PHYSIOLOGY OF THE CORONARY CIRCULATION



Three major determinants of myocardial oxygen consumption are contractility, heart rate, and wall tension. Myocardial wall tension is directly proportional to the pressure within the ventricular chamber and the radius of the ventricular chamber (Laplace relationship). The myocardial mass is a determinant of wall tension and therefore myocardial oxygen consumption; the larger the muscle mass, the more oxygen needed.

The coronary vascular bed is able to autoregu-late, enabling myocardial oxygen and substrate delivery to equal the demand. Coronary vascular resistance is normally determined by the arterioles and is influenced by neural and metabolic factors. Both the sympathetic and parasympathetic nervous systems innervate the coronary arteries. Alpha receptor stimulation Causes vasoconstriction while stimulation of the beta-2 receptor as well as the vagus causes vasodilation. Metabolic factors regulate regional perfusion. Several mediators including oxygen, carbon dioxide, and metabolites such as adenosine are probably important. However, when coronary perfusion pressure falls to below 60 to 70 mm Hg, the vessels become maximally dilated and flow depends on perfusion pressure alone, since capability for further autoregulation is lost. The normal coronary vascular bed has a capacity to increase its blood flow four- to fivefold during maximal exercise. Hemodynamic factors that affect coronary perfusion include arterial pressure (especially diastolic pressure, since coronary flow occurs primarily in diastole), the time spent in diastole, and the intraventricular pressure (which exerts tension on the myocardial walls and di­minishes coronary flow).





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