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Control of Stroke Volume

Under conditions of rest, the heart does not fill to its maximum capacity. If the heart were to fill more per beat then it could pump out more blood per beat, thus increasing stroke volume. Also, the ventricles of the heart empty only about 50% of their volume during systole. If the heart were to contract more strongly then the heart could pump out more blood per beat. In other words, a stronger contraction would lead to a larger stroke volume. During periods of exercise, the stroke volume increases because of both these mechanisms; the heart fills up with more blood and the heart contracts more strongly. Stroke volume is increased by 2 mechanisms: 1. increase in end-diastolic volume 2. increase in sympathetic system activity

End-diastolic Volume
An increase in venous return of blood to the heart will result in greater filling of the ventricles during diastole. Consequently the volume of blood in the ventricles at the end of diastole, called end-diastolic volume, will be increased. A larger end-diastolic volume will stretch the heart. Stretching the muscles of the heart optimizes the length-strength relationship of the cardiac muscle fibers, resulting in stronger contractility and greater stroke volume. Starling's Law Starling's Law describes the relationship between end-diastolic volume and stroke volume. It states that the heart will pump out whatever volume is delivered to it. If the end-diastolic volume doubles then stroke volume will double.

An Increase in Sympathetic Activity Increases Stroke Volume The cardiac muscle cells of the ventricular myocardium are richly enervated by sympathetic nerve fibers. Release of norepinephrine by these fibers causes an increase in the strength of myocardiall contraction, thus increasing stroke volume. Norepinephrine is thought to increase the intracellular concentration of

calcium in myocardial cells, thus facilitating faster actin/myosin cross bridging. Also, a general sympathetic response by the body will induce the release of epinephrine from the adrenal medulla. Epinephrine, like norepinephrine will stimulate an increase in the strength of myocardial contraction and thus increase stroke volume.

1. Preload Stretch - Frank - Starling law - the greater the stretch on


cardiac fibers just before they contract (draws myosin fibers closer together) increases their force of contraction, the more blood is ejected from the ventricle the heart is filled during diastole the greater the force of contraction 2. Contractility - strength of a contraction at any give preload. Substances that increase contractility (positive inotropic agents) include hormones (glucagons, thyroxine), catecholemines (epinephrine and norepinephrine), drugs (digitalis) and increased calcium concentration in the extracellular fluid. 3. Afterload - the pressure in the large arteries leaving the heart that must be overcome before the aortic semilunar valve can open. Increased afterload results in decreased stroke volume.

Extrinsic regulation:

Involves neural and hormonal control Autonomic Nervous system Sympathetic stimulation Fight or Flight"supplied by cardiac nerves, increases heart rate and force of contraction Sympathetic nerves include the cardiac accelerator nerves which extend out to the SA node, AV node and portions of the myocardium, releasing norepinephrine and epinephrine from adrenal medulla which increases heart rate and contractility

- Parasympathetic stimulation normally dominates resting heart rate - Parasympathetic nerves include the right and left Vagus (X) nerves. These fibers innervate the SA node, AV node and the atrial myocardium, releasing acetylcholine which decreases heart rate. There is always a balance between sympathetic and parasympathetic stimulation of the heart, but the parasympathetic dominates at rest.