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pulmonary edema and epi


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This may sound like a stupid question but why wouldn't you give epi 1:1 to the respiratory distress patient with pulmonary edema? Is it because the epi causes further vasoconstriction which could worsen the pulmonary edema and also counteract the nitro? Is there more to it than that?

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Epinephrine's alpha effects are a good place to start with why you wouldn't want to use it for the patient with pulmonary edema, but they are just the start.

Epinephrine is a potent beta agonist as well. The problem is you can't decide which beta effect you will get from it. Beta one effects will make the failing heart work harder, and worsen the MVO2. Beta two effects will create bronchodilation but it will also cause the coronary vessels to dilate.

Combine the beta two response with the alpha (peripheral vasoconstriction), and you will cause the pulmonary edema to become worse.

Nitrates/diuresis/NIPPV are the hallmark treatments for pulmonary edema. Epinephrine should be left until all other options have proven ineffective.

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Combine the beta two response with the alpha (peripheral vasoconstriction), and you will cause the pulmonary edema to become worse.

Not to mention the ß[sub:869e5d96a2]1[/sub:869e5d96a2] effects. With significant PE, your patient is already tachycardic, decreasing both filling time and stroke volume, as well potentially hypertensive. Both the inotropic and chronotropic effects would be detremental to the patient's condition.

And remember, ß[sub:869e5d96a2]2[/sub:869e5d96a2] is bronchodilation. The bronchioles aren't really the problem here. The primary problem is that the fluid is jamming up the alveoli. No matter how much more space you created in the airways, at the end of the line you still have alveoli too full of fluid to function.

If PE is a (oversimplified) case of too much fluid in the lungs, then increasing the size of the container doesn't address the problem of the fluid being there in the first place, nor does it address the reason it is there.

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Adrenaline would also increase peripheral vasoconstriction which would just add to the problem...and in a way totally counteract the effect that one hopes to achieve with Glyceryl trinitrate and morphine. One wants a recduction in the afterload to assist with the treatment of PE.

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And remember, ß[sub:4c456f5ab8]2[/sub:4c456f5ab8] is bronchodilation. The bronchioles aren't really the problem here. The primary problem is that the fluid is jamming up the alveoli. No matter how much more space you created in the airways, at the end of the line you still have alveoli too full of fluid to function.

Beta 2 receptors are not exclusive to the bronchi. They are found in all smooth muscle, with a predominance in the bronchi and coronary/cerebral vasculature. They are also in uterine smooth muscle, but that doesn't really apply to pulmonary edema very often. :D

When we combine the alpha response of peripheral vasoconstriction, with the beta 2 response of central vasodilation the result is a restriction of fluid movement out of the central circulation. This causes the failing heart to receive an increased workload without giving it someplace to move the fluid volume. Result: pulmonary edema worsens.

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