A Case of Severe Hyponatremia Unmasking Borderline Heart Failure With Preserved Ejection Fraction With Right Ventricular Dysfunction

TL;DR

A patient with severe low sodium levels revealed heart failure with preserved ejection fraction and right ventricular dysfunction, highlighting diagnostic challenges.

Contribution

This case emphasizes the role of right ventricular dysfunction in hyponatremia and the need for careful sodium correction in borderline heart failure.

Findings

Severe hyponatremia (97 mmol/L) was linked to right ventricular dysfunction and elevated atrial pressures.

HFpEF diagnosis was supported by advanced echocardiography despite borderline left ventricular ejection fraction.

Management required balancing sodium correction to avoid neurological risks and osmotic demyelination.

Abstract

Hyponatremia, characterised by a low serum sodium level, is the most common electrolyte abnormality encountered in clinical practice. Its diverse etiologies and varied clinical presentations can make diagnosis and management complex, especially in the context of borderline heart failure with preserved ejection fraction (HFpEF). We report the case of a 53-year-old male who presented with slurred speech, generalised weakness, shortness of breath, and bilateral leg swelling over eight weeks. Initial investigations revealed severe hypotonic hyponatremia (sodium = 97 mmol/L), elevated urine osmolality (515 mmol/kg) and low urine sodium (<20 mmol/L). Imaging demonstrated pulmonary oedema and cardiomegaly. Liver and renal studies excluded cirrhosis and nephrotic syndrome. Echocardiography showed an estimated borderline preserved left ventricular ejection fraction, severely dilated left atrium, and impaired right ventricular function. Advanced echocardiography parameters supported a diagnosis of HFpEF based on the European Society of Cardiology scoring algorithm, namely, an increased tricuspid regurgitation velocity of 3.0 m/second, a severely elevated left atrial volume index at 73.9 mL/m² and an increased left ventricular mass index at 142 g/m². The N-terminal pro-B-type natriuretic peptide level was measured at 752 pg/mL in the context of atrial fibrillation and obesity. The patient experienced acute neurological deterioration requiring intravenous hypertonic saline, intubation, and mechanical ventilation in the intensive care unit. After excluding other potential causes of hypervolemic hyponatremia, including liver cirrhosis, nephrotic syndrome, and chronic kidney disease, this case highlights the diagnostic challenges that arise when left ventricular function and natriuretic peptide levels are not markedly abnormal. In this patient, right ventricular dysfunction and elevated atrial pressures appeared to play a central role in the development of hyponatremia. Management required a careful balance: correcting sodium levels promptly to mitigate neurological risk, while avoiding overly rapid shifts that could precipitate osmotic demyelination syndrome. Clinicians should maintain a high index of suspicion for HFpEF in patients presenting with fluid overload and hyponatremia, even when traditional heart failure markers are equivocal. A comprehensive, multidisciplinary approach, integrating biochemical data, imaging, and clinical context, is essential for accurate diagnosis and safe, effective treatment.

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