β-adrenergic stimulation increases intracellular Ca2+ influx and pacemaker currents, leading to arrhythmias. Class II antiarrhythmic drugs are β-adrenoceptor antagonists that indirectly block Ca2+ channels to counteract β receptor stimulation. These drugs primarily depress phase 4 cardiac depolarization, reducing automaticity, prolonging AV conduction, and decreasing heart rate and contractility. Class II drugs vary in β1-selectivity, intrinsic sympathomimetic activity, membrane-stabilizing effects, and action potential prolongation. Nonselective β-blockers, such as propranolol, inhibit β2 -receptor-mediated hypokalemia and also block Na+ channels. However, they can cause bronchospasm. β1 -selective drugs like metoprolol have reduced bronchospastic effects. Other class II drugs include esmolol, a short-acting intravenous drug, and acebutolol, used to treat ventricular ectopic beats. Adverse effects of class II drugs include fatigue, bradycardia, bronchospasm, and hypotension. Abrupt discontinuation of these drugs can cause rebound symptoms, potentially worsening arrhythmias.