The Management of Acute Myocardial Infarction

Symposium on Circulatory Diseases

The Management of Acute Myocardial Infarction MILTON W. ANDERSON

diagnostic features, statistics as to incidence and prognosis, electrocardiographic evidence, and pathologic findings for a.cute myocardial infarction are well known and documented. Yet we must admit that at the present time the basic cause for the atherosclerotic disease which leads to myocardial infarction remains unknown despite intensive investigation of lipid metabolism and other supposed factors. In the absence of ability to prevent coronary atherosclerosis, there is continuing need for review of the management of the patient who has an acute heart attack. Evaluating critically the topics of recently published discussion concerning the management of acute myocardial infarction, however, one finds no contribution to compare with such medical advances as, for example, the employment of antibiotic drugs against infection. Controversy has been generated about such points as the length of hospitalization, rest in bed or arm-chair convalescence, and whether the use of anticoagulants is indicated for all patients. 2 • 3, 6 Although these controversial topics are interesting, the clinician is left with the realization that there is no specific therapy for the treatment of necrotic myocardium secondary to occlusive coronary disease, and that the outcome of disease depends mainly on two factors-first, the inherent capability of the injured heart to recover from its insult, and second, the doctors' ability to foresee and counteract disastrous complications of the myocardial infarction. . The physician has five basic aims or objectives in his management .of the patient with acute myocardial infarct. They cannot be accomplished by a routine, but require individualization in each case. Broadly ~ressed, they are (1) establishing the diagnosis, (2) controlling symp849

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tOffio, (3) preventing and treating cOlnplications, (4) encouraging healing and myocardial revascularization, and (5) supervising postinfarction convalescence and rehabilitation. ESTABLISHMENT OF DIAGNOSIS

It can be said generally that the suspicion that acute myocardial infarction has occurred is sufficient evidence for beginning treatment. If one uses this principle he is less likely to err in the direction of omission, and overzealousness is seldom criticized. One stipulation, however, must go with this therapeutic plan: the physician must not allow fear, shame, or stubbornness to keep him from informing his patient frankly if serial electrocardiograms and other diagnostic tests during a few days of hospital observation fail to confirm the suspicion of heart attack. The frequency with which one sees patients whose lives have been marred by anxiety from having the unfounded diagnosis of heart disease attached to them and not removed after an episode of chest-wall pain, pleuritis, or indigestion secondary to disease of the gastrointestinal or the biliary tract is disheartening. Suspicion that acute myocardial infarction has occurred is indication for either hospitalization or the prescription of rest in bed at home pending the assistance of electrocardiography or consultation for establishing a diagnosis. The period to be allowed for definitive diagnostic findings to develop can vary inversely with the depth of suspicion that infarction has occurred. If the pain and systemic reaction are typical, one's suspicion is greater; and it is not unreasonable to keep the patient inactive for a week before reassuring him that no heart attack has occurred. In the last few years other tests of diagnostic value for acute myocardial infarction have become available. These include measurement of certain enzymes and the other factors in the blood. A widely accepted and accurate test is the determination of serum glutamic-oxalacetic transaminase-or, more simply, the transaminase test. Both experimentally and clinically a high degree of correlation has been found between a significant rise in serum transaminase and myocardial injury. Following infarction the concentration of serum transaminase has been found to reach from two to 20 times normal in the first 48 hours. l This test is especially valuable for diagnosis in the patient who has an abnormal electrocardiographic pattern, such as that of left bundle-branch block, which can obscure a pattern diagnostic of infarction. Mention should be given also to the syndrome of impending myocardial infarction. This entity is manifested by progressive increase in the frequency, duration, and intensity of anginal pains, or the occurrence of nocturnal angina in a patient known to have coronary heart disease. Such symptoms may well be evidence of rapidly progressive occlusive atherosclerotic coronary disease or even of coronary thrombosis. Patients thus affected are in danger of sustaining extensive myocardial

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infarction, and pending subsidence of the progressive syInptoms should have the benefits of a program of rest and sedation, with administration of coronary vasodilators and anticoagulants. In these cases, which may present transitory electrocardiographic changes involving mainly the T waves, serum transaminase studies are helpful in determining the presence of true infarction. CONTROL OF SYMPTOMS

In emergency care of patients with acute heart attack the symptolns~ which include in varied degree pain, apprehension, dyspnea, and shockrequire attention first, since each of these symptoms may in itself aggravate the existing coronary insufficiency and increase the seriousness of the attaek. Pain

The physician should quickly evaluate the severity of the pain and administer either morphine sulfate or another opiate. One should not overdo in opiate therapy, however, nor overemphasize its specificity. If the pain has subsided spontaneously when the patient is seen, no need exists for giving a drug which possibly may cause a gastrointestinal upset or even be followed with an allergic reaction. When pain is mild, meperidine (Demerol) or codeine is adequate; but if pain is severe and terrifying to the patient, morphine sulfate given by intravenous injection may be required for its control. Repetition of opiate injections should depend on continuation of pain and should not be done on a routine order. Usually there is adequate time for tile physician to learn from the patient or his family whether he has a known intolerance to opiates. Unless there is a marked hypotensive reaction, it probably is wise to add atropine sulfate when morphine is administered. Apprehension

Besides reducing pain, the opiate will help to allay apprehension. '-fhis symptom, so frequent with cardiac patients, requires tact and reassurance on the part of the physician. The use of barbiturates or other sedative drugs is to be encouraged during the patient's hospitalization to insure his rest and ease his anxiety. Care should be taken, however, to give no more than is needed and also to withdraw the drug with the patient's improvement so that dependence is not acquired. Even in this early stage of the illness, attention must be devoted to prevention of later cardiac neurosis and to eventual rehabilitation. Dyspnea

As a symptom accompanying myocardial infarction, dyspnea can be mere reflexive tachypnea from pain or, in forms varying from mild orthopnea to severe pulmonary edema, it may represent myocardial

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failure. The milder types of dyspnea require and respond to elevation of the head of the patient's bed and control of his pain with opiate drugs. Against milder and more severe dyspnea, oxygen should b~ used. Oxygen therapy for acute myocardial infarction is well established; but like other routine procedures in treatment, it is overdone at times with resultant increase of expense and apprehension on the part of the patient. In the presence of persisting symptoms and signs, including pain, dyspnea, pulmonary congestion, cyanosis, or shock, the patient should be supplied with oxygen by means of a tent, mask, or nasal catheter, depending on which method is available and most comfortable. When these indications exist, the use of oxygen should be continued until their control is insured. In mild cases in which pain and other symptoms have disappeared by the time of hospitalization, there is no need to cause alarm by insisting on use of oxygen. Shock

In the presence of acute myocardial infarction, shock is an omen which enjoins a guarded imm~diate prognosis but still is not necessarily a sign of massive infarction incompatible with recovery. Most cardiologists can recall quickly instances of patients in profound shock who, after rallying from that state, went on to uncomplicated convalescence and recovery with a good cardiac reserve. Statistical studies have indicated that when shock does not spontaneously clear on control of pain and administration of oxygen the mortality rate is as high as 80 per cent. Since, despite this formidable prognosis, untreated shock still does not necessarily denote irreparable myocardial destruction, an energetic attack on this syndrome is justified, for continued hypotension further aggravates the coronary insufficiency. Loss of blood or fluid is not the basic cause of shock in acute myocardial infarction, and consequently infusion therapy is likely to be ineffectual. Indeed, intravenous infusions may be instrumental in overloading the damaged heart and lead to pulmonary edema. The recommended approach to the problem of shock associated with myocardial infarction is to insure coronary perfusion by restoration of aortic pressure through administration of vasopressor agents which make the peripheral vascular bed contract and act directly on the heart muscle to increase its contractility. Unfortunately, in the use of any of the vasopressor drugs there remains some risk of inducing cardiac arrhythmias; but the mortal risk of unrelieved shock warrants employment of a vasoconstrictor against such a condition. If the hypotensive reaction is not too alarming, usually the effect of ephedrine injected subcutaneously or of phenylephrine (Neo-Synephrine) given intramuscularly may be tried with the hope that shock may be averted. For severe shock, if that occurs, the most potent vasopressor available is levarterenol (Levophed), which is administered in dilute solution by slow intra-

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venous drip.4 The usual practice is to dilute one 4-cc. ampule of 1: 1000 solution in 1000 cc. of 5 per cent dextrose solution, and to regulate the rate of administration to accord with the blood pressure response. If a drip rate of more than 50 or 60 drops per minute is required to keep the pressure between 100 to 120 mm. of mercury, two or more ampules of Levophed may be put into the glucose solution so that the patient need not be given too much fluid. It must be remembered that Levophed is an extremely potent drug: administration of it must be under constant surveillance, and infiltration of the tissues by it will cause local necrosis and sloughing. Use of it should be continued as long as necessary, which may be merely a few hours or may be several days; and usually the patient must be carefully weaned from it to prevent a reactive hypotensive withdrawal effect. Mephentermine sulfate (Wyamine Sulfate) and metaraminol (Aramine), other vasopressor agents, are receiving favorable reports in the literature. These drugs apparently are not so potent as Levophed, but have the advantage that they may be administered either continuously by the intravenous route or intermittently by intramuscular injection. 5 The dosages recommended for these drugs are to be found among the directions which accompany the ampules. PREVENTION AND TREATMENT OF COMPLICATIONS

Any complication arising in a case of acute myocardial infarction entails worsening of the prognosis; in dealing with this factor, therefore, the emphasis should be placed on prevention rather than treatment. The complications which most frequently increase hazard to the patient include congestive heart failure, thrombo-embolism, arrhythmia, and myocardial rupture. Myocardial Rupture

No strongly effective prophylactic measures against myocardial rupture are known, and its occurrence invariably is fatal. An especially likely candidate for rupture of the heart is the patient who had hypertension before infarction and who presents electrocardiographic evidence of transmural involvement. His most hazardous period is the first week after the attack, during which time strict rest in bed, sedation to prevent disquietude, and avoidance of straining at stool, vomiting, and similar sudden acts are important prophylaxis. Arrhythmias

For the average person, occasional and even frequent extrasystoles are a benign symptom and seldom require other treatment than reassurance. In the patient who has had an acute myocardial infarction, however, they must be considered alarming as a manifestation of myocardial hyperirritability due to ischemia and as the harbinger of a major j~;disturbance of rhythm. In the presence of fairly frequent extrasystoles

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in such a patient, quinidine sulfate in doses of 3 to 6 grains given three to five times daily may prevent ventricular tachycardia or fibrillation. 'rwo hundred and fifty to 500 mg. of procainamide (Pronestyl) may be given orally instead of the quinidine if the patient is intolerant to the latter. In view of this occasionally encountered intolerance, the routine administration of quinidine sulfate to all patients with infarction does not seem justified, although the plan does have proponents. Despite careful observation and prophylaxis, the occurrence of ventricular tachycardia is not rare following myocardial infarction. It is a complication requiring rapid treatment to avoid terminal ventricular fibrillation or uncontrollable congestive failure. For the patient whose condition is satisfactory otherwise, an attempt can be made to bring about conversion of his rhythm with oral quinidine using 6 to 9 grains every two hours for five doses or until conversion occurs. Since the usual patient with myocardial infarction is critically ill, this complication usually calls for fast action such as is supplied by the intravenous administration of procainamide (Pronestyl). One gram of Pronestyl should be diluted with 5 per cent dextrose solution and be given not more rapidly than 100 mg. every minute or two, preferably with monitoring by means of a direct-writing electrocardiograph during the administration so that the injection can be stopped immediately on cessation of the ventricular tachycardia, or on appearance of electrocardiographic evidence of increasing conduction defect. Both quinidine and Pronestyl may be administered intramuscularly. When the rhythm has been restored to normal, prophylactic use of quinidine should be continued until the patient is definitely convalescent. Rapid disturbances of auricular rhythm, including fibrillation and flutt~r, constitute a hazard to cardiac compensation and also may be instrumental in loosening thrombotic material. In emergency care of the patient with an acute heart attack, the use of digitalis to control the rate is preferable to attempting conversion. Congestive Heart Failure

Rapid onset of the signs and syrnptoms of congestive heart failure is always to be feared and watched for. '-rhe patient may first experience slight dyspnea and orthopnea. Usually, however, the capable physician will note the appearance of a few moist rales over the lung fields or ft gallop rhythm, whieh indicates to hirn the need for preventive therapy. Restriction of sodium in the diet and administration of a mercurial diuretic, such as intramuscular injection of 1 or 2 cc. of mercaptomerin (Thiomerin) or meralluride (Mercuhydrin), will prevent or control the milder tendencies toward fluid retention. When frank congestive failure appears imminent despite these simpler measures, full treatment for congestive failure-employing digitalis, oxygen, and diuretics-should be instituted promptly. The developnlent of acute pulmonary edema

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requires heroic measures which in no way differ from those used against it in other situations. Thrombo-embolism

An important contribution of the last decade to the management of acute myocardial infarction is the use of anticoagulants for prevention of arterial and venous thrombo-embolism. Although evidence is lacking to suggest that there is any specific effect upon the coronary occlusion per se, nearly uniform experience points to lower mortality and lower morbidity, by virtue of the reduced incidence of thrombosis and embolism, among patients in whom adequate anticoagulant therapy was maintained during the acute episode. 6 If the physician develops a proper perspective in regard to the predictable benefits from anticoagulants and weighs these against the possible hazard of anticoagulant drugs for the specific patient in his particular locality, the decision concerning employment of this form of treatment should not be difficult. We can predict that with good therapeutic control anticoagulants will greatly inhibit the development of thrombophlebitis and subsequent pulmonary emboli, and also inhibit the separation of embolic material from mural thrombosis overlying the infarcted ventricular myocardium. Otherwise, one or more of these complications are likely to occur in the presence of severe or extensive infarction, especially if the patient suffers shock or congestive failure as a result of the infarction. The benefits to be obtained from anticoagulants must always be balanced against the possible hazards. l'he major contraindications to anticoagulant therapy are inexperience on the part of the prescribing physician and inaccuracy on the part of the clinical laboratory which is determining the prothrombin levels. The experienced physician will be aware of the hazards of using anticoagulants in patients with potential cerebral or gastrointestinal bleeding lesions, and without adequate laboratory control anticoagulant therapy is futile and dangerous. Although proponents of anticoagulant therapy for all patients are opposed by others who would exclude "good risk" patients, it seemingly would be nearly impossible when the patient is first seen with acute myocardial infarction to foretell accurately his clinical eourse; and therefore under ideal conditions every possible patient should have the theoretical benefits of anticoagulant therapy. r-rhe anticoagulant preparations in common usage are heparin and various eoumarin derivatives, of which bishydroxycoumarin (Dicumarol) is used most widely. The plan of attack with anticoagulants is variable, depending on the factors of the individual case. If the patient is still in pain when seen and hospitalized, or if he exhibits shock, arrhythmia, or congestive failure Upon admission, heparin and derivatives of coumarin are suitable medicaments. Treatment is started immediately with 300 mg. of Dicumarol and 900 or 1200 mg. of ethyl biscoumacetate (r-rrornexan) given by mouth

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and 50 mg. of heparin injected intravenously. l"'he dose of heparin is repeated every four hours until the effect of Tromexan and Dicumarol on the prothrombin time is noted 24 to 48 hours later. Dicumarol then is given in daily doses of sizes regulated to maintain prothrombin activity between 10 and 30 per cent of normal. Anticoagulant treatment, once begun, is continued throughout the period of hospitalization unless complications of such therapy cause cessation. Fortunately there is available an effective antidote in the form of vitamin KJ, which should be used if prothrombin activity is excessively depressed or if bleeding occurs. ENCOURAGEMENT OF HEALING AND MYOCARDIAL REVASCULARIZATION

That the discussion on encouragement of healing is a catch-all or wastebasket category in the presentation of over-all management of myocardial infarction implies the difficulty of dealing with the actual pathologic lesion, the occluded coronary artery, and the necrotic myocardium. It is depressing, yet literally true, that the physician has no specific approach to this phase of the coronary problem, but must depend upon nature's bounty, to which his assisting efforts are but ancillary. Ideally, the patient with acute myocardial infarction should be hospitalized throughout the initial period of its management. To fix limits for the length of hospitalization should not be attempted. It may be as short as two weeks for a patient with minor infarction and as long as three months for the severe, complicated case. The decision with respect to ambulation-and hence dismissal from the hospital-depends on clinical judgment supported by stabilization of the electrocardiographic pattern and normalization of the erythrocyte sedimentation rate. Rest occupies the key role in the encouragement of healing. There has been considerable discussion recently concerning the relative merits of chair rest versus bed rest. This controversy is unimportant, since the significant term here is rest, not chair or bed. A recommended practice is to ask patients with uncomplicated myocardial infarction to remain in bed for the first 10 to 14 days except for sitting up on the bedside toilet commode for bowel movements. This request is augmented with a frank explanation of the patient's existing pathology so he knows the purpose of the request. An occasional patient will be so restless, disturbed, or uncomfortable staying constantly in bed that permission to sit in a chair should be granted. As mentioned earlier, sedatives may be needed to insure rest therapy. Care must be given to dietary management also. In the early days of infarction a soft bland diet is prescribed. If the patient is at all overweight, caloric restriction is imposed and continued. Mild laxatives or even small enemas using warm tap water may be needed to guard against constipation and abdominal distention. The emphasis on the rest pro-

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gram must be implemented with patience and encouragement on behalf of the physician and nursing attendants. Some patients continue to have episodes of angina pectoris while at rest in the hospital. This symptom requires attempts at management. The inhalation of oxygen by mask after meals may have a helpful effect and is worthy of trial. If pain is frequent or persistent, aminophylline is frequently of benefit when administered by rectal suppository or by slow intravenous injection with 0.5 gm. aminophylline diluted in 200 cc. of 5 per cent dextrose solution. Similarly, papaverine in oral doses of 1 to 1}1 grains three or four times daily appears sometimes to have a coronary vasodilatory effect. Healing and cardiac revascularization are inherent in the patient's reparative ability, and the physician's responsibility is to provide the physical and emotional environmental situation in which that reparative process can best proceed. SUPERVISION OF POSTINFARCTION CONVALESCENCE AND REHABILITATION

Medical care of the patient who has had an acute myocardial infarction is not completed when he leaves the hospital. His convalescence at home must be one of gradual increase in activity, continuing at least four weeks and usually longer before it is advisable for him to return to work on even a part-time basis. During this convalescence regular rest during the day is encouraged. During this time also the overweight patient should be diligent with his reduction program. In general, at this phase in his convalescence the same advice should be given to the patient who has had a heart attack as is given to the one with angina pectoris. He and his phy~ician must work toward a philosophic acceptance of an illness which will require that he assume a lower level of activity in the future and adopt a less competitive attitude toward living. It is equally important that he be reassured so that he can approach the future affirmatively with the knowledge that his life can be enjoyable and productive. In the present state of knowledge the young man with coronary artery disease, particularly if he is obese or if he has elevated concentrations of serum lipids, should be asked to follow a low-fat diet indefinitely. Also, general advice should be given with regard to avoiding tobacco, eating small meals, resting after meals, and keeping regular habits of work and recreation. For the patient who has residual effort angina, nitroglycerin should be prescribed with appropriate directions. It may be helpful also to prescribe a course of 10 to 20 mg. of pentaerythritol (Peritrate) four times a day for two to three months, with the advice that the drug be discontinued at the end of that time if the patient is asymptomatic or if it appears to make no difference in his symptoms. Finally, a word should be said concerning long-term use of anticoagu-

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lants. 1"1he potential hazard with anticoagulants, the unpredictable response to a given dose even in the same person, and the inconvenience to the patient of frequent blood tests are sufficiently good reasons to make long-term anticoagulant therapy unfeasible as a routine measure for all patients who have recovered from acute myocardial infarction. In spite of this opinion, supporters of long-term treatment with anticoagulants can show strongly favorable statistical evidence from cases in which such therapy has been continued indefinitely. At the present time, long-term therapy should be used for selected patients, as, for example, those with repeated infarction, those with thrombosing tendency manifested by recurrent thrombophlebitis or pulmonary embolus, and some with superimposed congestive heart failure. The physician should keep his lnind open with respect to anticoagulant therapy. If larger series confirm the present impression regarding the benefits, and if safer drugs and simpler testing methods become available, the future may see widespread acceptance of long-term anticoagulant control. SUMMARY

The management of the patient with acute Inyocardial infarction is not a standardized or routine procedure, but one which must be carefully individualized within the limits of certain broad principles. Since specific therapy is not available, emphasis continues to be placed on careful attention to supporting the inherent ability of the human body to heal itself. Avoidance of complications, and prompt treatment to abolish them, reduce morbidity and mortality. A confident physicianpatient relationship is imperative for the optimal restoration of the patient to productivity within the limits of his cardiac reserve on recovery from his acute myocardial infarction. REFERENCES 1. LaDue, ,J. S. andWr6blewski, Felix: The Significance of the Seruln Glutamic

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Oxalacetic Transaminase Activity Following Acute Myocardial Infarction. Circulation 11: 871-877 (June) 1955. Levine, S. A. and Lown, Bernard: "Armchair" Treatment of Acute Coronary Thrombosis. J.A.M.A. 148: 1365-1369 (April 19) 1952. Russek, H. 1., Zohlnan, B. L., White, L. G. and Doerner, A. A.: Indications for Bishydroxycoumarin (Dicumarol) in Acute Myocardial Infarction. J.A.M.A. 145: 390-392 (Feb. 10) 1951. Sampson, J. J. and Zipser, Albert: Norepinephrine in Shock Following Myocardial Infarction: Influence Upon Survival Rate and Renal Function. Circulation 9: 38-47 (Jan.) 1954. WeB, M. H.: Clinical Studies on a Vasopressor Agent: Metaraminol (Aramine). 11. Observations on Its Use in the Management of Shock. Am. J. M. Se. 230: 357-369 (Oct.) 1955. Wright, I. S., Marple, C. D. and Beck, Dorothy F.: Myocardial Infarction: Its Clinical Manifestations and Treatment With Anticoagulants, a Study of 1031 Cases. New York, Grune & Stratton, 1954, 656 pp.