Prior investigations of inhaled nitric oxide (iNO) have focused on improved gas exchange of oxygen as reflected by arterial oxygenation. We hypothesized that a similar improvement in CO2 exchange would cause an increase in end-tidal carbon dioxide tension (PetCO2), which would serve as a marker for the efficacy of iNO therapy. We administered iNO 2-50 ppm to mechanically ventilated patients with pulmonary hypertension from PPHN, ARDS, or CHD. Monitoring included arterial oxyhemoglobin saturation, inspired NO concentration, inspired and exhaled O2, CO2, and N2 tensions, invasive arterial blood pressure and gas tensions. A positive response to iNO was defined as a 25% improvement in arterial O2 tension, arterial/alveolar O2 tension ratio, alveolar-arterial O2 tension gradient, shunt fraction, or oxygenation index. Data from 414 trials in 49 patients were analyzed by ANOVA and linear regression. The increase in PetCO2 was significantly greater in positive (n=231) than negative (n=183) trials (34±16% vs. 7±10%, p<0.02). The increase in SpO2 was highly related to the change in PetCO2(R=0.71, p<0.001). This data indicates that a positive response to iNO causes an increase in CO2 delivery to ventilated lung units, which can be detected by increased PetCO2. The mechanisms involved may include increased total pulmonary blood flow, redistribution of intrapulmonary regional flow, or reduced extrapulmonary shunt. Thus, PetCO2 provides immediate quantitative information about the response to iNO. Supported by the Children's Hospital Foundation and equipment by Ohmeda, Inc. Figure

figure 1

Figure 1