Determinants of Adult Blood Pressure - Lab Report Example

Q1. When one moves from the sitting or supine position, various vascular changes takes place. As one stands up gravitational pull acts on the extremities and reduce the venous return because blood is pulled towards the legs. This decreases the blood volume by about 300 to 800ml. Since the blood volume is decreased the venous return and End Diastolic Volume (Pre-load) are also decreased. Hence the myocardium is less stretched and according to Franks Starlings Hypothesis, the force of myocardial contraction depends upon the initial length of the contracting muscles, within physiologic limits. As the muscles are less stretched the force of contraction decreases which reduces the stroke volume. Decreased stroke volume results in decreased cardiac output and hence reduces blood pressure initially. This is also called orthostatic hypotension (reduced blood supply to brain due to reduced cardiac output causing fainting). However after sometimes, baroreceptor respond to this decreased blood volume and stimulates the cardio-accelerator center in Rostral Ventrolateral Medulla which cause noradrenergic discharge. Nor adrenaline then acts on Beta-2 adrenergic receptors on myocardium to increase the heart rate and force of contraction to increase the blood pressure to normal and thus maintaining homeostasis (Williams et al, 2004). Q2. Analyzing the blood pressure it becomes evident that although there was a drop in mean systolic blood pressure (114mm Hg sitting versus 111 mm Hg standing, but it was not statistically significant as p value was > 0.05), even mean diastolic blood pressure decreased (76.3 mm Hg sitting versus 73 mm Hg standing but again it was not statistically significant as p value was > 0.05). However the mean pulse pressure ( difference between systolic and diastolic) increased(84.6 mm Hg sitting versus 87 mm Hg, but this was also not statistically significant as p value was > 0.05). This means that out of 100 observations more than 5 observations has happened due to chance factors of random sampling and change in posture has not statistically altered their blood pressure. Though statistically insignificant it is clearly seen that clinically or physiologically there is reduction of blood pressure from sitting and standing postures as discussed in question 1. The increased pulse pressure was due to the fact to compensate the reduction in cardiac output and increase the peripheral circulation (Williams et al, 2004) (Blair et al, 1980). t tests are conducted to test the significance of difference between grouped observations. t score is a standard score and is calculated as : t= MX1-MX2/ standard error of difference between the means (where MX1 is the mean of one group and MX2 is the mean of another group e.g. In our test for systolic BP (sitting versus standing it is 114-111) . Standard error of difference (SEDM) between the means= square root [(standard deviation of group 1)2 / number of observations in that group + (standard deviation of group 2)2 / number of observations in that group)]. In the same example SEDM= 91.86. Thus computed t is 114-111/91.86=0.03. The computed t of 0.03 is much lesser than critical t at df =5 (n1 +n2 -1) where, n1and n2 are number of observations in each group and df= degree of freedom). As it is less than critical t the area beyond the computed t in the Unit normal curve is much greater than 0.05. Hence the probability of chance is considered (Null Hypothesis accepted) and it is considered there is no significant difference between two observations (in our example systolic blood pressure). The t test was conducted as unpaired t test with unequal variance (Blair et al, 1980). Q3. Considering the anatomy of a Giraffe and Human it will be evident that Giraffes will be less prone to orthostatic hypotension or fainting (reduced blood supply to brain due to reduced cardiac output). This is because special cardiovascular compensations take place to pull the blood to their heart and brain in-spite of pull of gravity. Normally Giraffes have a larger heart (hence more stroke volume) and hence increased blood pressure than humans. They also have tight skin and stronger muscles which influence venous return. The tight skin prevents the blood from getting pulled and the stronger muscles ensues adequate venous return, hence decrease in blood pressure is not so obvious unlike humans (Lawlor et al, 2005). Q4. Hypertension is defined as sustained elevation in arterial blood pressure beyond a certain range specified to age and population. The range of normal blood pressure is however fixed at 140 mm Hg (systolic blood pressure which represents the arterial blood pressure when the heart is in systole or during contraction) and 90 mm Hg at diastole (represents the arterial blood pressure when the heart is in diastole or during relaxation). However this range is valid for persons without any co -morbid disorders like diabetes or dyslipidemia. For persons with these disorders the target range of normal blood pressure as specified by JNC VI Guidelines is 135 mm Hg/85 mm Hg. Beyond this range the patient will be considered hypertensive. Normally blood pressure varies with time and activity but as such it is auto regulated within a range of 60 mm Hg and 180 mm Hg by the action of Baroreceptors and Chemo receptors. However in hypertensive patients this auto regulation fails in this range and the threshold range is fixed to higher levels beyond 180mm HG due to resetting of Baroreceptors and Chemo receptors (Arguedas et al,2009)( Williams et al, 2004). There are many causes for the same but two of the causes are: Increased Peripheral Resistance due to increased sympathetic stimulation: In conditions of stress and sustained anxiety, there is a release of Norepinephrine from the Locus Ceruleus – Norepinephrine System (LC-NE) or the sympathetic nervous system which releases Norepinephrine. This Norepinephrine acts on alpha adrenergic receptors on the endothelium of the arteries causing vasoconstriction which increases the peripheral resistance without increasing the cardiac output. This causes sustained elevated blood pressure as per the equation: Blood Pressure= Cardiac Output * Peripheral Resistance. Thus if peripheral resistance is increased blood pressure will increase (Arguedas et al,2009)( Williams et al, 2004). Hyperaldosteronism or Conn’s Syndrome: Due to release of excess aldosterone from the adrenal cortex (due to adreno- cortical tumors), it acts on the epithelial sodium channels (ENaC) channels in the Henle’s loop of the nephrons. Aldosterone causes increased reabsorbtion of sodium ions and hence water which follows the osmotic gradient of sodium is also reabsorbed. This cause’s reduced urine output and cause increase in blood volume and hence cardiac output. If cardiac output or hypervolemia occurs blood pressure increases since: Blood Pressure= Cardiac Output * Peripheral Resistance (Arguedas et al,2009)( Williams et al, 2004). Q5. Beta Blockers or Beta adrenergic blocking agents like atenolol or popanolol are used to manage hypertension. They block the Beta 1 adrenergic receptors of the myocardium and hence prevent the action of nor adrenaline or adrenaline on it. Nor –adrenaline released by the sympathetic nervous system in response to stress acts on these receptors and increase the chronotropic and ionotropic effects positively ( which means the rate and force of contraction of the myocardium is increased). This increases the cardiac output which cause increased Blood Pressure. Thus by blocking the actions of Nor –adrenaline it decreases chronotropic and ionotropic effects positively (thus the rate and force of contraction of the myocardium is decreased). This decreases the cardiac output which cause decreased Blood Pressure as Blood Pressure= Cardiac Output * Peripheral Resistance (Singer et al, 2008). However, Beta blockers are not used for treating asthma and diabetes. Beta blockers used are non selective which means along with blocking beta 1 receptors( found on heart muscles) they will also block beta- 2 receptors ( found on bronchiolar smooth muscles). Blocking of beta- 2 receptors in the lungs will prevent the action of adrenaline on it, but in bronchiole smooth muscles adrenaline acts opposite to myocardium muscles which means they cause relaxation of the bronchioles normally. Since asthma is an obstructive disease, blocking beta 2 receptors will cause further bronchoconstriction and exacerbate the obstructive conditions (that is air is trapped in alveoli and cannot be exhaled out easily) or asthmatic condition will be prolonged (Singer et al, 2008).In diabetics Beta blockers are not preferred because diabetic patients develop a condition called “Hypoglycemic Unawareness”, where although they have extremely low blood sugars they do not experience the symptoms like light headed or sweatiness to aware them of the problem. Beta blockers mask the issue of hypoglycemia more acute and aggravate the condition of “Hypoglycemic Unawareness” further(Singer et al, 2008). Q6. Angiotensin 1 Converting Enzyme Inhibitors (ACE I) like Ramipril acts by inhibiting Angiotensin 1 Converting Enzyme. Angiotensin 1 Converting Enzyme normally converts Angiotensin 1 to Angiotensin II in the lungs. Angiotensin II is a potent arterial vasoconstrictor, thus it can increase the peripheral resistance and blood pressure. Another mechanism is that it stimulates aldosterone from the adrenal cortex which causes increased reabsorbtion of sodium ions (in nephrons) and hence water which follows the osmotic gradient of sodium is also reabsorbed. This cause’s reduced urine output and cause increase in blood volume and hence cardiac output which indirectly increase blood pressure. Hence by inhibiting Angiotensin 1 Converting Enzyme, Angiotensin II formation is reduced and hence blood pressure is reduced too(Singer et al, 2008).Young patients respond to Angiotensin 1 Converting Enzyme Inhibitors because in them kidney etiology is the major reason for their essential hypertension than people over 55 years of age where the cause of hypertension stems from aging, obesity, sedentary lifestyle than kidney issues(Singer et al, 2008). Q7. Potassium channel activators like Nicorandil activates the ATP sensitive potassium channels and causes influx of K+ ions with respect to Na+ and this hyperpolarizes the cell (less excited state). Thus voltage gated Ca++ ions will not enter the cell and hence smooth muscle contraction of the vascular endothelium will not take place. Thus by inhibiting development of peripheral resistance and after load Potassium channel activators controls hypertension. Nitrates like Nitroglycerin also cause vasodilatation. This is because they are converted to Nitric Oxide by nitric oxide synthase found in the walls of blood vessels. They cause vasodilatation and improve blood flow. By increasing vasodilatation, they reduce peripheral resistance and hence blood pressure. However since they cause rapid vasodilatation, there is a chance of reflex tachycardia which can stress the heart and hence they are used as adjunct and not as first line treatment of hypertension. Although Potassium channel activators also cause vasodilatation but they do not rapidly does it and hence chance of reflex tachycardia is lesser than Nitrates (Singer et al, 2008). Graph Compare :Though the blood pressure and heart rates increased for all following exercise the pulse rate was less increased in fit individual than the other two because a fit person has an athletes heart( more volume of ventricles) and hence a larger stroke volume. So he can meet the demand of exercise cardiac output by increased stroke volume (Cardiac Output = Stroke volume * Heart Rate). But the other two Bela and Helen have to increase the Cardiac Output by increasing heart rate).The systolic and diastolic blood pressure came to normal within 3 minutes in Bella and Fit individual but took 4.5 in Helen. While the fit individual recovered quickly in heart rate (1.5min) but Bela and Helen took around 4.5 minutes as they do not have an athlete’s heart. Error bars represent standard error. References Arguedas, JA; Perez, MI; Wright, JM (2009). Arguedas, Jose Agustin, ed. "Treatment blood pressure targets for hypertension". Cochrane Database of Systematic Reviews (3): CD004349 Blair, R. Clifford; Higgins, James J. (1980). "A Comparison of the Power of Wilcoxons Rank- Sum Statistic to That of Students t Statistic Under Various Nonnormal Distributions". Journal of Educational Statistics 5 (4): 309–335. Lawlor, DA; Smith, GD (2005). "Early life determinants of adult blood pressure". Current Opinion in Nephrology and Hypertension 14 (3): 259–64 Singer DR, Kite A; Kite (2008). "Management of hypertension in peripheral arterial disease: does the choice of drugs matter?". European Journal of Vascular and Endovascular Surgery 35 (6): 701–8 Williams, B; Poulter, NR, Brown, MJ, Davis, M, McInnes, GT, Potter, JF, Sever, PS, McG Thom, S, British Hypertension, Society (2004). "Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV". Journal of Human Hypertension 18 (3): 139–85 Read More