Abstract
The myocardial effects of coronary occlusion are the immediate result of ischemia which may be defined physiologically as anoxia plus accumulation of products of anaerobic metabolism. This induces two dangerous conditions: It creates a functional state at or near the borders of the ischemic zones which favors production of ectopic beats which may lead to ventricular fibrillation and it eliminates contractile functions of the affected muscle, thereby throwing the burden of work in maintaining an adequate cardiac output on the remaining muscle. If this muscle is able to respond in accordance with physiologic rules, compensation occurs. If it does not or fails to maintain compensation, acute or progressive cardiac failure results which may lead to clinical symptoms and signs distinguished with difficulty from "shock" or circulatory failure of peripheral origin, but which are not due to such failure. The anoxia or chemical products of metabolism or both and possibly the mechanical stretching of the ischemic area excite pain endings and usually cause the suffering associated with coronary occlusion. The sequential changes which early or late may lead to a fatal outcome are schematized.