CardioVascular discussion

[Sieldan]

Ok, I need some help getting something straight. Were talking CardioVascular.

Given that CO = SV x HR
and that SV is composed of PreLoad, Contractility, and Afterload
and that Afterload is basically peripheral vascular resistance

Wouldnt anything that lowers PVR (ie, a vasodilator) also lower Preload? My theory is that vasodilators will dilate both the arterial and venous vessels. If you dilate the veins, you will reduce the already low pressures there, and cause a lower preload.


I thought I had a handle on this, but after a recent test in class and discussion with classmates, I'm not really sure if there is actually blood in the vasculature. :unsure:

 

[JPINFV]

Can you give us an idea of what the question asked?

 

[jrm818]

Try this explanation on for size...It is at least convincingly explained, although I haven't seen the data to back up the claim that increased CO and the baroreceptor effect quantitatively compensate for venous dilation and maintain preload, so reader beware unless you find some actual data.

good question

http://www.cvpharmacology.com/vasodilator/vasodilators.htm

 

[8jimi8]

My theory is that vasodilators will dilate both the arterial and venous vessels. If you dilate the veins, you will reduce the already low pressures there, and cause a lower preload.

not every drug lowers both arterial and venous vasculature. Be very careful that you are using the correct pharmacological intervention. This is a great example of why you must know your drugs inside and out, down to the molecular method of action.

 

[Sieldan]

Can you give us an idea of what the question asked?

You know, I cant for the life of me remember how it was stated. The test was Tuesday, and Ive been thru 4 clinical rotations since then. (ouch) I think it was something like "Reduced PVR will cause a reduction in <blank>?" And the answer was preload. IIRC

 

[Sieldan]

not every drug lowers both arterial and venous vasculature. Be very careful that you are using the correct pharmacological intervention. This is a great example of why you must know your drugs inside and out, down to the molecular method of action.

You are correct, and you happen to hit on one of my biggest weak spots. One that I am trying to eliminate. (or reduce )

 

[18G]

Wouldnt anything that lowers PVR (ie, a vasodilator) also lower Preload? My theory is that vasodilators will dilate both the arterial and venous vessels. If you dilate the veins, you will reduce the already low pressures there, and cause a lower preload.

Pretty much, yes. If you open up the pipes and drop the pressure, the volume of blood making it back to the heart is less. Less blood return (preload) means less stretch of the myocardium and with less stretch comes less stroke volume. Remember Starlings Law... the more the heart is stretched, the stronger its contraction up until a certain point. So less stretch from less pressure in blood return = lowered stroke volume.

This is one of the main reasons why we give nitro... it lowers blood pressure by dilating the vessels thus decreasing blood return (preload) making the heart have to work less hard by not having to pump as much blood and with much less force (reduces myocardial oxygen demand).

Keep in mind though that different vasodilators will effect the veins and arterioles differently. Nitro for example is primarily a preload reducer which predominantly effects the venous side with only slight effect or arterioles and afterload. Nitro also effects the coronary arteries too.

Nifedipine is a vasodilator used to mainly treat hypertension. It is a calcium channel blocker with strictly vasculature effect and no effect on heart rate like other calcium channel blockers. It exerts its effect by dilating the arterial side of the system.

So NTG is more of a preload reducer and Nifedipine is more of an afterload reducer. Both are vasodilators but work differently to achieve the desired effect.

And PVR is more affected by the arterial side.