Dopamine in Clinical Practice
Primary Recommendation
Dopamine should be reserved as a second-line vasopressor in highly selected patients (those with low risk of tachyarrhythmias and absolute or relative bradycardia), while norepinephrine remains the first-choice vasopressor for septic shock. 1 For inotropic support in acute heart failure, dopamine can be used at 3-5 mcg/kg/min, though dobutamine is generally preferred for augmenting cardiac output. 1, 2
Dose-Dependent Effects and Administration
Dopamine exhibits distinct pharmacologic effects based on infusion rate:
2-3 mcg/kg/min: Predominantly dopaminergic receptor stimulation with renal vasodilation, though clinical evidence shows limited effects on diuresis and no renal protection. 1, 2
3-5 mcg/kg/min: Beta-adrenergic stimulation producing inotropic effects with increased myocardial contractility and cardiac output. 1, 2, 3
>5 mcg/kg/min: Progressive alpha-adrenergic stimulation causing vasoconstriction and increased systemic vascular resistance, useful for maintaining blood pressure in hypotensive patients but potentially deleterious by increasing left ventricular afterload and pulmonary pressures. 1, 2
>10 mcg/kg/min: Predominantly vasopressor effects. 3
The FDA-approved regimen recommends starting at 2-5 mcg/kg/min in patients likely to respond to modest increments, or 5 mcg/kg/min in more seriously ill patients, with gradual increases in 5-10 mcg/kg/min increments up to 20-50 mcg/kg/min as needed. 4
Clinical Context: Septic Shock
The Surviving Sepsis Campaign explicitly recommends against using dopamine as a first-line vasopressor. 1 Norepinephrine is the first-choice agent (strong recommendation, moderate quality evidence), with dopamine relegated to an alternative only in highly selected patients with low risk of tachyarrhythmias or bradycardia (weak recommendation, low quality evidence). 1
This downgrade stems from evidence showing dopamine is associated with increased mortality in septic patients and increased arrhythmias compared to norepinephrine. 1 Low-dose dopamine should absolutely not be used for renal protection (strong recommendation, high quality evidence). 1
Clinical Context: Acute Heart Failure
For acute heart failure with peripheral hypoperfusion (hypotension, decreased renal function) refractory to diuretics and vasodilators, inotropic agents including dopamine are indicated. 1
Dopamine at 3-5 mcg/kg/min provides inotropic support, though dobutamine (starting at 2-3 mcg/kg/min, titrated to 15-20 mcg/kg/min) is generally preferred for augmenting cardiac output in chronic low-output cardiac failure. 1, 2 The European Society of Cardiology gives dopamine a Class IIb recommendation (level of evidence C) for this indication. 1
For patients with systolic blood pressure <90 mmHg, dopamine may be considered; for systolic blood pressure 90-100 mmHg, dobutamine or a vasodilator/inotrope combination is preferred. 2
Administration and Monitoring Requirements
Dopamine must be infused through a large vein whenever possible (antecubital fossa preferred over hand or ankle veins) because extravasation causes severe tissue necrosis and sloughing. 4 Central venous access is preferred, though peripheral large-bore or intraosseous access can be used if central access is unavailable or staff experience is limited. 1
Use only an infusion pump, preferably volumetric, not gravity-regulated apparatus. 4 Continuous monitoring requirements include:
- Blood pressure (invasive arterial catheter placement recommended as soon as practical for all patients requiring vasopressors) 1, 3
- Heart rate and continuous ECG telemetry 2, 3
- Urine output (should urinary flow decrease without hypotension, reduce dopamine dosage) 4
- Signs of organ perfusion and congestion 2
- Infusion site for extravasation 1, 4
Blood pressure should be measured every 5-15 minutes during infusion. 1
Critical Warnings and Adverse Effects
Dopamine carries significant risks that limit its clinical utility:
Tachycardia and arrhythmias: Use with extreme caution in patients with heart rate >100 bpm. 1 In cardiogenic shock, patients treated with norepinephrine versus dopamine had improved 28-day survival and fewer arrhythmias. 2
Increased myocardial oxygen demand: Potentially harmful as it increases oxygen consumption and calcium loading. 1
Vasoconstriction at higher doses: Alpha-adrenergic stimulation increases afterload, which may be deleterious in acute heart failure. 1
No renal protection: Despite historical use, low-dose dopamine does not prevent acute kidney injury or improve renal outcomes and should not be used for this purpose. 1, 5, 6, 7
Splanchnic effects: Evidence suggests low-dose dopamine may worsen splanchnic oxygenation and impair GI function. 7
Endocrine and immunologic impairment: Low-dose dopamine may impair endocrine and immune systems and blunt ventilatory drive. 7
Discontinuation Protocol
When discontinuing dopamine, gradually decrease the dose while expanding blood volume with intravenous fluids to prevent marked hypotension. 4 Withdraw inotropic agents as soon as adequate organ perfusion is restored and/or congestion reduced. 2
Key Pitfalls to Avoid
Do not use low-dose dopamine for "renal protection" - this practice is ineffective and potentially dangerous. 1, 6, 7
Do not use dopamine as first-line vasopressor in septic shock - norepinephrine is superior with lower mortality and fewer arrhythmias. 1
Do not administer through small peripheral veins - extravasation causes severe tissue necrosis. 4
Do not combine with alkalinizing substances - dopamine is inactivated in alkaline solution. 4
Do not ignore rising heart rate or new arrhythmias - these are indications to decrease or temporarily suspend dosage. 4
Monitor for disproportionate rise in diastolic pressure (marked decrease in pulse pressure), which indicates predominant vasoconstrictor activity requiring dose reduction. 4