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physio questions

Discussion in 'Medical Students - MD' started by Halaljello, Oct 24, 2002.

  1. Halaljello

    Halaljello Hot Oil
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    Can anyone please tell me if this is correct?

    an increase in venous retrun = increase in EDV = increase in preload = increase in tension (more crossbridges) = increased force of contraction ?


    p.s. aside from what I listed, what else increases force of contraction (besides digitalis, increased heart rate and affect of catecholimines)?

    p.s.s what mechanisim does ACH use to decrease heart rate?
     
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  3. tega

    tega Senior Member
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    ACH (via muscarinic receptors) raduces rate of depolarization in phase 4 of action potentials of SA and AV nodes. it does so by opening K+ channels. thus the AP does not attain its max quickly, and conduction velocity is reduced...and heart rate slows down.

    the stretch caused on ventricles by the increased EDV......enhances the myocytes affinity for calcium..thus contraction is stronger. however, i belive there is a limit...excessive preloads..may overlap actin molecules and contraction may be compromised (im not sure). almost like overstrectching a rubber band.
     
  4. uffda

    uffda Senior Member
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    overstretching would move you onto the descending limb of the length-tension curve - no force because the myosin heads cannot reach a thin filament - no matter how exposed the binding site is.


    PDE inhibitors -- (e.g. milrinone/Primacor) -- inhibit phosphodiesterase --> incr. cAMP --->-->--> incr. force of contraction (similar effect to epi/norepi)
     
  5. imtiaz

    imtiaz i cant translate stupid
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    the question is: is contractility affected by preload? ie. changing preload will change contractility or wont change it?
     
  6. uffda

    uffda Senior Member
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    sorry - I thought that was asked & answered - preload affects force of contraction - Frank-Starling Law of the Heart.
    fiber length is determined by how much blood enters the heart before the contraction starts. The heart normally operates on the ascending limb of the length-tension curve so more stretch=more force. so incr preload => increased stretch = incr sarcomere length => incr. force of contraction.

    if you want to consider velocity of contraction rather than force generated (force-velocity graph) ,
    - incr. preload = incr. velocity of shortening
    - incr. afterload = decr. velocity of shortening, no change to Vmax
    - incr. contractility = incr vel of shortening and incr Vmax

    defn. of contractility= force generating potential independent of load - think avail Ca++

    so - does preload affect contractility- I'd say no, it is a different and independent factor. It is affected by symp n.s.

    Does it affect force of contraction - yes. How - probably by making the TnC more sensitve to Ca++ - stretching may uncover more Ca++ binding sites so more x-bridge attach for same Ca++.

    so you have 3 variables to affect Stroke Volume:
    - preload
    - contractility
    - afterload
     
  7. imtiaz

    imtiaz i cant translate stupid
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    that was very consise, thanks!
     

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