Class Notes (837,696)
Canada (510,399)
Biology (2,229)
BIO271H1 (40)
Lecture 10

BIO271 2014 Lecture 10.pdf

11 Pages
Unlock Document

Christopher Garside

  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
More Less

Related notes for BIO271H1

Log In


Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.