Ventilatory Chemoreceptor Response in Parents of Children at Risk for Sudden Infant Death Syndrome

Abstract

Summary: We postulated that parents of infants who sustain near-death episodes associated with defective chemical regulation of breathing might share a similar defect. We, therefore, measured the ventilatory responses to progressive hypoxia and hypercapnia individually in eight sets of parents of infants who had sustained at least one near-death episode (apnea, cyanosis, pallor, limpness, and responsive only to mouth-to-mouth resuscitation); each infant had a ventilatory response to CO₂ which was more than 2 S.D. below the mean normal. Ventilatory function measured by vital capacity forced expiratory volume 1.0 and flow volume curves was normal in each group. Responses to hypercapnia and hypoxemia in both fathers and mothers were similar to 11 pairs of controls. Ventilation during CO₂ rebreathing normalized for surface area increased 0.87 liter/min/mm Hg in fathers, 0.94 in controls, 0.87 in mothers, and 0.75 in controls. Ventilation during progressive hypoxemia increased 88 liter/min/1/mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.

Speculation: Defective chemical regulation of breathing in infants at risk of sudden infant death syndrome is not shared by their parents. This suggests that environmental influences, perhaps in utero, are responsible for this defect.

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