Aortic stenosis

CrunchRN, ADN, RN · Nov 11, 2015

What is that drugs mechanism of action?

PaSSiNGaS, MSN · Nov 11, 2015

Look up the physiology of aortic stenosis and what is the most important aspect of coronary perfusion pressure. You can actually give any drug to a patient with AS but there are definitely better ones to choose.

RookieRoo · Nov 15, 2015

This AACN article has a good review of aortic stenosis, but doesn't mention nicardipine specifically.

http://www.aacn.org/wd/cetests/media/c132.pdf

However, this blurb from drugs.com I think offers some clues:

"Nicardipine does, however, have a negative inotropic effect in some patients with severe left ventricular dysfunction and could, in patients with very impaired function, lead to worsened failure." (Nicardipine - FDA prescribing information, side effects and uses)

Sooooo from what I gather, it would be unwise to administer cardene because of the possibility of it decreasing the force with which the ventricles contract and the left ventricle, in particular, which NEEDS to contract forcefully in order to overcome the resistance of the calcified aortic valve? Yes or no- now that I've done some "homework" I would love for a more experienced ICUer to weigh in and clarify, please. :)

PaSSiNGaS, MSN · Nov 15, 2015

Okay so with Aortic Stenosis you have a LV outflow obstruction which leads to diastolic dysfunction in the LV. This causes wall thickening in the LV because of the increased work of it to push through the stenotic valve. Laplace's law talks about wall thickness and diameter of a sphere and with increased wall thickness of the ventricle that causes increased oxygen demand. If you drop a patients pressure with severe AS with a drug like nicardipine it can cause an even further drop in coronary perfusion pressure. Classic signs of AS are syncope, DOE, and chest pain which are hallmark signs of decreased coronary perfusion and ischemia to the heart. By keeping the afterload (BP of the pt) up in a patient with AS you will keep perfusion to the coronary arteries up to limit ischemia.

MunoRN, RN · Nov 16, 2015

Okay so with Aortic Stenosis you have a LV outflow obstruction which leads to diastolic dysfunction in the LV. This causes wall thickening in the LV because of the increased work of it to push through the stenotic valve. Laplace's law talks about wall thickness and diameter of a sphere and with increased wall thickness of the ventricle that causes increased oxygen demand. If you drop a patients pressure with severe AS with a drug like nicardipine it can cause an even further drop in coronary perfusion pressure. Classic signs of AS are syncope, DOE, and chest pain which are hallmark signs of decreased coronary perfusion and ischemia to the heart. By keeping the afterload (BP of the pt) up in a patient with AS you will keep perfusion to the coronary arteries up to limit ischemia.

I know that used to be the assumption but I don't think there is broad agreement anymore that hypertrophy is the cause of myocardial ischemia in AS.:

The concentric LV hypertrophy typically associated with AS was initially believed to be the main cause of impaired CFR in these patients (12, 38). Rajappan et al. (34), however, recently reported that CFR correlates better with the hemodynamic indexes of AS severity, i.e., valve effective orifice area (EOA) and transvalvular pressure gradient, than with LV mass. Moreover, in patients with severe AS and no significant obstructive coronary artery disease, ischemic symptoms, such as angina, are generally relieved immediately after aortic valve replacement (AVR), whereas LV hypertrophy gradually regresses over several months. These findings, therefore, suggest that the abnormally high LV workload induced by the stenosis may be one of the key mechanisms responsible for impaired CFR and thus myocardial ischemia in AS.

ARTICLES | Journal of Applied Physiology

PaSSiNGaS, MSN · Nov 19, 2015

Might want to read my post and that article again. I stated you get a decrease in CPP due to a drop in after load. The article states just that. "CFR correlates better with the hemodynamic indexes of AS severity, i.e., valve effective orifice area (EOA) and transvalvular pressure gradient, than with LV mass."

I said in different words that this ischemia is based on the pressure gradient through the stenotic valve which will be increased if you cause an increase in the pressure gradient by giving a dilator and causing a drop in SVR.

I know that used to be the assumption but I don't think there is broad agreement anymore that hypertrophy is the cause of myocardial ischemia in AS.:
ARTICLES | Journal of Applied Physiology

Remember Coronary perfusion pressure = Aortic EDP - CVP. If you already decrease EDP in the aortic arch by dilating it and have an increased CVP or any kind of right heart failure due to the chronic diastolic dysfunction caused by AS you will only worsen the ischemia. One of the major hallmark signs of severe AS is angina and that is due to the ischemia seen in the coronaries.

Pheebz777, BSN, RN · Nov 24, 2015

To the OP. To simplify things, cardiac output (CO) is dependent basically on 3 key elements. Pre-load, AFterload and Contractility. The better the CO, the better coronary perfusion you achieve. Now, Calcium Channel blockers (CCB)s pharmacologic effect is to reduce afterload and slow down automaticity of the heart (Contractility). Now, with a stenosed aortic valve, the heart needs more force to push thru that tiny passage way, (like blowing thru a straw). You slow down the hearts contractility, and now you have problems with CO.

Reducing afterload to acceptable limits is key in reducing cardiac oxygen demands without diminishing contractility. So ACE inhibitors or ARBs are usually prescribed. Drugs that weaken contractility like beta-blockers are also avoided for the same reasons mentioned above.

However medical management can only do so much. For severe aortic stenosis, valve replacement would be needed.