The ability to switch from nasal to oral breathing in response to nasal obstruction is crucial for survival, and has been suggested to be an important mechanism in preventing sudden infant death syndrome (SIDS). To know whether the ability to switch from nasal to oral breathing is uniformly present during the early neonatal period, we examined the effects of slow and fast nasal occlusions on the establishment of oral breathing in preterm infants. Slow occlusions were used to mimic more closely occlusions occurring spontaneously. We studied 17 healthy preterm infants [birth weight, 1830 +/- 27 g (mean +/- SE); study weight, 1800 +/- 109 g; gestational age, 32 +/- 1 weeks; postnatal age, 12 +/- 2 days]. We used a nosepiece with a nasal occluder and a flow-through system to measure ventilation. A CO2 sampling catheter at the mouth was used to detect oral breathing. Of 58 occlusions, 29 were slow [resistance increasing slowly from 0 to infinite (occlusion)], and 29 were fast (infinite elastance applied in < 1 sec). Oral breathing was always established following slow and fast occlusions. In 44% of the slow occlusions, oral breathing started before complete occlusion. Arousal was observed in 12/58 (17%) of all occlusions, occurring primarily after initiation of oral breathing. Oxygen saturation and respiratory rate decreased significantly following occlusions, from 96 +/- 0.6 to 87 +/- 1.2% and 49 +/- 2.8 to 38 +/- 2 breaths/min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the influence of sleep state, respiratory pattern, and ventilation on cyclical fluctuations (CF) in cerebral blood flow (CBF) velocity (CBFV), we studied 21 ‘healthy’ preterm infants: birth weight 1,790 ± 162 g (SEM), study weight 1,960 ± 165 g, gestational age 32 ± 1 weeks, postnatal age 20 ± 4 (range 8–57) days. The CBFV was measured using on-line pulsed Doppler ultrasound by insonating the middle cerebral artery. Breathing was measured using a flow through system. The sleep state was monitored according to conventional criteria. Three hundred and seventy-five epochs of 1 min each were analyzed; 207 during quiet sleep (QS) and 168 during rapid eye movement (REM) sleep. CFs in CBFV were detected in all babies. The frequency of CF ranged from 0.5 to 6 cycles/min. The proportion of epochs showing CF was similar during both sleep states (56% QS vs. 59% REM; p = NS). Although the mean CBFV (cm/s) was similar in these two sleep states, the mean coefficient of variation, a measure of CF amplitude, was significantly higher during REM as compared with QS (6 ± 0.5 vs. 4.3 ± 0.2%; p < 0.05). Similarly, the mean CBFVs were similar with various respiratory patterns, but the coefficient of variation was significantly higher in periodic and apneic patterns as compared with regular and irregular respiratory patterns (5.6 ± 0.6% periodic, 5.6 ± 0.3% apneic, 3.6 ± 0.3% regular, and 4.1 ± 0.5% irregular; p < 0.05). The amplitude of CF was associated with the variability of the heart rate (p < 0.05), but not with the variability of the respiratory measurements. These findings suggest: (1) REM sleep is associated with a greater CBF variability than QS, and (2) periodic and apneic breathing are associated with a greater CBF variability than regular or irregular breathing. We speculate that sleep state and respiratory pattern do not determine but modulate the CBF. Our data suggest that in studies involving interpretation of CBFV data using the Doppler technique, breathing patterns should be taken into account in addition to sleep state.

We tested the hypothesis that in preterm infants, prolonged apneas (apneas > or = 20 sec) are not random events but are preceded by frequent and progressively longer respiratory pauses associated with changes in ventilatory variables. We studied 36 preterm infants with apnea [birth weight 1190 +/- 60 g (mean +/- SEM), study weight 1300 +/- 60 g, gestational age 28 +/- 1 weeks, and postnatal age 23 +/- 2 days]. A nosepiece with a flow-through system was used to measure ventilation and alveolar gases. Throughout the monitoring period for each infant we established 10-min moving "window of observation" followed by a 1-min interval examined for the detection of a prolonged apnea. Within the 10-min window, three variables were defined: the number of apneic episodes, the maximum length of a single apneic episode, and the total duration of apneic time. During the following minute (eleventh) the presence or absence of a prolonged apnea was determined. Chi-square test for a linear-trend in the rate of prolonged apnea and multiple logistic regression analysis showed that the relative risk of a prolonged apnea increases significantly from preceding periods without apnea to preceding periods containing the potential predictors of prolonged apnea. The strongest predictor was total duration of apneic time in the previous 10 min. When the 1 min before prolonged apnea was compared with the 1 min of similar sleep state not having prolonged apnea, minute ventilation decreased, primarily due to a decrease in respiratory frequency. Oxygen saturation decreased and alveolar PCO2 did not change. These findings suggest that prolonged apnea is not a random event but is preceded by a disturbance of the respiratory control system characterized by (1) frequent apneas of progressive duration, (2) decrease in respiratory minute volume and frequency, and (3) decreased O2 saturation.

Oral breathing is an important defense mechanism, yet its prevalence and relationship to behavioral activities have not been studied in preterm infants. We tested the hypothesis that oral breathing is rare in these infants and likely to be restricted to periods of body movements. Ten healthy preterm infants (birthweight 1300 +/- 100 g [SE]; gestational age 29 +/- 1 weeks; postnatal age 36 +/- 7 days) were studied. Ventilation was measured with a nose piece and screen flowmeter. Oral breathing was detected with a carbon dioxide sampler at the mouth. Movements were classified according to intensity into type I (localized, minor signal distortion) and type II (generalized, moderate signal distortion). Oral breathing was present 10% of the time, with a mean duration of 27 +/- 3 seconds. Of 104 episodes of oral breathing, 13 (13%) occurred during type I movement, 89 (86%; p < 0.01) during type II, and 2 (2%) in the absence of movement. The delay from beginning of movements to the beginning of oral breathing was 20 +/- 3 seconds. Nasal minute ventilation decreased from 0.203 +/- 0.013 L.min-1.kg-1 during movements in the absence of oral breathing to 0.167 +/- 0.013 L.min-1.kg-1 during movements plus oral breathing (p = 0.017). In 496 type I and II movements, the prevalence of oral breathing was 21 of 165 (13%) in quiet sleep, 37 of 194 (19%) in rapid eye movement sleep, 6 of 12 (50%) in transitional sleep, and 44 of 125 (35%) in indeterminate sleep (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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