Effects of Gravity on the Cardiovascular System
Gravity has a major influence on vascular pressures and on the distribution of blood.
– When a person is sitting or standing, arterial pressures progressively decrease above the heart and increase below the heart, reaching ~90 mm Hg higher in the feet than at heart level.
– Similarly, when upright, venous pressures above the heart become negative, causing collapse of the jugular veins.
– The extent of gravity-induced venous pressure change below the heart depends on muscular activity.
– Standing still for long periods allows pooling of blood in the lower extremities (due to the large capacitance of veins) and a rise in venous and capillary pressures (Pc); it also promotes edema. Edema causes a decrease in both blood volume and venous return to the heart. This, in turn, will cause a decrease in stroke volume and cardiac output (CO) via the Frank–Starling mechanism.
– Walking and running force peripheral blood toward the heart. Venous valves inhibit backflow, thereby preventing a large buildup of pressure and preserving venous return to the heart.
– Moving from the supine to the standing position shifts at least 0.5 L of blood from the pulmonary vessels to the lower body and lowers central venous pressure.
The baroreceptor reflex is usually able to compensate rapidly for the transient decrease in arterial pressure that occurs upon standing.
– Reduced afferent signals from the carotid sinus baroreceptors cause an increase in sympathetic outflow to the heart and blood vessels and a decrease in parasympathetic outflow to the heart. This results in
– Increased heart rate, contractility, and CO
– Constriction of arterioles, which increases total peripheral resistance (TPR)
– Constriction of large veins, which increases venous return
– Orthostatic hypotension is syncope (fainting) that occurs upon standing. It is caused by a transient reduction in venous return that is not adequately compensated by the baroreceptor reflex. It can be exacerbated by drugs (e.g., β-blockers) that inhibit the sympathetic outflow induced by the baroreceptor reflex.
Surgery with the patient in a sitting position, as done in some neurosurgical procedures, poses the threat of air embolism, which is the introduction of air into the vascular system. If central venous pressure is not high enough to support the column of blood from the heart to a site of vascular penetration above the heart, pressure becomes negative at the site and will draw in air. Venous air emboli travel to the heart, where they may be trapped and greatly impede pulmonary blood flow, or travel to the pulmonary microcirculation, unleashing a host of damaging actions. Large air emboli are often fatal.
Aerobic exercise causes cardiovascular changes that reflect a combination of central command effects and peripheral effects that are driven by the increase in metabolism in exercising muscle. These changes increase blood flow and oxygen delivery to skeletal muscle.
Central Command Effects
During exercise, central command receives input from the motor cortex or from mechanoreceptors in muscles and joints, leading to an increase in sympathetic outflow and a decrease in parasympathetic outflow. This, in turn, produces the following effects:
– Increased heart rate and contractility. This greatly increases CO with a modest increase in mean arterial pressure (MAP), as TPR is decreased by peripheral vasodilation.
– Increased venous return to match the increased CO. This is driven in part by the alternating contraction and relaxation of the exercising limbs and by venoconstriction.
– Vasoconstriction of the splanchnic vessels allows more of the CO to go to exercising muscle.
– Blood flow to the skin is initially reduced but soon rises to promote heat loss.
– Local peripheral vasodilation occurs due to the release of vasodilator metabolites, such as adenosine and lactate. This causes a decrease in TPR.
Effects of Hemorrhage on the Cardiovascular System
Hemorrhage causes a decrease in blood volume, CO, and MAP.
Hemorrhage invokes emergency responses (the sympathetic “fight-or-flight” response) that collectively act to keep MAP high enough to perfuse the brain and coronary vessels. This is accomplished by a combination of short-acting reflexes (baroreceptor reflex) and longer-term actions that promote retention of body fluid volume (Fig. 11.1).
– Reduced afferent signals from both the arterial and cardiopulmonary baroreceptors cause an increase in sympathetic outflow to the heart and blood vessels and a decrease in para-sympathetic outflow to the heart. This results in
– Increased heart rate and contractility
– Increased TPR caused by vasoconstriction of the splanchnic, skin, and renal vasculatures. This allows the limited CO to flow to the brain and coronary circulation.
– Constriction of large veins, which preserves venous return.
– The posterior pituitary secretes large amounts of vasopressin (antidiuretic hormone [ADH]), which raises TPR and causes the kidneys to reduce excretion of water.
– The renin–angiotensin−aldosterone system is activated, which provides additional peripheral vasoconstrictive actions via angiotensin II and reduced Na+ excretion. Increased Na+ reabsorption in the proximal tubule stimulated by angiotensin II and in the cortical collecting ducts stimulated by aldosterone are responsible for reduced Na+ excretion.
– Thirst centers in the hypothalamus are stimulated, increasing the drive to drink water.
In extreme cases of peripheral hypoperfusion, reduced anaerobic metabolism leads to lactic acidosis, which activates chemoreceptors. These add to the afferent signals, causing increased sympathetic outflow.
Fig. 11.1 Compensatory mechanisms when there is a risk of hypovolemic shock.
Hypovolemic shock may occur due to acute heart failure, hormonal causes, or volume deficit (e.g., hemorrhage). Compensation involves activation of the baroreceptor reflex and the renin–angiotensin−aldosterone system, which cause physiological changes that increase blood pressure and blood volume. (ADH, antidiuretic hormone; GFR, glomerular filtration rate)