In healthy neonates, the physiological CO 2 range is defined as 4.7–6.0 kPa (35.3–45.0 mmHg). Thus, the cerebral vasculature is highly sensitive to the level of circulating physiological gases with hypocapnia and hypercapnia capable of affecting brain oxygen levels indirectly through modulation of cerebral blood flow. 4 In contrast, hypocapnia leads to vascular constriction and reduced blood flow. Elevated CO 2 levels, which are frequently associated with hypoxia, also promote an increase in cerebral blood flow through dilation of cerebral arteries and arterioles. Given the brain’s significant demand for oxygen to maintain normal function, several adaptive cerebral vasodilatory mechanisms are elicited to promote and maintain cerebral blood flow under conditions of hypoxia. 3 The cerebral vasculature is very sensitive to physiological gases. Chronic responses to CO 2 can be elicited on a cellular level through CO 2-dependent changes in gene expression, e.g., genes associated with immune signalling. Acute responses to CO 2 are generally sensed through brain stem central chemoreceptors that modulate the rate and depth of breathing to try and maintain normocapnic partial pressures of CO 2. Adaptive responses to changes in CO 2 can be classified as being acute or chronic. 2 This is likely a consequence of local metabolic activity and alterations in local blood supply. 1 Importantly, the local microenvironment of cells and tissues can experience pCO 2 levels that differ markedly from systemic PaCO 2, e.g., in solid tumours.

Consequently, slightly higher pCO 2 values are associated with the venous circulation as CO 2-enriched blood is returned towards the lungs. In humans, normocapnia is defined as a pCO 2 of between 4.7 and 6.0 kPa (35.3–45.0 mmHg), with pCO 2 reflecting the balance between CO 2 production and removal. CO 2 is mainly removed from the body via the lungs and can accumulate in lung pathologies. Plasma CO 2 levels are tightly regulated under physiological conditions to maintain blood pH. Contradictory findings on the effectiveness of permissive hypercapnia highlight the need for further data on appropriate CO 2 parameters and correlation with outcomes.Ĭarbon dioxide (CO 2) is a physiological gas produced as a consequence of aerobic metabolism. For permissive hypercapnia, parameters described for bronchopulmonary dysplasia (BPD PaCO 2 6.0–7.3 kPa: 45.0–54.8 mmHg) and congenital diaphragmatic hernia (CDH PaCO 2 ≤ 8.7 kPa: ≤65.3 mmHg) were identified. Although PaCO 2 ranges were reported from 2.6 to 8.7 kPa (19.5–64.3 mmHg) in both term and preterm infants, there are little data on the safety of these ranges. As safe pCO 2 ranges were not explicitly concluded in the studies chosen, it was indirectly extrapolated with reference to pCO 2 levels that were found to increase the risk of neonatal disease. Permissive hypercapnia did not decrease periventricular leukomalacia (PVL), ROP, hydrocephalus or air leaks. Hypocapnia was associated with predominantly neurological side effects while hypercapnia was linked with neurological, respiratory and gastrointestinal outcomes and Retinpathy of prematurity (ROP). Covidence online software was employed to streamline relevant articles. Two hundred and ninety-nine studies were screened and 37 studies included. A systematic review was conducted in accordance with the PRISMA statement and MOOSE guidelines. We reviewed the effects of hypercapnia and hypocapnia and existing carbon dioxide thresholds in neonates. There is no consensus on the optimal pCO 2 levels in the newborn.

High co2 levels in blood