Dopamine is the precursor of epinephrine and norepinephrine.

​

• Dopaminergic effects (0.5 to 2 micrograms/kg per minute) directly activate dopaminergic receptors in the kidneys and splanchnic arteries, increasing renal blood flow, urine output, and sodium excretion.

​​

• Beta1 effects (2 to 10 micrograms/kg per minute) is a weak partial agonist of myocardial beta1 receptors. It causes the release of norepinephrine from the sympathetic nerve terminal (a tyramine-like effect), contributing to myocardial stimulation and a mild vasoconstrictor effect.

​​

• Alpha effects (> 10 micrograms/kg per minute) affect the peripheral alpha-adrenergic stimulation, resulting in vasoconstriction in all vascular beds and increasing mean arterial pressure and systemic vascular resistance. The vasoconstrictor effect overcomes the dopaminergic vasodilator effects, leading to decreased renal blood flow and urine output.

​

The use of dopamine in patients with heart failure

​

The dose required in acute decompensated heart failure to improve systemic and renal hemodynamics may be higher (4-6 micrograms/kg per minute) than the low dose.

 

The Renal Optimization Strategies Evaluation (ROSE) trial showed that low-dose dopamine (2 μg/kg/min) does not affect diuresis or renal function.

​

• The co-primary outcome of 72-hour urine volume was 8.5 L in the dopamine group compared to 8.3 L in the placebo group (p = 0.58).

• The co-primary outcome change in cystatin-C was 0.12 mg/L in the dopamine group versus 0.11 mg/dL in the placebo group (p = 0.72).

​

In patients experiencing severe cardiogenic shock, high doses of dopamine are used to increase systemic vascular resistance. These higher doses also raise left ventricular (LV) afterload more than the positive inotropic effect. The high dose may increase PCWP, peripheral vasoconstriction, and left and right afterload. The peripheral vasoconstriction increases venous return. 

​

The inotropic responses to dopamine may be reduced due to desensitization of the beta-adrenergic pathway and depletion of myocardial catecholamine stores, which is common in patients with chronic severe heart failure.

​

The Comparison of Dopamine and Norepinephrine in the Treatment of Shock (SOAP II) trial compared norepinephrine and dopamine in 1,679 patients with various shock causes. 

 

• The primary outcome showed no difference in survival at 28 days between patients treated with norepinephrine or dopamine. However, dopamine was linked to significantly higher arrhythmia rates (24% compared to 12.4% for norepinephrine), e.g., atrial fibrillation. Additionally, there was a higher incidence of severe arrhythmia with dopamine (6.1%) versus norepinephrine (1.6%). 

• In a pre-defined subgroup of patients with cardiogenic shock, comprising 280 patients (16.7%), dopamine use was associated with a notably increased mortality rate.  

• Based on this study's findings, norepinephrine is recommended as the preferred vasopressor for patients with cardiogenic shock. 

• In my humble opinion, due to various mechanisms of heart failure, norepinephrine is the preferred vasopressor for managing shock in acute pulmonary embolism, critical pulmonary hypertension, and in combination with inotropic agents for left ventricular failure. For patients with valvular heart disease, my preference depends on the hemodynamics associated with the valve condition. For instance, in cases of severe mitral valve stenosis caused by rheumatic disease, I usually prefer beta-blockers. In cases of valve regurgitation, I prefer arterial vasodilators with or without inotropic agents for hemodynamic support before valve interventions.

​​​​​​

Sinus tachycardia and tachyarrhythmia may be unwanted side effects. Other adverse effects of dopamine include digital gangrene in patients with PAD, and nausea at high doses, tissue necrosis at the site of infiltration. The local injection of the alpha-adrenergic antagonist phentolamine may counteract local infiltration.

​

​