THE PHYSIOLOGY OF THE CORONORY CIRCULATION

Abstract

A detailed report is presented which demonstrates the physiology of the coronary circulation based on the bubble flowmeter and nitrous oxide methods of measuring coronary blood flow in dog and human. The capillary density of the heart is considered to be 5 times that of the brain. Coronary flow[long dash]65-85 ml./100g. heart muscle/min. (200 ml. in adult male)[long dash]is not regulated by sympathetic or parasym-pathetic nerves but is detd. by the metabolic demands of the heart with oxygen as the probable key. Intra-arterial injn. of minute amts. of acetylcholine or epinephrine results in a prompt increase of coronary flow independent of changes in heart rate or blood pressure. Also the flow parallels the changes in mean arterial blood pressure. A reduction of cardiac output from 5000 to 500 ml./min. causes a compensatory percentile increase in flow from 4% to 14% although actual flow was reduced (from 200 ml./min. to 77 ml./min.). CO2 excess in arterial blood does not change coronary flow but a decrease of pH accelerates the flow. Coronary venous blood is black and contains 5 vol.% oxygen as compared with 14 vol.% found in mixed venous blood in the right ventricle. Thus the heart removes 75% of the oxygen delivered to it and is similar to striate muscle in this respect. Hypoxemia of coronary arterial blood produces a greater volume of coronary flow; as arterial oxygen is decreased from 18 to 4 vol.%, the flow increases 5-fold without any great change in cardiac work. Two main factors are paramount in the regulation of coronary flow alterations in arterial blood pressure (coarse adjuster) influence cardiac work, and metabolic (oxygen?) demands of the heart (fine adjuster). Clinical application in support of the thesis is applied to hypotension occurring under spinal anesthesia. Effects on normal and abnormal patients of such cardiovascular drugs as neosynephrine, papaverine, amino-phylline, coramine and nitroglycerine, are presented.