A model investigation of the impact of ventilation-perfusion mismatch on oxygenation during apnea in preterm infants.
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 (sigma) defined conventionally according to sigma=S.D. of the distribution of V/Q ratios. Average desaturation rate 10s 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.
Sands
Scott A
SA
Ritchie Centre for Baby Health Research, Monash Institute of Medical Research, Monash University, Victoria, Australia.
Edwards
Bradley A
BA
Kelly
Vanessa J
VJ
Davidson
Malcolm R
MR
Wilkinson
Malcolm H
MH
Berger
Philip J
PJ
D001049:Apnea / Q000503:physiopathology*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000502:physiology*; D008168:Lung / Q000098:blood supply / Q000503:physiopathology; D008954:Models, Biological; D010101:Oxygen Consumption; D012123:Pulmonary Ventilation / Q000502:physiology*; D012119:Respiration