Need help understanding coronary perfusion pressure

[oudoc08]

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A quick cardiac physio question that I can't wrap my mind around.

When figuring coronary perfusion pressure, I know that is systemic diastolic pressure minus LVEDP. I understand that since the coronaries fill during diastole that it should be the difference in the pressures present, but here's the thing. Since in diastole, the aortic valve is CLOSED, why does it matter if LVEDP is zero, 10 or 50? It would seem that the coronary perfusion pressure would be diastolic pressure - zero (since the valve is closed).
LVEDP would only seem to matter if the valve were open.

I know I'm missing something here, help please.

 

[InductionAgent]

A quick cardiac physio question that I can't wrap my mind around.

When figuring coronary perfusion pressure, I know that is systemic diastolic pressure minus LVEDP. I understand that since the coronaries fill during diastole that it should be the difference in the pressures present, but here's the thing. Since in diastole, the aortic valve is CLOSED, why does it matter if LVEDP is zero, 10 or 50? It would seem that the coronary perfusion pressure would be diastolic pressure - zero (since the valve is closed).
LVEDP would only seem to matter if the valve were open.

I know I'm missing something here, help please.

By pushing back against forces favoring perfusion, the pressure in the left ventricle opposes perfusion into the myocardium regardless of what is going on with the aortic valve. It's somewhat analagous to the force that tissue hydrostatic pressure exerts against perfusion in the systemic circulation.

 

[Trisomy13]

A quick cardiac physio question that I can't wrap my mind around.

When figuring coronary perfusion pressure, I know that is systemic diastolic pressure minus LVEDP. I understand that since the coronaries fill during diastole that it should be the difference in the pressures present, but here's the thing. Since in diastole, the aortic valve is CLOSED, why does it matter if LVEDP is zero, 10 or 50? It would seem that the coronary perfusion pressure would be diastolic pressure - zero (since the valve is closed).
LVEDP would only seem to matter if the valve were open.

I know I'm missing something here, help please.

I think what you're missing here is that even if the valve is closed, there is still a pressure exerted against it by the ventricle, acting against the systemic pressure. It is not zero when it is closed.


Disclaimer:
That's my simplistic post-call-should-be-asleep-now view, and I'm prone to errors in this state.

 

[oudoc08]

By pushing back against forces favoring perfusion, the pressure in the left ventricle opposes perfusion into the myocardium regardless of what is going on with the aortic valve. It's somewhat analagous to the force that tissue hydrostatic pressure exerts against perfusion in the systemic circulation.

Ah, this makes sense. So basically, it's the same force (i.e.- the pressure in the ventricle is essentially compressing the coronaries from the inside out) that prevents the left ventricle from being perfused during systole, but since it's much less in diastole, the coronaries are able to be perfused, and thus the less the pressure, the greater the perfusion.

Makes perfect sense. I was thinking of the pressure as having the effect at the valve instead of actually acting directly on the coronary arteries.

Thanks! You guys rock.

 

[amyl]

not sure if i am missing something or what the question is. my disclaimer is a glass of wine here in my sucky hotel room in between interviews and i am a light weight these days.... why would the LVEDP be zero?, closing the valve increases the pressure in the Lv. increased LVEDP will cut into coronary perfusion pressure....minimizing the pressure gradient between SDP-LVEDP decreasing the perfusion pressure. it matters what the LVEDP is because that is the force the perfusion pressure has to work against perfusing the myocardium...regardless of whether the valve is open or closed. does that make sense or should i skip that second glass of wine...?

 

[oudoc08]

not sure if i am missing something or what the question is. my disclaimer is a glass of wine here in my sucky hotel room in between interviews and i am a light weight these days.... why would the LVEDP be zero?, closing the valve increases the pressure in the Lv. increased LVEDP will cut into coronary perfusion pressure....minimizing the pressure gradient between SDP-LVEDP decreasing the perfusion pressure. it matters what the LVEDP is because that is the force the perfusion pressure has to work against perfusing the myocardium...regardless of whether the valve is open or closed. does that make sense or should i skip that second glass of wine...?

You have it right, I was misunderstanding how LVEDP affected coronaries.

The issue that I was having trouble with was why the pressure inside the LV would matter if the aortic valve was closed. I was thinking in terms of a spillway downstream of a dam. It doesn't make any difference to the spillway, how much water or how much pressure the dam is holding back. If the floodgate is closed, there's no effect downstream. That's how I was visualizing the problem. Hence, my confusion on why the amount of pressure in the ventricle (lake) would affect the pressure in the coronaries (spillway) since the aortic valve (floodgate) was closed.

The above clarification made me remember that the problem is not a linear set of events as the dam analogy. The fact that the coronaries are located in the distensible myocardium, and that the pressure inside the ventricle essentially compresses the coronaries, is the point I was missing. So since in systole, the pressure inside the ventricle is equal to the pressure in the aorta, and is also compressing the coronaries as the muscle is contracting, there is little to no flow. However, in diastole, due mainly to the aortic valve being present and competent, there is a gradient which accounts for the perfusion. The higher the diastolic pressure, and the lower the LVEDP, the greater that gradient and the greater the perfusion of the coronaries. So, that explains why aortic insuffficiency can cause such problems w/ coronary perfusion. It causes a interruption in the gradient and decreases coronary blood flow. It also explains why to increase coronary perfusion pressure, you either increase diastolic pressure or decrease LVEDP, thereby increasing the gradient.

If I'm missing something or getting this wrong, please comment.