Sodium 97 mmol/L: Profound Hyponatremia Unmasking Borderline HFpEF with RV Dysfunction

A 53-year-old man with no known prior medical history — and not taking any medications — presented to the emergency department with slurred speech, generalised weakness, progressive dyspnoea, and bilateral leg swelling over eight weeks. He had first noticed leg swelling during a transatlantic flight to Thailand and attributed increasing fatigue before the trip to work stress. He was obese, a heavy smoker, and consumed alcohol daily. His blood pressure in the ED was 210/112 mmHg with a heart rate of 108 bpm, respiratory rate 30/min, and bilateral pitting oedema to the knees.

Venous blood gas on arrival revealed a serum sodium of 97 mmol/L — one of the most severe hyponatraemia presentations compatible with consciousness, confirmed on formal biochemistry. The initial working diagnosis was symptomatic hypervolaemic hyponatraemia secondary to heart failure, and IV furosemide 40 mg was administered. A CT pulmonary angiogram was performed given the dyspnoea and tachycardia.

CT pulmonary angiography excluded pulmonary embolism but showed bi-basal interlobular septal thickening consistent with pulmonary oedema, cardiomegaly, and flattening of the interventricular septum — the last finding suggesting elevated right heart pressures. Brain CT, performed given the neurological presentation, was unremarkable.

Figure 1

CT Pulmonary Angiogram — Bi-Basal Interlobular Septal Thickening (Pulmonary Oedema)

CT pulmonary angiogram on admission demonstrating bi-basal interlobular septal thickening (blue arrows) consistent with hydrostatic pulmonary oedema from elevated left atrial pressures. Cardiomegaly and interventricular septal flattening were also noted. The interlobular septal thickening pattern — representing fluid accumulation in the interstitium — is the CT correlate of the plain X-ray Kerley B lines and reflects elevated capillary wedge pressure. In the context of profound hyponatraemia, this radiographic constellation strongly supports hypervolaemic hyponatraemia from heart failure.

The patient was admitted to the ICU for profound hyponatraemia with neurological compromise. Sodium correction was targeted at no more than 8 mmol/L per 24-hour period to prevent osmotic demyelination syndrome (ODS). Two boluses of 1.8% hypertonic saline at 2 mL/kg each were administered, with serial arterial blood gas monitoring after each bolus. Fluid intake was restricted to 1 L/day.

Echocardiography was performed in the ICU: borderline preserved LVEF (45–50%), severely dilated left atrium (LAVI 73.94 mL/m²), evidence of elevated left atrial pressures, impaired right ventricular systolic function (TAPSE 2 cm), maximum tricuspid regurgitation velocity 3.0 m/s, and right atrial dilation. Advanced echocardiographic parameters applied to the ESC 2019 HFpEF diagnostic algorithm scored 6 points — functional domain (TRV 3.0 m/s, 2 points), morphological domain (LAVI 73.9 mL/m², 2 points; elevated LVMI, 1 minor point), and biomarker domain (NT-proBNP 752 pg/mL with atrial fibrillation, major criterion threshold >365 pg/mL in AF, 2 points) — supporting a diagnosis of HFpEF despite the borderline LVEF.

Twenty-four hours into the ICU admission, the patient's consciousness deteriorated abruptly with inability to protect his airway, followed by hypoxic cardiac arrest. One cycle of CPR restored spontaneous circulation. He was intubated and mechanically ventilated. At the time of arrest, serum sodium was 111 mmol/L. Over the subsequent 48 hours, sodium improved from 111 to 126 mmol/L with further hypertonic saline boluses and fluid restriction. Neurological function recovered substantially and he was successfully extubated. He was transferred to the ward and discharged with serum sodium of 134 mmol/L.

Figure 2

Serum Sodium Trend — Admission to Discharge

Serial serum sodium values plotted from admission through ICU stay and ward transfer to discharge, demonstrating the controlled rate of correction achieved with hypertonic saline boluses and fluid restriction. The controlled correction rate (≤8 mmol/L per 24 hours) reflects adherence to ODS prevention guidelines. Note the point at which the cardiac arrest occurred (sodium 111 mmol/L), the subsequent ICU management, and the stable plateau before safe extubation. Discharge sodium of 134 mmol/L confirmed successful and safe correction without ODS.

Hospital complications included new-onset atrial fibrillation (treated with apixaban), hospital-acquired pneumonia (co-amoxiclav), and suspected obesity hypoventilation syndrome/obstructive sleep apnoea contributing to respiratory acidosis. Discharge medications included apixaban, bisoprolol, furosemide, and a fluticasone/vilanterol inhaler.

Discussion

This case demonstrates the pathophysiological cascade from undiagnosed HFpEF to profound hyponatraemia via neurohormonal activation. Elevated left atrial pressures from HFpEF — evidenced by the severely dilated left atrium, elevated LAVI, and high TRV — transmitted congestion to the systemic venous circulation, causing impaired renal perfusion. This activated the renin-angiotensin-aldosterone system and stimulated non-osmotic ADH release, producing water retention in excess of sodium retention: the mechanism of dilutional (hypervolaemic) hyponatraemia. Right ventricular dysfunction played an additional amplifying role — RV failure causes systemic venous congestion and renal hypoperfusion independent of LVEF, further stimulating neurohormonal water retention. Lee et al. have described a specific association between RV dysfunction and hyponatraemia in the Korean Heart Failure Registry, consistent with what we observe here. The borderline LVEF (45–50%) complicated phenotypic classification, but application of the ESC 2019 scoring algorithm confirmed HFpEF despite the ambiguous ejection fraction — emphasising that diagnostic algorithms are needed precisely when individual markers (EF, NP) fall in equivocal ranges.

The management of symptomatic hyponatraemia in the context of HFpEF requires navigating two competing urgencies: rapid enough sodium correction to halt neurological deterioration, while respecting the 8 mmol/L per 24-hour ceiling imposed by ODS risk. The therapeutic dilemma is further complicated by the fact that loop diuretics — the cornerstone of HFpEF decongestion — can paradoxically worsen hyponatraemia by depleting sodium more than water. Hypertonic saline bolus therapy, as used here, provides targeted sodium delivery without the diuretic-induced natriuresis that loop agents produce. The cardiac arrest that occurred at sodium 111 mmol/L — likely from cerebral oedema causing brainstem herniation — illustrates that neurological deterioration can occur faster than the typical correction algorithm predicts, particularly in patients with additional risk factors (alcohol use, obesity, obstructive sleep apnoea). Clinicians managing severe hyponatraemia should have a low threshold for escalation to intensive monitoring, with arterial blood gas sampling after every hypertonic saline bolus.