Early End-Tidal Carbon Monoxide Levels, Patency of the Ductus Arteriosus and Regional Cerebral Oxygenation in Preterm Infants

Abstract

Background: Carbon monoxide (CO), a relaxant regulator of muscle tone and marker of oxidative stress and inflammation, can be measured in exhaled air by determination of end-tidal CO corrected for CO in ambient air (ETCOc). Objective: Increased endogenous production of CO may influence patency of the ductus arteriosus, cerebral perfusion and, subsequently, cerebral oxygenation. The aim was to study the relation between early ETCOc levels, hemodynamically significant patent ductus arteriosus (hsPDA) and cerebral oxygenation (rScO₂) in preterm infants <32 weeks' gestational age and determine predictive values of ETCOc for hsPDA. Methods: ETCOc was measured in 91 infants within the first 24 h after birth. A hsPDA was diagnosed according to echocardiographic indices. In 78/91 infants, rScO₂ was monitored with near-infrared spectroscopy to assess cerebral oxygenation. Results: ETCOc values were significantly higher in infants who subsequently developed hsPDA (2.3 ± 0.7 ppm) vs. no-hsPDA (1.7 ± 0.6 ppm), p < 0.001. With a cut-off value of 2.5 ppm, positive and negative predictive values of ETCOc for hsPDA were 55 and 88%, respectively. rScO₂ values were not different between the two groups (64 ± 1 vs. 65 ± 3%, NS). Conclusions: The higher ETCOc values in hsPDA infants early after birth reflect the early relaxant state of ductal muscular tone. ETCOc <2.5 ppm within 24 h after birth may predict the subsequent absence of hsPDA. ETCOc showed no correlation with cerebral oxygenation in both groups.