Reviving Unconventional Interventions: Using Hyperdiuresis in Diuretic-Resistant Heart Failure

Introduction: Diuretics are an essential component of decompensated heart failure management. Yet, some patients develop diuretic resistance. Defined as inadequate response to escalating dosage of diuretics. Management includes increasing diuretic dosage, combination diuretic therapy and ultrafiltration. A less recognized approach is Hyperdiuresis, where loop diuretics are combined with hypertonic saline to enhance natriuresis and overcome diuretic resistance. We present a case of diuretic resistant heart failure responding to Hyperdiuresis.


Description: A 76-year-old male with a history of congestive heart failure presented with respiratory failure secondary to pneumonia and pulmonary congestion requiring intubation. Chest Xray showed pulmonary infiltrates and congestion. Despite completing antibiotics and receiving Bumex 2mg IV twice daily for congestion, patient failed weaning trials due to tachypnea and continued need for pressure support. Chest X-ray and CT showed persistent pulmonary congestion, BNP was 30,000 and urine output was ~1L with an intake of 2.7L. Bumex dose was increased to 2 mg three times daily, and metolazone 5 mg was added. Urine output improved to 2L. However, pulmonary congestion persisted. Considering serum sodium of 148 and Creatinine Clearance of 60 mL/min², decision was made to pursue Hyperdiuresis. Patient received 40 mg IV Lasix and 150 ml of 3% saline. Urine output increased to 5L over 24 hours. Patient was then resumed on Bumex 2 mg IV twice daily with an output of 3 liters. Patient was liberated from mechanical ventilation 2 days after Hyperdiuresis.


Discussion: Diuretic resistance poses a challenge in heart failure management. When increasing dosages of diuretics or combination therapy fail, interventions as ultrafiltration are often considered. Proposed pathophysiology of diuretic resistance includes renal hypoperfusion, neurohormonal activation and decreased sodium delivery to the distal nephron. The mechanism of Hyperdiuresis includes complementary effects on sodium reabsorption and renal blood flow, with hypertonic saline causing intravascular volume expansion, increasing sodium and chloride delivery to macula dense, inhibiting RAAS system and Lasix increasing renal blood flow, sodium and chloride delivery to macula dense, achieving both diuresis and natriuresis.