Inspiratory effort sensation to added resistive loading in patients with obstructive sleep apnea.

STUDY OBJECTIVES: Repeated episodes of upper-airway occlusion are the main characteristics of patients with obstructive sleep apnea (OSA) during sleep. It has been reported that an impairment in the sensation of detection and a depression of ventilatory compensation to added load could be observed in such patients. In this study, we examined patients with OSA to evaluate the inspiratory effort sensation (IES), ventilation, and mouth occlusion pressures during added resistive loading while awake and to determine whether they can be reversed by nasal continuous positive airway pressure (CPAP) treatment. DESIGN: A hospital-based case-control study. SETTING: A sleep laboratory of a medical unit in Japan. SUBJECTS: Seventeen patients with moderate to severe OSA and 10 control subjects were included in this study. MEASUREMENTS: All patients with OSA had undergone standard nocturnal polysomnography. Patients with OSA and control subjects were evaluated for IES measured by a modified Borg score, ventilation, and mouth occlusion pressure during control and inspiratory resistive loaded breathing. These tests were repeated in all patients with OSA after 2 weeks of nasal CPAP treatment. RESULTS: IES to inspiratory resistive loading was lower in patients with OSA than in control subjects. There were no differences in ventilation and mouth occlusion pressure between patients and control subjects during loaded breathing. After 2 weeks of nasal CPAP, the decreased IES was increased in patients with OSA. CONCLUSION: In patients with OSA, the decreased IES to inspiratory resistive loaded breathing is reversible with nasal CPAP. This could be one additional benefit of nasal CPAP in the treatment of OSA.

Oxygen consumption of respiratory muscles in patients with COPD.

We measured the oxygen consumption (VO2) of respiratory muscles in 8 COPD patients and 12 age-matched healthy subjects using a closed circuit device which allows a continuous increase in external dead space and is equipped with a 9-L Collins spirometer. Furthermore, we measured simultaneously mouth occlusion pressure at 0.1 s of inspiration (P0.1), minute ventilation (VE), and other ventilatory parameters during the measurement of total VO2 (VO2 tot). We found that the logarithm of VO2tot (logVO2tot) had a good correlation with VE in both groups. The mean slope of the regression line of logVO2tot and VE (delta logVO2tot/delta VE) of COPD patients was significantly higher than that of normal subjects (p < 0.001). However, the mean Y-intercept (metabolic VO2[VO2met]) of the regression lines did not differ between the two groups. The P0.1 in COPD patients was higher than that in normal subjects at the corresponding dead space loading. However, the VE did not differ between the two groups except for at rest and the first 1 min after dead space loading. These results suggest that the VO2 of respiratory muscles in patients with COPD is higher at given ventilation compared with that in age-matched normal subjects and that this increased VO2 partly may be due to an augmented ventilatory drive.

Decrease in functional residual capacity during inspiratory loading and the sensation of dyspnea.

The purposes of the present study were to determine the changes in functional residual capacity (FRC) during inspiratory loading and to examine their mechanisms. We studied seven normal subjects seated in a body plethysmograph. In both graded inspiratory elastic (35, 48, and 68 cmH2O/l) and resistive (21, 86, and 192 cmH2O.l-1.s) loading, FRC invariably decreased from control FRC and phasic expiratory activity increased. The reduction in FRC was greater with greater loads. A single inspiratory effort against an inspiratory occlusion at three different target mouth pressures (-25, -50, and -75 cmH2O) and durations (1, 2, and 5 s) also resulted in a decrease in FRC with an increase in expiratory electromyogram activity in the following expiration. The decrease in FRC was greater with greater target pressure and duration. This decrease in FRC is qualitatively similar to that during inspiratory loaded breathing, and we suspect that the same mechanisms are at work. Because neither vagal nor chemoreceptor reflex can account for these responses, we suspect conscious awareness of breathing or behavioral control to be responsible. In an additional study, the sensation of discomfort of breathing during elastic loading decreased with a decrease in FRC. These results suggest that the reduced FRC may be due to behavioral control of breathing to reduce the sensation of dyspnea during inspiratory loading.

The maximum expiratory flow rate and volume dependent respiratory resistance in small airway obstruction.

In 8 healthy subjects (group A) and 4 subjects with respiratory symptoms (group B), the lung pressure-volume curve (P-V curve), maximum expiratory flow-volume curve (MEFVC) and respiratory resistance (Rrs) at all vital capacities were measured. To avoid laryngeal artifact on a mouth pressure, an intratracheal catheter was used for measurement of Rrs which was obtained with 3 cycles/sec oscillatory forced pressure. Group B did not show a different elastic recoil from group A. In comparison of the maximum expiratory flow (Vmax) at 80, 70, 60 and 50% of the total lung capacity (TLC). Vmax of group B showed lower values than that of group A. Rrs was almost the same in both groups from 70% TLC upwards, but Rrs of group B was higher than that of group A from 65%TLC downwards. Since the lung elastic recoil pressures (Pst (1)) in the two groups were not different and Rrs's were different significantly only at low lung volumes, the decrease in Vmax of group B was supposed to be due to the increased Rrs which might reflect small airway obstruction.

Submental stimulation and supraglottic resistance during mouth breathing.

We studied submental stimulation on supraglottic resistance (Rsg) in 5 normals and 6 patients with obstructive sleep apnea. We then examined the most effective sites of stimulation in the submental regions, and the relationships between Rsg and stimulation frequency and voltage in the supine position. Inspiratory and expiratory Rsg's were obtained as the slope of the linear portion of the pressure-flow relation determined at zero flow. Before stimulation, inspiratory and expiratory Rsg's were 0.76 +/- 0.06 (means +/- SE) and 0.61 +/- 0.02 cmH2O.L-1.sec, respectively, in normals, and 1.04 +/- 0.20 and 0.92 +/- 0.29 cmH2O.L-1.sec, respectively, in patients. Stimulation in the proximal half submental region with surface electrodes 1 cm apart decreased inspiratory and expiratory Rsg's in patients, and inspiratory Rsg in normals. Inspiratory Rsg measured in this submental region showed a stimulation frequency-and voltage-dependency in both groups, but expiratory Rsg did not. These findings suggest that submental stimulation in the proximal half region widens the supraglottic airway during mouth breathing and probably involves the upper airway muscles.

[Relationship between apneic episodes and destruction of temporomandibular joints in patients with rheumatoid arthritis].

There have been only a few investigational reports of sleep apnea syndrome (SAS) in patients with rheumatoid arthritis (RA), although it may not be a rare condition and may be life-threatening occasionally. The factor precipitating SAS in such patients is thought to be destruction of the temporomandibular joints (TMJs) from RA processes. To assess the relationship of the degree of destruction of the TMJs to the frequency of apnea, we examined them in 10 RA patients who complained of snoring. Those patients were classified as classical RA according to the criteria of American Rheumatism Association. They consisted of 3 males and 7 females with a mean age of 57.8 + 11.0 years and a mean disease duration of 15.9 +/- 9.4 years. In order to numerically evaluate the degree of destruction of the mandibular rami, we quoted a method from the literature (Redlund-Johnell I, Scand J Rheumatol 16:355, 1987) and measured the vertical distance (= ramal height) from the mandibular angle to the palato-occipital line on the lateral view film of the cervical spine in each patient. The mean values of ramal height (RH) of the normal material (we studied in Japanese) are 46.0 mm in males and 38.3 mm in females. There were 8 cases of SAS out of the 10 RA patients studied. Their mean total apneic episode (TAE) was 289.9 mm with a range of 0-611. The mean ratio (%) of RH to mean value of the normal material (%RH) was 68.8 +/- 22.2% for all. There was a significant statistic correlation between TAE and %RH (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of CO2 responsiveness and breathing efficiency in determining exercise capacity of patients with chronic airway obstruction.

We examined the role of CO2 responsiveness and breathing efficiency in limiting exercise capacity in 15 patients with chronic airway obstruction (FEV1 = 0.88 +/- 0.25 L, mean +/- SD). Responses of minute ventilation and P0.1 (mouth pressure 0.1 s after the onset of occluded inspiration) to hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) were measured by rebreathing, and the ratio of the two (delta VE/delta P0.1) was defined as an index of breathing efficiency during hyperventilation. Exercise capacity was measured as symptom-limited, maximal oxygen consumption (VO2max/BW) in an incremental treadmill test and also as the 12-min walking distance (TMD). All patients discontinued the treadmill test because of dyspnea, and the exercise capacity correlated with the degree of airway obstruction, although there was a wide variability among patients with comparable FEV1. There were no significant correlations between the responses to CO2 and exercise capacity. However, there was a significant correlation between delta VE/delta P0.1 and VO2max/BW (r = 0.87, p less than 0.001) or TMD (r = 0.78, p less than 0.001), and these correlations remained significant even when the relational effects of FEV1 were taken out. These results support the hypothesis that airway obstruction and breathing efficiency are important, but that CO2 responsiveness is not a major factor in determining the exercise capacity of patients with chronic airway obstruction.

[New methods for measurement of peripheral airway resistance].

We have developed two new methods to evaluate the peripheral resistance of the lung. The first is a method for continuous measurement of the frequency dependence of dynamic compliance (Cdyn, f.d.) and pulmonary resistance (RL) from a single-breath cycle by Fourier-series analysis. In this method, we have found that procaterol my first dilate the central airway and then gradually dilate the peripheral airway in bronchial asthma. The second is a method for the direct measurement of peripheral resistance by the anterograde catheter system using a catheter tip micromanometer. The catheter tip was inserted into the 3 mm diameter small airway anterogradely and intrabronchial pressure was measured simultaneously with transpulmonary pressure and mouth flow. We have found that the values of peripheral resistance in patients with COPD are four to seven times higher than that of normal subjects. These results suggest that the behavior of the peripheral and central airway may differ between patients and that the peripheral airway may be important to examine the pathogenesis of COPD.

Respiratory muscle strength and gas exchange in neuromuscular diseases: comparison with chronic pulmonary emphysema and idiopathic pulmonary fibrosis.

To examine whether or not the respiratory muscle weakness is correlated with decrease in arterial oxygen tension (PaO2), respiratory muscle and pulmonary functions in 14 patients with neuromuscular diseases (NMD) were studied and compared with those of 12 patients with chronic pulmonary emphysema (CPE) and 15 patients with idiopathic pulmonary fibrosis (IPF). Respiratory muscle strength was assessed by maximal static inspiratory and expiratory mouth pressure at three lung volumes (RV, FRC and TLC). Although mean pulmonary functions in NMD showed virtually normal function, respiratory muscle strength was significantly less than the corresponding values in CPE and IPF. In NMD, maximal inspiratory mouth pressure at RV level (PImax) correlated positively with %TLC and %VC (r = 0.652 and r = 0.536, respectively). Moreover, PImax was significantly correlated with PaO2 (r = 0.561), but not with PaCO2. Maximal expiratory mouth pressure at TLC (PEmax) correlated positively with %TLC and %VC. In CPE and IPF, respiratory muscle strength had no correlation with PaO2 and PaCO2. These findings suggest that inspiratory muscle dysfunction in NMD may be one of the factors responsible for determination of the level of hypoxemia and lung volume.

Effects of posture on carbon dioxide responsiveness in patients with obstructive sleep apnoea.

BACKGROUND: It is well known that upper airway resistance increases with postural change from a sitting to supine position in patients with obstructive sleep apnoea (OSA). It is not known, however, how the postural change affects the ventilatory and occlusion pressure response to hypercapnia in patients with OSA when awake. METHODS: The responses of minute ventilation (VE) and mouth pressure 0.1 seconds after the onset of occluded inspiration (P0.1) to progressive hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) both in sitting and supine positions were measured in 20 patients with OSA. The ratio of the two (delta VE/delta P0.1) was obtained as an index of breathing efficiency. The postural changes in response to carbon dioxide (CO2) after uvulopalatopharyngoplasty (UPPP) were also compared in seven patients with OSA. RESULTS: There were no significant changes in the resting values of end tidal PCO2, P0.1, or VE between the two positions. During CO2 rebreathing, delta VE/delta PCO2 did not differ between the two positions, but delta P0.1/delta PCO2 was significantly higher in the supine than in the sitting position (supine, mean 0.67 (SE 0.09) cm H2O/mm Hg; sitting, mean 0.57 (SE 0.08) cm H2O/mm Hg), and delta VE/delta P0.1 decreased significantly from the sitting to the supine position (sitting, 4.6 (0.4) l/min/cm H2O; supine, 3.9 (0.4) l/min/cm H2O). In seven patients with OSA who underwent UPPP, delta VE/delta P0.1 improved significantly in the supine position and postural change in delta VE/delta P0.1 was eliminated. CONCLUSIONS: These results suggest that in patients with OSA the inspiratory drive in the supine position increases to maintain the same level of ventilation as in the sitting position, and that the postural change from sitting to supine reduces breathing efficiency. Load compensation mechanisms of patients with OSA appear to be intact while awake in response to the rise in upper airway resistance.

Noninvasive method for detecting laryngeal narrowing with low-frequency sound.

We measured laryngeal narrowing with low-frequency sound in human subjects. A low-frequency sound of 800 Hz was forced into the mouth, and sound-pressure amplitude above (SPAa) and below the vocal cord (SPAb) was detected using two separate microphones at the anterior neck. If the subject voluntarily narrowed the larynx at functional residual capacity, the increased respiratory resistance (Rrs) was only caused by increased laryngeal resistance, and SPAa was increased and SPAb was decreased. The percent changes of SPAa (SPAa%) minus that SPAb (SPAb%) from the initial values (SPAa% - SPAb% = Y) was proportional to the increase of Rrs from the initial control state (X, cmH2O X 1-1 X s); Y = 22.4 X1.20 (coef of correlation, r = 0.96, P less than 0.01). We confirmed similar proportions in dogs by manually narrowing the vocal cord. When laryngeal resistance was directly measured by tracheal puncture with a needle, the proportions between Y and X were not significantly dependent on the increase of Rrs below the vocal cord induced by methacholine inhalation in human subjects and histamine injection in dogs. We concluded that the increase of laryngeal resistance from the initial state could be detected noninvasively by using low-frequency sound.