Response of CVS to stimuli

Response of CVS to exercise: At the onset of exercise, there is increased sympathetic and decreased parasympathetic outflow to the CVS. This is done in order to meet increased metabolic demands of the exercising muscle. The stroke volume, cardiac output and heart rate increase. Arteriolar dilation in exercising muscle as a result of the action of local metabolites, leads to a drop in TPR which decreases the diastolic BP. The systolic BP is increased. As a result the pulse pressure increases. Arteriovenous oxygen difference which is the difference between arterial and venous O2 content, is increased as more O2 is being consumed by tissues. The venous return increases. More blood is diverted to the skeletal muscle vasculature from the skin, splanchnic, renal circulations and from inactive muscles.

Response of CVS to blood loss: Blood loss or hemorrhage will lead to reduced blood volume, reduced venous return and cardiac output and hence mean arterial pressure or MAP will decrease. The body responds to hemorrhage in a multipronged approach to maintain MAP in order to preserve vital tissue perfusion. It involves the baroreceptors, renin-angiotensin-aldosterone system, chemoreceptors and ADH . Decreased MAP will activate the carotid sinus baroreceptors which will lead to activation of sympathetic outflow to the heart and blood vessels , increased heart rate, contractility, conduction velocity, TPR (arteriolar constriction), venoconstriction with increased stressed volume, decreased unstressed volume and decreased venous capacitance. Redistribution of blood flow occurs so that coronary and cerebral circulations are maintained at the expense of gastrointestinal, renal and skeletal muscle beds.

Reduced renal perfusion will activate beta 1 receptors in the smooth muscle cells of the juxtaglomerular apparatus of the kidney leading to secretion of renin which activates the renin-angiotensin-aldosterone system. The resultant increase in angiotensin II will cause arteriolar constriction and increased TPR. Increased aldosterone will lead to sodium retention and increase in plasma volume.

Increased ADH secretion leads to increased reabsorption of water by the collecting ducts (V1 receptors) and arteriolar vasoconstriction (V2 receptors).

Activation of central and peripheral chemoreceptors leads to stimulation of sympathetic outflow augmenting the baroreceptor response.

Blood loss shifts the Starling forces to net absorption as the capillary hydrostatic pressure decreases.

Response of CVS to postural changes: Most drastic postural changes are seen when a person shifts from a lying down to upright position. There is a 14% drop in plasma volume after 20 minutes of standing. This happens due to venous pooling of blood in the lower extremities from gravity. Reduced venous return decreases the cardiac output and mean arterial pressure. This in turn activates the baroreceptor reflex ultimately causing increased heart rate, increased cardiac output and TPR, venoconstriction and increased contractility. In this way, the mean arterial pressure will be restored back to normal.