Nitrates and preload and/or afterload?

[tpsreport]

Hey guys

On the topic of nitrates

So FA2015 Page 305 notes that nitrates decrease preload >> afterload. When I think of nitrates, I think venodilation, whereas arteriolar dilation makes me think hydralazine.

Then I see this Uworld question where it makes me pick between the effects of nitrates: either only decreasing preload, or decreasing preload and after load the same amount.

Here's a snap of the two choices:

I'm concerned about picking the right one on test day, because this seems like a really important distinction.
Has anyone else had this mixup? What do you guys think?

Thanks in advance

---

Members don't see this ad.

 

[Jabbed]

Hey guys

On the topic of nitrates

So FA2015 Page 305 notes that nitrates decrease preload >> afterload. When I think of nitrates, I think venodilation, whereas arteriolar dilation makes me think hydralazine.

Then I see this Uworld question where it makes me pick between the effects of nitrates: either only decreasing preload, or decreasing preload and after load the same amount.

Here's a snap of the two choices:

I'm concerned about picking the right one on test day, because this seems like a really important distinction.
Has anyone else had this mixup? What do you guys think?

Thanks in advance

This is a question/answer highly specific to sodium nitroprusside, which has potent preload and afterload reducing effects. Nitroglycerin or isosorbide mono/dinitrates on the other hand have significantly greater preload reduction than afterload.

 

[tpsreport]

This is a question/answer highly specific to sodium nitroprusside, which has potent preload and afterload reducing effects. Nitroglycerin or isosorbide mono/dinitrates on the other hand have significantly greater preload reduction than afterload.

Thanks Jabbed, that makes sense to me. I didn't realize that nitroprusside is unique in that it does both. I thought that all nitrates act the same way (bioavailability aside)

Continuing on this topic, there was another question that asked about sublingual tablets (assuming this is nitroglycerin).

Patient came in with angina, and reported rapid relief of pain after taking a single tablet. Question asks about the major contributor to the drug effect observed.

I was 50/50 between either
1. Decreased LV volume (Actually picked this first and then changed my answer)
2. Increase in coronary blood flow

I thought angina was directly caused by a lack of sufficient blood flow and oxygen to the myocardium?
Yes nitrates decrease preload, which is the direct effect of the drug and would therefore decrease myocardial oxygen demand due to less of an emphasis on the Frank-Starling mechanism, but I thought that it's actually the increased coronary blood flow from the decreased volume and less squishing of the coronary vessels that provides the relief, especially when you have >80% lumen blockage?

I think that both of these mechanisms are involved in nitrates; am I placing the emphasis on the wrong thing?


Thanks again

 

[Jabbed]

Thanks Jabbed, that makes sense to me. I didn't realize that nitroprusside is unique in that it does both. I thought that all nitrates act the same way (bioavailability aside)

Continuing on this topic, there was another question that asked about sublingual tablets (assuming this is nitroglycerin).

Patient came in with angina, and reported rapid relief of pain after taking a single tablet. Question asks about the major contributor to the drug effect observed.

I was 50/50 between either
1. Decreased LV volume (Actually picked this first and then changed my answer)
2. Increase in coronary blood flow

I thought angina was directly caused by a lack of sufficient blood flow and oxygen to the myocardium?
Yes nitrates decrease preload, which is the direct effect of the drug and would therefore decrease myocardial oxygen demand due to less of an emphasis on the Frank-Starling mechanism, but I thought that it's actually the increased coronary blood flow from the decreased volume and less squishing of the coronary vessels that provides the relief, especially when you have >80% lumen blockage?

I think that both of these mechanisms are involved in nitrates; am I placing the emphasis on the wrong thing?


Thanks again

Recall that anginal chest pain is due to a mismatch of myocardial oxygen demand with myocardial oxygen availability. Work = energy.

The point of nitroglycerin in the treatment of angina is not to increase coronary perfusion (although you could make a case that it has non-negligible benefit), but to decrease the workload of the heart. Decreased venous return = decreased EDV = decreased wall tension of the ventricle. By decreasing the wall tension of the ventricle at end-diastole, we decrease the stress of the myocardium and decrease oxygen demand.

Think of preload not as the volume of blood at end-diastole, but rather the ventricular wall tension of the EDV. This helps keep the idea of preload as a work-force in perspective.

 

[tpsreport]

Recall that anginal chest pain is due to a mismatch of myocardial oxygen demand with myocardial oxygen availability. Work = energy.

The point of nitroglycerin in the treatment of angina is not to increase coronary perfusion (although you could make a case that it has non-negligible benefit), but to decrease the workload of the heart. Decreased venous return = decreased EDV = decreased wall tension of the ventricle. By decreasing the wall tension of the ventricle at end-diastole, we decrease the stress of the myocardium and decrease oxygen demand.

Think of preload not as the volume of blood at end-diastole, but rather the ventricular wall tension of the EDV. This helps keep the idea of preload as a work-force in perspective.

Thanks again for clarifying! To add some detail for those who are also interested, it turns out that I was also making the mistake in thinking that these clogged vessels would further dilate. In angina, the coronary vessels are already maximally dilated due to auto regulation forces, so any decrease in LVEDV would not really put anything towards further dilating the coronary vessels.