Intercostal muscle reflexes and sleep breathing patterns in the human infant

1980 ◽  
Vol 48 (1) ◽  
pp. 139-146 ◽  
Author(s):  
B. T. Thach ◽  
I. F. Abroms ◽  
I. D. Frantz ◽  
A. Sotrel ◽  
E. N. Bruce ◽  
...  

Breathing variability and apnea characteristic of rapid eye movement (REM) sleep was investigated in a newborn infant with complete interruption of intercostal to phrenic neural pathways due to intrapartem transection of the cervical spinal cord. Breath-to-breath variability in inspiratory duration (TI), breath duration (Ttot), tidal volume (VT), and ventilation (VI) was significantly greater in REM than in quiet sleep and was similar to the variability in these parameters seen in normal infants. In addition, brief periods of diaphragmeatic apnea were observed during REM sleep. The phenomenon of shortened TI during airway occlusion previously attributed to intercostal-to-phrenic reflexes was examined in the quadriplegic infant and in seven healthy term infants. The frequency of this response was increased when airway occlusion was delayed until after onset of inspiration. Shortening of TI by occlusion occurred no less frequently in the quadriplegic than in the control infants. The constant paradoxical inward movement of the rib cage during inspiration observed in the quadriplegic infant suggests that supraspinal innervation of intercostal muscle limits such paradoxical movements in the normal infant. The quadriplegic infant's end-expiratory volume was consistently above his passive functional residual capacity, as inferred from respiratory volume and pressure measurements.

1993 ◽  
Vol 264 (3) ◽  
pp. R638-R646 ◽  
Author(s):  
S. M. Pincus ◽  
T. R. Cummins ◽  
G. G. Haddad

Approximate entropy (ApEn), a mathematical formula quantifying regularity in data, was applied to heart rate data from normal and aborted-sudden infant death syndrome (SIDS) infants. We distinguished quiet from rapid-eye-movement (REM) sleep via the following three criteria, refining the notion of REM as more "variable": 1) REM sleep has greater overall variability (0.0374 +/- 0.0138 vs. 0.0205 +/- 0.0090 s, P < 0.005); 2) REM sleep is less stationary (StatAv = 0.742 +/- 0.110) than quiet sleep (StatAv = 0.599 +/- 0.159, P < 0.03); 3) after normalization to overall variability, REM sleep is more regular (ApEnsub = 1.224 +/- 0.092) than quiet sleep (ApEnsub = 1.448 +/- 0.071, P < 0.0001). Fifty percent of aborted-SIDS infants showed greater ApEn instability across quiet sleep than any normal infant exhibited, suggesting that autonomic regulation of heart rate occasionally becomes abnormal in a high-risk subject. There was an association between low ApEn values and aborted-SIDS events; 5 of 14 aborted-SIDS infants had at least one quiet sleep epoch with an ApEn value below the minimum of 45 normal-infant ApEn values.


1977 ◽  
Vol 42 (3) ◽  
pp. 362-367 ◽  
Author(s):  
R. Hagan ◽  
A. C. Bryan ◽  
M. H. Bryan ◽  
G. Gulston

We have studied two groups of eight preterm infants, relating chest wall afferent information to respiratory timing. Rib cage and abdominal motion were monitored by magnetometers and flow and tidal volume via a face mask. In the first group, studies were done in REM sleep when spontaneously occurring distortion of the rib cage occurred and a significant linear relationship between the rate of distortion of the chest wall and shortening of the inspiratory time (Ti) was found in all infants. Reduction in this distortion by the use of continuous positive airway pressure (CPAP) or continuous negative pressure at the body surface (CNeg) was associated with a significant (P less than 0.01) lengthening of Ti. Absence of changes in Ti when pressure was applied in quiet sleep suggested that lung volume or chemical changes were not involved. In the second group of infants we artificially generated the afferent inflow by using vibratory stimuli applied in one intercostal interspace and produced a significant (P less than 0.05) shortening in Ti. We suggest that the distortion of the rib cage in REM sleep generates afferent information from intercostal muscle spindles that is related to the rate of distortion and this, via a supraspinal reflex, inhibits phrenic motoneuron discharge. It may then be of importance in the etiology of apneic episodes in these infants. Applied pressure may be of benefit because it reduces an inhibitory afferent inflow.


2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee

The present study was designed to investigate breathing patterns across the sleep-wake state following a high cervical spinal injury in rats. The breathing patterns (e.g., respiratory frequency, tidal volume, and minute ventilation), neck electromyogram, and electroencephalography of unanesthetized adult male rats were measured at the acute (i.e., 1 day), subchronic (i.e., 2 wk), and/or chronic (i.e., 6 wk) injured stages after unilateral contusion of the second cervical spinal cord. Cervical spinal cord injury caused a long-term reduction in the tidal volume but did not influence the sleep-wake cycle duration. The minute ventilation during sleep was usually lower than that during the wake period in uninjured animals due to a decrease in respiratory frequency. However, this sleep-induced reduction in respiratory frequency was not observed in contused animals at the acute injured stage. By contrast, the tidal volume was significantly lower during sleep in contused animals but not uninjured animals from the acute to the chronic injured stage. Moreover, the frequency of sigh and postsigh apnea was elevated in acutely contused animals. These results indicated that high cervical spinal contusion is associated with exacerbated sleep-induced attenuation of the tidal volume and higher occurrence of sleep apnea, which may be detrimental to respiratory functional recovery after cervical spinal cord injury. NEW & NOTEWORTHY Cervical spinal injury is usually associated with sleep-disordered breathing. The present study investigated breathing patterns across sleep-wake state following cervical spinal injury in the rat. Unilateral cervical spinal contusion significantly impacted sleep-induced alteration of breathing patterns, showing a blunted frequency response and exacerbated attenuated tidal volume and occurrence of sleep apnea. The result enables us to investigate effects of cervical spinal injury on the pathogenesis of sleep-disordered breathing and evaluate potential therapies to improve respiration.


1983 ◽  
Vol 55 (4) ◽  
pp. 1113-1119 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan

The arousal and breathing responses to total airway occlusion during sleep were measured in 12 normal subjects (7 males and 5 females) aged 25-36 yr. Subjects slept while breathing through a specially designed nosemask, which was glued to the nose with medical-grade silicon rubber. The lips were sealed together with a thin layer of Silastic. The nosemask was attached to a wide-bore (20 mm ID) rigid tube to allow a constant-bias flow of room air from a blower. Total airway occlusion was achieved by simultaneously inflating two rubber balloons fixed in the inspiratory and expiratory pipes. A total of 39 tests were done in stage III/IV nonrapid-eye movement (NREM) sleep in 11 subjects and 10 tests in rapid-eye-movement (REM) sleep in 5 subjects. The duration of total occlusion tolerated before arousal from NREM sleep varied widely (range 0.9-67.0 s) with a mean duration of 20.4 +/- 2.3 (SE) s. The breathing response to occlusion in NREM sleep was characterised by a breath-by-breath progressive increase in suction pressure achieved by an increase in the rate of inspiratory pressure generation during inspiration. In contrast, during REM sleep, arousal invariably occurred after a short duration of airway occlusion (mean duration 6.2 +/- 1.2 s, maximum duration 11.8 s), and the occlusion induced a rapid shallow breathing pattern. Our results indicate that total nasal occlusion during sleep causes arousal with the response during REM sleep being more predictable and with a generally shorter latency than that in NREM sleep.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 860-864 ◽  
Author(s):  
Sally L. Davidson Ward ◽  
Daisy B. Bautista ◽  
Thomas C. Keens

Failure to arouse in response to hypoxia has been described in infants at increased risk for sudden infant death syndrome (SIDS) and has been suggested as a possible mechanism for SIDS. However, most SIDS victims are not in a high-risk group before death. Thus, if a hypoxic arousal disorder is an important contributor to SIDS, normal infants might fail to arouse from sleep in response to hypoxia. To test this hypothesis, the authors studied hypoxic arousal responses in 18 healthy term infants younger than 7 months of age (age 12.1 ± 1.7 [SEM] weeks; 56% girls). Hypoxic arousal challenges were performed during quiet sleep by rapidly decreasing inspired oxygen tension (Pio2) to 80 mm Hg for 3 minutes or until arousal (eye opening, agitation, and crying) occurred. Tests were performed in duplicate when possible. Only 8 infants (44%) aroused in response to one or more hypoxic challenges; arousal occurred during 8 (32%) of 25 trials. There were no significant differences in lowest Pio2 or arterial oxygen saturation during hypoxia between those infants who aroused and those who failed to arouse. All 18 infants had a fall in their end-tidal carbon dioxide tension during hypoxia, suggesting that each had a hypoxic ventilatory response despite failure to arouse in the majority. Periodic breathing occurred following hypoxia in only 1 (13%) of the 8 trials that resulted in arousal, compared with 16 (94%) of 17 trials without arousal (P &lt; .005). It is concluded that the majority of normal infants younger than 7 months of age fail to arouse from quiet sleep in response to hypoxia, despite the apparent presence of a hypoxic ventilatory response.


1984 ◽  
Vol 57 (5) ◽  
pp. 1531-1535 ◽  
Author(s):  
T. Aizad ◽  
J. Bodani ◽  
D. Cates ◽  
L. Horvath ◽  
H. Rigatto

To determine the effect of a single breath of 100% O2 on ventilation, 10 full-term [body wt 3,360 +/- 110 (SE) g, gestational age 39 +/- 0.4 wk, postnatal age 3 +/- 0.6 days] and 10 preterm neonates (body wt 2,020 +/- 60 g, gestational age 34 +/- 2 wk, postnatal age 9 +/- 2 days) were studied during active and quiet sleep states. The single-breath method was used to measure peripheral chemoreceptor response. To enhance response and standardize the control period for all infants, fractional inspired O2 concentration was adjusted to 16 +/- 0.6% for a control O2 saturation of 83 +/- 1%. After 1 min of control in each sleep state, each infant was given a single breath of O2 followed by 21% O2. Minute ventilation (VE), tidal volume (VT), breathing frequency (f), alveolar O2 and CO2 tension, O2 saturation (ear oximeter), and transcutaneous O2 tension were measured. VE always decreased with inhalation of O2 (P less than 0.01). In quiet sleep, the decrease in VE was less in full-term (14%) than in preterm (40%) infants (P less than 0.001). Decrease in VE was due primarily to a drop in VT in full-term infants as opposed to a fall in f and VT in preterm infants (P less than 0.05). Apnea, as part of the response, was more prevalent in preterm than in full-term infants. In active sleep the decrease in VE was similar both among full-term (19%) and preterm (21%) infants (P greater than 0.5). These results suggest greater peripheral chemoreceptor response in preterm than in full-term infants, reflected by a more pronounced decrease in VE with O2. The results are compatible with a more powerful peripheral chemoreceptor contribution to breathing in preterm than in full-term infants.


1992 ◽  
Vol 73 (6) ◽  
pp. 2368-2372 ◽  
Author(s):  
S. Duara ◽  
G. Silva Neto ◽  
N. Claure ◽  
T. Gerhardt ◽  
E. Bancalari

The influence of maturation on extrathoracic airway (ETA) stability during quiet sleep was determined in 13 normal preterm infants of 1.41 +/- 0.14 (SD) kg birth weight and 32 +/- 2 wk estimated gestational age. Studies began in the first week of life and were performed three times at weekly intervals. A drop in intraluminal pressure within the ETA was produced by external inspiratory flow-resistive loading (60 cmH2O.l-1 x s at 1 l/min); an increase in intrinsic resistance, indicating airway narrowing, was sought as a measure of ETA instability. Baseline total pulmonary resistance was not significantly different between weeks 1, 2, and 3 (88 +/- 35, 65 +/- 24, and 61 +/- 17 cmH2O.l-1 x s, respectively) but increased markedly above baseline with loading to 144 +/- 45 cmH2O.l-1.s during week 1 (P < 0.001), 89 +/- 28 cmH2O.l-1 x s at week 2 (P < 0.01), and 74 +/- 25 cmH2O.l-1 x s at week 3 (n = 10). The increment with loading was significantly greater during week 1 than during weeks 2 or 3 (P < 0.02). Similar studies were also done in seven full-term infants in the first week of life to evaluate the influence of gestational maturity on ETA stability. Despite a relatively greater drop in intraluminal pressure within the ETA of term vs. preterm infants with loading (P < 0.001), total pulmonary resistance failed to increase (68 +/- 21 to 71 +/- 32 cmH2O.l-1.s). These data reveal that ETA instability is present in preterm infants at birth and decreases with increasing postnatal age. Full-term neonates, by comparison, display markedly greater ETA stability in the immediate neonatal period.


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