Positive inotropic agents increase cardiac output in heart failure.

These drugs enhance sarcomere contractility by elevating free cytosolic  Ca²⁺ levels, boosting contraction force and output.

Cardiac glycosides are positive inotropic agents with a unique structure comprising a steroid nucleus linked to a lactone ring and sugars without ionizable groups.

They inhibit the Na⁺/K⁺ pump, raising intracellular Na⁺ concentrations while blocking Ca²⁺ extrusion. This improves myocardial contractility, cardiac output, and renal perfusion, ultimately alleviating cardiac stress.

These drugs' effects depend on their plasma concentration. Low levels enhance parasympathetic activity, while high concentrations cause calcium overload, mesenteric artery ischemia, and sinus rhythm disturbances.

Other inotropic agents include β₁-adrenoceptor agonists, glucagon, phosphodiesterase  III inhibitors, and steroid derivatives.

Their common side effects include gastrointestinal and neurotoxic symptoms. Electrolyte imbalances may trigger arrhythmias or toxicity.

Their narrow therapeutic window necessitates monitoring serum electrolytes and patient response to minimize risks.