The management of acute coronary insufficiency.
1. Coronary insufficiency is a pathophysiologic state that can initiate lethal cardiac arrhythmias in the absence of myocardial necrosis. Patients with suspected coronary insufficiency should be monitored until they are stabilized and a diagnosis is confirmed. 2. Early and adequate intravenous antiarrhythmic prophylaxis with lidocaine to raise the fibrillation threshold in the setting of coronary insufficiency can prevent primary ventricular fibrillation. Classic "warning arrhythmias" are not predictive of ventricular fibrillation. Their persistence during adequate antifibrillatory prophylaxis does not indicate therapeutic failure. 3. The isoenzyme of creatine phosphokinase, CPK-MB, is an extremely sensitive and specific indicator of myocardial necrosis if measured serially during the 24 hours following the onset of symptoms suggesting coronary insufficiency. It may prove most useful in eliminating the false positive diagnosis of myocardial infarction in  difficult clinical cases. 4. The management of heart failure in myocardial infarction requires an understanding of the relationship between ventricular preload and the cardiac output. The treatment of clinical manifestations of an elevated ventricular preload in asymptomatic patients is not justified and may be detrimental. In symptomatic patients, however, judicious manipulation of ventricular preload should be the first therapeutic consideration, and an optimal filling pressure should be achieved and maintained when other determinants of the cardiac output are manipulated. 5. Indications for the prophylactic insertion of a temporary transvenous pacing electrode for heart block associated with myocardial infarction must be individualized. Most authorities agree that prophylactic pacing may be justified in patients with evidence of new infranodal block involving two of the three fascicles. Patients with bifascicular block who progress to complete heart block transiently may benefit from permanent transvenous pacemaker insertion before discharge. 6. Hospitalized patients with persistent pain of suspected cardiac origin but without evidence of myocardial infarction can be studied safely with coronary angiography. A small percentage will be normal or have diffuse disease that is inoperable. Of those with operable disease, short-term mortality appears to be similar for medical and surgical therapy. 7. Patients with an uncomplicated myocardial infarction may be safely discharged from thehospital by day 7-10. 8. Experimental evidence indicates that modification of infarct size is possible. Application of these concepts to human subjects presently is limited by the absence of a proved method of measuring infarct size in vivo in humans.
D000208:Acute Disease; D000787:Angina Pectoris / Q000628:therapy; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000517:prevention & control; D001219:Aspartate Aminotransferases / Q000097:blood; D001794:Blood Pressure; D002302:Cardiac Output; D004796:Clinical Enzyme Tests; D003327:Coronary Disease / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D003402:Creatine Kinase / Q000097:blood; D006321:Heart / Q000503:physiopathology; D006327:Heart Block / Q000628:therapy; D006760:Hospitalization; D006801:Humans; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008012:Lidocaine / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000628:therapy; D010138:Pacemaker, Artificial; D014693:Ventricular Fibrillation / Q000209:etiology / Q000517:prevention & control
D000889:Anti-Arrhythmia Agents; D007527:Isoenzymes; D008012:Lidocaine; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase