Need help understanding compliance of Heart!

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echox184

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Hello,

Was hoping someone could explain this to me. Why when there is decreased compliance (increased stiffness), does ventricular pressure go up? I feel like if the ventricular walls are stiff and there is reduced EDV (less blood going into the ventricle, and less pressure when it contracts to push it out) the pressure would overall decrease since the volume going into the ventricle is smaller, and the ability for it to contract is also reduced so wouldn't the pressure go down? Am i thinking about this the wrong way?

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Contractility (and somewhat end-systolic pressure assuming a normal afterload) and end-diastolic pressure are independent of one another (one dealing with sarcomere shortening, one deal with sarcomere lengthening). In children with restrictive cardiomyopathy, their contractility is normal, but there end-diastolic pressure is high. Conversely, in dilated cardiomyopathy, the contractility is low, but the end-diastolic pressure is usually normal. The only reason a high end diastolic pressure would lead to less contractility is due to sustained high end diastolic pressures leading to reduced coronary perfusion in diastole (from high intramural wall pressure causing increased coronary resistance) and thus myocardial ischemia.

http://cvphysiology.com/Cardiac Function/CF014.htm
 
Last edited:
Hello,

Was hoping someone could explain this to me. Why when there is decreased compliance (increased stiffness), does ventricular pressure go up? I feel like if the ventricular walls are stiff and there is reduced EDV (less blood going into the ventricle, and less pressure when it contracts to push it out) the pressure would overall decrease since the volume going into the ventricle is smaller, and the ability for it to contract is also reduced so wouldn't the pressure go down? Am i thinking about this the wrong way?
Compliance is determined at the molecular level, son. In hypertrophic cardiomyopathy, you have thicker walls, and therefore higher EDP for any given EDV (see #1). In contrast, in dialated cardiomyopathy, you can have a **** ton of EDV but the dilated non-thickened walls dont allow for much increased in EDP (this is an example of a situation where you have increased compliance).

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doesn't the pressure in the ventricles have to do with how much the muscle cells can stretch out after filling? so if the muscle cells cant stretch due to hypertrophy, youre saying this is what causes the increase in ventricular pressure? so when a normal ventricle is in the filling phase of ventricular diastole, the ventricular pressure doesn't increase that much at all due to the ability of the ventricle to stretch, is that what youre telling me?
 
doesn't the pressure in the ventricles have to do with how much the muscle cells can stretch out after filling? so if the muscle cells cant stretch due to hypertrophy, youre saying this is what causes the increase in ventricular pressure? so when a normal ventricle is in the filling phase of ventricular diastole, the ventricular pressure doesn't increase that much at all due to the ability of the ventricle to stretch, is that what youre telling me?
Pressure is inversely related to radius. Review LaPlace's law of the heart. That's all I was trying to explain to you.
 
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