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3120 cardiovascular system

Mary Nguyen English 175 cards

Cards in this deck (175)

  1. 12 advantages for parallel arrangements of blood vessels1. amt of blood flow to individual vascular beds can be controlled separately by dilating or constricting the artery supplying a vascular bed
    2. contribute to relatively low resistance to blood flow, in turn, lowering the pressure requirement for blood flow and dec the work load on the heart
  2. 2how much blood in human body + its distribution5 L.
    15% = heart + pulmonary circulation
    10% = arteries of systemic circulation
    5% = systemic capillaries
    70% = venous system
  3. 32 types of myocardial cells in heartcardiac contractile ells (muscle), specialized excitatory/conductive cells
  4. 4structure of cardiac musclefilaments interdigitate and slide along e/o during contraction (same as skeletal muscle)
    cardiac muscle cells in series and have intercalated discs where they meet
    cardiac muscle branches and recombines and each fiber is surrounded by personal membrane
  5. 5electrical resistance of intercalated disc1/400th of resistance thru membrane of cardiac muscle fiber
  6. 6specialized excitatory/conducting cellscontract v weakly
    can self excite themselves to generate action potential
    provide system for heart to generate impulses and transmission system for rapid conduction of impulses thruout the heart
  7. 7special excitatory cellsSA, AV node
  8. 8special conductive cellsbundle of His, purkinje fibers
  9. 9SA nodewhere each heartbeat originates, fastest self excitation rate , has a slow response AP (ventricular muscle has fast response AP)
  10. 10why does ventricular muscle have different AP (fast) than SA?because the different cells use different ion channels
  11. 11functional syncytiumcardiac muscle cells are so tightly bound that when now of these cells become excited, the AP spreads to all of them, from cell to cell throughout the interconnections
  12. 122 functional syncytiaatrial syncytium, ventricular syncytium
  13. 13atrioventricular ringsurrounds the valvular openings bw atria and ventricles, however, APs can be conducted from the atrial syncytium to the ventricular syncytium by a the AV node and bundle of his. the division allows the atria to contract a short time ahead of ventricular contraction.
  14. 142 major characteristics of SA node for self excitability1. greater Na and Ca permeability during diastole
    2. decreasing K permeability during diastole
  15. 15resting membrane potential of SA nodal cellsdoes not exist, SA node cells sit at -60 mV not -90 (which it is in ventricular fiber)... there is only pre potential (the slow drift of the membrane potential)
  16. 163 phases of SA node action potential1. slow depol: membrane potential slowly becomes more positive: inc perm: Na+, T Ca2+, and some slow L type Ca2+, dec perm: K+
    2. depol: when threshold reached, close: Na+ funny, T type calcium, rest of L type Ca2+ open --> go to +20
    3. repolarization: slow L-type Ca2+ begin to close and K+ begin to open. back to -60 mV.
  17. 17why does SA node AP cycle repeat?during the next tenths/sec after AP is over, progressively more and more K+ begin to close and now inward Na and Ca overpower the outward flux of K+ --> fire AP
  18. 18do voltage gated K+ channels contribute to only pre potential?no VG K+ contribute to both prepotential and repolarization. during prepotential, dec perm, during repolarization, begin to open
  19. 19how to alter rate of discharge of AP by the SA node1. change slope of prepotential (diastolic depolarization)
    2. change mp from -60 mV (the degree of diastolic hyperpol)
  20. 20interatrial myocardial bandconducts impulses from the SA node directly to the left atrium
  21. 21anterior, middle and posterior internodal pathwayconducts impulses from SA node to AV node made of ordinary myocardial cells and specialized conducting fibers
  22. 22electrocardiogramwhen cardiac impulse generated @ SA nod passes thru carious parts of the heart, the electrical currents spread to surrounding tissues and a small proportion spreads all the way to the surface of the body... the ECG is the sum of all the electrical events in the heart. signals are vectors b/w movement of charge have 3d direction and magnitude
  23. 23P wavedepol of atria
  24. 24QRS complexrapid depolarization of right and left ventricles, overshadows P a lot of the time
  25. 25T waverepolarization of ventricles
  26. 26U waverepolarization of papillary muscles in ventricles
  27. 27PR interval0.18 is the average
    get atrial depolarization and conduction thru AV node, decreases as heart rate increases
  28. 28QRS intervalventricular depolarization
  29. 29QT intervalventricular depolarization and ventricular repolarization
  30. 30SR interval (QT --> QRS)ventricular repolarization
  31. 31the greater the amplitude of the action potential and the greater the rate of change of potential during depolarization, the ...more rapid is the conduction down the fiber
  32. 325 phases (0-14) of ventricular myocardial cells0: depolarization
    1: rapid repolarization
    2: plateau phase
    3: restoration of resting potential
    4: resting potential
  33. 330: depolarizationcurrent from AP opens fast VG Na+ channels --> 20 mv
  34. 341: rapid repolarizationrapid repolarization: at positive membrane potentials VG Na+ closes. perm inc: Cl-, K+
  35. 352: plateau phaseAP opens slow L type Ca2+ channels, neutralizes outward K+ and MP is steady
  36. 363: restoration of resting potential:slow (Ltype) Ca2+ close. inward movement of Ca2+ dec while K+ cont to move outwards to get normal MP (-90 mV)
  37. 37cardiac similarities to skeletalAP on cardiac cell membrane spreads to T tubules
    depol of T tubules cause Ca2+ release from SR into sarcoplasm
  38. 38cardiac differences from skeletalextracellular Ca2+ enters sarcoplasm during depolarization of sarcolemma
    Ca2+ interacts w SR to cause further release of Ca2+ from SR (Ca2+ induced Ca2+ release)
  39. 39mechanisms inc free intracellular Ca2+ in sarcoplasm1. depolarization induced Ca2+ influx from ECF thru slow, L type Ca2+ channels (DHPR) in the SL
    2. Ca+ from DHPR can interact w myofibrils or with ryanodine channels on SR, which cause them to open
    3. the Ca2+ released from ryanodine can also interact w other ryanodine to open
    4. Na+ Ca2+ exchanger (NCX) since pump is bidirectional
  40. 40importance of extracellular Ca2+1. not only essential for triggering Ca2+ release from SR
    2. maintain adequate levels of Ca2+ intracellular stores over the long run (lose from NCX)
  41. 41mechanisms of cardiac muscle relaxation80%: pumped back into lumen of SR by Ca ATPase
    5%: Ca ATPase pumps out into ECF
    15%: Na Ca2+ exchanger is bidirectional and will pump Ca2+ out when transmembrane gradients fit
  42. 42why can't you summate twitches in cardiac musclesb/c when the refractory period ends, more than 75% of the contractile response is over -- muscle has relaxed considerably.
  43. 43what causes ARPinactivation of Na+ channels
  44. 44what causes RRPefflux of K+
  45. 45what can you infer from a cardiac cycle diagrampressure changes in aorta, left atria, and left ventricle
    volume changes in left ventricles
    ECG
    phonocardiogram
  46. 467 phases in one cardiac cycle:atrial systole, isometric ventricular contraction, ejection, protodiastole, isometric ventricular relaxation, rapid inflow, diastasis
  47. 47what does it mean when lines crossvalves opening or closing
  48. 48atriale systoleP wave = atrial depolarization
    AV valves open and blood fills the ventricles, last 30%, EDV
  49. 49isovolumetric contractionQRS = ventricular depolarization and the start of contraction
    ventricular pressure exceeds atrial and AV valves close
    w all valves closed, there is no change in volume ... ventricular P < aortic still
  50. 50ejection periodventricles continue to contract and eventually the ventricular pressure exceeds aortic pressure
    aortic valve opens and blood leaves ventricles --> T wave (ventricular repol)
  51. 51protodiastoleventricles begin to relax
    ventricular pressure falls slightly since not a lot of blood left
    aortic pressure is higher than ventricular since blood has inertia and is still moving into aorta
    very little blood leaves, and at the end have the ESV
  52. 52isovolumetric ventricular relaxationventricles cont to relax causing pressure to cont dropping and the blood in the aorta reverses direction and the aortic valve closes
    ventricular pressure still greater than atrial pressure so AV valves closed --> no change in ventricular volume
  53. 53rapid inflowwhen ventricular pressure drops below atrial, AV valves open and blood rapidly enters the ventricles
  54. 54diastasisventricles relaxed and ventricular pressure still lower than atrial pressure so the AV valves are still open ... blood cont to enter ventricles but much more slowly
  55. 55lubcaused by sudden block of reverse blodo flow due to closure of AV valves
  56. 56dubcaused by sudden block of reversing blood fow due to closure of the aortic and pulmonary valves at the end of ventricular systole
  57. 57cardiac outputthe amount of blood pumped by the left ventricle per minute,
  58. 58cardiac output eqnCO = HR * SV
  59. 59cardaic output normal5L/min (HR = 72, SV = 70 mL)
  60. 60which areas of body get high levels of blood flowbrain, liver, kidneys (despite these organs representing only a small fraction of the body mass)
  61. 61brainto provide nutrition and to prevent CO2 nd H concentrations from being to high in body fluids
  62. 62liverto support high level of metabolic activity
  63. 63kidneysfor adequate excretion so as to maintain a safe body fluid composition
  64. 64skeletal muscle blood flowin inactie state not very much blood flow... but as muscles become active, metabolic rate inc as much as 50xx
  65. 65factors affecting COlevel of fitness,
  66. 66in most cases, postganglionic neurons of the SNS is noreadrenergic except when they secrete Ach1. sweat glands, piloerector
    2. vasodilator nerves to blood vessels of skeletal muscle
    3. preganglionic fibers to adrenal medulla secretes Ach which binds to N2 nicotinic receptors
  67. 67parasympathetic nerves distributionin SA node and AV node
  68. 68sympathetic nerves distributiondistributed to SA and AV but stronger representation to the ventricular muscle
  69. 69negative chronotropic responsedec in heart rate
  70. 70negative inotropic effectdec in force of contraction
  71. 71effects of parasympthetic (vagal) stimulationparasympathetic stimulation to the heart causes a decrease in heart rate (neg chronotropic) owing to decrease in SA node rhythm and velocity of AP conduction thru the AV node
  72. 72mechanism of parasympathetic effectsAch binds to muscarinic receptors to
    1. open special K+ channels causing an inc in K+ permeability.
    2. slow the opening of L type Ca2+ channel
    3. may close funny Na+ channels
    --> hyperpolarization
  73. 73what happens if you electrically stimulate vagus nervemay stop impulse generation or completely block transmission --> ventricular escape
  74. 74ventricular escapepurkinje takes over, develops its own rhythm of 15-40 bpm. before this, the ventricles would have stopped beating for 4-10 s.
  75. 75effects of sympathetic stimulationinc HR (positive chronotropic) and force (positive ionotropic). maximal stimulation of SNS can triple heart rate and double force of contraction.
  76. 76mechanism of sympathetic effectsnorepinephrine, released by sympathetic nerve endings, interacts w B1 adrenergic receptors,
    1. increasing the opening of slow L-type Ca2+ channels and
    2. funny Na+ channels.
    --> inc perm leads to inc rate of depol of the pre potential to reach threshold faster --> inc HR
    in AV node, inc perm makes it easier for each fiber to excite the succeeding fiber thereby decreasing conduction time b/w aria and ventricles
    in contractile cells, the inc in calcium perm inc Ca2+ influx and consequently inc force of contraction
  77. 77HR < 100 bpmPNS activated
  78. 78HR = 100 bpmnothing activated
  79. 79HR > 100 bpmSNS activated
  80. 80max HRHR = 220 - age
  81. 81stroke volumeamt of blood ejected by the ventricle on each contraction
  82. 82stroke volume= EDV - ESV
  83. 83EDVvolume of blood in left ventricle at the end of ventricular diastole
  84. 84ESVvolume of blood in left ventricle at the end of ventricular systole (right after contraction)
  85. 85stroke volume affected byinput from autonomic nervous system, preload, afterload
  86. 86how SNS stimulation inc HR1. release NE onto B1 adrenergic --> inc entry thru L type Ca2+ channels --> inc SV
    2. release Ach onto adrenal glands --> release E and NE
  87. 87PNS stimulation dec HRsome evidence that vagus nerve does innervate left ventricle --> resulting release of Ach closes a small number of slow L type calcium channels, causing a small dec in Ca2+ entry --> dec force of ventricular contraction, which would decrease stroke volume
  88. 88preloadthe extent of filling of a entricle before contraction... EDV can be used to measure preload.
  89. 89how does inc EDV (preload) inc force of contraction of the ventriclewhen EDV inc, there is more blood in the ventricles and they stretch, increasing the length of the ventricular muscle fiber. the stretched muscle has greater contractile force than the unstretched muscle b/c the force is proportional to the nubmer of cross bridges formed b/w actin and myosin and
    1. in heart muscle, max overlaps b/w actin and myosin filaments occurs only whne the muscle is stretched to its maximum physiological dimensions
    2. more Ca2+ enters
    3. troponin has higher affinity for Ca2+ when sarcomeres are longer
  90. 90frank starling law of the heartthe greater the heart is filled during diastole, the greater will be the quantity of blood pumped during systole
  91. 91how does preload inc? (3 ways)muscle pump
    respiratory pump
    ANS
  92. 92muscle pump inc preload inc SVduring exercise, muscles contract and expand laterally and intramuscular pressure exerted on veins pushes blood thru one way valves....
  93. 93respiratory pump inc preload inc SVwhen physical activity is inc, the intrathoracic pressure in chest cavity drops.... so air is pulled into the lungs and also blood is pulled back to the right atrium, increasing venous return, increasing EDV, and increasing SV and CO
  94. 94ANS inc preload inc SVsympathetic activation of the smooth muscle in the walls of the veins increases venomotor tone, causing them to constrict slightly.... this inc central venous pressure and inc venous return to the heart to ultimately inc cardiac output
  95. 95effect of afterload on stroke volumeafterload is the resistance against which the ventricles pump blood (the ventricular wall stress during systole)
  96. 96afterload faced by left ventriclepressure in aorta during systole
  97. 97afterload faced by right ventriclepressure in the pulmonary artery during systole
  98. 98how does an increase in afterload (aortic) affect stroke volumeleft ventricle would have to generate more pressure in order to open the aortic valve. so isometric contraction phase lengthens and there is less time during ejection period to eject blood. However, the stroke volume will only decrease initially... eventually will return to normal due to frank starling (EDV will start to build up).
  99. 99veins known as thecollection vessels
  100. 100arteries known as thedistribution vessels
  101. 101pulmonary circulationblood vessels that carry blood to and from the lungs
  102. 102systemic circulationall the vessels that carry blood to and from the rest of the body
  103. 103arterioles known asresistance vessels
  104. 104resistancefall in pressure is directly proportional to the vascular resistance (most due to friction of blood w inside wall of vessel)
  105. 105why is it that by the time blood reaches the atrium the pressure appraoches 0b/c there is a small but significant amount of resistance in the venous side of the circulation
  106. 106what is avg TPR17 mmHg/min/L
    given CO = 5 L
    P gradient = 100 mmHg
  107. 107in contrast to the systemic circulation, the pulmonary circulation is ...a low pressure low resistance circuit
  108. 108pulse pressuredifference between systolic and diastolic pressures
  109. 1092 factors affecting pulse pressure1. SV
    2. Compliance
  110. 110compliancethe distensibility (stretchiness) of arterial system
    greater compliance = less rise in pressure b/c stretches to accommodate rushing in flow
  111. 111aorta compliancegreatest compliance in the arterial system due to more elastin than smoothmuscle+collagen --> dampening pulsatile output of the left ventricle, reducing pulse pressure -- becomes stiff in atherosclerotic conditions
  112. 112mean arterial pressurethe average pressure throughout the cardiac cycle... slightly less than half way b/w systolic and diastolic b/w systole is shorter
  113. 113MAP eqn= diastolic pressure + 1/3 pulse pressure
  114. 114total peripheral resistanceall the resistance encountered by the blood in the entire systemic circulation
  115. 115rate pressure producta way to measure the workload on the heart
  116. 116rate pressure product eqnRPP = systolic pressure * HR, estimates how hard the heart is working at any one time ....
    working hard: force of contraction and resulting systolic pressure is as high as HR
  117. 117flow thru a blood vessel depends on 2 factors:1. pressure gradient
    2. vascular resistance
  118. 118poiseuille's eqn assumptions:1. tube is straight rigid and cylindrical, unbranched constant radius
    2. low is steady (not pulsatile)
  119. 119resistance eqn1/r^4
  120. 120blood flow eqn relating to delta P and rQ = deltaP*r^4
  121. 1213 layers of blood vessels1. inner tunica intima
    2. tunica media
    3. tunica adventitia
  122. 122tunica adventitiaouter layer made of entirely connective tissue
  123. 123tunica mediahas circularly arranged elastic tissue and smooth muscle
  124. 124inner tunica intimaendothelial cells
  125. 125venuleall connective (adventitia)
  126. 126autoregulationthe process by which individual vascular beds maintain relatively constant blood flow when moderate changes occur in pressure
  127. 1272 explanations for autoregulationmyogenic theory, metabolic theory
  128. 128myogenic theoryaka the bayliss effect
    when blood pressure is inc in the blood vessels and the blood vessels distend, they react in constriction... stretching of muscle membrane opens a stretch activated ion channel
    the cells depol and results in Ca2+ entry and triggers muscle contraction resulting in vasoconstriction --> NO AP (the level of entered ca2+ affects the level of contraction proportionally)
  129. 129metabolic theoryaccording to this theory, uatoregulation may occur as a result of locally induced vasomotion due to the presence or absence of vasodilator metabolites
  130. 130VDMsa dec in oxygen
    H+
    CO2
    temperature
    K+
    lactic acid
    adenosine
  131. 131VDMs during exerciseinc metabolic activity of tissue leading to inc production of VDM
    vessels dilate
    inc blood flow to active tissue
  132. 132metabolic/active hyperemiainc blood flow due to inc in activity of tissue (DURING EXERCISE) which releases VDMs.... different from reactive hyperemia
  133. 133reactive hyperemiainc in BF resulting from a brief period of occlusion or ischaemia .... allows for the build up of VDMS and the depletion of oxygen.
  134. 134kidneys + adenosinein the kidneys, adenosine will constrict afferent arteriole which is what you want during exercise (dec blood flow to kidney -- d/n care about visceral)
  135. 135humoral regulationregulation by substances present in blood: vasoconstrictor, vasodilators
  136. 136vasoconstrictors1. E, NE
    2. angiotensin II
    3. vasopressin
    4. endothelin
  137. 137E, NEsecreted by adrenal medulla, exert vasoconstrictor effects by binding to alpha adrenergic receptors
  138. 138angiotensin IIformed in blood,
    potent vasoconstrictor
    also does: perihperal vasoconstriction to inc arterial p
    - inc synthesis and secretion of NE @ sympathetic nerve endings to inc arterial p
  139. 139vasopressinformed in hypothalamus,
    has vasocontrictor effects
    promote water reabsorption in renal collecting tubules, high conc of it appears in blood following hemorrhage and produces vasoconstriction
  140. 140endothelinvasoconstrictor
    present in endothelium of most blood vessel
    released by blood vessels such as crushing tissues
  141. 141vasodilator agents (5)epinephrine
    bradykinin
    nitric oxide
    prostaglandins
    atrial natriuretic factor
  142. 142epinephrinecauses mild vasodilation in skeletal and cardiac muscle and in the liver by binding to beta2 adrenergic receptors --> smooth muscle relax --> vasodilation
  143. 143bradykinin and histamineformed in blood and body fluids
    histmine is released by every damaged tissue (eosinophils and mast cells) --> have vasodilator effects
  144. 144nitric oxidereleased by endothelial cells
    causes relaxation of smooth muscle in walls of blood vessels
  145. 145prostaglandinsproduced locally by endothelial cells... causes relaxation of vascular smooth muscle to produce vasodilation
  146. 146atrial natriuretic factorproduced by atrial muscle cells ... is powerful vasodilator
    released when atrium is stretched
  147. 147MAP eqnCO * TPR
  148. 148in general, activation of the cholinergic system results in a ...decrease in arterial pressure
  149. 149in general, activation of adrenergic system results inincrease in arterial pressure
  150. 150how does cholinergic (parasymp) control decrease MAPstimulation of PNS fibers to heart --> Ach --> decrease HR and SV --> dec CO --> dec MAP
  151. 151how does cholinergic (symp) control decrease MAPcholinergic vasodilator fibers to peripheral tissues --> release Ach --> dilate vlood vessels dilate in skeletal muscles --> dec TPR --> dec MAP
  152. 152how does adrenergic (symp, heart) inc MAPstimulation of symp fibers to heart --> release NE --> inc HR and SV --> inc CO --> inc MAP
  153. 153how does adrenergic (medulla) inc MAPreelase Ach onto adrenal gland, --> secrete E and NE into circulation --> inc HR and SV --> inc CO --> inc MAP
  154. 154how does adrenergic (symp, peri) inc MAP?stimulation of vasoconstrictor fibers to perihperal blood vessels (abdominal viscera, skin, renal vasculature) --> NE released which acts on alpha adrenergic receptor receptors --> vasoconstriction --> inc TPR --> inc MAP
  155. 155NE bindsalpha adrenergic to cause vasoconstriction
  156. 156does norepeinpehrine directly cause vasodilation?no b/c they don't generally bind B2 receptors, in blood vessels cause vasodilation
  157. 157B1 receptors in heartinc HR
  158. 158constricting effect of norpeinpherine can be blocked by...presence of VDMs, which are produced
  159. 159what is the only way that the sympathetic adrenergic system cause vasodilationremove sympathetic activation
    the constricting effect of nroepinephrine is blocked by VDMs
  160. 160SNS bind (norepi) alpha receptorswill cause general vasoconstriction by binding to alpha receptors even in skeletal muscle, but this is blocked by vasodilation
  161. 161sympathetic stimulation will cause the release of...norep from post ganglionic sympathetic fibers and will cause the release of ach from symp cholinergic vasodilator fibers, both at the same time... but the effect of sympathetic chol vasodilators is weak so overall, get vasoconstriction
  162. 162mechanoreceptors2 mechanoreceptors: pressure baroreceptors, low pressure volume receptors
  163. 163baroreceptorshigh pressure receptors located in the aortic arch and carotid sinuses to monitor changes in BP and relay info to the cardiovascular center in the brain stem to adjust CO and TPR.
    when BP inc, the wall of aorta and carotid sinuses stretch, and the baroreceptors are mechanically stimulated by this stretching and will inc the freq of AP generation back to the cardiovascular center in the brain stem.
  164. 164atrial volume receptorslow pressure receptors found in the left and right atrium and at the junction bw the veins and atria of the heart
    detect the fullness of the circulation and are part of a group of receptors that help regulate blood volume
    1. when detect p drop, a signal is transmitted from the receptors to the hypothalamus, which inc the production of ADH
    2. low volume also stimulates sympathetic nerves which stimulate renin release from the juxtaglomerular cells of the afferent arteriole in the kidneys... renin leads to the activation of angiotensin II --> vasoconstricting agent that inc BP.
  165. 165baroreceptor reflexmechanism for maintaining mean arterial pressure
    provides negative feedback loop in which an elevated blood pressure reflexively causes HR, SV, and TPR to de back to normal
    and vice versa
  166. 166the cardiovascular center components1. solitary tract nucleus 2. vagal center 3. vasomotor center
  167. 167solitary tract nucleusthe main receiving station for afferent information from the baroreceptors, is linked by interneurons to the vagal nucelus
    and by inhibitory interneurons to the vasomotor center
    when the soltiary tract nucelus receives info about a change in arterial pressure, it sends appropriate signals to both the vagal nucleus and vasomotor center (syanpse w preganglionic noradrenergic fibers to heart and blood essels)... resulting changes in vagal outflow from the vagal nucelsu and sympathetic outflow from the vasomotor center help to restore normal arterial pressure
  168. 168right vagus nerve innervatesSA node
  169. 169left vagus nerve innervatesAV node
  170. 170cardiovascular response to emotional stress involves:1. inc activity of cholinergic fibers to muscle arterioles, causing their dilation
    2. inc activity of cholinergic fibers to sweat glands causing sweating and skin vasodilation
    3. inc activity of the preganglionic symp fibers to medulla --> secrete NE + E
    4. reduced activity of the vagal nerve and inc activity of the sympathetic postganglionic fibers (Nor) to heart, resulting in inc HR and contractility
    5. inc symp outflow to capacitance vessels
    6. inc symp outflow to renal and splanchnic resistance vessels
  171. 1713 regulation of circulation during exercise1. local
    2. mechanical
    3. nervous
  172. 1721. exercise, local effectsresistance vessels dilate in active muscles due to products of metabolism, products also block the effects of the postganglionic sympathetic vasoconstrictor nerves to muscle vessels
  173. 1732. exercise, mechanical effectsduring dynamic exercise the muscle pump returns blood from the lower limbs to the central circulation, inc EDV, SV, CO
  174. 1743. exercise, nervous effects1. sympathetic outflow from heart and systemic blodo essels is increased --> vagal outflow to the heart decreases and this causes tachcardia, inc cardiac contratility and constriction of resistance vessels in kidney and aplanchinic bed and of splanchinic cpacitance vesels... --> inc symp outflow due in part to central command from cerebral cottex and activation of receptors in contracting skeletal muscles. mechanoreceptors prevent fluctuations in arterial p from normal values.
    2. temp sensitive cells in hypothal activated and inhibit symp outflow to skin vessels and stimulate cholinergic fibers to sweat glands --> dilatation of skin vessels and issipation of heat
  175. 1754. exercise, humoralif exercise is severe, cholinergic fibers to adrenal medulla activated and secrete... --> inc HR and contractility and constriction of veins and renal resistance vessels

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Flashcards on 3120 cardiovascular system, created by Mary Nguyen on 25/01/2016.
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