ventricular fibrillation in stokes-adams syndrome

REGISTRATION OF HEART BEAT 591

The foregoing are only some of the uses in clinical work. Graphic records are essential for the research worker. It is desirable that he should see immediately, on a screen such as a fluorescent screen with long after-glow, the traces of the phenomena which he is investigating, since this will give him an idea of what his finished photographic records will look like. If any change is called for it can be made then and there. It is too late when an experiment is completed and the graphic records developed, to find that the recorded results are poor.

Summary. Some modern methods for the graphic registration of the heart

beat, viz., phonocardiography, electrocardiography, sphygmography, the measurement of the velocity of the pulse wave, pneumoeardio- graphy, radiography, combined eineradiography and electrocardiography, and the author's general purpose apparatus for the registration of tile heart beat, are described. The advantages and dis- advantages of the various methods are discussed and special refer- ence is given to the clinical applications.

I wish to thank Dr. P. T. O'Farrell, President of tile Hedical Section of the Royal Irish Academy of Medicine, and Dr. Fitzgerald, Secretary, for their kindness and advice, and elso Dr. Russell J. Reynolds, Physician in Charge, Radiological Depart- ment, Charing Cross Hospital, for permission to reproduce the photograph of his apparatus for cineradiography.

References. J Kountz, Gilson and Smith. Am. Heart J. 20 : 667, 1941.

Smith, Gilson and Kountz. Am. Heart J. 21 : 17, 1941. Smith, Edwards and Kountz. Am. Heart J. 21 : 228, 1941.

4 Brarnwell, Hill and MeSwiney. Heart, 1923, voL X, p. 233. aReynolds, R . J . : Jo. Inst. Elect. Eng., 79, 478, 1936. e Reynolds, R. J. : Tuberc/e, June, 1936, 396.

Donovan, G. E. : Jo. Inst. E/oct. Eng., 90, 10, I I I , 38. Donovan, O. E. : Phono.electrocardioscopy. (Lanczt, in press).

VENTRICULAR FIBRILLATION iN STOKES-ADAMS SYNDROME.

By P. T. O'FARR~L.

V ENTRICULAR fibrillation is rarely detected in clinical practice for the simple reason that the onset of the irregularity is very frequently asseciated with sudden

death. There are, however, a few instances recorded in the literature where ventricular fibrillation has been identified electrecardio- graphically as a transient phenomenon as well as a terminal event. The ease herewith recorded is of some interest because the onset of ventrieular fibrillation occurred during the course of a Stokes- Adams seizure, followed later by the restoration of normal rhythm, yet terminating finally in death.

592 IRISH JOURNAL OF MEDICAL SCIENCE

I am indebted to my colleague, Dr. John Shiel, for having referred this pat ient to me in consultation and for his collaboration in treatment.

Mrs. M . . . , aged 64 years, of heavy build, and a big meat eater, complained of attacks of dizziness during September and October, 1942, for which she con- sulted Dr. Shiel. Her previous history was good and she had never complained of any illness. Her blood pressure was found to be over 300 mm. Hg. systolic, and 120 mm. Hg. diastolic. The heart was enlarged to the left ; the rate and rhythm were normal. There was a systolic murmur a t the aortic and mitral areas. Urine, slight trace of albumen. No history of anginal pain.

Towards the end of October, 1942, Dr. Shiel noticed a peculiar heart rhythm consisting of a few normal beats followed by a series of quick fluttering beats (extrasystoles) and then a long period of silence. This type of irregularity was repeated again and again.

I saw the patient, in consultation, on October 26th 1942, when the blood pressure was systolic 260ram. Hg. and diastolic 120mm.ttg. The heart rate was normal (76 per minute) and the rhy thm perfectly regular. The irregularity which had previously existed was no longer present. The patient was admit ted to a nursing home on Nov. 3rd, 1942, for observation and she was ordered theo- gardinal and rest,

On Nov. 5th, 1942, the cardiac irregularity was noticed again: it cones. ponded exactly to the description already given by Dr. Shiel. The irregularity continued on and off for most of the day. During this time the pat ient was in a dazed condition, sometimes semi.conscious ; a t other times she could be roused to a certain extent and could answer questions in a sleepy manner. She did not have any convulsive seizures, but she had occasional fibrillary twitchings. Towards evening her condition disimproved and the unconsciousness seemed to be more prolonged; she developed Cheyne-Stokes respiration, the muscles became flaccid, her pupils dilated and it appeared as if she had had a stroke. An electro.cardiogram was taken while the cardiac irregularity was present ; it disclosed the presence of complete heart block with ventricular fibrillation. She was ordered 3 grains of quinidine every four hours if she showed signs of returning consciousness.

Next morning, the irregularity had gone and the patient seemed to be much better ; she was able to tak~ nourishment and was well aware of her surroundings although she could not remember any of the events of the previous day. An electrocardiogram taken on this morning disclosed a normal heart rate with normal rhythm. Later in the day she had a return of unconscioumaess, and she died on Nov. 7th, in the early hours of the morning. Unfortunately no post. mortem examination could be obtained, but probably the cause of death was coronary atheroma, as indicated by the valvular lesions, Stokes.Adams seizures and the onset and recurrence of ventricular fibrillation.

Elec2xocardiographi~ Findings. First Electrocardiogram. Nov. 5th, 1942. (Fig. I). Lead I shows complete 4 : 1 heart block (auricular rate 120 per minute,

ventricular rate 30 per minute), followed by a period of ventricular fibrillation lasting about 2 seconds and then the resumption of the heart block rhythm. In addition the lead shows a few extrasystoles.

Lead II shows complete 4 : 1 heart block followed by a period of mixed extrasystoles and ventrieular fibrillation lasting about 2 seconds.

Lead I I I shows complete 8: 1 heart block (auricular rate 120 per minute, ventrieular rate 15 per minute), followed by a period of mixed extrasystoles and ventricular fibrillation.

Second Electrocardiogram. Nov. 6th, 1942. (Fig. 2). All leads show a normal rhythm. Auricular and ventricular rate 80 per minute.

Discussion.

Experimental ventricular fibrillation was first described by Hoffa and Ludwig (1850), who found that electrical stimulation of the mammalian heart produced an ineffective and an into-ordinate type of ventricular contraction leading to arrest of the circulation and death. Vulpian (1874) called the condition mouvement fibrillaire. McWilliam (1887) put forward the suggestion that ventricular fibrillation might be the mechanism responsible for some forms of sudden heart failure in man. McWilliam's hypothesis, however, could not be substantiated until electrocardiographic evidence of

VENTRICULAR FIBRILLATION 593

human ventricular fibrillation was forthcoming. Meanwhile it was found that experimental ventricular fibrillation in animals could a]so be induced by other agents apart from electrical stimulation. For instance, thermal, chemical and mechanical stimuli were found to produce the irregularity. Again attention was directed to McWilliam's hypothesis and some observers thought that ventricular fibrillation might be the responsible factor for sudden death in some clinical eases inwhich no obvious reason for death could be discovered at the autopsy examination. These kinds of sudden death included fatalities from anesthetics, from non-penetrating injuries or trauma of the chest wall and from electrical shocks.

Of still greater importance from the clinical viewpoint was the discovery that experimental ventrieular fibrillation could also be produced in conscious animals by ligation of a main branch of the coronary artery. From this it seemed possible to postulate a mechanism responsible for sudden death in some cases of coronary disease. In support of this contention there seemed to be a remark- able similarity between the symptoms exhibited by an animal dying of ventrieular fibrillation and those of a person dying suddenly from angina pectoris and coronary thrombosis.

Objective evidence of ventrieular fibrillation in man was later demonstrated by electrocardiographic methods, the tracings showing a close resemblance wi th those obtained in experimental animals. Human electrocardiograms of ventricular fibrillation were, however, difficult to obtain because they were only recorded by mere chance in moribund patients. This was in accord with experimental experience, for induction of the irregularity in larger mammals (dog, sheep, goat) was looked upon as an irreversible condition almost invariably leading to death. For instance Wiggers (1940) in his earlier researches witnessed only one recovery in over 400 experiments in dogs. Later observers, however, showed that both clinical and experimental ventricular fibrillation need not necessarily be a terminal event. In the dog, Hooker, Kouwenhoven and Langworthy (1933) succeeded in defibrillating the ventricle and restoring natural and co-ordinate beats by means of electrical counter-shocks. Other investigators have also had success with cardiac massage and the combined use of procaine, adrenaline and calcium intravenously. Defibrillation of the ventricle is now a standard procedure in the physiological laboratory. For instance, Wiggers (1940a) and his co-worker Wegria, by using a serial counter-shock method, were able to cause 327 revivals in 328 attempts, with success 41 times in one dog.

In human beings transient episodes of the irregularity have been ~ecorded eleetrocardiographically in several instances. Leaman (1939) is of opinion that not alone is complete recovery from clinical ventricular fibrillation possible, but that such occurrences are more frequent than the scant number of reports in the literature would indicate.

The possibility of recovery from clinical ventricular fibrillation has stimulated investigations in two directions, viz., one with a view to preventing its onset in cases where it might be anticipated


and the other which aims at correcting the irregularity once it has occurred.

Mechanism of Ventricular Fibrillation. Two main problems arise in this connection: (1) the processes which initiate the irregularity and (2) the nature of the irregularity itself once it has become established. These two problems have not as yet been completely solved, but animal experiments have yielded important information. According to Wiggers (1940a), to initiate fibrillation a noxious stimulus (within " the fibrillation threshold ") must be applied during the vulnerable period of late systole at a time when certain elements of the myocardium have passed out of the refractory phase. Such a stimulus excites impulses which weave their way slowly through local, non-refractory tissue to form a small wave front, from which a massive excitation wave sweeps over comparatively large portions of the myoeardium in sequential order. This constitutes the first premature beat which is the immediate pre- cursor of the irregularity. After this single premature systole the phenomenon of fibrillation is caused by re-entry of circulating wave fronts which involve smaller and smaller blocks of myocardium, each of which develops an independent excitation. As a result of the anoxia which develops progressively after the cessation of the coronary flow, conduction is slowed and the vigour of fractionate contractions decreases. The resultant of these changes causes in succession the undulatory, convulsive, tremulous and atonic stages of ventricular fibrillation.

Cltniced Aspects of Yentricular Fibrillation. The principal method of diagnosis is by means of the electrocardiograph. Some tracings, however, are difficult to interpret because they may simu- late those of high ventrieular taehyeardia; moreover, the two irregularities may sometimes follow one another. In ventricular fibrillation the deflections are always rapid and irregular, con- stantly varying in shape, size and amplitude so as to resemble an artifact rather than a natural electrocardiogram. The QRS-T waves are indistinguishable; as Levy (1929) aptly says, the appear- ance is one of " ventricular anarchy ". In high ventricular tachycardia, on the other hand, the very rapid deflections are regular and there is some reproduction of the QRS-T waves. I f there is any variation in the size and shape of the complexes they are found to occur in phases.

The clinical features of ventricular fibrillation have not as yet been clearly established, chiefly owing to the fact that so few eases are detected in ordinary practice. In fatal cases, the majority of which are due to coronary disease, events take place with such dramatic suddenness that there is little time to study the phenomenon or to carry out electrocardiographic investigations. The signs and symptoms, however, are very like those found in experimental ventricular fibrillation terminating fatally. In both there is a sudden onset of apncea with loss of consciousness, an abrupt fall of blood pressure to zero, cessation of the heart sounds and muscular relaxation, occasionally preceded by brief rigidity or convulsive movements. A few deep or gasping respirations and


dilatation of the pupils are the final events leading to death. This combination of symptoms and signs is also found in patients who die from " ventricular standstill ", and the only way to differen- tiate this mechanism from that of ventricular fibrillation is by the electrocardiogram.

Our chief knowledge of clinical ventrieular fibrillation is mainly derived from observations on patients who exhibit transient and repeated episodes of the irregularity. The number of such eases reported in the literature is still comparatively small, perhaps a score or more. Most of these patients had advanced heart disease, usually associated with complete aurieulo-ventricular heart block and the Stokes-Adams syndrome, but the irregularity has also been reported during the course of auricular fibrillation, particularly when the patients were undergoing treatment with quinidine.

Probably the most instructive eases of transient, repeated ventrieular fibrillation are those reported by Schwartz (1932), and Schwartz and Jezer (1932).

These were two women, aged 66 a n d 65 yea r s respect ively , b o t h o f w h o m h a d aur iculo-ven¢ricular hear~ block a n d ar te r ia l hype r t ens ion . T h e f irst p a t i e n t , while u n d e r obse rva t ion for s e v e n m o n t h s , h a d 67 seizures o f unconsc iousness , the d u r a t i o n o f wh ich va r ied f rom a l i t t le over one m i n u t e to s ix m i n u t e s a n d two seconds. E lec t roca rd iograms were ob ta ined in all or p a r t of 12 such seizures a n d in e a c h ins t ance t h e unde r ly ing m e c h a n i s m p roved to be ven t r i . cu l a r fibrillation. T h e second pa t i en t , u n d e r obse rva t ion for a per iod of fou r m o n t h s , d id n o t pass a single d a y w i t h o u t h a v i n g a t leas t one syncopa l a t t a c k ; in one 24 hour s she h a d as m a n y as 207 a t t a c k s of lmconsc iousness . T h e d u r a t i o n o f t h e a t t a c k s va r ied f r o m a few seconds to s ix m i n u t e s , t h e ave rage seizure las t ing 46 seconds, l~Iore t h a n 100 e lec t rocard iograms were t a k e n du r ing t h e syncopa l seizures, and t h e y inva r i ab ly revealed a cardiac m e c h a n i s m due to t r ans i en t ven t r i cu la r fibrills¢.ion.

As a result of further studies Schwartz (i936) divided transient recurrent ventricular fibrillation into pre-fibrillatory, fibrillatory and post-fibrillatory periods. The pre-fibrillatory period is characterised by a marked acceleration of the basic ventrieular rate and the occurrence of multiple and variable cxtrasystoles. The fibrillatory period shows a high rate of irregular bizarre complexes. In the post-flbriUatory period there is a variable period of ventricular standstill followed by ventricular tachyeardia before the restoration of the basio ventrieular rate and rhythm. The duration of the post-fibrillatory period depends on the antecedent period of ventricular fibrillation and may vary from a few seconds to as long as half an hour at one time. This sequence of events, particularly if repeated, should enable one to diagnose the onset and progre~ of ventricular fibrillation by clinical observation apart from the electrocardiographic findings.

During the actual attack of transient fibrillation the patient has a syneopal seizure, with marked pallor, the eyes fixed, the face expressionless, cyanosis of the lips, breathing motionless, stertorous or of the Cheyne-Stokes variety. There may be foaming at the mouth and convulsive seizures. The pulse cannot be felt, nor can the heart sounds be heard, and auricular contraction ceases (if seen previously in the jugular pulse). If the seizure is prolonged 1here


may be incontinence of urine and f~eces. Spontaneous revival from transient ventricular fibrillation is associated with a sudden flush- ing of the face, a forceful pulsation of the heart against the chest wall and with a barely perceptible beat of the pulse at the wrist. With these events tachycardia sets in, the eyes open and loud screaming may be followed by incoherent and unintelligible speech, and a very clouded sensorium. This in turn is followed by a progressive lowering of the heart rate to the original basic level before the onset of the fibrillation. Coma and a period of unconsciousness may then supervene and last as long as five hours after" a major syncopal attack.

All these symptoms and signs are so unique that the clinical diagnosis of transient ventrieular fibrillation may be suspected in an individual with syncopal seizures such as occur in the Stokes- Adams syndrome. Loss of consciousness in a Stokes-Adams attack is not always due to ventricular fibrillation ; indeed Parkinson, Papp and Evans (1941) have pointed out that it is more often due to ventricular standstill or to high ventricular tachyeardia, or a combination of both. By careful attention to the sequence of events, however, it should be possible to detect the presence of ventrieular fibrillation, although the final decision depends on the electrocardiographic findings.

Prognosis. As the irregularity is most frequently encountered as a terminal event in patients with advanced eardio-vaseular disease and is believed to be a common cause of sudden death in angina pectoris and ooronary occlusion the prognosis is necessarily very bad. In transient ventrieular fibrillation the outlook is also very grave because the majority of patients already have serious myocardial disease and seldom survive for more than a few weeks or months after the initial onset of the irregularity. The prognosis should be more favourable in patients who do not show any under- lying pathology of the myoeardium, but unfortunately methods of defibrillation are still undeveloped and the most one can hope for is spontaneous recovery.

Treatment. and Prevention. Defibrillation methods so far em- ployed in experimental animals can seldom be used successfully in human ventricular fibrillation because of insurmountable difficul- ties. To be of service, shock methods would need to be applied within two or three minutes of the onset of the irregularity, that is to say, before irretrievable damage had been done to the pace- makers and conducting system of the heart. In the time available it would be almost impracticable to take the diagnostic electrocardiogram and to have ready a sufficiently strong current (about 3,000 volts) for immediate use. The only hope of success might be if the patient was already on the operating table with the chest open.

The only way to restore vigorous pulsation to a fibrillating ventricle is to stimulate the coronary circulation to supply sufficient oxygen to the myoeardium, and the only way this can be done, as far as we know, is by cardiac massage. Drugs are completely ineffective because none of them will relieve the anox~emia of


fibrillation; moreover, they may even do harm by lessening the chance of spontaneous recover~¢.

The prospect of restoring normal beats in the fibrillation of coronary occlusion is exceedingly remote because it is impossible in man to relieve the occlusion, and without this one can hardly hope for an adequate supply of oxygen to the myocardium. This is borne out by experimental experiences, for defibrillation of the heart of normal dogs can seldom be accomplished unless the artifi- cial occlusion of the coronary artery is first of all relieved. As no other means, apart from cardiac massage, are at present known ~or supplying oxygen to the fibrillating ventricle attention has been directed to the more promising problem of preventing its onset by reducing the sensivity of the ventricle to agents which cause fibrillation. Morawitz and Hoehrein (1929) regarded quinidine as a highly successful prophylactic in the treatment of patients liable to sudden death from ventricular fibrillation. Stepp and Parade (1928) advocated its use as a means of preventing the irregnlarity. Smith and his co-workers (1940), on the other hand, found that quinidine was of little use in preventing the onset of fibrillation caused by experimental occlusion of the coronary artery in dogs: indeed it seemed to hasten the onset of the irregularity. It is also well known that the use of large doses of this drug in the treatment of heart disease has led to fatal ventricular fibrillation.

Although the problem of making the heal"t completely refractory to fibrillation has not yet been solved, there is still a hope that success may be attained at some future date.

Hoffa, M. and Ludwig, C. (1850) Ztschr. f. rat. Med. 9. 107. Hooker, Kouwenhoven and Langworthy. (1933) Amer. Jo. Physiol., 103 .444. Leaman, "W. (1939) Amer. Jo. Med. Sci., 197. 139. Levy, J. R. (1929) Lea anomalies du camplexe ver~riculaire ele~rifue. Masson,

Paris. Morawitz, P. and Hochrein, M. (1929) M~nch. rr~d. W c h ~ r . , 76, 1075. McWilliam, J. (1887) JK Physiol., 8, 296. Parkinson, J. Papp, C. and Evans, W. (1941) Br~. Heart ,To., 3. 171. Schwartz, S. P. (1932) A ~ . Ins. M.d., 49, 282. Schwartz, S. P. (1936) A ~ . ,7o. Meal. ,.%'i., 192, 153 and 808. Schwartz, S. P. and Jezor, A. (1932) Arch. Ins. M ~ . , 50. 450. Smith, MeEachern and Hall. (1940) A ~ . H~r$ Jo., 20, 620. Stepp, W. and Parade, C. W. (1928) M/b~ch. ~ed. W v h ~ . , 75, 1869. Wiggers, C. J. (1940) Amer. Hears Jo., 20, 399. Wiggers, C. J. (1940a) Amer. Hears Jo., 20, 413.

ventricular fibrillation in stokes-adams syndrome

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