No abstract

549 IN NEONATES, THE INCIDENCE OF APNEA DEPENDS ON A VARIETY OF FACTORS, SUCH AS BIRTH WEIGHT, 1 SEX, 2 GESTATIONAL AGE, 3 AND POSTNATAL AGE. 3,4 Central apnea is generally reported as occurring more frequently during active sleep than during quiet sleep. 2,3,[5][6][7] Many authors have pointed out that apnea incidence is also closely related to ambient temperature in both full-term [8][9][10] and preterm neonates 9,11,12 and that the rate of apneic events is increased by warm exposure (i.e., thermal drive). Although preterm neonates are more often exposed to cool stress than to warm stress, little is known about the influence of cool exposure on the incidence of apnea in the different sleep states. Bader et al 11 reported a lower rate of central apnea during transient decreases in incubator temperature from warm (29°C) to thermoneutral conditions (24°C) over 30 minutes, although this was only seen during quiet sleep for preterm infants and during active sleep for term infants.The mechanism linking thermal stress and apnea is unknown and thus warrants further investigation. On the basis of the above-cited studies, it can be supposed that suprapontine influences modify respiratory control, which must be considered as a multiple-interaction system. Abnormal functional interaction among the respiratory system, thermoregulatory system, and sleep processes may alter compensatory responses to autonomic cardiovascular or respiratory challenge and increase the likelihood of life-threatening events later in life. 13 The effect of thermal stress is usually assessed by monitoring the body's internal temperature (generally esophageal or rectal temperatures, which supposedly represent the core temperature) and/or mean skin temperature. 14 However, the central controller of the thermoregulatory system receives thermal inputs from thermosensitive structures distributed throughout the body. The regulated variable therefore results from a weighted sum of different body temperatures. 15 Hence, to fully understand the thermal influence on apnea incidence in cool environments, it is essential to quantify the magnitude of body cooling that is proportional to the radiant, convective, conductive, and evaporative heat losses (i.e., body heat loss) on the other. Any failure to maintain thermal balance stimulates the body's thermal control mechanisms and thus triggers regulatory adjustments. This approach may help clarify a hypothesis raised by Perlstein et al, 9 whereby apnea is not specifically induced by changes in air temperature but, rather, through processes controlling the overall body heat loss (BHL). Hence, in the present study, the role of thermal drive in the mechanisms underlying the genesis of central apnea in the sleeping neonate was assessed by taking into account BHL during mild warm and cool thermal exposures.Central apneic events were monitored in a group of 22 nearterm neonates. Indeed, there are few published studies on these infants, who are generally considered to be physiologically similar to term infants, even t...

ABSTRACT:Chemoreception is frequently involved in the processes underlying apnea in premature infants. Apnea could result from a decrease in carotid body effectiveness. However, increased carotid body activity could also initiate apnea through hypocapnia following hyperventilation when the receptors are stimulated. The aim of this study was to analyze the relationship between carotid body effectiveness and short apneic episodes in older preterm neonates. Carotid body effectiveness was assessed at thermoneutrality in 36 premature neonates (2.07 Ϯ 0.26 kg) by performing a 30-s hyperoxic test during sleep, the oxygen inhalation involving a ventilation decrease. Blood O 2 saturation (Sp O2 ) and ventilatory parameters were monitored before and during the hyperoxic test. Short episodes of apnea (frequency and mean duration) were recorded during the morning's 3-h interfeeding interval. Pretest Sp O2 was not related to any of the measured respiratory parameters. A higher frequency of short apneic episodes was linked to a greater ventilation decrease in response to the hyperoxic test ( ϭ Ϫ0.32; p ϭ 0.01). Increased carotid body response is correlated with greater apneic episodes frequency, even in the absence of concomitant oxygen desaturation. Fetal or early postnatal hypoxemia could have increased peripheral chemoreceptor activity, which could initiate a "overshoot/ undershoot" situation, which in turn could induce a critical P O2 /P CO2 combination and apnea. (Pediatr Res 62: 591-596, 2007) S hort apneic episodes [defined as a respiratory pause of at least 3 s (1,2)] are common respiratory events in premature neonates, with an incidence of 25% in infants weighing Ͻ2500 g at birth and 84% in those weighing Ͻ1000 g (3).After birth, apnea frequency decreases progressively once chemoreception control is sufficiently developed to initiate the appropriate ventilatory responses to changes in arterial blood gas status (3-6). Chemoreception control is carried out by central and peripheral chemoreceptors that differ in their anatomical location and type of stimulation: peripheral chemoreceptors (mainly carotid bodies) are sensitive to variations in the levels of O 2 and (to a lesser extent) CO 2 , whereas central chemoreceptors are especially sensitive to variations in CO 2 and pH.It is accepted that abnormal functioning of the peripheral chemoreceptors can promote apnea even though the mechanism underlying this altered chemoreceptor activity is still subject to much debate. Provision of oxygen to infants suffering from bronchopulmonary dysplasia delays the peripheral chemoreceptor response and might induce more apnea (7). In preterm neonates, an increase in the chemoreceptor gain during the postnatal period has also been suggested. The latter can initiate an "overshoot/undershoot" situation: the apnea results from a central depression in inspiratory motor drive, which is mainly due to hypocapnia. This concept has been described in adult dogs to explain periodic breathing (8) and extended to the newborn lamb (9), but physiolog...

Sudden infant death syndrome (SIDS) remains the main cause of postneonatal infant death. Thermal stress is a major risk factor and makes infants more vulnerable to SIDS. Although it has been suggested that thermal stress could lead to SIDS by disrupting autonomic functions, clinical and physiopathological data on this hypothesis are scarce. We evaluated the influence of ambient temperature on autonomic nervous activity during sleep in thirty-four preterm neonates (mean ± SD gestational age: 31.4±1.5 weeks, postmenstrual age: 36.2±0.9 weeks). Heart rate variability was assessed as a function of the sleep stage at three different ambient temperatures (thermoneutrality and warm and cool thermal conditions). An elevated ambient temperature was associated with a higher basal heart rate and lower short- and long-term variability in all sleep stages, together with higher sympathetic activity and lower parasympathetic activity. Our study results showed that modification of the ambient temperature led to significant changes in autonomic nervous system control in sleeping preterm neonates. The latter changes are very similar to those observed in infants at risk of SIDS. Our findings may provide greater insight into the thermally-induced disease mechanisms related to SIDS and may help improve prevention strategies.