Inotropicvasodilatory

Inotropicvasodilatory, commonly referred to as an inodilator, describes drugs that simultaneously increase myocardial contractility (inotropy) and induce vasodilation. This dual action is designed to raise cardiac output while reducing or redistributing vascular resistance, thereby improving perfusion without markedly increasing afterload.

Mechanisms and classes

Inodilators act through different but overlapping pathways. Phosphodiesterase III inhibitors, such as milrinone and inamrinone (inamrinone), raise intracellular cyclic AMP in cardiac myocytes and vascular smooth muscle. This enhances calcium availability for stronger contraction and promotes smooth muscle relaxation, producing vasodilation. Some beta-adrenergic agonists, notably dobutamine, mainly enhance contractility but can cause mild vasodilation through beta-2 receptor effects and reduced systemic resistance in certain settings. Levosimendan is another inodilator that works by calcium sensitization of the contractile apparatus and opening of potassium channels, contributing both inotropic support and vasodilation.

Clinical use

Inodilators are used primarily in hospital settings for acute decompensated heart failure and cardiogenic shock, especially when low cardiac output coexists with signs of elevated filling pressures. They are often employed as short- to intermediate-term therapy or as a bridge to recovery, stabilization, or transplantation. They are not typically used as long-term chronic therapy due to risks of tachycardia, hypotension, and arrhythmias, among other adverse effects.

Examples and considerations

Milrinone, amrinone, dobutamine, and levosimendan are notable examples. Selection depends on hemodynamic goals, blood pressure, renal function, and risk of arrhythmias. Monitoring includes continuous hemodynamic assessment, ECG surveillance, and electrolyte management to mitigate adverse effects.