In a critically ill patient with hypotension, on dopamine, dobutamine, and noradrenaline (norepinephrine) infusion, which vasopressor should be increased first to improve blood pressure?

Increase Norepinephrine First

You should increase norepinephrine first, as it is the first-line vasopressor for hypotension in critically ill patients, and both dopamine and dobutamine are inappropriate choices for primary blood pressure support. 1, 2

Critical Problem with Your Current Regimen

You have three agents running simultaneously that should not be used together in this manner:

• Dopamine should be discontinued immediately unless this patient has absolute bradycardia or documented low risk of tachyarrhythmias, as it is associated with higher mortality and significantly more arrhythmias compared to norepinephrine 1, 2
• Dobutamine is NOT a vasopressor—it is an inotrope that actually causes vasodilation and will worsen hypotension if used without adequate vasopressor support 1
• Norepinephrine is the only appropriate first-line vasopressor among these three agents 1, 2

Correct Vasopressor Management Algorithm

Step 1: Immediate Actions

• Discontinue dopamine and transition entirely to norepinephrine as your primary vasopressor 1, 2
• Titrate norepinephrine to achieve MAP ≥65 mmHg 1, 2
• Ensure central venous access for safe norepinephrine administration 1, 2
• Place arterial catheter for continuous blood pressure monitoring if not already present 1, 2

Step 2: If Norepinephrine Alone Fails to Achieve Target MAP

• Add vasopressin at 0.03 units/minute (do not exceed 0.03-0.04 units/min except as salvage therapy) to either raise MAP to target or decrease norepinephrine requirements 1, 2, 3
• Never use vasopressin as monotherapy—it must be added to norepinephrine 1, 3

Step 3: If Norepinephrine Plus Vasopressin Still Inadequate

• Add epinephrine (0.05-2 mcg/kg/min) as a third vasopressor agent rather than escalating vasopressin beyond 0.03-0.04 units/min 1

Step 4: Role of Dobutamine (Only After Blood Pressure is Stabilized)

• Keep dobutamine ONLY if there is persistent hypoperfusion (elevated lactate, oliguria, altered mental status) despite adequate MAP and vasopressor therapy, particularly when myocardial dysfunction is evident 1, 2
• Dobutamine dosing: 2.5-20 mcg/kg/min 1
• If blood pressure is the primary problem, dobutamine will make it worse by causing vasodilation 1

Why This Specific Sequence Matters

The evidence strongly supports norepinephrine over dopamine and epinephrine monotherapy:

• Norepinephrine vs. dopamine: Dopamine causes significantly more arrhythmias (ventricular arrhythmias RR 0.35; 95% CI 0.19-0.66) and higher mortality 1
• Norepinephrine-dobutamine vs. epinephrine: While both achieve similar hemodynamic goals, epinephrine causes transient lactic acidosis, higher heart rates, more arrhythmias, and inadequate gastric mucosal perfusion 4, 5
• The combination of norepinephrine-dobutamine is more predictable and safer than epinephrine alone when both vasopressor and inotropic support are needed 4, 5

Common Pitfalls to Avoid

• Do not use dopamine for "renal protection"—this is strongly discouraged and has no benefit 1, 2, 3
• Do not delay norepinephrine initiation waiting to complete entire fluid resuscitation if life-threatening hypotension is present 1, 2
• Do not rely solely on blood pressure numbers—monitor tissue perfusion markers including lactate clearance, urine output (≥0.5 mL/kg/hr), mental status, and capillary refill 1, 3
• Do not use phenylephrine except in specific circumstances (norepinephrine-induced serious arrhythmias, documented high cardiac output with persistent hypotension, or salvage therapy) 1, 2