Autonomic Cardiorespiratory Physiology and Arousal of the Fetus and Infant

Excerpt

Despite intensive research over the past decades, the mechanisms which lead to sudden infant death syndrome (SIDS) still remain elusive. SIDS is presumed to occur in an apparently healthy infant during a period of sleep (1). A failure of cardiorespiratory control mechanisms, together with an impaired arousal from sleep response, are believed to play an important role in the final event of SIDS. Sleep has a marked influence on respiratory and cardiovascular control in both adults and infants, although sleep states, sleep architecture, and arousal from sleep processes in infants are very different from those of adults and undergo significant maturation during the first year of life, particularly in the first six months when SIDS risk is greatest (2).

Arousal from sleep involves both physiological and behavioral responses and has long been considered a vital survival response for restoring homeostasis in reaction to various life-threatening situations, such as prolonged hypoxia or hypotension (3). There are two distinct arousal types defined in infants, subcortical activation and full cortical arousal, which reflect the hierarchical activation from the brainstem (including heart rate, blood pressure, and ventilation changes) to the cortex (4). Any impairment of these protective responses may render an infant vulnerable to the respiratory and cardiovascular instabilities that are common during infancy and that have been postulated to occur in SIDS. In support of this possibility, extensive physiological and neuropathological studies have provided compelling evidence that impaired cardiovascular control, with a concomitant failure to arouse from sleep, are involved in the final events leading to SIDS. The first six months of life are a critical period of development when rapid maturation of the brain, cardiorespiratory system, and sleep state organization are all taking place (2, 5). Thus, the investigation of sleep physiology in healthy infants during this high-risk period provides important insights into the likely mechanisms involved in the pathogenesis of SIDS.