The investigators' previous study has stressed that inhaled nitric oxide therapy might play an ameliorative role in patients with refractory hypoxemia after surgical treatment of type A acute aortic dissection. The possible reason might be the decreasing of intrapulmonary shunt because previous studies showed that inhaled nitric oxide could decrease intrapulmonary shunt by selectively dilating the pulmonary vessels in ventilated areas. As a result, the investigators designed this observational study to calculate the intrapulmonary shunt before and after inhaled nitric oxide therapy. Intrapulmonary shunt was calculated from oxygen content (CO2) of different sites ( artery, mixed venous, alveolar capillary) by Fick equation:(CaO2-CcO2)/(CvO2-CcO2). A FiO2 of 1.0 and tidal volume of 6~8 ml/kg were chosen. Oxygen content was calculated from hemoglobin (Hb), oxygen saturation (SO2) and oxygen partial pressure (PO2) by the following equation: CO2 = 1.34*Hb*SO2 + 0,0031*PO2. PaO2, SaO2, PvO2 and SvO2 were measured from arterial and mixed venous blood samples taken from the radial arterial catheter and from the pulmonary artery catheter. ScO2 was estimated to be 1.0 with a FiO2 of 100%. PcO2 was considered to be the same as PAO2 (partial pressure of oxygen in the alveoli), and was calculated from the alveolar gas equation with PAO2 = [(atmospheric pressure - 47) * (FiO2)] - PaCO2/0.8.Other variables such as hemodynamic variables from pulmonary artery catheter were also collected.
The purpose of this study was to clarify the possible mechanism of hypoxemia after surgical treatment of type A acute aortic dissection and the possible mechanism of the treatment role of inhaled nitric oxide in refractory hypoxemia.