Starling's Law

[~Shiva~]

HI AGAIN GUYS

Your expert opinions are desperately needed

Why is Starling's Law relevant to heart transplant patients?

Is it because cardiac transplant patients have no automonic nerve supply after the relationship, you can clearly see Starling's Law at work without any interfering factors?

This is my personal opinion but others disagree and say it's relevant because of heart failure would cause Starling's Law to be ruined because cardiac muscle is too stretched and fails to pump?

Any opinions appreciated Thank you

[Thestableboy]

Haha, looks like were alone in our quest for Q7 help! I think its more a case of putting foward your science, even if its flawed we will probs still get marks. Allen hasnt made things easy!
Good luck

[Diya]

Yes, I think it is because when your heart starts to fail, ur heart muscle compensates by hypertrophy and pumps harder but once it fails beyond a certain degree, the muscle dilates and contractility falls...putting Starling's law into that, the heart compensates for failing by increasing end diastolic volume so that cardiac output is maintained but eventually, it gets to the top of the curve and increasing EDV just makes the ventricles dilate more and CO falls

Is it really obvious that I have forgotten most of my physiology and the terminology? lol

[yeliab_cram]

Marc is thinking out loud... here is my logic:

cardiac output = stroke volume x heart rate

If the donor heart is not innervated by the host nervous system it cannot alter HR so must rely solely on its intrinsic response to ventricular filling (ie Starling's law) to maintain cardiac output.

[Will Watson]

I think with a slightly abstract question like that you can say either answer is correct...

[~Shiva~]

Thanks, no Diya you sound spot on! If the ventricles dilate beyond a certain point, do they loose their contractility function??? Does the Starling mechanism depend entirely on contractility? I understand the Starling mechanism in so far as the higher the End Diastolic Volume= greater ejection, but I'm not sure whether that's just because there's more blood, or it has better contractility.

Cheers Yeliab_cram, is that basically to mean because the heart has no nerve supply, it is tacycardiac (because it's normally under parasympathetic innervation)...therefore the end diastolic volume is "made" lower than normal, because otherwise the cardiac output would be too high??

Good luck with yours, Thestableboy!

[chicken66]

Originally Posted by Diya

Yes, I think it is because when your heart starts to fail, ur heart muscle compensates by hypertrophy and pumps harder but once it fails beyond a certain degree, the muscle dilates and contractility falls...putting Starling's law into that, the heart compensates for failing by increasing end diastolic volume so that cardiac output is maintained but eventually, it gets to the top of the curve and increasing EDV just makes the ventricles dilate more and CO falls

but you wouldn't use a heart in heart failure in a transplant...