ch19 Blood Vessels.pptx

Part 1 Blood Vessel Structure and Function Blood vessels: delivery system that work with lymphatic system to circulate fluids Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus Capillaries...

Part 1 Blood Vessel Structure and Function Blood vessels: delivery system that work with lymphatic system to circulate fluids Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus Capillaries: direct contact with tissue cells to serve cellular needs Veins: carry blood toward heart; deoxygenated except for pulmonary circulation and umbilical vessels of fetus Venous system Arterial system Large veins Heart (capacitance vessels) Elastic Large arteries lymphatic (conducting vessels arteries) Lymph node Muscular arteries Lymphatic (distributing system arteries) Small veins (capacitance vessels) Arteriovenous anastomosis Lymphatic capillaries Sinusoid Arterioles (resistance vessels) Terminal Postcapillary arteriole venule Thoroughfare Capillaries Precapillary Metarteriole channel (exchange sphincter © 2016 Pearson Education, Inc. vessels)  19.1 Structure of Blood Vessel Wall All vessels consist of a lumen, central blood-containing space, surrounded by a wall Walls of all vessels, except capillaries, have three layers, or tunics: 1. Tunica intima 2. Tunica media 3. Tunica externa Capillaries – Endothelium with sparse basal lamina Tunic a intima Endothelium Artery Vein Subendothelial layer Internal elastic membrane Tunic a media (smooth muscle and elastic fibers) External elastic membrane Tunic a externa (collagen fibers) Vasa vasorum Valve Capillary Lumen network Lumen Basement membrane Capillary Endothelial cells © 2016 Pearson Education, Inc.  19.1 Structure of Blood Vessel Wall Tunic a intima 1. Tunica intima Endothelium A rtery Vein Subendothelial layer Endothelium: simple squamous Internal elastic membrane epithelium that lines lumen of all Tunic a media (smooth muscle and vessels elastic fibers) External elastic membrane – Continuous with endocardium Tunic a externa – Slick surface reduces friction (collagen fibers) Vasa vasorum Subendothelial layer: connective Valve tissue basement membrane – Found only in vessels larger than 1 mm Capillary Lumen network 2. Tunica media Lumen Middle layer composed mostly of Basement membrane Capillary Endothelial cells smooth muscle and sheets of elastin Sympathetic vasomotor nerve fibers innervate this layer, for Vasoconstriction: and Vasodilation 3. Tunica externa (Adventitia) Composed of loose collagen fibers that protect, reinforce, and anchor walls to surrounding structures Infiltrated with nerve fibers, lymphatic vessels, and system of tiny blood vessels (Vasa vasorum) © 2016 Pearson Education, Inc. 1 4 2 5 3 6 Elastic Arteries act as pressure 1) Elastic tissue contains Elastin reservoirs that expand and recoil as 2) In elastic arteries smooth muscle, are inactive in blood is ejected from heart, which vasoconstriction allows for continuous blood flow 3) Smooth muscle in Mascular arteries are active ion downstream even between heartbeats vasoconstriction Arterioles (resistance arteries) control flow into capillary beds via vasodilation and vasoconstriction of smooth muscle  Capillaries Supply gases, nutrients, wastes, hormones, etc., between blood and interstitial fluid to almost every cell, except for cartilage, epithelia, cornea, and lens of eye only single RBC can pass through at a time Walls just endothelial cells, joined by tight junctions with gaps called intercellular clefts Pericytes: spider-shaped stem cells help stabilize capillary walls, control permeability, and play a role in vessel repair endothelial cells are © 2016 Pearson Education, Inc.  Capillary Beds Capillary bed: interwoven network of capillaries between arterioles and venules Microcirculation: flow of blood through bed Capillary beds consist of two types of vessels 1. Vascular shunt: channel that connects arteriole directly with venule (metarteriole– thoroughfare channel) 2. True capillaries: actual vessels involved in exchange © 2016 Pearson Education, Inc.  19.4 Veins - carry blood toward the heart Capillaries unite to form postcapillary venules – Consist of endothelium and a few pericytes – Very porous; allow fluids and WBCs into tissues Larger venules have one or two layers of smooth muscle cells Large lumen and thin walls make veins good storage vessels. Called capacitance vessels (blood reservoirs) because they contain up to 65% of blood supply Venous ® EDV ® SV ® CO Return Frank-Starling Law © 2016 Pearson Education, Inc.  Veins (cont.) Large-diameter lumens offer little resistance  Blood pressure lower than in arteries, so adaptations ensure return of blood to heart – Venous valves Prevent backflow of blood Most abundant in veins of limbs – Venous sinuses Flattened veins with extremely thin walls Composed only of endothelium Examples: coronary sinus of the heart and dural sinuses of the brain V e in V a lv e C a p illa r y n e tw o r k Lum en B a s e m e n t m e m b ra n e y © 2016 Pearson Education, Inc. E n d o t h e l i a l c e l ls  Anastomoses (interconnections of blood vessels) Arterial anastomoses: provide alternate pathways (collateral channels) to ensure continuous flow, even if one artery is blocked. They are common in joints, abdominal organs, brain, and heart; none in retina, kidneys, spleen Arteriovenous anastomoses: shunts in capillaries; example: metarteriole–thoroughfare channel Venous anastomoses: so abundant that occluded veins rarely block blood flow © 2016 Pearson Education, Inc.  Clinical – Varicose veins: dilated and painful veins due to incompetent (leaky) valves Factors that contribute include heredity and conditions that hinder venous return – Example: prolonged standing in one position, obesity, or pregnancy; blood pools in lower limbs, weakening valves; affects more than 15% of adults – Elevated venous pressure can cause varicose veins: straining to deliver a baby or have a bowel movement raises intra-abdominal pressure, resulting in varicosities in anal veins called hemorrhoids © 2016 Pearson Education, Inc.  Part 2 Physiology of Circulation 19.6 Flow, Pressure, and Resistance Definition of Terms Blood flow: volume of blood flowing through vessel, organ, or entire circulation in given period – Measured in ml/min, it is equivalent to cardiac output (CO) for entire vascular system – Varies at individual organ level, based on needs © 2016 Pearson Education, Inc.  Definition of Terms (cont.) Blood pressure (BP): force per unit area exerted on wall of blood vessel by blood – Expressed in mm Hg – Measured as systemic arterial BP in large arteries near heart – Pressure gradient provides driving force that keeps blood moving from higher- to lower-pressure areas © 2016 Pearson Education, Inc.  Definition of Terms (cont.) Resistance (peripheral resistance): opposition to flow – Measurement of amount of friction blood encounters with vessel walls, generally in peripheral (systemic) circulation – Three important sources of resistance Blood viscosity (R ~1/V) Total blood vessel length (R~L) Blood vessel diameter (R~1/radius4) © 2016 Pearson Education, Inc.  Definition of Terms (cont.) Blood vessel diameter Fluid close to walls moves more slowly than in middle of tube (called laminar flow) Small-diameter arterioles are major determinants of peripheral resistance. Radius of small arterioles changes frequently, in contrast to larger arteries that do not change often Abrupt changes in vessel diameter or obstacles such as fatty plaques from atherosclerosis dramatically increase resistance. Laminar flow is disrupted and becomes turbulent flow, irregular flow that causes increased resistance © 2016 Pearson Education, Inc.  Relationship between Flow, Pressure, and Resistance Blood flow (F) ( equals CO) is directly proportional to blood pressure gradient ( P) (mean arterial pressure, MAP) Blood flow is inversely proportional to peripheral resistance (R) F= P/R R is more important in influencing local blood flow because it is easily changed by altering blood vessel diameter © 2016 Pearson Education, Inc.  Arterial Blood Pressure 120 Blood pressure (mm Hg) Determined by two factors: Systolic pressure 1. Elasticity of arteries close to heart 100 Mean pressure 2. Volume of blood forced into them at any time 80 Blood pressure near heart is pulsatile 60 Systolic pressure: pressure exerted in aorta during Diastolic 40 pressure ventricular contraction (~120 mm Hg) 20 Diastolic pressure: aortic pressure when heart is at rest Pulse pressure: difference between systolic and 0 es ae ies rta les ies ins diastolic pressure iol av lar Ao nu ter Ve ter ec Ve pil Ar Pulse: throbbing of arteries due to difference in pulse Ar na Ca Ve pressures, which can be felt under skin Mean arterial pressure (MAP): pressure that propels blood to tissues – Pulse pressure phases out near end of arterial tree – Flow is nonpulsatile with a steady MAP pressure Heart spends more time in diastole, so not just a simple average of diastole and systole MAP is calculated by adding diastolic pressure + 1/3 pulse pressure – Example: BP = 120/80; Pulse Pressure = 120 − 80 = 40; so MAP = 80 + (1/3) 40 = 80 +  13 = 93 mm Hg Pulse pressure and MAP both decline with increasing distance from heart © 2016 Pearson Education, Inc.  Arterial Blood Pressure (cont.) Clinical monitoring of circulatory efficiency – Vital signs: pulse and blood Superficial temporal artery pressure, along with respiratory rate and body temperature Facial artery – Taking a pulse Radial pulse (taken at the Common carotid artery wrist): most routinely used, but there are other clinically Brachial artery important pulse points Pressure points: areas where Radial artery arteries are close to body surface Femoral artery – Can be compressed to stop blood flow in event of Popliteal artery hemorrhaging Posterior tibial artery Dorsalis pedis artery © 2016 Pearson Education, Inc.  Arterial Blood Pressure (cont.) – Measuring blood pressure Systemic arterial BP is measured indirectly by auscultatory methods using a sphygmomanometer 1.Wrap cuff around arm superior to elbow 2.Increase pressure in cuff until it exceeds systolic pressure in brachial artery 3. Pressure is released slowly, and examiner listens for sounds of Korotkoff with a stethoscope Systolic pressure: normally less than 120 mm Hg – Pressure when sounds first occur as blood starts to spurt through artery Diastolic pressure: normally less than 80 mm Hg – Pressure when sounds disappear because artery no longer constricted; blood flowing freely © 2016 Pearson Education, Inc.  Capillary Blood Pressure Ranges from 35 mm Hg at beginning of capillary bed to ∼17 mm Hg at the end of the bed Low capillary pressure is desirable because: 1. High BP would rupture fragile, thin-walled capillaries 2. Most capillaries are very permeable, so low pressure forces filtrate into interstitial spaces © 2016 Pearson Education, Inc.  Venous Blood Pressure Changes little during cardiac cycle Small pressure gradient, only about 15 mm Hg Low pressure is due to cumulative effects of peripheral resistance Low pressure of venous side requires adaptations to help with venous return: 1. Muscular pump: contraction of skeletal muscles “milks” blood back toward heart; valves prevent backflow 2. Respiratory pump: pressure changes during Venous valve breathing move blood toward heart by (open) squeezing abdominal veins as thoracic veins expand Contracted 3. Sympathetic venoconstriction: under skeletal sympathetic control, smooth muscles constrict, muscle pushing blood back toward heart Venous valve (closed) Vein Direction of blood flow © 2016 Pearson Education, Inc.  19.8 Regulation of Blood Pressure Maintaining blood pressure requires cooperation of brain, heart, blood vessels, and kidneys Three main factors regulating blood pressure – Cardiac output (CO) – Peripheral resistance (PR) – Blood volume © 2016 Pearson Education, Inc.  19.8 Regulation of Blood Pressure Remember: F= P/R since F = CO, so substituting gives CO =  P/R and rearranging,  P = CO R = MAP Shows that blood pressure (MAP) is directly proportional to CO and PR Recall that CO = SV HR ( where SV is a stroke volume), so if MAP = CO R, then MAP = SV HR R Anything that increases SV, HR, or R will also increase MAP – SV is effected by venous return (EDV) – HR is maintained by medullary centers – R is effected mostly by vessel diameter Stroke Heart Diameter of Blood Blood volume rate blood vessels viscosity vessel length Cardiac output Peripheral resistanc e © 2016 Pearson Education, Inc. Mean arterial pressure (MAP )  19.8 Regulation of Blood Pressure Factors can be affected by: – Short-term regulation: neural controls – Short-term regulation: hormonal controls – Long-term regulation: renal controls © 2016 Pearson Education, Inc.  Short-Term Regulation: Neural Controls Neural controls operate via reflex arcs that involve: – Cardiovascular center of medulla – Baroreceptors – Chemoreceptors – Higher brain centers Vasomotor center © 2016 Pearson Education, Inc.  Short-Term Regulation: Neural Controls Role of the cardiovascular center – Cardiovascular center: composed of clusters of sympathetic neurons in medulla – Consists of: Cardiac centers: cardioinhibitory and cardioacceleratory centers Vasomotor center: sends steady impulses via sympathetic efferents called vasomotor fibers to blood vessels – Cause continuous moderate constriction called vasomotor tone – Receives inputs from baroreceptors, chemoreceptors, and higher brain centers © 2016 Pearson Education, Inc.  Short-Term Regulation: Neural Controls Baroreceptor reflexes – Located in carotid sinuses, aortic arch, and walls of large arteries of neck and thorax – If MAP is high: Increased blood pressure stimulates baroreceptors to increase input to vasomotor center Inhibits vasomotor and cardioacceleratory centers Stimulates cardioinhibitory center Results in arterial vasodilation and Vasomotor center venodilation ( venous return and CO).  vagal tone  HR Baroreceptors adopts to high BP and cannot get activated if altered blood pressure is sustained Baroreceptor reflexes is response to low MAP is low reflex vasoconstriction is initiated that increases CO and BP, via Carotid sinus reflex ad Aortic reflex to maintains BP in systemic circuit  Short-Term Regulation: Neural Controls Baroreceptor reflexes (cont.) – If MAP is low: Reflex vasoconstriction is initiated that increases CO and blood pressure Example: when a person stands, BP falls and triggers: – Carotid sinus reflex: baroreceptors that monitor BP to ensure enough blood to brain – Aortic reflex maintains BP in systemic circuit Baroreceptors adopts to high BP and cannot get activated if altered blood pressure is sustained – Become adapted to hypertension, so not triggered by elevated BP levels © 2016 Pearson Education, Inc. Figure 19.10 Baroreceptor reflexes that help maintain blood pressure homeostasis. Slide 6 3 Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center. 4a Sympathetic impulses to heart cause HR, contractility, and CO. 2 Baroreceptors in carotid sinuses and aortic arch are stimulated. 4b Rate of vasomotor impulses allows vasodilation, 5 CO and R IM B causing R. return blood 1 Stimulus: AL AN CE pressure to Blood pressure homeostatic range. (arterial blood Homeostasis: Blood pressure in normal range pressure rises above normal range). 1 Stimulus: Blood pressure IM B (arterial blood AL AN CE pressure falls below 4b Vasomotor normal range). 5 CO and R return blood fibers stimulate pressure to vasoconstriction, homeostatic causing R. range. 2 Baroreceptors in carotid sinuses and aortic arch are inhibited 4a Sympathetic impulses to heart Cause HR, contractility, and 3 Impulses from baroreceptors CO. activate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center. © 2016 Pearson Education, Inc.  Short-Term Regulation: Neural Controls Chemoreceptor reflexes – Aortic arch and large arteries of neck detect increase in CO 2, or drop in pH or O2 – Cause increased blood pressure by: Signaling cardioacceleratory center to increase CO Signaling vasomotor center to increase vasoconstriction © 2016 Pearson Education, Inc.  Short-Term Regulation: Neural Controls Influence of higher brain centers – Reflexes that regulate BP are found in medulla – Hypothalamus and cerebral cortex can modify arterial pressure via relays to medulla – Hypothalamus increases blood pressure during stress – Hypothalamus mediates redistribution of blood flow during exercise and changes in body temperature medulla © 2016 Pearson Education, Inc.  Short-Term Mechanisms: Hormonal Controls Hormones regulate BP in short term via changes in peripheral resistance or long term via changes in blood volume Adrenal medulla hormones – Epinephrine and norepinephrine from adrenal gland increase CO and vasoconstriction Angiotensin II stimulates vasoconstriction Antidiuretic hormone: high levels can cause vasoconstriction Atrial natriuretic peptide decreases BP by antagonizing aldosterone, causing decreased blood volume © 2016 Pearson Education, Inc.  Long-Term Mechanisms: Renal Regulation Baroreceptors quickly adapt to chronic high or low BP so are ineffective for long-term regulation Long-term mechanisms control BP by altering blood volume via kidneys Kidneys regulate arterial blood pressure by: 1. Direct renal mechanism 2. Indirect renal mechanism (renin-angiotensin- aldosterone) © 2016 Pearson Education, Inc. Figure 19.11 Direct and indirect (hormonal) mechanisms for renal control of blood pressure. Direct renal mechanism Indirect renal mechanism (renin-angiotensin-aldosterone) Initial stimulus Arterial pressure Arterial pressure Physiological response Result Inhibits baroreceptors Sympathetic nervous system activity Filtration by kidneys Angiotensinogen Renin release from kidneys Angiotensin I Angiotensin converting enzyme (ACE) Angiotensin II Urine formation ADH release by Thirst via Vasoconstriction; Adrenal cortex posterior pituitary hypothalamus peripheral resistance Secretes Aldosterone Blood volume Sodium reabsorption Water reabsorption Water intake by kidneys by kidneys Blood volume Mean arterial pressure Mean arterial pressure © 2016 Pearson Education, Inc. Figure 19.12 Factors that increase MAP. Activity of Release Fluid loss from Crisis stressors: Vasomotor tone; Dehydration, Body size muscular of ANPP hemorrhage, exercise, trauma, bloodborne high hematocrit pump and excessive body chemicals respiratory sweating temperature (epinephrine, pump NE, ADH, angiotensin II) Conservation Blood volume Blood pH of Na+ and Blood pressure O2 water by kidneys CO2 Blood Baroreceptors Chemoreceptors volume Venous Activation of vasomotor and cardio- return acceleratory centers in brain stem Diameter of Blood Blood vessel Stroke Heart blood vessels viscosity length volume rate Cardiac output Peripheral resistance Initial stimulus Physiological response Mean arterial pressure (MAP) Result © 2016 Pearson Education, Inc. 19.8 Regulation of Blood Pressure Homeostatic Imbalances in Blood Pressure Transient elevations in BP occur during changes in posture, physical exertion, emotional upset, fever Age, sex, weight, race, mood, and posture may also cause BP to vary © 2016 Pearson Education, Inc. Homeostatic Imbalances in Blood Pressure Hypertension Sustained elevated arterial pressure of 140/90 mm Hg or higher Prehypertension if values elevated but not yet in hypertension range May be transient adaptations during fever, physical exertion, and emotional upset Often persistent in obese people Prolonged hypertension is major cause of heart failure, vascular disease, renal failure, and stroke Heart must work harder; myocardium enlarges, weakens, and becomes flabby Also accelerates atherosclerosis Primary hypertension --- 90% of Secondary hypertension --- Less common; hypertensive conditions; No underlying Commonly due to obstructed renal cause identified; Risk factors include arteries, kidney disease, and endocrine heredity, diet, obesity, age, diabetes disorders such as hyperthyroidism and mellitus, stress, and smoking; No cure Cushing’s syndrome; Treatment focuses but can be controlled on correcting underlying cause © 2016 Pearson Education, Inc. Homeostatic Imbalances in Blood Pressure (cont.) Hypotension Low blood pressure below 90/60 mm Hg Usually not a concern unless it causes inadequate blood flow to tissues Often associated with long life and lack of cardiovascular illness Orthostatic hypotension: temporary low BP and dizziness when suddenly rising from sitting or reclining position Chronic hypotension: hint of poor nutrition and warning sign for Addison’s disease or hypothyroidism Acute hypotension: important sign of circulatory shock Circulatory shock Hypovolemic shock results from large-scale blood loss Vascular shock results from extreme vasodilation and decreased peripheral resistance Cardiogenic shock results when an inefficient heart cannot sustain adequate circulation © 2016 Pearson Education, Inc. 19.9 Control of Blood Flow Functions of blood flow: 1. Delivery of O2 and nutrients to, and 750 removal of wastes from, tissue cells 2. Gas exchange (lungs) 750 3. Absorption of nutrients (digestive tract) Brain 750 12,500 4. Urine formation (kidneys) Heart 250 Rate of flow (RF) is precisely right amount to Skeletal 1200 provide proper function to that tissue or muscles organ. Thus, RF is controlled: Skin 500 5. Extrinsic control: sympathetic nervous system and hormones control Kidneys 1100 blood flow by act on arteriolar smooth muscle to reduce flow to regions that need it the least. Abdomen 1400 6. Intrinsic control: Autoregulation control of blood flow by varying 1900 resistance (diameter) of arterioles: Other 600 blood flow is adjusted locally to meet Total blood 600 specific tissue’s requirements. flow at rest 600 5800 ml/min 400 Total blood flow during strenuous exercise 17,500 ml/min © 2016 Pearson Education, Inc. Figure 19.14 Intrinsic and extrinsic control of arteriolar smooth muscle in the systemic circulation. Vasodilators Metabolic Neural O2 Sympathetic tone CO2 H+ Hormonal K+ Atrial natriuretic Prostaglandins peptide Adenosine Nitric oxide Extrinsic controls Intrinsic controls (autoregulation) Vasoconstrictors Neural or hormonal controls Maintain mean arterial pressure Metabolic or myogenic controls (MAP) Distribute blood flow to individual Redistribute blood during exercise organs and tissues as needed and thermoregulation Myogenic Neural Stretch Sympathetic tone Metabolic Hor monal Endothelins Angiotensin II Antidiuretic hormone Epinephrine Norepinephrine © 2016 Pearson Education, Inc. Autoregulation: Intrinsic (Local) Regulation of Blood Flow (cont.) Long-term autoregulation Occurs when short-term autoregulation cannot meet tissue nutrient requirements Long-term autoregulation may take weeks or months to increase blood supply Number of vessels to region increases (angiogenesis), and existing vessels enlarge Common in heart when coronary vessel occluded, or throughout body in people in high-altitude areas © 2016 Pearson Education, Inc. Blood Flow in Special Areas Skeletal muscles Blood flow varies with fiber type and activity At rest, myogenic and Exerc ising skeletal neural mechanisms muscle predominate; maintain flow at ∼1L /min Active or exercise O2, CO2, H+, and hyperemia: during muscle other metabolic factors in extracellular fluid activity, blood flow increases in direct proportion to metabolic activity Vasodilation of arterioles Local controls override (overrides sympathetic extrinsic sympathetic vasoconstriction; flow can input) increase 10 Initial stimulus Muscle blood Physiological flow (active response hyperemia) Result © 2016 Pearson Education, Inc. Blood Flow in Special Areas (cont.) Brain Blood flow to brain must be constant because neurons are intolerant of ischemia --- Flow averages ~750 ml/min. Brain vulnerable under extreme systemic pressure changes MAP < 60 mm Hg can cause syncope (fainting) MAP > 160 mm Hg can result in cerebral edema Control mechanisms are due to 1) Metabolic controls pH or  CO2cause marked vasodilation Very high CO2 levels depress Metabolic control 2) Myogenic controls  MAP causes cerebral vessels to dilate  MAP causes cerebral vessels to constrict © 2016 Pearson Education, Inc. Blood Flow in Special Areas (cont.) Skin Blood flow through venous plexuses below skin surface regulates body temperature Flow varies from 50 ml/min to 2500 ml/min, depending on body temperature Flow is controlled by sympathetic nervous system reflexes As temperature rises (e.g., from heat exposure, fever, vigorous exercise) Hypothalamic signals reduce vasomotor stimulation of skin vessels, causing dilation Warm blood flushes into capillary beds Heat radiates from skin As temperature decreases, blood is shunted to deeper, more vital organs Superficial skin vessels constrict strongly Blood in vessels may become trapped causing rosy cheeks in cold Vasomotion: intermittent flow of blood through capillaries Due to on/off opening and closing of precapillary sphincters © 2016 Pearson Education, Inc. Blood Flow in Special Areas (cont.) Lungs Pulmonary circuit is unusual; pathway is short Arteries/arterioles are more like veins/venules (thin walled, large lumens) Arterial resistance and pressure are much lower than in systemic circuit Averages  24/10 mm Hg versus 120/80 mm Hg Autoregulatory mechanisms are opposite Low O2 levels cause vasoconstriction, and high levels promote vasodilation Allows blood flow to O2-rich areas of lung © 2016 Pearson Education, Inc. Blood Flow in Special Areas (cont.) Heart Blood flow through heart is influenced by aortic pressures and ventricular pumping During ventricular systole, coronary vessels are compressed Myocardial blood flow ceases Stored myoglobin supplies sufficient oxygen During diastole, high aortic pressure forces blood through coronary circulation At rest, coronary blood flow is 250 ml/min Control is probably via myogenic mechanisms During strenuous exercise, coronary vessels dilate in response to local accumulation of vasodilators Blood flow may increase three to four times Important because cardiac cells use 65% of O2 delivered Other cells use only 25% of delivered O2 Increasing coronary blood flow is only way to provide more O2 © 2016 Pearson Education, Inc. 19.10 Capillary Exchange Velocity of Blood Flow Velocity of flow changes as blood travels through systemic circulation Fastest in aorta, slowest in capillaries, then increases again in veins Speed is inversely related to total cross-sectional area Capillaries have largest area so slowest flow Slow capillary flow allows adequate time for exchange between blood and tissues 120 Blood pressure (mm Hg) Relative cross- sectional area of Systolic pressure different vessels of the vascular bed 100 Mean pressure 5000 80 Total area 4000 (c m 2) of the 3000 60 vasc ular 2000 bed 1000 Diastolic 0 40 pressure 50 40 20 Veloc ity of 30 blood flow 20 (c m/s) 0 10 es ae ies rta les ies ins 0 iol av lar Ao nu ter Ve ae Ve ries pil es ter ies les ec rta ins Ve pil Ar av Ca riol ter nu la Ao Ar Ve na Ca ec te Ar Ve Ar na Ve © 2016 Pearson Education, Inc. Figure 19.17-2 Capillary transport mechanisms. Lumen Caveolae Pinocytotic vesicles Endothelial fenestration Intercellular (pore) cleft 4 Transport via vesicles or caveolae (large substances) Basement 3 Movement membrane through fenestrations 2 Movement (water-soluble 1 Diffusion through through substances) intercellular clefts membrane (water-soluble (lipid-soluble substances) substances) © 2016 Pearson Education, Inc. Fluid Movements: Bulk Flow Fluid is forced out clefts of capillaries at arterial end, and most returns to blood at venous end Extremely important in determining relative fluid volumes in blood and interstitial space Bulk fluid flow across capillary walls causes continuous mixing of fluid between plasma and interstitial fluid; maintains interstitial environment. Direction and amount of fluid flow depend on two opposing forces Hydrostatic pressures Colloid osmotic pressures © 2016 Pearson Education, Inc. Fluid Movements: Bulk Flow (cont.) Hydrostatic pressures Hydrostatic pressure (HP): force exerted by fluid pressing against wall; two types Capillary hydrostatic pressure (HPc): capillary blood pressure that tends to force fluids through capillary walls Greater at arterial end (35 mm Hg) of bed than at venule end (17 mm Hg) Interstitial fluid hydrostatic pressure (HPif): pressure pushing fluid back into vessel; usually assumed to be zero because lymphatic vessels drain interstitial fluid Colloid osmotic pressures Capillary colloid osmotic pressure (oncotic pressure, OPc) “Sucking” pressure created by nondiffusible plasma proteins pulling water back in to capillary Opc  26 mm Hg Interstitial fluid colloid osmotic pressure (OPif) Pressure is inconsequential because interstitial fluid has very low protein content OPif around only 1 mm Hg © 2016 Pearson Education, Inc. Fluid Movements: Bulk Flow (cont.) Hydrostatic-osmotic pressure interactions Net filtration pressure (NFP): comprises all forces acting on capillary bed NFP = (HPc + OPif) (HPif + OPc) Net fluid flow out at arterial end (filtration) Net fluid flow in at venous end (reabsorption) More fluid leaves at arterial end than is returned at venous end Excess interstitial fluid is returned to blood via lymphatic system © 2016 Pearson Education, Inc.  Arteriole The big picture Each day, 20 L of fluid filters from capillaries at their arteriolar end and flows through the interstitial space. Most (17 L) is reabsorbed at the venous end. Fluid moves through the interstitial space. For all capillary beds, 20 L of fluid is filtered out per day—almost 7 times the total plasma volume! 17 L of fluid per day is reabsorbed into the capillaries at the venous end. About 3 L per day of fluid (and any leaked proteins) are removed by the lymphatic Venule system (see Chapter 20). Lymphatic capillary Focus Figure 19.1-3 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid compartments, and maintains the interstitial environment. How do the pressures drive fluid flow across a capillary? Net filtration occurs at the arteriolar end of a capillary. Capillary lumen Boundary Interstitial fluid (capillary wall) Hydrostatic pressure in capillary HPc = 35 mm Hg (HPc) “pushes” fluid out of capillary. Osmotic pressure in capillary OPc = 26 mm Hg (OPc) “pulls” fluid into capillary. Let’s use what we know about pressures to determine the net filtration pressure (NFP) at any point. (NFP is the pressure Hydrostatic pressure driving fluid out of the capillary.) To do HPif = 0 mm Hg (HPif) in interstitial fluid this we calculate the outward pressures “pushes” fluid into (HPc and OPif) minus the inward capillary. pressures (HPif and OPc). So, OPif = 1 mm Hg Osmotic pressure (OPif) NFP = (HPc + OPif)  (HPif + OPc) in interstitial fluid “pulls” = (35 + 1) (0 + 26) fluid out of capillary. = 10 mm Hg (net outward pressure) As a result, fluid moves from the NFP = 10 mm Hg capillary into the interstitial space. © 2016 Pearson Education, Inc. Focus Figure 19.1-4 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid compartments, and maintains the interstitial environment. Net reabsorption occurs at the venous end of a capillary. Capillary lumen Boundary Interstitial fluid (capillary wall) Hydrostatic pressure in capillary “pushes” fluid out of capillary. HPc = 17 mm Hg The pressure has dropped because of resistance encountered along the capillaries. Osmotic pressure in capillary OPc = 26 mm Hg “pulls” fluid into capillary. Again, we calculate the NFP: HPif = 0 mm Hg Hydrostatic pressure in interstitial fluid “pushes” fluid into capillary. NFP = (HPc + OPif)  (HPif + OPc) = (17 + 1) (0 + 26) OPif = 1 mm Hg Osmotic pressure in = 8 mm Hg (net inward pressure) interstitial fluid “pulls” fluid out of capillary. Notice that the NFP at the venous end is a negative number. This means that reabsorption, not filtration, is occurring and so fluid moves from the NFP=  8 mm Hg interstitial space into the capillary. © 2016 Pearson Education, Inc. Clinical – Homeostatic Imbalance 19.2 Edema: abnormal increase in amount of interstitial fluid Caused by either an increase in outward pressure (driving fluid out of the capillaries) or a decrease in inward pressure An increase in capillary hydrostatic pressure accelerates fluid loss from blood. It could result from incompetent venous valves, localized blood vessel blockage, congestive heart failure, or high blood volume An increase in interstitial fluid osmotic pressure can result from an inflammatory response. Inflammation increases capillary permeability and allows proteins to leak into interstitial fluid, causes large amounts of fluid to be pulled into interstitial space. A decrease in capillary colloid osmotic pressure hinders fluid return to blood. It can be caused by hypoproteinemia, low levels of plasma proteins caused by malnutrition, liver disease, or glomerulonephritis (loss of plasma proteins from kidneys) © 2016 Pearson Education, Inc. Clinical – Homeostatic Imbalance 19.2 Edema also can be caused by decreased drainage of interstitial fluid through lymphatic vessels that have been blocked by disease or surgically removed Excess interstitial fluid in subcutaneous tissues generally causes pitting edema Edema can impair tissue function as a result of increased distance for diffusion of gases, nutrients and wastes between blood and cells Slow fluid losses can be compensated for by renal mechanisms, but rapid onset may have serious effects on the circulation © 2016 Pearson Education, Inc. Figure 19.18 Pitting edema. © 2016 Pearson Education, Inc. Part 3 Circulatory Pathways: Blood Vessels of the Body Vascular system consists of two main circulations: Pulmonary circulation: short loop that runs from heart to lungs and back to heart Systemic circulation: long loop to all parts of body and back to heart © 2016 Pearson Education, Inc. Figure 19.19a Pulmonary circulation. Pulmonary Pulmonary capillaries R. pulmonary L. pulmonary capillaries of the artery artery of the R. lung L. lung Pulmonary To trunk systemic circulation R. pulmonary veins From systemic RA LA circulation L. pulmonary veins RV LV Schematic flowchart. © 2016 Pearson Education, Inc. Figure 19.19b Pulmonary circulation. Left pulmonary artery Air-filled alveolus Aortic arch of lung Pulmonary trunk Right pulmonary O2 artery Three lobar arteries CO2 to right lung Pulmonary Gas exchange capillary Two lobar arteries Pulmonary to left lung veins Pulmonary Right veins atrium Left atrium Right ventricle Left ventricle Illustration. The pulmonary arterial system is shown in blue to indicate that the blood it carries is oxygen-poor. The pulmonary venous drainage is shown in red to indicate that the blood it transports is oxygen-rich. © 2016 Pearson Education, Inc. Figure 19.20 Schematic flowchart showing an overview of the systemic circulation. Common carotid Capillary beds of arteries to head head and and subclavian upper limbs arteries to upper limbs Superior vena cava Aortic arch Aorta RA LA RV LV Azygos Thoracic system aorta Venous Arterial drainage blood Inferior vena Capillary beds of cava mediastinal structures and thorax walls Diaphragm Abdominal aorta Capillary beds of Inferior digestive viscera, vena spleen, pancreas, cava kidneys Capillary beds of gonads, pelvis, and lower limbs © 2016 Pearson Education, Inc. Vascular System Important differences between systemic arteries and veins: 1. Arteries run deep, whereas veins are both deep and superficial Deep veins share same name with corresponding artery Superficial veins do not correspond to names of any arteries 2. Venous pathways are more interconnected Veins can have more than one name, making venous pathways harder to follow 3. The brain and digestive systems have unique venous drainage systems Brain contains dural venous sinuses Venous system of the digestive system drains into hepatic portal system, which perfuses through liver before returning to heart 4. Arteries and veins tend to run side by side, and, in many places, they also run with nerves 5. Systemic vessels do not always match on right and left sides of body Example: almost all vessels in head and limbs are bilaterally symmetrical, but some large, deep vessels of trunk are asymmetrical or unpaired © 2016 Pearson Education, Inc.