In experimental settings, carbon dioxide (CO2) blood levels affect the perfusion of various tissues. Hypocapnia-induced vasoconstriction impairs blood supply and severe hypocapnia may cause DNA fragmentation in cerebral neurons. In contrast, hypercapnia, acting as a vasodilator, increases mesenteric, renal and cerebral blood flow. Hypercapnia antagonises hyperoxia-induced retinal vasoconstriction but also augments oxygen-induced retinal microvascular degeneration that precedes proliferative retinopathy. In animal models of endotoxin-induced acute lung injury, hypercapnia improves compliance and attenuates alveolar neutrophil infiltration. Peripheral microvessel diameter, blood-flow velocity, and global cardiac output appear to increase with graded arterial hypercapnia up to 80–100 mm Hg, whereas all of these variables start to decrease at higher CO2 values. These findings are not apt to establish a safe range for target CO2 levels in ventilated preterm infants. Randomised trials of permissive hypercapnia in preterm infants cover an overall range from 35 to 65 mm Hg. A meta-analysis of all three trials published to date demonstrates the lack of any significant benefit or harm with respect to long-term outcomes such as death, bronchopulmonary dysplasia, retinopathy of prematurity, intravascular haemorrhage (IVH), periventricular leucomalacia (PVL), or neurodevelopmental impairment. In contrast, circumstantial but solid evidence suggests that moderately low CO2 levels (<30–35 mm Hg) in ventilated preterm infants are strongly associated with the development of PVL. Moreover, both CO2 extremes and the magnitude of CO2 fluctuations are associated with severe IVH. This suggests that avoiding rapid CO2 changes by meticulous and gentle ventilator adjustments may be even more important than absolute CO2 levels to prevent brain damage of preterm infants.
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