Synthetic catecholamine, β₁-agonist (inotropy)MONITORED CARE SETTINGREQUIRES MONITORING

Dobutamine

Dobutamin Hameln

Pure inotropy when the problem is the pump and not vascular tone. Strong β₁ effect with marked β₂ effect means that stroke volume increases while systemic vascular resistance falls at low doses — good in the cold, hypoperfused patient with an acceptable blood pressure, less so when blood pressure is already low. The dose threshold lies around 5 μg/kg/min: below that vasodilation predominates, above it the vascular effect shifts toward constriction.

BOXED WARNING

Dobutamine increases myocardial oxygen consumption and can precipitate ischaemia, tachyarrhythmia, and rapid ventricular rate in atrial fibrillation. Never given without continuous ECG and blood pressure monitoring, and not to a patient with uncorrected hypovolaemia.

Dosing in adults

By indicationuppdaterad 2026-08-22
IndicationRegimenComment
Cardiogenic shock and low cardiac output2–20 μg/kg/min iv, titrate in steps of 2–3 μg/kg/minbelow 5 μg/kg/min vasodilation; above 5 μg/kg/min vasoconstriction
Acute decompensated heart failure with hypoperfusion2,5–10 μg/kg/min ivshortest possible treatment duration, no prognostic benefit
Stress echocardiographyStart 5 μg/kg/min, increase every 3 minutes to 10, 20, 30 and 40 μg/kg/minatropine may be needed to achieve the target heart rate
Bradycardia (second-line)2–10 μg/kg/min ivafter atropine and while awaiting pacing
Maximum dose40 μg/kg/minarrhythmia and ischaemia are limiting factors far below this level
Renal impairment

No dose adjustment. Metabolites are inactive and accumulation has no clinical significance.

Hepatic impairment

No established dose adjustment. Titrate to effect.

Children

2–20 μg/kg/min; children likely tolerate a lower maximum dose than adults, titrate cautiously.

Pitfall

The effect is absent in a patient on non-selective beta-blockade — do not increase the dose in that situation, switch to an inotropic agent acting downstream of the beta receptor, such as levosimendan or milrinone. Also avoid in hypertrophic obstructive cardiomyopathy and in severe hypovolaemia, where increased contractility worsens the outflow obstruction or drains an already underfilled ventricle.

Pharmacokinetics

BIOAVAIL.
Intravenous only
ONSET
1–2 minutes
PEAK EFFECT
10–12 minutes
2 minutes
Vd
0,2 l/kg
METABOLISM
COMT to 3-O-methyldobutamine (inactive)
EXCRETION
Renal as conjugates
TOLERANCE
Receptor downregulation after 2–3 days

Adverse effects by frequency

≥ 10 %
Tachycardia, palpitations, blood pressure rise, headache
1–10 %
Ventricular ectopic beats, angina, hypotension at low dose, nausea, hypokalaemia
< 1 %
Sustained ventricular tachycardia, myocardial ischaemia and infarction, eosinophilic myocarditis, stress cardiomyopathy