Comprehensive treatment plan for the prevention of primary ventricular fibrillation in acute myocardial infarction

Comprehensive Treatment Plan for the Prevention of Primary Ventricular Fibrillation in Acute Myocardial Infarction

MILFORD G. WYMAN, MD, FACC LUCILLE HAMMERSMITH, RN

San Pedro, California

Fromthe Departmentof Cardiology, San Pedro and Peninsula Hospital, San Pedro, Calif. Manuscript accepted January 3, 1974. Address for reprints: Milford G. Wyman, MD, 1360 West Sixth St., Suite 120, San Pedro, Calf. 90732.

This report of 1,165 cases of acute myocardiaf infarction outlines a method for preventing primary ventricular fibriiiatbn in patients wfth this lesion. The plan of prevention begins in the emergency room, wfth every patient suspected of having myocardial infarction receiving an intravenous bolus injection of lidocaine, 75 mg, followed by a 2 mg/min infusion controlled by an infusion pump. If administration of iidocaine is ineffective (19 percent of cases), procainamide is given intravenously in a dose of 100 mg every 5 minutes, repeated as necessary to a maximum of 1 g and followed by an infusion of 2 to 6 mg/min. Ventrlcuiar tachycardia is rapidly converted to sinus rhythm by either drug or eiectrical therapy. Monitoring by telemetry Is continued after the patient’s discharge from the coronary care unit. A new episode of sustained chest pain requires the reinstitution of prophylactic lkiocaine therapy. Important precautions to control the toxic effects of these intravenous medications can be achieved in the community hospital where the nursing staff makes the decision to increase the dose of lidocaine or to substitute procainamide. There has been no recognized mortality from the use of these drugs as outlined. With this total system of care, the prevalence rate of primary ventricular flbriiiation has been decreased from 6.5 percent (9 of 139 cases) to 0.3 percent (3 of 1,026 cases) and no deaths have occurred.

Prevention and treatment of primary ventricular fibrillation during the course of an acute myocardial infarction are the most important functions of the coronary care unit. Despite the reduced incidence of this type of cardiac arrest since the advent of such units, continued reports emphasize both the occurrence and associated mortality of primary ventricular fibrillation.1-8 These studies have raised the following questions: (1)Is primary ventricular fibrillation always preceded by “premonitory” arrhythmias? (2) Once premonitory arrhythmias occur, is there sufficient time for the institution of drug therapy to prevent primary ventricular fibrillation? (3) Are the currently used drugs effective in suppressing these premonitory arrhythmias or preventing primary ventricular fibrillation? The purpose of this report is to answer these questions and describe a method for preventing primary ventricular fibrillation. The technique has been developed over the past 7 years in a community hospital with neither a full time unit director nor house staff. This plan of treatment has reduced the prevalence rate of primary ventricular fibrillation from 6.5 percent (9 of 139 cases) to 0.3 percent (3 of 1,026 cases).

May 1974

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Volume 33

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160

~

E.R.

PROVEN AMI

LIDOCAINE

infusion

LID.

dc’d.

may be

is

Discha from C%J m 3 Days

IS begun after I V medlcatlon dlscontlnued.

Ordl Procalnamlde

MEDICAL FLOOR

FIGURE 1. Sample treatment plan for 160 patients with suspected acute myocardial infarction. Of the 160 patients admitted to the coronary care unit, 100 will be dllgnosed as having had an acute myocardial infarction. The plan represents treatment given to the last 611 patients with proved infarction. AMI = acute myocardial infarction: boli = bolus injection; CCU = coronary care unit; E.R. = emergency room; I.V. = in~avenous; LID. = liiocaine; MED. = medical; PRDC = procainamide; PVB’s = premature ventricular beats; VT = ventricular tachycardia.

-b

SUSPECT AMI

Trans. from

Sustained Chest Pain

F’REVENTION OF PRIMARY VENTRICULAR FIBRILLATION-WYMAN

Methods The data were collected during a 7 year period in a 165 bed community hospital that has neither house staff nor a full time unit director. All patients (1,165) diagnosed as having an acute myocardial infarction since the inception of the unit in 1966 were included in the study. The criteria for the diagnosis of acute myocardial infarction have been previously described9 and were the same as those used for the diagnosis of myocardial infarction in the California Regional Medical Program Study. Analysis of the electrocardiograms revealed new or significant change in preexisting Q waves in 78 percent of cases and evolutionary S-T and T wave changes without Q waves in 22 percent. All patients had significant rises in serum enzyme levels with at least a 100 percent increase in serum glutamic oxaloacetic transaminase and creatine phosphokinase. In this series 23 percent of all deaths occurred in the group without Q waves. Primary ventricular fibrillation was defined as fibrillation occurring in the absence of pulmonary edema or shock. All cases of secondary fibrillation occurred as an agonal event or when the patient had profound shock or pulmonary edema. Only cases of primary ventricular fibrillation occurring in the coronary care unit were included. The average duration of stay in the unit was 4.5 days. Arrhythmias were documented in the coronary care unit with standard monitoring equipment utilizing an alarmtriggered electrocardiogram, a memory loop and, in selected cases, a 10 hour continuous tape. Both lidocaine and procainamide were administered to patients by the nurse, as directed by a set of standing orders. Ventricular tachycardia was immediately terminated electrically (direct-current capacitor discharge) by the nurse if clinical deterioration occurred. Serum potassium determinations were performed in all patients on admission to the unit, and potassium replacement was begun immediately if hypokalemia existed.

Treatment Plan In Group I (the first 139 patients with confirmed acute myocardial infarction), prophylactic treatment was limited to orally administered procainamide or quinidine when multiple premature ventricular beats were observed. The doses were 250 or 500 mg of procainamide or 200 or 400 mg of quinidine every 4 to 6 hours, as determined by the attending physician. Ventricular tachycardia was treated with an intravenous infusion of procainamide at a rate of 50 to 100 mg/min until the arrhythmia was abolished or 1 gram of procainamide had been given. Electrical conversion was used if clinical deterioration was evident or if the use of procainamide had been unsuccessful. In Group II, (the last 1,026 patients with confirmed acute myocardial infarction), prophylactic intravenous administration of lidocaine was begun, and, if unsuccessful, procainamide was given intravenously. In the first subgroup (IIA, 145 patients) the criteria for initiating a lidocaine drip infusion were as follows if premature ventricular beats: (1) occurred on the T wave, (2) occurred in bursts (two in succession), (3) were multifocal, or (4) exceeded a rate of B/min. In the second subgroup (IIB, 270 patients) prophylactic administration of lidocaine was begun when the first premature ventricular beat was observed. The third subgroup (IIC, 611 patients) reflects the current procedure of administering lidocaine to every patient with suspected myocardial infarction. The treatment plan for every patient with suspected myocardial infarction begins in the emergency room. The

AND HAMMERSMITH

doses of lidocaine, and procainamide if needed, are as follows: Lidocaine, 50 mg, is given intravenously as a bolus injection, followed by 25 mg over the next minute. A 2 mg/ min drip infusion is then begun and continued over the next 24 hours. It is then slowly diminished and discontinued over the next 6 hours if no premature ventricular beats are observed. The patient is then given procainamide, 250 mg orally, every 4 hours until discharge from the hospital. If the premature ventricular beats are not controlled by the 2 mg/min infusion of lidocaine, a second and, if necessary, a third bolus injection of lidocaine is given, and the infusion rate is increased to a maximum of 4 mg/min. If lidocaine is ineffective at this dose, intravenous administration of procainamide is started. An infusion of 100 mg is given every 5 minutes and repeated as necessary (not to exceed 1 gram) to suppress ventricular extrasystoles. This is followed by infusion at a rate of 2 mglmin, which may be increased to 6 mg/min. The two drugs given in combination have appeared at times to have a more suppressant effect than either alone. If ventricular tachycardia ensues (rates over lOO/min) and is sustained despite drug treatment, electrical conversion is immediately carried out. After the patient is discharged from the coronary care unit to the ward, an intravenous pathway is maintained for

48 hours. Monitoring by telemetry is continued during the convalescent period. A patient experiencing a new episode of sustained chest pain during the convalescent period again receives prophylactic intravenous infusions of lidoCaine. A flow chart of the entire treatment plan is shown in Figure 1. The dose of lidocaine or procainamide is halved if shock, serious congestive failure or renal failure is present, since lidocaine is primarily detoxified by the liver and procainamide by the kidney.lOJl Blood pressure and QRS duration are carefully monitored when procainamide is given. Administration of this drug is withheld in the presence of second or third degree atrioventricular (A-V) block if a pacing catheter has not been inserted. If muscular twitching or change in sensorium is noted during the administration of lidocaine, the dose is decreased. Premature or escape ventricular beats resulting from sinus bradycardia or bradycardia due to heart block require increasing the ventricular rate by administration of atropine or cardiac pacing. If the ectopic beats continue after the ventricular rate is increased, suppressant therapy will be given as previously outlined. The following rules have been developed ocaine toxicity:

to prevent

lid-

1. All patients receive lidocaine by infusion pump. 2. Lidocaine is not given at a rate higher than 4 mg/min. 3. The dose of lidocaine is halved in the presence of severe congestive failure or shock. 4. In uncontrolled atria1 arrhythmias, the ventricular rate is slowed before treatment with lidocaine is begun.isJs 5. If ectopic ventricular beats appear to be enhanced by lidocaine (a rare occurrence), intravenous infusion of procainamide is substituted.

Results Prevalence and clinical factors: The mortality rate for the total series of 1,165 patients with acute myocardial infarction was 10.2 percent. The mean age of all patients in the series was 63 years. Shock occurred in IO percent, and moderate or severe congestive failure in 25 percent. Time from onset of pain until hospital admission was calculated in each case.

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I

TABLE

Prevalence of Primary Ventricular Fibrillation Administration of Lidocaine or Procainamide

Before and After Use of Prophylactic

Intravenous

Patients with Proved AMI

Primary VF Criteria for Prophylaxis

(no.) Group

139

I

Multiple

AMI = acute myocardial

PVBs

Procainamide (orally)

.

1,026 145 270 611

Group II A B C

Prophylaxis Plan

PVB = premature

%

9

6.5

3 0 1 2

0.3

or quinidine

Lidocaine (intravenous bolus injection, then infusion to 4 mg/min); if unsuccessful, procainamide (intravenous bolus injection, then infusion to 6 mg/min)

“Standard” criteria 1st PVB On admission with suspected AMI

infarction;

(no. of cases)

ventricular

beat; VF = ventricular

Fifty-eight percent of patients were admitted within 4 hours of onset and 29 percent within 1 hour of onset. Pump failure was the cause of death in all cases except for one case of primary ventricular fibrillation. Primary ventricular fibrillation occurred in 12 patients in the entire series; 1 of the 12 died despite immediate defibrillation. The other 11 were discharged from the hospital and are alive 6 to 84 months after the event. Table I shows the prevalence

... ... ...

fibrillation.

of primary ventricular fibrillation before and after prophylactic use of lidocaine and, if necessary, procainamide. Before this procedure was adopted, the prevalence rate of primary ventricular fibrillation was 6.5 percent (9 of 139). After its adoption, primary ventricular fibrillation occurred 3 times in 1,026 cases (0.3 percent). Premonitory cardiac arrhythmias: Table II shows the characteristics of the 12 patients with ven-

TABLE II Characteristics

of Patients with Primary Ventricular

Fibrillation

Time (hours) From Pain to Fibrillation

From Pain to Admission

1 2

44M 45M

1 1

1 2

2 3

Inf Inf

3

53M

1

2 112

3 l/2

Inf

We of Infarct

5

54F 56M

1 1

1 15

2 16

Inf Inf

6 7

58M 60M

1 3

3 137

4 140

Ant Inf

4

8 9

63M 63M

2 12

10

69M

12

11

71F

3

12

77F

6

A = alive; Ant = anterior;

664

From Admission to Fibrillation

Age (yr) & Sex

Case no.

May 1974

10 20 113

3 D = died;

The Amerkan

12 32

Inf Ant

12

Ant

5

Ant

9

Inf

Inf = inferior;

PVB = premature

Journal of CARDIOLOBY

Volume 33

Premonitory Rhythm Sinus with PVBs Sinus tachycardia PVBs Sinus with PVBs

with

Sinus with PVBs Atrial flutter with rare PVB Sinus with no PVBs Atrial flutter with rare PVB

Sinus with Junctional PVB Sinus with (R on T) Sinus with (R on T) Junctional ventricular

Prophylactic Medication

Outcome

None None

A A

Lidocaine

A

(3 mg/min) Quinidine Digitalis; none None Procainamide

A D A A

rare PVB with rare

(orally); lidocaine (intravenously, 2 mg/min) None Quinidine

A A

rare PVB

None

A

rare PVB

Quinidine

A

with PVBs

None

A

beat.

PREVENTION OF PRIMARY VENTRCULAR

tricular fibrillation. More than half (7 of 12) were 60 years of age or less; the average age was 59. In 8 of the 12, ventricular fibrillation developed within 3 hours of the patient’s admission to the coronary care unit; in 6 of the 12, it occurred within 5 hours of the onset of pain. In seven, only a rare or no premature ventricular beat was noted before the onset of the fibrillation. No episode of primary ventricular fibrillation was immediately preceded by ventricular tachycardia or preceded at any time by sinus bradycardia, junctional bradycardia or A-V block. Two episodes occurred after inadequate control of atria1 flutter. The single death from primary ventricular fibrillation occurred before the use of lidocaine. This patient had atria1 flutter with a ventricular rate of 150/min. Digoxin was given intravenously, but shortly thereafter, with only a rare ectopic ventricular beat, ventricular fibrillation occurred. Defibrillation was unsuccessful. In one patient (Group IIB) with primary ventricular fibrillation there were no preceding ectopic ventricular beats, as documented with use of a 20 minute memory loop. This occurrence of primary ventricular fibrillation without any warning prompted the initiation of prophylactic lidocaine therapy to all patients with suspected myocardial infarction (Group IIC). One patient in this latter group had ventricular fibrillation on the fifth hospital day. His course was complicated by hypotension, heart failure, multiple pulmonary emboli and atria1 fibrillation and flutter. Despite intravenous administration of digitalis, the ventricular rate was not adequately slowed, and during one of many episodes of atria1 flutter, ventricular fibrillation ensued, which was converted to sinus rhythm by direct-current defibrillation. At the time of the ventricular fibrillation, the patient was receiving a 2 mg/min infusion of lidocaine. The second patient in Group IIC who demonstrated ventricular fibrillation was given a 3 mg/min infusion of lidocaine after a brief run of bigeminy. No ectopic ventricular beats were noted for 15 minutes before the occurrence of ventricular fibrillation. Treatment outside the coronary care unit: The prevalence data on primary ventricular fibrillation in this report have included only those documented cases occurring in the coronary care unit. The treatment program during the 7 years was expanded to include the emergency room area and the general medical floor. In those patients who received lidocaine therapy in the emergency room (last 611 cases), no cases of primary ventricular fibrillation occurred either in the emergency room, on the elevator or in the halls as the patient was transported to the unit. Three cases of primary ventricular fibrillation occurred in the emergency room before intravenous tubing could be inserted and lidocaine administered. Monitoring after discharge from the unit was used in the last 810 cases. Sudden death has rarely occurred since the addition of this step to the program. Five patients died suddenly on the medical floor, but the arrhythmia at the precise moment of clinical

FIBRILLATION-WYMAN

AND HAMMERSMTH

death was not recorded since the telemetric equipment has no memory loop. Two of these patients underwent autopsy; one had a large fresh pulmonary embolus in the left main pulmonary artery, and one a fresh occlusion of the left main coronary artery. Other treatment for ventricular arrhythmias: It was necessary to supplement or replace lidocaine with procainamide in 19 percent of patients because of inadequate control of the ectopic ventricular rhythms. In less than 1 percent of patients requiring procainamide, the ventricular rhythm still could not be controlled. Diphenylhydantoin, bretylium tosylate, propranolol hydrochloride or overdrive pacing was then used. Rapid ventricular tachycardia was quickly and successfully converted to sinus rhythm by chemical or electrical therapy. Accelerated idioventricular rhythm was generally controlled by administration of atropine. However, a gradual acceleration of the focus was commonly observed and, in these instances, lidocaine or procainamide proved effective. In two patients with an accelerated idioventricular rhythm, a 2:l exit block was recognized when the ventricular rate exceeded 160/ min. It should be pointed out that most ectopic ventricular rhythms occur in the first 24 hours of an acute myocardial infarction; in some instances, it is difficult to determine if time alone is as important as drug therapy in controlling the ventricular rhythms. In others, a prior history of ventricular premature beats is associated with difficulty in suppressing such a focus. Lidocaine and Procainamide Toxicity

Lidocaine: This agent has been used in more than 1,550 patients since the inception of the coronary care unit. Infarction was documented in approximately 950 patients; more than 550 patients were found to have had no infarction. The latter patients experienced no significant side effects from the administration of lidocaine (75 mg bolus injection and a 2 mg/min drip infusion). Minor transient central nervous system complaints could be elicited after the initial bolus injection; spontaneous complaints were unusual. In the patients with documented myocardial infarction, effects on the central nervous system were dose-related. Three patients early in the series had convulsions caused by a “runaway” infusion. This complication has since been prevented by the use of infusion pumps in all patients. No adverse hemodynamic effects were found. The effects of lidocaine on the sinus rate and P-R, QRS and Q-T durations were studied in 100 consecutive patients. These measurements were performed on the surface electrocardiogram every minute for the first 15 minutes after the initial 75 mg bolus injection, and then hourly for the ensuing 30 hours. No statistically significant effects were found. Twenty patients in this group had sinus rates of less than 60/min, and none manifested further slowing. Blood lidocaine levels were serially measured in 25 patients who had received the bolus injection plus the 2 mgl

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min infusion. The results showed that no patient demonstrated drug buildup after administration of lidocaine for a 30 hour period. Procainamide: Intravenously administered procainamide was used in 19 percent of patients because of the ineffectiveness of lidocaine. With this method of administration, serum procainamide levels did not exceed 10 mg/liter. Significant widening of the QRS duration was recognized in one case, and prolongation of the Q-T interval was frequently observed. Significant hypotension rarely occurred. Discussion As currently used throughout the world, lidocaine prophylaxis has reduced the mortality from acute myocardial infarction, but many patients still experience primary ventricular fibrillation and subsequently die. In many cases these deaths occur because the so-called premonitory ventricular rhythms are absent or unrecognized. I* Bennett and Pentecost? clearly d~umented the absence of electrocardiographic warning in 27 patients with primary ventricular fibrillation: Five (19 percent) had no warning at all, 2 (7 percent) had warning for less than 5 minutes, and 20 (74 percent) had fewer than five premature ventricular beats per minute. In our study, 7 of 12 patients with primary ventricular fibrillation had no premonitory ventricular arrhythmias. In other studies3e8 from 25 to 83 percent of such patients have had no warning arrhythmia. Factors in prevalence of ventricular fibrillation: Prevalence data on primary ventricular fibrillation have been documented in only a few reports and have generally been limited to instances in the coronary care unit. The rates have ranged from 2.4 to 10 percent. Data on the prevalence of primary ventricular fibrillation in the emergency room and after discharge from the coronary care unit are sorely needed. Because most of the published reports are from units with both house staff and full time director and data from large numbers of community hospitals are lacking, it is not possible to estimate the true incidence of this potentially lethal complication. In a recent 3 year study’5 conducted in 100 hospitals in California, the prevalence rate of primary ventricular fibrillation in the coronary care unit was 5 percent (793 of 15,031 cases), and 47 percent of these patients died. Of all the deaths that occurred in the entire study, 17 percent were due to a primary arrhythmia. Two major factors other than treatment may account for differences in the prevalence rate of primary ventricular fibrillation from one hospital to another. The first is definition of the arrhythmia; the second, the rapidity with which patients are hospitalized. Definition: The definition of primary ventricular fibrillation used in our study is more inclusive than that generally used. laf17 In our hospital patients who have ventricular fibrillation accompanied by moderate congestive failure are classified as having primary

899

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The American Journal of CARMOLOGY

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fibrillation; only patients with pulmonary edema or shock are considered to have secondary ventricular fibrillation. Time from onset of symptoms:The second factor that may influence the prevalence rate of primary ventricular fibrillation is the interval between onset of symptoms and hospitalization. In our study 58 percent of patients were hospitalized within 4 hours and 29 percent within 1 hour; this delay is generally less than that reported in other studies.3+1sJs Effect of treatment plan: Neither of the preceding factors accounts for the low prevalence rate reported here. Since our definition of primary ventricular fibrillation was more inclusive and our patients were hospitalized earlier during their acute myocardial infarction than in other reported series, the extremely low prevalence rate (0.3 percent) of primary ventricular fibrillation in our study must have resulted from the treatment plan. This plan takes into account the multiple conditions that predispose the patient to primary ventricular fibrillation and deals with each in a specific manner. The high prevalence rate during the first hours and the lack of warning arrhythmias are countered by the use of lidoeaine in every case of suspected myocardial infarction in the emergency room. There is evidence that lidocaine has a direct effect on the myocardium, decreasing its vulnerability to development of fibrillation.*O The ineffectiveness of lidocaine in approximately 19 percent of patients is dealt with by the early use of intravenously administered proeainamide. The danger of a rapid ventricular tachycardia degenerating into ventricular fibrillation is countered by rapid conversion to sinus rhythm by chemical or electrical means. The high rate of sudden death after a patient is transferred from the coronary care unit is prevented by telemetric monitoring until time of discharge, and reinstitution of prophylactic lidocaine therapy if a new episode of chest pain occurs or new bursts of ectopic ventricular beats are recognized. Reports of controlled trials with routine antiarrhythmic prophylaxis have shown a reduction in ectopic ventricular rhythms but not in primary ventricular fibrillation; this finding is expected.2i-23 The control patients in all of the reported studies were given lidocaine as soon as premonitory ventricular arrhythmias were recognized and were therefore removed from the control population. In addition, the number of cases in each trial was small. A controlled trial of a plan involving multiple steps, such as that presented here, would be a difficult undertaking in a single hospital. A cooperative study involving several institutions may be able to test this treatment program. We believe that primary ventricular fibrillation is a preventable complication of acute myocardial infarction, requiring a plan that recognizes the precise time the patient is most susceptible and, in the absence of the physician, the initiation of prophylactic measures by nursing personnel.

PREVENTION OF PRIMARY VIM-RKXJLAR

FIBRILLATION-WYMAN

AND HAMMERSMTH

References 1. Julian DG, Valentlne PA, Miller GO: Disturbances of rate, rhythm and conduction in acute myocardial infarction. Am J Med 37:915-927.1964 2. Ruck DC, Gken E, Pentecoel BL, et al: Natural history and clinical significance of arrhythmias after acute cardiac infarction. Br Heart J 29:170-1891967 3. Lawrfe GM, Hi@ns MR, Godman JM, et al: Ventricular fibrlfation complicating acute myocardial infarction. Lancet 2:523528, 1968 4. Lawrfe MH: Ventricular fibrillation in acute myocardiaf infarction. Am Heart J 781424-1425, 1969 5. Church 0, Blem RO: Intensive coronary care-a practical system for a small hospital without house staff. N Engl J Med 281: 1155-l 1591969 6. Dhurandhar RW, MacMillan RL, Brown KWO: Primary ventricular fibrillation complicating acute myocardial infarction. Am J Cardiil27:347-351, 1971 7. Becener MB: G~n~tive comparison of bretylium with other antifibrillatory drugs. Am J Cardiol 21:504-512, 1968 8. Bennett MA, Pentecost BL: Warning of cardiac arrest due to ventricular 8b~l~t~n and tachycardia. Lancet 1:1351-1352, 1972 9. Wyman MO, Hammersmlth L: Coronary care in the small community hospital. Dis Chest 53:584-59X 1968 10. Glanetly R, Von Ger Greeben JO, Sptvak AP, et al: Effect of Iiiocaine on ventricular arrhythmias in patients with coronary heart disease. N Enal J Med 277:1215-1219. 1967 11. Rigger JR Jr, Hel&nbuttet RH: The use of procainamfde and Rfocaine in the treatment of cardiac arrhythmias. Prog Cardiovast Dis 11:515-534, 1969 12. Kllllp 1: Discussion. In, Lidocaine in the Treatment of Ventricular A~~rn~s (Scott DB, Julian DG, ed). Edinbur~, E & S Living ston. 1971, p 227

13. Marriott HJL, Pleza Cl? Alarming ventricular acceleration after liiocaine administration. Chest 61:682-683. 1972 14. Romhllt DW, ~~ SS, Cbou T, et at: Unre~~bili~ of conventional electrocardiographic monitoring for arrhythmia detection in coronary care units. Am J Cardioi 31:457-46 I, 1973 15. Wyman MO, Swan HJC, Rapaport E, et al: Arrhythmia deaths in 15,000 acute myocardiil infarctions (abstr). Circulation 48: Suppl IV:IV-40, 1973 18. Gflver MP, Julian DO, Donald KW: Problems in evaluating coronary care units: their responsibilftes and their relation to the community. Am J Cardiil20:465-474, 1967 17. Jewltt D: The genesis of cardiac arrhythmias in acute myocardial infarction. In. Proaress in Cardioloov lYu PN. Goodwin JF. ed). Ph~~~~~w, Lea i Febfger, 1972, p6;-90 18. Lown B, Fakhro AM, Hood WB Jr, et al: The coronary care unit-new ptL*spective and directions. JAMA 199:188-198, 1967 19. Pentecost BL, Mayne NMC: Results of a general hospital coronary care service. Br Lied J 1:830-833, 1988 20. Spear JF, Moore EN, Gerstenblfth 0: Effect of lidocaine on the ventricular fibril~~~n threshold in the dog during acute ischemia and premature ventricular contractions. Circulation 46:65-73, 1972 21. Mogensen L: Ventricular tachyarrhythmias and lignocaine prophylaxis in acute myocardfi infarction: a clinical and therapeutic study. Acta Med Stand: Suppl513:1-80, 1970 22. Koch-Weeer J, Klein SW, Poe-Canto LL, et al: Anti-arrhythmic prophylaxis with procainamide in acute myocardiil infarction. N Engi J Med 261:1263-1260, 1969 23. Bloomfield SS, Romhlll DW, Chou T, et al: Quinidins for prophylaxis of arrhythmias in acute myocardial infarction. N Engl J Med 285:979-986, 197 1

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