Discuss the factors involved in the regulation of cardiac output.

Outline:

·        Intrinsic factors:

- Frank-starling mechanism

- myogenic

·        Autonomic control:

- heart rate

- myocardial contractility

- venous return

Essay:

            Cardiac output is the volume of blood pumped by the left ventricle into the aorta per minute. Cardiac output is a function of stroke volume and heart rate. Regulation of cardiac output is necessary to vary the blood flow to the tissues in accordance to their needs. Cardiac output varies between 4-6 L/min at rest to between 20-24L/min during strenuous activity. Variations in cardiac output can be produced by changes in heart rate or stroke volume.

            The heart rate is controlled primarily by the cardiac innervation, sympathetic increaseing the rate and parasympathetic stimulation decreasing it. The center of control of autonomic regulation of heart rate is exerted by groups of neurons in the medulla that are collectively called the vasomotor center. The afferent input to the vasomotor center comes from the baroreceptors, chemoreceptors, the cortex and hypothalamus. The baroreceptors are stretch receptors in the walls of the heart and blood vessels. Impulses generated in the baroreceptors inhibit the tonic discharge of the sympathetic nerves and excite the vagal innervation of the heart, resulting in a decrease in heart rate. Activation of chemoreceptors, due to hypoxia or hypercapnia, however, increases the rate of discharge of the sympathetic nerves, increasing the heart rate. There are descending tracts to the vasomotor center from the cerebral cortex that relay in the hypothalamus. These fibers are responsible for the increase in heart rate produced by emotions such as sexual excitement and anger. Other emotions such as fear and grief lowers the heart rate.

            Stroke volume is the amount of blood pumped per ventricle per contraction. Stroke volume is the difference between end-diastolic volume and end systolic volume. End systolic volume is determined by the force of cardiac contractions. Myocardial muscle is innervated by noradrenergic sympathetic nerve endings. Norepinephrine binds to b₁ receptors and the resulting increase in intracellular cAMP facilitates the opening of calcium and sodium channels, increasing the strength of myocardial contraction.

            End diastolic volume is determined chiefly by venous return. An increase in venous return will lead to increase in end diastolic volume. This is explained by the Frank-Starling mechanism. When an extra amount of blood flows into the ventricles, the cardiac muscle is stretched to a greater length. This in turn causes the muscle to contract with increased force because the actin and myosin filaments are then brought to a more optimal degree of interdigitation for force generation. In addition, stretch may also increase the sensitivity of the actin/myosin filaments to calcium or may increase the calcium entry into the cell with a depolarization stimulus. The stretched right atrium also initiates a nervous reflex called the Bainbridge reflex, passing first to the vasomotor center of the brain and then back to the heart by way of the sympathetic nerves and vagi.

            Venous return is a measure of the flow of blood back to the heart and it is equivalent of the cardiac output and therefore with reasonable limits, an increase or decrease in venous return will elicit the corresponding alteration in cardiac output. The most important determinant of venous return is total peripheral resistance which is in turn dependent on the diameter of the blood vessels (arterioles and venules). Noradrenergic fibers innervate the smooth musculature of all the peripheral vessels, exerting a tonic vasoconstrictive effect. An increase in the sympathetic discharge vasoconstricts the vessels, increasing the mean systemic filling pressure which increases the venous return.

            In short, the regulation of cardiac output involves mainly intrinsic mechanisms and neural control which is mediated by the vasomotor center in the medulla.