The role of arousal related brainstem reflexes in causing recovery from upper airway occlusion in infants

Abstract

During obstructive sleep apnea (OSA) in adults upper airway reopening coincides with a sudden burst in activity of pharyngeal dilating muscles. This has been attributed to arousal from sleep as indicated by increased EEG activity. Recovery from OSA in infants often occurs in the absence of cortical arousal. To investigate mechanisms involved in recovery, we performed experimental airway occlusions in sleeping infants. Based on past work, our hypothesis was that a sleep startle combined with an augmented breath and heart rate acceleration would occur during the occlusion, and that such brainstem mediated reflexes might provide an explanation for recovery from OSA in the absence of cortical arousal. However, this is contrary to expectations, since lung inflation is believed to be necessary for occurrence of an augmented breath. We studied 16 healthy infants during sleep. We recorded EEG, EOG, ECG, oxygen saturation, diaphragmatic, nuchal and limb electromyograms, face mask pressure, and airflow. A startle, accompanied by neck extension, limb and nuchal EMG activation, as well as heart rate acceleration occurred during all airway occlusions. The startle occurred simultaneously with a large biphasic inspiratory effort, having characteristics of an augmented breath (sigh). In more than a third of cases, this occurred without any evidence of cortical arousal activity. The magnitude of startles as well as the increase in heart rate correlated positively with peak airway negative pressure, indicating that arousal processes are graded in intensity. We conclude that the neck extension and pharyngeal dilating muscle activity associated with the startle and augmented breath may account for recovery of airway patency in infants as they do adults. Lung inflation is not a prerequisite for the reflex to occur.

Figure 1a

Placement of EEG, EOG, EKG, and EMG leads during the study

Figure 1b

Placement of facemask on the infant and arrangement of the flow meter and mask pressure tubing.

Figure 2

Polygraphic tracings showing effects of airway occlusion in an infant. On spontaneous recovery the mask seal was broken by infant's startle as reflected in the limb and nuchal EMG. Also note biphasic contour of the terminal inspiratory effort (recovery breath) diaphragm EMG. Startle EMG change begins immediately after phase I of the augmented inspiratory effort.

Figure 3

Summed data of all airway occlusions in NREM and REM sleep. Note the large decrease in airway pressure and inspiratory time occurring with sigh-startle complex. The negative pressure of this breath produced was outside of the P < 0.05 confidence interval determined from the preceding breaths. This was true for REM and NREM breaths. Also, note that pressures during REM are significantly less than those during NREM. These differences in pressures of pre-startle breath and augmented breath for REM and NREM were different (P < 0.01).

Figure 4

Latency of startle occurrence from occlusion onset related to infants age. Data for both REM and NREM.

Figure 5

Correlation of peak negative pressure of augmented breaths vs. startle intensity (NREM and REM).

Figure 6

Relation of startle intensity to increase in heart rate at termination of the occlusion.

Figure 7

Effect of infant age on startle intensity.

Figure 8

Data taken from tracings of adult OSA episodes and recovery from obstruction indicating similarities to findings in infants. A. Note inspiratory time for the recovery breath is much longer than preceding respiratory efforts. The recovery breath was distinctly biphasic, as in infants. Inspiratory peak pressures are not given because the pressure scale went off in the recovery breath. (Data extracted from ref # 17, Fig. 2). B. Note the increased duration as well as peak inspiratory pressure of the recovery breath. (Data extracted from ref # , Fig. 4b). C. In this example inspiratory time of recovery breath was not prolonged, but inspiratory pressure was distinctly elevated over that of preceding breaths. (Data extracted from ref # 5, Fig. 1a).