Perfusion and function in the normal and abnormal heart

The continuous work of the heart throughout life requires a high level of supply of nutrients. Because the heart has a limited and short-lived capacity for anaerobic metabolism, the functional adequacy of the coronary circulation depends on its ability to supply sufficient oxygen to meet metabolic requirements over a wide range of ventricular activity [1]. The necessary balance between myocardial oxygen demand and supply is illustrated schematically in Fig. 1.1. The primary physiologic factors governing myocardial oxygen demand include afterload, heart rate, and contractile state: 1 Afterload, the stress developed by myocardial fibers during shortening, is directly proportional to systolic pressure and the ventricular radius of curvature and inversely proportional to ventricular wall thickness. Systolic arterial pressure is a clinically useful surrogate for afterload, although it cannot account for changes in either ventricular cavity dimension or wall thickness. Wall tension, which takes chamber radius into account but pertains only to thin wall structures, is less frequently substituted for wall stress. 2 The effect of heart rate on myocardial oxygen demand depends primarily on the number of contractions per minute. Positive inotropic effects of increased rate are involved to a lesser degree. 3 Contractile state. Myocardial contractility is an additional important factor related to the strength of contraction. It remains difficult to evaluate quantitatively in humans (as reflected by the numerous indices that have been proposed to evaluate it). 4 Preload. Changes in ventricular volume can alter afterload (via changes in wall thickness) and contractile state (via the Starling effect). These four parameters normally account for approximately 80% of myocardial oxygen consumption. Stroke volume has a limited independent effect on oxygen usage. Another important factor when considering the need to balance oxygen demand and supply is the coronary circulation’s high degree (70–80%) of oxygen extraction under basal conditions. The heart has only limited ability to adjust to increasing oxygen demand by increasing transmyocardial oxygen extraction. Thus, changes in oxygen demand mandate changes in coronary blood flow on essentially a 1:1 basis. Because of the ease with which it can be measured, the “double product’’ of peak systolic blood pressure and heart rate continues to be used frequently as an index of left ventricular oxygen demand [2]. Experimental studies supporting the use of double product have been summarized elsewhere [3]. The index correlates usefully with left ventricular oxygen consumption during exercise [4] and other activities. It also remains valid in the presence of beta blockade [5]. As noted above, limitations may arise during interventions involving substantial changes in ventricular volume.