Collage of medicine Cardiovascular Physiology 3- Arterial and venous blood Pressure.

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1 University of Babylon Collage of medicine Dr. Ghafil Seyhood Hassan Al-Shujiari Cardiovascular Physiology 3- Arterial and venous blood Pressure. UArterial blood pressureu: Arterial pressure = COP X Peripheral resistance. Mean blood pressure = Diastolic pressure + 1/3 pulse pressure. Pulse pressure = Systolic pressure diastolic pressure. (Figure 1). The pressure falls very slightly in the large and medium-sized arteries because their resistance to flow is small, but it fall rapidly in the small arteries and arterioles, which are the main sites of peripheral resistance. Normal blood pressure is 120/ 70 mmhg. The pressure in any vessel below heart level is increased and above heart level is decreased by effect of the gravity 0.77 mmhg for each one cm. Figure (1): Arterial blood pressure curve. In general the blood pressure is lower in children than adult and women than men. Blood pressure may increase by exercise, emotion and pregnancy. Increase cardiac output lead to increase the systolic pressure. The blood pressure is higher in systemic than pulmonary circulation because pulmonary circulation is under lower resistance UMethods of measuring arterial blood pressure: 1- Direct method ( invasive method): A cannula is inserted into an artery, the arterial pressure can be measured directly with a mercury manometer. The wave recorded by this method is called pulse wave. Pressure at the highest point of each pulse is systolic pressure and the lowest point is diastolic pressure. 2- Indirect method (non invasive method): A- UPalpation method:u Letting the pressure fall and determining the pressure at which the radial pulse become palpable. This is a systolic pressure. This method is usually 2-5 mmhg, pressure lower than those measured by ausculatory method.

2 A-UAusculatory methodu: Inflatable cuff attached to mercury manometer (sphygmomanometer) is wrapped around the arm and a stethoscope is placed over the brachial artery at elbow. The cuff is rapidly inflated until pressure in it above expected systolic pressure. Artery is occluded by cuff and no sound is heard with stethoscope. The pressure in cuff is then lowered slowly, at point a tapping sound heard (Korotkoff sound phase 1), systolic pressure is recorded. Cuff pressure is lowest further, the sound become louder, dull, and muffled then disappear (Korotkoff sound phase 5), at this point diastolic pressure is recorded. A number of precautions must be obtained in measurement of arterial BP: 1- The cuff must be at heart level to obtain a pressure that is uninfluenced by gravity. 2- The size of the cuff suitable, as small cuff use in children and large cuff use in obese. 3- Do not leave the cuff inflate for long time as it may cause generalized reflex vasoconstriction. 4-Measure blood pressure from right and left arm. Regulation of arterial blood pressure I- Nervous mechanism: UA- Baroreceptor mechanism:u This is fast neural mechanism. Baroreceptors are stretch receptors located with in the wall of the carotid sinus near the bifurcation of the common carotid arteries and aortic arch in adventitia of vessels. Figure (2). Figure (2): Carotid sinus and aortic arch paroreceptors. UB- The chemoreceptors mechanism:u Chemoreceptors present in the carotid and aortic bodies. They have very high rate of O2 consumption and therefore are very

3 sensitive to hypoxia. A decrease in arterial pressure causes a decrease in O2 delivery to the chemoreceptors. Information is sent to vasomotor center. UC- Vasomotor center (VMC)U: It is group of neurons located in the medulla oblongata. It is composed of vasoconstrictor, vasodilator and sensory area. When blood pressure decreases, the informations reach VMC via vagus and glosopharyngeal nerves to increase sympathetic discharge to blood vessels and heart to increase HR, stroke volume and TPR. Conversely increase in blood pressure causes decrease in sympathetic and increase in parasympathetic discharge to cause vasodilatation of vessels and decrease heart rat. UII-Hormonal Mechanism: 1- URenin-angiotensin-aldosterone system:u It is a slow mechanism. Blood pressure regulated by blood volume. Renin is an enzyme that catalyzes the conversion of angiotensinogen to angiotensin I in plasma. It is secreted from the juxtaglomerular cells of the afferent arteriole in kidney during decrease in renal perfusion pressure. Angiotensin I is inactive. The angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE), primarily in the lungs. Angiotensin II is physiologically active. It is degraded by angiotensinase. Angiotensin II has two effects: 1- It stimulates the synthesis and secretion of the aldosterone by the adrenal cortex. Aldosterone increases sodium chloride ( Nacl) reabsorption by renal distal tubule, thereby increasing blood volume and arterial pressure. This action of aldosterone is slow because it requires new protein synthesis. 2- It causes vasoconstriction of the arterioles, thereby increasing TPR and mean arterial pressure. U2-Vasopressin or Antidiuretic hormone (ADHU): Atrial receptors respond to a decrease in blood pressure and cause the release of vasopressin from the posterior pituitary gland. Vasopressin has two effects that tend to increase BP toward normal. 1- It is a potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles. 2- It increases water reabsorption by the renal distal tubule and collecting ducts by activating V2 receptors. U3- Atrial natriuretic peptide (AVP):U It is released from the atria in response to an increase in atrial pressure, causes relaxation of vascular smooth muscle, dilatation of arterioles and decreased TPR. It causes increased excretion of salt and water by the kidney III- Capillary fluid shift mechanism: Any change in the arterial pressure usually associated with change in capillary pressure resulting in the movement of fluid across the capillary membrane between the blood and interstitial compartment so a new state of equilibrium will be achieved.

4 Venous blood pressure The pressure in the venules is about mmhg. It fails in the larger veins to about 5.5 mmhg in the great veins outside the thorax and 4.5 mmhg (central venous pressure) at their entrance the thorax. Peripheral venous pressure is affected by gravity. It is increased by 0.77 mmhg for each cm below the right atrium and decrease by 0.77 mmhg for each 1cm above the right atrium. UJugular venous pulses:u The changes in atrial pressure are transmitted to the great veins, producing three characteristic positive waves. The (a) wave is due to atria systole. The (c) wave concides with the onset of ventricular systole and results from tricuspid valve closure (Tricuspid bulging). The (v) wave indicates arise in pressure as venous blood return continously while tricuspid valve is closed. Figure (3). Figure (3): Normal jugular venous pulse. Effect of gravity on the body The following changes occur when an individual move from a supine position to standing position: 1- A significant volume of blood pools in the lower extremities due to of high compliance of the vein. Muscular activity would prevent this pooling. 2- Increase venous pressure in legs, increase filtered fluid into interstitium. Edema will occur. 3- Decrease venous return, both stroke volume and COP decrease (Frank-Starling relationship). 4- If COP decrease cerebral blood pressure becomes low, fainting may occur. Compensatory mechanism will attempt to increase blood pressure to normal. The carotid sinus baroreceptors respond to the decrease in arterial pressure by decreasing the firing of the carotid sinus nerves. Vasomotor center then increases sympathetic outflow to the heart and blood vessels and decreases parasympathetic outflow to heart. As a result, heart rate and TPR increase and blood pressure increases toward normal

5 from Effect of altitude on the body 1- The oxygen partial pressure decreases, hypoxia beginning at altitude of about 12,000 feet, symptoms of hypoxia are drowsiness, lassitude, mental and muscle fatigue, sometime headache. 2- Hypoxia stimulates arterial chemoreceptors to Uincrease alveolar ventilationu to a maximum of about 1.65 times 0f normal. This is an immediate compensation with in seconds. 3- It Uincreases red blood cell productionu, UhematocitU from a normal value of to an average of about UIncrease concentration of hemoglobin U a normal value 15 gm /dl to about 20 gm /dl. 5- It Uincreases diffusing capacity for O2 through the pulmonary membraneu 3 fold as much as during exercise. Normal capacity 21 ml / mmhg / minute. 6- UCOP increaseu as much as 30% immediately after a person ascends to high altitude but then decrease back toward normal as the blood hematocrit increases. 7- UIncrease in number of systemic circulatory capillaries U. 8- In animals native to altitude of 13,000 to 17,000 feet, Ucell mitochondria and cellular oxidative enzyme systems are slightly more plentiful than in sea-level inhabitants. Venous return Venous flow is aided by; 1- The heart beat. 2-The increase in the negative intrathoracic pressure during each inspiration. 3- Contraction of skeletal muscles that compress the vein (muscle pump) figure (4). 4-Venous valves prevent reverse flow, the blood moves toward the heart. 5-The diaphragm descend during inspiration, intra-abdominal pressure rises, and this also squeezes blood toward the heart. 6-During inspiration the intrapleural pressure falls from to 6 mmhg. This negative pressure is transmitted to great veins; venous pressure fluctuates from about 6 mmhg during expiration to 2 mmhg during inspiration. The drop in venous pressure during inspiration aids venous return. Figure (4): Venus return.