Dopamine

Endogenous catecholamine. Direct action on peripheral dopamine receptors and direct + indirect (via NE release) action on α- and β-adrenergic receptors. In dogs and cats, adrenergic activity is dose-dependent: 5–10 µg/kg/min predominantly β₁ (positive inotropy, increased contractility, HR, cardiac output); 10–15 µg/kg/min has both α₁ and β₁ effects with α₁ (vasoconstriction, increased SVR/PVR) progressively dominating. Half-life in dogs is ~11 minutes; metabolized by MAO and COMT in liver, kidney, and plasma.

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Clinical background

Dopamine is one of the older catecholamines but still earns a place in small-animal practice. It is dose-dependent across receptor families, which makes it more versatile than dobutamine but less predictable. In a general practice setting without echocardiography, dopamine is most useful as an inotrope-plus-mild-vasopressor for anesthesia-induced hypotension that has not responded to fluid therapy and lightening the plane.

Pharmacology

Endogenous catecholamine and immediate precursor of norepinephrine. Receptor activity is dose-dependent, and the dose ranges that produce each effect overlap, which is part of why dopamine is harder to titrate cleanly than dobutamine or norepinephrine:

• Low dose (≈1–3 µg/kg/min), historically described as “dopaminergic”: vasodilation in renal and mesenteric beds via DA₁ receptors. Newer human evidence has largely abandoned the idea of “renal-dose dopamine” providing meaningful kidney protection, and the “dopaminergic dose” framing is no longer recommended in the Surviving Sepsis literature.
• Mid dose (≈3–10 µg/kg/min), predominantly β₁: increased contractility and heart rate, increased cardiac output. This is the range used for inotropic support of anesthesia-induced hypotension in dogs.
• High dose (>10 µg/kg/min): α₁ vasoconstriction overtakes β effects. Systemic vascular resistance and blood pressure rise; heart rate and contractility remain elevated. The drug now resembles norepinephrine but with substantially more arrhythmogenicity.

Onset is within 5 minutes IV, duration 10 minutes after stop. Dopamine is metabolized by COMT and MAO; about 25% is converted to norepinephrine in the periphery. Does not cross the blood-brain barrier.

Indications

Primary use cases:

• Anesthesia-induced hypotension in dogs that has not responded to fluid bolus and lightening the anesthetic plane
• Hypotension during septic shock when norepinephrine is not available, though norepinephrine is preferred where available
• Bradycardia with hypotension where atropine has failed
• Adjunctive support of low cardiac output in dogs with congestive heart failure (less commonly used than dobutamine for this purpose)

The Surviving Sepsis Campaign positions norepinephrine as the first-line vasopressor for septic shock and dopamine as a second choice, the rationale is that dopamine produces more tachyarrhythmias for an equivalent pressure response. In small-animal practice, the same principle applies. Dopamine remains a reasonable choice in clinics where norepinephrine isn’t stocked, but if both are available, norepinephrine is generally preferred for sustained pressure support.

Cats

Cats deserve special mention. Plumb’s notes that dopamine in cats has been associated with arrhythmias and that the dosing range is narrower; the Wiese et al. work cited in Lumb & Jones further documents adverse cardiovascular effects in cats with hypertrophic cardiomyopathy specifically. The cat dose range in this calculator (5–20 µg/kg/min) starts higher than the dog range to reflect that low-dose effects are less reliable in cats; nevertheless, monitor ECG closely and avoid in cats with HCM.

Dosing

• Dogs: 3–20 µg/kg/min, titrated from the low end to effect
• Cats: 5–20 µg/kg/min, with extra caution above 10 µg/kg/min

Most patients responding to dopamine will respond at 5–10 µg/kg/min in dogs. Doses approaching 20 µg/kg/min should prompt reassessment of indication and contributing causes, at that point, switching to norepinephrine often provides more pressure with fewer arrhythmias.

Preparation

InfusionFox offers two preparation workflows for dopamine. They deliver the same drug, just compounded into different bag sizes; pick whichever fits the bags you have on hand.

The Plumb’s 6 × kg method is a simple bedside preparation: add (6 × patient weight in kg) milligrams of dopamine to a 100 mL bag of compatible carrier fluid. The resulting concentration produces a delivered rate where 1 mL/hr = 1 µg/kg/min, which makes pump-rate adjustments intuitive at the bedside. Use this when you have a 100 mL bag available; the InfusionFox 6×kg dopamine calculator does the math for you.

The standard CRI workflow uses fixed-concentration preps in 250 mL or 500 mL bags (200 mg dopamine in either bag size). It applies the standard CRI formula at the bedside rather than relying on the 6×kg identity. Use this when 100 mL bags aren’t available. The standard dopamine CRI calculator handles the math.

Administration

Dilute in 5% dextrose, 0.9% sodium chloride, or lactated Ringer’s. Compatible with most other infusions but incompatible with sodium bicarbonate, bicarbonate inactivates dopamine. Discard if the solution turns pink, yellow, or brown, which indicates oxidation.

A central line is preferred. Peripheral administration is acceptable for shorter infusions but the infusion site must be visible and checked frequently for extravasation, which can cause local tissue necrosis from α₁-mediated vasoconstriction.

Drug interactions

• Halogenated inhalant anesthetics (isoflurane, sevoflurane) sensitize the myocardium and increase arrhythmia risk during dopamine infusion, relevant because anesthesia hypotension is the most common veterinary CRI indication.
• Beta-blockers can produce unopposed α-mediated vasoconstriction with severe hypertension.
• MAO inhibitors and tricyclic antidepressants potentiate dopamine’s effects substantially; reduce starting dose by ≈90% if these are on board.
• Phenytoin plus dopamine has caused severe hypotension and bradycardia in humans, avoid the combination.

Adverse effects

• Tachyarrhythmias, sinus tachycardia, premature ventricular complexes, ventricular tachycardia. More common than with dobutamine or norepinephrine at equivalent inotropic effect.
• Excessive vasoconstriction at higher doses (>15 µg/kg/min), splanchnic, renal, and limb ischemia
• Hypertension, particularly at high doses
• Nausea and vomiting in awake patients
• Extravasation injury, tissue necrosis from local α₁ vasoconstriction
• Suppression of pituitary hormone secretion (TSH, prolactin) with prolonged infusions, usually clinically silent, but worth knowing in critically ill patients

Monitoring

• Continuous ECG, arrhythmias are common, particularly above 10 µg/kg/min
• Continuous or frequent blood pressure
• Urine output as a perfusion marker
• Lactate trend if shock is the indication
• Mucous membrane color, CRT, extremity temperature
• Serum potassium and magnesium, derangements amplify arrhythmia risk

Extravasation

Dopamine extravasation can cause severe local tissue necrosis, similar to norepinephrine. If it occurs, stop the infusion immediately, aspirate what you can through the catheter before removing it, and consider local infiltration with phentolamine.

Weaning

Wean by reducing the rate in 1–2 µg/kg/min increments every 10–15 minutes while monitoring blood pressure. Patients often tolerate weaning better than they did initiation, receptor down-regulation during the infusion means they need less drug to maintain pressure than they did to gain it. As with other catecholamine vasopressors, do not stop abruptly unless transitioning to another agent.

Sources

• Plumb’s Veterinary Drugs, dopamine monograph (current edition).
• Hart S, Silverstein DC. Catecholamines. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. 3rd ed. Elsevier; 2023:855–859. Chapter 147; Table 147.1.
• Wiese AJ, et al. Cardiovascular effects of dopamine in cats with hypertrophic cardiomyopathy. Cited in Lumb & Jones Veterinary Anesthesia and Analgesia 6th ed., Chapter 21.