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Chapter 14

Chapter 14. Cardiac Output, Blood Flow, and Blood Pressure. 14-1. Chapter 14 Outline Cardiac Output Blood & Body Fluid Volumes Factors Affecting Blood Flow Blood Pressure Hypertension Circulatory Shock. 14-2. Cardiac Output . 14-3. Cardiac Output (CO).

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Chapter 14

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  1. Chapter 14 Cardiac Output, Blood Flow, and Blood Pressure 14-1

  2. Chapter 14 Outline • Cardiac Output • Blood & Body Fluid Volumes • Factors Affecting Blood Flow • Blood Pressure • Hypertension • Circulatory Shock 14-2

  3. Cardiac Output 14-3

  4. Cardiac Output (CO) • Is volume of blood pumped/min by each ventricle • Heart Rate (HR) = 70 beats/min • Stroke volume (SV) = blood pumped/beat by each ventricle • Average is 70-80 ml/beat • CO = SV x HR • Total blood volume is about 5.5L 14-4

  5. Regulation of Cardiac Rate • Without neuronal influences, SA node will drive heart at rate of its spontaneous activity • Normally Symp & Parasymp activity influence HR (chronotropic effect) • Mechanisms that affect HR: chronotropic effect • Positive increases; negative decreases • Autonomic innervation of SA node is main controller of HR • Symp & Parasymp nerve fibers modify rate of spontaneous depolarization 14-5

  6. Regulation of Cardiac Rate continued Fig 14.1 • NE & Epi stimulate opening of pacemaker HCN channels • This depolarizes SA faster, increasing HR • ACh promotes opening of K+ channels • The resultant K+ outflow counters Na+ influx, slows depolarization & decreasing HR 14-6

  7. Regulation of Cardiac Rate continued • Vagus nerve: • Decrease activity: increases heart rate • Increased activity: slows heart • Cardiac control center of medulla coordinates activity of autonomic innervation • Sympathetic endings in atria & ventricles can stimulate increased strength of contraction 14-7

  8. 14-8

  9. Stroke Volume • Is determined by 3 variables: • End diastolic volume (EDV) = volume of blood in ventricles at end of diastole • Total peripheral resistance (TPR) = impedance to blood flow in arteries • Contractility = strength of ventricular contraction 14-9

  10. Regulation of Stroke Volume • EDV is workload (preload) on heart prior to contraction • SV is directly proportional to preload & contractility • Strength of contraction varies directly with EDV • Total peripheral resistance = afterload which impedes ejection from ventricle • SV is inversely proportional to TPR • Ejection fraction is SV/ EDV (~80ml/130ml=62%) • Normally is 60%; useful clinical diagnostic tool 14-10

  11. Frank-Starling Law of the Heart • States that strength of ventricular contraction varies directly with EDV • Is an intrinsicproperty of myocardium • As EDV increases, myocardium is stretched more, causing greater contraction & SV Fig 14.2 14-11

  12. Frank-Starling Law of the Heartcontinued • (a) is state of myocardial sarcomeres just before filling • Actins overlap, actin-myosin interactions are reduced & contraction would be weak • In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed Fig 14.3 14-12

  13. At any given EDV, contraction depends upon level of sympathoadrenal activity • NE & Epi produce an increase in HR & contraction (positive inotropic effect) • Due to increased Ca2+ in sarcomeres Fig 14.4 14-13

  14. Extrinsic Control of Contractility • Parasympathetic stimulation • Negative chronotropic effect • Through innervation of the SA node and myocardial cell • Slower heart rate means increased EDV • Increases SV through Frank-Starling law

  15. Fig 14.5 14-14

  16. Venous Return • Is return of blood to heart via veins • Controls EDV & thus SV & CO • Dependent on: • Blood volume & venous pressure • Vasoconstriction caused by Symp • Skeletal muscle pumps • Pressure drop during inhalation Fig 14.7 14-15

  17. Venous Return continued • Veins hold most of blood in body (70%) & are thus called capacitance vessels • Have thin walls & stretch easily to accommodate more blood without increased pressure (=higher compliance) • Have only 0-10 mm Hg pressure Fig 14.6 14-16

  18. Blood & Body Fluid Volumes 14-17

  19. Blood Volume • Constitutes small fraction of total body fluid • 2/3 of body H20 is inside cells (intracellular compartment) • 1/3 total body H20 is in extracellular compartment • 80% of this is interstitial fluid; 20% is blood plasma Fig 14.8 14-18

  20. Exchange of Fluid between Capillaries & Tissues • Distribution of ECF between blood & interstitial compartments is in state of dynamic equilibrium • Movement out of capillaries is driven by hydrostatic pressure exerted against capillary wall • Promotes formation of tissue fluid • Net filtration pressure= hydrostatic pressure in capillary (17-37 mm Hg) - hydrostatic pressure of ECF (1 mm Hg) 14-19

  21. Exchange of Fluid between Capillaries & Tissues • Movement also affected by colloid osmotic pressure • = osmotic pressure exerted by proteins in fluid • Difference between osmotic pressures in & outside of capillaries (oncotic pressure) affects fluid movement • Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure = 0 mm Hg 14-20

  22. Overall Fluid Movement • Is determined by net filtration pressure & forces opposing it (Starling forces) • Pc + Pi (fluid out) - Pi + Pp (fluid in) • Pc = Hydrostatic pressure in capillary • Pi = Colloid osmotic pressure of interstitial fluid • Pi = Hydrostatic pressure in interstitial fluid • Pp = Colloid osmotic pressure of blood plasma 14-21

  23. Fig 14.9 14-22

  24. Edema • Normally filtration, osmotic reuptake, & lymphatic drainage maintain proper ECF levels • Edema is excessive accumulation of ECF resulting from: • High blood pressure • Venous obstruction • Leakage of plasma proteins into ECF • Myxedema (excess production of glycoproteins in extracellular matrix) from hypothyroidism • Low plasma protein levels resulting from liver disease • Obstruction of lymphatic drainage 14-23

  25. Regulation of Blood Volume by Kidney • Urine formation begins with filtration of plasma in glomerulus • Filtrate passes through & is modified by nephron • Volume of urine excreted can be varied by changes in reabsorption of filtrate • Adjusted according to needs of body by action of hormones 14-24

  26. ADH (vasopressin) • ADH released by Post Pit when osmoreceptors detect high osmolality • From excess salt intake or dehydration • Causes thirst • Stimulates H20 reabsorption from urine • ADH release inhibited by low osmolality Fig 14.11 14-25

  27. Aldosterone • Is steroid hormone secreted by adrenal cortex • Helps maintain blood volume & pressure through reabsorption & retention of salt & water • Release stimulated by salt deprivation, low blood volume, & pressure 14-26

  28. Renin-Angiotension-Aldosterone System • Decreased BP and flow (low blood volume) • Kidney secreted Renin (enzyme) • Juxaglomerular apparatus • Angiotensin I to AngiotensinII • By angiotensin-converting enzyme (ACE) • Angio II causes a number of effects all aimed at increasing blood pressure: • Vasoconstriction, aldosterone secretion, thirst 14-27

  29. Angiotensin II • Fig 14.12 shows when & how Angio II is produced, & its effects 14-28

  30. Atrial Natriuretic Peptide (ANP) • Expanded blood volume is detected by stretch receptors in left atrium & causes release of ANP • Inhibits aldosterone, promoting salt & water excretion to lower blood volume • Promotes vasodilation 14-29

  31. Factors Affecting Blood Flow 14-30

  32. Vascular Resistance to Blood Flow • Determines how much blood flows through a tissue or organ • Vasodilation decreases resistance, increases blood flow • Vasoconstriction does opposite 14-31

  33. 14-32

  34. Physical Laws Describing Blood Flow • Blood flows through vascular system when there is pressure difference (DP) at its two ends • Flow rate is directly proportional to difference • (DP = P1 - P2) Fig 14.13 14-33

  35. Physical Laws Describing Blood Flow • Flow rate is inversely proportional to resistance • Flow = DP/R • Resistance is directly proportional to length of vessel (L) & viscosity of blood () • Inversely proportional to 4th power of radius • So diameter of vessel is very important for resistance • Poiseuille's Law describes factors affecting blood flow • Blood flow =DPr4() L(8) 14-34

  36. Fig 14.14. Relationship between blood flow, radius & resistance 14-35

  37. Extrinsic Regulation of Blood Flow • Sympathoadrenal activation causes increased CO & resistance in periphery & viscera • Blood flow to skeletal muscles is increased • Because their arterioles dilate in response to Epi & their Symp fibers release ACh which also dilates their arterioles • Thus blood is shunted away from visceral & skin to muscles 14-36

  38. Extrinsic Regulation of Blood Flow continued • Parasympathetic effects are vasodilative • However, Parasymp only innervates digestive tract, genitalia, & salivary glands • Thus Parasymp is not as important as Symp • Angiotensin II & ADH (at high levels) cause general vasoconstriction of vascular smooth muscle • Which increases resistance & BP 14-37

  39. Paracrine Regulation of Blood Flow • Endothelium produces several paracrine regulators that promote relaxation: • Nitric oxide (NO), bradykinin, prostacyclin • NO is involved in setting resting “tone” of vessels • Levels are increased by Parasymp activity • Vasodilator drugs such as nitroglycerin or Viagra act thru NO • Endothelin 1 is vasoconstrictor produced by endothelium 14-38

  40. Intrinsic Regulation of Blood Flow (Autoregulation) • Maintains fairly constant blood flow despite BP variation • Myogenic control mechanisms occur in some tissues because vascular smooth muscle contracts when stretched & relaxes when not stretched • E.g. decreased arterial pressure causes cerebral vessels to dilate & vice versa 14-39

  41. Intrinsic Regulation of Blood Flow (Autoregulation) continued • Metabolic control mechanism matches blood flow to local tissue needs • Low O2 or pH or high CO2, adenosine, or K+ from high metabolism cause vasodilation which increases blood flow (= active hyperemia) 14-40

  42. Aerobic Requirements of the Heart • Heart (& brain) must receive adequate blood supply at all times • Heart is most aerobic tissue--each myocardial cell is within 10 m of capillary • Contains lots of mitochondria & aerobic enzymes • During systole coronary vessels are occluded • Heart gets around this by having lots of myoglobin • Myoglobin is an 02 storage molecule that releases 02 to heart during systole 14-41

  43. Regulation of Coronary Blood Flow • Blood flow to heart is affected by Symp activity • NE causes vasoconstriction; Epi causes vasodilation • Dilation accompanying exercise is due mostly to intrinsic regulation 14-42

  44. Regulation of Blood Flow Through Skeletal Muscles • At rest, flow through skeletal muscles is low because of tonic sympathetic activity • Flow through muscles is decreased during contraction because vessels are constricted 14-43

  45. Circulatory Changes During Exercise • At beginning of exercise, Symp activity causes vasodilation via Epi & local ACh release • Blood flow is shunted from periphery & visceral to active skeletal muscles • Blood flow to brain stays same • As exercise continues, intrinsic regulation is major vasodilator • Symp effects cause SV & CO to increase • HR & ejection fraction increases vascular resistance 14-44

  46. Fig 14.19 14-45

  47. Fig 14.20 14-46

  48. Cerebral Circulation • Gets about 15% of total resting CO • Held constant (750ml/min) over varying conditions • Because loss of consciousness occurs after few secs of interrupted flow • Is not normally influenced by sympathetic activity 14-47

  49. Cerebral Circulation • Is regulated almost exclusively by intrinsic mechanisms • When BP increases, cerebral arterioles constrict; when BP decreases, arterioles dilate (=myogenic regulation) • Arterioles dilate & constrict in response to changes in C02 levels • Arterioles are very sensitive to increases in local neural activity (=metabolic regulation) • Areas of brain with high metabolic activity receive most blood 14-48

  50. Fig 14.21 14-49

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