Respiratory pulse pressure variation fails to predict fluid responsiveness in acute respiratory distress syndrome

INTRODUCTION: Fluid responsiveness prediction is of utmost interest during acute respiratory distress syndrome (ARDS), but the performance of respiratory pulse pressure variation (Δ(RESP)PP) has scarcely been reported. In patients with ARDS, the pathophysiology of Δ(RESP)PP may differ from that of healthy lungs because of low tidal volume (Vt), high respiratory rate, decreased lung and sometimes chest wall compliance, which increase alveolar and/or pleural pressure. We aimed to assess Δ(RESP)PP in a large ARDS population. METHODS: Our study population of nonarrhythmic ARDS patients without inspiratory effort were considered responders if their cardiac output increased by >10% after 500-ml volume expansion. RESULTS: Among the 65 included patients (26 responders), the area under the receiver-operating curve (AUC) for Δ(RESP)PP was 0.75 (95% confidence interval (CI(95)): 0.62 to 0.85), and a best cutoff of 5% yielded positive and negative likelihood ratios of 4.8 (CI(95): 3.6 to 6.2) and 0.32 (CI(95): 0.1 to 0.8), respectively. Adjusting Δ(RESP)PP for Vt, airway driving pressure or respiratory variations in pulmonary artery occlusion pressure (ΔPAOP), a surrogate for pleural pressure variations, in 33 Swan-Ganz catheter carriers did not markedly improve its predictive performance. In patients with ΔPAOP above its median value (4 mmHg), AUC for Δ(RESP)PP was 1 (CI(95): 0.73 to 1) as compared with 0.79 (CI(95): 0.52 to 0.94) otherwise (P = 0.07). A 300-ml volume expansion induced a ≥2 mmHg increase of central venous pressure, suggesting a change in cardiac preload, in 40 patients, but none of the 28 of 40 nonresponders responded to an additional 200-ml volume expansion. CONCLUSIONS: During protective mechanical ventilation for early ARDS, partly because of insufficient changes in pleural pressure, Δ(RESP)PP performance was poor. Careful fluid challenges may be a safe alternative.