Cardiac output (CO) is defined as the volume of blood pumped systemically by the left ventricle each minute. Physiologically, CO is a function of heart rate (HR) and stroke volume (SV), according to the following equation: CO = HR × SV. The SV usually ranges between 70 and 120 mL, thus producing a resting CO of 5.6 L/min in men and 4.9 L/min in women. Alternatively, to compensate for variability in body weight and body surface area (BSA), CO can also be expressed as the cardiac index (CI), according to the following equation: CI = CO/BSA. The normal range for an individual’s CI is usually between 2.5 and 4.2 L/min/m2.
Both HR and SV are directly proportional to CO, such that increases in either the HR or the SV produce an increase in CO. While the HR is controlled by the spontaneous depolarization of the sinoatrial (SA) node (which is controlled by the autonomic nervous system), SV is a function of the following four factors: (1) preload; (2) afterload; (3) contractility; and (4) wall motion abnormalities.
CARDIAC OUTPUT PHYSIOLOGY
The autonomic nervous system controls the automaticity and rate of spontaneous depolarization of the SA node, which in turn controls an individual’s intrinsic HR (usually ranges between 60 and 90 beats/minute). The sympathetic division of the autonomic nervous system increases the HR via stimulation of beta-1 adrenergic receptors, while the parasympathetic division of the autonomic nervous system decreases the HR by stimulating muscarinic M2 cholinergic receptors.
Four major factors affect SV:
Preload—The most important factors contributing to the ventricular preload (synonymous with the ventricular end-diastolic volume, EDV) include ventricular filling, ventricular compliance, and venous tone. As the venous tone and ventricular compliance increase, the blood volume that the left ventricle is able to accommodate increases, thus resulting in an increased EDV, which subsequently contributes to an increased SV according to the Frank–Starling Law (Figure 153-1).
Afterload—Ventricular wall tension during systole approximates the ventricular afterload, which can be defined as the pressure the left ventricle must overcome to generate a particular ejection fraction. Stroke volume and afterload have an inversely proportional relationship—thus, as the afterload (synonymous with the aortic systolic pressure) increases, the ventricular wall tension increases, resulting in a decreased SV and CO. In contrast, as the afterload decreases, both SV and CO increase.
Contractility—Inotropism or contractility is affected by the rate of myofibril shortening as well as by the rate of calcium release from the smooth sarcoplasmic reticulum. Faster rates of myofibril shortening and calcium release into the intracellular space contribute to an increased strength of contractility and augmentation of SV and CO (Figure 153-2). The sympathetic nervous system has the most profound effect on myocardial contractility as the ...