GENERAL MANAGEMENT OF MYOCARDIAL INFARCTION



Since approximately 50 per cent of patients who die from myocardial infarction do so within the first four hours after the onset of chest pain, often before they ever arrive at the hospital, the prehospital management of myocardial infarction is important. Many large cities employ emergency medical technicians who can recognize the symp­toms of myocardial infarction, initiate electrocar­diographic monitoring, and treat ventricular tachy-”arrhythmias, terminating them with electrical defibrillation if necessary. Airway management, intravenous drug delivery, and cardiopulmonary resuscitation may be administered, if needed. Pre­hospital emergency cardiac care, especially the rapid treatment of life-threatening ventricular ar­rhythmias, improves both early and late survival from myocardial infarction.

The coronary intensive care unit allows contin­uous electrocardiographic and hemodynamic monitoring, delivery of intensive nursing care, and immediate treatment of arrhythmias or other problems. The advent of the coronary care unit has improved survival of patients with myocar­dial infarction mainly by reducing mortality from arrhythmias. Prevention of death from hemody­namic deterioration has been less successful and accounts for most of the mortality in coronary care units. Future progress in this area will probably come from thrombolysis of acute coronary ob­structions.

Some general principles in treating patients with uncomplicated myocardial infarction in­clude sedation if necessary, a calm, quiet coronary care unit atmosphere, and control of pain to de­crease patient anxiety, sympathetic drive, and myocardial oxygen demand. Morphine can be ad­ministered intravenously in doses of 2 to 8 mg repeated at intervals of 5 to 15 minutes until pain is relieved or drug side effects (e.g., hypotension, respiratory depression, nausea, vomiting, or vagal side effects such as bradycardia) appear. Small IV doses of atropine treat the vagomimetic side ef­fects of morphine, and naloxone 0.4 mg IV at 5-minute intervals to a maximal dosage of 1.2 mg reverses respiratory depression if needed. After the acute severe pain is relieved, nitroglycerin can be used cautiously for recurrent angina, and chronic nitrate therapy may be initiated if angina persists. Oxygen can be omitted if the patient is not hypoxemic.

The patient with uncomplicated acute myocar­dial infarction should be confined to bed for the first 24 to 36 hours except for the use of a bedside commode. He should then be allowed to sit up out of bed for short periods of time and can be transferred out of the coronary care unit after three days, since life-threatening arrhythmias are un­common after 36 to 48 hours. Ambulation is usu­ally begun on the fourth to fifth day and is in­creased progressively so that at discharge the patient is able to walk up a flight of stairs. Early mobilization increases the patient’s psychological well-being, prevents deconditioning, and de­creases the incidence of thromboembolism. Many patients require stool softeners or laxatives to avoid constipation and straining at stool. Nausea and vomiting either from the infarction or drugs can be treated with a clear liquid diet. A gentle rectal examination in patients with acute my­ocardial infarction is not contraindicated.

The use of anticoagulation in acute myocardial infarction is controversial. If no contraindication exists, “minidose” heparin (5000 units subcuta-neously every 8 to 12 hours) may decrease the incidence of deep vein thrombosis and possibly systemic embolization. In patients who have a high risk of embolization, such as those who have a ventricular aneurysm with thrombus, past or present thrombophlebitis, or previous systemic or pulmonary embolism, full systemic antico­agulation may be reasonable in the absence of con­traindications. Systemic anticoagulation is contraindicated in patients with postinfarction pericarditis because of the risk of hemorrhage into the pericardium. Minidose heparin is stopped once the patient is ambulating, usually two to three days prior to hospital discharge. Continua­tion of systemic anticoagulation depends upon the original indication for therapy. Patients with left ventricular thrombi after myocardial infarc­tion are at high risk of embolization, and this risk may be decreased by prophylactic systemic an­ticoagulation for about six months.

In patients with known or suspected acute my­ocardial infarction, lidocaine effectively prevents many ventricular tachyarrhthmias. If it is admin­istered appropriately, side effects such as confu­sion, dizziness, and paresthesias can be mini­mized. Both the loading and maintenance doses of lidocaine should be decreased in elderly pa­tients, patients with congestive heart failure, and patients with liver disease. Although ventricular fibrillation should be easily treatable in the cor­onary care unit, many physicians feel that, given the safety of lidocaine, it is advisable to attempt to prevent ventricular fibrillation rather than have to electrically defibrillate it should it occur. How­ever, the prophylactic administration of lidocaine in this situation is still somewhat controversial. The dose of lidocaine should be increased if ven­tricular tachycardia occurs. Suppression of pre­mature ventricular contractions (PVC’s) is ques­tionable, since their value (including “R on T” PVC’s) as prognostic indicators or precipitators of the onset of more severe arrhythmias is question­able. Prophylactic lidocaine is continued for ap­proximately 48 hours, after which the risk of ven­tricular tachyarrhythmias is reduced.

Patients with uncomplicated courses are usu­ally discharged from the hospital between 7 and 12 days following infarction. The patient should gradually increase his activity but avoid isometric exercise (for example, lifting weights) and get ad­equate rest. He should be instructed in the use of sublingual nitroglycerin even if he requires no an­tianginal therapy on discharge. Many centers have formal rehabilitation programs in which the pa­tient is supervised during activity and his elec­trocardiogram monitored. Exercise testing in pa­tients after acute myocardial infarction helps determine what level of activity can be performed safely at home and is useful to identify those pa­tients at high risk for recurrent events by finding a positive ST response and/or chest pain within the first two stages of exercise. Some physicians perform a limited treadmill test (the heart rate achieved is only 70 per cent of predicted maxi­mum) just prior to hospital discharge, whereas others prefer a more normal stress test protocol six weeks after infarction. Patients who are con­sidered at high risk on the basis of their clinical course and/or treadmill exercise test results may subsequently undergo coronary arteriography.

Large studies with timolol, propranolol, and metoprolol have shown that these agents reduce overall mortality, sudden death, and/or reinfarc­tion if administered to patients after their first in­farction. This outcome may be related to anti-is-chemic effects, antianginal effects, or some other unknown effect of these drugs. Patients with con­traindications to beta-adrenergic receptor block­ers, especially heart failure, cannot receive these drugs; unfortunately, these patients are at the highest risk for a recurrent event. In addition, the mortality in the group of patients that can tolerate these drugs is relatively small, and thus even a 50 per cent reduction in sudden death or reinfarction does not represent a large proportion of the total patients. Despite these reservations, many phy­sicians feel that it is advisable to administer beta-adrenergic receptor blocking drugs in doses suf­ficient to blunt the heart rate response to exercise in postinfarction patients who have no contrain­dication, and the drug should be continued for approximately two years.Early ventricular tachyarrhythmias during acute myocardial infarction (i.e., first 24 to 48 hours) do not warrant chronic antiarrhythmic drug therapy. Patients with chronic complex ven­tricular ectopy, especially ventricular tachycar­dia, are at particularly high risk for sudden death in the first six months to a year after myocardial infarction. However, chronic antiarrhythmic ther­apy has not been shown to decrease mortality in patients with premature ventricular contractions (PVC’s) or ventricular tachycardia after infarction. Therefore, at the present time there appears to be no compelling evidence to support treating pa­tients with uniform or multiform PVC’s or pairs of PVC’s after infarction. In patients with episodes of nonsustained ventricular tachycardia after in­farction, it seems prudent to treat with a type I antiarrhythmic agent (i.e., quinidine) to eliminate the spontaneous tachycardia, although there are no objective data to support this approach.