Dobutamine is approved by the Food and Drug Administration (FDA) for short-term use in patients with decreased contractility due to heart failure or cardiac surgical procedures leading to cardiac decompensation. The agent has not demonstrated positive outcomes in the hospital or outpatient setting for patients with heart failure despite hemodynamically improving the patient’s condition.

Dobutamine can be used as temporary intravenous inotropic support until resolution of the acute inducing factors or the patient receives more definitive treatment, such as coronary revascularization, mechanical circulatory support, or heart transplant. Short-term intravenous inotropic support should be given to patients in cardiogenic shock to preserve systemic blood flow and protect from end-organ damage.

Patients can reasonably receive dobutamine in continuous intravenous form for inotropic support to bridge patients with late-stage heart failure, stage D, that is refractory to guideline-directed medical therapy until patients who are candidates for and awaiting cardiac transplantation or mechanical circulatory support receive the appropriate long-term treatment.

Continuous intravenous inotropic dobutamine support can reasonably be given in the short-term for those hospitalized patients with severe systolic dysfunction who present with low blood pressure and a significantly decreased cardiac output, to preserve systemic blood flow and protect from end-organ damage.

Continuous intravenous inotropic dobutamine support can reasonably be given for the long-term in palliative patients with late-stage heart failure, stage D, who are not candidates for mechanical circulatory support or cardiac transplantation for symptomatic control, regardless of guideline-directed medical therapy.

Intravenous inotropic dobutamine can be given off-label to patients to induce pharmacological stress during stress echocardiography if patients are not able to perform an exercise stress test.[1][2][3][4][5]

Dobutamine is used as a pharmacological agent because of its inotropic effects on the myocardium through binding and activating the beta-1 receptors. The medication is indicated clinically for decompensated congestive heart failure because of the sympathomimetic effects. Dobutamine increases contractility, which leads to decreased end-systolic volume and, therefore, increased stroke volume. The larger stroke volume leads to an increase in cardiac output of the heart. The changes in cardiac output allow for the baroreceptor mediated response to decrease the systemic vascular resistance and cause little to no change in the arterial blood pressure. In addition to the well-known beta-1 activity, dobutamine has shown to have some beta-2 activity, which contributes to the reduction in the systemic vascular resistance, and alpha-1 activity, to an even lesser extent, whose vasoconstrictive effects are negated by the baroreceptor mediated response and beta-2 activity.[6][7][8][9]

Dobutamineadministration is via intravenous access for inotropic support in decompensated congestive heart failure and stress echocardiogram testing. The dosage for cardiac decompensation in heart failure can begin with one-half to one mcg/kg/min and can increase up to a maximum of 40 mcg/kg/min. The lower doses of dobutamine can be prescribed at 2.5 to 5.0 mcg/kg/min, and the higher end of dobutamine doses can be 5.0 to 20.0 mcg/kg/min. The dose for the stress echocardiogram test is initiated at five mcg/kg/min and can be increased in intervals of 10 mcg/kg/min every 3 to 5 minutes until reaching the target heart rate. Dobutamine comes in a solution as a racemic mixture of both positive and negative enantiomers for intravenous administration. The positive enantiomer in the solution is predominately selective for the beta sympathetic receptors, mainly beta 1 and 2, whereas the negative enantiomer has been shown in studies to be selective for the alpha one receptors.

Dobutamine administration can lead to possible adverse reactions, mainly due to the sympathomimetic activity. The majority of patients taking this medication have experienced a rise in the systolic blood pressure of 10 to 20 mmHg and an increase of 5 to 10 beats per minute in their heart rate. There have been reports of further increases in systolic blood pressure and heart rate. In about 10% of the patients, there can be a rise of 30 beats per minute or more in the heart rate, and in about 7.5% of patients, there can be an increase of 50 mmHg or more in the systolic blood pressure. Patients with preexisting hypertension are more susceptible to the adverse effects on systolic blood pressure when using dobutamine.

Dobutamine increases the risk of rapid ventricular response in patients with preexisting atrial fibrillation. The recommendation is that these patients use a regimen of digoxin before starting dobutamine, to decrease the risk of developing atrial fibrillation with a rapid ventricular response. There has been an increased risk of developing premature ventricular beats during the administration of dobutamine. About 5% of patients experience premature ventricular beats.

Other adverse effects caused by this medication include hypotension rarely. While increases in systolic blood pressure is a common effect due to dobutamine, hypotension can occur, less frequently, due to the decreases in the systemic vascular resistance. Recommendations include decreasing the dose or stopping the drug to reverse the hypotensive effects.

Phlebitis at the site of the intravenous administration can occur, but it an uncommon reaction. Dobutamine can rarely reduce the potassium concentrations to hypokalemic levels. Other rare adverse effects have occurred in one to three percent of the patients, including nausea, headaches, chest pain, palpitations, and shortness of breath. Dobutamine contains sulfite, which can lead to reactions in rare patients with sulfite hypersensitivity.

Dobutamine use has been contraindicated, according to the Food and Drug Administration, in patients with a noted history of allergic reactions to either previous dobutamine use or any sulfite use. The medication is contraindicated in patients with a history of idiopathic hypertrophic sub-aortic stenosis.