Vasopressors IV: Dopamine

Start with Part I, Part II, and Part III. No skipping!

We’ve discussed our bedrock norepinephrine, the alternative epinephrine, the questionable phenylephrine, and the funky vasopressin. Now we can no longer avoid talking about…

Dopamine

Ah, dopamine. Pressor of our forefathers.

The history of dopamine goes back a long way. As a result, so do many of its fans. Not to put too fine a point on it, but many of the places you’ll find dopamine, and the people you’ll find using it, are favoring it for one simple reason: they always have.

Let’s rewind and clarify a few points. Those who paid attention in neurophysiology will recall the important role dopamine plays in the central nervous system, particularly for the Parkinsonians (or the psych patients with acute Haldol deficiency). This is not what we are talking about. Intravenous dopamine has no neurological effects, because IV dopamine does not cross the blood-brain barrier. (To reach the brain, you need to cross over using a prodrug like L-DOPA.) It is only active peripherally.

What does it do peripherally? Let’s discuss the standard teaching, and then explain why it’s wrong.

Dopamine has three classical dose ranges, each with distinct effects:

• Renal range: 1–3 mcg/kg/min. In this range, dopamine exerts a renoprotective effect, increasing GFR and renal perfusion by binding dopamine receptors in the renal vasculature.
• Inotrope range: 5–10 mcg/kg/min. In this range, dopamine primarily binds beta receptors. Hence, it acts as an inotrope, and can even have inodilator properties (due to beta-2 receptors in the vasculature), similar to dobutamine.
• Pressor range: 10–20 mcg/kg/min. In this range, alpha-1 binding dominates, and it acts primarily as a vasopressor. Although some inotropic effects persist they are overshadowed by vasoconstriction.

These dose ranges (albeit with some variation in the exact numbers) have been learned and taught for decades.

Unfortunately, renal range dopamine is BS. To use a more scientific term, it is nonsense. The concept has been roundly disproven, so definitively so—and at this point, so long ago—that anybody still using dopamine to “protect the kidneys” is being only slightly more progressive than bloodletting. Dopamine does not improve renal outcomes.

It does tend to increase urine output. Dopamine is a diuretic. If that’s what you’re after, then great. But it’s no better or worse than other diuretics, and just like all diuretics, it yields no intrinsic benefit for the kidneys, but can potentially harm them by creating volume depletion and prerenal injury.

Dopamine is a legitimate inochronotrope and vasopressor. However, its use for either purpose can be finicky. Due to its dose-dependent characteristics, which in real life are overlapping and never as neat as the textbooks present, it can be difficult to titrate for the desired effect. It is also among the worst culprits in our drug box when it comes to promoting tachycardia, and more importantly, tachyarrhythmias. (In comparison, epinephrine will cause sinus tachycardia, but seems to be less associated with malignant dysrhythmias. At least, that is the common perception, which may be unfair.)

It is also one of the relatively few pressors that has been shown inferior to another in head-to-head trials, specifically for sepsis when compared with norepinephrine. Do not use dopamine for sepsis. Use norepinephrine.

What is it good for? Well, it is traditionally considered one of the safer choices for peripheral administration, which may explain why it’s the pressor of choice in most prehospital systems. (It’s also quite shelf stable, even premixed, and so can sit around in ambulances and code carts for prolonged periods.) However, much like phenylephrine, this safety is probably a myth; like other pressors, dopamine should be run through a central line whenever possible.

It is still the first-line inotrope for some providers, particularly when they want a somewhat balanced inopressor (and don’t want to use epinephrine). This group includes some cardiac surgeons, who appreciate its diuretic effects. Neurosurgeons may like it for neurogenic shock, since bradycardia can accompany hypotension. Finally, it is used by those who mastered dopamine forty years ago and have stuck with it ever since.

For most other scenarios, the sun has set on this venerable drug. Dopamine is not evil, but we have reached the point where its role has become vanishingly small.

Tune in for Part V, where we’ll round things off by discussing the inodilator family.