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Babylon Medical College

Dr. Ahlam Kadhim

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blood pressure cardiovascular physiology arterial pressure medical

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This document provides lecture notes on cardiovascular physiology, focusing on blood pressure. It covers definitions, measurement methods, and regulatory mechanisms. The document targets an undergraduate level education.

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-Cardiovascular physiology -Dr.AhlamKadhim Lecture Objectives : -Definition of arterial blood pressure and the meaning of diastolic and systolic pressure -Methods of measurement of BP. -Demonstration of short and long time mechanism of regulation of BP. - Some notes abo...

-Cardiovascular physiology -Dr.AhlamKadhim Lecture Objectives : -Definition of arterial blood pressure and the meaning of diastolic and systolic pressure -Methods of measurement of BP. -Demonstration of short and long time mechanism of regulation of BP. - Some notes about venous pressure. Arterial blood pressure : means the force exerted by the blood against any unit area of the vessel wall. Blood pressure almost alwaysis measured in millimeters of mercury (mm Hg) because the mercury manometer has been used since antiquity as the standard reference for measuring pressure. The pressure in the aorta and in the brachial and other large arteries in a young adult human rises to a peak value (systolic pressure) of about 120 mm Hg during each heart cycle and falls to a minimum (diastolic pressure) of about 70 mm Hg. Systolic pressure is produced by ejection of blood into aorta during left ventricular systole while diastolic pressure is produced as a result of the elastic recoil of the aorta during ventricular diastole, fig.1..The arterial pressure is conventionally written as systolic pressure over diastolic pressure, for example, 120/70 mm Hg. Figure1 Ejection of blood during systole and Elastic recoil of aorta during diastole -Cardiovascular physiology -Dr.AhlamKadhim arterial pressure is the product of the cardiac output and the peripheral resistance, it is affected by conditions that affect either or both of these factors. BP=CO*PVR ( CO: cardiac output, PVR: peripheral vascular resistance) The pulse pressure, the difference between the systolic and diastolic pressures, is normally about 40 mm Hg.The mean blood pressure is the average pressure throughout the cardiac cycle. Mean BP=diastolic BP+1/3pulse pressure. Methods of Measuring Blood Pressure: 1-Invasive method: a cannula is inserted into an artery, the arterial pressure can be measured directly with a mercury manometer or a suitably calibrated strain gauge. 2-Non invasive methods: BP measured by sphygmomanometer. It includes : I-palpatory method. II-Auscultatory method Regulation of arterial blood pressure arterial pressure is not regulatednot by a single pressure controlling system but instead by several interrelated systems: Reflex mechansims for controlling arterial blood pressure (1) the baroreceptor feedback mechanism: Baroreceptors are stretch receptors that are extremely abundant in two locations: the aortic arch, and the carotid sinuses of the carotid arteries. Thus arterial baroreceptors are also called sinoaortic baroreceptors. These baroreceptors are placed -Cardiovascular physiology -Dr.AhlamKadhim because pressure in the aorta affects blood flow to every organ in the systemic circuit, and because pressure in the carotid arteries affects blood flow to the brain. Signals from the “carotid baroreceptors” are transmitted through glossopharyngeal nerves to the medulla. Signals from the“aortic baroreceptors” in the arch of the aorta are transmitted through the vagus nerves also to the medulla. When arterial BP increases cause stimulation of baroreceptors ,so signals transmitted to the medulla, secondary signals inhibit the vasoconstrictor centerof the medulla and stimulate cardiac inhibitory center(CIC) and vasodilator center(VDC). The net effects are (1) vasodilatationof the veins and arterioles. (2) decreased heartrate and strength of heart contraction. Therefore, excitation of the baroreceptors by high pressure in the arteries reflexly causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. Conversely, low pressure has opposite effects by inhibition of baroreceptors causing the pressure to rise back toward the normal.Figure-2. Decreased BP baroreceptors Vasomotor center vasoconstriction Increased HR and contractility of heart Increased BP Fig-2 Baroreceptor system for controlling arterial pressure. -Cardiovascular physiology -Dr.AhlamKadhim (2)The chemoreceptor mechanism: The chemoreceptors are chemosensitive cells to oxygen lack, carbon dioxide excess, and hydrogen ion excess. They are located in several small chemoreceptor organs (two carotid bodies, one of which lies in the bifurcation of each common carotid artery, and aortic bodies adjacent to the aorta). The chemoreceptors excite nerve fibers that pass through Hering nerve and vagus nerve into vasomotor center. Whenever the arterial pressure falls below a critical level, the chemoreceptors become stimulated because diminished blood flow causes decreased oxygen as well as excess buildup of carbon dioxide and hydrogen ions that are not removed by the slowly flowing blood.The signals transmitted from the chemoreceptors excite the vasomotor center, and this elevates the arterial pressure back toward normal. However, this chemoreceptor reflex is not a powerful arterial pressure controller until the arterial pressure falls below 80 mm Hg. (3) the central nervous system ischemic mechanism: when blood flow to the vasomotor center in the lower brain stem becomes decreased severely enough to cause cerebral ischemia—the vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond to the ischemia and maintain cerebral blood flow.This response is due to failure of slowly flowing blood to carry carbon dioxide away from vasomotor center. This excess CO2 has potent effect on sympathetic nervous control areas in the brain΄s medulla. It is a powerfull response.This CNS ischemic response occur when BP falls below 60mmHg. -Cardiovascular physiology -Dr.AhlamKadhim 4.Control of Blood Pressure by Low-Pressure receptors (Volume Receptors) In addition to the arterial baroreceptors, which monitor systemic arterial pressure, both the atria and pulmonary arteries have stretch receptors called low- pressure receptors. These receptors function in the same way as arterial baroreceptorsin that they have receptor endings that respond to stretch; because of their locations, however, they monitor pressure on the venous side of the systemic circulation and, therefore, act directly to detect changes in blood volume and elicit reflexes parallel to the baroreceptor to make potent control of arterial pressure. -Atrial reflexes to the kidneys : stretch of the atria causes reflex dilatation of afferent arterioles with resultant increase of filtration of fluid into the renal tubules. Signals from atrial reflexes cause reduction in secretion of Antidiuretic hormone that cause reduction in reabsorption from the renal tubules.The combination of these two effects causes rapid loss of fluid into the urine. Atrial reflex also causes release of atrial natriuretic peptide that acts on the kidneys and increase loss of fluid in urine. Atrial reflex control of heart rate called (Bainbridge reflex) that occurs due to increase blood volume and atrial stretching that cause increase in heart rate to prevent damming of blood in the veins ,atria and pulmonary circulation (this reflex has a different purpose from that of controlling arterial pressure). -Renal role in regulation arterial blood pressure: involves the renin-angiotensin system, rennin is synthesized and stored in the juxtaglomerular cells of the kidney, these cells located in the wall of the afferent arterioles proximal to the glomeruli. : decreased BP stimulate secretion of rennin enzyme from kidney this enzyme act on -Cardiovascular physiology -Dr.AhlamKadhim angiotensinogen (synthesized by the liver) forming angiotensinI which is converted to angiotensinII by angiotensin converting enzyme which is occur in the lung.this angiotensinII has potent vasoconstrictor effect.angiotensinII has two principal effects that can elevate arterial pressure. The first of these, vasoconstriction in many areas of the body, occurs rapidly. Vasoconstriction occurs intensely in the arterioles so increases the total peripheral resistance, thereby raising the arterial BP. The second principal means by which angiotensin increases the arterial pressure is to decrease excretionof both salt and water by the kidneys. This slowly increases the extracellular fluid volume, which then increases the arterial pressure during subsequent hours and days. AngiotensinII that is formed from rennin-angiotensin system causes the kidney retain both salt and water in two major ways: (fig-2) 1. AngiotensinII acts directly on the kidneys to cause salt and water retention. 2. AngiotensinII stimulates the adrenal glands to secrete aldosterone, and the aldosterone in turn increases salt and water reabsorption by the kidney tubules -Cardiovascular physiology -Dr.AhlamKadhim Decreased arterial pressure Renin(kidney) Angiotensinogen Angiotensin I ACE(lung) ACE(lung) AngiotensinII Secretion of Vasoconstriction U aldosterone Renal retention of from adrenal salt and water gland Increased arterial blood pressure Figure -2 Renin angiotensin system -Cardiovascular physiology -Dr.AhlamKadhim Veins: A Volume Reservoir the veins in the human body contain a substantially greater volume of blood than do the arteries , even though the pressure within veins is much lower than that within arteries. Factors That Influence Venous Pressure and Venous Return The driving force for venous return is the pressure gradient between the peripheral veins and the right atrium. Increases in venous pressure enhance venous return, four factors that affect venous pressure: the skeletal muscle pump, the respiratory pump, blood volume, and venomotor tone -Muscle pump: every time one moves the legs by contraction of the muscles which compress the veins adjacent to them and this squeezes the blood out of the veins. the valves in the veins are arranged so that the direction of venous blood flow can be only toward the heart. -Thoracic Pump: During inspiration, your diaphragm pulls downward and your rib cage expands, which lowers pressure in the thoracic cavity and raises pressure in the abdominal cavity. This action creates a pressure gradient that promotes the movement of blood from abdominal veins to the central veins located in the thoracic cavity, thereby increasing blood flow toward the heart. When you exhale, thoracic pressure rises and abdominal pressure falls. This creates a pressure gradient that would tend to favor the backward movement of blood from the central veins to the abdominal veins, but such backward flow is prevented by the closure of valves in the abdominal veins.the rise in thoracic pressure drives the forward movement of blood from the central veins to the heart. -Cardiovascular physiology -Dr.AhlamKadhim -Blood Volume The relationship between blood volume and venous pressure is a simple one: An increase in blood volume produces an increase in venous pressure, and a decrease in blood volume produces a decrease in venous pressure. -Venomotor Tone : The smooth muscle in the walls of veins contracts or relaxes in response to input from the sympathetic nervous system and certain chemical agents. In terms of neural control, venous smooth muscle contains _ adrenergic receptors and activity of the sympathetic nervous system triggers increased contractile activity, with a resulting rise in tension referred to as venomotor tone. Venous pressure in the venules is 12–18 mm Hg. It falls steadily in the larger veins to about 5.5 mm Hg in the great veins outside the thorax. The pressure in the great veins at their entrance into the right atrium (central venous pressure) averages 4.6 mm Hg. Central venous pressure: it is the pressure in the right atrium as Blood from all the systemic veins flows into the right atrium of the heart; Right atrial pressure is regulated by a balance between (1) the ability of the heart to pump blood outof the right atrium and ventricle into the lungs. (2)the tendency for blood to flow from the peripheral veins into the right atrium. If the right heart is pumping strongly, the right atrial pressure decreases. Conversely, weakness of the heart elevates the right atrial pressure. Also, any effect that causes rapid inflow of blood into the right atrium from the peripheral veins elevates the right atrial pressure. -Cardiovascular physiology -Dr.AhlamKadhim References : Ganong textbook of physiology , Guyton and Hall textbook of physiology. -principle of human physiology 5th edithion.

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