Pharmacological Management of Heart Failure

Loop diuretics block the sodium-potassium-2-chloride cotransporter in the thick ascending limb of the loop of Henle, a segment of the kidney that normally reabsorbs a large fraction of filtered sodium. Blocking this transporter produces a substantial loss of sodium and water in the urine, which reduces blood volume and lowers the elevated filling pressures responsible for the shortness of breath and swelling seen in decompensated heart failure.

Because this same transporter is involved in handling other electrolytes, blocking it also causes increased urinary loss of potassium, magnesium, and calcium. Patients on loop diuretics require monitoring for these electrolyte losses, and hypokalemia in particular increases the risk of dangerous arrhythmias.

Furosemide is the most widely used loop diuretic. Its absorption from the gut can be unreliable in patients with decompensated heart failure, since the same fluid overload that the drug is meant to treat can also cause swelling of the gut wall and reduce drug absorption. For this reason, intravenous administration is commonly used in the hospital for patients with significant fluid overload, since it bypasses this absorption problem entirely. Torsemide and bumetanide are alternative loop diuretics with more predictable oral absorption, and are sometimes preferred for long-term outpatient use.

Loop diuretics and aldosterone antagonists are frequently used in the same patient, and their opposite effects on potassium are an important practical consideration. Loop diuretics promote potassium loss, while aldosterone antagonists reduce potassium loss. When both are used together, as they often are alongside the renin-angiotensin-aldosterone system blockers from Module 2, the net effect on serum potassium depends on the balance between these opposing forces, and regular monitoring is required.