What is the initial dose and titration of dopamine (dopamine hydrochloride) for a patient in shock?

Dopamine Dosing in Shock

Dopamine should NOT be used as a first-line vasopressor in shock; norepinephrine is the preferred agent, with dopamine reserved only for highly selected patients with absolute or relative bradycardia and low risk of tachyarrhythmias. 1, 2

Initial Dosing Strategy

When dopamine is deemed appropriate (rare circumstances only):

• Start at 2-5 mcg/kg/min for patients likely to respond to modest increments of heart force and renal perfusion 3, 2
• For more seriously ill patients, begin at 5 mcg/kg/min and increase gradually using 5-10 mcg/kg/min increments up to 20-50 mcg/kg/min as needed 3
• Titrate every 15-30 minutes based on hemodynamic response, targeting a mean arterial pressure (MAP) of 65 mmHg 2

Dose-Dependent Pharmacologic Effects

Understanding dopamine's receptor activity guides dosing:

• <5 mcg/kg/min: Dopaminergic effects (renal and mesenteric vasodilation) 2
• 5-10 mcg/kg/min: β-adrenergic effects (increased cardiac contractility and heart rate) 2
• >10 mcg/kg/min: α-adrenergic effects (vasoconstriction) 2

Administration Requirements

Critical safety measures:

• Infuse into a large vein (antecubital fossa preferred) to prevent extravasation and tissue necrosis 3
• Use only an infusion pump (preferably volumetric), never gravity-regulated IV apparatus 3
• Place an arterial catheter as soon as practical for continuous blood pressure monitoring 1, 4
• Ensure adequate volume resuscitation first (minimum 30 mL/kg crystalloid) before initiating vasopressors 1

Titration End Points and Limitations

Target goals:

• MAP ≥65 mmHg 1, 2
• Urine output >40 mL/hr 5

Stop escalating or reduce dose if:

• Heart rate reaches 120-125 beats/min 5
• Arrhythmias develop (dopamine causes significantly more arrhythmias than norepinephrine: 24% vs 12%) 6, 7
• Disproportionate rise in diastolic pressure occurs (marked decrease in pulse pressure) 3
• Doses exceed 50 mcg/kg/min—at this point, check urine output frequently and consider switching agents 3

Why Dopamine Is NOT First-Line

Evidence against dopamine as initial therapy:

• Higher mortality in cardiogenic shock compared to norepinephrine (subgroup analysis showed increased 28-day mortality) 6
• Significantly more arrhythmic events: 24.1% with dopamine vs 12.4% with norepinephrine (P<0.001) 6
• No mortality benefit in septic shock compared to norepinephrine 6, 7
• Worsens myocardial oxygenation in ischemic myocardium (increases myocardial lactate production) 5

Discontinuation Protocol

Never stop abruptly:

• Gradually decrease the dose while simultaneously expanding blood volume with IV fluids 3, 2
• This prevents marked hypotension that can occur with sudden cessation 3

The Only Acceptable Indication

Dopamine may be considered only when:

• Patient has absolute or relative bradycardia (heart rate <60-70 bpm) 1, 2
• Low risk of tachyarrhythmias (no history of atrial fibrillation, ventricular arrhythmias, or ischemic heart disease) 1, 2
• Norepinephrine would be problematic due to the bradycardia 1

Common Pitfalls to Avoid

• Do NOT use low-dose dopamine (<5 mcg/kg/min) for "renal protection"—this has been definitively disproven and is strongly discouraged 1, 2
• Do NOT mix with sodium bicarbonate or alkaline solutions (dopamine is inactivated in alkaline pH) 3
• Do NOT use as first-line therapy in septic shock—norepinephrine is superior with fewer adverse events 1, 2, 4
• Do NOT continue escalating if arrhythmias develop—switch to norepinephrine 6, 7

When to Switch to Norepinephrine

Immediately transition if:

• Arrhythmias develop (sinus tachycardia >125 bpm, atrial fibrillation, ventricular ectopy) 6, 7
• Doses exceed 20 mcg/kg/min without achieving MAP goals 1
• Patient has cardiogenic shock (dopamine associated with worse outcomes) 6