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Cardiovascular system - Essay Example

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Demonstrate the adaptability of the cardiovascular system to autoregulate to two different, stressful conditions (1. Max test 2. Steady state exercise at 65% maximum oxygen level).The cardiovascular system has the capabilities to adapt to a number of external factors. …
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Cardiovascular system
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1. Demonstrate the adaptability of the cardiovascular system to autoregulate to two different, stressful conditions Max test 2. Steady exercise at 65% maximum oxygen level). Explain in detail how the different cardiovascular components such as heart rate, systolic blood pressure, diastolic blood pressure, total pulmonary resistance, stroke volume and blood flow, respond to these stressful conditions. Explain in detail the physiological mechanisms responsible for the changes observed. The cardiovascular system has the capabilities to adapt to a number of external factors. An example of the cardiovascular system's ability to adapt is seen in response to a max test. This test measures the volume of oxygen in the blood that the body uses in one minute of maximal exercise. A stationary exercise machine is used when administering the test. The first minute interval is done at a very easy level. As each minute passes the levels become increasingly more difficult until you reach a levels when you can no longer continue. The max test requires you to wear a mask and to breathe through your mouth. The mask is connected to an analyzer that looks at the levels of carbon dioxide and oxygen in the exhaled gas. You are also hooked up to a heart monitor. Using the information gathered you could figure out your cardiovascular fitness and define your maximum aerobic power. The max test causes an increase in heart rate, because there is an increased need by your muscles for oxygenated blood. Towards the end of the max test anaerobic activity occurs. Yu et al. said, "hypoxia induces pulmonary hypertension" (Impaired physiological responses, 1999). That means the pulmonary vascular resistance is increased and so is pressure on the right side of the heart. If this occurs on a regular, unregimented basis right ventricular hypertrophy may occur. This is not the case in an acute situation like a max test. In a max test the total pulmonary resistance decreases. Overall blood flow would increase due to the increase in heart rate as well as both systolic and diastolic blood pressure. Stroke volume is the amount of blood per contraction from both the right and left ventricle. Even though there is a decrease in total pulmonary resistance the stroke volume in this case would decrease due to the fact that the peripheral vessels, which have higher pressures, increases. The increased heart rate causes the ventricles to not fill as full, thus lowering the volume pumped out of the ventricles by each contraction. The final stage of the max test is anaerobic. This stage looks at how quickly the body can remove the lactic acid. The increased heart rate helps in the removal of lactic acid. If you have crossed this threshold you will be prematurely fatigued and may feel your muscles burn. Toga et al. states that "during hypoxia, the total" pulmonary "resistance decreased with increased blood flow" (Effects of hypoxia, 1998, 1003). Steady state exercise is different from the max text, because it does not increase in intervals. In the steady state test you also have the increase in systolic blood pressure, but there is no dramatic increase in diastolic blood pressure. When steady state exercise has been done over time the effects are a minimal change in blood pressure and a higher red blood cell count (blood is more easily saturated with oxygen). Once finished with steady state exercise the systolic blood pressure will drop to below normal levels for a brief period of time. Steady state exercise, when done on a regular basis, will decrease heart rate. A decrease in heart rate will allow the ventricles more time to fill. . Stroke volume is the volume of blood in the ventricles during diastole minus the volume of blood in the ventricles during systole of the same heartbeat. If the heart rate is slower it allows for more filling of the ventricles hence a larger stroke volume. There are other factors that also contribute to these different cardiovascular components. Khaksari et al. explained how the increase in both systolic and diastolic blood pressure during stress is higher in men than in women (Cardiovascular response to psychological, 1991, 185-197).The distensibility of the myocardium as well as the contractility of the ventricles are factors of stroke volume. Increased contractility leads to increased stroke volume. Increased distensibility leads .to an increased volume of blood in the ventricles which also leads to increased stroke volume. 2.Discuss the impact of a disease state where impaired autonomic function and vascular homeostasisis seen. How does this impact the CV system both at rest and during exercise The autonomic system is responsible for regulating cardiac functions such as heart rate, conductivity, and contractility. It also assists with constriction and relaxation of the vessels. Autonomic function consists of the sympathetic and the parasympathetic nervous system. The sympathetic nervous system acts as an accelerator. A sympathetic response is known as a fight or flight response. The sympathetic nervous system increases heart rate and electrical conductivity of the heart. The parasympathetic nervous system slows heart rate down by decreasing conductivity of both the atria and ventricles. Harris et al.conducted a study which showed that sympathetic nerves and endothelial cells share an functional antagonism in a normal state to keep the most efficient vessel tone (Interactions between autonomic, 2004). In a state where the autonomic system is impaired the vessels are unable to maintain homeostasis under extremely stressful situations. The autonomic and cardiovascular systems work with each other in an effort to maintain homeostasis. When there is impairment in autonomic function there is added stress on the body while it tries to compensate for the impairment. Varghese et al. said that " a sympatho-vagal imbalance with a prevalent parasympathetic dysfunction can result in a defective inhibitory vagal tone on the cardiac pacemaker. This will result in an acceleration of heart rate and an increase in cardiac output along with enhanced cardiac preload" (Does autonomic dysfunction, 2007, p.106). A study preformed by Gerritsen et al. shows that there is an increased mortality rate when there is impaired autonomic function (Autonomic dysfunction, 2001.). An example of that would be post myocardial infarction. There is damaged muscle cell as well as impaired autonomic function which leads to a lower ejection fraction. This means that the overall productivity and efficiency of the heart is reduced. With this in mind we address the issue of the impact on the cardiovascular system at rest and during exercise. There is less stress and demand on the cardiovascular system during rest. The effects of the imapired autonomic system will not be as obvious during rest because there is not as much work required of the cardiovascular system and vessels. When exercise is introduced into the equation dramatic problem arise within the cardiovascular system. There will be less control over heart rate with impaired autonomic function. This will negatively effect cardiac output. Less cardiac out put means the potential for congestive heart failure. 3.Discuss the possible sites within the cardiovascular system that could limit performance. Choose a side and argue if skeletal muscle is the master or slave of the cardiovascular system. The cardiovascular system has the capability to compensate for a number of external factors. When there is an increased need for oxygen the autonomic system speeds up the heart rate, pulmonary vessels dilate, and contractility of the myocardium increases, but all of these compensations have their limits. The heart can only beat so fast before the increased rate becomes more of a detriment rather than a solution. Tachycardia is when the heart beats around 120 beats per minute or more. Anything much faster will not allow for proper filling of blood into the ventricles and therefore a less than sufficient stroke volume. Over dilated pulmonary vessels can easily become distended especially when there is a chronic increased pressure in the system. Once over distended the vessels lose contractility and help the heart pump blood adequately throughout the body and lungs. When the myocardium is filled with more than it's normal workload it has to pump harder to remove the extra blood. This increased use of the left ventricular muscle causes the muscle to become hypertrophied, which is not always a bad thing. When aerobic exercise is preformed on a regular basis, there is left ventricular hypertrophy. This hypertrophy actually benefits the cardiovascular systems in terms of the ejection fraction. When this trend continues and the workload persists eventually this can lead to congestive heart failure. Skeletal muscle is the slave to the cardiovascular system. Striated muscle fibers, skeletal muscles, are dependent upon a constant flow of oxygenated blood. Skeletal muscle engages in the uptake and utilization of oxygen, which dramatically increases with the increase of muscle movement. They rely on the bloodflow to supply essential elements, especially oxygen, and remove lactic acid from the cells. Lactic acid build up in skeletal muscle cells results from inadequate levels of oxygen getting into the cells. The resulting anaerobic activity causes the cells to produce lactic acid. When there is less then optimal bloodflow there is lactic acid build-up, which causes the skeletal muscle cells to fatigue and become sore. If this pattern continues it will ultimately lead to death of the skeletal muscle cells. There are two types of skeletal muscle- type I and type II. Type I is able to store more oxygen so it would not be as quickly effected by a decrease or compromise in cardiovascular activity and oxygen supply. Type II skeletal muscle produces more lactic acid and would be more adversely effected by a compromised cardiovascular system and oxygen supply. As stated before skeletal muscle is definitely the slave to the cardiovascular system. Without the heart and lungs blood would not be properly oxygenated and it will not be circulated to all of the necessary destinations such as skeletal muscle fibers. Without the cardiovascular system skeletal muscles would be deprived of oxygen, fill up with lactic acid, deteriorate, and eventually die. 4. Compare and contrast the hemodynamic responses of isometric versus aerobic exercise. What are the major differences Do the control mechanisms differ There are several hemodynamic responses to isometric and aerobic exercise. Isometric exercise means the your exercise your muscle without changing the muscle length. You can do this by either pressing against an unmovable object or you can add weight to an already existing place with no motion of the muscles. With isometric exercise there is little increase in heart rate (initial increase for the first 90 seconds), total pulmonary resistance, and cardiac output. This is due to the fact that with isometric exercises there is less of a need for oxygen and the removal of lactic acid. This is the major variance when comparing the two types of exercise. The other difference is that during isometric exercise the cardiovascular changes are not directly connected to the volume of oxygen. Fisher et al. stated that isometric exercise "evoked a lesser increase in heart rate and cardiac output" than aerobic exercise. He also said that isometric exercise "resulted in a more potent systemic pressor response" (Hemodynamic responses, 1973,p.422). Blood pressure during isometric exercise increases to help the blood to get to the necessary areas. Aerobic exercise has more pronounced effects on hemodynamics. For someone who has been engaging in aerobic exercise for a while you will see a slower heart rate while resting. Aerobic exercise strengthens and enlarges your myocardium increasing contractility. Increased contractility means that your heart will pump more efficiently. Aerobic exercise improves circulation and, along with a stronger heart muscle pumping more efficiently, lowers resting blood pressure. You will also see very little change in blood pressure when you engage in ongoing aerobic exercise. This is, once again, due to the fact the myocardium is stronger and pumping more efficiently. The red blood cell count increases with regular aerobic exercise. This means the blood has a higher oxygen carrying capacity as opposed to someone who has not done aerobic exercises resulting in a lower hemoglobin count. With aerobic exercise there is a large change in heart rate, total pulmonary resistance, and cardiac output. This is due to the fact that the muscles are moving in much greater mass, when compared to isometric exercise. In aerobic exercise the cardiovascular changes are tightly coupled oxygen levels. There are two major control mechanisms that are responsible for the increase in heart rate during isometric exercises. The first control mechanism is the initial increase in heart rate which produces small changes in cardiac output and blood pressure. After the first 90 seconds the sympathetic system takes over using pressors to balance the system. In aerobic exercise there are several factors that contribute to the control mechanisms. After several months of constant aerobic exercise your heart has a stronger myocardium, higher red blood cell count, and more vessel elasticity. This means that the cardiovascular system is able to compensate better and the "vascular tone and reactivity" is increased (Rakobowchuk et al.,2005,2185).There is an increase in heart rate, but pressors are not the only key for regulating bloodflow in aerobic exercise.. 5. Explain how catecholamines affect myocardial contraction - what happens if you decrease intracellular calcium According to the Journal of Biological Chemistry catecholamines, such as epinephrine and norephinephrine, "induced a more rapid contraction rate" (Norephinephrine- and ephinephrine,2008, 807). When epinephrine is released the heart rate increases which, in turn, increases the rate of myocardial contraction. This can be a problem when you look at someone who has had a myocardial infarction or ventricular fibrillation, because there is damage to the myocardium and more then likely damage to the epicardium which houses the conduction system of the heart When someone has suffered damage to the myocardium that catecholamines could actually have a detrimental effect. Epinephrine causes an increase in myocardial oxygen consumption. There is also in increase in the left ventricular end diastolic pressure. This causes an increase in myocardial dysfunction that, in turn, causes a decrease in the rate of survival If intracellular calcium decreases the myocardium will begin to lose contractility, because .calcium is one of the three important elements to the action potential. With lowered levels of calcium entering the cells myocardial contraction is compromised. Hypocalcemia (low calcium levels) may cause cardiac arrhythmias, hypotension, and in some cases heart failure. Silver et al. points out that hypocalcemia "mediates" histamine release (Decreased intracellular calcium,2002, p.501). When there are low calcium levels, there is a reduction in the release of epinephrine. With no calcium for contraction and no histamine release one can see how, in severe cases, hypocalcemia can even lead to death. 6. Discuss how the endothelium contributes to vasodilatation - vasoconstriction - what happens if flow is not laminar The endothelium is able to release chemicals that have an impact on the vessels. The endothelium releases endothelin-1. Endothelin-1 is a powerful vasoconstrictor that helps with the maintenance of vessel tone (Evidence for endothelin-1, 1995. P.732). The journal talks about how lower levels of endothelin-1 are seen in people with hypertension. This tells us that the endothelium is able to not only produce the vasoconstrictor, endothelin-1, but also is able to regulate the release of endothelin-1. The endothelium is able to sense when the vessels are in need of vasoconstriction and dispense endothelin- 1. The endothelium is able to release endothelin-1 after a heart attack to constrict the vessels and help bring blood back to the heart. Endothelin-1 could also pose as a problem. An example of this would be when the body is in shock. Endothelin-1 would have an undesired effect in a case such as this. The second part of the question refers to blood flow. There are two types of blood flow- laminar an turbulent. The ideal flow of blood would be laminar. Laminar flow is when the pressure is at a level high enough to channel the blood to the center of the vessel, producing a more streamlined flow. Once the Reynolds number reaches 4,0000 the flow goes from laminar to turbulent. Turbulent flow means that the blood flow is chaotic. When the flow is turbulent you have a reduction in the amount of blood transported throughout the vessel as well as a reduction in the efficiency of bloodflow thru the vessel. This is due to the fact that the cells are no longer streamlined in flow, they flow chaotically at random. 7. Explain the difference in action potential between the SA node and regular myocardial muscle fibers. Action potential is generally the same throughout the body. There are a few differences between the action potential of the SA node and the myocardium. The first, and most important, difference is that the SA node has the ability to fire at will. Phase 4 of the SA node's action potential is called the spontaneous depolarization mode. In this phase the SA node exhibits pacemaker potential unlike the myocardium who is not able to contract at will. The myocardium is more controlled in it's depolarization. The myocardium has to go through all phases of the action potential in order for it to depolarize or contract. Another major difference between the SA nodal and myocardial action potentials is the sodium channels. In the myocardial action potential you have the opening of fast sodium channels. This causes an influx of calcium which leads to myocardial contraction. The myocardial action potential has to go through extra phases in order to contract. The SA node has a slow flow of sodium. The SA node does not need the influx of sodium because, as mentioned above, it is able to spontaneously depolarize. This means the flow of calcium into the SA node cells is not necessary for depolarization as it is in the myocardium. The electrical conductive system of the heart is the fastest electrical activity in the body. Fisher, M.L., Nutter, D.O., Jacobs, W., Schlant, R.C. (1973). Hemodynamic responses to isometric exercise (handgrip) in patients with heart disease. British Heat Journal. 35(4), 422-432. Gerritsen, J., Dekker, J.M., TenVoorde, B.J.,et al. (2001) Autonomic disfunction and increased morality: assesment by sinus arrythmia is as good as any other autonomic function tests.Diabetes Care. 24, 1793-1798. Harris, K., Matthews, M.S. & K. (2004) Interactions between autonomic nervous system activity and endothelial function: A model for the development of cardiovascular disease.American Psychosomatic Society. 66. 153-164. Kiowski, W., Sutsch G., Hunziker, P., Muller, P., Kim, J., Oeschslin, E.(1995). Evidence for endothelin-1- mediated vasoconstriction in severe chronic heart failure. The Lancet. 346. 732-736. Rakobowchuk, M., McGowan, C.L., de Groot, P.C., Hartman, J.W., Phillips, S.M., MacDonald, M.J. (2005). Endothelial function of young healthy males following whole body resistance training. Journal of Applied Physiology. 98. 2185-2190. Silver, R., Poonwasi, K., Seyedi, N., Wilson, S., Lovenberg, W., Levi, R. (2001) Decreased intracellular calcium mediates histamine H3 receptor induced attenuation of norepinephrine exocytosis from cardiac sympathetic nerve endings.PNAS. 99(1). 501-506. Tersman, Z. Collins, A., Eneroth, P., (1991) Cardiovascular response to phychological and physiological stress during menstrual cycle. Psychocom Med. 53. 185-197. Toga, H., Okazaki, H., Ishigaki, M. Noguchi, T., Huang, J., Fukunaga, t., et al. (1998) Effect of hypoxia on pulmonary blood flow-segmental vascular resistace relationship in perfused cat lungs. Journal of Applied Physiology.84. 1003-1010. Varghese, S.Balan, N., Caroline Selvi, K., Jayapalan, K. Jayanthi, V. (2007). Does autonomic dysfunction in cirrhosis liver influence variceal bleed.Annals of Hepatology. 6(2). 104-107. Wang, Y., De Arcangelis, V., Gao, X., Ramani, B., Jung, Y.S., Xiang, Y. (2008) Norepinephrine and epinephrein induced distinct beta2-adrenoceptor signaling is dictated by GRK2 phosphorylation in cardiomyocytes. The Journal of Biological Chemistry. 283(4). 1799-1807. Read More
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