Furosemide is given IV to a patient in acute pulmonary edema. Before significant diuresis occurs, the patient feels relief of dyspnea. This early benefit is due to:

• A Venodilatation (via PGE2 stimulation) reducing venous return and preload before the onset of diuresis ✓
• B Immediate inhibition of NKCC2 in the loop of Henle reducing GFR and tubular reabsorption
• C Reflex tachycardia increasing cardiac output and pulmonary blood flow
• D Bronchodilation mediated by beta-2 adrenoceptor stimulation

Explanation

When given IV, furosemide causes rapid venodilation by stimulating renal prostaglandin (PGE2) synthesis, which reduces systemic venous tone, decreases venous return, and reduces cardiac preload within minutes. This precedes the diuresis (which takes 15–30 minutes) and provides early symptomatic relief in pulmonary edema. Prostaglandin synthesis inhibitors (NSAIDs) can blunt this venodilatory effect of furosemide. The loop diuretic effect then provides sustained reduction in plasma volume.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.