This chapter discusses the actions, indications, pharmacokinetics,
dosing, and adverse effect profiles of vasopressor drugs that are
pertinent to emergency medicine practice. Specific medications also
are discussed. Please also see Chapter 25, Approach to the Patient in Shock.
Dobutamine (Dobutrex) is a synthetic sympathomimetic drug that
exerts potent inotropic and mild chronotropic activities. Dobutamine
is formulated as a racemic mixture with β1- and β2-adrenergic and α-adrenergic
agonist activities that are offset by α-adrenergic
antagonist activity (Table 24-1). The net
result is an increase in myocardial contractility and systemic vasodilation,
with minimal changes in heart rate. Doses of up to 20 micrograms/kg/min
will increase cardiac output, decrease peripheral vascular resistance,
and decrease pulmonary occlusive pressures. Conversely, doses >20
micrograms/kg/min will increase the heart rate
and induce arrhythmias.
24-1 Ability of Commonly Used Sympathomimetic Agents to
Stimulate Adrenergic Receptors
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The onset of action of dobutamine is 1 to 2 minutes, and the peak
response occurs within 10 minutes after IV administration. The apparent
volume of distribution (Vd) is 0.2 L/kg, and the drug is
metabolized primarily in tissue and the liver to inactive metabolites.
The elimination half-life is 1 to 2 minutes, with the majority of
the drug being eliminated within 48 hours in the urine as inactive
Dobutamine is indicated for short-term positive inotropic support
for the treatment of cardiovascular decompensation secondary to ventricular
dysfunction or low-output heart failure. It is the preferred agent
in septic shock with depressed cardiac output despite adequate left
ventricular filling pressures. Dobutamine is also usually the preferred
agent in the management of cardiogenic shock. It increases
cardiac output and renal and mesenteric blood flow without direct stimulation
of the heart rate and decreases systemic vascular resistance.
Dosing and Administration
Dobutamine is administered only as a continuous IV infusion.
The dosage range is 2 to 20 micrograms/kg/min; however,
most patients can be maintained on 10 micrograms/kg/min. Doses
larger than 20 micrograms/kg/min increase the
risk of tachyarrhythmia. To assess effectiveness of the dose administered,
patients should be monitored with a central venous pressure or pulmonary
artery catheter. Unlike many pressor agents, dobutamine may safely
be given peripherally.
The primary adverse effects of dobutamine are modest increases
in heart rate (increases >5 to 15 beats/min are uncommon),
blood pressure (increases >10 to 20 mm Hg are uncommon), and ectopic
arrhythmias (escape beats, unifocal and multifocal ventricular ectopic
beats, and ventricular bigeminy). Less common adverse effects include
headache, paresthesias, tremors, nausea, angina, and dyspnea. Heart rate
increases >10% may induce or exacerbate myocardial ischemia.
Dopamine (Intropin) is an endogenous catecholamine and a precursor
of norepinephrine and other endogenous catecholamines. It acts on dopaminergic, β1-
and α-adrenergic receptors. In low doses (0.5 to
5.0 micrograms/kg/min), dopamine causes vasodilation
in the renal, mesenteric, coronary, and intracerebral vasculatures
via stimulation of the dopaminergic receptors. This stimulation
results in an increase in renal blood flow, glomerular filtration
rate, sodium excretion, and urine output. However, the ability of
dopamine to prevent renal complications has not been demonstrated.
At intermediate doses (5 to 10 micrograms/kg/min),
dopamine stimulates β1-adrenergic receptors,
thereby improving myocardial contractility and cardiac output and
increasing sinoatrial nodal conduction. At these doses, dopamine
increasingly stimulates α-adrenergic receptors,
causing peripheral vasoconstriction and increasing blood pressure.
At doses >10 micrograms/kg/min, the α-adrenergic
effects dominate, causing peripheral vasoconstriction and vasoconstriction
of the mesenteric and renal vascular beds.
The onset of action of dopamine is 5 minutes, with a duration
of action of 10 minutes after IV administration. Dopamine is used
only as a continuous IV infusion. The apparent Vd is 1.8 to 2.5
L/kg. Dopamine is 75% metabolized by monoamine
oxidase (MAO) and catechol-O-methyltransferase
(COMT) in the liver, kidneys, and plasma to an inactive metabolite.
The remaining 25% is metabolized to norepinephrine in the
adrenergic nerve terminals. The elimination half-life is 2 minutes
and 80% is eliminated by the kidneys as the inactive metabolite and
norepinephrine. The elimination half-life may be prolonged in patients
with hepatic or renal insufficiency and in pediatric patients.
Dopamine is indicated for reversing hemodynamically significant
hypotension caused by myocardial infarction, trauma, heart failure,
and renal failure when fluid resuscitation is unsuccessful or not appropriate. Like
norepinephrine, it is considered first-line therapy for septic shock.1 Dopamine
is used to increase cardiac output, blood pressure, and peripheral
perfusion. It should not be used at low doses solely for the purpose
of renal protection or to increase urine output.
Dosing and Administration
Use the lowest dose of dopamine to maintain the desired blood
pressure. Most patients can be maintained on doses between 3 and
20 micrograms/kg/min (continuous infusion). Tachyphylaxis
may occur with larger doses because the actions of dopamine are
dependent on endogenous stores of norepinephrine and other catecholamines.
Do not infuse dopamine in the same IV line with alkaline infusions.
IV administration through a central line is recommended to prevent extravasation.
To discontinue dopamine, taper the dose and do not stop it abruptly.
Dopamine produces dose-dependent adverse ...