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Cardiovascular Physiology.pdf

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Department
Physiology
Course
PSL301H1
Professor
Gordon Richardson
Semester
Winter

Description
Cardiovascular  Physiology   Lecture  1   Goals   1. Understand  basic  science  of  heart   2. How  dysfunction  leads  to  disease     To  achieve  this   1. Overview  of  cardiovascular  system   2. Pressure,  volume,  flow  and  resistance   3. Cardiac  muscle  biochemistry   4. Consider  heart  as  functioning  pump  in  closed  system     Main  functions  of  circulatory  system   1. Transport  and  distribute  essential  substances  to  tissue   2. Remove  metabolic  byproducts   3. Adjustment  of  O  and  nu2rient  supply  in  different  physiological  states   4. Regulation  of  body  temperature   5. ‘Humoral’  communication     What  is  being  transport  and  where   Materials  entering  body   -­‐ O 2  moved  from  lungs  to  all  cells   -­‐ Nutrients  and  water  moved  from  intestinal  tract  to  all  cells   Materials  moved  from  cell  to  cell   -­‐ Wastes  moved  from  some  cells  to  liver  for  processing   -­‐ Immune  cells,  antibodies,  clotting  proteins  found  present  in  blood   continuously  to  available  to  any  cell  that  needs  them   -­‐ Hormones  moved  from  endocrine  cells  to  target  cells   -­‐ Stored  nutrients  moved  from  liver  and  adipose  tissue  to  all  cells   Materials  leaving  the  body   -­‐ Metabolic  wastes  moved  from  all  cells  to  kidney   -­‐ Heat  moved  from  all  cells  to  skin   -­‐ CO 2 from  all  cells  to  lungs     General  anatomy  of  Cardiovascular  System   -­‐ Is  a  closed  loop   -­‐ Heart  is  a  pump  that  circulates  blood  through  the  system   -­‐ Arteries  take  blood  away  from  heart   -­‐ Veins  carry  blood  back  to  heart     Structure  of  the  Heart   -­‐ Composed  mostly  of  myocardium   -­‐ Is  encased  within  membranous  fluid-­‐filled  sac  –  pericardium   -­‐ Two  sides  –  each  with  two  chambers   -­‐ Ventricles  occupy  bulk  of  heart   -­‐ Arteries  and  veins  all  attach  to  base  of  heart     Cardiovascular  System   -­‐ The  heart   o Bicuspid  (mitral)  valve   o Tricuspid  valve   o Pulmonary  valve   o Aortic  valve   -­‐ Atrioventricular  valves   o Occurs  between  atria  and  ventricles   o Tricuspid  valve  on  right  AV  junction   o Bicuspid  valve  on  left  AV  junction   o Valves  are  re-­‐enforced  by  chordae  tendinae  attached  to  muscular   projections  within  ventricles     Anatomy  of  the  Heart:  Major  vessels,  input  and  output   Heart   -­‐ Right  atrium  receives  blood  from  right  atrium  from  venae  cavae  and  sends   blood  to  right  ventricle   -­‐ Right  ventricle  receives  blood  from  right  atrium  and  sends  blood  to  lungs   -­‐ Left  atrium  receives  blood  from  pulmonary  veins  and  sends  blood  to  left   ventricle   -­‐ Left  ventricle  receives  blood  from  left  atrium  and  sends  blood  to  body  except   lungs   Vessels   -­‐ Venae  cavae  receives  blood  from  systemic  veins  and  sends  blood  to  right   atrium   -­‐ Pulmonary  trunk  (artery)  receives  blood  from  right  ventricle  and  sends   blood  to  right  atrium   -­‐ Pulmonary  vein  receives  blood  from  veins  of  lungs  and  send  blood  to  left   atrium   -­‐ Aorta  receives  blood  from  left  ventricle  and  sends  blood  to  systemic  arteries     Heart  Valves   -­‐ Heart  valves  ensure  one-­‐way  flow   -­‐ AV  valves  between  atria  and  ventricles   o Tricuspid  valve  on  R  side   o Bicuspid  on  L  side   -­‐ Semilunar  valves     o Between  ventricles  and  arteries   o Aortic  valve   o Pulmonary  valves   -­‐ During  ventricular  contraction  AV  valves  remain  closed  to  prevent  blood   flow  backward  into  atria   -­‐ Semilunar  valves  prevent  blood  flow  that  has  entered  arteries  from  flowing   back  into  ventricles  during  ventricular  relaxation     Passage  of  Blood  through  Heart   Blood  flows  this  sequence  through  heart:   à  SVC  and  IVC  à  R  atrium  à  tricuspid  valve  à  R  ventricle  à  pulmonary  trunk  and   arteries  to  lungs  à  pulmonary  veins  leaving  lungs  à  L  atrium  à  bicuspid  valve  à   left  ventricle  à  aortic  semilunar  valve  à  aorta  à  to  body     General  Terminology  of  Cardiovascular  System  Flow   -­‐ Coronary  circulation  –  circulation  of  blood  within  heart   -­‐ Pulmonary  circulation  –  flow  of  blood  between  heart  and  lungs   -­‐ Systemic  circulation  –  flow  of  blood  between  heart  and  cells  of  body     Blood  pressure  and  the  heart   -­‐ Blood  pressure  greatest  in  aorta   o Wall  of  L  ventricle  thicker  than  R  ventricle  –  generating  greater  force   to  pump  blood  to  entire  body   -­‐ BP  then  decreases  as  cross-­‐sectional  area  of  arteries  and  then  arterioles   increases   -­‐ Aorta  >  Arteries  >  Arterioles  >  Capillaries  >  Venules  >  Veins  >  Venae  Cavae     Physics  of  fluid  flow:  Hydrostatic  pressures   -­‐ Hydrostatic  pressure  is  pressure  exerted  on  walls  of  any  container  by  fluid   within  container   -­‐ Hydrostatic  pressure  is  proportional  to  height  of  water  column   -­‐ Once  fluid  begins  to  flow  through  system,  pressure  falls  with  distance  as   energy  is  lost  because  of  friction   -­‐ This  is  the  situation  in  cardiovascular  system   -­‐ Plug  pulled,  P  can  be  maintained  for  a  bit  but  changes  the  further  it  goes     Pressure  Change   -­‐ Pressure  created  by  contracting  muscles  is  transferred  to  BVs   -­‐ Driving  pressure  created  by  ventricles   -­‐ If  BVs  dilate,  BP  decreases   -­‐ If  BVs  constrict,  BP  increases   -­‐ Volume  changes  affect  BP  in  cardiovascular  system     Fluid  Flow  through  a  tube  depends  on  pressure  gradient   -­‐ Flow  is  directly  proportional  to  pressure  gradient   o Flow  α  ΔP   o Higher  pressure  gradient,  greater  fluid  flow   -­‐ Fluid  flows  only  if  there  is  positive  pressure  gradient  ΔP   -­‐ Flow  depends  on  pressure  gradient  (ΔP)  not  on  absolute  pressure  (P)   o ΔP=100-­‐75=25mmHg   o ΔP=40-­‐15=25mmHg     Resistance  of  vessel  can  affect  flow   -­‐ Flow  through  a  tube  is  inversely  proportional  to  resistance  (Flow  α  1/R)   o If  resistance  increases,  flow  decreases   o If  resistance  decreases,  flow  increases     Poiseuille’s  Law   -­‐ R  =  8Lη/πr  or  R α Lη/r   4 -­‐ Resistance  is  proportional  to  length  (L)  of  tube  (BV)   o Resistance  increases  as  length  increases   -­‐ Resistance  is  proportional  to  viscosity  (η),  or  thickness  of  fluid  (blood)   o Resistance  increase  as  viscosity  increases   -­‐ Resistance  is  inversely  proportional  to  tube  radius  to  fourth  power   o Resistance  decreases  as  radius  increases     When  vessel  radius  changes   -­‐ As  radius  of  tube  decreases,  resistance  to  flow  increases   Resistance  α  1/r   4 Flow  α  1/resistance     Flow  rate  is  not  the  same  as  velocity  of  flow   -­‐ Velocity  (v)  =  flow  rate  (Q)  /  cross-­‐sectional  area  (A)     Resistance  opposes  flow   -­‐ Small  change  in  radius  has  enormous  effect  on  resistance  to  blood  flow   o Vasoconstriction   § A  decrease  in  BV  diameter/radius  and  decreases  blood  flow   o Vasodilation   § An  increase  in  BV  diameter/radius  and  increases  blood  flow   -­‐ Flow  α ΔP/R   o Flow  of  blood  in  cardiovascular  system  is   § Directly  proportional  to  pressure  gradient   § Inversely  proportional  to  resistance  to  flow     Pressure,  flow  and  resistance   -­‐ Mean  arterial  pressure  α cardiac output x peripheral resistance -­‐ We  will  come  back  to  this…   o Vessel  size  can  change   o Blood  properties  can  change   o Cardiac  contractility  can  change   -­‐ Learn  to  calculate  and  interpret  this  in  detail     Heart   -­‐ In  order  to  generate  blood  flow,  need  to  generate  pressure  difference   -­‐ Do  this  with  cardiac  contraction   -­‐ Heart  is  simple  pump,  small  moving  parts     Cardiac  Muscle:  Central  piece  in  CV  physiology   -­‐ Myocardial  muscle  cells  are  branched,  have  single  nucleus  and  attached  to   each  other  by  specialized  junctions  (intercalated  disks)     Cardiac  Muscle:  Excitation-­‐contraction  coupling   How  an  electrical  signaling  lead  to  control   1. AP  enters  from  adjacent  cell   2+ 2+   2. Voltage-­‐gated  Ca  channels  open.  Ca enters  cell   3. Ca induces  Ca  release  through  ryanodine  receptor-­‐channels  (RyR)   4. Local  release  causes  Ca  spark   5. Summed  Ca  sparks  create  a  Ca  signal   2+ 6. Ca  ions  bind  to  troponin  to  initiate  contraction   7. Relaxation  occurs  when  Ca  unbinds  from  troponin   8. Ca  is  pumped  back  into  SR  for  storage   2+ + 9. Ca  +s  exchanged  with  Na  by  NCX  anti+orte+   10.Na  gradient  is  maintained  by  Na -­‐K -­‐ATPase     Cardiac  Muscle  versus  Skeletal  Muscle   -­‐ Smaller  and  have  single  nucleus  per  fiber   -­‐ Have  intercalated  disks   o Desmosomes  allow  force  to  be  transferred   o Gap  junctions  provide  electrical  connection   -­‐ T-­‐tubules  are  larger  and  branch  more   -­‐ SR  smaller   -­‐ Mitochondria  occupy  one-­‐third  of  cell     The  Electrocardiogram:  measuring  electrical  changes  in  heart   -­‐ Electrocardiogram  (ECG)   o Recording  of  electrical  changes  that  occur  in  myocardium  during  a   cardiac  cycle   -­‐ Atrial  depolarization  creates  P  wave,  ventricle  depolarization  creates  the  QRS   wave  and  repolarization  of  ventricles  produce  T  wave     Introduction  to  conduction  system  of  heart:  Electrical  signals  generated  and   propagated   -­‐ SA  (sinoatrial)  node/pacemaker     o Initiates  heartbeat  and  causes  atria  to  contract   -­‐ AV  (atrioventricular)  node   o Conveys  stimulus  and  initiate  contraction  of  ventricles     Lecture  2   Cardiac  Action  Potential   1. How  do  electrical  signals  release  Ca  and  cause  contraction?   2. How  do  these  signals  result  in  ECG?     Cardiac  Muscle:  Excitation-­‐contraction  coupling   1. AP  enters  from  adjacent  cell   2. Voltage-­‐gated  Ca  channels  open.  Ca enters  cell    3. Ca induces  Ca  release  through  ryanodine  receptor-­‐channels  (RyR)   2+ 4. Local  release  causes  Ca  spark   5. Summed  Ca  sparks  create  a  Ca  signal   6. Ca  ions  bind  to  troponin  to  initiate  contraction   7. Relaxation  occurs  when  Ca  unbinds  from  troponin   2+ 8. Ca  is  pumped  back  into  SR  for  storage   9. Ca  is  exchanged  with  Na  by  NCX  antiporter   10.Na  gradient  is  maintained  by  Na -­‐K -­‐ATPase     Cardiac  APs   -­‐ Two  general  types  of  cardiac  APs:   o Non-­‐pacemaker  APs   § Fast  response  APs   • Rapid  depolarization   § Throughout  heart  except  for  pacemaker  cells   o Pacemaker  cells  generate  spontaneous  APs   § Slow  response  APs   • Slower  rate  of  depolarization   § Found  in  SA  and  AV  nodes  of  heart     Cardiac  APs  are  unique   -­‐ Both  pacemaker  and  non-­‐pacemaker  APs  in  heart  differ  considerably  from   APs  found  in  neural  and  skeletal  muscle  cells   -­‐ Main  difference  is  duration:\   o Nerves  about  1ms   o Skeletal  muscle  cells  2-­‐5ms   o Cardiac  APs  range  from  200-­‐400  ms     Myocardial  Contractile  Cells  (non-­‐pacemaker  cells)   Phase   Membrane  channels   0   Na channels  open   +   1   Na channels  close   2   Ca  channels  open;  fast  K channels  close   3   Ca  channels  close;  slow  K channels  open   4   Resting  potential   -­‐ Refractory  period  in  skeletal  muscle   o Skeletal  muscle  fast-­‐twitch  fiber  –  refractory  period  is  very  short   compared  with  amount  of  time  required  for  development  of  tension   -­‐ Refractory  period  in  cardiac  muscle   o Cardiac  muscle  fiber  –  refractory  period  lasts  almost  as  long  as  entire   muscle  twitch     Action  Potentials   Comparison  of  APs  in  cardiac  and  skeletal  muscle     Skeletal  Muscle   Contractile   Autorhythmic   Myocardium   Myocardium   Membrane   Stable  at  -­‐70mV   Stable  at  -­‐90mV   Unstable   Potential   pacemaker   potential;  usually   starts  at  -­‐60mV   + + Events  leading  to   Net  Na  entry   Depolarization   Net  Na  entry   threshold   through  ACh   enters  via  gap   through  I f   potential   operated  channels   junctions   channels;   2+ reinforced  by  Ca   entry   Rising  phase  of  AP   Na  entry   Na  entry   Ca  entry   Repolarization   Rapid;  caused  by   Extended  plateau   Rapid;  caused  by   + 2+ + phase   K  efflux   caused  by  Ca   K  efflux   entry;  rapid  phase   caused  by  K  efflux   Hyperpolarization   Due  to  excessive   None;  resting   Normally  none;   K  efflux  at  high  K   potential  is  -­‐90mV,   when   permeability  when   equilibrium   repolarization  hits   K  channels  close;   potential  for  K   -­‐60mV,  If  channels   + + leak  of  K  and  Na   open  again.  ACh   restores  potential   can  hyperpolarize   to  resting  state   cell   Duration  of  AP   Short:  1-­‐2  msec   Extended:  200+   Variable;  generally   msec   150+  msec   Refractory  period   Generally  brief   Long  because   None   resetting  of  Na   channel  gates   delayed  until  end   of  action  potential     Autorhythmic  nature  of  cardiac  cells   -­‐ What  is  underlying  reason  that  heart  cells  contract?   o Unstable  membrane  potentials   o -­‐55  to  -­‐62mV  vs  -­‐85  to  -­‐90  mV   o Resting  membrane  potential  compared  to  pacemaker  potential   o Due  to  presence  of  funny  currents  I f   Action  Potentials  in  Cardiac  Autorhythmic  Cells   -­‐ If  channels  are  permeable  to  both  K  and  Na   -­‐ HCN:  Hyperpolarization-­‐activated  cyclic  nucleotide  gated  channel   o Pacemaker  potential  gradually  becomes  less  negative  until  it  reaches   threshold,  triggering  an  AP   o Ion  mvt  during  an  action  and  pacemaker  potential   o I  fa  influx  >  K  efflux   o States  of  various  ion  channels     Cardiac  APs  are  unique   -­‐ Role  of  Na  and  Ca  ions  in  depolarization   o Nerve  and  muscle  cells   § Depolarization  phase  caused  by  opening  of  sodium  channels   § Also  occurs  in  non-­‐pacemaker  cardiac  cells   o Cardiac  pacemaker  cells   § Ca  ions  are  involved  in  initial  depolarization  phase  of  AP   o Cardiac  non-­‐pacemaker  cells   § Ca  influx  prolongs  duration  of  AP  and  produces  a   characteristic  plateau  phase     Effect  of  pacemaker  activity   -­‐ This  mV  potential  is  then  transmitted  to  adjacent  cells  à  propagating  APs   causing  contraction   -­‐ Also  consider:   o Can  this  rate  of  pacemaker  be  changed?   o Control  HR?     Electrical  Conduction  in  Myocardial  Cells   -­‐ Depolarizations  of  autorhythmic  cells  rapidly  spreads  to  adjacent  contractile   cells  through  gap  junctions     Electrical  Conduction  in  Heart   1. SA  node  depolarizes   2. Electrical  activity  goes  rapidly  to  AV  node  via  internodal  pathways   3. Depolarization  spreads  more  slowly  across  atria.  Conduction  slows  through   AV  node   4. Depolarization  moves  rapidly  through  ventricular  conducting  system  to  apex   of  heart   5. Depolarization  wave  spreads  upward  from  apex     Overview  of  transmission   -­‐ APs  generated  by  SA  node   -­‐ Spread  throughout  atria   -­‐ Causing  atrial  contraction   -­‐ Impulse  travels  into  ventricles  via  AV  node   -­‐ Specialized  conduction  pathways  (bundle  branches  and  Purkinje  fibers)   within  ventricle   -­‐ Ventricular  contraction   -­‐ Normal  cardiac  rhythm  is  controlled  by  pacemaker  activity  of  SA  node     Electrical  Conduction   -­‐ SA  node   o Sets  pace  of  heartbeat  at  ~70bpm   o AV  node  (50  bpm)  and  Purkinje  fibers  (25-­‐40bpm)  can  act  as   pacemakers  under  some  conditions…  slower  pacemaker  activity   -­‐ AV  node   o Routes  direction  of  electrical  signals   o Delays  transmission  of  APs     Control  of  HR   -­‐ Decreased  heart  rate:   o Activation  of  vagus  nerve  innervating  SA  node   o At  rest,  significant  vagal  tone  on  SA  node  à  resting  heart  rate  is  btw   60  and  80  beats/min   o Atropine  –  muscarinic  receptor  antagonist,  leads  to  20-­‐40  beats/min   increase  in  HR   -­‐ Increased  heart  rate  (about  intrinsic  rate)   o Both   § Withdrawal  of  vagal  tone   AND   § Activation  of  sympathetic  nerves  innervating  SA  node     o Also  modified  by  circulating  catecholamines  acting  via  β -­‐ 1 adrenoceptors  located  on  SA  nodal  cells     Sympathetic  increase  in  HR   -­‐ β 1  receptor  activation  via  EPI  binding  cause  cAMP  production  within  cell   -­‐ Remember:   o I fchannels  or  HCN:  hyperpolarization-­‐activated  cyclic  nucleotide   gated  channel   -­‐ cAMP  increases  à  directly  increases  funny  current   -­‐ Result  in  Na  enters  cell  more  quickly   -­‐ And  cAMP  à  PKA   -­‐ PKA  phosphorylates  numerous  calcium  channels  (DHPR,  RyR,  SERCA)   further  increasing  calcium  conductance  into  cell   -­‐ Overall  result:  Both  Na  and  Ca  enter  cell  more  quickly,  threshold  is   reached  more  quickly  so  APs  are  generated  more  frequently     Parasympathetic  decrease  in  HR   -­‐ Pacemaker  cells  have  muscarinic  M  G-­‐protein2  ioupled  receptors   o ACh  acts  on  βγ  subunit  of  G-­‐protein   o Activates  K  channels   o Once  open,  cause  K  to  leak  out  and  cell  becomes  hyperpolarized   o Funny  current  also  reduced  by  ACh   § Inhibition  of  AC  decreases  cytosolic  cAMP  concentration   § Lower  cAMP  decreases  activity  of  ion  channel,  decreases   sodium  influx  =  takes  longer  for  cell  to  reach  threshold   -­‐ This  HR  slows   Control  HR  vs  Contraction  strength   -­‐ Vagus  nerves  (parasympathetic)  causes  decrease  in  SA  node  rate  (thereby   decreasing  HR)   -­‐ Parasympathetic  fibers  cannot  change  force  of  contraction  because  they  only   innervate  SA  and  AV  node   -­‐ Sympathetic  fibers  increase  SA  node  rates  (thereby  increasing  HR)   -­‐ Can  increase  force  of  contraction  because  in  addition  to  innervating  SA  and   AC  node,  they  also  innervate  atria  and  ventricles     The  Electrocardiogram   -­‐ Three  major  waves:  P  wave,  QRS  complex  and  T  wave     Electrical  activity   -­‐ Correlation  between  an  ECG  and  electrical  events  in  heart   -­‐ Comparison  of  an  ECG  and  myocardial  AP   -­‐ Normal  and  abnormal  electrocardiograms     Mechanical  Events  of  cardiac  cycle   1. Late  diastole  –  both  sets  of  chambers  are  relaxed  and  ventricles  fill  passively   2. Atrial  systole  –  atrial  contraction  forces  small  amount  of  additional  blood   into  ventricles   3. Isovolumic  ventricular  contraction  –  first  phase  of  ventricular  contraction   pushes  AV  valves  closed  but  does  not  create  enough  pressure  to  open   semilunar  valves   4. Ventricular  ejection  –  as  ventricular  pressure  rises  and  exceeds  pressure  in   arteries,  the  semilunar  valves  open  and  blood  is  ejected   5. Isovolumic  ventricular  relaxation  –  as  ventricles  relax,  pressure  in  ventricles   falls,  blood  flows  back  into  cusps  of  semilunar  valves  and  snaps  them  closed     Wiggers  Diagram   Next  page     Stroke  Volume  and  Cardiac  Output   -­‐ Cardiac  output  –  HR  x  Stroke  volume   -­‐ Average  5L/min     Lecture  3   Cardiac  AP  to  aortic  flow   -­‐ How  do  electrical  signals  initiate  contraction  and  cause  blood  mvt?     Recap:  Innervation  and  Heart  Control   -­‐ Heart  is  stimulated  by  sympathetic  cardioacceleratory  center   -­‐ Heart  is  inhibited  by  parasympathetic  cardioinhibitory  center     Autonomic  Neurotransmitters  Alter  HR   Cardiovascular  control  center  in  medulla  oblongata  à  Sympathetic  neurons  (NE   and  EPI)  à  β -­‐receptors  of  authrhythmic  cells  à  ↑  Na  and  Ca  influx  à  ↑  rate  of   1 repolarization  à  ↑  HR     Cardiovascular  control  center  in  medulla  oblongata  à  Parasympathetic  neurons   (ACh)  à  Muscarinic  receptors  of  autorhythmic  cells  à  ↑K  efflux;  ↓  Ca  influx  à   Hyperpolarizes  cell  and  ↓  rate  of  depolarization  à  ↓  HR     Catecholamines  Modulate  Cardiac  Contraction   Next  page     Mechanical  Pumping  Events  of  cardiac  cycle   1. Late  diastole  –  both  sets  of  chambers  are  relaxed  and  ventricles  fill  passively   2. Atrial  systole  –  atrial  contraction  forces  small  amount  of  additional  blood   into  ventricles   3. Isovolumic  ventricular  contraction  –  first  phase  of  ventricular  contraction   pushes  AV  valves  closed  but  does  not  create  enough  pressure  to  open   semilunar  valves   4. Ventricular  ejection  –  as  ventricular  pressure  rises  and  exceeds  pressure  in   arteries,  the  semilunar  valves  open  and  blood  is  ejected   5. Isovolumic  ventricular  relaxation  –  as  ventricles  relax,  pressure  in  ventricles   falls,  blood  flows  back  into  cusps  of  semilunar  valves  and  snaps  them  closed     Heart  Sounds   -­‐ First  heart  sound   o Vibrations  following  closure  of  AV  valves   o “Lub”   -­‐ Second  heart  sound   o Vibrations  created  by  closing  of  semilunar  valve   o “Dup”   -­‐ Auscultation  is  listening  to  heart  through  chest  wall  through  stethoscope     Control  system  –  Clinic  Pathologies   -­‐ Arrhythmias   o Uncoordinated  atrial  and  ventricular  contractions   -­‐ Ectopic  Foci   o Depolarization  (beat)  originates  someplace  other  than  SA  node   § May  be  triggered  by  high  caffeine  or  nicotine   § Most  common  cause  is  low  oxygen  to  region  of  heart   § Premature  Ventricular  contractions  (PVC’s)  most  serious   -­‐ Ventricular  Tachycardia   o Rapid  rate  stimulated  by  ventricular  ectopic  foci   -­‐ Ventricular  Fibrillation   o This  is  the  quivering  of  muscle  –  uncoordinated   o No  pumping  is  occurring   o Use  of  defibrillator  is  indicated  here   -­‐ Heart  Failure   o Walls  thinning,  loss  of  strength   o May  be  on  either  side  (R  or  L)   o If  on  left,  fluid  builds  up  in  lungs  (why?)   -­‐ Treatment   o Digitalis  –  from  poisonous  Foxglove  family  of  plants  –  slows  rate  but   increases  strength  (contractility)   o Beta-­‐blockers,  calcium  channel  blockers     Clinical  Application  –  Heart  Failure   -­‐ Heart  failure  caused  by   o Coronary  atherosclerosis   o Persistent  high  BP   o Multiple  myocardial  infarcts   o Dilated  cardiomyopathy  (DCM)   o Viral  Infection  (coxsackieB)     Running  Problem:  What  is  a  “Heart  attack”?   -­‐ Myocardial  infarction   -­‐ Ischemia  results  in   o Anaerobic  metabolism  –  lactic  acid  formation   2+ o Rising  acidity  hinders  ATPase  and  cannot  pump  out  Ca  then   o Gap  junctions  close  –  cells  electrically  isolated,  and   o If  ischemic  area  is  large,  heart  pumping  action  impaired   o Myocyte  death,  form  scar  tissue  =  non-­‐contractile     Further  applications  of  this  knowledge   -­‐ Normal  valve  operation   o Valve  closes  after  left  ventricle  pumps  blood  into  aorta   -­‐ Leakage  of  valve     o Valve  does  not  close  completely,  leaking  blood  into  heart     Fetal  Heart  Development   1. Ventricular  septal  defect  –  superior  part  of  interventricular  septum  fails  to   form;  thus,  blood  mixes  between  two  ventricles  but  because  left  ventricle  is   stronger,  more  blood  is  shunted  from  L  to  R   2. Coarctation  of  aorta  –  part  of  aorta  is  narrowed,  increasing  workload  on  L   ventricle   3. Tetralogy  of  Fallot  –  multiple  defects  (tetra=four):  pulmonary  trunk  too   narrow  and  pulmonary  valve  stenosed,  resulting  in  hypertrophied  R   ventricle;  ventricular  septal  defect;  aorta  opens  from  both  ventricles;  wall  of   R  ventricle  thickened  from  overwork     Cardiac  AP  to  aortic  flow  –  Summary   1. Electrical  signals  originate  in  SA  node  and  are  propagated  through  heart  –   can  be  regulated   2. These  signals  are  translated  by  contractile  cells  to  generate  force  and  pump   blood   3. A  very  ordered  electrical  and  contractile  mechanism   4. We  can  monitor  these  signals  and  sounds  to  accurately  assess  cardiac   function   5. Systems  needs  to  work  and  near  100%  effectiveness     Lecture  4   Cardiac  Cycle   -­‐ What  is  the  cardiac  cycle?   o Sequences  of  events  that  occur  when  heart  beats   -­‐ There  are  two  phases  of  this  cycle   o Diastole  –  ventricles  are  relaxed   o Systole  –  ventricles  are  contracted   -­‐ Overall  aim:  understand  and  integrate  electrical  activity,  contraction  and   blood  flow  in/out  of  heart   General  principles   -­‐ Contraction  generates  pressure  changes   o Orderly  movement  of  blood   -­‐ Blood  flows  high  pressure  à  low  pressure   -­‐ Events  on  R  and  L  side  of  heart  are  same  but  pressure  lower  on  R     Cardiac  performance  in  ventricles   -­‐ ESV  =  end  systolic  volume  (~65ml)   -­‐ EDV  =  end  diastolic  volume  (~135ml)   -­‐ Stroke  volume   o SV=EDV-­‐ESV   o Amount  of  blood  pumped  by  1  ventricle  in  1  contraction   -­‐ Cardiac  out   o CO  =  HR  x  SV   o Amount  of  blood  pumped  per  ventricle  per  unit  time   o ~5L/min  (~70  beats/min  *  65  ml/beat  =  4.6L/min)   o Normal  blood  volume  is  ~5L   -­‐ Cardiac  reserve   -­‐ Difference  between  resting  and  maximal  CO     Frank-­‐Starling  Law  of  the  Heart  (what  affects  SV?)   -­‐ Preload  of  cardiac  muscle  cells  is  critical  factor  controlling  stroke  volume   o Preload  –  increase  in  venous  return  to  heart  increases  filled  volume   (EDV)  of  the  ventricle   o Afterload  –  pressure  that  ventricle  must  generate  in  order  to  eject   blood  into  aorta   -­‐ Slow  heartbeat  and  exercise  increase  venous  return  to  heart  increasing  SV   -­‐ Blood  loss  and  extremely  rapid  heartbeat  decrease  SV     Stroke  Volume   -­‐ Frank-­‐Starling  law  states   o Stoke  volume  increases  as  EDV  increases   -­‐ EDV  affected  by  venous  return   -­‐ Venous  return  is  affected  by  
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