Abstract
The hypothesis that the primary defect in infants dying of the Sudden Infant Death Syndrome (SIDS) lies in the control of ventilation has provoked much interest. We have used the measurement of occlusion pressure as an index of the neuromechanical output of the respiratory system to investigate the response of infants to hyperoxic hypercapnia All measurements were made on unsedated infants during quiet sleep as defined by EEG and EOG recordings. Infants breathed through a facemask and pneumotachograph with a shutter attachment. Progressive hypercapnia was achieved by using a rebreathing bag with an initial pCO2 at 38 mmHg. The shutter was activated every 20-30 seconds and airway pressure was recorded from the facemask, until either the infant aroused or the pCO2 reached 65 mmHg. Pressure was measured 100 msec following the onset of inspiratory effort (P0.1). The slope of P0.1 against pCO2 was plotted for each subject. Seventeen infants below the age of 20 weeks (4 ‘near-misses’ for SIDS, 5 siblings of SIDS, 8 normal infants) were studied. The slope of P0.1 against pCO2 in the normal infants ranged from 0.08 to 0.47 cmH2O.mmHg−1 and the P0.1 at 55 mmHg ranged from 4.05 to 15.5 cmH2O. The values from the other groups of infants, who might be thought to be at increased risk for SIDS, all lay within these normal ranges. In conclusion, no significant differences were found between the three study groups under these defined circumstances.
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