Bedside acetone breath analysis in differentiating acute heart failure from acute respiratory failure: an observational study in the emergency department

Observational studies have shown increased exhaled acetone concentrations in patients with heart failure (HF), related to the increased breakdown of fatty acids and subsequent production of ketone bodies.

The present study aims to assess the diagnostic discriminative value of exhaled acetone in differentiating acute heart failure (AHF) from acute respiratory failure (ARF) in patients presenting with acute dyspnoea.

Exhaled breath acetone was sampled using a point-of-care prototype acetone device in 26 patients with acute dyspnoea admitted to the emergency department. AHF was diagnosed in 10 patients (mean age: 76 ± 8 years, mean left ventricular ejection fraction (LVEF): 48 ± 11%), ARF in 10 patients (mean age: 53 ± 19 years, mean LVEF: 59 ± 3%), and a combination of AHF and ARF in 6 patients (mean age: 72 ± 15 years, mean LVEF: 55 ± 12%). To evaluate the relationship between haemodynamics (left- and right-sided filling pressures and cardiac index) and breath acetone levels, we enrolled an additional 29 patients (mean age: 72 ± 11 years, mean LVEF: 55 ± 8%) with stable HF scheduled for invasive evaluation.

Average breath acetone levels were higher in patients with acute dyspnoea compared to patients with stable HF: 0.94 ± 0.7 ppm vs. 0.11 ± 0.09 ppm (p < 0.0001). However, there were no significant differences between the study groups: 0.81 ± 0.67 ppm for AHF, 0.92 ± 0.55 ppm for ARF, and 1.19 ± 1.03 ppm for combined AHF and ARF (p = 0.6; Figure 1). The diagnostic power of breath acetone to differentiate AHF from ARF was poor, with an area under the ROC curve of 0.56 (p = 0.665). There was no correlation between breath acetone levels and haemodynamics (R-values < 0.2).

Breath acetone levels were increased in patients with AHF and ARF compared to patients with stable HF, but without significant differences between the two pathologies. Our data suggest that an increased adrenergic state, rather than haemodynamics, drives the increased ketone production in patients with acute dyspnoea.Figure 1.

Median breath acetone levels.