Physiology and metabolism, cardiovascular system, MacMan computer simuklation - Essay Example

Physiology and metabolism, cardiovascular system, MacMan computer simuklation Physiology and Metabolism Macman – Computer Simulation Report Institution Introduction Physiological homeostasis in the cardiovascular system is maintained depending on baroreceptor and chemoreceptor reflexes. Baroreceptor reflexes respond to changes in blood pressure and chemoreceptor reflexes respond to changes in pH, which are usually caused by an increase or decrease in blood CO2 (Scanlon & Sanders, 2011). (will insert diagrams here) In this computer simulation, changes of the internal and external environments such as arterial resistance, venous resistance, cardiac pump resistance, and blood volume, were conducted using the MacMan software. The aim was to investigate how the cardiovascular system reacts to such changes. The reference values for heart, peripheral circulation and arterial baroreceptor function are shown in table 1. Table 1: Normal values of a simulation of heart, peripheral circulation and arterial baroreceptor function of a normal average adult man. Systolic pressure: 121.0 mmHg Diastolic pressure: 75.1 mmHg Right atrial pressure: 1.7 mmHg Mean capillary pressure: 12.7 mmHg Heart rate: 69.7 /min Stroke volume: 71.5 ml Cardiac output: 5.0 l/min Total arterial resistance: 16.0 mmHg.l/min Cardial contractility: 1.3 l/min/mmHg In each of the following exercises, the results will be compared to the normal values from Table 1. Exercise 1: Table 2: Arterial resistance was increased to 150% of normal. Showing results after 180 seconds: Systolic pressure: 132.8 mmHg Diastolic pressure: 82.2 mmHg Right atrial pressure: 2.1 mmHg Mean capillary pressure: 11.2 mmHg Heart rate: 51.8. /min Stroke volume: 79.7 ml Cardiac output: 4.1 l/min Total arterial resistance: 21.8mmHg.l/min Cardial contractility: 1.0 l/min/mmHg Question 1: What happens to the blood pressure and heart rate? The systolic blood pressure is increased to 132.8 mmHg and the diastolic pressure is increased to 82.2 mmHg. The heart rate is decreased to 51.8/min (table 1). When arterial resistance is increased, the vessels experience vasoconstriction, which leads to an increase in blood pressure and a decrease in heart rate. Changing the heart rate resulted into a change in the time of the systole and that of the cardiac relaxation. The alteration in the blood pressure and cardiac output displayed a plateau, but increased by a small margin. At low heart rates, the existence of pericardial constraints causes a limitation in the viscous pressure (Her, Mandy, & Bairamian, 2005). A decrease in the heart rate led to the redistribution of the thoracic compartment from the extracic hence causing a reduction in the blood pressure. Question 2: What might give rise to the altered arterial resistance in a natural situation? The result of altered arterial resistance is increased high blood pressure (hypertension). Systolic pressure ranging between 125 and 139 mmHg and diastolic pressure that range between 60 and 80 mmHg are often considered prehypertension. This can be caused by stress, smoking, and high level of salt consumption (Her, Mandy, & Bairamian, 2005). Exercise 2: Table 3: Arterial resistance was increased to 200% of normal. Results after 180 seconds: Systolic pressure: 144.9 mmHg Diastolic pressure: 91.5 mmHg Right atrial pressure: 2.2 mmHg Mean capillary pressure: 10.3 mmHg Heart rate: 45.6 /min Stroke volume: 80.2 ml Cardiac output: 3.7 l/min Total arterial resistance: 27.6mmHg.l/min Cardial contractility: 0.9 l/min/mmHg Question: Can you suggest real situations where the changes you have made would be likely to occur? (See question 1) The Arterial pressure levels will exert mechanical stress on the walls of the arteries. Increased pressure leads to an increase in the workload of the heart. In effect, it causes the progression of the unhealthy growth of the tissues within the arterial walls. As the pressure increases, the stress on the walls increases leading to the progression of the atheroma. In the event, the heart muscle to thickens, and in the process become weak. Any persistence in hypertension result into complication such as stroke, heart failure, or heart attack (Zapol, & Snider, 977). The observed changes would occur in a hypertensive emergency case. This is so because of the levels of blood pressure being higher than normal. Table 4: Arterial resistance is decreased to 75% of normal. Results after 180 seconds: Systolic pressure: 110.5 mmHg Diastolic pressure: 69.7 mmHg Right atrial pressure: 1.4 mmHg Mean capillary pressure: 13.6 mmHg Heart rate: 90.6 /min Stroke volume: 61.0 ml Cardiac output: 5.5 l/min Total arterial resistance: 13mmHg.l/min Cardial contractility: 1.6 l/min/mmHg Question: Can you suggest real situations where the changes you have made would be likely to occur? Decreasing the arterial resistance, causes a corresponding decrease in the arterial pressure upstream from the blood flow resistance. The Arterial pressure levels will exert less mechanical stress on the walls of the arteries. Decreased pressure leads to reduced workload of the heart. As the pressure decreases, the stress on the walls decreases (Zapol, & Snider, 1977). This makes the heart muscle to thin. The blood pressure and the cardiac output reduced. Such observation may occur in a normal situation. This is so because, the desired blood pressure is classified at values higher than 90/60 and lower than 130/80. Normal pressure values may fluctuate over a twenty-four hour cycle, with the lowest reading at night, while a higher reading during the afternoon (Zapol, & Snider, 1977). 3. Venous resistance increased a) Venous resistance increased to 125% of normal b) Results: Systolic pressure: 114.6 mmHg Diastolic pressure: 73.6 mmHg Right atrial pressure: 1.1 mmHg Mean capillary pressure: 13.6 mmHg Heart rate: 78.8 /min Stroke volume: 57.8 ml Cardiac output: 4.6 l/min Total arterial resistance: 16.6 mmHg.l/min Cardinal contractility: 1.5 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? The changes in the venous resistance did not have any effect on the blood pressure and cardiac function. There was a tremendous reduction in the blood pressure and cardiac output when the venous resistance was increased. This means that a decrease in the venous pressure would result into an increase in the blood pressure and cardiac output. The existence of pericardial constraint led to the limitation of the cardiac output after the venous resistance was altered to levels below the control value. Different from the effect to the cardiac output, the changes in the venous resistance had minimum influence to the blood pressure (Zapol, & Snider, 1977). The observed changes would occur in a normal situation. This is so because, the desired blood pressure is classified at values higher than 90/60 and lower than 130/80. Normal pressure values may fluctuate over a twenty-four hour cycle, with the lowest reading at night, while a higher reading during the afternoon. 4. Venous resistance decreased a) Venous resistance decreased to 50% of normal b) Results after 180 seconds: Systolic pressure: 135.5 mmHg Diastolic pressure: 77.2 mmHg Right atrial pressure: 3.6 mmHg Mean capillary pressure: 10.1 mmHg Heart rate: 55.5 /min Stroke volume: 107.4 ml Cardiac output: 6 l/min Total arterial resistance: 14.9 mmHg.l/min Cardial contractility: 1.1 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? The observed changes would occur in a prehypertensive case. This is so because the levels of blood pressure are between 120/60 mmHg and 139/89 mmHg. Decreasing the venous resistance reduced the blood pressure as a result of the volume transferred from the systemic towards the compartment of the thorax (Zapol, & Snider, 1977). 5. Cardiac pump performance a) Cardiac pump performance increased to 125% of normal b) Results after 180 seconds: Systolic pressure: 124 mmHg Diastolic pressure: 76.2 mmHg Right atrial pressure: 1.4 mmHg Mean capillary pressure: 12.8 mmHg Heart rate: 68 /min Stroke volume: 76.5 ml Cardiac output: 5.2 l/min Total arterial resistance: 15.6 mmHg.l/min Cardial contractility: 1.5 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? Increasing the performance of the cardiac pump will increase the volume of blood that flows in other organs. This in turn will lead to a slight increase in blood pressure and the cardiac output as observed. In this experiment the blood pressure increased to 124/76.2mmHg (Zapol, & Snider, 1977). 6. Cardiac pump performance decreased a) Cardiac pump performance decreased to 50% of normal b) Results after 180 seconds: Systolic pressure: 107.4 mmHg Diastolic pressure: 69.8 mmHg Right atrial pressure: 3 mmHg Mean capillary pressure: 12.1 mmHg Heart rate: 80.7 /min Stroke volume: 51.2 ml Cardiac output: 4.1 l/min Total arterial resistance: 17.5 mmHg.l/min Cardial contractility: 0.8 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? Reducing the performance of the cardiac pump will reduce the blood pressure. This is as a result of a weakened heart that can no longer pump sufficient blood to other organs. This may reduce the functioning of other internal organs like the brain, kidneys and liver. 6. Intrathoracic pressure a) Intrethoracic pressure altered to 0 mm Hg b) Results after 120 seconds: Systolic pressure: 109.9 mmHg Diastolic pressure: 72.1 mmHg Right atrial pressure: 2.8 mmHg Mean capillary pressure: 12.1 mmHg Heart rate: 85.5 /min Stroke volume: 49.9 ml Cardiac output: 4.3 l/min Total arterial resistance: 17 mmHg.l/min Cardial contractility: 1.5 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? The pressure was reduced to 109.9/72 mmHg which was a slight deviation from the normal values. The observed changes would occur in a normal situation. This means that altering the Intrathoracic pressure has some influence on the blood pressure and the cardiac output. This value though classified as a desired blood pressure (higher than 90/60 and lower than 130/80), is slightly lower than the normal. Normal pressure values may fluctuate over a twenty-four hour cycle, with the lowest reading at night, while a higher reading during the afternoon 7. Blood volume a) Blood volume increased to 6 liters b) Results after 180 seconds: Systolic pressure: 134.8 mmHg Diastolic pressure: 78 mmHg Right atrial pressure: 3.3 mmHg Mean capillary pressure: 15.6 mmHg Heart rate: 55.2 /min Stroke volume: 101.8 ml Cardiac output: 5.6 l/min Total arterial resistance: 14.8 mmHg.l/min Cardial contractility: 1.1 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? Increase in the blood volume will give a linear blood pressure increase. For a human who is intact, the increasing v may be as a result of a reduction in the capacitance or the volume infusion. A small increase in the blood pressure and the cardiac output was observed when the blood volume was increased. Increase in volume above 6000ml may not have a further effect on the arterial pressure and the cardiac output especially in the presence of the pericardial constraint. In the study, there was a slight upward increase in the blood pressure after increasing the blood volume giving out a concave curve. The systolic pressure reached 134.8mmHg showing a huge effect on the blood pressure with the blood volume changes. Increase in blood pressure was limited by the pericardial restriction. The observed changes would occur in a prehypertension case. This is so because the levels of blood pressure are between 120/80 mmHg and 139/89 mmHg. 8. Blood volume a) Blood volume decreased to 3 liters b) Results after 240 seconds: Systolic pressure: 26.2 mmHg Diastolic pressure: 18.0 mmHg Right atrial pressure: 0.7 mmHg Mean capillary pressure: 2.9 mmHg Heart rate: 111.7 /min Stroke volume: 8.8 ml Cardiac output: 1.0 l/min Total arterial resistance: 20.2 mmHg.l/min Cardial contractility: 0.4 l/min/mmHg c) Question: Can you suggest real situations where the changes you have made would be likely to occur? The observed results will occur in a hypotensive case. This is so because the blood pressure is below 90/60 mmHg level. Decreasing the blood volume reduced the blood volume to 26.2/18 mmHg. Exercise 3 Results after 240 seconds Class I haemorrhage: decrease blood volume by 15% (1000-750 ml) Systolic pressure: 108 mmHg Diastolic pressure: 71.1 mmHg Right atrial pressure: 0.7 mmHg Mean capillary pressure: 10.3 mmHg Heart rate: 90.3 /min Stroke volume: 48.1 ml Cardiac output: 4.3 l/min Total arterial resistance: 17.3 mmHg.l/min Cardial contractility: 1.6 l/min/mmHg Class II haemorrhage: decrease blood volume by 30% (1500 ml) Systolic pressure: 88.2 mmHg Diastolic pressure: 61.7 mmHg Right atrial pressure: -0.4 mmHg Mean capillary pressure: 7.0 mmHg Heart rate: 137.1 /min Stroke volume 24.7 ml Cardiac output: 3.4 l/min Total arterial resistance: 19.3 mmHg.l/min Cardial contractility: 2.2 l/min/mmHg Class III haemorrhage: decrease blood volume by 40% (2000 ml) Systolic pressure: 26.2 mmHg Diastolic pressure: 18.0 mmHg Right atrial pressure: 0.7 mmHg Mean capillary pressure: 2.9 mmHg Heart rate: 111.7 /min Stroke volume: 8.8 ml Cardiac output: 1.0 l/min Total arterial resistance: 20.2 mmHg.l/min Cardial contractility: 0.4 l/min/mmHg Class IV haemorrhage: decrease blood volume by more than 40% (above 2000 ml – here 3000 ml) No recordings. Subject dead in less than a minute. c) Question: Does it make any difference if the blood loss is fast or slow? Yes. It makes a big difference when the loss of blood is slow or fast. The less blood volume in the body, the lesser the blood return rate to the heart and the output of cardiac. Whenever blood is lost at a fast rate, the blood return rate towards the heart will reduce at a faster rate, while a slow loss of blood would make the blood return rate to the heart to reduce at a slower rate (Brody, Stemmler, & DuBois, 2000). Question: What is the eventual cause of death? The eventual cause of death is as a result of a fast rate of blood loss. High volumes of blood loss will substantially reduce the amount of blood that returns to the heard, hence death. Exercise 4: 1. a) Multiple changes in blood volume / cardiac pump performance: Blood volume: 4000 ml; cardiac pump performance: 50% b) Results after 240 seconds: Systolic pressure: 89.4 mmHg Diastolic pressure: 61.4 mmHg Right atrial pressure: 1.1 mmHg Mean capillary resistance: 8.5 mmHg Heart rate: 112.5 /min Stroke volume: 29.7 ml Cardiac output: 3.3 l/min Total arterial resistance: 19.3 mmHg.l/min Cardial contractility: 1.1 l/min/mmHg 2. a) a) Multiple changes in blood volume / cardiac pump performance: Blood volume: 3500 ml; cardiac pump performance: 50% b) Results after 240 seconds: Systolic pressure: 22.9 mmHg Diastolic pressure: 15.8 mmHg Right atrial pressure: 2.5 mmHg Mean capillary pressure: 4.2 mmHg Heart rate: 107.2 /min Stroke volume: 7.4 ml Cardiac output: 0.8 l/min Total arterial resistance: 20.2 mmHg.l/min Cardial contractility: 0.2 l/min/mmHg c) Question: How much more serious is severe blood loss in a person with only 50% normal cardiac performance? Blood loss to a person with 50% normal performance of the cardiac will result into a hypotension condition. It results into the reduction of the arterial pressure together with the flow of blood beyond the normal point (Brody, Stemmler, & DuBois, 2000). This decreases the brain perfusion as a result of insufficient supply of blood causing fainting, dizziness, weakness, or light-headedness. Exercise 5: 1. a) Arterial resistance changed to 150% b) Results after 180 seconds: Systolic pressure: 132.8 mmHg Diastolic pressure: 82.1 mmHg Right atrial pressure: 2.1 mmHg Mean capillary pressure: 11.2 mmHg Heart rate: 51.8 /min Stroke volume: 79.7 ml Cardiac output: 4.1 l/min Total arterial resistance: 21.8 mmHg.l/min Cardial contractility: 1.0 l/min/mmHg 2. a) Arterial resistance changed to 150% and baroreceptor nerves cut b) Results after 180 seconds: Systolic pressure: 788.0 mmHg Diastolic pressure: 0.0 mmHg Right atrial pressure: 0.7 mmHg Mean capillary pressure: 15.0 mmHg Heart rate: 161.8 /min Stroke volume: 2700.3 ml Cardiac output: 436.9 l/min Total arterial resistance: 30.3 mmHg.l/min Cardial contractility: 2.4 l/min/mmHg c) Question: Would this kill the subject and if so, what would be the eventual cause of death. Yes. This will kill a person as a result of the increased blood pressure. High amounts of arterial pressure will increase the amount of pressure that is exerted on the arterial walls. This high pressure makes the workload of the heart to increase leading to the unhealthy tissue growth progression in the arteries. Such a high pressure will increase the stress, hence increasing the atheroma and the thickening of the heart muscle. When this condition persist, it may result into heart failure, stroke, heart attack or death (Brody, Stemmler, & DuBois, 2000). Summary From the study, it is true to conclude that altering the selected values of the venous resistance together with compliance while establishing minimum alteration in other cardiovascular parameters tremendously changes the blood pressure as a result of the ventricular chance response, heart rate, or venous resistance. Setting the venous resistance at low values would reduce the ventricular function together with the heart rate. This means that the increasing venous resistance has minimum influence on the blood pressure. Setting the venous resistance at high values may alter the blood pressure. These variations of the blood pressure on the different parameters has been reported on many studies on the return function and the cardiac function and determination of the performance of the circulatory system. This study shows that the debate should narrow down on the fact that the venous resistance has some effect to the cardiovascular system. References: Brody, Stemmler, J., & DuBois, A. 2000. “Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins.” Journal of Clinical Investigation; 47(4):783-99. · 12.81 Impact Factor. Her,C., Mandy, S., & Bairamian, M. 2005. “Increased pulmonary venous resistance contributes to increased pulmonary artery diastolic-pulmonary wedge pressure gradient in acute respiratory distress syndrome.” Anesthesiology Impact Factor: 5.16. 04. Scanlon, V.C and Sanders, T. 2011. Essential of Anatomy and Physiology, 6th edition, F. A. Davis Company, Philadelphia, United States of America Zapol, K, & Snider, M. 1977. Pulmonary hypertension in severe acute respiratory failure. New England Journal of Medicine; 296(9):476-80. · 51.66 Impact Factor Read More