Ventilation and Ventilatory Pattern During Sleep in Aborted Sudden Infant Death Syndrome

Abstract

T o assess ventilatory control during sleep in infants at risk for the sudden infant death syndrome (SIDS), we made serial measurements of resting tidal volume (Vt), respiratory cycle time (Ttot), and the ventilatory changes resulting from inhalation of 2% Con in aborted S l D S infants in rapid eye movement and quiet sleep and compared them to a group of normal infants during the first 4 months of life. Ventilation was measured by the barometric method, and sleep was staged using electroencephalogram, electrooculogram, and electromyogram and behavioral criteria.Although resting instantaneous minute ventilation (Vt/Ttot) was virtually the same in both groups of infants, Vt tended to be smaller (by up to 50% in the first 2 months) and Ttot tended to be shorter in aborted S l D S than in normal infants in both rapid eye movement and quiet sleep. The increase in the mean Vt/Ttot with 2% COz is greater by about 5 to 20% in aborted SIDS than in normal infants at 3 and 4 months of age in both sleep states. These findings, together with our previous findings that aborted S l D S infants have an increase in heart rate and a shortening of the QT interval, provide indirect evidence that infants a t high risk for S l D S may have increased sympathoadrenal activity.

Cardiorespiratory Patterns in Infants Presenting with Apparent Life-Threatening Episodes

“…Although the higher frequency of apnoeic pauses and periodic breathing have been previously reported in such infants [2,12], a lower respiratory rate has not been identified. Therefore, our find ings clearly do not agree with those of Had dad et al [5] who found higher respiratory rates during quiet sleep in 'near-miss' cases. It is quite possible that the lower respiratory rates and increased numbers of short ap noeic pauses are linked, as previously dis cussed by Richards et al [7], The higher inci dence of periodic breathing patterns in the ALE cases may also be relevant to the excess of low frequency heart rate oscillation identi fied by Gordon et al [13] in their study of 'near-miss' patients who subsequently died.…”

“…Previous studies of breathing and heart rate patterns in otherwise healthy infants who have suffered from cyanotic or pro longed apnoeic episodes (apparent lifethreatening events, ALE) [1] have yielded conflicting results [2][3][4][5]. Some of this confu sion has undoubtedly arisen through the varying severities and causes for ALE occur ring in the infants studied.…”

Sudden Infant Death Syndrome (SIDS): An Integration of Ontogenetic Pathologic, Physiologic and Epidemiologic Factors1

“…Reports in the literature indicate that one infant who subsequently died of SIDS and one near-miss for SIDS exhibited hyperpnea in the neonatal period compared to control infants (Thoman et al 1977). Haddad et al (1981) demonstrated increased respiratory rates in near-miss infants monitored during sleep. In contrast, Ke/ly et al (1979,1980) reported increased rates of periodic breathing in near-miss and subsequent siblings, a finding not substantiated by our own data or those of Guilleminault et al (1980).…”

“…A transient seleetive aecelerated maturation ofthe forebrain is of partieular interest in light of a postulated inhibitory influence of this area upon brainstem respiratory centers If inereased respiratory rates in siblings reflect a eompensatory response to mild chronic hypoxia in some infants this could be expected to result in an altered ehemoreeeptor sensitivity. Shannon et al (1977) reported a significant hypoventilatory response to CO2 in near miss infants, a finding not substantiated by Brady et al (1980) or Haddad et al (1981). The latter authors advance three reasons for the diserepancy in results; monitoring over a prolonged period of time, use of a barometrie method which avoids facial stimulation known to alter breathing (Askanazi et al 1980) and differences in CO2 pereentages administered.…”

Sudden Infant Death Syndrome and Apnea of Infancy

“…The data to support this hypothesis were initially inferred from assessments of patients with symptomatic apnea (apnea of infancy) and from assessments of asymptomatic infants at increased epidemiologic risk for SIDS, a few of whom subsequently died of SIDS. Although on occasion yielding contradictory results, [4][5][6][7] most studies of cardiorespiratory control have identified one or more of the following abnormalities in groups considered to be at increased risk for SIDS: prolonged sleep apnea, 8 increased frequency of brief inspiratory pauses, 9 excessive periodic breathing, 10 diminished ventilatory sensitivity to hypercapnia or hypoxia, [11][12][13] and impaired arousal responsiveness to hypercapnia or hypoxia. 12,[14][15][16] Consistent with the presence of an arousal deficit, SIDS infants have retrospectively been reported by parents to have been more difficult to awaken and to have a behavioral pattern of apathy and sleepiness compared to control infants.…”