{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T15:16:02Z","timestamp":1773933362382,"version":"3.50.1"},"reference-count":30,"publisher":"Danish Medical Association","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dan Med J"],"abstract":"<jats:p>INTRODUCTION. While the diuretic effect of loop diuretics in acute heart failure (AHF) is well established, it remains debated whether furosemide exerts any extrarenal decongestive effects. This study aimed to examine the acute effects of furosemide on pulmonary congestion, diuresis and haemodynamics in patients hospitalised with AHF.\n\nMETHODS. We conducted a prospective interventional study including 20 AHF patients, each receiving 80 mg of intravenous furosemide at baseline. Diuresis, perfusion index, echocardiography and pulmonary fluid via remote dielectric sensing (ReDS) were assessed at predefined time points until 360 minutes. The primary endpoint was a change in ReDS within 30 minutes.\n\nRESULTS. The cohort had a mean age of 78 \u00b1 9 years, with 65% diagnosed with heart failure with reduced ejection fraction. Baseline ReDS was 35.3 \u00b1 1.8%. No significant reduction in ReDS was observed at any time point; a non-significant decrease of 1.7% was observed at 20 minutes (p = 0.32). Diuresis reached 134 \u00b1 56 ml by 20 minutes (p = 0.02). Perfusion index declined significantly by 25 minutes (p = 0.03) and remained stable until 120 minutes. No other haemodynamic parameters changed significantly.\n\nCONCLUSIONS. Intravenous furosemide did not acutely reduce pulmonary fluid before diuresis, suggesting no immediate extrarenal effect. Haemodynamic changes occurred only after diuresis, indicating its primary acute action is diuretic, with later responses likely being secondary to volume loss.\n\nFUNDING. None.\n\nTRIAL REGISTRATION. 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