocyanine green dye. At rest the cardiac output was 3.8 L. per minute; the cardiac index was 2.0 L. per square meter per minute. The oxygen consumption was 214 ml. per minute, and the heart rate was 60 per minute with a stroke volume of 64 ml. When he walked a level treadmill at 3 m.p.h., his

Fig. 4. Patient 4, G. B., a 6.5year-old man. The electr-ocardiogram o E Feb. 24, 1965, shows sinus arrhythmia with sinus bradycardia. The electrocardiogram was otherwise within normal limits.

Lead

I

7-22-68

Transvenous

Demand

Pacemaker

Fig. 5. Patient 4. The electroc&iogram or june 5, 1968, shws shus ns-dtiycardia, with .1-V dissociation by interference. In the fifth QRS complex the atrium captures the ventricle. The electt-ocardiogram of July 22, 1968, was made after implantation of a transvenous demand pacemaker; alternate QRS complexes were activated by the pacemaker.

oxygen cous\lruptiou ilrcteased to 1,189 1111.l)et rrrirrlrte. The heart rate was 92 per minute. His cardiac index increased to 3.6 L. per square meter per minute, and the cardiac output increased to ‘1.3 L. per minute. This value is well below the normal of 8.6 L. per minute calculated from the oxygen consumption and regression equation of Granath and associates.6 This equation estimates the normal exercise-induced cardiac output increase of men aged 61 to 83 years. His cardiac output increased 351 ml. per 100 ml. increase in oxygen consumption per minute. Because of the absence of syncope, congestive heart failure, or renal failure, an electronic cardiac pacemaker was not recommended. He had a syncopal attack in January and again in May, 1968. Examination on June 6, 1968, showed his heart rate to be 30 to 40 per minute. There was no cardiac enlargement. There were no murmurs, and there was no evidence of congestive heart failure. An electrocardiogram showed a slow atria1 rate with A-V dissociation (Fig. 5). The patient was admitted to the Christian R. Holmes Hospital in Cincinnati on June 11. The BUN was 16 mg. per 100 ml., and the serum potassium was 4.2 mEq. per liter. A pervenous demand cardiac ventricular pacemaker was inserted (Fig. 5). On the fourth postoperative day,

atria1 flutter ~rl)pe~~ed .uId he WLLSgiven digitAlis. The rhythm reverted spontaneously to his previous rhythm. G. B. was last seen by his personal physician in early February, 1969. At that time there was no fatigue or syncope and the pacemaker was functioning normally. His energy seemed greatly improved. Except during atria1 flutter, none of the patient’s electrocardiograms showed atrioventricular block. Petient 5. H. O’B.I a SO-year-old man, was admitted to Christ Hospital, Cincinnati, Ohio, on Oct. 28, 1968, because of syncope. Since March, 1959, he had had left anterior chest pain, not typical of angina pectoris. Electrocardiograms in March, 1959, and in October, 1968, were normal except for low T waves. One hour following the initial syncopal episode, blood pressure was 135/90, and the pulse was 80 per minute and regular. He was semicomatose, but he could be aroused. The physical examination was otherwise normal. Three and a half hours later, a generalized convulsive seizure occurred, but the heart was not examined. Phenobarbital, 30 mg. three times a day, and Dilantin, 0.1 Gm. three times a day, were begun. He gradually became more alert. Sinus bradycardia, with rates between 50 and 60 per minute, was observed.

Fig. 6. Patient 6, D. P., a 75-year-old man. The electrocardiogram of May 31, 1967, shows sinus bradycardia, with periods of sinus arrest and junctional escape rhythm. The second QRS complex is followed by evidence of retrograde activation of the atria. On July 19, 1967, there is A-V junctional rhythm, Type III. On July 28, the atria were paced electronically by pervenous right atria1 stimulation at a rate of 60 per minute. The P-R interval was prolonged, being 0.28 second.

On the fourth hospital da,y, syncope recurred, and a physician found him pulseless for a few seconds. Seizure activity was not described. Electrocardio.~ graphic monitoring showed sinus bradycardia; at one time the sinus rate fell to 28 per minute. On November 4, prolonged sinus arrest with syncope was observed. On November 5, temporary pervenous demand pacemaking was instituted. The sinus rate gradually increased. No further syncope or convulsions were observed. The pacemaker was removed on November 21. The patient became ambulatory on November 27 and was discharged on Dec. 2, 1948. At no time did he receive digitalis. Electrocardiograms on October 28, 29, and 30 showed no change from earlier records. On November 4, 6, and 7 there were negative T waves in Leads VS and VS, but no abnormal Q waves appeared. Serum glutamic oxalacetic transaminase and lactic dehydrogenase were normal on Nov. 5 and 6, 1968. Carotid sinus massage on either side caused a slight decrease of the heart rate from 72 to 64 per minute. There was no change in A-V conduction time and no symptoms were produced. Cardiac fluoroscopy and a barium study of the esophagus were normal. The patient returned to work in January, 1969, and has worked steadily up to the present (May, 1969). He had several episodes of lightheadedness in early March, 1969, but was unaware of slowing of his pulse. Patient 6. D. P. was first admitted to Cincinnati Veterans Hospital in 1956 at the age of 63 years for inguinal hernia repair. The pulse (76 per minute) and blood pressure (114/75 mm. Hg) were normal. No electrocardiogram was recorded. In Mav. 1967. he had an occlusion of the left common iliac artery, and a vein graft was placed from the right femoral to the left femoral artery. An electrocardiogram showed marked sinus bradycardia with periods of sinus arrest (Fig. 6). The serum PBI was 7.1 hue Der 100 ml.. a,nd the T-3 resin test was 26 per &,~both normal values. On July 18, 1967, he was readmitted because of pain in the right calf and foot. The blood pressure was 150/70 mm. Hg and the pulse was 46 per minute and irregular (Fig. 6). The next day he was obtunded and appeared moribund. The skin was mottled and cyanotic; the blood pressure was 160/90; and the pulse was 40. Right atria1 electronic pacing at a rate of 60 per minute was started (Fig. 6). The patient became more alert, but bradycardia and signs of circulatory insufficiency reappeared whenever pacing was interrupted. The cardiac output on Aug. 1, 1967 (measured by indocyanine green dye and a Gilford spectrophotometer), was 2 L. per minute without pacing (intrinsic rate N 40 per minute). The cardiac output increased to 2.7 L. per minute with atria1 pacing at 60 per minute and fell to 2.3 L. per minute when the pacing rate was increased to 80. On Aug. 1, 1967, a General Electric fixed-rate pacemaker (GE No. A2072PA) was implanted, and a transjugular bipolar pacing electrode was positioned in the right ventricle. On Aug. 7, 1967, paroxysmal atria1 tachycardia appeared. After 1.5 mg. digoxin orally, A-V block increased, and the pacemaker again captured the

ventricles, although the atria1 arrhythmia persisted. By Aug. 19, 1967, the patient was walking. The pacemaker continued to function well, a.nd on Aug. 23, 1967, the patient was discharged. On Sept. 5? 1967, he was admitted to the hospitai in coma, thought by his physician to have been caused by cerebral thrombosrs. He died approximately one week later. No autopsy was done. Discussian

Sinoatrial bradycardia may occur in a variety of settings, and from the resting heart rate alone, it may be difficult to distinguish between health and disease. In athletes, the resting heart rate may be as slow as 36 to 40 beats per minute, with an increased cardiac stroke volume.4 The resting heart rate tends to decrease with age.” Presumably, the response of the heart rate and cardiac output to graded exercise might be of value in estimating the significance of resting sinoatrial bradycardia. In one of our patients, G. E., the response of the heart rate and cardiac output to exercise was tested and found to be less than normal.‘j Jose and Stitt 7a8found that decrease of the intrinsic heart rate could be related to impaired myocardial performance in patients and in experimental animals. The intrinsic heart rate was that obtained after pharmacologic denewation of the heart with propranolol and atropine. However, autonomic nerve function was not evaluated in our patients, so that we cannot conclude that their bradycardia was necessarily related to impaired myocardial contractility. Sinoatrial bradycardia may result from such medication as digitalis,g quinidine,lO propranoloi and other beta-sympathetic blocking agents,l’ or reserpine.l” It is of interest that 2 of our 6 patients, P. S. and M. J., were receiving reserpine as treatment for systemic hypertension at the time of hospitalization because of syncopal attacks. However, the persistence of bradycardia after

discontinuance

of reserpine

indicated

that this agent was not responsible for the sinoatrial bradycardia and syncope. Only one of these 6 patients, H. N., had received digitalis, and that was given rarily. Sinoatrial bradycardia prior to digitalis administration

only

tempo-

had existed and

was

still present two years after the drug was terminated. None of our 6 patients had received quinidine.

Volume Number

SO 3

Sinus bradycardia may occur in myxedema.13The serum PBI was measured and found to be normal in M. J., P. S., and D. P. Thyroid function tests were not specifically evaluated in the other three patients, but myxedema was not suspected from clinical examination. Sinus bradycardia may complicate either hyperkalemia or hypokalemia.l* Serum potassium values were normal in five of our six subjects at a time when sinus bradycardia existed and was slightly below normal in M. J. Sinoatrial bradycardia may result from vagal stimulation under a variety of circumstances. These include increased intracranial pressure, esophageal diverticulum, vasodepressor syncope, and carotid sinus stimulation.15 The chronic rather than paroxysmal nature of the sinoatrial bradycardia in our patients seemed to militate against the possibility of paroxysmal vagal stimulation. Barium esophagrams were not carried out in these patients. Sinoatrial bradycardia may result from organic disease of the sinoatrial node, the atria1 musculature, or its conducting pathways. Sinoatrial bradycardia may occur in 20 per cent of patients with acute cardiac infarction.3s16 In this setting, the bradycardia may result from morphine or may be a reflex mechanism triggered by pain or fear, or it may be caused by ischemia or infarction of the atrium or sinoatrial node. Sinoatrial bradycardia may occur with acute myocarditis and may result from neoplastic invasion of the atrium. JamesI’ has commented on the importance in the genesisof cardiac arrhythmias of diseaseof the small coronary arteries supplying the S-A node and the conduction system. Such diseasemay result from coronary embolism, the connective tissue diseases,hematologic disorders, amyloidosis, or hereditary medial necrosis, in addition to arteriosclerotic heart disease. Of our 6 subjects, only one, H. N., had a clear-cut history of angina pectoris, and an anterolateral myocardial infarction was documented in January, 1969. H. O’B. had a history suggestive of angina pectoris. In the others, two, P. S. and M. J., had received treatment for systemic hypertensive disease. None was diabetic and none had shown evidence of malignant disease. Except for the arrhythmia, numerous elec-

Syncope and cerebral dysfunction

309

trocardiograms were within normal limits in the five patients other than H. N. It is of interest that so many of these 6 patients showed possible additional evidence of atria1 disease by displaying a paroxysmal atria1 arrhythmia. G. B. had atria1 fibrillation in 1964 at the time of his exercise study and developed a-trial flutter in 1968 following insertion of a pervenous pacemaker. P. S. developed transient atria1 fibrillation following insertion of an Atricor pacemaker. D. P. developed paroxysmal atria1 tachycardia 6 days after implantation of a pervenous right ventricular pacemaker. M. S. developed paroxysmal atria1 flutter prior to cardiac pacemaker insertion and again transiently 8 days following implantation of the pacemaker. Although the etiology of the sinoatrial bradycardia in these 6 patients cannot be stated with certainty, the ages of the patients at the onset of symptoms (P. S. 73 yr., H. N. 69 yr., M. J. 68 yr., G. B. 65 yr., H. O’B. 50 yr., and D. P. 74 yr.), and the absence of other apparent cause suggest that coronary artery disease or a nonspecific degeneration of the S-A node or atria1 musculature was most likely responsible. When the intrinsic sinoatrial nodal rate falls below a certain value, there is a tendency for the ventricles to be driven by a lower pacemaker. This pacemaker is usually located near the A-V junction and fires at a rate slower than the normal sinus rate unless accelerated by drugs, electrolyte imbalance, or inflammation. Each of our patients at times displayed evidence of an escape A-V jun’ctional pacemaker when the atria1 rate was exceptionally slow. Sometimes there resulted A-V dissociation by interference or A-V junctional rhythm with retrograde atria1 activation. In none of our 6 patients wa.s there documentation of bundle branch block. Only one showed a transient escape ventricular rhythm. In none was second- or third-degree A-V block demonstrated during normal or slow atria1 rates. Although sinoatrial bradycardia has been often reported as a temporary cause of decreased cardiac output during the course of acute myocardial infarction,3,16~18~1g it has not been commonly described as a cause of syncope. In a recent report of cardiogenic

S~~CO~JC, 3 d 32 patierils Ilad S~UUS imdp cardia or nodal rhythm, 2 had atria1 fibrillation, and 21 had A-V block.” The cardiac mechanism during syncope was documented in three of our patients, P. S., M. Ja, and H. O’B. In each there was atria1 and ventricular asystole which lasted more than 5 seconds. In patients with ventricular bradycardia caused by acquired complete A-V block, the cardiac output is usually below normal at rest, and since the patient is unable to increase his heart rate with exercise, the cardiac output response to exercise is subnormal.2o In such patients syncope may be related to ventricular slowing or standstill, to ventricular fibrillation, or to ventricular tachycardia.21 Other symptoms may be those of effort fatigue, renal failure, heart failure, or impaired cerebral function.22 Syncope occurred in 5 of our 6 patients with sinoatrial bradycardia, and the other (D. P.) had symptoms of impaired perfusion of the brain and of the lower extremities, which were improved when the heart rate was increased by electronic atria1 pacing. Another patient, 6. B., had in addition to two bouts of syncope, symptoms of effort fatigue, and dyspnea, which were improved by atria1 pacing. Cardiac or renal failure were not documented in our 6 patients with sinoatrial bradycardia. Treatment

In sinoatrial bradycardia which complicates acute cardiac infarction, atropine may be given intravenously in doses of 0.3 to 2 mg. which may be repeated at 3 to 4 hour intervals.3 Alternatively, isoproterenol infusion may be employed,3 but this agent may provoke a junctional or ventricular arrhythmia. If there is no prompt improvement as a result of atropine or isoproterenol or the arrhythmia persists, temporary pervenous right atria1 pacing is probably indicated.ls When chronic sinoatrial bradycardia, unrelated to drugs or metabolic disorders, produces symptoms related to decreased cardiac output or syncope, it is essential to improve the cardiac mechanism. Atropine was used successfully in one reported instance in a young man who had syncope with cardiac slowing during at-

f.;iCkti

Ol

g~ojs~~~,ii;tr~-ll~ca~

il~lil~;i~$?,~~~.‘~”

1 iO\t

ever, atropine may be poorly tolerated in the patient over 50 years of age, and its effects may be unpredictable. Vagotomy was used successfully in the treatment of a 34-year-old man with syncope related to sinus bradycardia .24Isoproterenol by intravenous infusion may be effective in the management of acute sinoatrial bradycardia complicating acute cardiac infarction. Oral isoprotereno1 has been used for chronic sinus bradycardia with syncope.’ However, because of its brief duration of action, it may not be practical for the treatment of chronic sinoatrial bradycardia. Hence, cardiac electronic pacing is the rnost effective form of treatment now avail&je.2,25,26

Atria1 pacing has been used in the suppression of ventricular tachyarrhythmias, often in conjunction with quinidine, propranolol, or procaine amide.“7sX8It has a potential hemodynamic advantage over ventricular pacing, and the normal route of activation and repolarization of the ventricular musculature may render reentry tachycardia less likely.27*2gAlthough atria1 pacing is an effective form of temporary management of symptomatic sinoatrial bradycardia, there are considerations which limit its long-term use. It is difficult to obtain long-term effective atria1 pacing without a thoracotomy, although occasionally this is possible.28 The atria1 pacing catheter may be placed pervenously in the right atria1 appendage or in the coronary sinus.2sHowever, such placements are not without hazard, and the pacing catheter often becomes dislodged.sOStimulation of the right phrenic nerve with contraction of the right hemidiaphragm may be a complication of right atria1 pacing.28 Another theoretical limitation to atria1 pacing in the treatment of sinoatrial bradycardia is the possibility that atrioventricular block may develop,26 and thus the ventricles might fail to respond to cardiac pacing. Hence, we prefer transvenous ventricular pacing in the treatment of chronic symptomatic sinoatria1 bradycardia at the present time. Although the right ventricle may be paced by a fixed-rate pervenous catheter pacemaker,2 the danger of competition with the patient’s intrinsic activation impulse exists,

Syncope and cerebral dysjunclion

and this variety of pacing may possibly evoke ventricular tachycardia or fibrillation if the competing ventricular impulse falls within the ventricular vulnerable period.2” Hence, at this time we prefer pervenous right ventricular demand pacing to fixedrate right ventricular pacing in the treatment of chronic symptomatic sinoatrial bradycardia. An alternative is to employ an implanted epicardial right atria1 fixedrate pacemaker, if the possibility of A-V block can be excluded.26

5.

6.

7.

8.

Summary

In this paper six patients, aged 50 to 74 years, with chronic symptomatic sinoatrial bradycardia are described; none had more than first degree A-V block. The cause of the bradycardia was not evident except in one, who had coronary artery diseasewith myocardial infarction. Five patients suffered from syncopal attacks, which in 3 were documented to be related to cardiac slowing or arrest. One patient had evidence of effort fatigue, and another had symptoms of impaired cerebral and peripheral circulation. Electronic cardiac pacing was effective in improving cardiac output and relieving symptoms. Chronic sinoatrial bradycardia is much lesscommon than A-V block as a cause of cardiogenic syncope but must be considered in the differential diagnosis of fainting. We are grateful to Dr. David Frankel who referred Patient H. N.; to Dr. David Hamilton of Wilmington, Ohio, who referred Patient G. B.; to Dr. Clayton Sikes, who referred Patient H. O’B.; to Dr. Stephen Lewis, who referred Patient M. J.; to Dr. William Page of Sarasota, Fla., who kindly gave permission to report on Patient P. S.

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10.

11.

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13.

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15. 16.

17. 18.

REFERENCES Nissen, N. I., and Thomsen, ,4. C.: Oral treatment of A-V block and other bradycardias with sustained action isoprenaline, Brit. Heart J. 27:926, 1965. Hornbaker, J. H., Jr., Humphries, J. O., and Ross, R. S. : Permanent pacing in the absence of heart block: An approach to the management of intractable arrhythmias, Circulation 39:189, 1969. Shillingford, J., and Thomas, M.: Treatment of bradycardia and hypotension syndrome in patients with acute myocardial infarction, AMER. HEART J. 75:843, 1968. Hanson, J. S., and Tabakin, B. S.: Comparison of the circulatory response to upright exercise

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men and 9 distance runners, in 2j “normal” Brit. Heart J. 27:211, 196.5. Brandfonbrener, M., Landowne, M., and Shock, N. W.: Changes in cardiac output with age, Circulation 12:X7, 195.5. Granath, A., Jonsson, B., and Strandell, T.: Circulation in healthy old men, studied by right heart catheterization at rest and during exercise in supine and sitting position, Acta Med. Stand. 176:425, 1964. Jose, A. D.: Effect of combined sympathetic and parasympathetic blockade on heart rate and cardiac function in man, Amer. J. Cardiol. 18:476, 1966. Jose, A. D., and Stitt, F.: Cardiac function after combined beta-adrenergic and cholinergic blockade. Relationship of intrinsic rate to contractile force of the heart in dogs, Circulation Res. 21 (Suppl. 3):231, 1967. Dubnow. M. H.. and Burchell. H. B.: A comparison of digitalis intoxication in two separate periods, Ann. Intern. Med. 62:956, 1965. James, T. N., and Nadeau, R. A.: The mechanism of action of quinidine on the sinus node studied by direct perfusion through its artery, AMER. HEART i. 67:804. 1964. Cohen, L. S., and Braunwald, E.: Amelioration of angina pectoris in idiopathic hypertrophic subaortic stenosis with beta-adrenergic blockade, Circulation 35:847, 1967. Alper, M. H., Flacke, W., and Krayer, 0.: Pharmacology of reserpine and its implications for anesthesia, Anesthesiology 24:524, 1963. Graettinger, J. S., Muenster, J. J*, Checchia, C. S., Grissom, R. L., and Campbell, J. A.: A correlation of clinical and hemodynamic studies in patien.ts with hypothyroidism, J. Clin. Invest. 37:502, 1958. Surawicz, B.: Relationship between electrocardiogram and electrolytes, AMER. HEART J. 73:814, 1967, Ebert, R. V.: Syncope, Circulation 27:1148, 1963. Fluck, D. C., Olsen, E., and Mounsey, J. P. D.: Bradycardia in acute myocardial infarction, Brit. Heart T. 28:430. 1966. James, T. N.: Review. Pathology of small coronary arteries, Amer. J. Cardiol. 20:679, 1967. Thomas, M., and Woodgate, D.: Effect of atropine on bradycardia and hypotension in acute myocardial infarction, Brit. Heart J. 28:409, 1966. Bruce, R. A., Blackman, J. R., Cobb, L. A., and Dodge, H. T.: Treatment of asystole or heart block during acute myocardial infarction with electrode ca.theter pacing, AMER. HEART J. 69:460, 1965. Adolph, R. J., Holmes, J. C., and Fukusumi, H.: Hemodynamic studies in patients with chronically implanted pacemakers, ANER. HEART J. 76:829, 1968. Sacolick, S. L., Stein, W. G., and Friedberg, C. K. : Complete heart block with Adams-Stokes seizures from ventricular fibrillation, Arch. Intern. Med. 110:299, 1962. Burchell, H. B., Connolly, D. C., and Ellis,

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