Factors affecting cerebrovascular reactivity to CO2 in premature infants

Abstract

Abstract 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 (tcPCO2) 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 tcPCO2 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. tcPCO2 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; β = 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 tcPCO2 (β = 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.