Resuscitation from cardiac arrest due to acute coronary thrombosis.

Introduction Death from coronary heart disease may be due to a disorganization of rhythm resulting in arrest more often than it is due to actual failure or to rupture of the myocardium.4’5 This probably means that some cases of death from coronary thrombosis could be saved if cardiac massage were available at the time of the fatal heart attack. Lending support to this idea are two recent reports of cardiac arrests secondary to myocardial infarction with successful resuscitation by Beck2 and Regan8. This article reports a similar case in which a hospital employee stricken in the hospital corridor was resuscitated from a cardiac arrest secondary to myocardial infarction. Mr. C. S., an Ancker Hospital orderly, was found unconscious in the main hallway of the hospital on March 19, 1956, at 4:53 P.M. Although his fall was not witnessed, he was discovered almost immediately because of heavy traffic in the hail. First examination revealed no respirations and no heart sounds. He was given artificial respiration and immediately taken to the receiving room where oxygen was administered by mask. Again no heart sounds were audible so 1 cc. of 1:1000 epinephrine was injected directly into the left ventricle but there were still no heart tones. The chest was then opened through a left thoracotomy incision in the third interspace. The pericardium was incised and the heart observed to be in standstill. Cardiac massage was begun at a time estimated to be three and one-half minutes after arrest occurred. After a few minutes of massage, ventricular fibrillation set in so molar sodium lactate was injected into the left ventricle’ and electric defibrillation carried out.8 Regular pulsations began promptly and persisted. Spontaneous respirations started as soon as cardiac massage was initiated. After closing the chest, he was taken to the post-operative ward, but it was necessary to reopen the wound one hour later because of a bleeding vessel in the wound. Forty-eight hours later he responded to questions and was able to talk coherently. He became oriented and it was felt that he suffered little, if any, brain damage. But in spite of intensive antibiotic therapy, his wound became infected. Chest x-ray films were essentially clear until March 31, 1956, when evidence of pneumonia was seen. Tracheotomy and secondary closure of the infected wound were carried out on March 31, but on April 1 he expired. Electrocardiogram on March 24, the sixth day after the attack, revealed an S-T elevation in Lead 1 and in the right precordial leads. This was interpreted as suggesting a possible recent anterior infarction. (Leads 1 and Vi, V2, V3, V4.) Post mortem examination revealed bilateral bronchopneumonia, atelectasis, pulmonary congestion and edema. The coronary arteries showed areas of occlusion in the left circumflex branch and the posterior descending branch of the right coronary. There was an area of hyperemic mottling in the base of the anterior portion of the interventricular septum. Discussion