Abstract
Hypoxaemia during apnoea develops earlier and progresses faster in children than in adults. Ethical and practical considerations prevent detailed investigation of the issue. We used the Nottingham Physiology Simulator, an integrated, computational model of the respiratory and cardiovascular systems, to model four healthy virtual children (ages: 1 month, 1, 8 and 18 yr) and exposed them to apnoea after a variety of preoxygenation periods (0, 1 and 3 min) and with open and obstructed airways during apnoea. The rate of oxygen desaturation of haemoglobin from 90 to 40% was similar across the ages studied, being approximately 30% min(-1). The greatest difference between ages was found in the speed of early desaturation (i.e. between the onset of apnoea and the acceleration of haemoglobin desaturation); in the absence of preoxygenation and with an open airway, this time was 6.6 s in the 1-month-old and 33.6 s in the 8-yr-old. Preoxygenation had a substantial effect on the speed of early desaturation, but less effect on the time for SaO2 to decrease from 90 to 40%. Preoxygenation substantially delayed dangerous desaturation in all age groups, although the rapidity of denitrogenation in the very young (caused by the large ratio of minute ventilation to functional residual capacity) resulted in lengthy preoxygenation having little benefit over brief preoxygenation. Airway obstruction during apnoea accelerated every child's hypoxaemia through prevention of mass flow addition to oxygen stores and through intrathoracic depressurization. On average, haemoglobin desaturation from SaO2 90 to 40% was 33% min(-1) with an obstructed airway and 26% min(-1) with an open airway; all ages were similarly susceptible to this effect.
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