Hyponatraemia in heart failure: a mechanistic approach to contemporary management.

Hyponatraemia remains the most prevalent electrolyte disturbance in heart failure, complicating clinical management and correlating with adverse outcomes. While traditionally viewed as a biomarker of disease severity, mounting evidence suggests that hyponatraemia reflects specific pathophysiological mechanisms that demand targeted intervention alongside standard decongestion strategies. This mini review synthesises contemporary evidence to provide clinicians with an updated, mechanistically grounded approach to hyponatraemia in heart failure. We emphasise the critical distinction between dilutional hypervolaemic states driven by arginine vasopressin dysregulation and depletional hypovolaemic states arising from aggressive diuresis or sodium losses. Recent trials challenge longstanding practices: fluid restriction in stable chronic heart failure shows no quality-of-life benefit despite guideline recommendations, whilst emerging biomarkers such as early urine chloride offer promise in identifying diuretic resistance. We critically appraise the role of vasopressin antagonists, which correct sodium biochemically but lack mortality benefit, and explore oral urea as a pragmatic alternative supported by recent observational data. For acute severe presentations, we detail hypertonic saline protocols with strict correction limits and discuss proactive desmopressin strategies to prevent osmotic demyelination. Important knowledge gaps persist, including optimal diagnostic algorithms in diuretic-exposed patients, patient-centred outcome data for sodium-correcting therapies, and validation of safe-correction protocols. Overall, this review equips clinicians to integrate mechanistic understanding with evidence-based practice whilst identifying priorities for future investigation.