Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study

BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO(2) = 95 ± 16 mmHg, PEEP = 0, FiO(2) = 1.0), and eight patients with ARDS and septic shock (PaO(2) = 88 ± 11 mmHg, PEEP = 0, FiO(2) = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO(2) of at least 40 mmHg, at FiO(2) 1.0 and PEEP 10 cmH(2)O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (Q(VA)/Q(T)), and a dose-dependent increase in PaO(2)/FiO(2) (P ≤ 0.012). Dose-response of MPAP and PVRI were similar in both groups with a plateau effect at 4.5 ppm. Dose-response of PaO(2)/FiO(2) was influenced by the presence of septic shock. No plateau effect was observed in patients with septic shock and PaO(2)/FiO(2) increased by 173 ± 37% at 150 ppm. In patients without septic shock, an 82 ± 26% increase in PaO(2)/FiO(2) was observed with a plateau effect obtained at 15 ppm. In both groups, dose-response curves demonstrated a marked interindividual variability and in five patients pulmonary vascular effect and improvement in arterial oxygenation were dissociated. CONCLUSION: For similar NOinduced decreases in MPAP and PVRI in both groups, the increase in arterial oxygenation was more marked in patients with septic shock.