An Experimental Study in Pulmonary Embolism
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Bishop, John J. Jr.
In the past, references have been made to pulmonary embolizations which were fatal even though the extent of the occlusion of the pulmonary circulation was not considered to be sufficient to cause death. (15,18,24 25,30,31,32,35) De Takata and Jesser (4), in a study of 72 cases of fatal pulmonary embolism, found that in 27 per cent of the group there was a patent main pulmonary artery, only the left or right artery, or a small branch being obstructed. In an effort to explain the mechanism of death in such embolizations, various reflexes were considered. These reflexes included a pulmonocoronary reflex, a pulmonopulmonary reflex, a pulmonobronchial reflex, and reflex vagal inhibition of the heart and of the tone of the peripheral vascular system. The pulmonocoronary reflex has been considered to be the most vital reflex mechanism involved. This reflex was believed to cause contraction of the coronary arteries or arterioles and in this manner cause a coronary insufficiency. Evidence supporting this view was found in the fact that an electrocardiographic pattern simulating that seen after coronary occlusion occurs in pulmonary embolism, both clinically and experimentally.(15,24,35) Also, the symptom complex seen in pulmonary embolism is frequently indistinguishable from the clinical picture seen in coronary occlusion with myocardial infarction. Horn, Back, and Friedberg (15) felt that if pulmonary embolism caused coronary insufficiency and myocardial ischemia there should be resulting structural changes in the myocardium. They studied the hearts in 42 cases of fatal pulmonary embolism and found acute ischemic myocardial damage in 8 of them. In no instance was there any evidence of coronary occlusion. Master, Back, and Grisham (26) investigated 40 cases of pulmonary embolism and found that 17 cases showed electrocardiographic changes attributable to acute coronary occlusion. At autopsy, there was anatomical evidence of coronary insufficiency in the form of subendothelial necrosis or infarction in 25 per cent of these cases. This evidence seems to indicate clearly that there is a coronary insufficiency in many cases of pulmonary embolism. This coronary insufficiency could, be explained by a reflex contraction of the coronary arteries or arterioles, the afferent arm of the reflex originating in the pulmonary artery. The pulmonocoronary reflex would be initiated by the presence in a pulmonary artery of an embolus consisting of clotted blood.
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