11 Orthostatic Pressure physiology PDF

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Response to Change in Posture

1. 1. Orthostatic hypotension is the phenomenon whereby arterial pressure decreases when one stands up. 2. When a person suddenly moves from a supine (lying) position to a standing position, blood pools in the veins of the legs. 3. (Because the capacitance, or compliance, of the veins is high, they can hold large volumes of blood.) 4. This pooling decreases venous return to the heart, which decreases cardiac output by the Frank-Starling mechanism. 5. The Frank-Starling mechanism describes the relationship between venous return and cardiac output. 6. Increases in venous return lead to increases in cardiac output. 7. Conversely, decreases in venous return lead to decreases in cardiac output. 8. Because arterial pressure is affected by the volume of blood in the arteries, a decrease in cardiac output (i.e., less blood is pumped into the arterial system) causes a decrease in arterial pressure b. 1. When someone stands up quickly, they feel light-headed because a brief period of cerebral ischemia occurred as a result of the decrease in arterial pressure. 2. The autoregulatory range for cerebral blood flow is 60 to 140 mm Hg. 3. In other words, cerebral blood flow is maintained constant as long as arterial pressure is greater than 60 mm Hg and less than 140 mm Hg. 4. When someone stands up, their arterial pressure briefly decreases below this critical autoregulatory range. 5. As a result, cerebral blood flow decreased, and they felt light-headed.

3. a. Baroreceptors located in the carotid sinus and the aortic arch senses the decrease in arterial pressure. b. The baroreceptor reflex then orchestrate a series of compensatory responses, including increased sympathetic outflow of the heart and blood vessels. c. There are four consequences of this increased sympathetic outflow. i. 1) Increased HR (the sensation of a racing heart), a positive chronotropic effect mediated by beta1-adrenergic receptors in the sinoatrial node ii. 2) Increased contractility of the ventricles, a positive inotropic effect mediated by beta-adrenergic receptors in the ventricular muscle. iii. 3) Increased arteriolar constriction, mediated by alpha-1 adrenergic receptors on vascular smooth muscle of the arterioles. iv. 4) Increased venoconstriction, mediated by alpha-1 adrenergic receptors on vascular smooth muscle of the veins. 3.

a. b. Standing → Pooling of blood → Decrease venous return → Decrease Pa → Decrease stretch on carotid sinus baroreceptors → Decrease firing rate of carotid sinus nerve → Increase sympathetic outflow → 1) Increase HR and contractility; 2) constriction of arterioles ; 3) Construction of veins → 1) Increase cardiac output; 2) increase TPR; 3) Increase venous return → INCREASE Pa towards normal c. Pa = cardiac output (CO) x TPR i. Pa = mean arterial pressure (MAP) ; YES, Pa = MAP ii. CO = volume of blood ejected from the left ventricle per min iii. TPR = total peripheral resistance b. In words, arterial pressure depends on the volume of blood pumped into the arteries from the left ventricle and the resistance of the arterioles c. (it may be helpful to think of arteriolar resistance as holding blood on the arterial side of the circulation). d. Increased HR and contractility combined to produce an increase in CO. e. The increased CO caused an increase in arterial pressure. f. The increased arteriolar constriction produced an increase in TPR, which also increased the arterial pressure. g. Finally, venoconstriction lead to decreased capacitance of the veins, which increased venous return to the heart and increased the cardiac output (by the Frank-Starling mechanism)

3. a. As someone walks, the muscular activity compressed the veins in their legs and decreased venous capacitance (i.e., the volume of blood the veins can hold). b. This compression, combined with sympathetic venoconstriction, increased venous return to the heart and cardiac output....