Case Reports

Cardiac Resuscitation from Recurrent

Ventricular Fibrillation Occurring in a

Physician’s Office

Report of a Case*

_\SHER BLACK, M.D. and MARTIN M. BLACK, M.D.

Syracuse, New York

D EATH from myocardial infarction within the first few days is usually the result of

ventricular standstill or ventricular fibrillation. Although ischemic myocardium is particularly susceptible to ventricular fibrillation1 which often causes death, in most instances ventricular fibrillation itself does not necessarily indicate severe cardiac damage and may be reversible. Viability of cardiac muscle persists after cessa- tion of heart beat, and the ability of the myo- cardium to contract can be restored if fibrillation is abolished and spontaneous rhythmic electric stimulationrenewed. Cardiac resuscitationmust, therefore, be tried when this complication arises in an otherwise salvable heart. This has been accomplished successfully during opera- tions,2 diagnostic procedures3v4 and hospitaliza- tions for myocardial infarction.s-‘0

Myocardial infarction with “mechanism death,” frequently ventricular fibrillation, often occurs outside a hospital. The ability to restore useful life without severe deterioration of the central nervous system depends on prompt resuscitatory measures and maintenance of effective cardiac and respiratory functions until spontaneous cardiac action occurs. The neces- sity for open-chest cardiac massage has been circumvented by the method described by Kouwenhoven et al.” and maintenance of effective cardiac output by this means for as long as 45 minutes has been described.r2

The following report describes a case of cardiac

arrest which occurred in a physician’s office. Resuscitation and transfer to a hospital facility produced a successful outcome.

CASE REPORT

A 40 year old white mail carrier noticed some upper abdominal pain, back pain and bilateral arm ache while delivering mail at about 1:30 P.M. on May 15, 1962. This pain became progressively more severe. He became nauseated and vomited, and was faint. He was transported to the office at 2:30 P.Mi

On the examination table he suddenly became un- conscious: gasped several times and stopped breath- ing. Mild cyanosis developed; pupils dilated widely; and carotid and femoral pulses disappeared. No heart sounds were detected. Mouth-to-mouth respira- tion and external cardiac massage were started at once, Epinephrine, 0.5 cc. of 1 :l,OOO solution, was administered intravenously. Within one minute, the pupils were no longer dilated. Within three to four minutes, some movement of the extremities was noted, and his color improved. Mouth-to-mouth respira- tion and external cardiac massage were continued in the office until the ambulance arrived 30 minutes later, and was kept up en route to the hospital.

The cardiac resuscitation unit awaited the arrival of the patient at the hospital. Tracheal intubation was performed while external massage was main- tained. An electrocardiogram on admission revealed ventricular fibrillation (Fig. 1A). He was externally shocked with 450 volts. Fibrillation stopped, and an idioventricular rhythm with bizarre QRS complexes for several seconds developed (Fig. 1B). The rhythm then reverted to the ventricular fibrillation (Fig. lC),

* From the Department of Medicine, St. Joseph’s Hospital, Syracuse, N. Y.

JANUARY 1964 71

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FIG. 1. Electrocardiograms during treatment in emerpq room. A, ven- tricular fibrillation on admission. B, initial idioventricular rhythm. C, re- version to ventricular fibrillation. D, idioventricular rhythm with reversion to coarse ventricular fibrillation. E, cardiac arrest, then ventricular tachy- cardia. F, nodal rhythm.

and he was again shocked at the same vo!tage. ‘l‘he same sequence of events occurred, but the idio- ventricular complexes appeared less bizarre. A third shock at 550 volts produced idioventricular rhythm followed by a quick return to ventricular fibrillation (Fig ID). Epinephrine, 0.5 cc. of 1 :I,000 solution diluted to 5 cc., was administered intravenously, and a shock of 550 volts was again applied. Cardiac ar- rest ensued for several seconds, followed by ventricular tachycardia for 30 seconds (Fig. lE), with subsequent reversion to ventricular fibrillation. Pronestyl, 500 mg., was then administered intravenously. He was again shocked at 550 volts. A nodal rhythm de- veloped, and in lead III a distinct pattern of acute infarction of the inferior wall (Fig. 1F). This nodal rhythm was maintained, and femoral and carotid pulsations were easily detected. Blood pressure, which was previously unobtainable, was now 70/56 mm. Hg. At this point, the patient was able to breathe alone. Suddenly, a generalized convulsion appeared which lasted for 50 seconds. Shortly after this convulsion, some movements of the extremities were noted. Respirations were maintained by the patient without assistance from the anesthetist. He now became conscious and recognized his attending physician, whom he called by name. He had been unconscious about 55 minutes.

Forty minutes were consumed from the initial

period of unconsciousness to arrival at the Emergency Room. The period of unconsciousness in the Emer- gency Room was 15 minutes. Aramine@ was given intravenously and oxygen through a nasal catheter. Before arrival at the intensive care unit an x-ray film of the chest revealed no pneumothorax or fractured ribs.

In the intensive care unit he remained conscious and cooperative, complaining of chest pain in the anterior wall. He was attached to a monitor unit with stand-by pacemaker connection. At 7 P.M., a slight irregularity of the pulse was noted. An eIectrocardiogram revealed nodal rhythm without irregularities. Ventricular fibrillation then developed. Again, mouth-to-mouth respirations and external cardiac massage were instituted. Defibrillated with one shock at 450 volts, he reverted to the original nodal rhythm. This episode of cardiac arrest lasted 15 minutes. Thereafter he appeared to be confused for 30 minutes.

His subsequent course was stormy with nodal and sinus tachycardia, intermittent periods of hypo- tension, oliguria for 48 hours, and blurred vision for 72 hours. Retrograde amnesia for the events of the day of admission to the hospital developed.

In 72 hours his vital signs stabilized and improved. A harsh friction rub was noted on May 20 and per- sisted for 36 hours. On May 17 rhythm reverted to

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(Iardiac Kesuscitatiorl from L7entricular Fibrillation

regular sinus rhvthln at a rate of 100 with typical changes of an infarction of the inferior wall (Fig. 2). On May 19 nodal tachycardia (Fig. 3) again de- veloped, and digitalization was augmented. The next day he was in regular sinus rhythm. A repeated electrocardiogram on May 24 demonstrated reg- ular sinus rhythm at a rate of 88 and classic evolution ary changes of an infarction of the inferior wall (Fig. 4). He was discharged from the hospital on June 10.

Laboratory studies (Table I) showed the serum

cnz; mt’s. st~~un glutamic oxalacctic transaminase and lacnc dehydrogenase drawn two hours after his in- farction wrre very high and remained so for four days and seven days. respectively. ‘I’he white blood count became elevated on the second day-; the sedimenta- tion rate on the third and fourth days.

DISWSSION

This case represents reversal of “apparent death” by the prompt action on the scene by

TABLE I

Laboratory Studies During Hospitalization

May May May May May May May May May Test 15 16 17 18 19 21 22 24 28

WBC 8,500 21,700 15,300 I..

Sed. rate 3 27 40

BUN 31 41 42 ._. 23 21

SGOT 620 700 420 380 126 80 48 . . 26

LDH 1,000 1,280 2,200 1,880 1,450 1,040 760 560 160

WBG = white blood cells; Sed. rate = sedimentation rate; BUN = blood urea nitrogen; SGOT = serum glutamic oxalacetic transaminase; and LDH = lactic dehydrogenase.

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74 Black and Black

FIG. 3. Electrocardiogram showing nodal tachycardia 96 hours after admission.

physicians who know how to maintain artificial ventilation and circulation until spontaneous cardiac action can be established. It is remark- able that external cardiac massage could deliver cardiac output sufficient to maintain life for as long as described. However, when one con- siders that in severe aortic stenosis, stroke output has been estimated to be as little as 10 to 15 cc. in ambulatory patients, maintenance of ade- quate cardiac output by external cardiac mas- sage seems reasonable and feasible.

The indications for external cardiac massage are sudden death manifested by apnea, gasping or convulsions and the abrupt disappearance of pulse and heart sounds in a person who has previously been well or has the possibility of regaining worthwhile life. This would exclude terminally ill patients or those dying from incurable illness such as cancer, leukemia and the like.

A limiting factor in initiating treatment is a lapse of time following arrest. To effectively prevent permanent brain damage, resuscitative measures must provide adequate cerebral oxy- genation within four to six minutes.r3J4 Signs such as reversal of fixed dilated pupils or spon-

taneous movements after starting resuscitation indicate a possibly favorable outcome. Only after resuscitative measures are in effect should one attempt to diagnose the true cause of cardiac arrest, i.e., ventricular fibrillation or ventricular standstill.

During resuscitation many complications may occur, such as rib fractures, hepatic lacerations, pneumothorax and aspiration of regurgitated stomach contents. Skillful massage may min- imize these complications. Postresuscitative measures such as tracheal suction, administra- tion of oxygen, vasopressor therapy, anti- arrhythmic drugs and digitalization may all be vital. Hypothermia is recommended for pa- tients not awakening promptly after cardiac resuscitation.‘5 Experimental findings suggest less neurologic injury following cardiac arrest with the use of hypothermia.‘6Jr

Once normal rhythm is established by the presently accepted resuscitative measures, care- ful monitoring is essential, preferably by cardiac monitoring devices. Recurrent ven- tricular fibrillation, as occurred twice in the case reported here, if anticipated and detected promptly, may be of much shorter duration

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Cardiac Resuscitation from Ventricular Fibrillation 75

FIG. 4. Fkctrocardiogram on ninth hospital day.

and more susceptible to successful conversion. Arrhythmias following cessation of ventricular fibrillation should be anticipated and treated with the usual pharmacologic agents. In our patient, procaine amide was twice employed successfully in postfibrillatory ventricular tachy- cardia. The recent advent of direct current electroshock may offer further help in refractory arrhythmias and even ventricular fibrillation.‘8

Cerebral function following resuscitation may be temporarily impaired as noted by the confusion and amblyopia displayed in the described case. Brain edema occurring within a few minutes of circulatory arrest may be reversible. Intravenous ureaI and hypother- mia,l5*20 advocated as treatments for this complication, were not employed because of initial prompt awakening and significant im- provement within two to three hours. The transient neurologic defects sometimes noted should not be misconstrued as poor prognostic signs. Guarded optimism and attempted sal- vage should be the rule.

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SUMMARY

Cardiac resuscitation in a 40 year old man with acute myocardial infarction who had a sudden cardiac arrest in a physician’s office is described.

Successful external defibrillation was ac- complished 55 minutes after onset of cardiac arrest. The postfibrillatory course was com- plicated by cardiac arrhythmias, recurrence of ventricular fibrillation, central nervous system manifestations of convulsions, confusion and amblyopia.

Eight months after the onset of infarction, the patient is asymptomatic and preparing to return to his occupation as a mail carrier.

REFERENCES

1. BROFMAN, B. L., LEIGHNINCER, D. S. and BECK, C. S. Electrical instability of the heart: The concept of the current of oxygen differential in coronary artery disease. Circulation, 13: 161,1956.

2. HINTON, J. W., STEPHENSON, H. E. and DEL MISSIER, P. A. Cardiac arrest, a resume of experimental and clinical data. J. Not. M. A., 49 : 11, 1957.

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3. SASAHARA, A. A., RUDOLPH, A. M., HOFFMAN, J. I. E. and HAUCK, A. J. Ventricular fibrillation dur- ing catheterization of the right side of the heart terminated successfully by external defibrillation. New England J. Med., 261: 26, 1959.

4. RYAN, N. J. and CAYLER, G. G. Ventricular tibril- lation during cardiac catheterization. Am. J. Cardiol., 10: 120, 1962.

5. BLOOMFIELD, D. K. and MANNICK, .J. A. Successful resuscitation in acute myocardial infarction with ventricular fibrillation; report of case. Nezc England J. Med., 258: 1244, 1958.

6. BECK, C. S., WECKESSER, E. C. and BARRY, F. M. Fatal heart attack and successful defibrillation. J.A.M.A., 161:434, 1956.

7. TURRELL, D. J. and HUSNI, E. A. Cardiac resusci- tation after documented myocardial infarction. Am. J. Cardiol., 7: 736, 1961.

8. THAL, J. F., CERNEY, M. E., CONLON, D. J., TUSSMAN, M. A. and IRWIN, R. H. Closed-chest cardiac resuscitation in acute myocardial infarc- tion. Am. J. Cardiol., 7: 731, 1961.

9. SUSSMAN, I. Successful thoracotomy and cardiac massage in case of apparent sudden death due to acute myocardiaJ infarction. Am. J. Cordial., 10: 124, 1962.

10. Moss, A. J. et al. Closed-chest cardiac massage in the treatment of ventricular fibrillation complicat- ing acute myocardial infarction. New England J. Med., 267: 679, 1962.

11. KOUWENHOVEN, W. B., JUDE, J. R. and KNICKER- BOCKER, G. G. Closed-chest cardiac massage. J.A.M.A., 178: 1063, 1960.

12. SEIDE, M. J. Cardiac arrest; report of a case sur- viving closed-chest cardiac massage for 45 minutes outside the hospital. Hartford Hosp. ButI., 17: 16, 1962.

13. COLE, S. I,. and CORDAY, E. Four minute limit for cardiac resuscitation. J.A.M.A., 161: 1454, 1956.

14. NAST, P. R., PENNYPACKER, C. S. and WAGNER, J. A. Successful external electrical defibrillation in acute myocardial infarction; report of a case. Circula- tiorr, 22: 138, 1960.

15. WILLIAMS, G. R., JR. and SPENCER, F. C. The clinical use of hypothermia following cardiac ar- rest. Ann. Surg., 118: 462, 1958.

16. MARSHALL, S. B., OWENS, J. C. and SWAN, H. Tem- porary circulatory occlusion to the brain of the hypothermic dog. Arch. Surg., 72: 98, 1956.

17. MCMURREY, J. D., BERNHARD, W. F., TAREN, J. A. and BERING, E. A. Studies on hypothermia in monkeys. I. The effect of hypothermia on the prolongation of permissible time of total occlusion of the afferent circulation of the brain. sq., Gynec. @ Obst., 102 : 75, 1956.

18. LOWN, B., NEWMAN, J., AMARASINGHAM, R. and BERKOVITS, B. V. Comparison of alternating cur- rent with direct current electroshock across the closed chest. Am. J. Cardiol., 10: 223, 1962.

19. JAVID, M. Urea. New use of an old agent: Re- duction of intracranial and intraocular pressure. S. Clin. North America, 38 : 907, 1958.

20. BENSON, D. W., WILLIAMS, G. R., JR., SPENCER, F. C. and YATES, A. J. The use of hypothermia after cardiac arrest. Anesth. & A&g., 38: 423, 1959.

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