Effect of inhaled nitric oxide on venous admixture depends on cardiac output in patients with acute lung injury and acute respiratory distress syndrome

Background: It has been shown that inhaled nitric oxide (NO) reduces intrapulmonary venous admixture (Q(VA)/Q(T)) and improves oxygenation in patients suffering from acute respiratory distress syndrome (ARDS). The change in Q(VA)/Q(T) during NO inhalation varies individually. Factors known to influence the respiratory response to NO are the NO conceritration and the level of shunt before NO administration. Other factors that may modify the effect on gas-exchange during NO breathing are unknown. Methods: We studied the effect of 40 ppm inhaled NO on pulmonary gas-exchange and haemodynamics in 37 patients with acute lung injury (ALI) and ARDS, respectively, and factors that may influence the respiratory response to NO. Results: Inhalation of 40 ppm NO produced a decrease in mean pulmonary artery pressure (MPAP) from 33.1+/-7.2 to 30.2+/-6.8 (mean+/-SD) mmHg (P<0.0001) while pulmonary artery wedge pressure (PAWP), cardiac output and mean arterial pressure remained constant. Change in Q(VA)/Q(T) during NO inhalation depended on the preinhalation cardiac output and had no association with mixed venous oxygen tension, MPAP-PAWP, and Q(VA)/Q(T) before NO delivery. Q(VA)/Q(T) decreased in 26 patients (group 1) and increased in 11 patients (group 2) during NO inhalation. In group 1, cardiac output was lower than in group 2 (8.6 vs. 12.2 l . min(-1); P<0.0005). Conclusion: We conclude that the change in venous admixture during inhalation of SO ppm NO depends on cardiac output. If preinhalation cardiac output is high, 40 ppm NO can adversely affect gas exchange in patients with ALI and ARDS.