Blood pressure regulation.pdf

Blood pressure regulation Dr.Husam Elmehrik Physiology Department [email protected] At the end of this lecture ,students should be able to: Define blood pressure and state its normal value. Describe the classification of blood pressure. Describe the factors af...

Blood pressure regulation Dr.Husam Elmehrik Physiology Department [email protected] At the end of this lecture ,students should be able to: Define blood pressure and state its normal value. Describe the classification of blood pressure. Describe the factors affecting normal blood pressure. Explain the different mechanisms of blood pressure regulation. Describe the abnormalities of blood pressure (Hypertension).  BLOOD PRESSURE The body’s blood pressure is a measure of the pressures within the cardiovascular system during the pumping cycle of the heart. It is influenced by a vast number of variables, and can alter in either direction for various reasons. Everyone’s blood pressure is slightly different and can change throughout the day depending on activity.  There is a range of normal blood pressures that we consider as acceptable. When blood pressure is outside of this normal range of values, people can start to have problems in both the long and short term. Blood pressure can be calculated as Flow x Resistance Arterial blood pressure = cardiac output x total peripheral vascular resistance N ~ 120/80 mmHg Mean arterial blood pressure (MAP) = DP + 1/3(SP – DP) or MAP = DP + 1/3(PP) ~ 100 mmHg Pulse pressure(PP): - is the difference between systolic blood pressure and diastolic blood pressure. - a normal pulse pressure range is between 40 and 60 mmHg. - a pulse pressure reading is considered low when it's less than 40 mmHg indicates decreased cardiac output.  Blood pressure is measured manually using a stethoscope and sphygmomanometer. Sphygmomanometer: is a blood pressure monitor, or blood pressure gauge, a device used to measure blood pressure BP is given as two values ( 120/80 mmHg) in average, measured in “millimetres of mercury(mmHg)”: 1- Systolic pressure – the first number (120 mmHg in the example) is the pressure of the blood during the heart contraction. 2- Diastolic pressure – the second number (80 mmHg in the example) is the pressure of the blood after one contraction but before the next contraction (heart relaxation). Can be measured manually by :Aneroid or mercury Sphygmomanometer. Aneroid Vs Mercury manometer  Blood pressure also can be measured digitally using an automated blood pressure monitor: - involves recording several blood pressure readings using a fully automated oscillometric sphygmomanometer. - It is may be inaccurate in 5-15% of patients. invasive blood pressure measurement: involves direct measurement of arterial pressure by placing a cannula in an artery (usually radial but femoral, dorsalis pedis or brachial arteries may also be used). The arterial cannula is connected to non-compressible tubing containing a continuous column of heparinized saline. classification of blood pressure (Adult)  REGULATION OF ARTERIAL PRESSURE The most important mechanisms for regulating arterial pressure are : 1- Fast, neurally mediated baroreceptor mechanism(Short-Term Regulation). 2- Slower, hormonally regulated renin–angiotensin–aldosterone mechanism (long -Term Regulation). Fast Slow  Short-Term Regulation of Blood Pressure Short-term regulation of blood pressure is controlled by the autonomic nervous system. Changes in blood pressure are detected by BARORECEPTORS. These are located in the Arch of the aorta (Aortic bodies) and the Carotid sinus ( i.e same location as for Chemoreceptors which are sensitive to arterial levels of oxygen, carbon dioxide (CO2), and pH, while BARORECEPTORS are stretch receptors sensitive to Changes in blood pressure). Both receptors travel their signals to the CNS via the same nerve bundles. Increased arterial pressure stretches the wall of the blood vessel, triggering the mechanical baroreceptors. These baroreceptors then feedback negatively to the autonomic nervous system. ANS acts to reduce the heart rate and cardiac contractility via the efferent parasympathetic fibres (vagus nerve) thus reducing blood pressure. Decreased arterial pressure is detected by baroreceptors, which then trigger a sympathetic response. This stimulates an increase in heart rate and cardiac contractility leading to an increased blood pressure. Baroreceptors cannot regulate blood pressure in a long-term manner. This is because the mechanism of triggering baroreceptors resets itself once an adequate blood pressure is restored. Baroreceptor reflex includes fast neural mechanisms. is a negative feedback system that is responsible for a minute-to-minute regulation of arterial blood pressure, i.e it induces an INHIBITORY effect on vasomotor centre controlling blood pressure by stimulating parasympathetic NS While inhibiting sympathetic NS. Baroreceptors are stretch receptors located within the walls of the Carotid sinus near the bifurcation of the common carotid arteries. Steps in the baroreceptor reflex: As example; a decrease in arterial pressure: Neural mechanism a. This will decrease the stretch on the walls of the carotid sinus. Because the baroreceptors are most sensitive to changes in arterial pressure, rapidly decreasing arterial pressure produces the greatest response. Note: Additional baroreceptors in the Aortic arch respond to increases, but not to decreases, in arterial pressure. b. Decreased stretch decreases the firing rate of the carotid sinus nerve [Hering’s nerve, a branch of cranial nerve IX (The glossopharyngeal nerve), which carries information to the vasomotor centre in the brain stem. c. The set point for mean arterial pressure in the vasomotor centre is about 100 mmHg. Therefore, if mean arterial pressure is less than 100 mmHg, a series of autonomic responses is coordinated by the vasomotor centre. These changes will attempt to increase blood pressure toward normal (100 mmHg). d. The responses are decreased parasympathetic (vagal) outflow to the heart (M2 at SA node) and increased sympathetic outflow to the heart (B1 and B2 at SA node and heart muscle) and blood vessels (alfa1 receptors).  The following four MECHANICAL EFFECTS attempt to increase the arterial pressure to normal: (1) ↑ heart rate, resulting from decreased parasympathetic tone and increased sympathetic tone to the SA node of the heart. (2) ↑ contractility and stroke volume, resulting from increased sympathetic tone to the heart. Together with the increase in heart rate, the increases in contractility and stroke volume produce an increase in cardiac output that increases arterial pressure. (3) ↑ vasoconstriction of arterioles, resulting from the increased sympathetic outflow. As a result, total peripheral resistance (TPR) and arterial pressure will increase. (4) ↑ vasoconstriction of veins (Venoconstriction), resulting from the increased sympathetic outflow. Constriction of the veins causes a decrease in unstressed volume and an increase in venous return to the heart. The increase in venous return causes an increase in cardiac output by the Frank– Starling mechanism by increase PRELOAD. Role of the baroreceptor reflex in the cardiovascular response to hemorrhage. Pa = mean arterial pressure; TPR = total peripheral resistance.  Application of the baroreceptor mechanism: Valsalva maneuver (Testing baroreceptor function) The integrity of the baroreceptor mechanism can be tested with the Valsalva maneuver (i.e., expiring against a closed glottis). Expiring against a closed glottis causes an increase in intrathoracic pressure, which decreases venous return. The decrease in venous return causes a decrease in cardiac output and arterial pressure (Pa). If the baroreceptor reflex is intact, the decrease in Pa is sensed by the baroreceptors, leading to an increase in sympathetic outflow to the heart and blood vessels. In the test, an increase in heart rate would be noted. When the person stops the manoeuvre, there is a rebound increase in venous return, cardiac output, and Pa. The increase in Pa is sensed by the baroreceptors, which direct a decrease in heart rate. If test is negative means baroreceptor mechanism is not intact. That can be seen in cases with autonomic system dysfunctions like in diabetes mellitus neuropathy patients.  Long-Term Regulation of Blood Pressure There are several physiological mechanisms that regulate blood pressure in the long-term: Renin-angiotensin-aldosterone system (RAAS). Vasopressin (Antidiuretic hormone ADH). Atrial natriuretic peptide (ANP).  Renin-Angiotensin-Aldosterone System (RAAS) There are several physiological mechanisms that regulate blood pressure in the long-term, the first of which is the renin-angiotensin-aldosterone system (RAAS). Renin is a peptide hormone released by the granular cells of the juxtaglomerular apparatus in the kidney. It is released in response to: Sympathetic stimulation Reduced sodium-chloride delivery to the distal convoluted tubule Decreased blood flow to the kidney Renin facilitates the conversion of angiotensinogen (from liver) to angiotensin I which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) released mainly by type II alveolar epithelial cells. Angiotensin II is a (1)potent vasoconstrictor. It acts directly (2)on the kidney to increase sodium reabsorption in the proximal convoluted tubule. Sodium is reabsorbed via the sodium-hydrogen exchanger. Angiotensin II also promotes release of(3) aldosterone.  ACE also (4)breaks down a substance called bradykinin which is a potent vasodilator. Therefore, the breakdown of bradykinin potentiates the overall constricting effect (V.C). Aldosterone (5) promotes salt and water retention by acting at the distal convoluted tubule to increase expression of epithelial sodium channels. Furthermore, aldosterone increases the activity of the basolateral sodium- potassium ATP-ase, thus increasing the electrochemical gradient for movement of sodium ions. More sodium collects in the kidney tissue and water then follows by osmosis. This results in decreased water excretion and therefore increased blood volume and thus blood pressure.  Steps in the renin–angiotensin–aldosterone system a. A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin. b. Renin is an enzyme that catalyses the conversion of angiotensinogen to angiotensin I in plasma. c. Angiotensin-converting enzyme (ACE) catalyses the conversion of angiotensin I to angiotensin II, primarily in the lungs. d. Angiotensin I is inactive. Angiotensin II is physiologically active. Angiotensin II is degraded by angiotensinase. One of the peptide fragments is Angiotensin III, has some of the biologic activity of angiotensin II. ACE inhibitors (e.g., captopril) block the conversion of angiotensin I to angiotensin II and, therefore, decrease blood pressure. Angiotensin receptor (AT1) antagonists (e.g., losartan) block the action of angiotensin II at its receptor and decrease blood pressure.  Clinical Relevance - Hypertension Hypertension is defined as a sustained increase in blood pressure. It may be primary (of an unknown cause) or secondary to another condition such as chronic renal disease or Cushing’s syndrome. Hypertension causes damage to the walls of blood vessels, making them weaker. This leads to a number of pathologies including Atherosclerosis, Thromboembolism (progressing to MI or stroke) and Aneurysms. Hypertension also damages the heart itself by increasing the afterload of the heart. The heart is pumping against greater resistance, leading to left ventricular hypertrophy. This increases the risk of heart failure in the future. Hypertrophy of the cardiac muscle also increases the heart’s oxygen demand, predisposing to myocardial ischaemia and ultimately angina. (Hypertensive crisis) WHY? REFERENCES  Ganong WF, 2009. Review of Medical Physiology. 23rd Ed. Appleton & Lange: USA.  Lauralee Sherwood. 2004. Human Physiogy. 5th Ed. Thomson, Brooks/Cole: USA.  Eric P. Widmaier. 2007. Vander’s Human Physiology –The mechanism of body function. 11th. McGraw-Hill: USA.  Robert M. Berne. 2004. Physiology. 5th Ed. Mosby,Elsevier Sc.: USA.  John T. Hansen. 2003. Netter’s Atlas of Human Physiology. 1st Ed. MediMedia: USA.