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Chapter 14 Lecture Outline
See separate PowerPoint slides for all figures and tables pre-inserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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I. Cardiac Output
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Introduction Cardiac output – the volume of blood pumped each minute by each ventricle: cardiac output = stroke volume X heart rate (ml/minute) (ml/beat) (beats/min) Average heart rate = 70 bpm Average stroke volume = 70−80 ml/beat Average cardiac output = 5,500 ml/minute
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Regulation of Cardiac Rate
Spontaneous depolarization occurs at SA node when HCN channels open, allowing Na+ in. Open due to hyperpolarization at the end of the preceding action potential Sympathetic norepinephrine and adrenal epinephrine keep HCN channels open, increasing heart rate. Parasympathetic acetylcholine opens K+ channels, slowing heart rate. Controlled by cardiac center of medulla oblongata that is affected by higher brain centers
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Regulation of Cardiac Rate, cont
Actual pace comes from the net affect of these antagonistic influences Positive chronotropic effect – increases rate Negative chronotropic effect – decreases rate
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Effects of ANS on the SA Node
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. = Pacemaker potential Control Threshold –50mV Sympathetic nerve effect –50mV Parasympathetic nerve effect –50mV 250 500 750 1000 Time (msec)
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Effects of ANS Activity on the Heart
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Regulation of Stroke Volume
Regulated by three variables: End diastolic volume (EDV): volume of blood in the ventricles at the end of diastole Sometimes called preload Stroke volume increases with increased EDV. Total peripheral resistance: Frictional resistance in the arteries Inversely related to stroke volume Called afterload
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Regulation of Stroke Volume, cont
Contractility: strength of ventricular contraction Stroke volume increases with contractility. Normally, about 60% of the EDV is ejected – ejection fraction
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Frank-Starling Law of the Heart
Increased EDV results in increased contractility and thus increased stroke volume. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Frank-Starling law Increased contractility caused by sympathetic nerve stimulation Stroke volume (ml) Ventricular end-diastolic volume (ml)
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Intrinsic Control of Contraction Strength
Due to myocardial stretch Increased EDV stretches the myocardium, which increases contraction strength. Due to increased myosin and actin overlap and increased sensitivity to Ca2+ in cardiac muscle cells
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Intrinsic Control of Contraction Strength, cont
Adjustment for rise in peripheral resistance Increased peripheral resistance will decrease stroke volume More blood remains in the ventricles, so EDV increases Ventricles are stretched more, so they contract more strongly
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Frank-Starling Law of the Heart
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Resting sarcomere lengths A I I H (d) 2.4 μm (d) Actin Z Z Myosin (c) Tension (g) Stretch (c) 2.2 μm (b) (a) (b) 2.0 μm 500 1000 msec Time (a) 1.5 μm
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Extrinsic Control of Contractility
Contractility – strength of contraction at any given fiber length Sympathetic norepinephrine and adrenal epinephrine (positive inotropic effect) can increase contractility by making more Ca2+ available to sarcomeres. Also increases heart rate. Parasympathetic acetylcholine (negative chronotropic effect) will decrease heart rate which will increase EDV increases contraction strength increases stroke volume, but not enough to compensate for slower rate, so cardiac output decreases
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Effect of muscle length & epinephrine on contractility
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 100 Skeletal muscle Cardiac muscle with epinephrine (inotropic effect) 80 Cardiac muscle without epinephrine 60 Relative tension (%) 40 20 50 60 70 80 90 100 Length of muscle (as percent of optimum at 100%)
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Regulation of Cardiac Output
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Total peripheral resistance and mean arterial pressure Cardiac output = Cardiac rate X Stroke volume Contraction strength Sympathetic nerves End- diastolic volume (EDV) Parasympathetic nerves Stretch Frank- Starling
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Venous Return End diastolic volume is controlled by factors that affect venous return: Total blood volume Venous pressure (driving force for blood return) Veins have high compliance - stretch more at a given pressure than arteries (veins have thinner walls). Veins are capacitance vessels – 2/3 of the total blood volume is in veins They hold more blood than arteries but maintain lower pressure.
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Distribution of blood at rest
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lungs (10%–12%) Heart (8%–11%) Small veins and venules Systemic arteries (10%–12%) Systemic veins (60%–70%) Capillaries (4%–5%) Large veins
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Factors in Venous Return
Pressure difference between arteries and veins (about 10mm Hg) Pressure difference in venous system - highest pressure in venules vs. lowest pressure in venae cavae into the right atrium (0mm Hg) Sympathetic nerve activity to stimulate smooth muscle contraction and lower compliance Skeletal muscle pumps Pressure difference between abdominal and thoracic cavities (respiration) Blood volume
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Factors in Venous Return
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. End-diastolic volume Venous return Negative intrathoracic pressure Blood volume Venous pressure Breathing Urine volume Tissue-fluid volume Venoconstriction Skeletal muscle pump Sympathetic nerve stimulation
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II. Blood Volume
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Body Water Distribution
2/3 of our body water is found in the cells (intracellular). Of the remaining, 80% exists in interstitial spaces and 20% is in the blood plasma (extracellular). Osmotic forces control the movement of water between the interstitial spaces and the capillaries, affecting blood volume. Urine formation and water intake (drinking) also play a role in blood volume. Fluid is always circulating in a state of dynamic equilibrium
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Body Water Distribution
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Intracellular 27–30 L Extracellular 14–16.5 L Water excretion per 24 hrs Cell membrane Capillary wall Kidneys 0.6–1.5 L Interstitial fluid volume 11–13 L Blood plasma volume 3.0–3.5 L Lungs 0.3–0.4 L Cytoplasm Skin (sweat glands) 0.2–1.0 L Water intake per 24 hrs (drink + food) 1.5–2.5 L H2O GI tract Feces 0.1–0.2 L H2O
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Tissue/Capillary Fluid Exchange
Net filtration pressure is the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of the fluid outside the capillaries Hydrostatic pressure at arteriole end is 37 mmHg and at the venule end is 17 mmHg Hydrostatic pressure of interstitial fluid is 1 mmHg Net filtration pressure is 36 mmHg at arteriole end and 16 mmHg at venule end
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Colloid osmotic pressure
Due to proteins dissolved in fluid Blood plasma has higher colloid osmotic pressure than interstitial fluid. This difference is called oncotic pressure. Oncotic pressure = 25 mmHg This favors the movement of fluid into the capillaries.
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Starling Forces Combination of hydrostatic pressure and oncotic pressure that predicts movement of fluid across capillary membranes Fluid movement is proportional to: (pc + πi) - (pi + πp) fluid out fluid in pc = Hydrostatic pressure in capillary πi = Colloid osmotic pressure of interstitial fluid pi = Hydrostatic pressure of interstitial fluid πp = Colloid osmotic pressure of blood plasma
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Starling Forces, cont Starling Forces predict the movement of fluid out of the capillaries at the arteriole end (positive value) and into the capillaries at the venule end (negative value). The return of fluids on the venous end is not 100%; 10% - 15% remains in the interstitial spaces and will enter the lymphatic capillaries and ultimately return to the venous system
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Distribution of fluid across walls of a capillary
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tissue fluid Net filtration Net absorption Capillary Blood flow Net force out Net force out Net force in Net force in Arteriole Venule Arterial end of capillary Venous end of capillary (Pc + πi) – (Pi + πp) (Fluid out) (Fluid in) (37 + 0) – (1 + 25) (17 + 0) – (1 + 25) = 11 mmHg = –9 mmHg Net filtration Net absorption Where Pc = hydrostatic pressure in the capillary πi = colloid osmotic pressure of interstitial fluid Pi = hydrostatic pressure of interstitial fluid πp = colloid osmotic pressure of blood plasma
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Edema Excessive accumulations of interstitial fluids
May be the result of: High arterial blood pressure Venous obstruction Leakage of plasma proteins into interstitial space Myxedema (excessive production of mucin in extracellular spaces caused by hypothyroidism) Decreased plasma protein concentration Obstruction of lymphatic drainage
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Causes of Edema
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Severe Edema of Elephantiasis
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Regulation of Blood Volume by Kidneys
The formation of urine begins with filtration of fluid through capillaries in the kidneys called glomeruli. 180 L of filtrate is moved across the glomeruli per day, yet only about 1.5 L is actually removed as urine. The rest is reabsorbed into the blood. The amount of fluid reabsorbed is controlled by several hormones and the sympathetic nervous system in response to the body’s needs.
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Role of the sympathetic nervous system
Increased blood volume in the atria stimulates stretch receptors that leads to increased sympathetic stimulation to the heart and decreased stimulation to the kidneys Kidney arterioles dilate, increasing blood flow and increases urine production that will decrease blood volume
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Antidiuretic Hormone (ADH or vasopressin)
Produced by the hypothalamus and released from the posterior pituitary when osmoreceptors detect increased plasma osmolality. Plasma osmolarity can increase due to excessive salt intake or dehydration. Increased plasma osmolarity also increases thirst. ADH stimulates water reabsorption.
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Antidiuretic Hormone, cont
Increased water intake and decreased urine formation increase blood volume. Blood becomes dilute, and ADH is no longer released. Stretch receptors in left atrium, carotid sinus, and aortic arch also inhibit ADH release. Stretch receptors in the atria also stimulated the release of atrial natriuretic peptide which increases excretion of salt and water from kidneys to reduce blood volume
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Negative Feedback Control of Blood Volume by ADH
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Dehydration ( Blood volume) Stimuli Salt ingestion Sensor Blood osmolality Integrating center Effector Osmoreceptors in hypothalamus Posterior pituitary Thirst ADH Water retention by kidneys Drinking Negative feedback responses Blood volume Blood osmolality
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Regulation by Aldosterone
Secreted by adrenal cortex indirectly when blood volume and pressure are reduced Stimulates reabsorption of salt and water in kidneys Does not change blood osmolality since both salt and water are involved Regulated by renin-angiotensin-aldosterone system
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Renin-angiotensin-aldosterone system
When blood pressure is low, cells in the kidneys (juxtaglomerular apparatus) secrete the enzyme renin Angiotensinogen is converted to angiotensin I by renin Angiotensin I is converted to angiotensin II by ACE enzyme.
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Renin-Angiotensin-Aldosterone System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Blood pressure Stimuli Blood flow to kidneys Juxtaglomerular apparatus in kidneys Sensor Integrating center Effector Renin Angiotensinogen Angiotensin I ACE Angiotensin II Adrenal cortex Vasoconstriction of arterioles Aldosterone Salt and water retention by kidneys Negative feedback responses Blood volume Blood pressure
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Regulation by aldosterone, cont
Angiotensin II has many effects that result in a raise in blood pressure: Vasoconstriction of small arteries and arterioles to increase peripheral resistance Stimulates thirst center in hypothalamus Stimulates production of aldosterone in adrenal cortex Can also work the opposite direction to reduce blood pressure
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Regulation by atrial natriuretic peptide
Produced by the atria of the heart when stretch is detected from high volume or increased venous return Promotes salt and water excretion in urine in response to increased blood volume Inhibits ADH secretion Antagonist of aldosterone
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increased blood volume
Negative feedback correction of increased venous return Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sensor Water immersion or increased blood volume Integrating center Effector Negative feedback Venous return Stretch of left atrium Blood volume Vagus nerves Brain Urine volume Atrial natriuretic peptide (ANP) Posterior pituitary NaCl and H2O excretion Antidiuretic hormone (ADH) Kidneys H2O reabsorption
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III. Vascular Resistance to Blood Flow
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Blood Flow to the Organs
Cardiac output is distributed unequally to different organs due to unequal resistance to blood flow through the organs.
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Estimated Distribution of Cardiac Output at Rest
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Physical Laws Describing Blood Flow
Blood flows from a region of higher pressure to a region of lower pressure. The rate of blood flow is proportional to the differences in pressure.
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Blood Flow is produced by a pressure difference
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pressure = 0 mmHg RA LA RV LV ΔP = 100 – 0 = 100 mmHg Pressure = 120/80 (mean mmHg) = ~
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Physical Laws describing Blood Flow, cont
The rate of blood flow is also inversely proportional to the frictional resistance to blood flow within the vessels. ΔP blood flow = resistance ΔP = pressure difference between the two ends of the tube
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Physical Laws Describing Blood Flow, cont
Resistance is measured as: Lη resistance = r4 L = length of the vessel η = viscosity of the blood r = radius of the blood vessel
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Poiseuille’s Law adds in physical constraints
ΔPr4(π) blood flow = ηL(8) Vessel length (L) and blood viscosity (η) do not vary normally. Mean arterial pressure and vessel radius (r) are therefore the most important factors in blood flow. Vasoconstriction of arterioles provides the greatest resistance to blood flow and can redirect flow to/from particular organs
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Relationship Between Blood Flow, Vessel Radius, and Resistance
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Radius = 1 mm Resistance = R Blood flow = F Arterial blood Radius = 1 mm Resistance = R Blood flow = F (a) Radius = 2 mm Resistance = 1/16 R Blood flow = 16 F Arterial blood Radius = 1/2 mm Resistance = 16 R Blood flow = 1/16 F (b)
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Pressure Differences in Different Parts of Systemic Circulation
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Small arteries and arterioles Left ventricle Large arteries Large veins Capillaries Venules 120 100 80 Pressure (mmHg) 60 40 20 Resistance vessels Exchange vessels Capacitance vessels
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Total Peripheral Resistance
The sum of all vascular resistance in systemic circulation Blood flow to organs runs parallel to each other, so a change in resistance within one organ does not affect another. Vasodilation in a large organ may decrease total peripheral resistance and mean arterial pressure. Increased cardiac output and vasoconstriction elsewhere make up for this.
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A Diagram of Systemic and Pulmonary Circulation
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lungs Vena cava Hepatic artery Splenic artery Liver Hepatic vein Mesenteric artery (from intestine) Hepatic portal vein Kidney Renal afferent arterioles Renal efferent arterioles
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Extrinsic Regulation of Blood Flow
Autonomic and endocrine control of blood flow Sympathetic nerves Increase in cardiac output and increase total peripheral resistance through release of norepinephrine onto smooth muscles of arterioles in the viscera and skin to stimulate vasoconstriction (alpha-adrenergic). Acetylcholine is released onto skeletal muscles, resulting in increased vasodilation to these tissues (cholinergic)
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Sympathetic nerves, cont
Adrenal epinephrine stimulates beta-adrenergic receptors for vasodilation During “flight or fight”, blood is diverted to skeletal muscles
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Extrinsic Control of Vascular Resistance and Blood Flow
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Extrinsic Regulation of Blood Flow, cont
Parasympathetic nerves (cholinergic) Acetylcholine stimulates vasodilation. Limited to digestive tract, external genitalia, and salivary glands Less important in controlling total peripheral resistance due to limited influence
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Paracrine Regulation of Blood Flow
Molecules produced by one tissue control another tissue within the same organ. Example: The tunica interna produces signals to influence smooth muscle activity in the tunica media. Smooth muscle relaxation influenced by bradykinin, nitric oxide, and prostaglandin I2 to produce vasodilation Endothelin-1 stimulates smooth muscle contraction to produce vasoconstriction and raise total peripheral resistance.
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Intrinsic Regulation of Blood Flow
Used by some organs (brain and kidneys) to promote constant blood flow when there is fluctuation of blood pressure; also called autoregulation. Myogenic control mechanisms: Vascular smooth muscle responds to changes in arterial blood pressure.
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Metabolic control mechanisms
Local vasodilation is controlled by changes in: Decreased oxygen concentrations due to increased metabolism Increased carbon dioxide concentrations Decreased tissue pH (due to CO2, lactic oxide, etc.) Release of K+ and paracrine signals
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Intrinsic Regulation of Blood Flow, cont
Reactive hyperemia – constriction causes build-up of metabolic wastes which will then cause vasodilation (reddish skin) Active hyperemia – increased blood flow during increased metabolism (reddish skin)
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IV. Blood Flow to the Heart and Skeletal Muscles
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Aerobic Requirements of the Heart
The coronary arteries supply blood to a massive number of capillaries (2,500–4,000 per cubic mm tissue). Unlike most organs, blood flow is restricted during systole. Cardiac tissue therefore has myoglobin to store oxygen during diastole to be released in systole. Cardiac tissue also has lots of mitochondria and respiratory enzymes, thus is metabolically very active.
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Aerobic Requirements of the Heart, cont
Large amounts of ATPase are produced from the aerobic respiration of fatty acids, glucose, and lactate. During exercise, the coronary arteries increase blood flow from 80 ml to 400 ml/ minute/100 g tissue.
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Regulation of Coronary Blood Flow
Norepinephrine from sympathetic nerve fibers (alpha-adrenergic) stimulates vasoconstriction, raising vascular resistance at rest. Adrenal epinephrine (beta-adrenergic) stimulates vasodilation and thus decreases vascular resistance during exercise. Vasodilation is enhanced by intrinsic metabolic control mechanisms – increased CO2, K+, paracrine regulators
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Exercise training Increased density of coronary arterioles and capillaries Increased production of NO to promote vasodilation Decreased compression of coronary arteries during systole due to lower cardiac rate
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Regulation of Blood Flow Through Skeletal Muscles
Arterioles have high vascular resistance at rest due to alpha-adrenergic sympathetic stimulation Even at rest, skeletal muscles still receive 20−25% of the body’s blood supply. Blood flow does decrease during contraction and can stop completely beyond 70% of maximum contraction. Vasodilation is stimulated by both adrenal epinephrine and sympathetic acetylcholine. Intrinsic metabolic controls enhance vasodilation during exercise
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Changes in Skeletal Muscle Blood Flow Under Rest and Exercise
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Circulatory Changes During Dynamic Exercise
Vascular resistance through skeletal and cardiac muscles decreases due to: Increased cardiac output Metabolic vasodilation Diversion of blood away from viscera and skin Blood flow to brain increases a small amount with moderate exercise and decreases a small amount during intense exercise.
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Circulatory Changes During Dynamic Exercise, cont
Cardiac output can increase 5X due to increased cardiac rate. Stroke volume can increase some due to increased venous return from skeletal muscle pumps and respiratory movements Ejection fraction increases due to increased contractility
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Endurance training Lower resting cardiac rate due to greater inhibition of the SA node Increase in stroke volume because of the increase in blood volume Improved O2 delivery
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Circulatory Changes During Exercise
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 25 L/min Cardiac output = 25 L/min 100% 3%–5% 4%–5% 2%–4% 0.5%–1% 3%–4% 80%–85% Heavy exercise ~20 L/min Heavy exercise Rest ~0.75 L/min Rest 100% 20%–25% 4%–5% 20% 3%–5% 15% 4%–5% 15%–20% 5 L/min Cardiac output = 5 L/min
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Cardiovascular Adaptations to Exercise
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Cardiac output Blood flow to skeletal muscles Cardiac rate Stroke volume Metabolic vasodilation in muscles Sympathetic vasoconstriction in viscera Sympathoadrenal system Improved venous return Skeletal muscle activity Deeper breathing
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Cardiovascular Changes During Exercise
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V. Blood Flow to the Brain and Skin
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Introduction Cerebral flow primarily controlled by intrinsic mechanisms and is relatively constant; the brain can not tolerate much variation in blood flow. Cutaneous flow primarily controlled by extrinsic mechanisms and shows the most variation; can handle low rates of blood flow
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Cerebral Circulation Held constant at about 750 mL/min flow
Unless mean arterial pressure becomes very high, there is little sympathetic control of blood flow to the brain. At high pressure, vasoconstriction occurs to protect small vessels from damage and stroke.
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Myogenic Regulation When blood pressure falls, cerebral vessels automatically dilate. When blood pressure rises, cerebral vessels automatically constrict. Decreased pH of cerebrospinal fluid (buildup of CO2) causes arteriole dilation. Increased pH of cerebrospinal fluid (drop in CO2) causes constriction of vessels.
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Metabolic Regulation The most active regions of the brain must receive increased blood flow (hyperemia) due to arteriole sensitivity to metabolic changes. Active neurons release K+, adenosine, NO, and other chemical that cause vasodilation Astrocytes may play a role
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Changing Patterns of Blood Flow in the Brain
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. (a) (b) (c) (d) (all): © Niels A. Lassen, Copenhagen, Denmark
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Cutaneous Blood Flow The skin can tolerate the greatest fluctuations in blood flow. The skin helps control body temperature in a changing environment by regulating blood flow = thermoregulation. Increased blood flow to capillaries in the skin releases heat when body temperature increases. Sweat is also produced to aid in heat loss. Bradykinins in the sweat glands also stimulate vasodilation in the skin.
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Cutaneous Blood Flow, cont
Vasoconstriction of arterioles keeps heat in the body when ambient temperatures are low. This is aided by arteriovenous anastomoses, which shunt blood from arterioles directly to venules. Cold temperatures activate sympathetic vasoconstriction. This is tolerated due to decreased metabolic activity in the skin.
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Cutaneous Blood Flow, cont
At average ambient temperatures, vascular resistance in the skin is high, and blood flow is low. Sympathetic stimulation reduces blood flow further. With continuous exercise, the need to regulate body temperature overrides this, and vasodilation occurs.
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Sympathetic Stimulation, cont
May result in lowered total peripheral resistance if not for increased cardiac output However, if a person exercises in very hot weather, he or she may experience extreme drops in blood pressure after reduced cardiac output. This condition can be very dangerous. Emotions can affect sympathetic activity and cause pallor or blushing
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Circulation in the Skin
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Epidermis Dermis Capillary loop Arteriovenous anastomosis Venule Arteriole Vein Artery
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VI. Blood Pressure
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Blood Pressure Affected by blood volume/stroke volume, total peripheral resistance, and cardiac rate Increase in any of these will increase blood pressure. Vasoconstriction of arterioles raises blood pressure upstream in the arteries. Arterial blood = cardiac X total peripheral pressure output resistance
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Effect of Vasoconstriction on Blood Pressure
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Increased pressure Decreased pressure Constriction
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Blood Pressure, cont The blood pressure of blood vessels is related to the total cross-sectional area Capillary blood pressure is low because of large total cross-sectional area. Artery blood pressure is high because of small total cross-sectional area
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Relationship between blood pressure and cross-sectional area of vessels
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 5,000 4,000 3,000 Area (c2) 2,000 1,000 120 100 80 Pressure (mmHg) 60 40 20 Capillaries Arterioles Venules Arteries Veins Aorta Vena cava
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Blood Pressure Regulation
Kidneys can control blood volume and thus stroke volume. The sympathoadrenal system stimulates vasoconstriction of arterioles (raising total peripheral resistance) and increased cardiac output.
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Baroreceptor Reflex Activated by changes in blood pressure detected by baroreceptors (stretch receptors) in the aortic arch and carotid sinuses Increased blood pressure stretches these receptors, increasing action potentials to the vasomotor and cardiac control centers in the medulla. Most sensitive to drops in blood pressure The vasomotor center controls vasodilation and constriction. The cardiac center controls heart rate.
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Effect of Blood Pressure on the Baroreceptor Response
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 180 160 140 120 Action potentials Mean arterial pressure (mmHg) 100 80 60 40 Resting potential Time
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Structures involved in the Baroreceptor Reflex
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sensory neuron Cerebrum Sympathetic neuron Carotid sinus Parasympathetic neuron Common carotid artery Sensory fibers Arch of aorta Hypothalamus Medulla oblongata Parasympathetic vagus nerve SA node AV node Spinal cord Sympathetic cardiac nerve Sympathetic chain
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Baroreceptor Reflex, cont
Fall in blood pressure = Increased sympathetic and decreased parasympathetic activity, resulting in increased heart rate and total peripheral resistance Rise in BP has the opposite effects. Good for quick beat-by-beat regulation like going from lying down to standing
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Baroreceptor Reflex Going from laying to standing position Venous
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Going from laying to standing position Venous return End-diastolic volume Stroke volume Cardiac output Stimuli Blood pressure Sensor Baroreceptors Integrating center Effector Sensory neurons Medulla oblongata Sympathetic Parasympathetic Vasoconstriction of arterioles Cardiac rate Total peripheral resistance Cardiac output Negative feedback response Blood pressure
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Atrial Stretch Reflexes
Activated by increased venous return to: Stimulate reflex tachycardia Inhibit ADH release; results in excretion of more urine Stimulate secretion of atrial natriuretic peptide; results in excretion of more salts and water in urine
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Blood Pressure Measurement
Measured in mmHg by an instrument called a sphygmomanometer. A blood pressure cuff produces turbulent flow of blood in the brachial artery, which can be heard using a stethoscope; called sounds of Korotkoff. The cuff is first inflated to beyond systolic blood pressure to pinch off an artery. As pressure is released, the first sound is heard at systole and a reading can be taken.
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Blood Pressure Measurement, cont
The last Korotkoff sound is heard when the pressure in the cuff reaches diastolic pressure and a second reading can be taken. The average blood pressure is 120/80.
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Blood Flow & Korotkoff Sounds
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. No sounds First Korotkoff sounds Sounds at every systole Last Korotkoff sounds Cuff pressure = 140 Cuff pressure = 120 Cuff pressure = 100 Cuff pressure = 80 Systolic pressure = 120 mmHg Diastolic pressure = 80 mmHg Blood pressure = 120/80
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Indirect, or Auscultatory, Method of Blood Pressure Measurement
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Cuff pressure No flow Turbulent flow Laminar flow 120 mmHg First sound Sound Last sound Artery silent Artery silent Systole Blood pressure Diastole 80 mmHg
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Five Phases of Blood Pressure Measurement
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Blood flows during systole only (turbulent flow) systole and diastole Blood flows during (laminar flow) No blood flows 14 mmHg 20 mmHg 130 120 5 mmHg 110 5 mmHg 100 90 80 70 1 2 3 4 5 Silence Snapping sounds Murmurs 60 Muffling Silence Thumping Cuff pressure (mmHg) Relative intensity of sounds
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Pulse Pressure “Taking the pulse” is a measure of heart rate. What the health professional feels is increased blood pressure in that artery at systole. The difference between blood pressure at systole and at diastole is the pulse pressure. If your blood pressure is 120/80, your pulse pressure is 40 mmHg. Pulse pressure is a reflection of stroke volume
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Mean Arterial Pressure
The average pressure in the arteries in one cardiac cycle is the mean arterial pressure. This is significant because it is the difference between mean arterial pressure and venous pressure that drives the blood into the capillaries. Calculated as: diastolic pressure + 1/3 pulse pressure
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VII. Hypertension, Shock, and Congestive Heart Failure
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Hypertension Hypertension is high blood pressure.
Incidence increases with age It can increase the risk of cardiac diseases, kidney diseases, and stroke. Hypertension can be classified as “essential” or “secondary.” Essential or primary hypertension is a result of complex and poorly understood processes Secondary hypertension is a symptom of another disease, such as kidney disease.
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Blood Pressure Classification in Adults
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Possible Causes of Secondary Hypertension
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Essential Hypertension
Most people fall in this category. The cause is difficult to determine and may involve any of the following: Increased salt intake coupled with decreased kidney filtering ability Increased sympathetic nerve activity, increasing heart rate Responses to paracrine regulators from the endothelium Increased total peripheral resistance
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Dangers of Hypertension
Vascular damage within organs, especially dangerous in the cerebral vessels and leading to stroke Ventricular overload to eject blood due to abnormal hypertrophy, leading to arrhythmias and cardiac arrest Contributes to the development of atherosclerosis
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Treatments for Hypertension
Lifestyle modification: limit salt intake; limit smoking and drinking; lose weight; exercise K+ (and possibly calcium) supplements Diuretics to increase urine formation Beta blockers to decrease cardiac rate ACE inhibitors to block angiotensin II production
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Mechanisms of Action of Selected Antihypertensive Drugs
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Circulatory Shock Occurs when there is inadequate blood flow to match oxygen usage in the tissues Symptoms result from inadequate blood flow and how our circulatory system changes to compensate. Sometimes shock leads to death.
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Signs of Shock
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Cardiovascular Reflexes to Compensate for Circulatory Shock
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Hypovolemic Shock Due to low blood volume from an injury, dehydration, or burns Characterized by decreased cardiac output and blood pressure Blood is diverted to the heart and brain at the expense of other organs. Compensation includes baroreceptor reflex, which lowers blood pressure, raises heart rate, raises peripheral resistance, and produces cold, clammy skin and low urine output.
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Septic Shock Dangerously low blood pressure (hypotension) due to an infection (sepsis) Bacterial toxins (endotoxins) induce NO production, causing widespread vasodilation. Mortality rate is high (50−70%).
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Other Causes of Circulatory Shock
Severe allergic reactions can cause anaphylactic shock due to production of histamine and resulting vasodilation. Spinal cord injury or anesthesis can cause neurogenic shock due to loss of sympathetic stimulation. Cardiac failure can cause cardiogenic shock due to significant myocardial loss.
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Congestive Heart Failure
Occurs when cardiac output is not sufficient to maintain blood flow required by the body Caused by myocardial infarction, congenital defects, hypertension, aortic valve stenosis, or disturbances in electrolyte levels (K+ and Ca2+) Similar to hypovolemic shock in symptoms and response
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Types of congestive heart failure
Left-side failure – raises left atrial pressure and produces pulmonary congestion and edema causing shortness of breath Right-side failure – raises right atrial pressure and produces systemic congestion and edema
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