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anim_vascular_regulation_answer_key.doc

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Contributor: Maria
Category: Anatomy
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Vascular Regulation To complete this worksheet, select: Module: Distribution Activity: Animations Title: Vascular Regulation Introduction 1. a. How do Mean Arterial Blood Pressure (MABP) and Systemic Vascular Resistance (SVR) factor together to produce the total Cardiac Output (CO)? Cardiac output is equated to mean arterial blood pressure (MABP) divided by the system vascular resistance (SVR). CO = MABP/SVR. b. What systems both influence and regulate MABP and SVR thereby impacting CO? Hormones and the central nervous system both influence and regulate MABP. Primary Factors That Affect Circulation 2. Name the three primary factors that influence circulation. Arterial blood pressure, systemic vascular resistance and cardiac output. 3. Blood moves from areas of high pressure toward areas of lower pressure. Describe how the right atrial and aortic pressures affect blood movement. Blood moves from high to low pressures. The pressure gradient is determined by differences in blood ejected from the heart (MABP, and that entering the right atrium (right atrial pressure) determines systemic blood flow. Right atrial pressure is so low that blood flow is directly proportional to only MABP. 4. Define Systemic Vascular Resistance (SVR). Systemic vascular resistance is the natural dampening of blood flow. The greater the resistance the harder it is to move through a vessel. 5. Identify and describe three factors that increase SVR. Vasoconstriction - the smaller the radius the greater the systemic vascular resistance. Polycythemia or Dehydration - the thicker the blood the greater the systemic vascular resistance. Vessel Length - the greater the length the greater the systemic vascular resistance. 6. Cardiac Output (CO) is a product of heart rate and stroke volume. What three factors influence heart rate and stroke volume? The influencing factors are: venous return, also known as preload; contractile strength of the heart; and metabolic demands. Structures and Functions 7. Summarize how each of the following affect blood flow. Heart – the heart generates blood pressure. Arterioles – the arterioles produce resistance thereby regulating blood flow to tissues. Veins & Kidneys – the veins and kidneys regulate blood volume and both affect venous return and cardiac output. 8. Explain ventricular importance in maintaining blood pressure. The contraction of the ventricles determined the force of blood ejection and blood pressure that drives circulation. 9. a. Describe ventricular activity during each of the following. Systole – BP is the highest during systole and the highest during cardiac muscle contraction. Diastole – Diastolic BP is the lowest pressure during cardiac muscle relaxation. b. What are normal systolic and diastolic pressures for a resting adult? Normal systolic pressure is 120 mm/Hg. Normal diastolic pressure is about 80 mm/Hg. c. What is the importance of blood vessel elasticity? Elastic vessels allow for capacitance and decrease the resistance to flow and thus can decrease blood pressure by stretching to accommodate a greater volume and/or pressure. 10. If normal resting blood pressure is 120/80, then why is MABP 93? Because BP is defined as the systolic pressure over the diastolic BP. The MABP is equated to the diastolic pressure + 1/3 (systolic BP – diastolic BP). 11. Explain how, and why, arterioles and small arteries affect SVR? Small arteries and arterioles have smooth muscle walls that can regulate their diameter. Changes in the diameter of these blood vessels will change SVR. 12. How does vasoconstriction affect SVR and local blood flow? Vasoconstriction increases SVR and decreases local blood flow. 13. How does vasodilation affect SVR and local blood flow? Vasodilation decreases SVR and increases local blood flow. 14. Define venous return of blood. Venous return is the amount of blood retuned to the heart per unit time. 15. In what way(s) does venous return of blood affect cardiac output? Increased venous return leads directly to a greater preload which increases cardiac output. Conversely, a decrease in venous return results in a decreased cardiac output. 16. How does increased water reabsorption by the kidneys affect blood volume and venous return? Increased water reabsorption on the part of the kidneys increases overall blood volume and blood pressure, which in turn causes an increase in venous return. 17. How does decreased water reabsorption by the kidneys affect blood volume and venous return? Decreased water reabsorption on the part of the kidneys decreases overall blood volume. As a consequence of a decrease in blood volume there is a decrease in venous return. 18. What is the body’s primary blood reservoir? Systemic veins. 19. Define venous tone. Venous tone is the degree of contraction of smooth muscle in the walls of the vein. 20. a. Explain the effect of venoconstriction. Venoconstriction is an increase in venous tone. This decreases venous storage and increase return and cardiac output. b. Explain the effect of venodilation. Venodilation is a decreased venous tine. This increases venous storage and decreases venous return and cardiac output. 21. Describe how venous valves and muscular movements affect venous blood flow. During exercise the contraction of skeletal muscle causes veins in the muscles to become compressed. This process milks the blood towards the heart, increasing venous return. Valves in the veins ensure that blood flows in one direction. 22. Explain how breathing contributes to venous blood flow. During inhalation the diaphragm moves inferiorly. Pressure in the thoracic cavity drops and pressure in the abdominal cavity increases; Abdominal vessels are compressed pumping more blood toward the heart. This increases venous return and cardiac output. Neural Regulation of Blood Pressure 23. Generally describe the role of the following receptors relative to blood pressure monitoring. BP monitoring is reflexive and is monitored by Baroreceptors that monitor changes in pressure and chemoreceptors that monitor changes in blood chemistry. 24. Describe each of the following neural reflexes. Baroreceptor Reflexes – these are major short-term reflex mechanisms that regulate MABP. These receptors are stimulated by changes in the stretch of the carotid sinus wall and they send impulses to the medulla oblongata. Carotid Sinus Reflex – this reflex helps maintain normal blood pressure to the brain. Aortic Reflex – This reflex maintains general systemic blood pressure. The baroreceptors located in the ascending aorta and the aortic arch send impulses via the vagus nerve. 25. Describe physiological adjustments in response to dropping MABP. Sympathetic Signals – Increases in sympathetic impulses increases heart rate, myocardial contractility, venous tone and cardiac output. Parasympathetic Signals – decreases in parasympathetic impulses increase heart rate and cardiac output. Heart Rate, Contractility, Venous Tone, Cardiac Output - hart rate, muscle contractility, venous tone and cardiac output all increase in response to a dropping MABP. Vasoconstriction – vasoconstriction of small arteries and arterioles increase systemic vascular resistance. 26. Describe physiological adjustments in response to rising MABP. When MABP rises stretch receptors impulses also increases. The sympathetic impulses decrease and parasympathetic impulses decreases. Decreases in both cardiac output and systemic vascular resistance cause MABP to decrease and return to normal ranges. . 27. How do chemoreceptors in the carotid and aortic bodies contribute to re-establishing homeostasis during hypoxia, acidosis, or hypercapnia? Receptors in the carotid and aortic bodies detect chemical changes of oxygen, carbon dioxide and hydrogen ions in the blood. Such conditions as hypoxia (decreased oxygen levels) acidosis (increased hydrogen ions) or Hypercapnea (increased carbon dioxide) stimulates the receptors to send impulses to the cardiovascular center in the medulla. The CV center then increases sympathetic stimulation to arterioles and veins. Hormonal Regulation of Blood Pressure 28. Neural regulation of blood pressure is short-term and quick in response. What about hormonal regulation of blood pressure? There are several hormones that aid in the regulation of blood pressure and volume. These are renin-angiotensin-aldosterone (RAA) system, Antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP). Hormonal regulation general last longer than neural regulation. 29. What activates the RAA system? Activated by a drop in BP. 30. Describe the role of each of the following hormones. Name their source, too. Renin – originates at the juxtaglomerular cells of the kidneys and is used to convert angiotensinogen in the liver. Angiotensinogen – found in the liver and is converted to angiotensin I by renin. Angiotensin I – Angiotensin I is converted to angiotensin II by angiotensin converting enzyme. Angiotensin II – located in the blood is a potent vasoconstrictor and increase systemic vascular resistance. 31. How does angiotensin II affect cells in the proximal convoluted tubules in kidney nephrons? At the PCT there is an increase in the reabsorption of sodium and chloride ions. This establishes an osmotic gradient that favors the retention of water. The end result is a decrease in urine volume and increases in blood volume and pressure. 32. a. How does angiotensin II affect target cells in the adrenal cortex? Increases the production of aldosterone that increases the reabsorption of sodium ion and water by the kidneys. This also decreases urine production and increases blood volume which subsequently results in an incease in MABP. b. How does this affect cardiac output? The increase in volume increases cardiac output and raises mean arterial blood pressure. 33. How does angiotensin II affect sensations of thirst? How does this contribute to blood pressure homeostasis? Dehydration increases thirst and activates the RAA system. Angiotensin II targets the thirst centre of the brain prompting for water intake. Responses increase blood volume and venous return. Increased cardiac output raises MABP back to normal. 34. What stimulates the release of Anti-Diuretic Hormone (ADH)? ADH responds to high blood osmotic pressure which is caused by decreases in blood volume. . 35. Where is ADH produced and secreted? It is produced in the hypothalamus and released from the posterior pituitary. 36. How does ADH affect smooth muscle in arteriole walls? The vasopressin component of ADH causes vasoconstriction. 37. How does ADH affect the kidneys? How does this contribute to blood pressure homeostasis? ADH binds to principle cells in the walls of the kidney nephrons. ADH Stimulates the tubules to add water pores, also known as aquaporins, to surface membranes thus, increasing permeability of the kidney tubules to water. This increases the reabsorption of water and increases blood volume. 38. How does ADH affect sweat glands? How does this contribute to blood pressure homeostasis? ADH binds to sweat glands and inhibits sweating allowing for greater water retention and increased blood volume which increase cardiac output and raises MABP. 39. What stimulates ANP secretion? ANP is released when increased blood volume stretches cells in the atria. 40. How does ANP affect the kidneys and what ultimate affect that that have on blood volume? ANP lowers MABP via vasodilation, sodium and water excretion, and reduced blood volume. The PCT cells of the kidney are targeted with a n increase in urine production by the inhibition of sodium ions and water. Less water retention lower blood volume and returns MABP to normal.

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