A basic grasp of normal cardiac function sets the stage for understanding the patho-physiologic processes leading to HF and selecting appropriate therapy for HF. CO is defined as the volume of blood ejected per unit of time (liters per minute) and is a major determinant of tissue perfusion. CO is the product of heart rate (HR) and stroke volume (SV): CO = HR x SV. The following describes how each parameter relates to CO.

HR is controlled by the autonomic nervous system, where sympathetic stimulation of P-adrenergic receptors results in an increase in HR and CO. SV is the volume of blood ejected with each systole. SV is determined by factors regulating preload, af-terload, and contractility. Preload is a measure of ventricular filling pressure, or the volume of blood in the left ventricle (also known as LV end-diastolic volume). Preload is determined by venous return as well as atrial contraction. An increase in venous return to the left ventricle results in the stretch of cardiomyocyte sarcomeres (or contractile units) and a subsequent increase in the number of cross-bridges formed between actin and myosin myofilaments. This results in an increase in the force of contraction based on the Frank-Starling mechanism.6 Afterload is the resistance to ventricular ejection and is regulated by ejection impedence, wall tension, and regional wall geometry. Thus, elevated aortic and systemic pressures result in an increase in afterload and reduced SV. Contractility, also known as the inotropic state of the heart, is an intrinsic property of cardiac muscle incorporating fiber shortening and tension development. Contractility is influenced to a large degree by adrenergic nerve activity and circulating catecholamines such as epinephrine and norepinephrine.

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