Reducing ventilatory response to carbon dioxide by breathing cold air

To study the effect of cooling of nasal receptors on breathing we had 10 normal male volunteers rebreathe through their noses 8% CO2 in oxygen at "warm" (23 to 30 degrees C) and at "cold" (-4 to 10 degrees C) temperatures. In order to further examine the effect of nasal receptors on the control of breathing, 11 subjects had their nasal response to CO2 measured at the warm temperature before and after topical nasal anesthesia. To exclude an increase in nasal resistance as the cause of the reduced response to CO2, 10 subjects had their nasal resistance measured before and after nasal rebreathing of cold 8% CO2 in oxygen. To also exclude increased bronchial resistance, forced expiratory volume in one second (FEV1) was measured in 12 subjects before and after nasal breathing of cold oxygen for 3 min. The mean ventilatory response to CO2 was reduced from 3.0 +/- 1.6 L/min/mmHg to 2.5 +/- 1.1 L/min/mmHg (p less than 0.05) by the cold air. Topical nasal anesthesia increased the response to CO2 at the warm temperature from 2.4 +/- 0.7 to 2.7 +/- 0.9 L/min/mmHg. The effect of nasal breathing of 8% CO2 in oxygen at the cold temperature was to reduce nasal inspiratory resistance at 1 L/s from 4.3 +/- 3.0 cm H2O L/s to 2.6 +/- 1.0 cm H2O L/s (p less than 0.05). Expiratory resistance at 1 L/s fell from 3.7 +/- 1.5 cm H2O L/s to 2.4 +/- 0.7 cm H2O L/s (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Moderate alcohol ingestion increases upper airway resistance in normal subjects

Apnea during sleep has been associated with both increased pharyngeal resistance and nasal obstruction. Alcohol can worsen obstructive sleep apnea, but its influence on pharyngeal resistance and nasal patency has not been evaluated. Accordingly, we determined the effects of alcohol on pharyngeal and nasal resistances in 11 normal awake subjects on 2 separate days. Baseline pharyngeal resistance prior to placebo and alcohol was not significantly different. After placebo, pharyngeal resistance did not change significantly. However, after alcohol, pharyngeal resistance increased from 1.9 +/- 0.5 (SEM) to 3.3 +/- 0.8 cm H2O/L/s at 45 min (p less than 0.05) and returned to near baseline level by 90 min. Baseline nasal resistance varied considerably within subjects on the 2 days, but the mean values for baseline nasal resistance on alcohol and placebo days were not significantly different. Nasal resistance did not change after placebo, but after alcohol, nasal resistance increased from 2.4 +/- 0.9 at baseline to 3.7 +/- 0.8 at 45 min (NS) and to 4.3 +/- 1.2 cm H2O/L/s at 90 min (p less than 0.05). We conclude that a decrease in pharyngeal airway size and an increase in nasal resistance may account for alcohol's ability to worsen obstructive sleep apnea.     

Sulfur dioxide does not acutely increase nasal symptoms or nasal resistance in subjects with rhinitis or in subjects with bronchial responsiveness to sulfur dioxide

We examined whether brief exposures to moderately high concentrations of sulfur dioxide (SO2) causes acute increases in nasal symptoms and nasal resistance in subjects with chronic rhinitis. We studied 19 subjects with allergic rhinitis and 3 subjects with chronic intermittent rhinorrhea, nasal congestion, and sneezing without any other manifestation of allergy. We found that the change in nasal resistance and symptoms caused by nasal inhalation of 4 ppm of SO2 for 10 min was no greater than the changes caused by nasal inhalation of conditioned room air. In a second set of experiments, we examined whether allergic subjects with demonstrable bronchomotor responsiveness to SO2 also had nasal responsiveness to the gas. We studied 8 subjects with a history of both asthma and allergic rhinitis. Each subject developed symptoms of dyspnea or wheezing and an increase in specific airway resistance of at least 8 L x cm H2O/L/s after breathing 1 or 2 ppm of SO2 by mouthpiece at 20 L/min, and did not develop these changes after breathing room air under the same conditions. No subject, however, developed more nasal symptoms or a greater increase in nasal airway resistance after tidally breathing SO2 through the nose than after breathing room air, even when the concentration of SO2 delivered to the nose was double the concentration delivered through the mouthpiece to the lower airways. We conclude that brief exposure to SO2 at a concentration of 4 ppm or less is unlikely to cause significant nasal dysfunction in most subjects with chronic rhinitis, and that in subjects with both allergic rhinitis and asthma, responsiveness to SO2 is not uniform throughout the respiratory tract.     

Effects of nasal prongs on nasal airflow resistance

STUDY OBJECTIVES: The aim of this study was to investigate whether nasal prongs, which have been proposed to assess nasal flow during sleep, affect nasal airflow resistance (NR). DESIGN: NR was estimated by posterior rhinomanometry at a 0.5 L/s flow, under eight conditions: in the basal state, and with seven different nasal prongs. PARTICIPANTS: The study was performed in 17 healthy supine subjects, 8 of whom had basal NR values within the normal range (< or = 2 cm H(2)O.L(-1).s, group 1), and 9 had increased basal NR values (> 2.5 cm H(2)O.L(-1).s, group 2), because of nare narrowness and/or deviated nasal septum. Measurements and results: NR increased significantly while breathing with nasal prongs (p < 0.0001 in both groups). The changes in NR (DeltaNR) induced by the different nasal prongs were characterized by large intersubject and intrasubject variability, with a maximum DeltaNR of 24.2 cm H(2)O.L(-1).s. Significant differences were found between the DeltaNR induced by the different nasal prongs (p < 0.001 in group 1, and p < 0.0003 in group 2), and for six of them, DeltaNR was significantly higher in group 1 than in group 2 (p < 0.02). CONCLUSIONS: This study demonstrates that nasal prongs can markedly increase NR in subjects presenting with nare narrowness and/or deviated nasal septum. Further investigations that would include nocturnal polysomnography are still required to evaluate the possible influence of nasal prongs on the diagnosis of obstructive sleep apnea syndrome and its severity.     

Combined effects of a nasal dilator and nasal prongs on nasal airflow resistance

STUDY OBJECTIVES: Nasal prongs (NPs), when used to assess nasal flow, can result in dramatic increases in nasal airflow resistance (NR). The aim of this study was to investigate whether the NP-induced increases in NR could be corrected by the simultaneous use of an internal nasal dilator (ND). DESIGN: NR was estimated by posterior rhinomanometry, in the basal state (NRb), and while breathing with NP (NRp), with ND (NRd), and with both ND and NP (NRd + p). PARTICIPANTS: The study was performed in 15 healthy subjects. Measurements and results: NR (mean NRb [+/- SEM], 2.5 +/- 0.4 cm H(2)O/L/s) significantly decreased with ND (NRd = 1.4 +/- 0.2 cm H(2)O/L/s; p < 0.001) and significantly increased with NP (NRp = 3.8 +/- 0.8 cm H(2)O/L/s; p < 0.001). A significant logarithmic relationship was found between NRd and NRb (r(2) = 0.95; p < 0.0001), and a significant exponential relationship was found between NRp and NRb (r(2) = 0.99; p < 0.0001). While breathing with both ND and NP, NRd + p was significantly lower than NRb (1.9 +/- 1.4 cm H(2)O/L/s; p < 0.02). CONCLUSIONS: Our results demonstrate that the ND tends to slightly overcorrect the NP-induced increase in NR and suggest that, in view of the possible effects of NPs on upper airway resistance, the combination of both devices might be used for nasal airflow monitoring during nocturnal polysomnography in patients presenting with highly resistive nares.     

Evaluation of nasal impedance using the forced oscillation technique in infants

By applying oscillations to the respiratory system through a rigid face mask, the infant-adapted Lándsér forced oscillation technique measures impedance of the total respiratory system including the nose, at frequencies from 4 to 52 Hz. The present study was aimed at evaluating nasal impedance in infants from consecutive forced oscillation measurements through both nostrils and each nostril separately, using a simple electrical model. In 30 asthmatic infants with varying degrees of nasal obstruction, aged 1-16 months, calculated nasal resistance (Rn) at 24 Hz ranged from 1 to 16 cm H2O.L-1.s. The ratio of Rn to total respiratory system resistance varied between 1 and 48% (mean: 16%). In seven non-asthmatic infants, aged 0-12 months, Rn was between 1 and 11 cm H2O.L-1.s. Nasal patency (evaluated clinically) was correlated with the calculated Rn (P less than 0.05). Rn showed almost no frequency dependence between 24 and 48 Hz as demonstrated by a mean slope of -0.09 +/- 0.08 cm H2O.s2/L for the asthmatic and of -0.08 +/- 0.07 for the non-asthmatic infants. In seven of the asthmatic infants the differences between two Rn determinations at a 45 min interval ranged from -1.7 to 3.8 cm H2O.L-1.s-1 at 24 Hz and from -3.6 to 1.0 at 48 Hz. Changes in Rn did not correlate with changes in total respiratory system resistance (P greater than 0.05). In conclusion, nasal impedance can be approximated from three consecutive measurements through both nostrils and through each nostril separately.     

Static and dynamic upper airway obstruction in sleep apnea: role of the breathing gas properties

Increased upper airway collapsibility in the sleep apnea/hypopnea syndrome (SAHS) is usually interpreted by a collapsible resistor model characterized by a critical pressure (Pcrit) and an upstream resistance (Rup). To investigate the role played by the upstream segment of the upper airway, we tested the hypothesis that breathing different gases would modify Rup but not Pcrit. The study was performed on 10 patients with severe SAHS (apnea-hypopnea index: 59 +/- 14 events/hour) when breathing air and helium-oxygen (He-O2) during non-REM sleep. The continuous positive airway pressure that normalized flow (CPAPopt) was measured. Rup and Pcrit were determined from the linear relationship between maximal inspiratory flow VImax and nasal pressure (PN):VImax = (PN - Pcrit)/Rup. Changing the breathing gas selectively modified the severity of dynamic (CPAPopt, Rup) and static (Pcrit) obstructions. CPAPopt was significantly (p = 0.0013) lower when breathing He-O2 (8.44 +/- 1.66 cm H2O; mean +/- SD) than air (10.18 +/- 2.34 cm H2O). Rup was markedly lower (p = 0.0001) when breathing He-O2 (9.21 +/- 3.93 cm H2O x s/L) than air (15.92 +/- 6.27 cm H2O x s/L). Pcrit was similar (p = 0.039) when breathing He-O2 (4.89 +/- 2.37 cm H2O) and air (4.19 +/- 2.93 cm H2O). The data demonstrate the role played by the upstream segment of the upper airway and suggest that different mechanisms determine static (Pcrit) and dynamic (Rup) upper airway obstructions in SAHS.     

Older individuals have increased oro-nasal breathing during sleep.

Breathing route during sleep has been studied very little, however, it has potential importance in the pathophysiology of sleep disordered breathing. Using overnight polysomnography, with separate nasal and oral thermocouple probes, data were obtained from 41 subjects (snorers and nonsnorers; 25 male and 16 female; aged 20-66 yrs). Awake, upright, inspiratory nasal resistance (Rn) was measured using posterior rhinomanometry. Each 30-s sleep epoch (not affected by apnoeas/hypopnoeas) was scored for presence of nasal and/or oral breathing. Overnight, seven subjects breathed nasally, one subject oro-nasally and the remainder switched between nasal and oro-nasal breathing. Oral-only breathing rarely occurred. Nasal breathing epochs were 55.79 (69.78) per cent of total sleep epochs (%TSE; median (interquartile range)), a value not significantly different to that for oro-nasal (TSE: 44.21 (68.66)%). Oro-nasal breathing was not related to snoring, sleep stage, posture, body mass index, height, weight, Rn (2.19 (1.77) cm H2O x L(-1) x sec(-1)) or sex, but was positively associated with age. Subjects > or = 40 yrs were approximately six times more likely than younger subjects to spend >50% of sleep epochs utilising oro-nasal breathing. Ageing is associated with an increasing occurrence of oro-nasal breathing during sleep.     

The nose and sleep-disordered breathing: what we know and what we do not know

The relationship between sleep-disordered breathing (SDB) and nasal obstruction is unclear. In order to better understand, we performed an extensive computer-assisted review and analysis of the medical literature on this topic. Data were grouped into reports of normal control subjects, patients with isolated nasal obstruction, and those with SDB. We conclude that SDB can both result from and be worsened by nasal obstruction. Nasal breathing increases ventilatory drive and nasal occlusion decreases pharyngeal patency in normal subjects. Nasal congestion from any cause predisposes to SDB. Although increased nasal resistance does not always correlate with symptoms of congestion, nasal congestion typically results in a switch to oronasal breathing that compromises the airway. Moreover, oral breathing in children may lead to the development of facial structural abnormalities associated with SDB. We postulate that the switch to oronasal breathing that occurs with chronic nasal conditions is a final common pathway for SDB.     

Nasal and pharyngeal resistance after topical mucosal vasoconstriction in normal humans

Phenylephrine, an alpha-adrenergic agonist, increases pharyngeal cross-sectional area when applied topically to the nasal and pharyngeal mucosa, as determined by magnetic resonance imaging. In this study, we examined the possibility that the increase in area results from either a decrease in transmural collapsing pressure, as a result of a decrease in upstream (nasal) resistance, or an increase in upper airway muscle activity. In eight normal, awake men we measured inspiratory pharyngeal and nasal resistance and the electrical activity of the genioglossus (EMGGG) and alae nasi (EMG(AN) before and after pharyngeal and nasal + pharyngeal instillation of 1 ml of either 0.25% phenylephrine or normal saline; phenylephrine and saline were tested on separate days. Under control eucapnic conditions, pharyngeal resistance was 0.43 +/- 0.03 cm H2O/L/s, and nasal resistance was 2.43 +/- 0.14 cm H2O/L/s. Pharyngeal resistance was 0.29 +/- 0.03 cm H2O/L/s after nasal + pharyngeal instillation of phenylephrine and 0.98 +/- 0.13 cm H2O/L/s after saline; nasal resistance was 2.18 +/- 0.13 cm H2O/L/s after nasal + pharyngeal instillation of phenylephrine and 3.15 +/- 0.21 cm H2O/L/s after saline. Thus, phenylephrine decreased both nasal and pharyngeal inspiratory resistance. The change in pharyngeal resistance was not dependent on the change in nasal resistance. Eucapnic EMGGG and EMGAN activities did not change after phenylephrine or saline. We conclude that phenylephrine decreased pharyngeal resistance independent of a change in nasal resistance of upper airway muscle activity, and we believe that the changes in resistance we observed reflect a direct effect of phenylephrine on the pharyngeal mucosa and a consequent enlargement of pharyngeal size.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nasal or oral breathing route on upper airway resistance during sleep.

Healthy subjects with normal nasal resistance breathe almost exclusively through the nose during sleep. This study tested the hypothesis that a mechanical advantage might explain this preponderance of nasal over oral breathing during sleep. A randomised, single-blind, crossover design was used to compare upper airway resistance during sleep in the nasal and oral breathing conditions in 12 (seven male) healthy subjects with normal nasal resistance, aged 30+/-4 (mean+/-SEM) yrs, and with a body mass index of 23+/-1 kg x m2. During wakefulness, upper airway resistance was similar between the oral and nasal breathing routes. However, during sleep (supine, stage two) upper airway resistance was much higher while breathing orally (median 12.4 cmH2O x L(-1) x s(-1), range 4.5-40.2) than nasally (5.2 cmH2O x L(-1) x s(-1), 1.7-10.8). In addition, obstructive (but not central) apnoeas and hypopnoeas were profoundly more frequent when breathing orally (apnoea-hypopnoea index 43+/-6) than nasally (1.5+/-0.5). Upper airway resistance during sleep and the propensity to obstructive sleep apnoea are significantly lower while breathing nasally rather than orally. This mechanical advantage may explain the preponderance of nasal breathing during sleep in normal subjects.     

Effect of a Soft Boston Orthosis on pulmonary mechanics in severe cerebral palsy.

Spinal braces such as the Soft Boston Orthosis (SBO) help stabilize scoliosis and improve sitting, positioning, and head control in individuals with cerebral palsy. However, their impact on pulmonary mechanics in this population has not been studied. We examined the effect of a Soft Boston Orthosis on the pulmonary mechanics and gas exchange in 12 children and young adults (5-23 years of age) with severe cerebral palsy. Pulmonary resistance, compliance, tidal volume, minute ventilation, work of breathing, oxygen saturation, and end-tidal CO2 tension were measured with the subjects seated both with and without the orthosis and in the supine position without the orthosis. There were no significant differences in the measured parameters when comparing subjects with and without their orthoses in the sitting or in the supine position. As would be expected in individuals with severe cerebral palsy, pulmonary resistance was increased (7.33 cm H2O/L/s) and compliance was decreased (0.12 L/cm H2O) compared to reported normal values. Work of breathing was greatest in the sitting position without the orthosis (1.2 dynes/cm), suggesting that the improved positioning achieved with the orthosis may decrease the work of breathing. We conclude that the application of a Soft Boston Orthosis does not impact negatively on pulmonary mechanics and gas exchange in young people with severe cerebral palsy.     

Fluid shift by lower body positive pressure increases pharyngeal resistance in healthy subjects

INTRODUCTION: Fluid displacement into nuchal and peripharyngeal soft tissues while recumbent may contribute to narrowing and increased airflow resistance of the pharynx (Rph), and predispose to pharyngeal collapse in patients at risk for obstructive sleep apnea. OBJECTIVES: To determine whether displacement of fluid from the lower body to the neck will increase both neck circumference and Rph in healthy subjects. METHODS: In 11 healthy, nonobese subjects, studied while awake and supine, leg fluid volume, neck circumference, and Rph were measured at baseline. Subjects were then randomized to a control period or to application of lower body positive pressure (LBPP) of 40 mm Hg via antishock trousers to displace fluid from the legs, after which they crossed over to the other arm. Baseline measurements were repeated at 1 and 5 min during the control and LBPP periods. RESULTS: Compared with the control period, application of LBPP caused a significant reduction in leg fluid volume (p < 0.001) and a significant increase in neck circumference (p = 0.004). Rph remained stable during the control period, but increased significantly from baseline after 1 and 5 min of LBPP (from 0.43 +/- 0.10 to 0.60 +/- 0.11 cm H(2)O/L/s, p = 0.034, and to 0.87 +/- 0.19 cm H(2)O/L/s, p < 0.001, compared with baseline, respectively). CONCLUSIONS: Fluid displacement from the legs by LBPP increases neck circumference and Rph in healthy subjects. These findings suggest the hypothesis that fluid displacement to the upper body during recumbency may predispose to pharyngeal obstruction during sleep, especially in fluid overload states, such as heart and renal failure.     

Combined effects of a mechanical nasal dilator and a topical decongestant on nasal airflow resistance.

The goal of this study was to compare the isolated and combined effects of two treatments being used to reduce nasal airflow resistance (NR): an internal nasal mechanical dilator (Nozovent; Prevancure; Sté Pouret, Paris, France) and a topical decongestant, fenoxazoline hydrochloride (Aturgyl; Synthelabo; Le Plessis-Robinson, France). The study was performed in 17 healthy subjects. NR was estimated by active posterior rhinometry at a 0.5 L/s flow under four conditions: in the basal state, with the internal nasal mechanical dilator, after treatment with fenoxazoline hydrochloride, and with both fenoxazoline hydrochloride and the mechanical dilator. The mean NR (+/- SD) decreased from 1.65+/-0.54 cm H2O/L/s in the basal state to 1.02+/-0.27 cm H2O/L/s with the mechanical dilator (p < 0.001), 1.03+/-0.47 cm H2O/L/s with fenoxazoline hydrochloride (p < 0.001), and 0.48+/-0.15 cm H2O/L/s with both the mechanical dilator and fenoxazoline hydrochloride (p < 0.001). The decreases in NR observed after using either the mechanical dilator (deltaNR(N)) or fenoxazoline hydrochloride (deltaNR(A)) were not significantly different. The decrease in NR observed with both (deltaNR(N + A)) was not significantly different from the sum deltaNR(N) + deltaNR(A): 1.16+/-0.53 cm H2O/L/s vs 1.25+/-0.63 cm H2O/L/s, respectively (p > 0.05). deltaNR(N + A) strongly correlated with deltaNR(N) + deltaNR(A): deltaNR(N + A) = 0.80 (deltaNR(N) + deltaNR(A)) + 0.15 (r = 0.96; p < 0.0001). However, the slope of the regression line of deltaNR(N + A) vs deltaNR(N) + deltaNR(A) was significantly lower than unity (p < 0.003). These results demonstrate that, although not totally additive, the effects of using the mechanical dilator and fenoxazoline hydrochloride are cumulative. Further studies that include patients with nasal obstruction would allow us to better evaluate the benefit of a therapy combining both treatments.     

Partitioning of pulmonary responses to inhaled methacholine in subjects with asymptomatic asthma.

To partition the central and peripheral airway resistance, a catheter-tip micromanometer sensing lateral pressure of the airway was wedged into the right lower lobe of a bronchus with a 3 mm inner diameter in 10 patients with asymptomatic asthma. We simultaneously measured mouth flow, transpulmonary pressure (PL) and intra-airway lateral pressure during tidal breathing. Total pulmonary resistance (RL) was calculated from PL and mouth flow, and central airway resistance (RC) was calculated from intra-airway lateral pressure and mouth flow. Peripheral airway resistance (Rp) was obtained by subtraction of RC from RL. Therefore, our measurement of Rp included lung tissue resistance. The technique permitted identification of the site of changes in airway resistance. The baseline values of resistances were 2.3 +/- 0.2 cm H2O/L/s in RL, 1.5 +/- 0.1 cm H2O/L/s in RC, and 0.8 +/- 0.1 cm H2O/L/s in Rp, respectively. To determine the site of airway hyperresponsiveness, dose-response curves of central, peripheral, and total airways to inhaled methacholine were separately constructed. Bronchial responsiveness was evaluated by a log methacholine unit requiring a 35% decrease (PC35) and a 50% decrease (PC50) in pulmonary conductance (a reciprocal of RL). We calculated the increase of resistances in total (delta RL), central (delta RC), and peripheral (delta Rp) airways from the baseline values at either PC35 or PC50.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bedside assessment of respiratory viscoelastic properties in ventilated patients.

Viscoelasticity represents an important component of respiratory mechanics, being responsible, in some cases, for most of the pressure dissipated during breathing. Hitherto the methods available for determining the viscoelastic properties have been simplified, but are still time-demanding and depend on a great deal of calculation. In this study, a simple means of determining respiratory viscoelastic properties during mechanical ventilation was introduced. The viscoelastic constants of the respiratory system, modelled as a Maxwell body, were studied in 17 normal subjects and seven patients with acute lung injury (ALI) using two end-inspiratory occlusions; one with a short inspiratory time (tI) to determine the elastic component of viscoelasticity and the other with a long tI to assess the resistive component of viscoelasticity. The results were reproducible and similar to those provided by the previously described multiple-breath method (MB). The mean+/-SD viscoelastic resistance was 5.31+/-1.50 cm H2O x L(-1) x s with the proposed method and 5.71+/-1.87 cm H2O x L(-1) x s with the MB method in normal subjects, and 8.93+/-2.82 cm H2O x L(-1) x s and 10.36+/-3.13 cm H2O x L(-1), respectively in ALI patients. The mean+/-SD viscoelastic elastance was 3.92+/-0.84 cm H2O x L(-1) and 4.94+/-1.01 cm H2O x L(-1) in normal subjects and 7.08+/-2.01 cm H2O x L(-1) and 8.21+/-1.16 cm H2O x L(-1) in ALI patients, respectively. The mean+/-SD viscoelastic time constant was 1.36+/-0.24 s and 1.17+/-0.34 s in normal subjects and 1.26+/-0.35 s and 1.24+/-0.23 in ALI patients, respectively. The method was easy to perform and applicable at the bedside in clinical routine.     

Abbreviated method for assessing upper airway function in obstructive sleep apnea

STUDY OBJECTIVES: Previous studies have shown that the level of flow through the upper airway in patients with obstructive sleep apnea (OSA) is determined by the critical closing pressure (Pcrit) and the upstream resistance (RN). We developed a standardized protocol for delineating quasisteady-state pressure-flow relationships for the upper airway from which these variables could be derived. In addition, we investigated the effect of body position and sleep stage on these variables by determining Pcrit and RN, and their confidence intervals (CIs), for each condition. DESIGN: Pressure-flow relationships were constructed in the supine and lateral recumbent positions (nonrapid eye movement [NREM] sleep, n = 10) and in the supine position (rapid eye movement [REM] sleep, n = 5). SETTING: University Hospital Antwerp, Belgium. PATIENTS: Ten obese patients (body mass index, 32.0+/-5.6 kg/m(2)) with severe OSA (respiratory disturbance index, 63.0+/-14.6 events/h) were studied. INTERVENTIONS: Pressure-flow relationships were constructed from breaths obtained during a series of step decreases in nasal pressure (34.1+/-6.5 runs over 3.6+/-1.2 h) in NREM sleep and during 7.8+/-2.2 runs over 0.8+/-0.6 h in REM sleep. RESULTS: Maximal inspiratory airflow reached a steady state in the third through fifth breaths following a decrease in nasal pressure. Analysis of pressure-flow relationships derived from these breaths showed that Pcrit fell from 1.8 (95% CI, -0.1 to 2.7) cm H(2)O in the supine position to -1.1 cm H(2)O (95% CI, -1.8 to 0.4 cm H(2)O; p = 0.009) in the lateral recumbent position, whereas RN did not change significantly. In contrast, no significant effect of sleep stage was found on either Pcrit or RN. CONCLUSIONS: Our methods for delineating upper airway pressure-flow relationships during sleep allow for multiple determinations of Pcrit within a single night from which small yet significant differences can be discerned between study conditions.     

Weber's law and resistive load detection

The threshold of detection for added resistive loads to breathing (delta R50) was measured in 4 normal subjects at 4 different background resistances (Ro). Under normal conditions (Ro = 2.26 +/- 0.16 (SEM) cm H2O/L/s), the mean delta R50 was 0.53 +/- 0.17 cm H2O/L/s and the Weber fraction (delta R50/Ro) was 0.24 +/- 0.07. When the background resistance was increased, the threshold of detection increased proportionately, so that the Weber fraction did not change significantly. The background resistance was also decreased by having the subject breathe heliox. Although this did not result in a change in delta R50 (0.68 +/- 0.1 cm H2O/L/s), the Weber fraction increased to 0.49 +/- 0.08. These results show that although the Weber fraction is relatively constant over a wide range of background resistances, it rises sharply at low levels of background resistance, a finding that is similar to other sensory modalities.     

Effects of added resistance to breathing during exercise in obstructive lung disease

Forty-nine men performed progressive submaximal treadmill exercise to determine the cardiopulmonary and subjective response to added resistance to breathing. Twenty subjects (controls), FEV1/FVC% = 79.2 +/- 1.4 (mean +/- SEM), were compared with 19 mildly obstructed men (OB1), FEV1/FVC% = 66.9 +/- 0.5, and 10 with moderate obstruction (OB2), FEV1/FVC% = 53.7 +/- 1.9. Separate exercise trials were performed with no added resistance (NAR), R1 = 3.5 cm H2O/L/s inspiratory and 1.5 cm H2O/L/s expiratory resistance, and R2 = 5 cm HKO/L/s inspiratory and 1.5 cm H2O/L/s expiratory resistance. Analysis of cardiopulmonary parameters was made at an oxygen consumption rate of VO2 = 1.5 L/min for all 3 obstruction groups at all 3 resistances. With NAR, all 3 groups had similar respiratory rate (RR), tidal volume (VT), minute ventilation (VE), end-tidal PCO2 (PETCO2), respiratory exchange ratio (R), heart rate (HR), and mouth pressure swing (Poral). With both R1 and R2 compared with NAR, control and OB1 subjects (at VO2 = 1.5 L/min) had reduced RR, VE, and R, and increased VT and Poral (p less than 0.01 for all). Changes with added resistance for OB2 subjects were in the same directions, but were significant only for VE and with R1 for RR. Heart rate did not change; PETCO2 increased in control subjects and with R2 in OB1 subjects. Separate analysis showed that except for the smaller increase in PETCO2 in OB2 subjects, none of the changes with added resistance in the OB1 or OB2 groups were different from changes in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nasal airflow dynamics: mechanisms and responses associated with an external nasal dilator strip.

The adhesive external nasal dilator strip (ENDS) is widely advocated for prevention of snoring and promotion of nasal breathing during exercise. In the present study, the effects of the ENDS on nasal airflow resistance (Rn) in normal subjects were examined and factors determining individual responses to the ENDS explored. Using posterior rhinomanometry, 20 healthy Caucasian adults (10 males, 10 females; age: 18-56 yrs) were studied during quiet tidal breathing and voluntary hyperpnoea with (ENDS) and without (control) ENDS and with a placebo strip (placebo) before and after application of a topical nasal decongestant (oxymetazoline hydrochloride). During tidal breathing, only nine subjects showed a significantly (p<0.05) decreased inspiratory and/or expiratory Rn with the ENDS ("responders"). During the control, inspiratory Rn (at 0.4 L x s(-1)) was higher in "responders" than "nonresponders" (3.28+/-0.16 versus 2.60+/-0.08 cmH2O x L(-1) x s; p=0.04). The effects of nasal decongestant and the ENDS were additive. During voluntary hyperpnoea, inspiratory Rn (at 1.0 L x s(-1)) and the hysteresis of the inspiratory transnasal pressure/flow curve were decreased with the ENDS in most subjects. It is concluded that the external nasal dilator strip influences nasal airflow dynamics by both dilation of the nasal valve and stabilization of the lateral nasal vestibule walls and may be more effective in subjects with a high resting nasal airflow resistance.