Hemodynamic implications of carbon monoxide (CO) and nitrogen oxide (NO) during living donor liver transplantation

Abstract

Carbon monoxide (CO) and nitrogen oxide (NO) affect vasodilation and cause hemodynamic change. Hemodynamic instability due to liver transplantation may result in poor prognosis of graft. This study investigated the hemodynamic implications of CO and NO levels measured using carboxyhemoglobin (COHb) and methemoglobin (MetHb) during living donor liver transplantation (LDLT). The hemodynamic instability with a pressor dose (norepinephrine equivalent) was estimated 1 hour after graft reperfusion. COHb and MetHb were used as indexes of CO and NO, and were measured using an arterial blood gas analyzer. One hundred and ten recipients who underwent LDLT from May 2011 to July 2013 were selected. Recipients were divided into high (≥ 1.9%) and low (< 1.9%) COHb groups with COHb concentrations at 5 minutes after reperfusion. Recipients were also divided into high (≥ 0.4%) and low (< 0.4%) MetHb groups with MetHb concentrations at 30 minutes after reperfusion. Data are presented as mean ± standard deviation or number (percentage). Model for End-stage Liver Disease (MELD) scores were different for the two COHb groups (low: 13.4 ± 9.0 vs. high: 19.7 ± 10.6, p < 0.001), and pressor doses adjusted by MELD scores were also different between the two COHb groups (low: 0.09 ± 0.01 μ g/kg/min vs. high: 0.14 ± 0.01 μ g/kg/min, p = 0.029). By contrast, pressor doses and MELD scores were not different between the two MetHb groups. In conclusion, CO rather than NO has hemodynamic implications during LDLT. Therefore, the increase in COHb during LDLT is predictive of hemodynamic instability.