Table 3.8-3. Use of IV inotropic agents in patients with acute heart failure





1) <3 microg/kg/min

2) 3-5 microg/kg/min

3) >5 microg/kg/min (max, 30 microg/kg/min)

– Low doses (1) mainly cause vasodilation of the visceral, renal, and coronary vascular beds; intermediate doses (2) increase myocardial contractility and cardiac output via adrenergic stimulation; high doses (3) increase peripheral vascular resistance through alpha-adrenergic stimulation (this may cause clinical deterioration in patients with AHF due to an increase in LV and right ventricular afterloads)

– May be used in patients with AHF and low BP

– Low-dose dopamine is often used in combination with higher doses of dobutamine

– Survival on dopamine may be worse compared with norepinephrine in case of cardiogenic shock (hypotension and hypoperfusion)Evidence 17Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to subgroup analysis of a randomized controlled trial with unclear classification of the type of shock. De Backer D, Biston P, Devriendt J, et al; SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 4;362(9):779-89. doi: 10.1056/NEJMoa0907118. PubMed PMID: 20200382.


2-20 microg/kg/min

– Used to increase cardiac output

– Stimulates beta1-receptors, increases myocardial contractility, increases heart rate; lower doses cause vasodilation while higher doses cause vasoconstriction

– Infusion over >24-48 h is associated with the development of tolerance and partial loss of hemodynamic effects

– Discontinuation may be difficult because of recurrent low BP, congestion, or kidney failure, which is why the infusion rates should be reduced gradually (by 2 microg/kg/min per day) and used together with optimized vasodilator therapy (eg, oral ACEIs)

– May cause ventricular or supraventricular arrhythmia and chest pain in patients with IHD


Bolus 25-75 microg/kg over 10-20 min followed by infusion of 0.375-0.75 microg/kg/min

– Phosphodiesterase inhibitor (inhibits cAMP degradation); has positive inotropic effects and facilitates myocardial relaxation and vasodilation

– Indicated in patients with peripheral hypoperfusion and normal BP with or without pulmonary congestion in whom diuretic and vasodilator treatment was ineffective

– May be used instead of dopamine in patients treated with beta-blockers in the case of inadequate response to dobutamine

– May have proarrhythmic effects and should be used with caution in patients with IHD


0.2-2 microg/kg/min

– Use (with caution!) only in patients with cardiogenic shock and BP <90 mm Hg when organ perfusion is inadequate in spite of other interventions

– May be indicated in shock patients with AHF and sepsis

– May be combined with each of the above inotropic agents (use with caution in combination with dopamine)


1 mg every 3-5 min (only during CPR); 0.05-0.5 microg/kg/min

Use only during CPR in patients with cardiac arrest or in the case of dobutamine resistance and persistent hypotension


Loading dose 0.5-1 mg, followed by 0.125-0.375 mg/d (monitor serum drug levels)

Effective in patients with AHF caused by tachyarrhythmia (eg, AF); not recommended in patients with AHF after acute MI because of its proarrhythmic effects

ACEI, angiotensin-converting enzyme inhibitor; AF, atrial fibrillation; AHF, acute heart failure; BP, blood pressure; cAMP, cyclic adenosine monophosphate; CPR, cardiopulmonary resuscitation; IHD, ischemic heart disease; IV, intravenous; LV, left ventricular; MI, myocardial infarction.