In Response.

Abstract

We thank Dr A. K. Jha1 for his valuable comments regarding our article.2 Although there is a correlation between the relative perfusion to the operative lung as assessed by lung scans and the partial pressure of oxygen in arterial blood (Pao2), it is unclear whether this variable is clinically relevant for patients undergoing thoracic surgery.3 Because not all the patients enrolled in our trial underwent lung perfusion scans, we did not perform a between-group comparison. We also did not measure Pao2 levels by arterial blood gas analysis during 2-lung ventilation (TLV). Because the Pao2 level during 1-lung ventilation (OLV) strongly and positively correlates with Pao2 during TLV, we were able to predict hypoxemia during OLV for patients in both groups that presented with an average room air saturation of 93% before general anesthesia. Nonetheless, we acknowledge that the TLV parameters and preoperative perfusion scans may give more insight on the impact of OLV, peak inspiratory pressure (PIP) and Pao2/fractional inspiration of oxygen (Fio2) (P/F) ratio. Hypoxic pulmonary vasoconstriction (HPV) during OLV mitigates the shunt fraction. HPV is blunted by sevoflurane and suppressed by the pathologic effects of chronic obstructive pulmonary disease (COPD). Although we did measure sevoflurane concentrations, we administered balanced anesthesia that included a remifentanil infusion. Thus, the actual concentration of sevoflurane was probably less than 1 minimum alveolar concentration (MAC), a concentration thought to have limited impact on HPV.4 Also, the treatment of OLV-induced increase in pulmonary hypertension may have been beneficial, as Dr A. K. Jha1 commented in the letter. Unfortunately, as we mentioned in the limitation section, we can only speculate there was an OLV-induced rise in pulmonary artery pressure because it was not possible to obtain accurate measurements of pulmonary arterial pressure in our clinical practice. We agree with the view that iloprost-induced pulmonary arteriolar vasodilation in the ventilated lung resulted in blood diversion from nonventilated lung to the ventilated lung with physiological dead space reduction and P/F ratio augmentation. Indeed, as our study results indicate, inhaled iloprost improves oxygenation and dead space ventilation during OLV in COPD patients with poor lung oxygenation. Considering that atelectasis in the operated lung persists in the postoperative period,5 it can be deduced that the difference in P/F ratio in the postanesthetic care unit in both groups may be due to the residual intrapulmonary shunt fraction and the residual effects of iloprost inhalation, which ameliorates the ventilation/perfusion matching. In this regard, we speculate that the beneficial effects of iloprost during OLV may persist even after TLV or spontaneous ventilation is restored, but this needs to be clarified. We think that the comments provided by Dr A. K. Jha1 are valuable and should be considered when planning further studies. Namo Kim, MD, PhDDepartment of Anesthesiology and Pain MedicineAnesthesia and Pain Research InstituteYonsei University College of MedicineSeoul, Republic of Korea Su Hyun Lee, MDDepartment of Anesthesiology and Pain MedicineYonsei Sarang HospitalSeoul, Republic of Korea Young Jun Oh, MD, PhDDepartment of Anesthesiology and Pain MedicineAnesthesia and Pain Research InstituteYonsei University College of MedicineSeoul, Republic of Korea[email protected]