Cardiovascular System Worksheet PDF

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Cardiovascular system...

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BIOL 3040

Case Study 2

I. What is mean arterial pressure (MAP) and why is it important? Mean arterial pressure is the average blood pressure in the arteries across the cardiac cycle. MAP is important as its maintenance ensures proper perfusion to the organs of the body. For physiologists, MAP is important as it allows them to ignore the pulsatile nature of blood pressure and instead apply the simple physical principles of fluid flow. II. Identify three factors that maintain MAP. Cardiac output (CO), total peripheral resistance (TPR), heart rate (HR), stroke volume (SV) & end-diastolic volume (EDV). III. What role does the heart play in regulating MAP? The heart plays a role in maintaining MAP by varying its cardiac output, which can be altered through the heart rate & the stroke volume. By increasing the cardiac output, the heart increases MAP & by decreasing it, the the heart decreases MAP. IV. What role does peripheral resistance play in maintaining MAP? The total peripheral resistance, alongside the cardiac output, is varied by the body to regulate the mean arterial pressure. Peripheral resistance is directly related to the mean arterial pressure, if resistance increases, so does the mean arterial pressure, and the same is true the other way around. Peripheral resistance is in-turn affected by the state of the arterioles, such that vasoconstriction increases the resistance, whilst vasodilatation decreases it. V. What effect would acute heart failure have on MAP? Since the acute heart failure would likely reduce the heart’s ability to pump, there would be a decrease in mean arterial pressure. VI. What effect does angiotensin II of RAAS have on blood volume and pressure and how does it achieve this? Angiotensin II of RAAS is activated during low blood volume or pressure, it stimulates several pathways which increase blood volume & pressure. The overall pathway begins when renal blood flow is reduced, this causes the juxtaglomerular cells in the kidneys to convert prorenin into renin and secrete it directly into circulation. The plasma renin then converts angiotensinogen, released by the liver, to angiotensin I. Then, the Angiotensin-converting enzyme (ACE), catalyses the conversion of the circulating peptide, angiotensin I to angiotensin II, which in-turn binds to the AT1 receptor (GCPR) on vascular smooth muscle. The bound-AT1 receptor then activates phospholipase C, producing IP3 , which then activates Ca2+ channels in the ER, this increases the intracellular Ca2+ concentration and

ultimately causes contraction and increased blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which causes the renal tubules to increase the reabsorption of sodium, causing the reabsorption of water into the blood, thus increasing blood volume. VII. What is antidiuretic hormone (ADH)? What effect does it have on blood volume and pressure, and what stimulates its secretion and what are its actions? Antidiuretic hormone (ADH) is a peptide hormone formed in the hypothalamus, it is then transported to the posterior pituitary gland, from where it is secreted into the blood stream. ADH is activated during low blood volume & pressure, it stimulates several pathways to increase volume & pressure. Antidiuretic hormone has a pathway which is similar to that of Angiotensin II. ADH binds to the V1 receptors (GPCR) on vascular smooth muscles & causes vasoconstriction via the IP3 signal transduction pathway, which increases the intracellular Ca2+ concentration and ultimately causes contraction and increased blood pressure & volume. VIII.What effect would the change in MAP due to heart failure have on RAAS and ADH? How and why? After the heart failure, the MAP levels will decrease and this will trigger activation of the RAAS and release of ADH. RAAS and ADH, which stimulate multiple pathways to increase volume/pressure, are usually activated during low blood volume or pressure. Following the heart failure, there will be a reduction in the heart’s ability to pump, resulting in a decrease in blood pressure & volume, and so, RAAS and ADH will be activated. IX. What effect would activation of angiotensin II and ADH have on blood flow to the heart and pressure in the heart chambers? Activation of both angiotensin II & ADH would increase the blood flow to the heart and increase the pressure inside of the chambers. X. There are many factors that can contribute to left ventricle heart failure. Based on what you have read above and after reviewing Mark’s history, life style and physical examination, what risk factors do you think are contributing to Mark’s heart failure and should be addressed as treatment? Contributing risk factors include excess weight, smoking, drinking, lack of exercise, high blood-pressure, senior age & male gender. Via treatment, Mark’s excess weight & high blood pressure should be addressed through physical activity and his tobacco & alcohol use should be completely omitted.

XI. The echocardiogram reveals a low ejection fraction and dilated left ventricle. What do the results of this test tell you about the efficiency of the heart? The results show that efficiency of the heart, as well as its capacity to act as a pump, have been greatly reduced.

XII. The x-ray shows an enlarged heart and edema around the lungs. What is the cause of the edema of the lungs and throughout the body? The edema of the lungs, which is likely a cardiogenic pulmonary edema, is caused by the inability of the left ventricle of the heart to remove blood adequately from the pulmonary circulation, this resulted in fluid accumulation of the lung tissue & air-space. XIII.Why would a change in MAP and blood distribution due to heart failure cause body fatigue? Due to the reduced MAP & inadequate blood distribution that results from heart failure, parts of body would experience inadequate perfusion. Certain regions of the body would exhibit reduced oxidative capacities for skeletal muscles, alterations in the metabolism of skeletal muscles, and an overall impairment in muscle strength. Together, these factors would contribute to body fatigue. XIV.BNP is elevated in Mark’s blood. What effect does BNP have on blood volume and pressure and how does it achieve this? Brain natriuretic peptide (BNP) is a hormone secreted by the cardiomyocytes in response to the stretching that occurs during increased ventricular blood volume. BNP stimulates multiple pathways to decrease blood volume & pressure. Like ANP, BNP induces a decrease in total peripheral resistance & central venous pressure, the overall effect of this is a decrease in blood pressure due to the decrease in total peripheral resistance resistance. Additionally, due to the overall decrease in blood pressure, there is also a decrease in cardiac output. XV. Sacubitril is used to keep brain natriuretic peptide (BNP) levels in the blood elevated. What beneficial effect does sacubetril have on a person with left ventricle heart failure? By maintaining elevated levels of BNP, sacubetril essentially amplifies the effect of the BNP, which is to decrease blood pressure & volume. The effect of sacubetril is beneficial in individuals with left ventricle heart failure as it reduces the mechanical stress on their already weakened heart muscles, reducing the chances of further myocardial injury. Sacubitril functions by inhibiting the enzyme neprilysin, which is responsible for the degradation of BNP.

XVI.Valsartan is used to inhibit the release of angiotensin II. Why would you want to inhibit the production of angiotensin II by valsartan in a person with left ventricular heart failure? Angiotensin II stimulates several pathways which increase blood volume & pressure, this would be harmful for an individual with left ventricular heart failure as it would induce even more mechanical stress on their already weakened heart muscles, increasing the chances of further myocardial injury. Thus, by preventing the release of angiotensin II, Valsartan is reducing the mechanical stress on the weakened heart muscles. XVII.What role do the kidneys play in the RAAS and BNP system? In regards to RAAS, the synthesis of angiotensin II & signal transduction of the IP3 pathway takes place due to the detection of the reduced renal blood flow. From here, the secretion of aldosterone is what triggers the renal tubules to increase the reabsorption of sodium by the kidneys, causing the reabsorption of water into the blood & thus increasing blood volume. In regards to BNP, a reduction in renal sodium reabsorption by the kidneys results in a decreased blood volume.

XVIII.Describe the homeostatic mechanism in this patient with acute heart failure. Mark is overweight & of a senior age, he likely has vascular plaque built up (high blood pressure) & a vast vascularization network which is required to adequately perfuse his additional body mass. Consequently, his heart was under a lot of additional mechanical stress and eventually developed an acute heart failure, which reduced its ability to ability to pump blood adequately. This must have led to a reduction in Mark’s MAP and an activation of RAAS & ADH to maintain proper levels, but eventually the blood pressure must have reach extreme levels leading to activation of ANP & BNP as a compensatory measure, this is his current state....