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Pathophysiology of Brain & Body - USSJJQ-20-3. Venous Excess: a new approach to cardiovascular control and its teaching. BAJ Reddi & RHS Carpenter J App Physiol , August 2004 Pathophysiology of Brain & Body Tutorial. p356. Circularity of the circulation CO  VR  CO  VR

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pathophysiology of brain body ussjjq 20 3

Pathophysiology of Brain & Body - USSJJQ-20-3

Venous Excess: a new approach to cardiovascular control and its teaching

  • BAJ Reddi & RHS Carpenter
  • J App Physiol, August 2004
  • Pathophysiology of Brain & Body Tutorial
slide2

p356

  • Circularity of the circulation
    • CO  VR  CO  VR
    • Mixing of ‘cause & effect’
      • Independent vs dependent variables
  • Arterial vs venous
    • Arterial ‘distributive’, venous ‘collective’
  • Arterial Pressure as ‘error signal’
    • AP reflects supply vs demand
      • ↑ demand  vasoldilation  ↓ TPR (+ ↓ vol)  ↓ AP
      • Baroreceptors ↑ HR and ↑ vasoconstriction
      • ↑ AP (classic –ve feedback, sustained by error sig)
  • Control via venous side less obvious
    • However, all agree that CO influenced by venous side of circulation
slide3

p357

  • Venous Return
    • Units? Quantity vs flow?
    • How is it measured?
    • If it’s flow into heart, then it must = CO
      • If it’s flow anywhere in venous system then = CO
      • So what use is it to talk about VR controlling heart when it is a consequence of CO?
  • Starling (1912)
    • Isolated heart
    • ↑ ven ‘head’  ↑ RAP (distension)  ↑ SV  ↑ CO
      • ‘guarantees’ that what is delivered to heart is expelled
    • (But it’s easy to think it’s the ↑ flow (VR) that is driving the ↑ CO)
slide4

p357-8

  • Seeing ↑ CO ‘obviously’ implies ↑ VR
  • ↑ VR came to be seen as the cause rather than a consequence of this effect
  • Confusing as CO and RAP ‘easily’ measured
    • VR not so (no such thing as a venousreturnometer)
  • AP = CO x TPR
    • Equivalent relationship on venous side??
    • Eg VP = VR x Venous resistance??
  • Strictly, ‘pressure’ is ‘pressure difference’
    • Can ignore difference on arterial side (aortic P >> capillary)
    • But pressure difference is important on venous side
      • Pressure at ‘start’ (venules) similar to ‘end’ (RAP)
slide5

p358

  • AP = CO x TPR
    • Implies correct causal relationship
      • Aaaaaaargh! – dependant!!!
    • Eg CO = AP / TPR gives wrong impression
  • For venous side, Guyton’s VR curves imply…
    • VR = (MSFP – RAP) / Venous resistance
    • VR a consequence of RAP (all others being =)
    • But is this correct?
      • In the experiments, VR was the controlled (independent) variable, and RAP was the measured (dependent) variable
      • As ↑ flow, RAP ↓
    • Curves led to the view that ↓ RAP, by ↑ (MSFP – RAP), ‘sucked’ more blood in
    • In reality, ↑ CO  shift in blood to the arterial side
      • which leads to a ‘venous deficit’ ↓ RAP
      • ie importance of ‘capacity’ and ‘volume’ – hooray!
slide6

p359

  • Fig 1
    • Must be true in the steady-state
    • But when things are changing, the mismatch between inflow and outflow will affect RAP
  • Summary of confusion…
    • ↑ RAP  ↓ VR (Guyton curves)
    • ↑ RAP  ↑ CO (Starling’s Law)
    • Yet VR = CO !!
slide7

p359-60

  • Capacitance
    • Simple haemodynamic equations use pressure, flow, and resistance
    • Tend to ignore volumes and capacity
    • Not that important on the arterial side
    • Dominant feature on venous side
      • So VR = (MSFP – RAP) / Venous resistance misleading
      • Resistance is not very important
        • Ievenoconstriction  ↑ RAP  ↑ CO
        • Volume/capacity effects, not resistance, dominates
slide8

p360

  • ‘Venous Excess’ as error signal
    • Volume, not flow, controls RAP (and so CO)
    • Any mismatch between VR and CO represents an accumulating/reducing volume which will affect RAP (and so CO)
      • Basis for keeping VR = CO
    • Figs 1b and 1c appear contradictory
      • But 1b superimposed on ‘classic’ Guyton curve
        • ‘cause and effect’ wrong
      • Fig 1c implies proper causal mechanism
        • ↑ VAR  ↑ RAP ( ↑ CO )
slide9

p361

  • Exercise
    • ↑ CO shift blood to the arterial side
    • So VE goes negative
    • So how is RAP maintained/enhanced?
      • By ↓ venous capacity
        • Sympathetic venoconstriction
        • ‘Crushing’ action of muscle contraction
  • Haemorrhage
    • ↓ venous volume
    • ↓ venous volume due to ↑ HR shifting blood to the arterial side
    • Venous deficit ↓ SV
    • Sympathetic stimulation helps reverse deficit
slide10

p362

  • Volume vs pressure as SV regulator
    • Volume, via ‘stretch’ changes heart function/hormone release
    • Pressure changes are the consequence of volume changes, so volume is the primary stimulus
  • Volume changes
    • ↓ CO  ↓ VR
    • But while the direction may be the same, the magnitude may not
      • So a positive VE will help bolster a failing heart