Role of respiratory muscles in upper airway narrowing induced by inspiratory loading in preterm infants

1994 ◽  
Vol 77 (1) ◽  
pp. 30-36 ◽  
Author(s):  
S. Duara ◽  
G. Silva Neto ◽  
N. Claure

Extrathoracic airway (ETA) narrowing is induced in preterm infants by inspiratory flow-resistive loading (IRL), which reduces intraluminal pressure within the region. Neuromuscular load compensation was evaluated over time in 10 infants [body wt 1.5 +/- 0.17 (SD) kg, gestational age 33 +/- 2.3 wk, age 12 +/- 5.2 days] during quiet sleep. Baseline (BL) studies were followed by IRL (125 cmH2O.l–1.s at 1 l/min). Minute ventilation, changes in esophageal pressure (Pes) and proximal airway pressure, and moving time averages of posterior cricoarytenoid (PCA), submental genioglossus (SM), and diaphragm (DIA) electromyograms were obtained during BL and 1 and 5 min of IRL. Total respiratory resistance was calculated from pressure and flow changes and was used to estimate ETA narrowing: there was an increase in total respiratory resistance from 90 +/- 15 to 120 +/- 34 and 151 +/- 86 cmH2O.l–1.s after 1 and 5 min of IRL, respectively (P < 0.05, 1-min IRL vs. BL), in association with a sustained decline in minute ventilation (P < 0.05) and increases in Pes and proximal airway pressure (P < 0.05). Phasic PCA activity was always present, but its duration was only transiently prolonged with IRL (P < 0.05, 1-min IRL vs. BL). SM activity was present in only one infant during BL and was recruited in two additional infants during IRL. The decline in Pes from 1 to 5 min of IRL occurred despite continuing increases in peak and average activities of the DIA moving time average, which may reflect an onset of DIA fatigue. The transient prolongation of phasic PCA activity and occasional recruitment of SM activity with sustained loading explain, in part, the ETA instability detectable by moderate IRL in sleeping preterm 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.


1987 ◽  
Vol 63 (4) ◽  
pp. 1539-1543 ◽  
Author(s):  
S. Duara ◽  
T. Gerhardt ◽  
E. Bancalari

Extrathoracic airway (ETA) stability was tested in 10 preterm infants during sleep with a drop in intraluminal pressure produced by the application of an external inspiratory flow-resistive load (IRL, 125 cmH2O.1–1.s at 1 l/min). An increase in total pulmonary resistance was sought as the measure of airway narrowing. The role of the ETA in the increased pulmonary resistance with loading was examined by testing the same infants while endotracheally intubated and after extubation. Total pulmonary resistance decreased with loading during the intubated studies (102.5 +/- 41.2 to 82.4 +/- 33.3 cmH2O.1–1.s, P less than 0.05), whereas a significant increase in pulmonary resistance was seen with loading in the extubated studies (101 +/- 58.1 to 128 +/- 68.6 cmH2O.1–1.s, P less than 0.01). Intraluminal pressure in the ETA, measured by the lowest proximal airway pressure, fell significantly with loading in both conditions, with values changing from -0.7 +/- 0.3 to -4.7 +/- 2.7 cmH2O in the intubated infants and from -0.9 +/- 0.3 to -4.6 +/- 0.9 cmH2O) in the extubated infants (P less than 0.01). The results suggest ETA narrowing with loading in extubated infants despite the absence of overt obstructive apnea. Measurements of total pulmonary resistance with IRL can be used as a simple test of ETA stability.


1988 ◽  
Vol 65 (6) ◽  
pp. 2434-2439 ◽  
Author(s):  
W. A. Carlo ◽  
R. J. Martin ◽  
J. M. Difiore

Because neonatal apnea is frequently associated with airway obstruction, we compared relative changes in activity between various upper airway muscles and the diaphragm during hypercapnic stimulation. The technique of hyperoxic CO2 rebreathing was employed in 17 healthy, sleeping preterm infants studied at a postnatal age of 32 +/- 12 days. Surface diaphragm (DIA) electromyograms (EMGs) were recorded in all infants, and noninvasive measurements of posterior cricoarytenoid (PCA), genioglossus (GG), and alae nasi (AN) EMGs were analyzed in 11, 9, and 8 infants, respectively. During the control period, consistent phasic EMGs were recorded from the DIA in all infants and from the PCA in 8 infants, but from the GG and AN each in only one infant. During CO2 rebreathing, minute ventilation and end-tidal CO2 increased linearly as CO2 rose from 31 +/- 5 to 51 +/- 5 Torr. DIA and PCA EMGs also had proportional and comparable increases throughout rebreathing. In contrast, both GG and AN responses differed from the DIA and PCA (P less than 0.001) and exhibited minimal or absent responses at low levels of hypercapnia. Consistent GG and AN EMGs appeared at comparable levels of end-tidal CO2 (47 +/- 5 and 45 +/- 5 Torr, respectively) and subsequently increased linearly in most infants. We conclude that during CO2 rebreathing the initially delayed and subsequently linear responses of the GG and AN EMGs indicate a high CO2 threshold for these muscles.


1990 ◽  
Vol 68 (3) ◽  
pp. 1041-1047 ◽  
Author(s):  
W. A. Carlo ◽  
J. M. DiFiore

Upper airway muscles and the diaphragm may have different quantitative responses to chemoreceptor stimulation. To compare the respiratory muscle responses to changes in CO2, 10 ventilator-dependent preterm infants (gestational age 28 +/- 1 wk, postnatal age 40 +/- 6 days, weight 1.4 +/- 0.1 kg) were passively hyperventilated to apnea and subsequently hypoventilated. Electromyograms from the genioglossus, alae nasi, posterior cricoarytenoid, and diaphragm were recorded from surface electrodes. Apneic CO2 thresholds of all upper airway muscles (genioglossus 46.8 +/- 4.3 Torr, alae nasi 42.4 +/- 3.6 Torr, posterior cricoarytenoid 41.6 +/- 3.2 Torr) were higher than those of the diaphragm (38.8 +/- 2.6 Torr, all P less than 0.05). Above their CO2 threshold levels, responses of all upper airway muscles appeared proportional to those of the diaphragm. We conclude that nonproportional responses of the respiratory muscles to hypercapnia may be the result of differences in their CO2 threshold. These differences in CO2 threshold may cause imbalance in respiratory muscle activation with changes in chemical drive, leading to upper airway instability and obstructive apnea.


2010 ◽  
Vol 108 (6) ◽  
pp. 1619-1624 ◽  
Author(s):  
Danny J. Eckert ◽  
Julian P. Saboisky ◽  
Amy S. Jordan ◽  
David P. White ◽  
Atul Malhotra

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately −16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31 ± 4 vs. 31 ± 6 ms and peak amplitude 318 ± 55 vs. 314 ± 26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54 ± 7 ms, nadir amplitude 64 ± 6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253060
Author(s):  
M. Nicholas Musselwhite ◽  
Tabitha Y. Shen ◽  
Melanie J. Rose ◽  
Kimberly E. Iceman ◽  
Ivan Poliacek ◽  
...  

The role of the cerebellum in controlling the cough motor pattern is not well understood. We hypothesized that cerebellectomy would disinhibit motor drive to respiratory muscles during cough. Cough was induced by mechanical stimulation of the tracheobronchial airways in anesthetized, spontaneously breathing adult cats (8 male, 1 female), and electromyograms (EMGs) were recorded from upper airway, chest wall, and abdominal respiratory muscles. Cough trials were performed before and at two time points after total cerebellectomy (10 minutes and >1 hour). Unlike a prior report in paralyzed, decerebrated, and artificially ventilated animals, we observed that cerebellectomy had no effect on cough frequency. After cerebellectomy, thoracic inspiratory muscle EMG magnitudes increased during cough (diaphragm EMG increased by 14% at 10 minutes, p = 0.04; parasternal by 34% at 10 minutes and by 32% at >1 hour, p = 0.001 and 0.03 respectively). During cough at 10 minutes after cerebellectomy, inspiratory esophageal pressure was increased by 44% (p = 0.004), thyroarytenoid (laryngeal adductor) muscle EMG amplitude increased 13% (p = 0.04), and no change was observed in the posterior cricoarytenoid (laryngeal abductor) EMG. Cough phase durations did not change. Blood pressure and heart rate were reduced after cerebellectomy, and respiratory rate also decreased due to an increase in duration of the expiratory phase of breathing. Changes in cough-related EMG magnitudes of respiratory muscles suggest that the cerebellum exerts inhibitory control of cough motor drive, but not cough number or phase timing in response to mechanical stimuli in this model early after cerebellectomy. However, results varied widely at >1 hour after cerebellectomy, with some animals exhibiting enhancement or suppression of one or more components of the cough motor behavior. These results suggest that, while the cerebellum and behavior-related sensory feedback regulate cough, it may be difficult to predict the nature of the modulation based on total cerebellectomy.


1982 ◽  
Vol 53 (4) ◽  
pp. 805-814 ◽  
Author(s):  
S. F. Al-Shway ◽  
J. P. Mortola

Kittens, puppies, cats, and dogs were anesthetized with pentobarbital sodium and tracheotomized. The ventilatory pattern was recorded before, during, and after the delivery of steady flows of room air of 20 or 50 ml X s-1 X kg-1 in the expiratory direction through a cannula inserted just below the larynx. In the newborn, a reduction in breathing frequency, mainly due to a prolongation of the expiratory time, and a decrease in tidal volume contributed to a reduction in minute ventilation particularly with the higher flows; in some instances apnea resulted. Small or no effects were observed in the adult. The ventilatory inhibition was still present when humidified 37 degrees C warmed airstreams were delivered, and it was unchanged when airflows of 4.9% CO21.5% O2–82.6% N2 were applied. After local anesthesia of the laryngeal region or after bypassing the larynx, the ventilatory inhibition disappeared. By closure of a nostril at any given airflow, the upper airway pressure was substantially increased; however, this maneuver did not enhance the respiratory depression. We conclude that airflow through the upper airways can inhibit ventilation in newborn kittens and puppies presumably through the stimulation of airflow-sensitive laryngeal receptors.


1992 ◽  
Vol 72 (1) ◽  
pp. 116-120 ◽  
Author(s):  
Z. Weintraub ◽  
R. Alvaro ◽  
K. Kwiatkowski ◽  
D. Cates ◽  
H. Rigatto

To discover whether increases in inhaled O2 fraction (FIO2; up to 40%) decrease apnea via an increase in minute ventilation (VE) or a change in respiratory pattern, 15 preterm infants (birth weight 1,300 +/- 354 g, gestational age 29 +/- 2 wk, postnatal age 20 +/- 9 days) breathed 21, 25, 30, 35, and 40% O2 for 10 min in quiet sleep. A nosepiece and a flow-through system were used to measure ventilation. Alveolar PCO2, transcutaneous PO2, and sleep states were also assessed. All infants had periodic breathing with apneas greater than or equal to 3 s. With an increase in FIO2 breathing became more regular and apneas decreased (P less than 0.001). This regularization in breathing was not associated with significant changes in VE. However, the variability of VE, tidal volume, and expiratory and inspiratory times decreased significantly. The results indicate that the more regular breathing observed with small increases in FIO2 was not associated with significant changes in ventilation. The findings suggest that the increased oxygenation decreases apnea and periodicity in preterm infants, not via an increase in ventilation, but through a decrease in breath-to-breath variability of VE.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P &lt; .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P &gt; .1), but the intercept was shifted to the right (P &lt; .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P &lt; .05). In addition, transcutaneous Po2 increased during administration of CPAP (P &lt; .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.


PEDIATRICS ◽  
2003 ◽  
Vol 112 (4) ◽  
pp. 907-913 ◽  
Author(s):  
S. L. Tonkin ◽  
C. G. McIntosh ◽  
W. Hadden ◽  
C. Dakin ◽  
S. Rowley ◽  
...  

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