OBJECTIVE: We tested the hypothesis that NO contamination of hospital compressed air also improves PaO(2) in patients with acute lung injury (ALI) and following lung transplant (LTx). DESIGN: Prospective clinical study. SETTING: Cardiothoracic intensive care unit. PATIENTS: Subjects following cardiac surgery (CABG, n=7); with ALI (n=7), and following LTx (n=5). INTERVENTIONS: Four sequential 15-min steps at a constant FiO(2) were used: hospital compressed air-O(2) (H1), N(2)-O(2) (A1), repeat compressed air-O(2) (H2), and repeat N(2)-O(2) (A2). MEASUREMENTS AND RESULTS: NO levels were measured from the endotracheal tube. Cardiorespiratory values included PaO(2) were measured at the end of each step. FiO(2) was 0.46+/-0.05, 0.53+/-0.15, and 0.47+/-0.06 (mean+/-SD) for three groups, respectively. Inhaled NO levels during H1 varied among subjects (30-550 ppb, 27-300 ppb, and 5-220 ppb, respectively). Exhaled NO levels were not detected in 4/7 of CABG (0-300 ppb), 3/6 of ALI (0-140 ppb), and 3/5 of LTx (0-59 ppb) patients during H1, whereas during A1 all but one patient in ALI and three CABG patients had measurable exhaled NO levels (P<0.05). Small but significant decreases in PaO(2) occurred for all groups from H1 to A1 and H2 to A2 (132-99 Torr and 128-120 Torr, P <0.01, respectively). There was no correlation between inhaled NO during H1 and exhaled NO during A1 or the change in PaO(2) from H1 to A1. CONCLUSIONS: Low-level NO contamination improves PaO(2) in patients with ALI and following LTx.
OBJECTIVE: We tested the hypothesis that NO contamination of hospital compressed air also improves PaO(2) in patients with acute lung injury (ALI) and following lung transplant (LTx). DESIGN: Prospective clinical study. SETTING: Cardiothoracic intensive care unit. PATIENTS: Subjects following cardiac surgery (CABG, n=7); with ALI (n=7), and following LTx (n=5). INTERVENTIONS: Four sequential 15-min steps at a constant FiO(2) were used: hospital compressed air-O(2) (H1), N(2)-O(2) (A1), repeat compressed air-O(2) (H2), and repeat N(2)-O(2) (A2). MEASUREMENTS AND RESULTS: NO levels were measured from the endotracheal tube. Cardiorespiratory values included PaO(2) were measured at the end of each step. FiO(2) was 0.46+/-0.05, 0.53+/-0.15, and 0.47+/-0.06 (mean+/-SD) for three groups, respectively. Inhaled NO levels during H1 varied among subjects (30-550 ppb, 27-300 ppb, and 5-220 ppb, respectively). Exhaled NO levels were not detected in 4/7 of CABG (0-300 ppb), 3/6 of ALI (0-140 ppb), and 3/5 of LTx (0-59 ppb) patients during H1, whereas during A1 all but one patient in ALI and three CABG patients had measurable exhaled NO levels (P<0.05). Small but significant decreases in PaO(2) occurred for all groups from H1 to A1 and H2 to A2 (132-99 Torr and 128-120 Torr, P <0.01, respectively). There was no correlation between inhaled NO during H1 and exhaled NO during A1 or the change in PaO(2) from H1 to A1. CONCLUSIONS: Low-level NO contamination improves PaO(2) in patients with ALI and following LTx.
Authors: Robert Lindwall; Mats E Svensson; Claes G Frostell; Staffan Eksborg; Lars E Gustafsson Journal: Intensive Care Med Date: 2006-10-17 Impact factor: 17.440