What is the evidence for using hypertonic saline (hypertonic sodium chloride) bolus in the management of acute heart failure?

Evidence for Hypertonic Saline Bolus in Acute Heart Failure Management

Hypertonic saline bolus therapy has limited evidence supporting its use in acute heart failure, with current data suggesting it may be beneficial when combined with loop diuretics but should not be used as monotherapy for this indication. 1

Efficacy in Acute Heart Failure

• Hypertonic saline is not recommended as a standalone treatment for acute heart failure, as there is insufficient high-quality evidence supporting this approach 2
• When combined with furosemide, hypertonic saline has shown promising results in treating acute decompensated heart failure with fluid overload, demonstrating improved outcomes compared to furosemide alone 1, 3
• Meta-analyses of randomized controlled trials have shown that combination therapy with hypertonic saline and furosemide is associated with lower all-cause mortality (RR 0.55; 95% CI, 0.46-0.67) and reduced heart failure-related readmissions (RR 0.50; 95% CI, 0.33-0.76) compared to furosemide alone 1

Hemodynamic Effects

• Hypertonic saline has been shown to be probably beneficial in non-obstructive cardiogenic shock (Grade C evidence), though the evidence is limited 2
• Studies in cardiac surgery patients have confirmed beneficial effects of hypertonic saline on hemodynamics, with increases in cardiac output and blood pressure, and reduced systemic vascular resistance 2
• However, it remains unclear whether the improvement in cardiac output is due to preload effect or direct inotropy, and safety in patients with impaired ventricular function has not been well established 2

Clinical Outcomes with Combination Therapy

• Combination therapy with hypertonic saline and furosemide has demonstrated:
  • Shorter hospital length of stay (mean difference -3.28 days) 1, 4
  • Increased daily diuresis (mean difference 583.87 mL) 1, 4
  • Greater weight loss (mean difference -1.76 kg) 1, 4
  • Improved renal function with decreased serum creatinine (mean difference -0.46 mg/dL) 1, 3
  • Higher 24-hour urine sodium excretion (mean difference 61.10 mEq) 1

Limitations and Caveats

• The evidence for hypertonic saline alone in acute heart failure is insufficient, with most positive studies examining combination therapy with loop diuretics 2, 3
• There is heterogeneity among studies regarding the concentration of hypertonic saline used (ranging from 1.7% to 30%), making standardized recommendations difficult 2
• Current evidence cannot be extrapolated to conditions other than fluid overload states in acute decompensated heart failure 1, 5
• The mechanism behind the paradoxical benefit of adding sodium (via hypertonic saline) to patients who are already fluid overloaded requires further investigation 5

Safety Considerations

• Serum sodium levels should be monitored closely when administering hypertonic saline, as significant increases can occur (mean difference 6.89 mEq/L) 1
• In studies using bolus doses, the majority of patients had peak sodium levels <155 mmol/L, with levels typically returning to normal within 24 hours 2
• The highest recorded sodium level in a survivor from bolus studies was 169 mmol/L, though this was potentially influenced by high blood alcohol levels affecting analyzer function 2
• No evidence of osmotic demyelination syndrome has been reported in studies of hypertonic saline use for heart failure when properly monitored 2

Clinical Application

• Hypertonic saline should be considered as an adjunct to loop diuretics in patients with diuretic-resistant acute decompensated heart failure rather than as monotherapy 1, 3
• The optimal concentration of hypertonic saline and dosing regimen for heart failure remains undefined, with studies using various concentrations and protocols 2, 1
• Future adequately powered, multi-center, randomized controlled trials are needed to better define the role of hypertonic saline in acute heart failure management, particularly in patients with renal dysfunction 3
• While promising, this approach should be used cautiously until further validation in diverse patient populations and in those on optimal current heart failure treatment 3, 4