Abnormal Regulation of Ventilation in Infants at Risk for Sudden-Infant-Death Syndrome

Abstract

To test whether alveolar hypoventilation and an abnormal ventilatory response to inhaled carbon dioxide explains some episodes of sudden-infant-death syndrome, we assessed ventilatory control during quiet sleep in 12 normal infants and 11 infants who had required at least two resuscitations because of prolonged apnea (greater than 20 seconds) during sleep (aborted form of the syndrome). Infants with the aborted syndrome hypoventilated during quiet sleep (alveolar partial pressure of carbon dioxide, 38.9+/-3.5 mm Hg) as compared to normal infants (35.1+/-1.9, P less than 0.01). In addition, the ventilatory response to carbon dioxide breathing during quiet sleep was impaired (mean change in minute ventilation per change in partial pressure of carbon dioxide 22.1+/-8.9, as compared to 63.1+/-19.1 ml per kilogram per minute per millimeter of mercury in controls [p less than 0.001]). Three infants with the "aborted syndrome" subsequently died during sleep at home; autopsy, done in two, revealed no apparent cause of death. We conclude that infants who have had an episode consistent with sudden-infant-death syndrome have a defect in the regulation of alveolar ventilation.

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

“…Thus, the 5-HT system may be very important for responding to these exogenous stressors, so that a defect in this system could compromise a vulnerable individual. These observations may be relevant to sudden infant death syndrome, which has previously been linked to abnormalities in the 5-HT system (Paterson et al, 2006), and has been associated with defects in control of body temperature and breathing (Shannon et al, 1977;Hunt et al, 1981;Dunne and Matthews, 1988).…”

Prenatal to Early Postnatal Nicotine Exposure Impairs Central Chemoreception and Modifies Breathing Pattern in Mouse Neonates: A Probable Link to Sudden Infant Death Syndrome

“…Although the causes of SIDS are still unknown, most of the evidence points to failures in the generation of the respiratory rhythm or its modulation by chemosensory input (Nattie and Kinney, 2002). Infants who died from SIDS had previously shown alterations of their breathing pattern during sleep (Schechtman et al, 1991;Kahn et al, 1992), reduction of chemoreflexes (Shannon et al, 1977), central apnea (Kahn et al, 1988;Schechtman et al, 1991), and impairment in spontaneous and evoked arousability .…”

Sudden Infant Death Syndrome Is Not Associated with the Mutation of PHOX2B Gene, a Major Causative Gene of Congenital Central Hypoventilation Syndrome

“…In addition, rebreathing of expired hypercapnic gases has been hypothesized as one of the major pathophysiological mechanisms underlying the risk due to prone position. SIDS and near-miss SIDS infants are considered to have a defect in hypoxic and hypercapneic response similar to CCHS (Shannon et al 1977;Hunt et al 1981).…”