Response of CVS to exercise: At the start of exercise, sympathetic outflow to the cardiovascular system (CVS) increases and parasympathetic outflow decreases. This helps meet the increased metabolic demands of exercising muscle.
- Heart rate, stroke volume, and cardiac output increase.
- Arterioles in exercising muscle dilate due to local metabolites. This lowers total peripheral resistance (TPR), which tends to decrease diastolic blood pressure (BP).
- Systolic BP increases.
- Because systolic BP rises while diastolic BP falls, pulse pressure increases.
- Arteriovenous oxygen difference (the difference between arterial and venous O2 content) increases because tissues extract and consume more O2.
- Venous return increases.
- Blood flow is redistributed toward skeletal muscle and away from the skin, splanchnic and renal circulations, and inactive muscles.
Response of CVS to blood loss: Blood loss (hemorrhage) reduces blood volume. This decreases venous return and cardiac output, so mean arterial pressure (MAP) falls. The body responds through multiple mechanisms to maintain MAP and preserve perfusion of vital tissues. These include baroreceptors, the renin-angiotensin-aldosterone system, chemoreceptors, and ADH.
- A decrease in MAP activates carotid sinus baroreceptors. This increases sympathetic outflow to the heart and blood vessels, leading to:
- Increased heart rate
- Increased contractility
- Increased conduction velocity
- Increased TPR (arteriolar constriction)
- Venoconstriction with increased stressed volume, decreased unstressed volume, and decreased venous capacitance
- Blood flow is redistributed so that coronary and cerebral circulations are maintained at the expense of gastrointestinal, renal, and skeletal muscle beds.
Reduced renal perfusion activates beta 1 receptors in the smooth muscle cells of the juxtaglomerular apparatus of the kidney, which stimulates renin release and activates the renin-angiotensin-aldosterone system.
- Increased angiotensin II causes arteriolar constriction and increases TPR.
- Increased aldosterone causes sodium retention, which increases plasma volume.
Increased ADH secretion leads to:
- Increased reabsorption of water by the collecting ducts (V1 receptors)
- Arteriolar vasoconstriction (V2 receptors)
Activation of central and peripheral chemoreceptors stimulates sympathetic outflow, which augments the baroreceptor response.
Blood loss also shifts Starling forces toward net absorption because capillary hydrostatic pressure decreases.
Response of CVS to postural changes: The most significant postural change occurs when a person moves from lying down to an upright position. After about 20 minutes of standing, plasma volume can drop by about 14%. This occurs due to venous pooling in the lower extremities under the effect of gravity.
- Venous pooling reduces venous return.
- Reduced venous return decreases cardiac output and MAP.
- The fall in MAP activates the baroreceptor reflex, which increases:
- Heart rate
- Cardiac output and TPR
- Venoconstriction
- Contractility
These responses restore MAP toward normal.
