L31: Arterial Blood Pressure Regulation (PDF)

L31:Regulation of Arterial blood pressure Learning objectives: 1. Identify the relation between COP , peripheral resistance and ABP 2. Analyse the factors affecting the ABP 3. Discuss nervous reflexes as short term regulatory mechanisms of ABP 4. Interpret the role of capillary fluid shift and hormo...

L31:Regulation of Arterial blood pressure Learning objectives: 1. Identify the relation between COP , peripheral resistance and ABP 2. Analyse the factors affecting the ABP 3. Discuss nervous reflexes as short term regulatory mechanisms of ABP 4. Interpret the role of capillary fluid shift and hormones in regulation of ABP. 5. Relate the adjustment of body fluids and blood volume to the long term regulatory mechanisms of ABP Definitions Blood pressure (BP) It is the force exerted by the blood against any unit area on a vessel wall (measured in mmHg). The Bp fluctuates during the cardiac cycle reaching a max value of ~120mmHg during systole and dropping to ~80 mmHg during diastole. Note: Blood pressure represents the driving force that moves blood through the circulation and perfuses tissues. Systolic BP is the maximum pressure exerted in the arteries when blood is ejected into them during systole (range 100-140 mm Hg). Diastolic BP is the minimum pressure within the arteries when blood is draining off into the remainder of the vessels during diastole (range 60-90 mm Hg). The arterial BP is conventionally written as systolic pressure over diastolic pressure e.g. 120/80 mm Hg. The pulse pressure is the difference between the systolic and diastolic pressures (systolic pressure – diastolic pressure), normally about 40 mmHg. Pulse pressure correlates to the volume of blood ejected during a contraction of the left ventricle of the heart to the aorta. Pulse pressure directly relates with compliance /elasticity of aorta. Elastic of aorta maintains a normal PP range. The mean arterial pressure (MAP) is the average pressure throughout the cardiac cycle (normally about 93 mm Hg). Because systole is shorter than diastole, the mean pressure is slightly less than the value halfway between systolic and diastolic pressure. An approximation to MAP can be obtained by applying the following equation: 1 Mean arterial pressure = 2/3 diastolic pressure + 1/3 systolic pressure Mean arterial pressure = 53.3 + 40 = 93 mmHg Physiological variations of Blood pressure : Age: both systolic and diastolic BP rises with advancing age. Sex: BP is lower in young women than young men until age 55-65, after which they become comparable. Anxiety: anxiety raises BP especially systolic (due to increased sympathetic stimulation) Circadian variation: BP normally falls up to 20 mm Hg during sleep. Meals: the systolic BP increases slightly after meals due to vasodilation in the splanchnic area, which increases both the venous return and cardiac output. Exercise: systolic BP increases markedly during exercise; the diastolic BP does not change or even decreases by endurance exercise. Obesity: there is an association between obesity and hypertension. Gravity: On standing, the force of gravity increases the mean arterial pressure (as well as the venous pressure) below a reference point in the heart (in the right atrium) and decreases them above that point by about 0.77 mm Hg/cm in each case. Patient position: BP should be measured in sitting position. Patient should sit for 5 minutes before measuring BP. arm levelled with the mid-sternum and sphygmomanometer at eye level. In elderly, supine and standing position can be used to detect postural Effect of gravity on blood pressure hypotension. Time of measurement: Use multiple readings at different times during the waking hours of the patient. For patient taking antihypertensive medications monitoring of blood pressure should be done before taking the scheduled dose. Factors determining the arterial blood pressure Arterial pressure (∆P) = Cardiac output (Q) x Peripheral resistance (R) Arterial BP acts as the driving force for blood flow through the tissues of the body. For blood to flow through a vascular bed there must be a pressure gradient between the arterial and venous ends of this bed. The size of that gradient (∆P) equals the rate of blood flow (F) times the resistance to flow (R) i.e. ∆P = F x R 2 Applying this to the systemic circulation, ∆P is the pressure gradient between the aorta and the right atrium. Since atrial pressure is close to zero, ∆P is equal to the arterial BP. The total blood flow through the systemic circulation is the cardiac output. This is an important relationship because it indicates that BP may be regulated through changes in either cardiac output or peripheral resistance. (1) Cardiac output: The arterial BP is directly proportionate to the cardiac output, which is equal to stroke volume x heart rate. a. Effect of changes in stroke volume: an increase the stroke volume raises mainly the systolic BP with no significant change in diastolic Effect of changes in heart rate: an increase in heart rate raises mainly the diastolic BP due to shortening of the diastolic period (which prevent fall of the diastolic pressure to the normal level). Figure 2: Factors determining blood pressure 3 (2) The peripheral resistance It is the total resistance to blood flow through the systemic circulation. The peripheral resistance is essential for maintenance of arterial BP particularly the diastolic. It is produced mainly in the arterioles and is determined by the radius of the vessel, blood viscosity and length of vessel. Normally, adjusting the arteriolar diameter can modify it, because the other 2 factors are normally kept constant. Effect of arteriolar diameter on arterial blood pressure) REGULATION OF THE ARTERIAL BLOOD PRESSURE It is important that arterial pressure is maintained quite constant , as a fall in pressure below a critical level leads to underperfusion of the brain and the subject faint. A sustained rise in arterial blood pressure (hypertension) Leads to pathological changes in blood vessels. Various sensors located within the body continuously monitor arterial blood pressure. Whenever arterial pressure varies from normal, multiple reflex responses are initiated which cause the adjustments in cardiac output and total peripheral resistance needed to return arterial pressure to its normal value. (A) SHORT-TERM MECHANISMS (NERVOUS): These are potent rapidly-acting pressure control mechanisms. They start acting within few seconds after alteration of the BP, and their action lasts for several hours then declines. They are mostly nervous reflexes. These adjustments are brought about by changes in the activity of the autonomic nerves supplying the heart and peripheral vessels. They include: 1. Arterial baroreceptor reflexes (pressure buffer system) They are located in the aortic arch and carotid sinuses. They respond to changes in the mean arterial blood pressure within a range varing between 60 and 160 mm Hg. Any drop in systemic arterial pressure decreases the discharge in the buffer nerves leading to a compensatory rise in blood pressure and cardiac output. In opposite, any rise in pressure produces dilation of the arterioles and decreases cardiac output until the blood pressure returns to its previous baseline level. 4 2. Atrial stretch receptor reflexes An increase in arterial blood pressure causes distention of atrial stretch receptors type B by volume stimulates the vagi. The efferent impulses are carried to the SA node to increase the heart rate with a negligible effect on ventricular contractility. It also decreases the secretion of vasopressin (antidiuretic hormone) by the posterior pituitary gland to increase urine output and decrease blood volume and pressure. Moreover, It also causes atrial natriuretic peptide (ANP) to be released from storage granules within atrial myocytes which has potent diuretic and natriuretic effects on the kidneys. 3. Peripheral chemoreceptor reflexes Peripheral arterial chemoreceptors activated by reduction in partial pressure of oxygen (PaO2), Hemorrhage that produces hypotension leads to chemoreceptor stimulation due to decreased blood flow to the chemoreceptors and consequent hypoxia. Their activation leads to vasoconstriction to increase blood pressure back to normal. 4. Cushing's reflex (or reaction) The blood pressure rise is proportional to the increase in intracranial pressure to restore the blood flow to the medulla. 5. The central nervous system (CNS) ischemic response In cases of severe reduction of the arterial BP, brain ischemia occurs. The resulting low blood flow causes buildup of carbon dioxide in the vasomotor centers (RVLM), resulting in generalized vasoconstriction. B) INTERMEDIATE-TERM MECHANISMS These mechanisms control the arterial BP by adjusting the vascular capacity and resistance as well as the blood volume. They start acting within few minutes and their action lasts for several days then declines. They include: 1. Capillary fluid shift mechanism An increase in the blood volume increases the capillary hydrostatic pressure, and this helps fluid filtration into the tissue spaces, thus the blood volume is decreased leading to reduction of the arterial BP toward the normal level. The opposite occurs when the blood volume is decreased. 2. Hormonal regulation This mechanism regulates the arteriolar diameter and the peripheral resistance. It includes Catecholamine, vasopressin, and renin angiotensin system, which are previously discussed. 5 (C) LONG-TERM MECHANISMS: "control urine output" These mechanisms control the arterial BP by renal-body fluid mechanism (i.e. by adjusting the body fluids and blood volumes through modifying the excretion of water and salt by the kidneys. This occurs by variation of (a) Glomerular filtration rate (b) Secretion of the aldosterone hormone. A fall of the arterial BP reduces renal blood flow and hence glomerular filtration and urine flow, so the renal excretion of water and salt is decreased. At the same time, renin is secreted and angiotensin II is formed which in addition to producing vasoconstriction, it also stimulates aldosterone secretion from the adrenal cortex, which increases sodium reabsorption by the kidney. All these effects eventually lead to increase in the body fluids and blood volume, which raise the arterial BP back to normal level. renin angiotensin aldosterone mechanism On the other hand, a rise of the arterial BP increases blood flow to the kidney and consequently glomerular filtration and urine flow, thus producing pressure diuresis, which leads to excessive loss of water and salt in the urine. At the same time, renin secretion is inhibited and angiotensin II is not formed, thus aldosterone secretion is inhibited, leading to loss of sodium and water in the urine. The renin- angiotensin-aldosterone system is the most important mechanism in long-term regulation of blood pressure. 6