What are the determinants of myocardial oxygen consumption (demand)?

What are the determinants of myocardial oxygen consumption (demand)?

Heart rate, contractility, and myocardial wall tension are the three major determinants of myocardial oxygen consumption. 

Heart rate is probably the most important parameter regulating the myocardial oxygen supply-demand balance. Decreasing heart rate both increases oxygen supply by prolonging diastole and decreases oxygen demand. The association between tachycardia and myocardial ischemia is well documented. Severe bradycardia should be avoided, however, as this will cause decreased diastolic arterial pres-sure and increased left ventricular end-diastolic pressure. β-Adrenergic blocking drugs are commonly used to main-tain a mild bradycardia in patients with CAD.

Myocardial contractility is loosely defined as the intrinsic ability of the myocardium to shorten. This is a very difficult parameter to measure and is poorly described by the cardiac output or even the left ventricular ejection fraction. Decreased myocardial contractility is associated with decreased myocardial oxygen demand. Thus, “myocardial depression” may be beneficial in patients with CAD. Specifically, agents that depress myocardial contractility but are not potent vasodilators may be beneficial as long as coronary perfusion pressure is maintained. Thus, potent volatile anesthetic agents (halothane, enflurane, and isoflu-rane) are examples of “myocardial depressants” that could be useful for patients with CAD as long as coronary perfusion pressure is maintained.

Myocardial oxygen supply and demand are kept in balance by properly managing left ventricular preload, afterload, heart rate, and contractility. Major increases in preload (left ventricular end-diastolic volume) add to the volume work of the heart (increased demand) and decrease coronary perfusion pressure because of the asso-ciated increase in left ventricular end-diastolic pressure (decreased supply). Nitrates assist in maintaining a normal to low preload (see below). Excessive increases in afterload result in increased pressure work of the heart (wall tension) during systole (increased demand) despite the increase in coronary perfusion pressure. At the other end of the spectrum, extreme vasodilatation (decreased afterload) will lower the diastolic arterial pressure and decrease myocardial oxygen supply (see Table 2.1).