Negative Airway Pressure Research Articles

Tube Law of the Pharyngeal Airway in Sleeping Patients with Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is characterized by repetitive pharyngeal collapse during sleep. However, the dynamics of pharyngeal narrowing and re-expansion during flow-limited breathing are not well described. The static pharyngeal tube law (end-expiratory area versus luminal pressure) has demonstrated increasing pharyngeal compliance as luminal pressure decreases, indicating that the airway would be sucked closed with sufficient inspiratory effort. On the contrary, the airway is rarely sucked closed during inspiratory flow limitation, suggesting that the airway is getting stiffer. Therefore, we hypothesized that during inspiratory flow limitation, as opposed to static conditions, the pharynx becomes stiffer as luminal pressure decreases. Upper airway endoscopy and simultaneous measurements of airflow and epiglottic pressure were performed during natural nonrapid eye movement sleep. Continuous positive (or negative) airway pressure was used to induce flow limitation. Flow-limited breaths were selected for airway cross-sectional area measurements. Relative airway area was quantified as a percentage of end-expiratory area. Inspiratory airway radial compliance was calculated at each quintile of epiglottic pressure versus airway area plot (tube law). Eighteen subjects (14 males) with OSA (apnea-hypopnea index = 57 ± 27 events/h), aged 49 ± 8 y, with a body mass index of 35 ± 6 kg/m(2) were studied. A total of 163 flow limited breaths were analyzed (9 ± 3 breaths per subject). Compliances at the fourth (2.0 ± 4.7 % area/cmH2O) and fifth (0.0 ± 1.7 % area/cmH2O) quintiles were significantly lower than the first (12.2 ± 5.5 % area/cmH2O) pressure quintile (P < 0.05). The pharyngeal tube law is concave (airway gets stiffer as luminal pressure decreases) during respiratory cycles under inspiratory flow limitation.

Can ventilator settings reduce the negative effects of endotracheal suctioning? Investigations in a mechanical lung model.

BackgroundThe insertion of suction devices through endotracheal tubes (ETTs) increases airway resistance and the subsequent suctioning may reduce airway pressures and facilitate atelectasis.The aim of this study was to investigate how airway pressures and tidal volumes change when different combinations of suction equipment and ETT sizes are used, and to what extent unfavorable effects can be ameliorated by choice of ventilator settings.MethodsA mechanical ventilator was connected to a lung model by ETTs of 9 mm, 8 mm or 7 mm internal diameter (ID) with a pressure transducer inserted distal to the ETT. The effects of suction procedures with bronchoscope and closed catheter systems were investigated during pressure controlled ventilation (PCV) and volume controlled ventilation (VCV). In each mode, the effects of changes in inspiration:expiration (I:E) ratio, trigger sensitivity and suction pressure were examined.ResultsThe variables that contributed most to negative model airway pressures and loss of tidal volume during suctioning were (in descending order); 1) Small-size ETTs (7–8 mm ID) combined with large diameter suction devices (14–16 Fr); 2) inverse I:E ratio ventilation (in VCV); 3) negative ventilator trigger sensitivity; and 4) strong suction pressure. The pressure changes observed distal to the ETTs were not identical to those detected by the ventilator.ConclusionsNegative model airway pressure was induced by suctioning through small-size ETTs. The most extreme pressure and volume changes were ameliorated when conventional ventilator settings were used, such as PCV mode with short inspiration time and a trigger function sensitive to flow changes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-016-0196-z) contains supplementary material, which is available to authorized users.

Mechanisms contributing to the response of upper-airway muscles to changes in airway pressure.

This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine (r(2) = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.

Brachycephalic obstructive airway syndrome: a growing problem

Brachycephalic obstructive airway syndrome: a growing problem

Submental Ultrasound Measurement of Dynamic Tongue Base Thickness in Patients with Obstructive Sleep Apnea

Dynamic tongue base thickness (TBT) may be an important anatomic factor in airway narrowing in patients with obstructive sleep apnea (OSA). The development of an accurate clinical assessment of the retroglossal airway in patients with OSA is still evolving. Submental ultrasound was used to investigate the association between measurements of TBT in response to negative airway pressure and the existence of OSA. Twenty OSA patients and 20 control participants underwent ultrasound measurement of TBT on eupneic breathing and with the Mueller maneuver, as well as clinical and polysomnographic assessments. Logistic regression analyses indicated that after adjustment for confounding factors, independent predictors of OSA included TBT in response to negative airway pressure, as measured by submental ultrasound with the Mueller maneuver (odds ratio: 2.11, 95% confidence interval: 1.15–3.87, p < 0.05), and the difference between TBT with the Muller maneuver and that without the Mueller maneuver (odds ratio: 2.47, 95% confidence interval: 1.09–5.58, p < 0.05). Ultrasound measurement of TBT during the Mueller maneuver provides a quantitative assessment of the retroglossal airway in OSA patients with minimal invasiveness and easy accessibility.

Obstructive sleep apnea and cardiovascular comorbidities: a large epidemiologic study.

Obstructive sleep apnea (OSA) is a common disorder, characterized by cyclic cessation of airflow for 10 seconds or more. There is growing awareness that OSA is related to the development and progression of cardiovascular disease. However, only a few studies have associated OSA directly to major cardiovascular events. The aim of this study was to evaluate the relationship between OSA and cardiovascular morbidity in a well defined population of patients.The electronic database of the central district of a major health management organization was searched for all patients diagnosed with OSA in 2002–2010. For each patient identified, an age- and sex-matched patient was randomly selected from the members of the same health management organization who did not have OSA. Data on demographics, socioeconomic status, and relevant medical parameters were collected as well.The study population included 2797 patients, average age 58.1, in which 76.6% were males. There was a significant correlation between OSA and the presence of ischemic heart disease (P < 0.001), pulmonary hypertension (P < 0.001), congestive heart failure (P < 0.001), cardiomyopathy (P = 0.003), and arrhythmia (P < 0.001). OSA was also significantly correlated with low socioeconomic status (P < 0.001).OSA and cardiovascular disease were strongly correlated. As such, early diagnosis and treatment of OSA may change the course of both diseases. We suggest that sleep disordered breathing should be routinely assessed in patients with cardiovascular problems. An ear–nose–throat evaluation may also be important to rule out anatomic disorders that cause upper airway obstruction.

Human hypoglossal motor unit activities in exercise

The genioglossus (GG) muscle is considered the principal protruder muscle of the tongue that dilates and stiffens the pharyngeal airway. We recorded whole muscle and single motor unit (MU) activities in healthy adults performing progressive intensity exercise on a cycle ergometer. Tungsten microelectrodes were inserted percutaneously into the GG of 11 subjects (20-40 years) to record electromyographic (EMG) activities and pulmonary ventilation (VI) at rest and at workload increments up to 300 W. Increases in respiratory drive were associated with increases in VI, mean inspiratory flow (Vt/Ti) and tonic and phasic components of the GG EMG activity. In contrast, individual MUs typically showed expiration-related decreases in firing as exercise intensity increased. We suggest the decrease in MU activity may occur secondary to afferent feedback from lungs/chest wall and that compensation for more negative inspiratory airway pressures generated during heavy exercise occurs primarily via recruitment of previously silent MUs.

Validation of a measurement to predict upper airway collapsibility during sedation for colonoscopy

Techniques to quantify the effects of sedation on upper airway collapsibility have been used as research tools in the laboratory and operating room. However, they have not been used previously in the usual clinical practice environment of colonoscopy sedation. The propensity for upper airway collapsibility, quantified as the critical pharyngeal pressure (P(crit)), was hypothesized to correlate with the need for clinical intervention to maintain ventilation. Twenty patients scheduled for colonoscopy with sedation were prospectively recruited to undergo measurement of upper airway collapsibility using negative airway pressure (NAP) provocation with a minimum pressure of -18 cmH(2)O. The P(crit) was the negative pressure that collapses the airway, either directly or by extrapolation from the pressure-flow relationship. An exponential transformation was applied to the P(crit) data for statistical analysis. A clinical intervention score (CIS) was used to quantify required interventions by the sedation nurse. The measurement of the P(crit) during sedation was significantly larger (less negative) than both the baseline ("awake") (P = 0.0029) and late recovery (P = 0.01) values. The CIS was not predicted by the transformed baseline or sedated P(crit) with or without including demographics associated with sleep apnea syndrome. Although the NAP technique showed the expected changes with sedation in this clinical situation, we did not find that it predicted the need for clinical intervention during endoscopy. Our study was not large enough to test for subpopulations in which the test might be predictive; further studies of these particular groups are needed to determine the clinical utility of the NAP measurement.

Increased sensitivity to endothelin‐1 in posterior cerebral arteries from obstructive sleep apnea rats

Obstructive sleep apnea (OSA) has been identified as a significant risk factor for stroke. However, little is known regarding the effects of OSA on the cerebral circulation. The repetitive airway closures associated with OSA lead to intermittent hypoxia/hypercapnia and reoxygenation, increased negative intrathoracic pressures, and arousals. In order to model the physiological consequences of OSA and examine the affect on cerebral circulation, we have chronically instrumented rats with inflatable endotracheal obstruction devices. Rats underwent 30 apneas/ hour for 8 hours/ day (sleep phase). We observed significant decreases in pO2 and pH accompanied by an increase in pCO2 (p&lt;0.05). Additionally, apneas caused a 5‐fold increase in negative airway pressure (p&lt;0.05). Following 2 weeks of apnea OSA rats exhibited a 24‐hour blood pressure (BP) pattern similar to non‐dipping hypertensives (i.e., BP drops &lt;10% during sleep; p&lt;0.05). Using the pressurized cerebral artery preparation, we observed no difference between OSA and sham‐vessels when endothelin (ET‐1) was administered through the lumen of the vessel. However, 1 month of OSA led to significantly increased ablumenal sensitivity to ET‐1 (p&lt;0.05). These data demonstrate that our novel rat model of OSA exhibits characteristics similar to those observed in OSA patients and results in increased sensitivity of cerebral vessels to ET‐1. Funded by R21HL102778

Cerebrovascular Consequences of Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is an independent risk factor for stroke. However, little is known about how OSA affects the cerebral circulation. The goal of this project was to test the following hypothesis: Chronic exposure to apnea produces hypertension and alters nitric oxide (NO) mediated dilation in cerebral arteries. For these studies, we developed a novel model of OSA in rats. Airway obstruction was induced by a chronically implanted, inflatable endotracheal obstruction device. We induced 30 apneas (8 sec duration each)/hr during 8 hrs of the sleep cycle in free‐ranging rats. Apnea caused significant alterations in blood gasses [baseline vs. end apnea‐ pO2 (mmHg): 127 ± 2 vs. 67 ± 2; pCO2 (mmHg): 43 ± 1 vs. 51 ± 1; and pH: 7.46 ± 0.002 vs. 7.38 ± 0.01; n=5, p≤0.003]. Apnea decreased hemoglobin O2 saturation by 12 ± 1% (n=5, p=0.001 vs. Sham) and produced exaggerated negative airway pressures (−16 ± 0.7 mmHg; n=7, p&lt;0.001 vs. Sham). Two weeks of apnea produced a 24‐hr mean blood pressure (BP) pattern similar to non‐dipping hypertensives (i.e. ‐ &lt;10% BP dip during the sleep phase). After one month of apnea, NO‐mediated dilations to ATP in isolated cerebral arteries were attenuated by 20 ± 2% (n=4, p&lt;0.02 vs. Sham). Using a novel model of OSA, which recapitulates OSA in humans, we demonstrate that endothelial dysfunction occurs by one month, likely increasing the vulnerability of the brain during stroke.Funded by NIH R21 HL102778

Influence of negative airway pressure on upper airway dynamic and impact on night-time apnea worsening

Negative airway pressure loading such as seen during obstructive apnea/hypopnea may influence upper airway (UA) mechanical properties. We measured the effects of such loading on UA mechanical properties during wakefulness and assessed the potential link with night-time apnea worsening. Twitch stimulations of the phrenic nerve were applied before and after a step-by-step increase in UA suction flow in 10 sleep apnea and 10 control males. Inspiratory closing pressure was lower in control than in apneic subjects. No consistent changes were observed in UA mechanical properties before and after the trial. In apneic patients, changes in the apnea index from the beginning to the end of the night correlated with changes in inspiratory closing pressure following suction flow. (1) Apnea phenotype does not influence the impact of negative airway pressure on UA dynamic properties during wakefulness and (2) worsening of sleep apnea frequency during the night may relate to the exposure to recurrent UA negative pressure.

Neuroventilatory efficiency and extubation readiness in critically ill patients

IntroductionBased on the hypothesis that failure of weaning from mechanical ventilation is caused by respiratory demand exceeding the capacity of the respiratory muscles, we evaluated whether extubation failure could be characterized by increased respiratory drive and impaired efficiency to generate inspiratory pressure and ventilation.MethodsAirway pressure, flow, volume, breathing frequency, and diaphragm electrical activity were measured in a heterogeneous group of patients deemed ready for a spontaneous breathing trial. Efficiency to convert neuromuscular activity into inspiratory pressure was calculated as the ratio of negative airway pressure and diaphragm electrical activity during an inspiratory occlusion. Efficiency to convert neuromuscular activity into volume was calculated as the ratio of the tidal volume to diaphragm electrical activity. All variables were obtained during a 30-minute spontaneous breathing trial on continuous positive airway pressure (CPAP) of 5 cm H2O and compared between patients for whom extubation succeeded with those for whom either the spontaneous breathing trial failed or for those who passed, but then the extubation failed.ResultsOf 52 patients enrolled in the study, 35 (67.3%) were successfully extubated, and 17 (32.7%) were not. Patients for whom it failed had higher diaphragm electrical activity (48%; P < 0.001) and a lower efficiency to convert neuromuscular activity into inspiratory pressure and tidal volume (40% (P < 0.001) and 53% (P < 0.001)), respectively. Neuroventilatory efficiency demonstrated the greatest predictability for weaning success.ConclusionsThis study shows that a mixed group of critically ill patients for whom weaning fails have increased neural respiratory drive and impaired ability to convert neuromuscular activity into tidal ventilation, in part because of diaphragm weakness.Trial RegistrationClinicaltrials.gov identifier NCT01065428. ©2012 Liu et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure.

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.

Use of titanium mesh in laryngotracheal reconstruction: an experimental study on rabbits

Titanium mesh may be an alternative material to be used in laryngotracheal reconstruction. Twenty New Zealand rabbits were divided into two groups. Group A underwent laryngotracheoplasty with titanium mesh-buccal mucosa-muscle complex, and Group B received auricular cartilage grafts. All animals survived without complications. The animals were killed at 60 days, and laryngotracheal regions were evaluated. There was no subglottic collapse at physiologic and supraphysiologic negative airway pressures in Group A and mild-moderate collapse in Group B. Macroscopically the average antero-posterior and lateral diameters were not statistically different among two groups. Light microscopic examination revealed no fibrosis, necrosis or new cartilage formation in both groups. Inflammation and granulation were more pronounced in Group A. The lumens in both groups were moderately obstructed. Reconstruction of the upper airway with titanium mesh may be used in very selected cases where autologous grafting materials are inadequate and unsatisfactory.

Development of atelectasis and arterial to end-tidal Pco2-difference in a porcine model of pneumoperitoneum

Intraperitoneal insufflation of carbon dioxide (CO2) may promote collapse of dependent lung regions. The present study was undertaken to study the effects of CO2-pneumoperitoneum (CO2-PP) on atelectasis formation, arterial oxygenation, and arterial to end-tidal PCO2-gradient (Pa-E'(CO2)). Fifteen anaesthetized pigs [mean body weight 28 (SD 2) kg] were studied. Spiral computed tomography (CT) scans were obtained for analysis of lung tissue density. In Group 1 (n=5) mechanical ventilation (V(T)=10 ml kg (-1), FI(O2)=0.5) was applied, in Group 2 (n=5) FI(O2) was increased for 30 min to 1.0 and in Group 3 (n=5) negative airway pressure was applied for 20 s in order to enhance development of atelectasis. Cardiopulmonary and CT data were obtained before, 10, and 90 min after induction of CO2-PP at an abdominal pressure of 12 mmHg. Before CO2-PP, in Group 1 non-aerated tissue on CT scans was 1 (1)%, in Group 2 3 (2)% (P<0.05, compared with Group 1), and in Group 3 7 (3)% (P<0.05, compared with Group 1 and Group 2). CO2-PP significantly increased atelectasis in all groups. PaO2/FI(O2) fell and venous admixture ('shunt') increased in proportion to atelectasis during anaesthesia but CO2-PP had a varying effect on PaO2/FI(O2) and shunt. Thus, no correlation was seen between atelectasis and PaO2/FI(O2) or shunt when all data before and during CO2-PP were pooled. Pa-E'(CO2), on the other hand correlated strongly with the amount of atelectasis (r2=0.92). Development of atelectasis during anaesthesia and PP may be estimated by an increased Pa-E'(CO2).

Opioid‐induced suppression of genioglossal muscle activity: is it clinically important?

Opioid‐induced suppression of genioglossal muscle activity: is it clinically important?

Long‐term facilitation of upper airway muscle activity induced by episodic upper airway negative pressure and hypoxia in spontaneously breathing anaesthetized rats

Obstruction of the upper airway (UA) is associated with episodes of hypoxia and upper airway negative pressure (UANP). In the companion paper it is shown that episodic hypoxia elicits long-term facilitation (LTF) of tongue protrudor, retractor and respiratory pump muscle activity. However, whether repeated exposure to UANP also induces LTF is unknown. We hypothesized that repetitive exposure to UANP would induce LTF of UA and respiratory pump muscle activity and when coupled with hypoxia, as occurs when the UA obstructs, would lead to an even greater facilitation of muscle activity and the response to UANP. Experiments were performed in 24 anaesthetized, spontaneously breathing rats with intact vagi. To induce LTF, UANP stimuli (-10 cmH(2)O) of 5 s duration were delivered every 30 s for 3 min (+/- hypoxia). This was repeated eight times over 1 h, each 3 min episode separated by 5 min of normoxia. Genioglossus (GG), hyoglossus (HG) and diaphragm (Dia) muscle activity was recorded before, during and for 1 h following the last exposure to episodic UANP alone (n = 8), UANP and hypoxia together (n = 8) or normoxia alone (n = 8). During the final hour, single pulses of UANP were applied at 1 min and every 10 min thereafter to determine whether LTF of the response to UANP had been induced. Our results show that LTF of GG muscle activity and its response to UANP was induced following exposure to episodic UANP stimuli alone and UANP applied during hypoxia. However, there was no significant difference between these responses. Episodic UANP alone also induced LTF of HG muscle activity but this effect did not manifest until 40 min following the last episode of repeated UANP stimulation. In the presence of hypoxia, no LTF of HG muscle response to UANP was found. In conclusion, episodic UANP stimulation induces LTF of UA dilator and retractor tongue muscles, but no further facilitation occurs when coupled with hypoxia. This response may serve as an important protective mechanism of respiratory homeostasis during sleep, particularly in patients who suffer from obstructive sleep apnoea.

Breathing cardiovascular variability and baroreflex in mechanically ventilated patients

Heart rate and blood pressure variations during spontaneous ventilation are related to the negative airway pressure during inspiration. Inspiratory airway pressure is positive during mechanical ventilation, suggesting that reversal of the normal baroreflex-mediated pattern of variability may occur. We investigated heart rate and blood pressure variability and baroreflex sensitivity in 17 mechanically ventilated patients. ECG (RR intervals), invasive systolic blood pressure (SBP), and respiratory flow signals were recorded. High-frequency (HF) amplitude of RR and SBP time series and HF phase differences between RR, SBP, and ventilatory signals were continuously computed by Complex DeModulation (CDM). Cross-spectral analysis was used to assess the coherence and the gain functions between RR and SBP, yielding baroreflex sensitivity indices. The HF phase difference between SBP and ventilatory signals was nearly constant in all patients with inversion of SBP variability during the ventilator cycle compared with cycling with negative inspiratory pressure to replicate spontaneous breathing. In 12 patients (group 1), the phase difference between RR and ventilatory signals changed over time and the HF-RR amplitude varied. In the remaining five patients (group 2), RR-ventilatory signal phase and HF-RR amplitude showed little change; however, only one of these patients exhibited a RR-ventilatory signal phase difference mimicking the normal pattern of respiratory sinus arrhythmia. Spectral coherence between RR and SBP was lower in the group with phase difference changes. Positive pressure ventilation exerts mainly a mechanical effect on SBP, whereas its influence on HR variability seems more complex, suggesting a role for neural influences.

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

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.

Lower body positive pressure increases upper airway collapsibility in healthy subjects

We previously showed that rostral fluid displacement by lower body positive pressure (LBPP) narrows the upper airway (UA) and increases UA resistance, but effects on UA collapsibility remained unknown. To test if LBPP increases UA collapsibility, 13 healthy men were randomized into a control or LBPP arm then crossed over into the other arm with a 30-min washout in between. LBPP was applied by inflating anti-shock trousers wrapped around both legs to 40 mmHg. UA collapsibility was assessed by determining UA critical closing pressure (P crit) during application of different negative airway pressures. P crit and leg fluid volume were measured at baseline and after 5 min during both periods. LBPP caused a significant increase in P crit associated with a reduction in leg fluid volume. We conclude that rostral fluid displacement by LBPP increases UA collapsibility in healthy men, suggesting that fluid shift into the neck could increase UA collapsibility during sleep and thereby predispose patients with fluid overload states to obstructive sleep apnea.