A model investigation of the impact of ventilation–perfusion mismatch on oxygenation during apnea in preterm infants

Abstract

Ventilation–perfusion ( V/ Q) mismatch is a prominent feature of preterm infants and adults with lung disease. V/ Q mismatch is known to cause arterial hypoxemia under steady-state conditions, and has been proposed as the cause of rapid arterial oxygen desaturation during apnea. However, there is little evidence to support a role for V/ Q mismatch in the dynamic changes in arterial oxygenation that occur during apnea. Using a mathematical model, we quantified the effect of V/ Q mismatch on the rate of desaturation during apnea to ascertain whether it could lead to rates of up to 10% s –1 as observed in preterm infants. We used a lung–body model for the preterm infant that incorporated 50 parallel alveolar–capillary units that were ventilated and perfused with the severity of V/ Q mismatch ( σ) defined conventionally according to σ=S.D. of the distribution of V/ Q ratios. Average desaturation rate 10 s from apnea onset was strongly elevated with worsening V/ Q mismatch as a result of an earlier desaturation of low V/ Q units compared with high V/ Q units. However, V/ Q mismatch had little impact after apnea onset, with peak desaturation rate only substantially increased if mismatching caused a lowered resting arterial O 2 saturation. In conclusion, V/ Q mismatch causes a more immediate onset of desaturation during apnea, and therefore places preterm infants and adults with lung disease at risk of hypoxemic dips. However, V/ Q mismatch does not accelerate desaturation rate beyond apnea onset and cannot, therefore, explain the rapid desaturation observed during recurrent apnea in preterm infants.