Background: During lung transplantation (LT) as well as living-donor lobar lung transplantation (LDLLT), patients undergo significant changes in gas exchange, and therefore, arterial carbon dioxide partial pressure (PaCO2) monitoring is crucial; however, transcutaneous carbon dioxide partial pressure (PtcCO2) monitoring is not performed perioperatively. We reviewed our early experiences with continuous PtcCO2 monitoring in LDLLT to evaluate its feasibility in LT. Methods: This retrospective study included 13 cases of LDLLT performed between July 2009 and July 2011. Thirteen patients underwent nocturnal preoperative and intraoperative PtcCO2 monitoring in living-donor lobar lung transplantation (LDLLT). Under anesthesia, each patient was managed according to their preoperative PtcCO2. End-tidal carbon dioxide partial pressure (PETCO2) was also measured during LDLLT. The nocturnal preoperative and intraoperative PtcCO2 data were reviewed. Furthermore, clinical data were collected from medical charts, anesthesia records, and laboratory tests. Results: In all the patients, anesthesia was maintained safely by continuous PtcCO2 monitoring, especially at the induction of anesthesia. There were no complications related to continuous PtcCO2 monitoring. According to the preoperative arterial blood gas analysis, the median PaCO2 was 57 mmHg (range, 40-77). PtcCO2 and arterial carbon dioxide partial pressure (PaCO2; range, 39-192 mmHg) showed significant correlations at several time points (p < 0.0001, r2 = 0.978, n = 37, PtcCO2 = 0.95 × PaCO2 + 4.56). The agreement between these 2 variables was estimated with acceptable precision. Although the relationship between PETCO2 and PaCO2 was significant, their differences varied widely with low coefficient of determination (p = 0.0095, r2 = 0.258, n=25, PETCO2 = 0.26 × PaCO2 + 26.36). The awake stable PaCO2 was 58.0±13.4 mmHg, and the maximal preoperative PtcCO2 was 77.5±31.9 mmHg, possibly because of sleep hypoventilation. The overall maximal PtcCO2 did not surpass the maximal preoperative PtcCO2 in 4 patients. In 4 other patients, the maximal PtcCO2 at induction surpassed the maximal preoperative PtcCO2, but it decreased thereafter to the acceptable range; the mean difference between these 2 values was 10 mmHg (range, 1-22 mmHg). In 2 other patients, PtcCO2 did not decrease below the maximal preoperative PtcCO2 (maximal difference, 28 and 39 mmHg, respectively), but they tolerated the relatively high PtcCO2 levels and low pH-related hemodynamic instability. In these 10 patients, hilar dissection was performed safely without the need of cardiopulmonary bypass (CPB). However, in 3 patients, PtcCO2 reached the maximal value at induction and continued to rise despite modification of the ventilator settings. The mean difference between the maximal PtcCO2 in LT and the maximal preoperative PtcCO2 was 65 mmHg (range, 29-85 mmHg). These patients needed CPB or extracorporeal membrane oxygenation (ECMO) as soon as possible because of the hemodynamic instability related to hypercapnia after the induction of anesthesia. The maximal preoperative PtcCO2 was significantly correlated with the maximal PtcCO2 at induction (p = 0.0076, r2 = 0.49) and overall (p = 0.005, r2 = 0.52). Conclusions: Continuous PtcCO2 monitoring is feasible and recommended because the intraoperative PaCO2 trend can be predicted from the preoperative PtcCO2 trend and timely assessed.
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