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THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS BLOOD VESSEL STRUCTURE AND FUNCTION BLOOD VESSELS • Three major types: – Arteries: blood away from the heart – Capillaries: exchange between blood and tissues – Veins: blood toward the heart • Heart—arteries—arterioles— capillaries—venules— veins—Heart • Altogether, the blood vessels in the adult human stretch for about 100,000 km (60,000 miles) through the internal body landscape BLOOD VASCULAR SYSTEM and LYMPHATIC SYSTEM STRUCTURE OF BLOOD VESSEL WALLS • The walls of all blood vessels except the smallest consist of three layers: – Tunica interna (intima): lining of slick simple squamous epithelium that reduces friction between the vessel walls and blood – Tunica media: mostly circularly arranged smooth muscle cells and sheets of elastin that controls vasoconstriction and vasodilation of the vessel – Tunica externa (adventitia): contains woven collagen fibers that protects, reinforces, and anchors the vessel to surrounding structures GENERALIZED STRUCTURE of ARTERIES, VEINS, and CAPILLARIES ARTERIAL SYSTEM Elastic (Conducting) Arteries • Elastic, or conducting, arteries contain large amounts of elastin, which enables these vessels to withstand and smooth out pressure fluctuations due to heart action – Thick-walled arteries near the heart – The abundant elastin enables these arteries to withstand and smooth out large pressure fluctuations by expanding when the heart forces blood into them, and then recoiling to propel blood onward into the circulation when the heart relaxes – Arteriosclerosis: blood vessels become hard and less elastic • Increases blood pressure • Without the pressuresmoothing effect of the elastic arteries, the walls of arteries throughout the body experience higher pressure – Battered by high pressure, the arteries eventually weaken and may balloon out or even burst ARTERIAL SYSTEM Muscular (Distributing) Arteries • Distally the elastic arteries give way to the muscular, or distributing, arteries • Muscular, or distributing, arteries deliver blood to specific body organs, and have the greatest proportion of tunica media of all vessels, making them more active vasoconstriction • Their tunica media contains relatively more smooth muscle and less elastic tissue than do elastic arteries – More active in vasoconstriction and less distensible ARTERIAL SYSTEM Arterioles • Arterioles are the smallest arteries and regulate blood flow into capillary beds through vasoconstriction and vasodilation • Lead into capillary beds: – When constricted, the local capillaries (tissues) served are largely by-passed – When dilated, blood flow into the local capillaries (tissues) increases dramatically Capillaries • Capillaries are the smallest vessels (microscopic) and allow for exchange of substances between the blood and interstitial fluid – Thin walls consist of just a thin tunica • In some cases, one endothelial cell forms the entire circumference of the capillary wall • Along the outer surface of the capillaries are spider-shaped pericytes, smooth muscle-like cells that stabilize the capillary wall • Diameter just large enough for red blood cells to slip through in single file • Most tissues have a rich capillary supply – Exceptions: • Tendons and ligaments are poorly vascularized • Cartilage and epithelia lack capillaries – Receive nutrients from blood vessels in nearby connective tissues • Cornea and lens of eye: avascular – Receive nutrients from aqueous humor TYPES of CAPILLARIES (a)Continuous Capillary • • • • Most common and allow passage of fluids and small solutes Abundant in the skin and muscles They are continuous in the sense that their endothelial cells provide an uninterrupted lining, adjacent cells being joined laterally by tight junctions – These junctions are usually incomplete and leave gaps of unjoined membrane called intercellular clefts, which are just large enough to allow limited passage of fluids and small solutes (exception in the brain) Endothelial cell cytoplasm contains numerous pinocytotic vesicles believed to ferry fluids across the capillary wall (a)Continuous Capillary • Brain capillaries are unique: – Tight junctions are complete and extend around the entire perimeter of the endothelial cells, constituting the structural basis of the blood-brain barrier CAPILLARY (b)Fenestrated Capillary • Endothelial cells are riddled with oval pores (fenestrations) • More permeable to fluids and solutes than continuous capillaries • Found wherever active capillary absorption or filtrate formation occurs: – Small intestine – Endocrine glands – kidneys CAPILLARY (c)Sinusoidal Capillary • • • • • • Highly modified, leaky capillaries that allow large molecules to pass between the blood and surrounding tissues Found only in the liver, bone marrow, lymphoid tissues, and some endocrine organs Irregularly shaped lumens Usually fenestrated Endothelial lining has fewer tight junctions Larger intercellular clefts than ordinary capillaries – Allow large molecules and even blood cells to pass between the blood and surrounding tissues (c)Sinusoidal Capillary • In the liver, the endothelium of the sinusoids is discontinuous and large macrophages called Kupffer cells, which remove and destroy any contained bacteria, form part of the lining • In the spleen, phagocytes located just outside the sinusoids stick cytoplasmic extensions through the intercellular clefts into the sinusoidal lumen to get at their “prey” CAPILLARY Capillary Beds • • Interwoven microcirculatory networks Consists of two types of vessels: – 1. A vascular shunt (metarteriolethoroughfare channel) • – • Short vessel that directly connects the arteriole and venule at opposite ends of the bed 2. True capillaries, which function as the exchange vessels The terminal arteriole feeding the bed leads into a metarteriole (a vessel structurally intermediate between an arteriole and a capillary), which is continuous with the thoroughfare channel (intermediate between a capillary and a venule) – The thoroughfare channel, in turn, joins the postcapillary venule that drains the bed Capillary Beds True Capillaries • Number from 10 to 100 per capillary bed, depending on the organ or tissues served • Usually branch off the metarteriole (proximal end of the shunt) and return to the thoroughfare channel (distal end) Capillary Beds True Capillary • A cuff of smooth muscle, called a precapillary sphincter, surrounds the root of each true capillary at the metarteriole and acts as a valve to regulate blood flow into the capillary – Open during digestion in gastrointestinal organs when you are relaxing – Closed in the gastrointestinal organs during exercising (open in the muscle) • Cramps when vigorous exercise after a meal GENERALIZED STRUCTURE of ARTERIES, VEINS, and CAPILLARIES CAPILLARY BED Venous System • Blood is carried from the capillary beds toward the heart by veins Venules • • • Venules are formed where capillaries converge The smallest venules, the postcapillary venules, consist entirely of endothelium around which a few pericytes congregate They are extremely porous (more like capillaries than veins in this way), and allow fluid and white blood cells to move easily between the blood and tissues – A sign of inflammation is adhesion of WBC to the postcapillary venule endothelium, followed by their migration through the wall into the inflamed tissue Venules/Veins • Venules join to form veins, which are relatively thin-walled vessels with large lumens containing about 65% of the total blood volume Veins • Walls are thinner and their lumens larger than those of corresponding arteries • Large lumens and thin walls • Three distinct layers: – Tunica externa • Thickest layer • Collagen and elastic networks – Tunica media • Relatively little smooth muscle and elastin • thin – Tunica interna • Forms venous valves Veins • Blood pressure low • Venous valves: – Resemble semilunar valves of heart – Abundant in veins of the limbs, where the upward flow of blood is opposed by gravity – Absent in the ventral body cavity GENERALIZED STRUCTURE of ARTERIES, VEINS, and CAPILLARIES HOMEOSTATIC IMBALANCE • Varicose veins: – Veins that have become dilated because of incompetent valves • Blood pools in the lower limbs, and with time, the valves weaken and the venous walls stretch and become floppy • Elevated venous pressure: – Straining to deliver a baby or have a bowel movement » Hemorrhoids VASCULAR ANASTOMOSES • Most organs receive blood from more than one arterial branch, and arteries supplying the same territory often merge, forming arterial anastomoses – Provide alternate pathways (collateral channels), for blood to reach a given body region • If one branch is cut or blocked by a clot, the collateral channel can supply the area with adequate blood supply • Venous anastomoses: – Interconnect much more freely than arteries • Example: skin on the dorsum of your hand – Occlusion of a vein rarely blocks blood flow or leads to tissue death PHYSIOLOGY OF CIRCULATION Circulatory Dynamics • To sustain life, blood must be kept circulating (blood flow, blood pressure, and resistance) – – – – – – – Heart: pump Aorta: pressure reservoir Arteries: conduits Arterioles: resistance vessels Capillaries: exchange sites Venules: exchange sites and conduits Veins: conduits and blood reservoirs BLOOD FLOW • Blood flow is the volume of blood flowing through a vessel, organ, or the entire circulation in a given period, and may be expressed as ml/min • Under resting conditions it is relatively constant • At any given moment, it may vary BLOOD PRESSURE • Blood pressure (BP) is the force per unit area exerted by the blood against a vessel wall, and is expressed in millimeters of mercury (mm Hg) – For example: a blood pressure of 120 mm Hg is equal to the pressure exerted by a column of mercury 120 mm high • Usually measure systemic arterial blood • It is the pressure gradient—the difference in blood pressure within the vascular system—that provides the driving force that keeps blood moving—always from an area of higher pressure to an area of lower pressure—through the body RESISTANCE • Opposition to flow • Measure of the amount of friction blood encounters as it passes through the vessels • Measure of the friction between blood and the vessel wall, and arises from three sources: blood viscosity, blood vessel length, and blood vessel diameter • Because most friction is encountered in the peripheral (systemic) circulation, well away from the heart, we generally use the term peripheral resistance RESISTANCE BLOOD VISCOSITY • Internal resistance to flow that exists in all fluids and is related to the thickness or “stickiness” of a fluid • The greater the viscosity, the less easily molecules slide pass one another and the more difficult it is to get and keep the fluid moving • More viscous than water (formed elements and plasma proteins): hence flows more slowly • Polycythemia: excessive RBC count – Increase viscosity • Anemia: low RBC count – Resistance declines RESISTANCE VESSEL LENGTH • Longer the vessel—the greater the resistance – An extra pound or two of fat requires that miles of small vessels be added to service the extra tissue • Increases the peripheral resistance RESISTANCE VESSEL DIAMETER • Because blood viscosity and vessel length are normally unchanging, the influence of these factors can be considered constant in healthy people – Changes in blood vessel diameter are frequent and significantly alter peripheral resistance • • • Fluid close to the wall of a vessel is slowed by friction as it passes along the wall, whereas fluid in the center of the vessel flows more freely and faster The smaller the vessel, the greater the friction, because relatively more of the fluid contacts the vessel wall where its movement is impeded Resistance varies inversely with the fourth power of the vessel radius (1/2 the diameter) – Example: • If the radius of a vessel is doubled, the resistance drops to 1/16 of its original value – R4 = 2x2x2x2=16 and 1/r4 = 1/16 • Thus, the large arteries close to the heart, which do not change dramatically in diameter, contribute little to peripheral resistance, and the small-diameter arterioles, which can enlarge or constrict in response to neural and chemical controls, are the major determinants of peripheral resistance RESISTANCE VESSEL DIAMETER • When blood encounters either an abrupt change in the vessel size or rough or protruding areas of the vessel wall (fatty plaques of atherosclerosis), the smooth laminar blood flow is replaced by turbulent flow, that is, irregular fluid motion where blood from the different laminae mixes – Turbulence dramatically increases resistance Relationship Between Flow, Pressure, and Resistance – If blood pressure increases, blood flow increases; if peripheral resistance increases, blood flow decreases • Blood flow (F) is directly proportional to the difference in blood pressure (∆P) between two points in the circulation, that is, the blood pressure, or hydrostatic pressure, gradient – When ∆P increases, blood flow speeds up – When ∆P decreases, blood flow declines • Blood flow is inversely proportional to the peripheral resistance (R) in the systemic circulation – If R increases, blood flow decreases – If R decreases, blood flow increases • F = ∆P/R – Peripheral resistance is the most important factor influencing local blood flow, because vasoconstriction or vasodilation can dramatically alter local blood flow, while systemic blood pressure remains unchanged SYSTEMIC BLOOD PRESSURE • • • • Blood flows through the blood vessels along a pressure gradient, always moving from higher-to lower-pressure areas The pumping action of the heart generates blood flow Pressure results when blood flow is opposed by resistance Systemic blood pressure is highest in the aorta, and declines throughout the pathway until it reaches 0 mm Hg in the right atrium – The steepest drop in blood pressure occurs in the arterioles, which offer the greatest resistance to blood flow ARTERIAL BLOOD PRESSURE • Arterial blood pressure reflects how much the arteries close to the heart can be stretched (compliance, or distensibility), and the volume forced into them at a given time – When the left ventricle contracts, blood is forced into the aorta, producing a peak in pressure called systolic pressure (120 mm Hg) • – Blood moves forward into the arterial bed because the pressure in the aorta is higher than the pressure in the more distal vessels Diastolic pressure occurs when blood is prevented from flowing back into the ventricles by the closed semilunar valve, and the aorta recoils (70-80 mm Hg) • Elastic arteries are pressure reservoirs that operate as auxiliary pumps to keep blood circulating throughout the period of diastole, when the heart is relaxing ARTERIAL BLOOD PRESSURE – The difference between diastolic and systolic pressure is called the pulse pressure • It is felt as a throbbing pulsation in an artery (a pulse) during systole, as the elastic arteries are expanded by the blood being forced into them by ventricular contraction – Increased stroke volume and faster blood injection from the heart cause temporary increases in the pulse pressure – Pulse pressure increased by arteriosclerosis (thickening of the walls of the arterioles, with loss of elasticity and contractility) because the elastic arteries become less stretchy » Atherosclerosis: the most common form of arteriosclerosis, marked by cholesterol-lipid-calcium deposits in the walls of arteries ARTHEROSCLEROSIS PLAQUE ARTERIAL BLOOD PRESSURE • • Because aortic pressure fluctuates up and down with each heartbeat, the important pressure to consider is the mean arterial pressure The mean arterial pressure (MAP) represents the pressure that propels blood to the tissues – Because diastole usually lasts longer than systole the MAP is roughly equal to the diastolic pressure plus 1/3 of the pulse pressure (systolic pressure-diastolic pressure) • MAP = diastolic pressure + pulse pressure/3 • Thus a person with a systolic blood pressure of 120 mm Hg and a diastolic pressure of 80 mm Hg: – MAP = 80 mm Hg + 40 mm Hg/3 = 93 mm hg » ***remember you are adding factions • MAP and pulse pressure both decline with increasing distance from the heart – The MAOP loses ground to the never-ending friction between the blood and the vessel walls, and the pulse pressure is gradually phased out in the less elastic muscular arteries (elastic rebound of the vessels ceases to occur) – At the end of the arterial tree, blood flow is steady and the pulse pressure has disappeared BLOOD PRESSURE CAPILLARY BLOOD PRESSURE • By the time blood reaches the capillaries, blood pressure has dropped to approximately 40 mm Hg and by the end of the capillary bed is only 20 mm Hg or less – Which protects the capillaries from rupture, but is still adequate to ensure exchange between blood and tissues BLOOD PRESSURE VENOUS BLOOD PRESSURE • Unlike arterial pressure, which pulsates with each contraction of the left ventricle, venous blood pressure is steady and changes very little during the cardiac cycle • The pressure gradient in the veins, from venules to the termini of the venae cavae, is only about 20 mm Hg (that from the aorta to the ends of the arterioles is about 60 mm Hg) – If a vein is cut, the blood flows evenly from the wound; a lacerated artery produces rapid spurts of blood • Very low pressure reflects the cumulative effects of peripheral resistance, which dissipates most of the energy of blood pressure (as heat) during each circuit VENOUS BLOOD PRESSURE • • Too low to promote adequate venous return Two functional adaptations are important to venous return – 1. Respiratory “pump”: • Pressure changes occurring in the ventral body cavity during breathing create the respiratory pump that moves blood up toward the heart – – Inhale, abdominal pressure increases, squeezing the local veins and forcing blood toward the heart » At the same time, the pressure in the chest decreases, allowing thoracic veins to expand and speeding blood entry into the right atrium 2. Muscular “pump”: Skeletal muscle activity is the most important pumping mechanism • As the skeletal muscles surrounding the deep veins contract and relax, they “milk” blood toward the heart, and once blood passes each successive valve, it cannot flow back OPERATION OF MUSCLE PUMP for VENOUS BLOOD FLOW MAINTAINING BLOOD PRESSURE • Maintaining a steady flow of blood from the heart to the toes is vital for proper organ function: – Making sure a person jumping out of bed in the morning does not keel over from inadequate blood flow to the brain requires the finely tuned cooperation of the heart, blood vessels, and kidneys—all supervised by the brain MAINTAINING BLOOD PRESSURE • Blood pressure varies directly with changes in blood volume and cardiac output, which are determined primarily by venous return and neural and hormonal controls: – BP = Force/area – F = ∆P/R – CO = ∆P/R – ∆P = CO x R – Blood pressure varies directly with CO, R, and blood volume • In theory, a change (increase or decrease) in any of these variables causes a corresponding change in blood pressure • HOWEVER, what really happens in the body is that changes in one variable that threaten blood pressure homeostasis are quickly compensated for by changes in the other variable Major Factors Enhancing Cardiac Output Summary of Factors causing an increase in Mean Systemic Arterial Blood Pressure Neural Controls of Blood Pressure • Short-term neural controls of peripheral resistance (blood pressure), mediated by the nervous system and blood borne chemicals, alter blood distribution to meet specific tissue demands, and maintain adequate MAP by altering blood vessel diameter • Neural controls of peripheral resistance are directed at two main goals: – 1. Altering blood distribution to respond to specific demands of various organs • Example: during exercise blood is shunted temporarily from the digestive organs to the skeletal muscles – 2. Maintaining adequate MAP by altering blood vessel diameter Neural Controls of Blood Pressure Role of Vasomotor Center • The vasomotor center is a cluster of sympathetic neurons in the medulla that controls changes in the diameter of blood vessels – Integrates blood pressure control by altering cardiac output and blood vessel diameter – Nerves innervate smooth muscles of blood vessels, mainly arterioles which are almost always in a state of moderate constriction (vasomotor tone) • Most vasomotor fibers release norepinephrine, which is a potent vasoconstrictor • Rise in blood pressure – Decreased sympathetic activity allows the vascular muscle to relax causing blood pressure to decline – In skeletal muscle, vasomotor fibers release acetylcholine causing vasodilation • Modified by inputs from: – 1. Baroreceptors (pressure-sensitive mechanoreceptors that respond to changes in arterial pressure and stretch) – 2. Chemoreceptors (receptors that respond to changes in blood levels of oxygen, carbon dioxide, and H+) – 3. Higher brain centers – 4. Hormones – 5. Bloodborne chemicals Neural Controls of Blood Pressure Baroreceptor-Initiated Reflexes • • When arterial blood pressure rises, it stretches baroreceptors, neural receptors located in the: – Carotid sinuses (carotid arteries: blood supply to the brain) – Aortic arch (brain, neck, upper limbs) – Walls of nearly every large artery of the neck and thorax When stretched baroreceptors send impulses to the vasomotor center, inhibiting its activity and promoting vasodilation of arterioles and veins – Decline in blood pressure Baroreceptor Reflexes that help to maintain Blood Pressure Neural Controls of Blood Pressure Baroreceptor-Initiated Reflexes • While dilation of the arterioles substantially reduces peripheral resistance, venodilation shifts blood to the venous reservoirs, causing a decline in both venous return and cardiac output • Stimulates parasympathetic activity and inhibits the cardioacceleratory center, reducing heart rate and contractile force – A decline in MAP initiates reflex vasoconstriction and increases cardiac output, causing blood pressure to rise – Thus, peripheral resistance and cardiac output are regulated in tandem so that changes in blood pressure are minimized Neural Controls of Blood Pressure Baroreceptor-Initiated Reflexes • The function of rapidly responding baroreceptors is to protect the circulation against short-term (acute) changes in blood pressure, such as those occurring when you change your posture – Example: blood pressure falls (head) when one stands up after reclining Neural Controls of Blood Pressure Chemoreceptor-Initiated Reflexes • When the oxygen content or pH of the blood drops sharply or the carbon dioxide levels rise, chemoreceptors in the aortic arch and large arteries of the neck transmit impulses to the cardioacceleratory center, which then increases cardiac output, and to the vasomotor center, which causes reflex vasoconstriction – The rise in blood pressure that follows speeds the return of blood to the heart and lungs • The most prominent chemoreceptors are the carotid and aortic bodies located close by the baroreceptors in the carotid sinus and aortic arch • More important in regulating respiratory rate than blood pressure Neural Controls of Blood Pressure Influence of Higher Brain Centers • The cerebral cortex and hypothalamus can modify arterial pressure by signaling the medullary centers – Example: fight-or-flight response Controls of Blood Pressure Short-Term Mechanisms Chemical Controls • Chemical controls influence blood pressure by acting on vascular smooth muscle or the vasomotor center – Adrenal medulla hormones: • Norepinephrine and epinephrine promote an increase in cardiac output and generalized vasoconstriction (except in skeletal and cardiac muscle, where it generally causes vasodilation) – Both hormones enhance the sympathetic fight-or-flight response – Nicotine mimics these hormones causing intense vasoconstriction – Atrial natriuretic peptide (ANP): • Hormone produced by the atria of the heart • Causes blood volume and blood pressure to decline • Acts as a vasodilator and an antagonist to aldosterone (hormone produced by the adrenal cortex which stimulates the kidneys to increase sodium reabsorption) – Prods the kidney to excrete more sodium and water from the body causing blood volume to drop • Causes a generalized vasodilation and reduces cerebrospinal fluid formation in the brain Controls of Blood Pressure Short-Term Mechanisms Chemical Controls • Antidiuretic hormone (ADH): – Hormone produced by the hypothalamus and stimulates vasoconstriction and water conservation by the kidneys, resulting in an increase in blood volume • Angiotensin II: – When renal nutrient (blood) supply is inadequate, the kidneys release renin, an enzyme – Release of renin causes the generation of angiotensin II which: • Acts as a vasoconstrictor promoting a rapid rise in systemic blood pressure • Promotes the release of aldosterone and antidiuretic hormone which act in long-term regulation of blood pressure by enhancing blood volume Controls of Blood Pressure Short-Term Mechanisms Chemical Controls • Endothelium (lining of blood vessels) is the source of several chemicals that: – Promote vasoconstriction, and are released in response to low blood flow • Example: – Endothelin: most potent vasoconstrictor known by enhancing calcium entry into vascular smooth muscle – Nitric oxide (NO): • Produced in response to high blood flow or other signaling molecules, and promotes systemic and localized vasodilation • Inflammatory chemicals, such as histamine, prostacyclin, and kinins, are potent vasodilators – They also promote fluid loss from the bloodstream by increasing capillary permeability • Alcohol inhibits antidiuretic hormone (ADH) release by the Hypothalamus – Depresses the vasomotor center – Results in vasodilation especially in the skin (flushed appearance) – Drop in blood pressure MAINTAINING BLOOD PRESSURE Long-Term Mechanisms • The long-term controls of blood pressure, mediated by renal mechanisms, counteract fluctuations in blood pressure not by altering peripheral resistance (as in short-term controls) but rather by altering blood volume • Renal mechanisms usually maintain blood volume close to 5L (varies with age, body size, and sex) – Increased in blood volume is followed by an increase in blood pressure • Example: excessive salt intake • The dynamic system will eventually stimulate the kidneys to eliminate water, which reduces blood volume and consequently blood pressure – Decrease in blood volume is followed by a decrease in blood pressure • Example: dehydration during exercise • The dynamic system responds to falling blood volume triggering renal mechanisms that increase blood volume and blood pressure – Blood pressure can be stabilized or maintained within normal limits only when blood volume is stable MAINTAINING BLOOD PRESSURE Long-Term Mechanisms • The kidneys act both directly and indirectly to regulate pressure and provide the major long-term mechanism of blood pressure control MAINTAINING BLOOD PRESSURE Long-Term Mechanisms – The direct renal mechanism counteracts an increase in blood pressure by altering blood volume, which increases the rate of kidney filtration (as blood volume goes, so goes the arterial blood pressure) • When either blood volume or blood pressure rises, kidney filtration is speeded up (increase urination) – Blood volume and blood pressure falls • When blood pressure or blood volume is low, water is conserved and returned to the bloodstream, and blood pressure rises Slowly Acting Renal Hormonal Mechanisms for Blood Pressure Control Summary of Factors causing an increase in Mean Systemic Arterial Blood Pressure MAINTAINING BLOOD PRESSURE Long-Term Mechanisms • The indirect renal mechanism is the renin-angiotensin mechanism – – When arterial blood pressure declines, the kidneys release the enzyme renin into the blood Renin triggers a series of reactions that produce angiotensin II (potent vasoconstrictor) • • – Increases systemic blood pressure Increases the rate of blood delivery to the kidneys and the rate of renal perfusion (passing of fluid through tissues) Also stimulates the adrenal cortex to secrete aldosterone, a hormone that enhances renal reabsorption of sodium, and prods the posterior pituitary to release ADH (antidiuretic hormone), which promotes more water reabsorption: • • Sodium moves into the bloodstream, water follows Both blood volume and blood pressure rise Slowly Acting Renal Hormonal Mechanisms for Blood Pressure Control Monitoring Circulatory Efficiency • Efficiency can be assessed by taking pulse and blood pressure measurements • Accomplished by measuring pulse and blood pressure; these values together with respiratory rate and body temperature are called vital signs – Vital signs: • • • • Pulse Blood pressure Respiratory rate Body temperature Monitoring Circulatory Efficiency Pulse • • The alternating expansion and recoil of elastic arteries during each cardiac cycle create a pressure wave—a pulse—that is transmitted through the arterial tree You can feel a pulse in any artery that lies close to the body surface by compressing the artery against firm tissue, and this provides an easy way to count heart rate – Radial pulse: radial artery in wrist • Routinely used to take a pulse measurement since it so accessible (DO NOT use thumb) – There are other clinically important arterial pulse points: • These same points are compressed to stop blood flow into distal tissues during hemorrhage • Called pressure points Body sites where Pulse is most easily palpated Monitoring Circulatory Efficiency Blood Pressure • Systemic blood pressure is measured indirectly in the brachial artery of the arm by using the ascultatory method – Which relies on the use of a blood pressure cuff (sphygmomanometer) to alternately stop and reopen blood flow into the brachial artery of the arm • Inflated to a point that exceeds systolic pressure – Blood flow is stopped and the brachial pulse cannot be heard • Cuff pressure is gradually reduced • Examiner listens (auscultates) with a stethoscope for sounds in the brachial artery – First soft tapping sounds heard (the first point at which a small amount of blood is spurting through the constricted artery) is systolic pressure • Cuff pressure is reduced further – Sounds become louder and more distinct (sounds of Korotkoff) • When the artery is no longer constricted and blood flows freely, the sounds can no longer be heard – Pressure at which the sounds disappear is the diastolic pressure Monitoring Circulatory Efficiency Blood Pressure • Normal adult at rest: – Systolic pressure: between 110 and 140 mm Hg – Diastolic pressure: between 75 and 80 mm Hg • Cycles over a 24-hour period: – Waning and waxing according to the amount of retinoic acid (vitamin A derivative) in blood – Blood vessels like certain brain cells contain “clock” proteins that regulates circadian rhythms in response to retinoic acid (used in treatment of cystic acne) • Varies with age, sex, weight, race, mood, physical activity, posture, and socioeconomic status • What is normal for you may not be normal for someone else Alterations in Blood Pressure • Hypotension: – Low blood pressure – Systolic pressure below 100 mm Hg – In many cases simply reflects individual variations and is no cause for concern • Low blood pressure is often associated with long life and an old age free of illness HOMEOSTATIC IMBALANCE HYPOTENSION • Orthostatic hypotension: – Elderly – Temporary low blood pressure and dizziness when they rise suddenly from a reclining or sitting position • Aging sympathetic nervous system does not respond as quickly • Blood pools briefly in the lower limbs, reducing blood pressure and delivery to the brain • Making postural changes slowly to give the nervous system time to adjust usually prevents this problem • Chronic hypotension: – – – – – – • Poor nutrition Often anemic and inadequate levels of blood proteins Blood viscosity low Warning of Addison’s disease (inadequate adrenal cortex function) Hypothyroidism Severe tissue wasting Acute hypotension: – One of the most important signs of circulatory shock • Threat to patients undergoing surgery and those in intensive care units Alterations in Blood Pressure • Hypertension: – High blood pressure – Transient: short-lived • Elevations in systolic pressure occur as normal adaptations during fever, physical exertion, and emotional upset – Persistent: long-lived • Common in obese people because the total length of their blood vessels is relatively greater than in thinner individuals HOMEOSTATIC IMBALANCE HYPERTENSION • Chronic: long duration: – Common and dangerous disease that warns of increased peripheral resistance – Estimated 30% of people over 50 years – Silent killer • Usually asymptomatic for the first 10 to 20 years • Slowly but surely strains the heart and damages the arteries • Major cause of heart failure, vascular disease, renal failure, and stroke – Heart is forced to pump against greater resistance, it must work harder, and in time the myocardium enlarges • Finally strained beyond its capacity to respond, the heart weakens and its walls become flabby – Ravages blood vessels • Small tears in the endothelium • Accelerates the progress of atherosclerosis – Vessels become increasing blocked – Elevated arterial pressure of 140/90 or higher • Higher the pressure, the greater the risk for serious cardiovascular problems • Elevated diastolic pressures are more significant medically, because they always indicate progressive occlusion (closure) and/or hardening of the arterial tree HOMEOSTATIC IMBALANCE Primary (Essential) Hypertension • No underlying cause has been identified • Following factors are believed to be involved – Diet: • High sodium, saturated fat, cholesterol intake • Deficiencies in certain metal ions: K+, Ca2+, Mg2+ – Obesity – Age: • Clinical signs of the disease usually appear after age 40 – Race: • Varies in different populations – Higher in Africans – Heredity – Stress – Smoking: • Nicotine enhances the sympathetic nervous system’s vasoconstrictor effects HOMEOSTATIC IMBALANCE Primary (Essential) Hypertension • Cannot be cured – Must adjust life style – Drugs: • Antihypertensive – – – – Diuretics Beta-blockers Calcium channel blockers Angiotensin-converting enzyme (ACE) inhibitors » Suppresses the renin-angiotensin mechanism HOMEOSTATIC IMBALANCE Secondary Hypertension • • • • • Accounts for 10% of cases Due to identifiable disorders Excessive renin secretion by the kidneys Arteriosclerosis Endocrine disorders – Hyperthyroidism – Cushing’s disease • Excessive production of adrenocorticotropic (ACTH) hormone from the anterior pituitary • Influences the activity of the adrenal cortex – High sugar – Loss in muscle and bone protein – Edema: water and salt retention • Treatment is directed toward the cause BLOOD FLOW THROUGH BODY TISSUE: TISSUE PERFUSION • • • Tissue perfusion is involved in delivery: – Of oxygen and nutrients to tissue cells – Removal of wastes from tissue cells – Gas exchange in the lungs – Absorption of nutrients from the digestive tracts – Urine formation in the kidneys Rate of blood flow to each tissue and organ is almost exactly the right amount to provide for proper function—no more, no less During exercise, nearly all of the increased cardiac output flushes into the skeletal muscles and blood flow to the kidneys and digestive organs is reduced Distribution of blood flow to selected body organs at rest and during strenuous exercise Velocity of Blood Flow • Velocity or speed of blood flow changes as it passes through the systemic circulation; it is fastest in the aorta, and declines in velocity as vessel diameter decreases – • Fastest in the aorta and other large arteries, slowest in the capillaries, and then picks up speed again in the veins Inversely related to the crosssectional area of the blood vessels to be filled – Blood flows fastest where the total cross-sectional area is least • • As the arterial system branches, the total cross-sectional area of the vascular bed increases, and the velocity of blood flow declines proportionately Slow capillary flow is beneficial because it allows adequate time for exchange between the blood and tissue cells Relationship between blood flow velocity and total cross-sectional area in various blood vessels of the systemic circulation BLOOD FLOW THROUGH BODY TISSUE: TISSUE PERFUSION Autoregulation: Local Regulation of Blood Flow • Autoregulation is the automatic adjustment of blood flow to each tissue in proportion to its needs, and is controlled intrinsically by modifying the diameter of local arterioles feeding the capillaries – Metabolic controls of autoregulation are most strongly stimulated by a shortage of oxygen at the tissues • Vasodilation of the arterioles serving the capillary beds of the “needy” tissue • Temporary increase of blood flow to the area – Myogenic control involves the localized response of vascular smooth muscle to passive stretch (increased intravascular pressure) with increase tone (resistance of muscle to passive stretch) • Resist the stretch and causes vasoconstriction – Long-term autoregulation develops over weeks or months, and involves an increase in the size of existing blood vessels and an increase in the number of vessels in a specific area, a process called angiogenesis • Example: – Common in the heart when a coronary vessel is partially occluded – Occurs throughout the body in people who live in high-altitude areas, where the air contains less oxygen BLOOD FLOW in SPECIFIC AREAS • Blood Flow in Special Areas: – Blood flow to skeletal muscles varies with level of activity and fiber type • When muscles become active, blood flow increases (hyperemia) in direct proportion to their greater metabolic activity (active or exercise hyperemia) • Capillary density and blood flow is greater in red (slow oxidative) fibers than in white (fast glycolytic) fibers – Muscular autoregulation occurs almost entirely in response to decreased oxygen concentrations BLOOD FLOW in SPECIFIC AREAS • Brain: – Cerebral blood flow is tightly regulated to meet neuronal needs, since neurons cannot tolerate periods of ischemia – Most metabolically active organ in the body, it is the least able to store essential nutrients – Sensitive to declining pH, and increased blood carbon dioxide levels causing marked vasodilation • Skin: – – – – Blood supplies nutrients to the cells Aids in body temperature regulation Provides a blood reservoir Local autoregulatory events control oxygen and nutrient delivery to the cells – Neural mechanisms control the body temperature regulation functions BLOOD FLOW in SPECIFIC AREAS – Lungs: • Autoregulatory controls of blood flow to the lungs are the opposite of what happens in most tissues – Low pulmonary oxygen (air sacs) causes vasoconstriction, while higher oxygen (air sacs) causes vasodilation – Heart: • Movement of blood through the coronary circulation (vessels of the heart) is influenced by aortic pressure and the pumping of the ventricles – When the ventricles contract and compress the coronary vessels, blood flows through the myocardium stops – As the heart relaxes, the high aortic pressure forces blood through the coronary circulation – Abnormally rapid heartbeat seriously reduces the ability of the myocardium to receive adequate oxygen and nutrients during diastole • Any event that decreases the oxygen content of the blood causes release of a vasodilator that adjust the oxygen supply – Increasing the blood flow is the only way to make sufficient additional oxygen available to a more vigorously working heart Blood Flow Through Capillaries and Capillary Dynamics • Blood flow through capillary networks is slow and intermittent – This phenomenon, called vasomotion, the slow, intermittent flow of blood through the capillaries, reflects the action of the precapillary sphincters (opening and closing) in response to local autoregulatory controls Capillary Exchange of Respiratory Gases and Nutrients • Capillary exchange of nutrients, gases, and metabolic wastes occurs between the blood and interstitial space through diffusion – Movement always occurs along a concentration gradient—one substance moving from an area of its higher concentration to an area of its lower concentration Capillary Exchange of Respiratory Gases and Nutrients • • • • • Direct diffusion: oxygen, carbon dioxide, nutrients, metabolic waste Intercellular clefts and sometimes fenestrations: small water-soluble solutes, such as amino acids and sugars Direct diffusion through the lipid bilayer of the endothelial cell plasma membrane: lipidsoluble molecules, such as respiratory gases Caveoli: translocate some larger molecules, such as small proteins Pinocytotic vesicles: imbibe solute-containing fluid Capillary Transport Mechanisms Blood Flow Through Capillaries and Capillary Dynamics • Fluid Movements: – While nutrient and gas exchanges are occurring across the capillary walls by diffusion, bulk fluid flows are also going on • Fluid is forced out of the capillaries through the clefts at the arterial end of the bed, but most of it returns to the bloodstream at the venous end – Direction and amount of fluid that flows across the capillary walls reflect the balance between two dynamic and opposing forces— hydrostatic and colloid osmotic pressures Blood Flow Through Capillaries and Capillary Dynamics Hydrostatic Pressures • Hydrostatic pressure (HP) is the force exerted by a fluid against a membrane – Capillaries: hydrostatic pressure is the same as capillary blood pressure (pressure exerted by blood on the capillary wall) • Capillary hydrostatic pressure (HPc) tends to force fluids through the capillary walls – Higher at the arterial (35 mm Hg) – Lower at the venous end (17 mm Hg) • In theory, blood pressure—which forces fluid out of the capillaries—is opposed by the interstitial fluid hydrostatic pressure (HPif) acting outside the capillaries and pushing fluid in Blood Flow Through Capillaries and Capillary Dynamics Hydrostatic Pressures • Net hydrostatic pressure acting on the capillaries at any point is the difference between HPc and HPif – There is usually very little fluid in the interstitial space, because any fluid there is constantly withdrawn by the lymphatic vessels – HPif may vary from slightly negative to slightly positive, traditionally it is assumed to be zero • The net effective hydrostatic pressures at the arterial and venous ends of the capillary bed are essentially equal to HPc (in other words, to blood pressure) at those locations Forces responsible for fluid flows at Capillaries Blood Flow Through Capillaries and Capillary Dynamics Colloid Osmotic Pressures • Colloid osmotic pressure (OP): – Force opposing hydrostatic pressure • Force created by the presence in a fluid of large nondiffusible molecules, such as plasma proteins, that are prevented from moving through the capillary membrane – Such molecules draw water toward themselves – These molecules encourage osmosis whenever the water concentration in their vicinity is lower than it is on the opposite side of the capillary membrane Blood Flow Through Capillaries and Capillary Dynamics Colloid Osmotic Pressures • The abundant plasma proteins in capillary blood (primarily albumin molecules) develop a capillary colloid osmotic pressure (OPc), also called oncotic pressure (26 mm Hg) – Because interstitial fluid contains few proteins, its colloid osmotic pressure (OPif) is lower—from 0.1 to 5 mm Hg • A value of 1 mm Hg is used • • Unlike HP, OP does not vary from one end of the capillary bed to the other Net osmotic pressure that pulls fluid back into the capillary blood is: – OPc – OPif = 26 mm Hg – 1 mm Hg = 25 mm Hg Forces responsible for fluid flows at Capillaries Hydrostatic-Osmotic Pressure Interactions • To determine whether there is a net gain or net loss of fluid from the blood, you have to calculate the net filtration pressure (NFP) – Fluids will leave the capillaries if net HP exceeds net OP, but fluids will enter the capillaries if net OP exceeds net HP Hydrostatic-Osmotic Pressure Interactions • Hydrostatic forces dominate at the arterial end: – NFP = (HPc – HPif) – (OPc – OPif) – – (35 – 0) - (26 1) (35 – 25) = 10 mm Hg – A pressure of 10 mm Hg (net excess of HP) is forcing fluid out of the capillary Hydrostatic-Osmotic Pressure Interactions • Osmotic forces dominates at the venous end: – NFP = (HPc – HPif) – (OPc – OPif) – (17 - 0) - (26 - 1) – (17 – 25) = -8 mm Hg – The negative pressure value indicates that the NFP (due to net excess of OP) is driving fluid into the capillary bed Hydrostatic-Osmotic Pressure Interactions • Thus, net fluid flow is out of the circulation at the arterial ends of capillary beds and into the circulation at the venous ends • The fluid that does not return to the blood enters the lymph system which eventually returns this fluid to the blood Forces responsible for fluid flows at Capillaries Circulatory Shock Hypovolemic Shock • Any condition in which blood vessels are inadequately filled and blood cannot circulate normally – • Inadequate blood flow to meet tissue needs Hypovolemic shock results from a large-scale loss of blood: – – – – – Acute hemorrhage Severe vomiting Severe diarrhea Extensive burns Characterized by: • • • • • Drop in blood volume Weak pulse Intense vasoconstriction (shifting of blood from various reservoirs) An elevated heart rate trying to correct problem Drop in blood pressure Events and signs of compensated (nonprogressive) hypovolemic shock Circulatory Shock Vascular Shock • Blood volume is normal and constant • Poor circulation as a result of an abnormal expansion of the vascular bed caused by extreme vasodilation – Huge drop in peripheral resistance followed by rapidly falling blood pressure – Loss of vasomotor muscle tone • Most common causes: – Anaphylactic shock: systemic allergic reaction in which bodywide vasodilation is triggered by the massive release of histamine – Neurogenic shock: failure of autonomic nervous system regulation – Septic shock: septicemia • Severe systemic bacterial infection • Bacterial toxins are notorious vasodilators Circulatory Shock Transient/Cardiogenic • Transient vascular shock is due to prolonged exposure to heat, such as while sunbathing, resulting in vasodilation of cutaneous blood vessels – If you stand up abruptly, blood pools because of gravity into the dilated blood vessels of the lower limbs – Blood pressure falls – Dizziness: signal that the brain is not receiving enough oxygen • Cardiogenic shock: pump failure – Occurs when the heart is too inefficient to sustain normal blood flow, and is usually related to myocardial damage, such as repeated myocardial infarcts CIRCULATORY PATHWAYS: BLOOD VESSELS OF THE BODY • Two distinct pathways travel to and from the heart: • Pulmonary circulation: – Runs from the heart to the lungs and back to the heart • Systemic circulation: – Runs to all parts of the body before returning to the heart CIRCULATORY PATHWAYS PULMONARY CIRCULATION SYSTEMIC CIRCULATION Differences Between Arteries and Veins • There is one terminal systemic artery: – Aorta • But two terminal systemic veins: – Superior and inferior vena cava PULMONARY CIRCULATION SYSTEMIC CIRCULATION Differences Between Arteries and Veins • Arteries run deep and are well protected • Veins are both deep and superficial: – Deep, which run parallel to the arteries • In most cases – Superficial, which run just beneath the skin MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION THE VENAE CAVAE AND THE MAJOR VEINS OF THE SYSTEMIC CIRCULATION Differences Between Arteries and Veins • Arterial pathways tend to be clear, but there are often many interconnections in venous pathways, making them difficult to follow • There are at least two areas where venous drainage does not parallel the arterial supply: – The dural sinuses draining the brain – The hepatic portal system draining from the digestive organs to the liver before entering the main systemic circulation Aorta and Major Arteries of the Systemic Circulation • Four paired arteries supply the head and neck: – Common carotid arteries – Three branches of the subclavian artery • Vertebral arteries • Thyrocervical trunks • Costocervical trunks ARTERIES OF THE HEAD, NECK, AND BRAIN THE AORTA AND MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION Aorta and Major Arteries of the Systemic Circulation ARTERIES OF THE HEAD AND NECK ARTERIES OF THE BRAIN Aorta and Major Arteries of the Systemic Circulation • The upper limbs are supplied entirely by arteries arising from the subclavian arteries MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION THE AORTA AND MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION ARTERIES OF THE UPPER LIMBS AND THORAX ARTERIES OF THE RIGHT UPPER AND THORAX Aorta and Major Arteries of the Systemic Circulation • The arterial supply to the abdomen arises from the aorta THE AORTA AND MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION ARTERIES OF THE ABDOMEN ARTERIES OF THE ABDOMEN ARTERIES OF THE ABDOMEN ARTERIES OF THE ABDOMEN Aorta and Major Arteries of the Systemic Circulation • The internal iliac arteries serve mostly the pelvic region • The external iliacs supply blood to the lower limb and abdominal wall THE AORTA AND MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION ARTERIES OF THE ABDOMEN ARTERIES OF THE ABDOMEN ARTERIES OF THE ABDOMEN ARTERIES OF THE PELVIS AND LOWER LIMBS ARTERIES OF THE PELVIS AND LOWER LIMBS Venae Cavae and the Major Veins of the Systemic Circulation • The venae cavae are the major tributaries of the venous circulation THE VENAE CAVAE AND THE MAJOR VEINS OF THE SYSTEMIC CIRCULATION THE VENAE CAVAE AND THE MAJOR VEINS OF THE SYSTEMIC CIRCULATION Venae Cavae and the Major Veins of the Systemic Circulation • Blood drained from the head and neck is collected by three pairs of veins: – External jugular veins: • Empty into the subclavians – Internal jugular veins: • Drains into the Brachiocephalic veins – Vertebral veins: • Drains into the Brachiocephalic veins VEINS OF THE HEAD AND NECK VEINS OF THE HEAD AND NECK Venae Cavae and the Major Veins of the Systemic Circulation • The deep veins of the upper limbs follow the paths of the common arteries VEINS OF THE UPPER LIMBS AND THORAX THE VENAE CAVAE AND THE MAJOR VEINS OF THE SYSTEMIC CIRCULATION VEINS OF THE UPPER LIMBS AND THORAX Venae Cavae and the Major Veins of the Systemic Circulation • Blood draining from the abdominopelvic viscera and abdominal walls is returned to the heart by the inferior vena cava VEINS OF THE ABDOMEN THE VENAE CAVAE AND THE MAJOR VEINS OF THE SYSTEMIC CIRCULATION VEINS OF THE ABDOMEN VEINS OF THE ABDOMEN Venae Cavae and the Major Veins of the Systemic Circulation • Most deep veins of the lower limb have the same names as the arteries they accompany Deep Veins and Arteries Deep Veins and Arteries VEINS OF THE PELVIS AND LOWER LIMB VEINS OF THE PELVIS AND LOWER LIMB DEVELOPMENTAL ASPECTS OF THE BLOOD VESSELS • • • • • • • The vascular endothelium is formed by mesodermal cells that collect throughout the embryo in blood islands, which give rise to extensions that form rudimentary vascular tubes By the fourth week of development, the rudimentary heart and vessels are circulating blood Fetal vascular modifications include shunts to bypass fetal lungs (the foramen ovale and ductus arteriosus), the ductus venosus that bypasses the liver, and the umbilical arteries and veins, which carry blood to and from the placenta At birth, the fetal shunts and bypasses close and become occluded Congenital vascular problems are rare, but the incidence of vascular diseases increases with age, leading to varicose veins, tingling in fingers and toes, and muscle cramping Atherosclerosis begins in youth, but rarely causes problems until old age Blood pressure changes with age: the arterial pressure of infants is about 90/55, but rises steadily during childhood to an average 120/80, and finally increases to 150/90 on old age