Heart failure reduces kidney perfusion, activating neurohumoral mechanisms, including RAAS.

These mechanisms increase cardiac filling pressure, causing ventricular dilation. However, without adequate cardiac force, fluid overload causes pulmonary and peripheral edema.

Diuretics alleviate these symptoms by increasing natriuresis and decreasing edema.

They decrease cardiac workload and oxygen demand without affecting contractility, effectively treating symptomatic congestive heart failure.

Loop diuretics block the Na⁺-K⁺-2Cl cotransporter in the ascending limb of Henle's loop  and are potent diuretics.

Thiazide  diuretics are comparatively less potent. However, in the case of loop diuretic-related refractoriness, thiazide combination therapy enhances the effect of loop diuretics.

K⁺-sparing diuretics directly inhibit apical Na⁺ channels in distal tubules. They help treat heart failure-associated hypertension when combined with other diuretics.

Mineralocorticoid receptor antagonists inhibit aldosterone and mitigate gene expression of Na⁺ channels, effectively lowering blood pressure and decreasing effects of heart failure.