Preload, Afterload, or Contractlity based on Med help.

  1. So I am looking for some help regarding a homework question. The meds that are part of the question are Dopamine, Hydrochlorothiazide, Nipride, and Epinephrine. How do I determine how each of these meds affect the heart in terms of preload, afterload, and contractility. I think I'm starting to understand, but I would like a little help with the subject.

    This is what I have so far, but we are just learning this stuff and it's driving me crazy!

    -Dopamine is a vasopressor, so does it increase afterload only?

    -Hydrocholorothiazide is a diuretic so since it decreases volume does it decrease preload and afterload?

    -Epi is a vasoconstrictor so that would have to increase afterload.

    -Nipride is a vasodilator, so does this decrease afterload only. (Or, would it decrease preload as well since there would be more blood in the periphery due to the vasodilation?)

    Am I understanding this or am I way off?? I feel like I'm starting to get the basics, but a little push in the right direction would be greatly appreciated, thanks!!
    Last edit by Joe1984 on Jan 22, '13
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  3. by   Esme12
  4. by   Esme12
    It is actually really simple......

    Preload is stretch. The amount of volume being returned to the right side of the heart from systemic circulation.
    Afterload is squeeze. The amount of resistance the left side of the heart has to overcome in order to eject blood.

    Just look at the mechanism of action with different drugs to see what they do. e.g. a dilator will decrease, so the pressure comes down and the heart has less resistance to overcome, the catch is that it can also lead to less venous return, hypotension, ischemia. A pressor will increase, hopefully leading to better return to the heart. But it can also create too much resistance, which also can lead to problems.

    Drugs that dilate the vasculature thus reducing blood return to the heart effect pre-load... for example nitroglycerin by making the venous side bigger. There is some effect on arterial side which reduces afterload not not as much as venous / preload. Fluid boluses increase preload.

    Drugs that increase afterload are sympathomimetics like epinephrine, dopamine, levophed, etc. They increase systemic vascular resistance and clamp down on the arterial side which increases the pressure making it harder for the heart to overcome and be able to eject its blood volume. ACE inhibitors offer afterload reduction.
  5. by   nurseprnRN
    Some drugs do more than one thing.

    When you read about dopamine, you will see that it affects the CV system in two ways. So does epi (and epi is a real double-edged sword: Why?). Look to see what those are and let us know what you find out!

    Good idea on the nitroprusside-- exactly right.

    We LOOOOVE cardiovascular physiology, Esme and I. We could talk about it all night.