I’m not talking about the dopamine already present in your system that allows you to like things and enjoy life. I’m talking about the intravenous drip used as an inotrope in the intensive care unit.

Dopamine is a primitive drug.

I mean that literally. Also, it smells bad. Seriously. Open the bag and take a whiff–sulfur, yum.

Dopamine is the precursor to norepinephrine and epinephrine. It’s a neurotransmitter that acts centrally and peripherally, once metabolized, on the sympathetic nervous system. The sympathetic nervous system is that fight-or-flight response we all remember from the last time we did CPR.

We used dopamine all the time when I was growing up as a nurse. The doctors would write for “renal dose dopamine” and we knew that meant 1-3 mcg/kg/min, titrate to urine output greater than 50cc/hr.

We ran it in septic patients all the time, based on the theory it would protect the kidneys and the gut from the low perfusion state induced by sepsis. We would run it before levophed–back then, levophed was the last drug you reached for. We’d use it to give our fresh hearts a little kick to get them extubated and make their numbers look good, help them have adequate urine output without lasix.

So how does dopamine induce diuresis?

It causes “diuresis” by decreasing aldosterone secretion in the adrenal cortex. Aldosterone is what encourages your kidneys to retain sodium at the distal renal tubule. This causes water retention. If you block aldosterone, you prevent the retention of sodium and water. It also, at low doses, increases renal blood flow & GFR, promoting the excretion of sodium. As we know, H2O can’t think for itself but merely follows sodium every where it goes.

It also inhibits insulin secretion. This is one reason why patients (particularly type 2 diabetics or patients who have received anesthetic medications) on dopamine drips will have a higher serum glucose. We didn’t worry about it much back then, because all of our patients were on insulin drips anyway.

Dopamine has another strange effect: it affects the release of thyroid-stimulating hormone and inhibits prolactin release. Consider hypo- or hyperthyroidism if your patient begins exhibiting unexplained heart rate/blood pressure changes while on a dopamine drip that hasn’t been titrated.

The effects of dopamine are dose-dependent.

  • Low dose effects (1-2 mcg/kg/min) include vasodilation of the renal and mesenteric blood vessels by acting on the dopaminergic 1 & 2 receptors.
  • Moderate dose effects (2-10 mcg/kg/min) are primarily beta-1, enhancing contractility and heart rate.
  • Higher doses than 10 mcg/kg/min act overwhelmingly on the alpha-1 receptors, causing vasoconstriction.

PRIMARY CONSIDERATIONS: causes tachyarrhythmias, particularly in hypovolemic patients. At high doses, profound vasoconstriction will occur, which can cause necrosis, gangrene, and even compartment syndrome if infused through a peripheral IV.


Author: Mitochondrial Eve

CCRN-CMC/CSC I know less than half as much as I'd like to, and say more than half as much as I should.

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