This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator.In a randomised double-blind crossover study, 23 patients with COPD (mean¡SEM forced expiratory volume in one second 42¡3% of the predicted value) inhaled salmeterol 50 mg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate.After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175¡52%, inspiratory capacity (IC) increased by 11¡2% pred and functional residual capacity decreased by 11¡3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (V9O 2 ) and carbon dioxide output. Salmeterol increased peak exercise endurance, V9O 2 and ventilation by 58¡19, 8¡3 and 12¡3%, respectively. Improvements in peak V9O 2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT.Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance. Several recent studies have shown that improvements in exertional dyspnoea following bronchodilator therapy in chronic obstructive pulmonary disease (COPD) correlate well with reductions in lung hyperinflation, as indicated by increases in inspiratory capacity (IC) [1][2][3][4][5]. However, the relationship between bronchodilator-induced increases in IC and improvements in symptoms and exercise performance is complex and poorly understood. Given the multifactorial nature of dyspnoea and exercise limitation in COPD, it remains unclear why small increases in resting IC (in the order of 0.3 L) appear to be clinically important. The current study extends previous studies conducted in the present authors9 laboratory using ipratropium bromide by, in addition, examining the effect of a bronchodilator (salmeterol) on plethysmographic lung volume components at rest and on breathing pattern and ventilatory capacity during exercise. Moreover, the study was designed to advance understanding of the mechanisms of bronchodilatorinduced dyspnoea relief, especially the role of reduced mechanical restriction.It has previously been shown that acute-on-chronic hyperinflation during exercise severely constrains tidal volume (VT) expansion, and that this dynamic mechanical restriction makes ...

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?m 2 . 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 In a recent publication the authors described, for the first time, partitioning of inhaled ventilation between the nose and mouth during sleep in healthy subjects with normal nasal resistance [1]. The main finding of the latter study was that the oral fraction of inhaled ventilation during sleep was very small, averaging only 4% for the group of 10 subjects, and several subjects did not breathe through their mouth at all during sleep. Furthermore, the inhaled oral fraction did not change significantly between different non-rapid eye movement sleep stages or between rapid eye movement (REM) and non-REM sleep.The physiological explanation for the marked predominance of nasal ventilation over oral ventilation during sleep in normal subjects is unknown. Since total airway resistance while awake and breathing through the mouth is typically 2-4 cmH 2 O?L -1 ?s -1 [2] and the normal nasal resistance alone is of similar magnitude [3], it is not intuitively obvious why healthy subjects should choose to breathe almost exclusively through the nasal route during sleep. Specifically, there are no published measurements describing the effect of oral versus nasal breathing on upper airway resistance during sleep.It is important to understand the influence of the breathing route (oral or nasal) on upper airway resistance during sleep from the perspective of understanding normal respiratory physiology during sleep, but this information may also provide an insight into the relationship between the breathing route and upper airway obstruction during sleep. The authors hypothesised that the observed preponderance of nasal over oral ventilation in normal subjects during sleep would reflect a mechanical advantage of the nasal breathing route. To test this hypothesis, the authors compared upper airway resistance during nasal breathing and during oral breathing in healthy sleeping subjects with normal nasal resistance. Methods Study designA randomised, single blind, crossover study was conducted to compare upper airway resistance during sleep when nose breathing with that when mouth breathing. Subjects underwent a single overnight polysomnogram at Kingston General Hospital Sleep Laboratory, Ontario. The night was divided into two parts, oral breathing and nasal breathing, the order being randomised...

No abstract

The effect of posture on upper airway dimensions was assessed for two reasons. First, some patients with untreated sleep apnea/hypopnea syndrome (SAHS) report they sleep better sitting upright. Second, to allow comparison of the differing techniques used to determine the site of maximal airway narrowing in awake patients with SAHS, as some are carried out in the erect and others in the supine posture. Lateral cephalometry was therefore carried out in 33 nonsnoring normal subjects and in 29 patients with obstructive SAHS (mean apneas plus hypopneas, 46 per hour; range, 17 to 103). In both normal subjects and patients, uvular width was increased (p less than 0.05) in the supine posture, and this was associated with significant narrowing of the retropalatal airway in the patients with SAHS (erect, 5.0 +/- SD 2.6 mm; supine, 3.6 +/- 2.8 mm; p less than 0.01). In both normal subjects and patients, the retroglossal hypopharynx widened (p less than 0.05) in the supine posture (e.g., in patients with SAHS, posterior airway space was: erect, 11.5 +/- 4.5 mm; supine, 13.4 +/- 4.8 mm; p = 0.003). In the supine posture there was anterior movement of the hyoid and neck flexion in both groups. However, a study of the effect of neck flexion in the erect posture showed that neck flexion produced no changes in airway caliber. Thus, posture is an important determinant of upper airway dimensions.

No abstract

No abstract

An association between mouth breathing during sleep and increased propensity for upper airway collapse is well documented, but the effect of treatment for nasal obstruction on mouth breathing during sleep and simultaneous obstructive sleep apnoea (OSA) severity has not been described previously.A randomised single blind placebo-and sham-controlled crossover study of treatment (topical decongestant and external dilator strip) for nasal obstruction was carried out in 10 patients (nine males; mean¡SEM 46¡5 yrs) with nasal obstruction and OSA. All patients had normal acoustic pharyngometry. The effect of treatment on nasal resistance, mouth breathing during sleep and OSA severity was quantified.Treatment of nasal obstruction was associated with a dramatic and sustained reduction in nasal resistance and the oral fraction of ventilation during sleep (mean (95% confidence interval) absolute reduction in oral fraction 30% (12-49)). Improvements in sleep architecture were observed during active treatment, and there was a modest reduction in OSA severity (change in apnoea-hypopnoea index 12 (3-22)).In conclusion, treating nasal obstruction reduced mouth breathing during sleep and obstructive sleep apnoea severity, but did not effectively alleviate obstructive sleep apnoea.

The Canadian Thoracic Society (CTS) published an executive summary of guidelines for the diagnosis and treatment of sleep disordered breathing in 2006⁄2007. These guidelines were developed during several meetings by a group of experts with evidence grading based on committee consensus. These guidelines were well received and the majority of the recommendations remain unchanged. The CTS embarked on a more rigorous process for the 2011 guideline update, and addressed eight areas that were believed to be controversial or in which new data emerged. The CTS Sleep Disordered Breathing Committee posed specific questions for each area. The recommendations regarding maximum assessment wait times, portable monitoring, treatment of asymptomatic adult obstructive sleep apnea patients, treatment with conventional continuous positive airway pressure compared with automatic continuous positive airway pressure, and treatment of central sleep apnea syndrome in heart failure patients replace the recommendations in the 2006⁄2007 guidelines. The recommendations on bariatric surgery, complex sleep apnea and optimum positive airway pressure technologies are new topics, which were not covered in the 2006⁄2007 guidelines.