Increasing the Functional Residual Capacity May Reverse Obstructive Sleep Apnea

Transcription

1 Sleep 11(4): , Raven Press, Ltd., New York 1988 Association of Professional Sleep Societies ncreasing the Functional Residual Capacity May Reverse Obstructive Sleep Apnea F. Series, Y. Cormier, N. Lampron, and J. La Forge Centre de Pneumologie, H6pital Laval, Sainte-Foy, Quebec, Canada Summary: We describe the reversal of obstructive sleep apnea with a 0.5 L increase in the functional residual capacity (FRC) in a patient with sleep apnea syndrome. The patient had been treated with medroxyprogesterone acetate for 8 months. The increase in FRC was obtained by applying a constant negative extrathoracic pressure (NEP) with a poncho-type respirator. With pulmonary inflation, there was a dramatic decrease in the apnea index and the percent apnea time, and an improvement in sleep architecture. At all sleep stages, the desaturation duration was shorter with NEP. The exact mechanisms by which pulmonary expansion improved sleep apnea in this patient remain unclear; lung volume dependence of upper airway patency and the improvements in apneainduced de saturation may be contributing factors. Our observation illustrates that lung volumes may be an important factor in the pathophysiology of obstructive sleep apnea, especially in the apnea onset and in the apneic-induced desaturation. Key Words: Obstructive sleep apnea-functional residual capacity-negative extrathoracic pressure-lung volumes. Lung volume may play an important role in the pathophysiology of sleep apnea; it is involved in the degree of hemoglobin de saturation and in apnea frequency (1). The pharyngeal cross-sectional area is lung-volume dependent (2). The pharynx of patients with obstructive sleep apnea (OSA) is smaller than that of control subjects at all lung ~ volumes and decreases more abruptly between functional residual capacity (FRC) and residual volume (RV) (3). The efficacy of continuous positive airway pressure (CPAP) in the treatment of OSA results mostly from a splinting of the pharynx by the positive pressure, but an upper airway opening secondary to pulmonary expansion could also be a contributing factor. We report the case of a patient with OSA in whom a 500-ml pulmonary inflation resulted in a dramatic reduction in the number of obstructive.. apneic events. CASE REPORT A 57-year-old man was referred for the evaluation of severe daytime hypersomnolence increasing over the last 3 years. He was an habitual loud snorer. He had stopped Accepted for publication December Address correspondence and reprint requests to Dr. Y. Cormier, Centre de Pneumologie, Hopital Laval, 2725, chemin Ste-Foy, Ste-Foy, Quebec, Canada 01V

2 350 F. SERES ET AL. smoking 2 years ago, took no medication, and had minimal alcohol consumption. Physical examination revealed marked obesity 043 kg, in cm), smau oropharynx with a.j large uvula, and tonsil and tongue hypertrophy. Pulmonary function tests showed mild airflow obstruction (FEV} = 2.51 L, = 90% of predicted, FEV1FVC = 71%); there was no evidence of extrathoracic airway obstruction on the flow-volume loop. Arterial gas analysis identified a hypoxemia (52 mm Hg) with hypercapnia (47 mm Hg) (sitting position). His ventilatory response to CO 2 (closed circuit) was 0.5 Llminlmm Hg CO 2 ; thyroid function tests were normal. The diagnosis of OSA was confirmed by a polysomnographic study that included determination of sleep stages, measurement of oxygen saturation with a Biox- ear oximeter, nasal and mouth flows by thermocouples, end-expiratory lung volumes and thoracoabdominal movements with an inductance vest (calibrated with the least squares method), and esophageal pressures. Sleep stage scoring and respiratory patterns were defined by standard criteria (4). Results of the initial sleep study are reported in Table 1. Mter the first sleep study, medroxyprogesterone acetate (MPA) was started at 20 mg four times daily. On this medication the patient noted significant clinical improvement, including a 25-kg weight loss and a marked reduction in his daytime hypersomnolence. A second sleep study was performed 8 months later while on progesterone (MPA study, Table 1). This second study showed no improvement in sleeprelated breathing abnormalities. Without changing therapy, two additional polysomnographic studies were done on consecutive nights with the subject sleeping in a ponchotype respirator (Emerson) one night with, and one without, pulmonary inflation. The lung inflation was obtained by applying a constant negative extrathoracic pressure (NEP) into the poncho. The poncho was sealed at the hips, the arms, and the base of the neck, just above the sternal fork. The level of subatmospheric pressure that increased FRC by 0.5 L was determined in the awake supine position using a closedcircuit Collins spirometer; a negative pressure of - 7 cm H 2 0 was needed. Results of TABLE 1. Comparative data of the initial diagnostic sleep study, the follow-up study, or MPA study (8 months therapy with medroxyprogesterone acetate), the control (in the poncho without pressure applied), and the negative extra thoracic pressure (NEP) polysomnographic studies Diagnostic MPA Control NEP study study study study Treatment None MPA 80 mgday MPA 80 mgday MPA 80 mgday Sleep period time (h) Total sleep time (h) Stage - (% TST) 84% 85% 91% 74% Stage -V (% TST) 0% 0% 5% 14% Stage REM (% TST) 16% 15% 4% 12% Apnea index Apnea-hypopneaindex Percent apnea time Mean apnea duration (s) Time in obstructive apnea! total apnea time 99.2% Time in mixed apnea! 99.0% 99.1% 100% total apnea time Time in central apnea! 0.8% 1.0% 0.9% 0% total apnea time 0% 0% 0% 0% TST, total sleep time. Sleep, Vol. 11, No.4, 1988

3 FUNCTONAL RESDUAL CAPACTY 351 the control and NEP night studies are reported in Table 1, while the cumulative distribution of time spent under each Sa0 2 value during the two nights is shown in Fig. 1. NEP night resulted in a reduction in stage and sleep and an increase in stage and V. Apnea index, apnea-hypopnea indexes (number of these respiratory abnormalities per hour of sleep), and percent apnea time (total duration of apnea divided by sleep time) were reduced, while the mean apnea duration increased from 19 to 36 s. During NEP night, the increase in sleep time spent in REM sleep compared to the control study was responsible for the apparent worsening of the cumulative distribution of total sleep time (TST) at Sa02 values less than 82% (Fig. 1), the most severe events occurring in stage REM. Comparing the percentage of REM spent under each Sa02 value, less time was spent under each de saturation level during the NEP night than during the control night. n other words, for a similar REM sleep duration, the Sa02 fall was deeper on the control night. Similar results were obtained considering only non REM sleep. DSCUSSON Pulmonary inflation was accompanied by a significant reduction in the total number of sleep-disordered breathing events with a dramatic improvement of the apnea index, which fell to within the normal range. When NREM and REM sleep stages were taken separately, less time was spent under each de saturation value when the negative extrathoracic pressure was applied. %TST Control night NEP night "",;'!l ~--~----~~~~~r---,---~----~--~--sa02% ~60 ~65 ~70 ~75 ~80 ~85 ~90 ~95 ~100 FG. 1. Cumulative distribution of total sleep time (TST) spent under each saturation (Sa0 2 ) value for the control and NEP nights. Sleep, Vol. 11, No.4, 1988

4 352 F. SERES ET AL. The first three night studies (diagnostic study, MPA study, and control study) were very similar in the sleep architecture and the characteristics of the apneic events (Tabie 1). t is unlikely, therefore, that the reduction in the apnea index and percent apnea time seen with NEP occurred spontaneously. We believe that our data could be explained by two mechanisms: (a) a volume dependence of upper airway dilatation, and (b) an improvement in the end-apnea Sa0 2. These two mechanisms could be involved separately or acting in concert. Supine position is known to reduce lung volume (5), especially in obese subjects. Using the helium dilution method, FRC in our patient was reduced by 370 cc by the supine position. The reduction or loss of muscle tone that accompanies sleep will increase thoracic compliance and may contribute to a further reduction of end-expiratory lung volumes (6), since lung compliance is not modified during sleep (7). By applying a constant negative extrathoracic pressure during sleep, the actual pulmonary inflation could have been greater than the 500 cc calculated awake. Since the end-expiratory lung volume monitoring with an inductance vest in the DC mode cannot be used for a long time and is not accurate in positions different from the calibration one, we could not determine the exact value of pulmonary expansion during sleep. We believe, therefore, that the FRC during NEP night must have been kept at a value at least as high as that in the awake, upright state. The cross-sectional pharyngeal area is highly lung-volume dependent in the awake state (2), but this dependence has not been studied during sleep. t is reasonable to assume that any change in FRC during sleep would similarly influence this area. We hypothesize that this increase in FRC by NEP sufficiently opened the pharyngeal area to prevent its collapse during sleep, therefore decreasing the number of obstructive apneas and hypopneas. Similar results were reported with end-expiratory positive airway pressure (EPAP) of 10 cm H 2 0 (8). EPAP increases lung volumes as well as expiratory pressure. Since upper airway expiratory resistances have been found to decrease during the two last breaths before an apnea (9), these results could be attributed to the maintenance of a positive expiratory pressure andor to pulmonary inflation. NEP did not directly modify upper airway pressures like CPAP or EPAP; therefore, it seems that thoracopulmonary expansion can reverse OSA by itself. A second possible explanation for the reduction of apnea events by NEP is the improvement in Sa0 2 Lung volumes seem to have an important role in the de saturation process during an apnea or hypopnea event: the higher the FRC, the less the Sa0 2 fall (10,.11). This could be related to airway closure occurring at low lung volumes, resulting in V AlQ mismatch or shunting, and to the role of lung volume in the oxygen stores (10). A similar reduction in apnea events is seen with oxygen therapy. ndeed, during acute hyperoxia, some patients show a significant decrease in apnea frequency (12). The exact mechanisms by which improvement in Sa0 2 reduces sleep-disordered breathing are not clear. f central, mixed, and obstructive apneas are different manifestations of a single mechanism, apneas may be the result of a sleep-induced instability of the respiratory control system. The postapneic rebound hypocapnea is believed to decrease diaphragmatic and upper airway stimulation, leading to obstructive apnea. As with oxygen, the reduced degree of hypoxemia under NEP could improve the control system stability: a reduced hypoxic-hypercapnic ventilatory drive leading to less hyperventilation and subsequently less reduction in the carbon dioxide tension. This would he accompanied by less depressed diaphragmatic and upper airway stimulation. Lung volume dependence of upper airway patency and respiratory control stability J Sleep, Vol. ]], No.4, 1988

5 FUNCTONAL RESDUAL CAPACTY 353 may be involved separately or together. Whatever the mechanisms, it appears that lung volume was a determinant factor in apnea frequency and apnea-induced de saturation in our subject. Acknowledgment: This work was supported by La Fondation J. D. Begin de l'universite Laval. REFERENCES 1. bnal E, Leech TA, Lopata M. Relationship between pulmonary function and sleep-induced respiratory abnormalities. Chest 1985;8714: Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal cross-sectional areajn patients with obstructive sleep apnea. Am Rev Respir Dis 1984;130: Brown, Taylor R, Hoffstein V. Obstructive sleep apnea reversed by increased lung volume? Eur J Respir Dis 1986;68: Martin RJ (Chairman). ndications and standards for cardiopulmonary sleep studies. Sleep 1985;8: Agostini E, Mead J. Respiration. n: Fenn WO, Rahn H, eds. Handbook of physiology. Washington, D.C.: American Physiological Society, 1964: Hudgel DW, Devadatta P. Decrease in functional residual capacity during sleep in normal humans. J Appl Physiol 1984;57: Hudgel DW, Martin RT, Johnson B, Hill P. Mechanics of the respiratory system and breathing pattern during sleep in normal humans. J Appl Physio1984;56: Mahadevia AK, bnal E, Lopata M. Effects of expiratory positive airway pressure on sleep induced respiratory abnormalities in patients with hypersomnia-sleep apnea syndrome. Am Rev Respir Dis 1983; 128: Sanders MH, Moore SE. nspiratory and expiratory partitioning of airway resistance during sleep in patients with sleep apnea. Am Rev Respir Dis 1983;127: Findley LJ, Rics AL, Tisi GM, Wagner PD. Hypoxemia during sleep in normal subjects: mechanisms and impact of lung volume. J Appl Physiol 1983;55: Bradley TD, Martinez D, Rutherford R, et al. Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea. J Appl Physiol 1985;59: i3~. 12. Martin RJ, Sanders MH, Gray BA, Pennock BE. Acute and long term ventilatory effects of hyperoxia in the adult sleep apnea syndrome. Am Rev Respir Dis 1982;125: Sleep, Vol. ll, No.4, 1988