Abstract
The heart is a pump built for quick adjustment of its performance to changing load. It has a low mechanical efficiency in terms of the energy cost of its external useful work. It is primarily a compression pump and the cyclic variations of its pressure-volume relationships define a measure of the compression work that it does. The heart has no fixed initial length, or rather, since it is a hollow viscus, no fixed initial volume. Certain peculiarities in its performance depend on the geometric relationship between mechanical events taking place in the walls of the heart and the resulting effects upon the blood in its chamber. These include the influence of velocity and duration of contraction on its size and the influence of size on its performance. The heart's minute output is determined not only by its diastolic size but also by its systolic residue and the frequency of the beat. It is likely that both of these latter parameters are altered in the physiologic regulation of the heart beat. While the frequency of the heart beat and the level of the blood pressure against which the heart works are closely linked to the oxygen that it consumes, its stroke output has practically no influence on its oxygen consumption. Hence, the product of blood pressure and heart rate constitutes a good first approximation of an index of the heart's oxygen consumption. The directions in which a better index should be sought are outlined. Factors that determine variations of the ratio between cardiac oxygen consumption, on the one hand, and the product of heart rate and blood pressure, on the other, are considered in trying to give meaning to the significance of changes in the mechanical efficiency of the heart's external useful work. Under ordinary conditions, the oxygen consumed by the heart cannot be altered by induced variations in coronary flow. Nevertheless, coronary flow is found to be finely attuned to cardiac oxygen consumption. This relationship constitutes a paramount meta-bolically induced autoregulation of coronary flow. This homeostatic mechanism is accompanied by a surprising degree of constancy of both the coronary venous oxygen content and the per cent of oxygen extracted by the heart from each unit of the coronary blood. Oxygen availability is finely attuned to the oxygen demands of the heart by the coronary flow autoregulation over a wide range of effort and during hypoxemia. Coronary flow can determine the oxygen consumption of the heart when the coronary flow is relatively insufficient. Under these abnormal circumstances, coronary flow operates to set the level of the heart's performance. Mechanical factors can modify the coronary flow independently of the metabolic regulation, as is manifested by variation in the level of the venous oxygen content, in the per cent of cardiac oxygen extraction, and by the development of an excess of oxygen availability in relation to the oxygen consumed by the heart. Certain humoral agents and drugs also can modify coronary flow independently of this metabolic regulation. The manifestations of their action are revealed in the same way as in the case of the mechanical factors.

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