physiology 1 -blood

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physiology 1 -blood
2010-10-28 22:45:39
sgu physiology blood

blood pressure packet
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  1. blood pressure
    • generated by heart
    • ventricle contracts and pushes blood by force into adjacent artery
  2. Hydrostatic pressure
    • generated by static force
    • 1. stretching of elastic elements of a compartement filled w/ fluid
    • 2. weight of fluid - gravity - zero at top and highest force at the bottom
  3. blood pressure and hydrostatic pressure
    • physical forces of same quality
    • hydrostatic pressure can also be used for blood pressure
  4. highest blood pressure
  5. when would there be higher pressure than in the arteries
    stenosis of aortic valve would cause the heart to have a higher blood pressure than arteries
  6. arterial pressure is
    • left heart
    • systemic
    • 98 mm Hg
  7. pulmonary pressure is
    • right heart
    • to lungs
    • 13 mmHg
  8. hemodynamic
    effects the absolute highest pressure is found in the larger artieris connected to the aorta
  9. blood pressure in arteries
    • oscillates between max systolic and min diastolic pressure
    • oscillation dies out in arterioles and not found in caps and veins
  10. mean pressure
    • replacement of systolic/diastolic oscillations by a continuous pressure
    • decreases gradually between aorta and vena cava
  11. systolic pressure definition
    • max pressure in sytole
    • normal 120 mm Hg
  12. diastolic pressure definition
    • min pressure during diastole
    • 80 mm Hg
  13. mean pressure definition
    • average pressure over whole cardiac cycle (continuous pressure)
    • 100 mmHg
  14. pulse pressure definition
    systolic - diastolic pressure = pulse pressure
  15. arterial sclerosis
    • high systolic
    • low diastolic
  16. calculation of mean pressure
    diastolic + 1/3 pulse pressure
  17. perfusion pressure
    • difference in pressure between the inlet side and the outlet side
    • (through all types of vessel)
  18. perfusion pressure in organs
    aortic pressure - vena cava pressure
  19. perfusion pressure of caps
    pressure at its inlet - pressure at its outlet
  20. systemic circulation of perfusion pressure
    • aorta 98 mmHg - vena cava 5 mm Hg = 93 mmHg (perfusion pressure)
    • decrease in pressure when goes away from heart
  21. pulmonary circulation perfusion pressure
    • pulmonary a. 13 mmHg - pulmonary v. 5 mmHg = 8 mmHg perfusion pressure
    • decrease in pressure when goes away from heart

    (8mmHg = 104 mm H20)
  22. blood pressure eqilibriates
    • when there is no pumping arterial side and venous side blood pressure equilibriates
    • filling pressure slightly higher(7 mm Hg) than barometric pressure
  23. filling pressure at equilibrium
    filling pressure slightly higher(7 mm Hg) than barometric pressure
  24. restarting heart causes
    • arterial pressure to rise to 91 mmHg
    • venous pressure to decrease by 4 mm Hg
  25. higher arterial pressure at heart restarting b/c
    arteries have lots of elastic and muscle less in veins
  26. Compliance
    • proportion of increase in volume and related increase in pressure
    • change volume/change in pressure = compliance
    • same amount of blood in arteries and veins but veins are better distensible(increase in blood with a lower increase in pressure)
  27. volume of blood shifted from the venous side to the arterial side
    • small decrease in pressure at the venous side
    • larger increase at the arterial side
  28. compliance in veins
    • is much higher that arteries
    • veins cope better
  29. pressure reservoirs
    • arteries
    • accept high pressure during systole and hold it durning diastole
  30. Windkessel function
    arteries creates a continuous flow
  31. arteries
    "pressure vessels" of the circulatory system
  32. veins
    • Volume reserviors (75%)
    • receive and release large volumes with only minor changes in pressure
    • reservoir for adjusting to varying demands in blood volume (exercise, hyper and hypovolaemia)
    • "volume vessels"
  33. Starling Experiment
    • heart - can respond to changes in the external conditions
    • Afterload - increase resistance - left ventricle affected
    • Preload - increase blood flow - both sides of heart affected - increased output of heart
    • Conclusion - heart can change in seconds, both venticles independently able to compensate for deviations
  34. Conclusion of Starling Experiment
    heart can work w/o cardiovascular center, autonomic control and humoral control
  35. After load part of Starling experiment
    • increase resistance to blood flow by reducing diameter
    • left ventricle responds by increasing the blood pressure
    • blood flow return to almost initial value
  36. Preload part of the Starling experiment
    • increase blood flow into right atrium heart responds by increasing output
    • caused increase in filling and resistance - increased retention of blood in the left ventricle
    • increased the size of the ventricle
    • longer cardiac muscle fibers generate more force of contraction
    • increased force causes - left side increases pressure and maintain output
    • right side increases the output in order to match the increased input
  37. Preload
    • right preload - generated by returing blood to the atrium
    • left preload - generated by blood returning to left atrium
    • presure measured in the atrium
    • increase in preload = increase in stoke volume
  38. Problems with Preload
    heart can become overstretched if preload is to large for a long time and will lose strenght instead of gaining it
  39. Afterload
    • measure of workload of the heart generated by the peripheral tissues
    • pressure is measured in the arteries that are directly connected to the ventricles
    • aortic pressure - left afterload
    • pulmonary artery - right afterload
    • higher the afterload the higher the work on the heart(usually b/c of higher demand it tissues) ex. exercise
  40. Hypertension - Afterload problem
    • pathological condition - increase in afterload
    • arterioles are dominated by vasoconstriction hormones
    • causes increase in total peripheral resistance (TPR), then need to increase aortic pressure in order to overcome TPR
  41. Pulmonary ciculation
    • arterial pressure vs. hydrostatic pressure
    • Zone 1, 2, and 3
  42. Hydrostatic pressure
    determined by the height of the blood column copared to the level of the heart
  43. Zone 1
    • min pressure to open vessels agains opposeing barometric pressure
    • systolic pressure is lower than the required pressure
    • barometris pressure keeps vessles closed
    • no profusion (gas exchange)
    • no blood flow
  44. Zone 2
    • blood pressure exceeds the required hydrostatic pressure only during the systole
    • not during diastole
    • resting - only profused during the systole
    • intermittent blood flow
  45. Zone 3
    • both systolic pressure as well as diastolic pressure exceed required hydrostatic pressure
    • resting - is always perfused during systole and diastole
    • contiuous blood flow
  46. Exercise affects on the Zones
    • Zone 1 - gets smaller
    • Zone 2 - increases
    • Zone 3 - increases (full lung perfusion)
  47. Venous side of circulation
    • low pressure - need larger diameter for adequate blood flow
    • +5 to -5 mmHg
  48. Absolute pressure of veins
    • higher or lower than blood pressure b/c of gravity
    • blood below heart - weight of blood column adds to the blood pressure and increse the total pressure
    • blood above hear - decreases total pressure
  49. anatomy of vein
    • thinner muscular layer
    • less elastic
    • more flexible than arteries
    • easily adjust to varying blood volumes by changing shape
  50. volume vessels = veins
    • storage of blood
    • during exercise blood shifted to the arterial side from the venous side
  51. Skeletal muscle pump
    • when increase in demand of blood from rest muscle pumps are needed
    • valves on veins open towards the heart
    • muscle contractions puts pressure on the vein and blood is pushed out of the segment and towards the heart
    • distal valve closes and prevents flow in wrong direction
    • muscle relaxes - decrease in pressure and proximal valves close to prevent back flow, distal valve opens for filling
  52. shematic of skeletal muscle pump
    • muscle contracts - distal valve closes - proximal valve open - decrease in blood
    • muscle relaxes - proximal valve closes - distal valve open - increase in blood
  53. Respiratory pump Inspiration
    • intrathoracic pressure decreases and intraabdominal pressure increases blood sucked from abdomen to thorax
    • increased blood to lungs
  54. Respiratory Pump Expiration
    • venous valves prevent backflow
    • increased pressure forces the blood to flow towards the heart
    • blood pushed from lungs
  55. Central Venous pressure
    • pressure in the right atrium
    • controlled - output of the right ventricle, and blood volume returning from peripheral tissue
    • normal : 0...5 mmHg
    • min : -3...-5 mmHg
    • max : 20...30 mmHg (b/c of pathological conditions like heart failure)
  56. blood flow meets the needs of tissues
    • active tissues need more blood than resting tissue
    • microvessels monitor needs
    • blood flow is controlled by metabolism and nerves
  57. cardiac output is mainly controlled by local tissue flow
    heart responds and adjusts to the demands of tissues
  58. arterial pressure is controlled independently by either
    • local blood flow in tissues
    • or
    • control of the cardiac output
  59. controllable convection system
    • for tansport purposes to maintain an appropriate environment
    • nutrients, 02, co2, waste products, hormones, immological cells and proteins, water
  60. driving force
    • blood flow is the pressure difference between arteries and veins
    • pressure is potential energy
  61. Control and adjustment
    throguh increase or decrease of cardiac output and resistance of vessels to meet varying demands
  62. Arteries "pressure vessels"
    • respond to volume changes with steep pressure changes (LOW compliance)
    • mainly controled by arterioles - thick muscular wall and able to change diameter
    • Poiseuille's law
  63. Poiseuille's Law
    changes in diameter have a strong effect on the resistance and consequently on the flow of blood
  64. Veins "volume vessels"
    • volume reservoirs
    • at rest holds 2/3 of total blood volume
    • most of volume in small veins and venules
    • cope better
    • can handle increase and decrease in blood with minor effects on venous pressure
  65. diameter and velocity
    • diameter decreases on the arterial side = velocity decreases
    • increase number of vessels results in an increase in the total cross-sectional area
  66. lowest velocity
    • capillaries
    • for better exchange
  67. Stop and go flow
    very energy consuming
  68. Windkessel function
    • less energy consumption
    • circulatory system pressure and volume are stored during pumping stroke (systole)
    • aorta -high pressure, increase blood volume, increase pressure
    • used during refilling(diastole)
    • aortic blood pressure (diastole) - stored blood leaves the aorta and the large arteries again
    • Continuous flow
  69. Continuous flow
    is more energy efficient than stop and go flow
  70. Laminar flow
    • concentric layers of same velocity
    • smooth flow
    • low friction against walls b/c of low velocity of outer layers
    • less energy required
    • aorta, vena cava
  71. Turbulent flow
    • no layers, same velocity
    • chaotic movements in and along the vessels
    • high friction against the wall
    • more energy required
    • valves
  72. Bolus flow of capillaries
    • RBC become bell shaped to squeeze through vessels that have a smaller diameter than theirs
    • aggregate
    • move in single file(bolus flow) reducing viscosity of blood
    • flow resistance is reduced
    • turbulent flow of plasma facilitates metabloic exchanges w/ tissues
  73. Cardiac Output
    • heart never empties completely
    • volume of blood ejected per min by one ventricle
    • stroke volume times the number of strokes per minute = heart rate
    • stroke volume x heart rate = cardiac output
  74. heart rate varies
    • 75 - 150 beats/min man
    • 1000 beats/min humming bird
  75. Stroke volume
    • volume ejected by on ventricle during a systole
    • end-diastolic volume - end-systolic volume = stroke volume
  76. Stroke volume depends on
    • preload, after load, and contractility
    • 70 - 140 mL in man
  77. Cardiac reserve
    Cardiac output max / Cardiac output rest = cardiac reserve

    man (25L/min) / (5L/min) = 5
  78. Cardiac output at rest
    • man 5 L/min
    • cow 30 L/min
  79. Max Cardiac output
    man 25 L/min
  80. perfusion pressure
    • driving force of flow
    • independent on diameter of vessels
    • inlet pressure - outlet pressure = perfusion pressure (change in pressure)
  81. FLow
    • is determined by perfusion pressure and the resistance of a vessel
    • resistance depends on the diameter
  82. Ohm's Law
    • FLow = (change in pressure) / (resistance)
    • small tube, low flow = high resistance
    • large tube, high flow = low resistance
  83. Poiseuille's Law
    • resistance of a vessle is determined by
    • diameter
    • length
    • fluid viscosity
    • Radius- determines mainly the resistance of flow, only variable that changes
    • (8 x velocity x 1) / (pi x r^4) basically 1/r^4
  84. importance of raidus
    • radius resistance
    • 1 1/1
    • 2 1/16
    • 4 1/256
  85. arterioles
    • arterioles control the blood flow in tissues by adjusting their diameter
    • highest resistance
  86. Total Peripheral Pressure (TPR)
    • total resistance to blood flow of all vessels of the systemic circulation
    • (mean aortic pressure - vena cava pressure) / cardiac output = TPR

    (systemic perfusion pressure) / cardiac output = TPR

    mmHg / L min - units of TPR
  87. Determining factors of TPR
    • radius of vessels (power of 4)
    • number of vessels
    • length (minor influence)
    • blood velocity
  88. Ohm's Law
    • Flow=change pressure / resistance
    • same as
    • cardiac output = perfusion pressure / TPR
    • (perfusion pressure = arterial pressure - venouse pressure) neglect vena cava too low
    • Cardiac output = blood pressure / TPR
    • Blood Pressure = Cardiac output x TPR
  89. Perfusion pressure = mean aortic pressure = blood pressure
  90. Mean Aortic Pressure
    determined by only the cardiac output and the TPR
  91. Hermaticrit
    per cent of blood that is cells
  92. Higher hematocrite (PCV)
    • higher the friction between cells, plasma and wall
    • normal - 45%
    • anemia - <45% about 14
    • polycythemia - >45% about 65
  93. Friction
    • Determines the viscosity of blood
    • anemia - less friction
    • normal - 3
    • polycythermia - higher friction
  94. Anemia
    • decrease in resistance
    • faciciltates perfusion of tissure
    • low hermatocrit
    • Low viscosity
  95. Polycythemia
    • high hermatocrit
    • living in high altitude
    • dehydatration
    • impeding
    • hihg viscosity
    • might lead to cessation of flow in capillaries and cause blood clotting
  96. Friction determines viscosity
  97. small vessels the viscosity
    • is lower than in larger vessels
    • RBC in single file and not touching walls = less friction
  98. small vessels the viscosity
    • increases when velocity decreases
    • formation of larger aggregates
    • increase viscosity
    • can lead to blood clotting
  99. Ficks Law of diffusion
    • exchange between capillaries and ECF
    • CO2 diffuses 20 times better that O2 - b/c higher diffusion coeficient
    • rate of diffusion = (diffusion coeficient x area x change in ICF & ECF) / (change in Distance)
    • hypoxia and hypercapnia
    • lower molecular weight = higher permeability
  100. Hypoxia
    • deficiency in O2
    • more likely
    • less diffusion
  101. Hypercapnia
    • excess in CO2
    • less likely b/c high diffusion
  102. Permeability of Capillary Membranes
    • depends on molecular size
    • larger less permeability
    • impermeable - albumin and myoglobin
    • permeable - water and salt
  103. Permeability of Lung caps
    • high permeability
    • intersitial protein con almost same as in cap blood
    • fast diffusion can cause edema quickly with heart failure
  104. Permeability of Liver capillaries
    • high permeability
    • high rate of synthesis and decomposition of proteins
  105. Permeability of Brain capillaries
    • LOW
    • protection of brain from toxic substances
  106. Blood side filtration
    blood pressure filters fluid and solutes into intersititium
  107. Blood side resorption
    • Oncotic pressure
    • generated by blood proteins
    • resorption of fluid and solutes from the intersititium back to blood
  108. Intersititial Side filtration
    • hydrostatic pressure
    • push back into the blood
    • opposes blood pressure
  109. Intersititial side Resorption
    • Oncotic pressure
    • pulls from blood
    • opposes blood oncotic pressure
  110. Oncotic pressure
    • resorption into side it is on
    • only proteins of blood
  111. Net Pressure
    • sum of all 4 pressures
    • direction is determined by polarity ( + filtration, - resorption)
    • rate of transport is determined by its value
  112. Equation for net pressure
    (Pblood - Poncotic) - (Phydrostat - P oncotic) = net P
  113. Oncotic pressure = constant
  114. arterial side
    • filtration into interstitium b/c blood pressure is higher than oncotic
    • net pressure : 10 mmHg
    • net 1 to venous side to more filtration
  115. venous side
    • resorption b/c oncotic pressure is higher than blood pressure
    • Net pressure : - 9 mmHg
  116. Liters of blood in 24 hrs
    • ~7,000 liters a day
    • 5 Liters per min
    • 20 Liters to intersititium
  117. Starling Equation
    net pressure = hydrostatic pressure - oncotic pressure
  118. Starling - non lung
    • net pressure favors filtration into interstitium
    • net flow from caps into interstitium
    • net 1 mmHg on arterial side
  119. Starling - Lung
    • net pressure = hydrostatic pressure = oncotic pressure
    • net pressure 10 times higher then other tissuses
    • 10 mmHg
    • higher permeability to plasma proteins
    • protein concentration in ECF almost as high as in capillary blood
  120. Lymph system - net pressure
    causes a contiunuous flow of water, solutes and proteins from capillaries into the interstitium
  121. Lymph system - Accumulation
    in interstitium (water, solutes, and proteins) would be lethal w/in 24 hr
  122. Lymph system -
    maintains homeostasis by removing excess water, solutes and proteins from the interstitium
  123. return of lymph
    • through lymphatic vessels to the right ventricle
    • catchment areas(lymph nodes)
    • flows back to right atrium via ductus thoracicus or ductus lymphaticus dexter and joins venous blood
  124. pig lymph vessels
    • lymphocentrum lumbale
    • iliosacrale
    • inguinale profundum
  125. terminal lymph capillaries
    • cells are not connected, they overlap
    • causing valves between intersititium and lymph duct
    • fluid from interstitium is called lymph
    • valves direct the lymph toward the heart
  126. lymphatic vessels
    • passage of high molecular weight substances possible
    • valves prevent reverse flow and limit hydrostatic pressure
  127. lymph vessel in intestinal villus
  128. intrinsic pumping by lymph vessels
    • stretch of lymph vessels by fluid
    • contraction of smooth muscles
    • pressure up to 50 mmHg
  129. Extrinsic pumping by compression
    • contraction of muscles
    • movement of body parts
    • arterial pulsations
    • compression of tissues from outside
  130. Lymphatic capillar pump
    • movement of surrounding tissue enlarge and fill capillaries
    • capillary valves prevent reverse flow and dircet lymph
  131. Factors increaseing hydrostatic pressure in the ECF
    • increases cap blood pressure
    • decreases cap oncotic pressure (less into blood)
    • increased cap permeability
    • increased interstitial fluid protein
  132. Lymph prevents
    • accumulations of fluid in interstitium
    • to much fluid would increase the distance between cap and cells = less exchange
    • edema
  133. Lymph transport capacity
    • limited
    • values above 1 mmHg flow cant increase and is at max value
    • increase from -6 to 0 = 12 fold increase
    • increase from 0 to 1 = 7 fold increase
  134. Tissues and blood
    • has bility to control its own local blood flow in proportion to its needs
    • autoregulation can be superseded by central control
  135. Local tissue controls
    • perfusion is controlled by diameter of vessels
    • diameter of vessels controlled by - local effects, neural activity, and hormonal signals
  136. increase metabolic rate of tissue
    increase release of vasodilators (high O2 consumption)- increase concentration of vasodilators (decrease in concentration of O2) - arteriol constriction and resistance - increase in blood flow and number of open caps - increase in blood flow and surface area of caps w/ decrease in diffusion distance - concentration of vasodilators decreases - negative feed back
  137. Vasodilators
    • Potassium
    • CO2
    • Adenosine
  138. increase in metabloic rate
    • decrease in oxygen and nutrients
    • increase in metabloic wastes
  139. release of vasodilators
    • increases blood flow through dilation of arterioles
    • potassium
    • CO2
    • Adenosine
  140. Negative feedback
    • limits the increase in blood flow
    • increase in O2
    • decrease in concentration of vasodilators
    • to much blood arterioles close
  141. Intrinsic Control of Blood flow
    • from inside = tissue itself
    • critical tissue
    • brain, heart, working skeletal muscle
  142. Extrinsic control of blood flow
    • from outside
    • non-critical tissues
    • kidney, stomach, intestines, liver, resting skeletal muscle
  143. Hyperaemia
    excessive blood volume in a tissue
  144. Raynaud Phenomenon
    • episodic color changes of fingers and toes in response to cold and stress
    • vasospasm - white fingers
    • compensatory vasodilation - red areas
  145. active or functional hyperaemia
    • metabolism in tissue increases (exercise) cells produce more vasodilators (K, CO2, adenosine)
    • increased vasodilators - aterioles dilate, increase blood flow
    • vasodilation continues - removal of vasodilators by blood meets production of tissue cells, production and removal match, arterioles remain in opening stage, tissue has increased volume of blood
  146. Active hyperaemia
    • normal blood flow - supply in and demand match
    • metabolism increases - decrease in supply of O2 and relief of wastes
    • feedback on arterioles - causes dilation, increase blood flow, now supplied at higher level
    • increased profusion based on increase in metabolism
    • longer blood flow adjustment to meet metabolic tissue demands
  147. reactive Hyperaemia
    • blockage of blood flow - no supply and relief of cells stops
    • increase in waste and vasodilators increases
    • vasodilators have no effect b/c of the block
    • when block is removed blood perfuses the tissue through dilated arteries
    • vasodilators are washed away w. increased blood flow, arterioles constict
    • balance
  148. reactive hyperaemia
    • interruption of blood flow - cessation of O2 supply and relief of wastes
    • increase in vasodilators, blockage removed more blood flow through dilated arterioles, vasodilator level in interstitial fluid returns to normal and supply and relief levels are normal
    • increased perfusion caused by a decrease in blood flow
    • temporary increase of blood flow to cover the metabolic dept b/c of vasuclar occlusion
  149. After ischemia
    • blood flow usually returns to normal within minutes
    • shorter time w/ blood loss = resupply w/ less blood flow for a shorter length of time
    • longer time w/ blood loss = resupply w/ higher blood flow for a longer period
  150. response to sudden decrease in blood pressure
    • perfusion pressure decreases sharply
    • blood flow initially decreases too then returns to inital value in a short period of time
    • steep decrease in perfusion pressure causes steep decrease in blood flow
    • returns it almost to initial value
  151. response to sudden increase to blood pressure
    • perfusion pressure increases steeply
    • blood flow initially increases too, returns almost the initial value within a chort period of time
    • steep increase in perfusion causes initially an increase blood flow, deviation is compensated in seconds
  152. Autoregulation of the brain
    • wide range of perfusion pressue 60 - 190 mmHg
    • corresponding blood changes are very small
    • if perfusion pressure drops below 60 mmHg = critical level, bad
  153. Principles of autoregulation after a pressure increase
    • blood pressure increases (no change in metabolic rate)
    • blood flow increases
    • number of open capillaries increases
    • increase in O2
    • decrease in vasodilator concentration
    • increase in arteriolar vasoconstriction
    • increase in vascular resistance
    • negative feedback
  154. Principles of autoregulation after a pressure increase
    • metabolic control mechanism also accounts for autoregulation
    • increase or decrease of the cencentration of vasodilators in the EFC changes the vascular resistance and thus the blood flow
  155. Metabolic theory
    • metabolism of tissue controls its perfusion
    • slow but continuous
  156. Myogenic theory
    • increase of blood pressure streches the muscle fibers in the vascular wall
    • muscle fibers respond with contraction
    • responds faster
    • protects the capillaries from excessively high blood pressures
  157. limitaton to coronary blood flow
    • diastole - cardiac muscle is best supplied w/ nutrients (mostly from left ventricle), longer that systole
    • shorten diastole - increased heart rate, less supply, limits max achievable heart rate
  158. Acute changes of blood flow
    • compensated w/in a few seconds
    • some deviations remain
  159. Long-term regulation of blood flow
    • over a period of hours to weeks
    • more precise
  160. changes between 50 - 250 mmHg cause only a small change in blood flow
  161. Long term regulation through tissue vasculatity
    • Low pressure - increase in size and number of vessels
    • increase in metabloism has same effect as low pressure
    • high pressure - decrease in siz and number of vessels
  162. Reconstrustion of tissure vasculature
    • fast in young animals (days)
    • fast in cancerous tissue
    • slow in older tissure (months to years)
  163. angiogenesis
    development of blood vessels
  164. long term regulatio through angiogenesis
    • angiogenic factors
    • released from ischemic tissue
    • rapidly growing tissues
    • tissue with a high metabolic rate
    • 3 factors
    • Endothelia growth factor
    • Fibroblast growth factor
    • angiogenin
  165. vasoconstiction factors
    • Nor and Epi
    • Angiotensin
    • Antiduretic
  166. Norepi and Epi
    • vasoconstrictor
    • norepi more powerful
    • (epi can also dilate)
  167. Angiotensin
    • vasoconstrictor
    • one of the most powerfull
    • 1 microgram increase blood pressure more than 50 mmHg
    • Renin - from kidney, angiotensinogen (liver), angiotensin (lung), aldosteron (hypothalamus)
  168. Antidiuretic hormone ( vasopressin)
    • vasoconstrictor
    • most powerful
    • small quanitites released
    • pressure regulation, important to kidneys which then reabsorb water
    • stops urin production
  169. Vasodilators
    • Bradykinin
    • Histamine
    • Prostaglandin
  170. Bradykinin
    • vasodilator
    • arteriolar dilation and increase permability of capillaries
    • formed in tissue fluid
    • (kallikrein converts kallidin to bradykinin)
    • (constricts smooth muscle)
  171. Histamine
    • vasodilator
    • released in all tissues
    • (damage, inflammation, allergic reaction)
    • causes arteriolar dilation and increased capillary permeability
    • fluid leaks out = edema
  172. Prostaglandins
    • vasodilation
    • almost each tissue
    • some cause constriction, most dilation
    • importance in circulatory regulation not completely clear
  173. vasoconstriction Ions
    • Calcium
    • increase cause constriction
    • stimulation of smooth muscles (contraction)
    • stimulation = contraction of smooth muscle
  174. Vasodilation Ions
    • Potassium
    • Magnesium
    • Sodium
    • Hydrogen ions
    • Carbon dioxide
    • Dilation = inhibit smooth muscle contraction
  175. Potassium
    • increase causes vasodilation
    • results from ability to inhibit smooth m. contraction
  176. Magnesium
    • increase causes powerful vasodilation
    • inhibits smooth muscle generally
  177. sodium
    • increase causes mild vasodilation
    • results from ability to inhibit smooth m. contraction
    • (vasomotor in brain)
  178. Hydrogen ions, Carbon Dioxide
    • vasodilation
    • CO2 can cause constriction effect on vasomotor center
  179. Neural control of Circulation
    • normally little to do with adjustment of blood flow in individual tissue
    • blood flow is usually controlled locally
    • Controls global functions- redistributes blood flow, adjustment of cardiac output, reapid control of arterial blood pressure
  180. ANS
    cardiovascular centers in the medulla oblongata and formation reticularis
  181. Sympathetic nerve - effect on cardiovascular system
    • norepi
    • alpha 1 and 2 - all organs, arterioles, abdomenal organs and veins - vasoconstriction (inside cells)
    • Beta 1 - heart and cardiac muscle cells - increase activity
  182. Circulating Catecholamines
    • Epi and norepi
    • beta 2 - heart coronary arterioles and skeletal muscle arterioles - vasodilation
  183. Parasympathetic nerve
    • acetylcholine
    • M 2 - heart, SA, AV, atrial cells - decrease heart rate
    • M 3 - heart coronary arterioles - vasodilation
  184. Beta 1 blocker - nitroglycerine pills
    decrease heart activity b/c of high blood pressure
  185. Coronary arteries dilate
    b/c dont want them to constrict which would decrease blood to cardiac muscle
  186. Humoral beta 2 stimulation can overpower neural alpha 1 stimulation
    causes - vasodilation in coronary circulation and skeletal muscles
  187. Humoral stimulation
    • circulating epi and norepi
    • beta 2 receptors
    • vasodilation
  188. Neural Stimulation
    • norepi from sympathetic nerve
    • alpha 1 receptor
    • vasoconstriction
  189. 2 reflexes regulate blood pressure and blood volume
    • arterial baroreceptor reflex
    • atrial volume receptor reflex
  190. Arterial Baroreceptor Reflex
    • responds to pressure changes (by sensing stretch or distortion of wall of vessels)
    • location - carotid and aortic arch
    • nerves - carotid sinus (glossopharyng), aortic arch (vagus)
  191. Arterial Baroreceptor Reflex
    • decrease in mean aortic blood pressure
    • decrease in baroreceptor activity
    • cardiovascular center in medualla oblongata
    • increase sympathetic output - more Norepi
    • Arterioles (alpha receptors)....... Ventricles(beta1 receptors)................SA node (Beta 1)
    • increase vasoconstriction.......... increase force of contraction............... increase Ht rate
    • increase peripheral resistance.... increase CO.......................................increase CO
    • increase blood pressure
  192. Arterial Barorecptor reflex
    • decrease in mean aortic blood pressure
    • decrease in baroreceptor activity
    • cardiovascular center in medualla oblongata
    • Parasymp output - Acetyle
    • mescarinic receptor
    • SA node
    • increase heart rate
    • increase cardiac output
    • increase in blood pressure
  193. Atrial Volume Receptor Reflex
    • responds to volume changes (senses stretch of distortion of wall of an atrium)
    • location - walls of the left and right atria
    • nerve - vagus
    • (cant measure pressure)
  194. arterial baroreceptor reflex - blocking the pressure receptors
    • inhibiting reflex causes wide variations in arterial blood pressure
    • there is no long term adjustment
    • standing up quickly from a lying position causes a drop in the pressure b/c of a change in the distribution of blood
    • barorecptor responds immediately to change and returns blood pressure to its normal level
  195. Arterial barorecptor reflex
    • afferent fibers of para
    • receptors located in carotid arteries and aortic arch
    • responds to stretch of arterial wall (baro = pressure)
    • high speed of response
    • requency of AP is proportional to arterial blood pressure - low pressure = low frequency
    • slow adaptation to long term changes in blood pressure
  196. volume receptor reflex
    • decrease in blood volume
    • decrease in atrial stretch
    • decrease volume receptor activity
    • cardiovascular center in medulla oblongata
    • increase sym & decrease para
    • increase renin, increase in ADH, increase in thirst
    • increase Na resporption, increase water resportion, increase water intake
    • increase in blood volume
  197. short-term and long-term effects of atrial volume receptor reflex
    • immediate - use reserve venous volume in vessels = decrease in systemic volume (vasoconstriction, increase in cardiac activity) can use the 20L of fluid in ECF to supplement blood volume
    • Long term - secure resources and replace losses (thirst, reduced Na excretion, stop urin production)
  198. Atrial volume receptor reflex
    • afferent fibers of para
    • receptors located in right and left atrium
    • responds to stretch of atrial wall (more volume = more stretch)
    • high speed response
    • frequency of AP is proportional to the filling of the atria (low volume = low pressure = low frequency)
    • immediate adaptation via sym and para activity
    • long- term adjustment (kidneys)
  199. decrease in blood volume
    • shift from venous to arterial to maintain pressure
    • decrease in atrial pressure causes response from atrial volume receptor response
    • sever blood loss - systemic pressure cant be maintained arterial baroreceptors respond too
  200. defense reaction
    • activates sym
    • increase cardiac activity - increase in blood pressure, vasoconstriction, pale skin, dry mouth, mydriasis
    • hormones - ADH, angiotensin, corticotropin
    • central control - overpowers non-central control, baroreceptor reflex set to an elevated leve
  201. initiation of exercise
    • decrease in supply and relief cells by blood
    • dilation of arterioles in skeletal muscles
    • decrease in TPR
    • decrease in systemic blood pressure
    • decrease in baroreceptor activity
    • increase sym, decrease para
    • increase cardiac output (increase in CO, increase respiration and muscle pump)
  202. blood transport by muscle pump
    • contraction increases blood pressure in veins
    • proximal values open - blood pushed to heart
    • relation - closes proximal valves, distal open and fill
  203. blood transport by respiratory pump
    • inspiration - decrease in pressure, pull veins from abdomen, lungs expand and fill w/ blood
    • expiration - incease pressure and blood goes to heart
  204. limitations to exercise ability
    • heavy exercise - CO can increase 4-5 times resting level (RESERVE CAPACITY)
    • CO limits exercise
    • no limitation of respiratory system, or metabloism of skeletal muscles
    • heart failure - exercise intolerance
  205. Hypertension
    • long term increase in blood pressure for a give output
    • increase constriction of arterioles - increase in vascular resistance
    • heart is forced to generate higher pressure
    • occurs in pulmonary or sytemic circulation or both
  206. Primary hypertension
    • occurs w/o underlying reasons
    • frequent in humans (~95%)
    • rare in animals
  207. Secondary hypertension
    • b/c of another primary disease
    • Dog - renal failure and hyperadrenocorticism, angiotensin causes vasoconstriction and aldosterone via NaCl retention an increase in blood volume, causing increase in blood pressure
    • Cat - renal failure and hyperthyroidism, thyroxine enhaces the effects of epinephrine and nore, increases blood pressure
  208. local edema
    impressions remain after crushig the edema
  209. Puerperal Gaseous Edema
    • from clostridium novyi infection
    • anaerobic bacteria - produces toxins and gas, toxins cause edema (increase profusion of fluid)
  210. eyelid edema
    • bilateral edema - after long time in bed in horizontal position
    • insect bite
  211. Edema definition, Aetiology, Pathology
    • clinically noticilble excess of intersitial fluid
    • imbalance between filtration and resorption + lymph
    • increase cap hydrostatic pressure (out of caps)
    • decrease in plasma oncotic pressure (into caps)
    • lesion of capillary cell membrane
    • decrease of lymph flow
  212. Exchange in capillary bed
    • arterial - hydrostatic pressure > oncotic pressure
    • out of cap into interstitium, filtration

    • venous - oncotic pressure > hydrostatice pressure
    • into cap from interstitium, resorption
  213. normal dynamics of cpa bed
    • 20 L per day are filtered from plasma into EFC
    • 18 L return to plasma
    • 2 L (10%) return to the circulation by lymphatic system
  214. imbalance in filtration and resorption
    • increase in venous side
    • decrease plasma oncotic pressure (hypoproteinemia)
    • filtration exceeds resorption plus lymph flow = Edema
  215. 3 ways to limit edema
    • 1. filtration limited- increase interstitial hydrostatic pressure
    • 2. filtration reduced - decrease of interstitial oncotic pressure
    • 3. lymph flow promoted - increase of interstitial hydrostatic pressure
  216. increase venous pressure - edema
    • cardiac failure - left: lung(fluid filtered into alveoli and air spaces, cough of frothey fluid) right: abdomen
    • increase venous pressure
    • increase cap hydrosatice pressure
    • increase filtration
    • increase interstitial fluid volume (edema)
    • increase intersitial fluid pressure
    • increase lymph flow
    • decrease concentration on interstitial protein
  217. Hypoproteinaemia = edema
    • malnutrition - Kwashiorkor, humand ascites, fluid in abdomen dont get enough protein, protien holds water, no absorption, use own body protein
    • loss of proteins - nephrotic syndrome (glomerula permeable to proteins), sever burns (loss of through damaged capillaries) decrease in protein concentration of blood
    • decrease protein concentration
    • decrease blood oncotic pressure
    • increase filtration Net
    • increase interstitial fluid volume = edema
    • increase interstitial fluid pressure
    • increaser lymph flow
    • decrease intersitital protein concentration
  218. Hypoxia = edema
    • mountain sickness - limited O2 transport capacity, 8-24 hr after first arrival(>3,000m)
    • decrease O2
    • increase areriolar dilation in brain
    • increase cap blood pressure
    • increase filtration
    • increase intersitial fluid volume = edema
    • increase fluid pressure
    • increase lymph
    • decrease intersitial protein concentration
  219. Lymphatic obstruction = edema
    • lymphedema - tumor, location depends on tumor
    • parasites, disease - microfilaria(obstruct lymph vessels), elephantiasis, tuberculosis, pneumonia
    • lymphatic obstruction
    • decrease lymph flow
    • increase interstitial protein concetration
    • increase filtration
    • increase intersitial fluid volume = edema
    • increse interstitial fluid pressure
  220. Haemorrhage
    decrease - blood volume, central venous pressure, cardiac output, arterial pressure, haematocrit, nutrients, O2
  221. Haemorrhage - immediate control mechanism
    • goal - return arterial blood pressure Survival
    • Sym and para
    • baroreceptors
    • volume receptors
    • CNS ischemic mechanism
    • Chemoreceptors for O2
  222. Hemorrhage - intermediate control
    • Conservation
    • vasoconstriction - decrease in renal flow, renin, decrease in loss of NaCl, antiburetic released
    • vasodilation - stress relaxation mechanism, protect against too high blood pressure,
    • (caonstiction maybe to stong and cut off circulation to an area so that is why dilation is needed so that tissues done die from full constiction)
    • Capillary fluid shift - low cap hydrostatic pressure, fluid shift from interstitium to blood
  223. Hemorrhage - long term
    • restoration
    • renal body fluid controls
    • decrease in renal blood flow
    • renin release
    • thirse - baroreceptor reflex, atrial volume reflex, hypothalumus (1-2days) thirst
    • replacement of blood components - plasma proteins (liver, several days), blood cells (bone marrow, erythorpoetin) weeks
  224. effectivnesss of renin-angiotensin system
    • ex - blood pressure at 50 mmHg
    • pressure compensation in min
    • w/o angiotensin and renin - 60mmHg
    • w/ 83 mmHg
  225. Ciculatory shock
    generalized inadquacy of blood flow throughout the body to the extent that the tissues are damaged b/c of too little flow
  226. ciculatory shock clinical signs
    • vasoconstriction - cold limbs (exception : septic shock), pale skin
    • Hypoxia - cyanosis, (blue tonguem blue conjunctivae)
    • Low blood pressure - pulse thread like, oliguria (reduced urin formation)
    • Sypathetic activity - mydriasis (dilation of the pupil)
  227. Hypovolaemic shock
    external or internal bleeding
  228. tramatic shock
    burn, sever bruises - loss of plasma
  229. Dehydration shock
    • loss of body fluid
    • diarrhea, peritonitis
  230. anaphylatic shock
    allergic reaction - loss of plasma
  231. toxic shock
    • vasomotor paralysis - smooth m. of vessels
    • produced from bacteria
  232. Stage 1 : Non Progressive
    centralisation of blood circulation
    • depending on severity - full recovery w/o treatment
    • vasoconstriction by ANS, Catecholamines (nor and epi), hormones reduces blood supply to non-vital organs
    • heart - barorecptor reflex (lower AP b/c of lower aortic pressure)
    • kidney - renin...angiotensin
    • hypothalamus - ADH (vasopressin)
    • suprarenal gland - cateholamines
    • Increase in carbonic acid - decrease in pH = death of tissues
    • dogs - 40 % of blood loss
  233. Stage 2 : Progressive Stage
    Decentalization of blood circulation
    • depending on severity - will fully recover possible with treatment
    • nerval depression - O2 deficiency affects CNS : clouding of consciousness
    • Cardiac depression - decrease arterial pressure, decreases coronary cirulation
    • Vasomotor failure - O2 deficiency, nutrient deficiency, increase of metabolic wates in tissues : damage to cap membranes(arteriole smooth m. cant constrict), plasma shift to interstitium, decrease in blood volume, increase in viscosity, danger of thrombus
  234. Stage 3 : Irreversible Stage
    Decompensation of blood circulation
    • No return possible - regardless of treatment = eventual death
    • cardiac failure and failure of cardiovascular centers
    • too much tissue damage
    • too many destructive enzymes released into body fluids
    • too much acidosis has developed
    • even restoration of blood pressure in an irreverisble shock can't prevent death