Amp Up Your Heart Knowledge 2026 – Master Cardiac Electrophysiology & Heart Failure!

The main idea is inotropism with a secondary reduction in myocardial workload. Digoxin increases contractility (positive inotropy) by inhibiting the Na+/K+ ATPase in cardiac myocytes. This raises intracellular sodium, which reduces the activity of the Na+/Ca2+ exchanger, leading to more intracellular calcium and stronger contractions. At the same time, digoxin enhances vagal tone, slowing AV nodal conduction and lowering heart rate, which cuts myocardial oxygen demand and workload. In heart failure with reduced ejection fraction, this combination improves stroke volume and exercise tolerance.

The other drugs mainly help by unloading or vasodilation rather than boosting contractility. Lisinopril reduces afterload and tends to improve symptoms and remodeling without increasing force of contraction. Spironolactone lowers preload and fibrosis, offering survival and symptom benefits but not a direct inotrope. Hydralazine reduces afterload as a vasodilator without enhancing contractility.