Nitrates: chemistry that gives the heart a rest
Angina is chest pain when the heart's oxygen demand outstrips its supply. A nitrate such as glyceryl trinitrate (GTN) is turned into nitric oxide in the vessel wall, raising cyclic GMP and relaxing smooth muscle. It dilates veins most, so less blood returns to the heart, which then has less to pump — its workload and oxygen demand fall, and the pain eases. It is a targeted vasodilator acting through the body's own signalling.
Antiarrhythmics: steadying the electrical beat
Each heartbeat is an electrical wave carried by sodium, calcium and potassium currents. When that wiring misfires, an antiarrhythmic dampens the wayward signal. The classic Vaughan-Williams scheme sorts them by which current they target: Class I block sodium channels, Class II are the beta-blockers, Class III block potassium channels, and Class IV are the heart-slowing calcium-channel blockers.
Cardiac glycosides: more force, tiny safety margin
A cardiac glycoside like digoxin blocks the cell's sodium-potassium pump. Sodium then builds inside the cell, which indirectly raises intracellular calcium — so each beat squeezes harder. Digoxin is a positive inotrope used in some heart failure and to slow the rate in atrial fibrillation. It is an old drug, originally from the foxglove plant.
Digoxin's famous problem is its razor-thin therapeutic index: the toxic dose sits barely above the effective dose. Toxicity brings nausea, visual disturbances and dangerous arrhythmias, and low potassium makes it worse — which is why diuretic-induced potassium loss is so risky here. Because it is cleared by the kidney, dosing falls in kidney impairment, and levels are checked with therapeutic drug monitoring.