In heart failure, a decrease in blood pressure causes baroreceptors to trigger compensatory sympathetic mechanisms. These mechanisms increase heart rate and contractility to maintain blood pressure.

The released catecholamines stimulate vasoconstriction, enhancing venous return and preload to improve cardiac output.

However, these actions increase cardiac workload, worsening heart failure symptoms.

β -blockers counteract this sympathetic overstimulation by reducing the heart rate and, contraction force, and relaxing cardiomyocytes. They also inhibit renin production and catecholamine-induced mitogenicity, curbing cardiac remodeling.

Among these drugs, carvedilol —a nonselective third generation β-blocker, and nebivolol  —a β₁ -selective agent— have vasodilatory properties.

These drugs benefit clinically stable patients with symptomatic heart failure or left ventricular dysfunction, reducing morbidity.

However, nonselective agents may induce adverse effects like bradycardia, peripheral vasoconstriction, and bronchoconstriction.

This necessitates careful dose titration, starting with low doses and a gradual increase based on patient tolerance and vital signs.