Aims & Objectives:
p50, the paO2 when the oxygen saturation is 50%, reflects the haemoglobin-oxygen affinity. Acidosis, hypercapnia and fever, common in critical illness, increase p50. This encourages Haemoglobin-oxygen dissociation, hence oxygen delivery, in tissues. This same p50 shift may reduce oxygen uptake from alveolar gas. Understanding and even manipulating this balance may assist with optimizing oxygen delivery. We aimed to characterize the trajectory of p50 in critically-ill children and to compare cases with and without acute lung injury.
We conducted a retrospective observational study of all children with arterial blood gas data admitted to a single PICU over a 2-year period. Mean p50 values according to day of admission were evaluated using multi-level linear regression. The trajectory of p50 was compared between children with and without acute lung injury (ALI), defined as those who had a PF ratio of < and >300 (or SF ratio < and > 263 if PF unavailable) at admission.
Over the 2-year period, 837/2029 (41.2%) children had arterial blood gas analysis; 349/827 (42.2%) had acute lung injury. The mean p50 was higher than the normal value of 3.53kPa, decreased over the first 3–4 days and then increased back towards normal (Figure). The trajectory was significantly different between those with and without ALI, with lower initial values in those with ALI (LR chi-square 6.25, p 0.01).
Critically-ill children initially decrease and subsequently increase haemoglobin oxygen affinity. The difference in trajectory between children with and without ALI may suggest adaptive mechanisms to optimize oxygen delivery.