Cardio questions...

A couple of links for you:

http://www.medscape.com/resource/heartfailure

http://www.chfpatients.com/ace.htm

http://www.uptodate.com/contents/ace-inhibitors-in-heart-failure-due-to-systolic-dysfunction-therapeutic-use

up to date is a great reference, so is Medscape. Medscape is a free registration site and you can get nursing CEU's if you need them. I'd normally go into more detail but I'm so sorry, I'm off to bed due to early dayshift tomorrow.

Another great reference is Drugs for the Heart, by Opie and Gersh. TONS of pharm info that I've found invaluable. I hope these will at least point you in the right direction

ACE inhibitors work by preventing the conversion of Angiotensin I to Angiotensin II (Angiotensin Converting Enzyme inhibitor). Remember the AT II is a powerful vasoconstrictor, especially on the aterial side of things.

Now, let's consider what diastolic blood pressure represents. It is the pressure left in the arteries after systole, and is indicative of systemic vascular resistance (also fluid state and preload, but discard that for now). So it would make sense that if giving an afterload reducer (afterload being equal to SVR) that the DBP would be lower.

As far as adjusting a med for an asymptoticly low DBP, if it's asymptotic why adjust it? All your doing is adjusting numbers to make yourself feel better. I'm doubtful 38 was accurate though.

ACE inhibitors work by preventing the conversion of Angiotensin I to Angiotensin II (Angiotensin Converting Enzyme inhibitor). Remember the AT II is a powerful vasoconstrictor, especially on the aterial side of things.

ACEi are vasoDILATORS. They reduce afterload. Especially in systolic heart failure they improve mortality. The data on efficacious treatments for diastolic dysfunction are lacking.

Much of diastolic dysfunction is caused by hypertension (among other causes). As such, ACEi would be effective to a certain extent. Unfortunately the hypertrophy of the ventricle has already been done so reducing afterload will help only improve SV. The filling of the ventricle (the problem in diastolic dysfunction or HFpEF- heart failure with preserved ejection fraction) is going to be relatively unaffected.

For heart failure the MDs often want the pressure low like what you are seeing. If they have significant HF, then having them hypertensive is going to easily overwork their heart, meet their starling's curve, and possibly cause some issues like pulmonary edema. And yes, the ACEi is to lower afterload. And often on Beta blockers too to help reduce BP more, and control the heart rate. They often use these to prevent the body's normal compensatory mechanisms, but in doing so is also why these patients often turn south really quickly and really badly, they can't mount a compensatory response.

I should also add that beta blockers are also used to prevent remodeling of the heart.

ACEi are vasoDILATORS. They reduce afterload. Especially in systolic heart failure they improve mortality. The data on efficacious treatments for diastolic dysfunction are lacking.

Much of diastolic dysfunction is caused by hypertension (among other causes). As such, ACEi would be effective to a certain extent. Unfortunately the hypertrophy of the ventricle has already been done so reducing afterload will help only improve SV. The filling of the ventricle (the problem in diastolic dysfunction or HFpEF- heart failure with preserved ejection fraction) is going to be relatively unaffected.

I think you misread, usalsfyre wasn't saying the ACEi is a vasocontrictor, they were explaining how it works to prevents the conversion of angiotensin 1 to 2, which 2 is a powerful vasocontrictor