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Cardiovascular physiology - House Of Sticks

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					Cardiovascular
Physiology
  http://www.houseofsticks.net


                     Brian Stickle
          Aberdeen Royal Infirmary
                                    2

Cardiovascular physiology
 Cellular ionic physiology
 Cardiac action potential
 Excitation contraction coupling
 Cardiac output
  – Preload
  – Contractility
  – Afterload
 MVO2
 The cardiac cycle
                                                   3

Cellular Ionic Physiology
 RMP is determined primarily by:
 1.The concentration of ions on the inside
   and outside of the cell
 2.The activity of electrogenic pumps
     •   (e.g., Na+/K+-ATPase and Ca++ transport
         pumps)

 3.The permeability of the cell membrane to
   those ions
     •   (i.e., ion conductance)
                                                  4


Nernst equation
 Determines the electrical potential
  across the membrane for individual
  ions




   R = The gas constant
   T = Temperature (absolute) oK
   z = Valence of the ion          25.6 (for z= +1)
   F = The Faraday constant
                                            5

Nernst Equation




 Stated as Intracellular / Extracellular
 ∴ Invert equation and change sign
 EK = -25.6 ln [K+]i / [K+]o = -96 mV
 ENa = -25.6 ln [Na+]i / [Na+]o = +50 mV
                                                      6

Goldman Equation
  Combines Nernst potentials for each ion and
   calculates the overall potential (Em)
  Weights according to permeability




                     or

Em = g'K+(-96 mV) + g'Na+(+50 mV) + g'Ca++(+134 mV)
                                                 7

Non-Pacemaker Action potentials
                                     Purkinje
 +20            1      2             fibre &
   0                                 myocytes

        0                       3



  -80                                     4
            0                       250
                    Time (ms)
                                  8

Non-Pacemaker Action potentials
                                       9

Action potentials
Sinoatrial nodal tissue
 +20

  0

       0     3             Threshold
 -40
                 4

 -80

           Time (ms)
                       10

Pacemaker potentials
                                            11


How is rate altered?
 Slope of pacemaker potential
 Symp  g’K+ and g’Ca++ and g’Na+
 Parasymp g’K+ and g’Ca++ and g’Na++
                            12

Normal Cardiac Conduction
 Note relative
  speeds

 Conduction
  speeds
  varied with
  Autonomic
  tone.
                                  13

Excitation contraction coupling
                                                14

Ca ++ Flux
  Cardiac muscle requires extracellular Ca++
   to contract
     • cf skeletal muscle

  Ca++ dependent Ca++ release


       Ca++                    Ca++ release
      crosses               from sarcoplasmic
    sarcolemma                  reticulum
                                        15

Excitation Contraction Coupling
  Intracellular Ca++ rises
  Ca++ binds to Troponin C
  Conformational change exposes
   binding site on actin molecule
  Actin binds myosin ATPase
  “Ratcheting” – shortens sarcomeres
  Continues as long as Ca++ remains
   high
                                                                 16

Ca ++ control

  Control of cytosolic Ca++ controls:
      • ATP hydrolysis
      • Force generated
      • Velocity of shortening

  -adrenergic receptor stimulation
      • Inc adenylate cyclase activity via G-protein  cAMP
      • Protein kinase activity increased
      • Phosphorylates ryanodine receptor
          –  Ca++ release from SR and Ca++ uptake
              »  Force and velocity of contraction (Inotropy)
          – activity of Ca++/Mg++ ATPase on SR wall.
              » Removes Ca++ at end of contraction
              »  diastolic relaxation (Lusitropy)
                                  17

Control of Cardiac Output
Simply:
   • Rate x Stroke volume (SV)


SV = EDV – ESV
   • EDV = End diastolic volume
   • ESV = End systolic volume
                                                             18

Control of Cardiac Output
Venous inflow                             Arterial Outflow

                   Heart & Lungs
 Preload                                   Afterload




           Sympathetic           Parasympathetic

            Functional state of heart-lung unit
                  (contractility and rate)
                                   19

Preload
Filling pressure of right heart
Reflected in increased EDV
Stretching of sarcomeres
Increased force of contraction
Increased SV
                               20

What determines preload?
Venous return influenced by
Intravascular volume
Position
Intra-thoracic pressure
Venous system tone
                                                         21

Venous return
                     Mean systemic        Right atrial
Right atrial       = filling pressure   - pressure
filling pressure
Venous return & CO   22

curves
                                                           23

Starlings law of the heart
 Energy of contraction  Starting length of muscle fibre
                                               24

Contractility / Rate
  Intrinsic property of myocardium
  Dependant on outside influences
   – -adrenergic stimulation
   – Drugs
   – Local factors
     • pH, adenosine, temperature, ischaemia
  Global contractility:
   – Deformity, dysrhythmias
                                     25

HR and CO
Small increase in rate
 – Shortened diastasis only
 – EDV preserved
 – CO increased

Large increase in rate
 – Shortens period of rapid inflow
 –  EDV decreased
 –  Lesser increase in CO
                                  26

HR and CO
Interval-strength effect

Treppe, Staircase, Bowditch
 effect.

Increased contractility at HR

Linked to common sympathetic
 influence
                                     27

Afterload
The resistance to the emptying of
 the left ventricle
= SVR + LVOT resistance

Increases:-
  – ESV  EDV  SV  ESV
               Starling effect
                                                           28

Determinants of MVO2
 Ventricular wall tension
         – Tension = Pressure x radius (laplace)
     • Large amount of ATP required to generate wall
       tension
     • BP  inc MVO2
 Contractility
     • Force x time = work = ATP utlisation
 Rate
     •  rate =  time in systole
 Stroke volume
     • Relatively small increases in work
     • i.e. Volume work uses less ATP than pressure work
          29
Cardiac
Cycle
All done


 Questions?

				
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