Dopamine (Intropin, Revimine)

Dose-dependent receptor activity - dopamine's effects shift dramatically with dose — dopaminergic (DA1/DA2) predominance at low doses, β1 dominance at moderate doses, and α1 vasopressor effects at high doses; understanding this spectrum is essential for clinical titration.

Low dose (1–3 mcg/kg/min) - DA1/DA2 receptor stimulation causes renal, splanchnic, coronary, and cerebral vasodilation; minimal effect on HR, BP, or CO — note: the concept of a 'renal protective dose' is not supported by outcome data.

Moderate dose (3–10 mcg/kg/min) - β1 receptor activation predominates; increased contractility, HR, and CO; modest increase in BP through inotropy rather than vasoconstriction.

High dose (>10 mcg/kg/min) - α1 adrenergic effects dominate; systemic vasoconstriction increases SVR and MAP; pulmonary vascular resistance also increases. This range provides true vasopressor support but increases afterload and myocardial oxygen demand.

Arrhythmia risk - dopamine carries a higher risk of tachyarrhythmias (AF, SVT, PVCs) than norepinephrine at equivalent vasopressor doses — a key reason to consider norepinephrine first in most shock states. For tachyarrhythmia, reduce or stop the infusion; consider esmolol or metoprolol for refractory tachycardia — note: beta-blockade will also reduce dopamine's inotropic effect.

Sulphite content - commercial formulations contain sodium metabisulphite — exercise caution in patients with known sulphite sensitivity or severe asthma.

Can suppress hypoxic ventilatory response - even low-dose dopamine can suppress hypoxic ventilatory response by acting on carotid body DA receptors — clinically relevant in spontaneously breathing patients with hypoxic drive (e.g., COPD).

Extravasation tissue necrosis - Use a central venous line whenever possible. Dopamine causes severe local vasoconstriction and tissue ischemia if it extravasates; if extravasation occurs, immediately infiltrate the area with phentolamine (5–10 mg in 10 mL NS).

Hypertensive Crisis - If a dopamine infusion causes a hypertensive crisis, administration of an alpha-adrenergic blocker is recommended (e.g., phentolamine 5 mg IV); nitroprusside or nicardipine can also be used for acute BP management.

Nausea and vomiting - dopaminergic stimulation of the chemoreceptor trigger zone (CTZ) can cause nausea, particularly at lower doses; antiemetics may be needed.

Increased IOP and mydriasis - dopaminergic effects may raise intraocular pressure; exercise caution in patients with narrow-angle glaucoma.

Catecholamine-depleted states - Since dopamine acts partly by releasing stored norepinephrine from presynaptic terminals, it can lose efficacy in catecholamine-depleted states (e.g., prolonged shock, chronic heart failure).

Drug Interactions - concurrent use of MAO inhibitors is contraindicated; MAO inhibition dramatically prolongs and intensifies catecholamine effects, risking hypertensive crisis and cardiovascular collapse — reduce dopamine to one-tenth the usual dose if MAOIs cannot be avoided. Halogenated agents (sevoflurane, desflurane, isoflurane) sensitize the myocardium to catecholamine-induced arrhythmias; Watch closely for dysrhythmias when dopamine runs alongside volatile anesthesia. IV phenytoin combined with dopamine has caused severe hypotension and bradycardia; β-adrenergic blockers blunt the inotropic and chronotropic effects of moderate-dose dopamine; α1-mediated vasoconstriction is unaffected and may even be relatively enhanced. Combined use of ergot alkaloids (methylergonovine or ergometrine) can cause severe peripheral vasoconstriction and gangrene.

OB - Dopamine is generally avoided in obstetric hypotension (e.g., spinal hypotension for cesarean); phenylephrine or ephedrine are preferred as they have a more established safety profile for uteroplacental perfusion. High-dose dopamine-mediated vasoconstriction may reduce uteroplacental perfusion; if used in a hemodynamically unstable obstetric patient, fetal monitoring is essential.

Absolute - Pheochromocytoma or paraganglioma (catecholamine-secreting tumors); concurrent or recent MAOI use; uncorrected ventricular fibrillation or tachyarrhythmias.

Relative - Hypertrophic obstructive cardiomyopathy (HOCM) — increased inotropy worsens outflow obstruction; uncorrected hypovolemia — vasopressors do not substitute for volume resuscitation; atrial fibrillation with rapid ventricular response.

Caution - Known CAD or active myocardial ischemia (increased O2 demand); occlusive vascular disease (peripheral or mesenteric ischemia risk at high doses); patients with sulphite sensitivity (formulation contains sodium metabisulphite)

1-3 mcg/kg/min (Low Dose — Dopaminergic)

3-10 mcg/kg/min (Moderate Dose — Inotropic)

10-20 mcg/kg/min (High Dose — Vasopressor)

50 mcg/kg/min (MAX dose). Marginal clinical benefit above 20 mcg/kg/min; transition to norepinephrine or vasopressin should be strongly considered

Allow 10–15 min between titrations

Typical Preparation - 400 mg in 250 mL D5W (1600 mcg/mL) or 800 mg in 500 mL D5W (1600 mcg/mL)

Directly stimulates dopaminergic and adrenergic receptors AND indirectly releases stored norepinephrine from presynaptic terminals, amplifying adrenergic effects; receptor predominance shifts from DA → β1 → α1 as dose increases.

Hepatic, renal, and plasma. Active metabolites contribute to adrenergic effects. Active metabolites include Homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC), and norepinephrine.

Renal

None. Management of overdose should warrant rapid discontinuation of the infusion; effects resolve within ~10 minutes due to short half-life

Septic Shock - norepinephrine is now preferred over dopamine as the first-line vasopressor for septic shock per current Surviving Sepsis guidelines; dopamine's higher arrhythmia burden drives this preference.

Hepatic or renal impairment - does not significantly prolong effect given the very short plasma half-life; however, metabolite accumulation is possible with prolonged infusions in critically ill patients

The 'renal dose dopamine' myth - low-dose dopamine (1–3 mcg/kg/min) was historically used to protect renal function; multiple RCTs have shown no benefit in preventing AKI or reducing the need for renal replacement therapy — this practice is no longer recommended.