Factors affecting cerebrovascular reactivity to CO2 in premature infants

Background: Hypercarbia increases cerebral blood flow secondary to cerebral vasodilatation, while hypocarbia can lead to vasoconstriction with a subsequent decrease in cerebral blood flow. The aim of this study was to examine CO2 cerebral vasoreactivity in a cohort of premature infants and to identify factors which influence this reactivity. Methods: We prospectively studied a cohort of hemodynamically stable premature infants [birth weight (BW) <1500 g and gestational age (GA) >= 34 weeks]. Subjects underwent two studies, one in the first 72 h and the second after 1 week of life. Infants were continuously monitored via a physiology station that included transcutaneous CO2 (tcPCO(2)) monitor, near-infrared spectroscopy (NIRS), arterial pulse oximetry and heart rate. The total hemoglobin (Hb-T) signal of NIRS was used as an indicator of cerebral blood volume (CBV). Correlation between tcPCO(2) and Hb-T was performed in each 1-h period using Pearson's correlation. Factors affecting the CO2 cerebrovascular reactivity were examined using bivariate and linear regression analyses. Results: A total of 3847 1-h epochs were obtained from 140 studies of 72 premature infants. tcPCO(2) correlated positively with Hb-T in 42% of epochs. In regression analysis, factors associated with increased percentage of positive correlation epochs were male sex and younger postmenstrual age (PMA; beta = 0.176, 0.169 and P-value = 0.036, 0.047 respectively). Factors associated with increased strength of positive correlation were mechanical ventilation and increased average tcPCO 2 (beta = 0.198, 0.220 and P-value = 0.024, 0.011 respectively). Conclusion: Increased prematurity, male sex, mechanical ventilation and hypercarbia are associated with stronger PCO2 cerebrovascular reactivity in premature infants. This association may explain their role in the pathogenesis of brain injury.