Physiology Of Circulation


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Physiology Of Circulation

  1. 1. Cardiac Output, Blood Flow, and Blood Pressure 14-1
  2. 2. <ul><li>Outline </li></ul><ul><li>Cardiac Output </li></ul><ul><li>Blood & Body Fluid Volumes </li></ul><ul><li>Factors Affecting Blood Flow </li></ul><ul><li>Blood Pressure </li></ul><ul><li>Hypertension </li></ul><ul><li>Circulatory Shock </li></ul>14-2
  3. 3. Cardiac Output 14-3
  4. 4. <ul><li>Is volume of blood pumped/min by each ventricle </li></ul><ul><li>Heart Rate (HR) = 70 beats/min </li></ul><ul><li>Stroke volume ( SV ) = blood pumped/beat by each ventricle </li></ul><ul><ul><li>Average is 70-80 ml/beat </li></ul></ul><ul><li>CO = SV x HR </li></ul><ul><li>Total blood volume is about 5.5L </li></ul>Cardiac Output (CO) 14-4
  5. 5. Regulation of Cardiac Rate <ul><li>Without neuronal influences, SA node will drive heart at rate of its spontaneous activity </li></ul><ul><li>Normally Symp & Parasymp activity influence HR ( chronotropic effect ) </li></ul><ul><ul><li>Mechanisms that affect HR: chronotropic effect </li></ul></ul><ul><ul><ul><li>Positive increases; negative decreases </li></ul></ul></ul><ul><li>Autonomic innervation of SA node is main controller of HR </li></ul><ul><ul><li>Symp & Parasymp nerve fibers modify rate of spontaneous depolarization </li></ul></ul>14-5
  6. 6. Regulation of Cardiac Rate continued <ul><li>NE & Epi stimulate opening of pacemaker HCN channels </li></ul><ul><ul><li>This depolarizes SA faster, increasing HR </li></ul></ul><ul><li>ACh promotes opening of K + channels </li></ul><ul><ul><li>The resultant K+ outflow counters Na+ influx, slows depolarization & decreasing HR </li></ul></ul>Fig 14.1 14-6
  7. 7. <ul><li>Vagus nerve: </li></ul><ul><ul><li>Decrease activity : increases heart rate </li></ul></ul><ul><ul><li>Increased activity: slows heart </li></ul></ul><ul><li>Cardiac control center of medulla coordinates activity of autonomic innervation </li></ul><ul><li>Sympathetic endings in atria & ventricles can stimulate increased strength of contraction </li></ul>Regulation of Cardiac Rate continued 14-7
  8. 8. 14-8
  9. 9. Stroke Volume <ul><li>Is determined by 3 variables: </li></ul><ul><ul><li>End diastolic volume ( EDV ) = volume of blood in ventricles at end of diastole </li></ul></ul><ul><ul><li>Total peripheral resistance ( TPR ) = impedance to blood flow in arteries </li></ul></ul><ul><ul><li>Contractility = strength of ventricular contraction </li></ul></ul>14-9
  10. 10. <ul><li>EDV is workload ( preload ) on heart prior to contraction </li></ul><ul><ul><li>SV is directly proportional to preload & contractility </li></ul></ul><ul><li>Strength of contraction varies directly with EDV </li></ul><ul><li>Total peripheral resistance = afterload which impedes ejection from ventricle </li></ul><ul><ul><li>SV is inversely proportional to TPR </li></ul></ul><ul><li>Ejection fraction is SV/ EDV ( ~80ml/130ml=62%) </li></ul><ul><ul><li>Normally is 60%; useful clinical diagnostic tool </li></ul></ul>Regulation of Stroke Volume 14-10
  11. 11. Frank-Starling Law of the Heart <ul><li>States that strength of ventricular contraction varies directly with EDV </li></ul><ul><ul><li>Is an intrinsic property of myocardium </li></ul></ul><ul><ul><li>As EDV increases, myocardium is stretched more, causing greater contraction & SV </li></ul></ul>Fig 14.2 14-11
  12. 12. Frank-Starling Law of the Heart continued <ul><li>(a) is state of myocardial sarcomeres just before filling </li></ul><ul><ul><li>Actins overlap, actin-myosin interactions are reduced & contraction would be weak </li></ul></ul><ul><li>In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed </li></ul>Fig 14.3 14-12
  13. 13. <ul><li>At any given EDV, contraction depends upon level of sympathoadrenal activity </li></ul><ul><ul><li>NE & Epi produce an increase in HR & contraction ( positive inotropic effect ) </li></ul></ul><ul><ul><ul><li>Due to increased Ca 2+ in sarcomeres </li></ul></ul></ul>Fig 14.4 14-13
  14. 14. Extrinsic Control of Contractility <ul><li>Parasympathetic stimulation </li></ul><ul><ul><li>Negative chronotropic effect </li></ul></ul><ul><ul><ul><li>Through innervation of the SA node and myocardial cell </li></ul></ul></ul><ul><ul><li>Slower heart rate means increased EDV </li></ul></ul><ul><ul><ul><li>Increases SV through Frank-Starling law </li></ul></ul></ul>
  15. 15. Fig 14.5 14-14
  16. 16. Venous Return <ul><li>Is return of blood to heart via veins </li></ul><ul><li>Controls EDV & thus SV & CO </li></ul><ul><li>Dependent on: </li></ul><ul><ul><li>Blood volume & venous pressure </li></ul></ul><ul><ul><li>Vasoconstriction caused by Symp </li></ul></ul><ul><ul><li>Skeletal muscle pumps </li></ul></ul><ul><ul><li>Pressure drop during inhalation </li></ul></ul>Fig 14.7 14-15
  17. 17. Venous Return continued <ul><li>Veins hold most of blood in body (70%) & are thus called capacitance vessels </li></ul><ul><ul><li>Have thin walls & stretch easily to accommodate more blood without increased pressure (=higher compliance ) </li></ul></ul><ul><ul><ul><li>Have only 0- 10 mm Hg pressure </li></ul></ul></ul>Fig 14.6 14-16
  18. 18. Blood & Body Fluid Volumes 14-17
  19. 19. Blood Volume <ul><li>Constitutes small fraction of total body fluid </li></ul><ul><li>2/3 of body H 2 0 is inside cells ( intracellular compartment ) </li></ul><ul><li>1/3 total body H 2 0 is in extracellular compartment </li></ul><ul><ul><li>80% of this is interstitial fluid; 20% is blood plasma </li></ul></ul>Fig 14.8 14-18
  20. 20. Exchange of Fluid between Capillaries & Tissues <ul><li>Distribution of ECF between blood & interstitial compartments is in state of dynamic equilibrium </li></ul><ul><li>Movement out of capillaries is driven by hydrostatic pressure exerted against capillary wall </li></ul><ul><ul><li>Promotes formation of tissue fluid </li></ul></ul><ul><ul><li>Net filtration pressure = hydrostatic pressure in capillary (17-37 mm Hg) - hydrostatic pressure of ECF (1 mm Hg) </li></ul></ul>14-19
  21. 21. Exchange of Fluid between Capillaries & Tissues <ul><li>Movement also affected by colloid osmotic pressure </li></ul><ul><ul><li>= osmotic pressure exerted by proteins in fluid </li></ul></ul><ul><ul><li>Difference between osmotic pressures in & outside of capillaries ( oncotic pressure ) affects fluid movement </li></ul></ul><ul><ul><ul><li>Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure = 0 mm Hg </li></ul></ul></ul>14-20
  22. 22. Overall Fluid Movement <ul><li>Is determined by net filtration pressure & forces opposing it ( Starling forces ) </li></ul><ul><ul><li>P c +  i (fluid out) - P i +  p (fluid in) </li></ul></ul><ul><li>P c = Hydrostatic pressure in capillary </li></ul><ul><li> i = Colloid osmotic pressure of interstitial fluid </li></ul><ul><li>P i = Hydrostatic pressure in interstitial fluid </li></ul><ul><li> p = Colloid osmotic pressure of blood plasma </li></ul>14-21
  23. 23. Fig 14.9 14-22
  24. 24. Edema <ul><li>Normally filtration, osmotic reuptake, & lymphatic drainage maintain proper ECF levels </li></ul><ul><li>Edema is excessive accumulation of ECF resulting from: </li></ul><ul><ul><li>High blood pressure </li></ul></ul><ul><ul><li>Venous obstruction </li></ul></ul><ul><ul><li>Leakage of plasma proteins into ECF </li></ul></ul><ul><ul><li>Myxedema (excess production of glycoproteins in extracellular matrix) from hypothyroidism </li></ul></ul><ul><ul><li>Low plasma protein levels resulting from liver disease </li></ul></ul><ul><ul><li>Obstruction of lymphatic drainage </li></ul></ul>14-23
  25. 25. Regulation of Blood Volume by Kidney <ul><li>Urine formation begins with filtration of plasma in glomerulus </li></ul><ul><li>Filtrate passes through & is modified by nephron </li></ul><ul><li>Volume of urine excreted can be varied by changes in reabsorption of filtrate </li></ul><ul><ul><li>Adjusted according to needs of body by action of hormones </li></ul></ul>14-24
  26. 26. ADH (vasopressin) <ul><li>ADH released by Post Pit when osmoreceptors detect high osmolality </li></ul><ul><ul><li>From excess salt intake or dehydration </li></ul></ul><ul><ul><li>Causes thirst </li></ul></ul><ul><ul><li>Stimulates H 2 0 reabsorption from urine </li></ul></ul><ul><li>ADH release inhibited by low osmolality </li></ul>Fig 14.11 14-25
  27. 27. Aldosterone <ul><li>Is steroid hormone secreted by adrenal cortex </li></ul><ul><li>Helps maintain blood volume & pressure through reabsorption & retention of salt & water </li></ul><ul><li>Release stimulated by salt deprivation, low blood volume, & pressure </li></ul>14-26
  28. 28. Renin-Angiotension-Aldosterone System <ul><li>Decreased BP and flow (low blood volume) </li></ul><ul><li>Kidney secreted Renin (enzyme) </li></ul><ul><ul><li>Juxaglomerular apparatus </li></ul></ul><ul><li>Angiotensin I to AngiotensinII </li></ul><ul><ul><li>By angiotensin-converting enzyme (ACE) </li></ul></ul><ul><li>Angio II causes a number of effects all aimed at increasing blood pressure: </li></ul><ul><ul><ul><li>Vasoconstriction, aldosterone secretion, thirst </li></ul></ul></ul>14-27
  29. 29. <ul><li>Fig 14.12 shows when & how Angio II is produced, & its effects </li></ul>Angiotensin II 14-28
  30. 30. Atrial Natriuretic Peptide (ANP) <ul><li>Expanded blood volume is detected by stretch receptors in left atrium & causes release of ANP </li></ul><ul><ul><li>Inhibits aldosterone, promoting salt & water excretion to lower blood volume </li></ul></ul><ul><ul><li>Promotes vasodilation </li></ul></ul>14-29
  31. 31. Factors Affecting Blood Flow 14-30
  32. 32. Vascular Resistance to Blood Flow <ul><li>Determines how much blood flows through a tissue or organ </li></ul><ul><ul><li>Vasodilation decreases resistance, increases blood flow </li></ul></ul><ul><ul><li>Vasoconstriction does opposite </li></ul></ul>14-31
  33. 33. 14-32
  34. 34. Physical Laws Describing Blood Flow <ul><li>Blood flows through vascular system when there is pressure difference (  P ) at its two ends </li></ul><ul><ul><li>Flow rate is directly proportional to difference </li></ul></ul><ul><ul><li>(  P = P 1 - P 2 ) </li></ul></ul>Fig 14.13 14-33
  35. 35. Physical Laws Describing Blood Flow <ul><li>Flow rate is inversely proportional to resistance </li></ul><ul><ul><li>Flow =  P/R </li></ul></ul><ul><ul><li>Resistance is directly proportional to length of vessel (L) & viscosity of blood (  ) </li></ul></ul><ul><ul><ul><li>Inversely proportional to 4th power of radius </li></ul></ul></ul><ul><ul><ul><ul><li>So diameter of vessel is very important for resistance </li></ul></ul></ul></ul><ul><li>Poiseuille's Law describes factors affecting blood flow </li></ul><ul><ul><li>Blood flow =  Pr 4 (  ) </li></ul></ul><ul><ul><ul><ul><ul><li> L(8) </li></ul></ul></ul></ul></ul>14-34
  36. 36. Fig 14.14. Relationship between blood flow, radius & resistance 14-35
  37. 37. <ul><li>Sympathoadrenal activation causes increased CO & resistance in periphery & viscera </li></ul><ul><ul><li>Blood flow to skeletal muscles is increased </li></ul></ul><ul><ul><ul><li>Because their arterioles dilate in response to Epi & their Symp fibers release ACh which also dilates their arterioles </li></ul></ul></ul><ul><ul><ul><li>Thus blood is shunted away from visceral & skin to muscles </li></ul></ul></ul>Extrinsic Regulation of Blood Flow 14-36
  38. 38. <ul><li>Parasympathetic effects are vasodilative </li></ul><ul><ul><li>However, Parasymp only innervates digestive tract, genitalia, & salivary glands </li></ul></ul><ul><ul><li>Thus Parasymp is not as important as Symp </li></ul></ul><ul><li>Angiotensin II & ADH (at high levels) cause general vasoconstriction of vascular smooth muscle </li></ul><ul><ul><li>Which increases resistance & BP </li></ul></ul>Extrinsic Regulation of Blood Flow continued 14-37
  39. 39. Paracrine Regulation of Blood Flow <ul><li>Endothelium produces several paracrine regulators that promote relaxation: </li></ul><ul><ul><li>Nitric oxide ( NO ), bradykinin , prostacyclin </li></ul></ul><ul><ul><ul><li>NO is involved in setting resting “tone” of vessels </li></ul></ul></ul><ul><ul><ul><ul><li>Levels are increased by Parasymp activity </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Vasodilator drugs such as nitroglycerin or Viagra act thru NO </li></ul></ul></ul></ul><ul><li>Endothelin 1 is vasoconstrictor produced by endothelium </li></ul>14-38
  40. 40. Intrinsic Regulation of Blood Flow (Autoregulation) <ul><li>Maintains fairly constant blood flow despite BP variation </li></ul><ul><li>Myogenic control mechanisms occur in some tissues because vascular smooth muscle contracts when stretched & relaxes when not stretched </li></ul><ul><ul><li>E.g. decreased arterial pressure causes cerebral vessels to dilate & vice versa </li></ul></ul>14-39
  41. 41. <ul><li>Metabolic control mechanism matches blood flow to local tissue needs </li></ul><ul><li>Low O 2 or pH or high CO 2 , adenosine, or K + from high metabolism cause vasodilation which increases blood flow (= active hyperemia ) </li></ul>Intrinsic Regulation of Blood Flow (Autoregulation) continued 14-40
  42. 42. Aerobic Requirements of the Heart <ul><li>Heart (& brain) must receive adequate blood supply at all times </li></ul><ul><li>Heart is most aerobic tissue--each myocardial cell is within 10 m of capillary </li></ul><ul><ul><li>Contains lots of mitochondria & aerobic enzymes </li></ul></ul><ul><li>During systole coronary vessels are occluded </li></ul><ul><ul><li>Heart gets around this by having lots of myoglobin </li></ul></ul><ul><ul><ul><li>Myoglobin is an 0 2 storage molecule that releases 0 2 to heart during systole </li></ul></ul></ul>14-41
  43. 43. Regulation of Coronary Blood Flow <ul><li>Blood flow to heart is affected by Symp activity </li></ul><ul><ul><li>NE causes vasoconstriction; Epi causes vasodilation </li></ul></ul><ul><li>Dilation accompanying exercise is due mostly to intrinsic regulation </li></ul>14-42
  44. 44. Regulation of Blood Flow Through Skeletal Muscles <ul><li>At rest, flow through skeletal muscles is low because of tonic sympathetic activity </li></ul><ul><li>Flow through muscles is decreased during contraction because vessels are constricted </li></ul>14-43
  45. 45. Circulatory Changes During Exercise <ul><li>At beginning of exercise, Symp activity causes vasodilation via Epi & local ACh release </li></ul><ul><ul><li>Blood flow is shunted from periphery & visceral to active skeletal muscles </li></ul></ul><ul><ul><li>Blood flow to brain stays same </li></ul></ul><ul><li>As exercise continues, intrinsic regulation is major vasodilator </li></ul><ul><li>Symp effects cause SV & CO to increase </li></ul><ul><ul><li>HR & ejection fraction increases vascular resistance </li></ul></ul>14-44
  46. 46. Fig 14.19 14-45
  47. 47. Fig 14.20 14-46
  48. 48. Cerebral Circulation <ul><li>Gets about 15% of total resting CO </li></ul><ul><li>Held constant (750ml/min) over varying conditions </li></ul><ul><ul><li>Because loss of consciousness occurs after few secs of interrupted flow </li></ul></ul><ul><li>Is not normally influenced by sympathetic activity </li></ul>14-47
  49. 49. Cerebral Circulation <ul><li>Is regulated almost exclusively by intrinsic mechanisms </li></ul><ul><ul><li>When BP increases, cerebral arterioles constrict; when BP decreases, arterioles dilate (= myogenic regulation ) </li></ul></ul><ul><ul><li>Arterioles dilate & constrict in response to changes in C0 2 levels </li></ul></ul><ul><ul><li>Arterioles are very sensitive to increases in local neural activity (= metabolic regulation ) </li></ul></ul><ul><ul><ul><ul><li>Areas of brain with high metabolic activity receive most blood </li></ul></ul></ul></ul>14-48
  50. 50. Fig 14.21 14-49
  51. 51. Cutaneous Blood Flow <ul><li>Skin serves as a heat exchanger for thermoregulation </li></ul><ul><li>Skin blood flow is adjusted to keep deep-body at 37 o C </li></ul><ul><ul><li>By arterial dilation or constriction & activity of arteriovenous anastomoses which control blood flow through surface capillaries </li></ul></ul><ul><ul><ul><li>Symp activity closes surface beds during cold & fight-or-flight, & opens them in heat & exercise </li></ul></ul></ul>Fig 14.22 14-50
  52. 52. Blood Pressure 14-51
  53. 53. Blood Pressure (BP) <ul><li>Arterioles play role in blood distribution & control of BP </li></ul><ul><li>Blood flow to capillaries & BP is controlled by aperture of arterioles </li></ul><ul><li>Capillary BP is decreased because they are downstream of high resistance arterioles </li></ul>Fig 14.23 14-52
  54. 54. Blood Pressure (BP) <ul><li>Capillary BP is also low because of large total cross-sectional area </li></ul>Fig 14.24 14-53
  55. 55. Blood Pressure (BP) <ul><li>Is controlled mainly by HR , SV , & peripheral resistance </li></ul><ul><ul><li>An increase in any of these can result in increased BP </li></ul></ul><ul><li>Sympathoadrenal activity raises BP via arteriole vasoconstriction & by increased CO </li></ul><ul><li>Kidney plays role in BP by regulating blood volume & thus stroke volume </li></ul>14-54
  56. 56. Baroreceptor Reflex <ul><li>Is activated by changes in BP </li></ul><ul><ul><li>Which is detected by baroreceptors (stretch receptors) located in aortic arch & carotid sinuses </li></ul></ul><ul><ul><ul><li>Increase in BP causes walls of these regions to stretch, increasing frequency of APs </li></ul></ul></ul><ul><ul><ul><li>Baroreceptors send APs to vasomotor & cardiac control centers in medulla </li></ul></ul></ul><ul><li>Is most sensitive to decrease & sudden changes in BP </li></ul>14-55
  57. 57. Fig 14.26 14-56
  58. 58. Fig 14.27 14-57
  59. 59. Atrial Stretch Receptors <ul><li>Are activated by increased venous return & act to reduce BP </li></ul><ul><li>Stimulate reflex tachycardia (slow HR) </li></ul><ul><li>Inhibit ADH release & promote secretion of ANP </li></ul>14-58
  60. 60. Measurement of Blood Pressure <ul><li>Is via auscultation (to examine by listening) </li></ul><ul><li>No sound is heard during laminar flow (normal, quiet, smooth blood flow) </li></ul><ul><li>Korotkoff sounds can be heard when sphygmomanometer cuff pressure is greater than diastolic but lower than systolic pressure </li></ul><ul><ul><li>Cuff constricts artery creating turbulent flow & noise as blood passes constriction during systole & is blocked during diastole </li></ul></ul><ul><ul><li>1st Korotkoff sound is heard at pressure that blood is 1st able to pass thru cuff; last occurs when can no long hear systole because cuff pressure = diastolic pressure </li></ul></ul>14-59
  61. 61. Measurement of Blood Pressure continued <ul><li>Blood pressure cuff is inflated above systolic pressure, occluding artery </li></ul><ul><li>As cuff pressure is lowered, blood flows only when systolic pressure is above cuff pressure, producing Korotkoff sounds </li></ul><ul><li>Sounds are heard until cuff pressure equals diastolic pressure, causing sounds to disappear </li></ul>Fig 14.29 14-60
  62. 62. Fig 14.30 14-61
  63. 63. Pulse Pressure <ul><li>Pulse pressure = (systolic pressure) – (diastolic pressure) </li></ul><ul><li>Mean arterial pressure ( MAP ) represents average arterial pressure during cardiac cycle </li></ul><ul><ul><li>Has to be approximated because period of diastole is longer than period of systole </li></ul></ul><ul><ul><li>MAP = diastolic pressure + 1/3 pulse pressure </li></ul></ul>14-62
  64. 64. Hypertension 14-63
  65. 65. Hypertension <ul><li>Is blood pressure in excess of normal range for age & gender (> 140/90 mmHg) </li></ul><ul><li>Afflicts about 20 % of adults </li></ul><ul><li>Primary or essential hypertension is caused by complex & poorly understood processes </li></ul><ul><li>Secondary hypertension is caused by known disease processes </li></ul>14-64
  66. 66. Essential Hypertension <ul><li>Constitutes most of hypertensives </li></ul><ul><li>Increase in peripheral resistance is universal </li></ul><ul><li>CO & HR are elevated in many </li></ul><ul><li>Secretion of renin, Angio II, & aldosterone is variable </li></ul><ul><li>Sustained high stress (which increases Symp activity) & high salt intake act synergistically in development of hypertension </li></ul><ul><li>Prolonged high BP causes thickening of arterial walls, resulting in atherosclerosis </li></ul><ul><li>Kidneys appear to be unable to properly excrete Na + and H 2 0 </li></ul>14-65
  67. 67. Dangers of Hypertension <ul><li>Patients are often asymptomatic until substantial vascular damage occurs </li></ul><ul><ul><li>Contributes to atherosclerosis </li></ul></ul><ul><ul><li>Increases workload of the heart leading to ventricular hypertrophy & congestive heart failure </li></ul></ul><ul><ul><li>Often damages cerebral blood vessels leading to stroke </li></ul></ul><ul><ul><li>These are why it is called the &quot;silent killer&quot; </li></ul></ul>14-66
  68. 68. Treatment of Hypertension <ul><li>Often includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na + intake, increased K + intake </li></ul><ul><li>Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, & Angio II-receptor blockers </li></ul>14-67
  69. 69. Circulatory Shock 14-68
  70. 70. Circulatory Shock <ul><li>Occurs when there is inadequate blood flow to, &/or O 2 usage by, tissues </li></ul><ul><ul><li>Cardiovascular system undergoes compensatory changes </li></ul></ul><ul><ul><li>Sometimes shock becomes irreversible & death ensues </li></ul></ul>14-69
  71. 71. Hypovolemic Shock <ul><li>Is circulatory shock caused by low blood volume </li></ul><ul><ul><li>E.g. from hemorrhage, dehydration, or burns </li></ul></ul><ul><ul><li>Characterized by decreased CO & BP </li></ul></ul><ul><li>Compensatory responses include sympathoadrenal activation via baroreceptor reflex </li></ul><ul><ul><li>Results in low BP, rapid pulse, cold clammy skin, low urine output </li></ul></ul>14-70
  72. 72. <ul><li>Refers to dangerously low blood pressure resulting from sepsis (infection) </li></ul><ul><li>Mortality rate is high (50-70%) </li></ul><ul><li>Often occurs as a result of endotoxin release from bacteria </li></ul><ul><ul><li>Endotoxin induces NO production causing vasodilation & resultant low BP </li></ul></ul><ul><ul><li>Effective treatment includes drugs that inhibit production of NO </li></ul></ul>Septic Shock 14-71
  73. 73. Other Causes of Circulatory Shock <ul><li>Severe allergic reaction can cause a rapid fall in BP called anaphylactic shock </li></ul><ul><ul><li>Due to generalized release of histamine causing vasodilation </li></ul></ul><ul><li>Rapid fall in BP called neurogenic shock can result from decrease in Symp tone following spinal cord damage or anesthesia </li></ul><ul><li>Cardiogenic shock is common following cardiac failure resulting from infarction that causes significant myocardial loss </li></ul>14-72
  74. 74. Congestive Heart Failure <ul><li>Occurs when CO is insufficient to maintain blood flow required by body </li></ul><ul><li>Caused by MI (most common), congenital defects, hypertension, aortic valve stenosis, disturbances in electrolyte levels </li></ul><ul><li>Compensatory responses are similar to those of hypovolemic shock </li></ul><ul><li>Treated with digitalis, vasodilators, & diuretics </li></ul>14-73