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Lecture 10

BIO271 2014 Lecture 10.pdf
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Department
Biology
Course
BIO271H1
Professor
Christopher Garside
Semester
Winter

Description
  Lecture  10:  Circulatory  Systems  –  Regulation  of  Blood  Pressure  and  Flow;   Blood  Composition   Electrocardiogram  (ECG  or  EKG)   -­‐ NOT  an  action  potential   à  signal  measured  is  a  composite  of  all  electrical  activity  taking   place  in  the  heart   -­‐ Composite  recording  of  action  potentials  in  cardiac  muscle     • P  wave   o Atrial  depolarization   o No  P  wave?  SA  nodes  aren’t  working  (triggers  atrial  depolarization)   § SA  nodes  initiate  atrial  depolarization   § No  depolarization?  No  communication  of  myocytes  in  atrium  =  no  P   waves   • QRS  complex   o Ventricular  depolarization  +  atrial  repolarization   • T  wave   o Ventricular  repolarization     -­‐ Used  for  clinical  diagnosis  of  problems  with  conducting  system       Integration   • In  ventricular  diastole:   § Filling  of  the  atria   § AV  valves  are  opened,  semilunar  valves  are  clo sed   § Increase  in  volume  in  the  atria   § Pressure  in  atria  is  higher  than  the  ventricles  =  why  AV  valves  are  opened   • When  we  initiate  atrial  systole   § Pressure  increases  in  atrium   § Ventricular  contraction  (isovolumetric  contraction)  can  trigger  increase  in  pressure  in  ventricles  =  closing  of   AV  valves,  semilunar  valves  still  closed  (brief  period)   § All  valves  remain  closed  until  pressure  in  ventricles  are  higher   than  the  pressure  in  the  aorta   § Semilunar  valves  then  open  (only  in  left  side),  blood  is  ejected   into  aorta   § Pressure  continues  to  rise  thorough  ventricular  systole,  and   then  starts  to  fall     • After  ventricular  systole,  you’ll  have  isovolumetric  relaxation     § All  valves  are  closed  because  pressure  in  ventricles  >  pressure  in   atria,  and  Pressure  in  aorta  >  pressure  in  ventricles   § All  remain  closed  until  pressure  in  ventricle  drops  below  the   pressure  in  the  atrium   • Atrial  systole:  P  wave   • Isovolumetric  contraction:  QRS  wave   • Ventricular  relaxation:  T  wave   • Heart  functions  as  an  integrated  organ   § Electrical  and  mechanical  even ts  are  correlated     § Changes  in  pressure  and  volume  of  blood  in  chambers     § Blood  flow  through  chambers     § Heart  sounds  detected  through    stethoscope  are  due  to:     § Opening  and  closing  of  valves   • 1st  sound  =  AV  valves  shutting   • 2nd  sound  =  Aortic  valve  closing       Cardiac  Output   • Cardiac  output  (CO)   o Volume  of  blood  pumped  per  unit  time   o CO  =  HR  X  SV   § Heart  rate  X  stroke  volume  (amount  of  blood  ejected/heart  beat)   • Cardiac  output  can  be  modified  by  regulating  heart  rate  and/or  stroke  volume       o Heart  rate   -­‐ Modulated  by  autonom ic  nerves  and  adrenal  medulla   -­‐ Decreased  HR  (bradycardia)   -­‐ Increased  HR  (tachycardia)     • Stroke  volume   o Modulated  by  various  nervous,  hormonal,  and  physical  factors       Control  of  Stroke  Volume   Extrinsic  Control  (outside  the  muscle  cell)   -­‐ the  nervous  and  endocrine  system  can  also  cause  the  heart  to  contract  more  forcefully  and  consequently  pump   more  blood  with  each  beat  (increase  in  SV)   § in  addition  to  HR  –  fast  depolarization  (T-­‐type  Ca2+  channel  and  “funny”  channels)   -­‐ norepinephrine/epinephrine  released  from  the  ad renal   medullaà  binds  to  beta-­‐adrenergic  receptors  à  activates   G-­‐protein  à  activation  of  adenylyl  cyclase   à  ATP  à  cAMP   à  activation  of  PKA  à  phosphorylates  T-­‐type  Ca2+  and   funny  channels  à  increase  in  pacemaker  potential  à   increase  in  heart  rate   -­‐ PKA  also  phosphorylates  L-­‐type  Ca2+  channels   -­‐ PKA  also  phosphorylates  the  Ryanodine  receptor  (RyR)  a   calcium  channel  in  the  sarcoplasmic  reticulum  =  increasing   concentration  of  Ca2+  in  the  cytoplasm   -­‐ Also  need  to  get  rid  of  Ca2+  after  stimulating  a  strong   contraction   -­‐ So  PKA  also  phosphorylates  calcium  ATPase   à  calcium   back  out  of  cytoplasm  =  prepare  for  next  contraction   -­‐ PKA  phosphorylates  the  myosin  ATPase  =  increases  rate  of   cross-­‐bridge  cycling     -­‐ Stronger  and  more  rapid  contractions  =  both  stimulated  by   the  nervous  system   -­‐ These  effects  are  as  a  result  of  stimulation  from  the  sympathetic  nervous  system   -­‐ This  increases  stroke  volume  (the  amount  of  blood  pumped  into  the  heart/beat)   Intrinsic  control  (inside  the  muscle  cell)   -­‐ Frank-­‐Starling  effect  –  an  increase  in  EDV  results  in  a  more  forceful  contraction  of  the  ventricle  and  an  increase  in   SV   • Greater  EDV  =  stretch  of  cardiomyocytes   • Due  to  length-­‐tension  relationship  for  muscle   • Heart  automatically  compensates  for  increases  in  the  amount  of  blood  returning   to  the  heart  (autoregulation)   -­‐ Autoregulation  àif  more  blood  comes  back  to  the  heart  (increasing  EDV),   you  will  automatically  pump  more  forcefully  (no  external  signals)   -­‐ As  you  stretch  (increasing  EDV  =  increasing  stroke  volume)  =  optimal   crossover  =  increasing  myosin  heads   -­‐ Simple  increase  of  blood  in  heart  =  stretches  heart   muscle  =  increasing   efficiency  of  contraction  due  to  length-­‐tension  relationship   • This  autoregulation  relationship  is  also  effected  by  sympathetic  activity   -­‐ Increase  sympathetic  activity  =  shift  of  length -­‐tension  curve  up   -­‐ Any  give  EDV  +  any  sympathetic  activity  =  higher  stroke  volume     § More  blood  pumped  out   -­‐ decrease  sympathetic  activity  =  reduce  stroke  volume   • Intrinsic  regulation   • Skeletal  muscles  at  rest,  have  optimal  cross -­‐overs  between  actin  and  myosin   • Cardiomyocytes  are  not  at  the  optimal  cross-­‐over  between  actin  and  myosin   -­‐ Level  of  sympathetic  activity  shifts  the  position  of  the  cardiac  muscle  length -­‐tension   relationship   -­‐ Extrinsic  control  (sympathetic  activity)  on  top  of  the  Frank -­‐Starling  effect  (intrinsic  control)     Myosin  and  Actin  Review       -­‐ each  arrow  head  =  myosin  heads   -­‐ when  the  cell  is  too  short,  no  optimal  crossover   -­‐ myosin  thick  filaments  are  bashing  again  the  Z -­‐lines  of   the  sarcomere   -­‐ no  optimal  contraction   -­‐ as  you  increase  the  length  of  the  sarcomere  (s tretching  the   muscle),  you  will  have  optimal  crossover   -­‐ the  more  overlap  between  the  thick  and  thin  filaments  =  more   force   -­‐ maximal  force  at  optimal  sarcomere  length   -­‐ at  rest,  cardiomyocytes  are  NOT  at  their  optimal  crossover   -­‐ sarcomere  too  long  =  insufficient  overlap  between  myosin  and  actin  filaments     Regulation  of  Blood  Flow   -­‐ pressure  as  blood  leaves  heart  provide  the  primary  driving  force  for  flow  through  circulatory  system   -­‐ must  be  maintained  within  appropriate  limits   -­‐ to  supply  blood  to  all  tissues   -­‐ ability  to  regulate  distribution  to  tissues/organs   -­‐ flow  must  be  diverted  more  to  highly  aerobically  active  tissues   -­‐ arterioles  (small  arteries,  thinned  wall)  control  blood  distribution   -­‐ because  arterioles  are  arranged  in  parallel,  they  can  alter  blood  flow  to  various  organs   § rapidly  respond  à  just  muscles  surrounding  the  endothelium   § vasoconstriction  and  vasodilation   • changes  in  resistance  alter  flow   • constrict  =  increase  in  resistance,  decrease  flow   -­‐ control  of  vasoconstriction  and  vasodilation  (regulation  of  the  diameter  or  radius  of  the  arterioles)     1) autoregulation   • direct  response  of  the  arteriolar  smooth  muscle   • stretch  sensitive  smooth  muscle  cells  contract  when  blood  pressure  rises   2) intrinsic  (local)  factors   • metabolic  state  of  the  tissue   • most  important   3) extrinsic  factors   • nervous  and  endocrine  systems     Myogenic  Autoregulation   -­‐ some  smooth  muscle  cells  in  arterioles  are  sensitive  to  stretch  and  contract  (to  control  flow)  when  blood  pressure   increases   -­‐ act  as  negative  feedback  loop   -­‐ keeps  flow  constant;  prevents  excessive  flow  o f  blood  into  tissue   -­‐ metabolic  activity  must  override  myogenic  control     Metabolic  Activity  of  Tissues   –  Intrinsic   -­‐ intrinsic  control  due  to  metabolic  activity  of  the  cells  itself   -­‐ if  you  have  increased  metabolic  rate  of  the  tissues  (ex.  Muscles)  =  decrease  pa rtial   pressure  of  O2,  increase  the  partial  pressure  of  CO2  =  increase  waste  product  (H+)  =   activates  arteriole  smooth  muscles  to  vasodilate  =  decreasing  resistance  =  increase   blood  flow  =  offsetting  low  PO2  and  high  PCO2  =  negative  feedback  leads  to  increa se  in   O2  and  decrease  in  CO2  and  H+     -­‐ smooth  muscle  cells  in  arterioles  are  sensitive  to  conditions  of  extracellular  fluid   -­‐ levels  of  metabolites  alter  vasoconstriction/vasodilation   § O2,  CO2,  H+   -­‐ blood  flow  matched  to  metabolic  requirements   -­‐ paracrine   -­‐ e.g.  NO,  adenosine  à  vasodilators  released  to  active  muscle  tissue     Extrinsic:  Neural  and  Endocrine  Control  of  Flow   -­‐ Sympathetic  stimulation  causes  arteriolar  vasoconstriction       o Norepinephrine  from  sympathetic  nerves   o Sympathetic  nervous  system  is  always  releasing  som e  NE,  always  causing  some  constriction   -­‐ Intrinsic  factors  override  in  active  tissues   -­‐ Decreased  sympathetic  vasomotor  tone  causes  vasodilation   -­‐ Extrinsic  (nervous  and  endocrine)  and  Intrinsic  (paracrine  signals  related  to  metabolic  activity)  work  together  to   influence  arteriolar  diameter  and  blood  flow.   -­‐ Other  hormones  affect  vascular  smooth  muscle   o Vasopressin  (ADH)  from  the  posterior  pituitary  causes  generalized  vasoconstriction   § Antidiuretic  –  retains  water  à  increases  blood  pressure     o Angiotensin  II  produced  in  response  to  decreased  blood  pressure  causes  generalized  vasoconstriction     § Kidney  is  also  important!   o Atrial  natriuretic  peptide  (ANP)   produced  in  response  to  increased  blood   pressure  promotes  generalized  vasodilation       Pressure  in  Vertebrate  Circulatory   Systems   -­‐ BP  in  left  ventricle  changes  with  systole  and  diastole     -­‐ Pressure  decreases  as  blood  moves  through  system   à  fluctuations  decrease  as  we   go  through  the  circulatory  system  =  consistency  of  flow   • Massive  left  ventricular  fluctuations  are  due  to  ventricu lar  systole  and   diastole   • As  soon  as  you  move  into  arteries  and  arterioles,  pressure  fluctuations  start   to  decrease   -­‐ Decrease  in  blood  pressure  as  it  reaches  the  veins   -­‐ As  you  reach  the  veins,  there  is  actually  little  driving  force  for  the  blood  to  get   back  to  the  heart  à  easy  to  get  blood  to  arterial  system   -­‐ Pressure  and  pulse  decrease  in  arterioles  due  to  high  resistance   -­‐ Arterioles  are  primarily  responsible  because:   1) Relatively  narrow  (vs  arteries)   à  increased  resistance  compared  to   arteries   2) Relatively  few  (vs  capillaries)     o Low  cross-­‐sectional  area  à  leads  to  rapid  decrease  in  blood  pressure   as  blood  moves  across  arterioles   à  velocity  drops  in  capillaries  =  good   for  gas  exchange  =  increase  cross-­‐sectional  area  in  capillaries     -­‐ both  leads  to  a  rapid  decrease  in  b lood  pressure  as  blood  moves  across  the   arterioles   -­‐ Velocity  of  blood  highest  in  arteri es,  drops  to  its  lowest  in  capillaries  (due  to  increased  cross  sectional  area  in  the   capillaries),  and  intermediate  in  veins  (decreased  cross-­‐sectional  area  of  blood  vessels)   • Flow  stays  the  same  across  any  give  point,  but  velocity  changes   • Velocity  of  blood  increases  as  it  exits   • V  =  Q/A     Arteries  Act  as  Pressure  Dampers   -­‐ pressure  fluctuations  in  arteries  are  smaller  than  those  in  left  ventricle   -­‐ arteries  that  exit  the  aorta   has  high  resistance  à  expansion  of  the  aorta  =   blood  backing  up  =  why  we  have  thick  walls  in  the  aorta   -­‐ aorta  acts  as  pressure  reservoir   • relatively  low  resistance  structure   short,  large  diameter  –  but  smaller  arteries  exit  the  aorta  =  has  high   resistance   • allows  for  continuous  blood  flow  throughout  the  body   • elasticity  of  vessel  wall   § lots  of  collagen   § expands  during  systole   § elastic  recoil  during  diastole   • dampens  pressure  fluctuations   • also  have  thick  walls  (aorta  especially  –  have  thick  tunica  externa)   § reduce  stress   -­‐ Law  of  LaPlace  à  tension  is  why  we  have  such  thick  walls  in  the  aorta       o T  =  Pr/W   -­‐ After  contraction  à  closing  of  semilunar  valves  =  elastic  recoil     Moving  Blood  Back  to  the  Heart   -­‐ blood  in  veins  is  under  low  pressure   -­‐ 2  pumps  assist  in  moving  venous  blood  back  to  the  heart   1) skeletal  muscle   • contractions  of  muscle  squeezes  veins ,  sending  blood  back  to  heart   2) respiratory  muscle   • pressure  changes  in  thoracic  cavity  during  ventilation   • when  we  inhale,  we  increase  volume  in  thoracic  cavity  =  decreases   intrapleural  pressure  =  decrease  in  right  atrial  pressure   • decrease  of  pressure  in  right  atrium  <  decrease  of  intrapleural  pressure   o therefore,  transmural  pressure  gradient  pulls  open  the  right  atrium  of   the  heart   o reduction  in  intrapleural  pressure  =  expansion  of  the  lung s  AND   expansion  of  right  atrium  (sucking  blood  back  to  the  heart)   • Atria  are  thin  walled  structure   à  expands  like  the  lungs   o When  it  expands,  it  reduces  pressure  and  sucks  blood  into  the  cavity   -­‐ valves  in  veins  assure  unidirectional  flow   -­‐ Only  veins  have  on  wa y  valves,  arteries  don’t   -­‐ Q  =  ΔP/R     Veins  Act  as  a  Volume  Reservoir     -­‐ Compliance  =  ΔP/ΔV   -­‐ thin,  compliant  walls   o small  increase  in  blood  pressure  leads  to  large  changes  in  volume   o not  true  in  arteries,  only  true  in  veins   -­‐ in  mammals,  veins  hold  more  than  60%  of  blood   -­‐ vein  volume  (and  nervous  return)  controlled  by  sympathetic  nerves   o venomotor  tone   o increased  in  sympathetic  activity  =  more  blood           Mean  Arterial  Pressure  (MAP)   -­‐ average  arterial  pressure  over  time   • MAP  at  rest  =  2/3  diastolic  pressure  +  1/3  systolic   pressure   o Heart  spends  more  time  in  diastole   • If  heart  is  beating  rapidly,  then  ½  diastolic,  ½  systolic  is  more  accurate   -­‐ MAP:  pressure  in  artery   –  central  venous  pressure  (but  so  low  it  can  be  neglected)     Regulation  of  Blood  Pressure   • Mean  Arterial  Pressure   o CO=MAP/TPR   o MAP  =  CO  x  TPR   • Body  varies  cardiac  output  (CO)  and  total  peripheral  resistance  (TPR)  to  maintain  a  near  constant  mean  arterial   pressure  (MAP)     • Pressure  is  the  primary  driving  force  for  blood  flow  so  maintaining   MAP  is  the  fundamental  requirement   o TPR  –  state  of  vasoconstriction/vasodilation   –  determined  by  metabolic  state  of  tissue  (overrides  extrinsic   effects);  summed  resistances  of  all  blood  vessels     o CO  varies  in  response  to  changes  in  TPR  to  maintain  MAP  in  narrow  range     § To  maintain  flow,  you  ch ange  the  pressure   § To  maintain  the  pressure  (if  resistance  changes)  you  change  the  cardiac  output   • Actions  of  sympathetic  nervous  system,  intrinsic  factors,  maintains  a  near  constant  arterial  pressure   –  regardless   of  physiological  state   • Thus,  metabolic  demand  of  tissues  is  ultimate  regulator         Homeostatic  Regulation  of  Blood  Pressure   -­‐ MAP  =  CO  X  TRP   -­‐ CO  =  heart  rate  X  stroke  volume   o Heart  rate  can  be  decreased  by   parasympathetic  nervous  system,   acetylcholine  (closure  of  T -­‐type  Ca2+   channels,  increase  in  K+  conductance)   o Heart  rate  can  be  increased  by  the   sympathetic  nervous  system  =  increasing   opening  of  T-­‐type  Ca2+  channels  and   funny  channels   § Also  inc
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