Lung (1992) 170:281-290
©Sprin~ger~ NewYorkInc.1992
Influence of Continuous Positive Airway Pressure on Sleep Apnea-Related Desaturation in Sleep Apnea Patients F. S6ri6s, Y. Cormier, and J. Laforge Unit6 de Recherche, Centre de Pneumologie de l'H6pital Laval, Universit4 Laval, 2725 Chemin Ste. Foy, Ste Foy (PQ), GIV 4G5 Qu6bec, Canada
Abstract. To investigate the influence of nasal continuous positive airway pressure (CPAP) on apnea-related desaturation, we c o m p a r e d the sleep apnea-related desaturations obtained during a polysomnographic study before and during nasal C P A P in 15 sleep apnea patients. An individual desaturation curve was determined with a regression analysis by plotting the lowest SaO 2 value reached during each apnea against its duration; these data were collected throughout the night. At baseline, we only considered the apneas with a preapneic SaO 2 value greater than 90% and a minimal SaO 2 value a b o v e or equal to 60%. F o r the CPAP study, the preapneic S a O 2 value also had to be within 2% the baseline value for the apneas to be retained. Due to the restriction criteria imposed to characterize apnea-related SaO 2 falls, residual apneas still had to be recorded with CPAP. These data were analyzed separately for obstructive a p n e a for non-rapid eye m o v e m e n t (REM) and R E M sleep stages. A desaturation curve was obtained f r o m 10 sec to a variable u p p e r limit that c o r r e s p o n d e d to the longest apnea duration commonly reached during both baseline and CPAP for a given a p n e a - t y p e and sleep stage. The individual apnea-related SaO 2 fall was characterized by measuring a desaturation area corresponding to the area under the curve. It was e x p r e s s e d in % SaO2/sec of apnea. CPAP reduced the n u m b e r of apneas per hour of sleep f r o m 37.5 + 6.5 (mean _+ SEM) to 14.3 + 3.7 (p = 0.001), and i m p r o v e d the whole night S a O 2 level as estimated by a cumulative SaO2 curve. The m e a n a p n e a duration was reduced from 22.9 _+ 1.5 sec at baseline to 16.8 + 0.5 sec during C P A P therapy (p = 0.005). The preapneic SaO 2 value was 94.8 -+ 0.3% at baseline and 95.5 +_ 0.2% during CPAP (p = 0.5). The desaturation area decreased from 267 _+ 48% SaO2/sec at baseline to 152 +- 41% SaO2/sec during C P A P (p < 0.001). We conclude that CPAP i m p r o v e s the apnea-related desaturation independently of the shortening of apneas and of any difference in the preapneic S a O 2 value. Offprint requests to: F. S6ri~s
282
F. S6ri~s et al.
Key words: Desaturation curve--Apnea length--Oxygen stores, Lung volu m e - S l e e p apnea.
Introduction
Repetitive nocturnal desaturations are frequently observed in sleep apnea patients [23]. The severity of these transient decreases in SaO2 depends on the preapneic SaO2 level, the percentage of the total sleep time spent in apnea, and the supine value of the expiratory reserve volume [4]. Continuous positive airway pressure (CPAP) is commonly used in the treatment of sleep apnea; it is accompanied by a dramatic decrease in the number of apneic events [22], with resumption of a normal sleep architecture, and an improvement in the mean SaO 2 during sleep [12, 16, 22, 26]. This improvement is mainly due to the disappearance of apneic events, but it is generally observed that the apnearelated desaturations of the remaining apneas are less severe during CPAP therapy. Since lung volume is an important determinant of apnea-related desaturations [1, 13, 20], the CPAP-induced increase in lung volume can theoretically account for this improvement. However, CPAP can also modify the apnea length [1, 16], the preapneic SaO 2 level [17], and the composition of the apnea time within the different apnea types (obstructive, central, mixed) [l 1]. Since these different factors are known to determine the severity of apnea-related desaturations [4, 18], they may be involved in this CPAP effect, but their respective influence has not been determined. We have recently described a method of analyzing the sleep apnea-related desaturations that characterizes the postapneic SaO 2 level, taking the duration of each apnea, the apnea type, and the preapneic SaO 2 value into account [18]. The aims of the present study were to characterize the changes in apnea-related SaO 2 fall induced by CPAP independently of the variations in apnea lengths, apnea types, and preapneic SaO2 values. Methods
Subjects: Fifteen sleep apnea patients (12 male, 3 female) were included in the study. The diagnosis of sleep apnea syndrome (SAS) was based on clinical findings and on the results of polysomnographic studies (apnea index > 5, and/or apnea-hypopnea index > 10). To be included in the study, the baseline SaO2 value (stable pre- and postapneic SaO 2value) had to be greater than 90%. Due to the restriction criteria imposed to characterize the apnea-related desaturations, a minimum number of apneas had to be collected during the sleep studies (see below); therefore the persistence of apneas despite maximum tolerated CPAP was required for a patient to be included in the study. No patient had bronchopulmonary or cardiac disease, and none was treated for sleep apnea or had already received CPAP prior to the study.
Pulmonary Function Measurements of lung volume, expiratory flow, and arterial blood gases were done in the sitting
CPAP and Postapneic Desaturation
283
position. Lung volumes were measured by body plethysmography. Normal values were those of Grimby [9].
Polysomnographic Studies Baseline and CPAP sleep studies included the determination of sleep stages (electroencephalogram [EEG], electro-oculogram [EOG], electromyogram [EMG]), the recording of nasal and mouth flows with 3 thermistors (1 below each nostril, and 1 in front of the mouth), SaO 2 with an ear oximeter (Criticare 504, CSI), thoracoabdominal movements with an inductance vest (Respitrace, ambulatory monitoring), calibrated by the least-square method [5]. During the baseline (diagnostic) sleep recording, intrathoracic pressures were measured with an esophageal balloon. These signals were continuously displayed on a polygraph (Grass instruments 78 D, Quincy, MA) at a paper speed of 10 mm/sec. Sleep stages and respiratory abnormalities were scored according to standard criteria [14, 15]. The length of apneas was measured from the end of an expiration to the beginning of the next inspiration. During the CPAP study, apneas' duration was determined according to the absence of flow on the thermistors and Sum Respitrace signals. Apneas were defined as obstructive in type (OA) if there were persistent inspiratory efforts and/or thoracoabdominal paradoxes during the apnea. The nasal CPAP study was done the night immediately following the initial diagnostic sleep study. Positive airway pressure was applied via a Healthdyne Tranquility CPAP nasal system. The study was initiated at a 5 cmH20 pressure. This pressure was progressively increased up to 15 cmH20 until apnea was no longer observed, or the patient complained of discomfort. The pressure level was determined within the first hour, and was then kept constant for the rest of the night. During the sleep study, the stability of the positive pressure level was verified with a Bird manometer.
Characterization of Apnea-Related SaO 2 Fall Postapneic desaturations were quantified as previously described [18]. For each subject the apnearelated desaturations were characterized by determining an individual desaturation curve. This was obtained by collecting the value of the lowest SaO2 following an apnea and the length of this apnea throughout the night recordings. The desaturation curve was obtained by a regression model between these two variables (see section on statistical analysis). This curve included all the apneic events in which the preapneic SaO2 was constant and equal to the baseline SaO2 value (by definition > 90%) and within 2% of the baseline value during the CPAP study, and the lowest SaO 2 value was -> 60%. Data were analyzed separately for the different apnea types and sleep stages during the baseline and the CPAP sleep studies. During the CPAP night, we only analyzed respiratory events that occurred after the stable level of CPAP had been reached. For the different sleep stages (stage I-II: non-REM and REM sleep) a minimum of 10 OA meeting the above restriction criteria had to be retained for a desaturation curve to be determined. This was done with a second-degree polynomial regression model passing through the origin. Since differences in the apnea lengths between baseline and CPAP studies could influence the characteristics of the desaturation curve, the curve was determined only up to the maximal apnea duration reached during both studies. From the equation of the desaturation curve obtained in each apnea category, we determined a desaturation area, defined as the area under the curve between 10 sec and the individual's upper time limit of the desaturation curve. The desaturation area was expressed in % SaO2/sec of apnea.
Statistical Analysis Since minimum SaO 2 decreased curvilinearily with increasing apnea duration, the correlation between these 2 variables was analyzed with a second-degree polynomial regression model passing through the origin. There was always a significant relationship between the postapneic SaO 2 value and the apnea length. The individual baseline values of the desaturation areas obtained for non-
284
F. S~ri6s et al.
Table 1. Anthropometric characteristics and results of the pulmonary function tests of the 15 patients studied. Age (yr) Body mass index (Kg/m2) FEV 1(L) (% predicted) FVC (L) (% predicted) TLC (L) (% predicted) FRC (L) (% predicted) ERV (L) (% predicted) PaO2 (mmHg) PaCO2 (mmHg)
55 _+3 47.0 -+ 3.6 2.7 -+ 0.2 (82.7 -+ 3.8) 3.6 -+ 0.2 (81.8 -+ 3.0) 5.7 _+0.4 (100.2 + 4.2) 2.7 -+ 0.1 (102 _+4.7) 0.4 -+ 0.05 (77.8 + 3.0) 84.1 + 1.4 41.4 -+ 1.0
FEV I, forced expiratory volume in 1 sec; FVC, forced vital capacity; TLC, total lung capacity; FRC, functional residual capacity; ERV, expiratory reserve volume (mean -+ SEM)
REM OA and REM OA were paired compared to the respective values measured during the CPAP study. Since our data were not normally distributed, the results of the 2 polysomnographicstudies were compared by the Wilcoxon signed-rank test.
Results The anthropometric characteristics of our subjects and the results of the pulmonary function tests are given in Table I. The mean effective C P A P level applied was 9 c m H 2 0 (range, 5-15 cmH20). There was no difference between the baseline and C P A P total sleep time values (6.7 -+ 0.3 hr and 6.4 - 0.4 hr, respectively; mean -+ SEM). As illustrated in Table 2, the frequency of the sleep-related breathing abnormalities and the percentage of total sleep time spent in apnea significantly decreased with CPAP. There was no significant difference in the composition of the total apnea time within the different apnea types between the baseline and C P A P sleep studies. The mean apnea duration was 22.9 -+ 1.5 sec at baseline and 16.8 -+ 0.5 sec with C P A P (p = 0.001). The severity of the nocturnal desaturations was estimated by the cumulative SaO 2 curve representing the percentage o f total sleep time (TST) spent at each 5% SaO 2 value (Fig. 1). The curve obtained during CPAP was shifted d o w n w a r d and to the right, the difference being significant for SaO 2 values greater than 75% (Fig. 1). There was a highly significant relationship between the postapneic SaO2 value and the apnea length during both baseline (r range, 0.61-0.94; mean r, 0.8; p = 0.0001) and C P A P studies (r range, 0.68-0.90; mean r, 0.79; p = 0.0001). As illustrated in Fig. 2 for a typical subject, the desaturation area obtained during C P A P was less than that measured at baseline. The individual values of the preapneic SaO2 and the desaturation area obtained without and with C P A P are reported in Table 3. There was no significant difference in the preapneic SaO 2 value between these 2 conditions. The improvement in the apnea-related desaturation observed with nasal CPAP seemed to be greater
285
CPAP and Postapneic Desaturation Table 2. Characteristics of the sleep-related breathing abnormalities observed during the baseline and CPAP sleep studies.
Apnea index (n/hr) Apnea ÷ hypopnea index (n/h) Total apnea-time (% TST) Obstructive apnea time (% TAT)
Baseline
CPAP
37.5 63.8 24.4 67.7
14.3 19.6 7.2 59.4
_+ 6.5 + 8.3 + 4.6 + 7.7
+ 3.7* -+ 4.4* +- 1.9" -+ 6.9
The total apnea-time (TAT) is the percentage of the total sleep time (TST) spent in apnea. The apnea and apnea + hypopnea indices and the total apnea time improved significantly with CPAP Mean + SEM, *p - 0.001
during non-REM than during REM sleep. For the whole group, the desaturation area measured with CPAP was significantly lower than at baseline.
Discussion
Our results demonstrate that the improvement in sleep apnea-related desaturations observed with nasal CPAP is independent of apnea duration and of an observed difference in the preapneic S a O 2. The postapneic changes in SaO2 were measured with an individual desaturation curve that characterizes the overnight apnea-related desaturation of each category of apnea. To reduce the influence of the differences in the preapneic S a O 2 value between the baseline and the CPAP studies, the apneas included in the regression model were very similar in term of preapneic SaO2 value. It can be argued that the small increase in the baseline S a O 2 value observed with CPAP may have contributed to the improvement in the apnea-related desaturation, as suggested by the significant increase in the preapneic PaO 2 values (estimated from the oxyhemoglobin dissociation curve by assuming a normal P50) with CPAP (79 -+ 2 mmHg) compared to baseline (75 -+ 2 mmHg, p < 0.05). However, the improvement in the apnea-related desaturation was observed even in the 8 patients whose preapneic SaO2 value did not change with CPAP (Table 3). Therefore, even if the CPAP-induced increase in the oxygen partial pressure had helped to improve desaturation, this parameter cannot entirely account for our results. Since the apnea-desaturation relationship is curvilinear, the decrease of apneas' length observed with CPAP could, theoretically, by itself improve the severity of apnea-induced desaturation. However, our study design controlled for this variable by including only the apneas within the time range seen under both conditions (baseline and CPAP); therefore, this parameter cannot account for the difference observed. The selection criteria for an apnea to be included in the analysis and for a desaturation curve to be determined reduced the categories of apnea that could
286
F. S6ri6s et al.
% Total sleep time
I
=
I --o---
Baseline CPAP
40 35 30 25 20 15 10 5 0
* ~C -
©Sprin~ger~ NewYorkInc.1992
Influence of Continuous Positive Airway Pressure on Sleep Apnea-Related Desaturation in Sleep Apnea Patients F. S6ri6s, Y. Cormier, and J. Laforge Unit6 de Recherche, Centre de Pneumologie de l'H6pital Laval, Universit4 Laval, 2725 Chemin Ste. Foy, Ste Foy (PQ), GIV 4G5 Qu6bec, Canada
Abstract. To investigate the influence of nasal continuous positive airway pressure (CPAP) on apnea-related desaturation, we c o m p a r e d the sleep apnea-related desaturations obtained during a polysomnographic study before and during nasal C P A P in 15 sleep apnea patients. An individual desaturation curve was determined with a regression analysis by plotting the lowest SaO 2 value reached during each apnea against its duration; these data were collected throughout the night. At baseline, we only considered the apneas with a preapneic SaO 2 value greater than 90% and a minimal SaO 2 value a b o v e or equal to 60%. F o r the CPAP study, the preapneic S a O 2 value also had to be within 2% the baseline value for the apneas to be retained. Due to the restriction criteria imposed to characterize apnea-related SaO 2 falls, residual apneas still had to be recorded with CPAP. These data were analyzed separately for obstructive a p n e a for non-rapid eye m o v e m e n t (REM) and R E M sleep stages. A desaturation curve was obtained f r o m 10 sec to a variable u p p e r limit that c o r r e s p o n d e d to the longest apnea duration commonly reached during both baseline and CPAP for a given a p n e a - t y p e and sleep stage. The individual apnea-related SaO 2 fall was characterized by measuring a desaturation area corresponding to the area under the curve. It was e x p r e s s e d in % SaO2/sec of apnea. CPAP reduced the n u m b e r of apneas per hour of sleep f r o m 37.5 + 6.5 (mean _+ SEM) to 14.3 + 3.7 (p = 0.001), and i m p r o v e d the whole night S a O 2 level as estimated by a cumulative SaO2 curve. The m e a n a p n e a duration was reduced from 22.9 _+ 1.5 sec at baseline to 16.8 + 0.5 sec during C P A P therapy (p = 0.005). The preapneic SaO 2 value was 94.8 -+ 0.3% at baseline and 95.5 +_ 0.2% during CPAP (p = 0.5). The desaturation area decreased from 267 _+ 48% SaO2/sec at baseline to 152 +- 41% SaO2/sec during C P A P (p < 0.001). We conclude that CPAP i m p r o v e s the apnea-related desaturation independently of the shortening of apneas and of any difference in the preapneic S a O 2 value. Offprint requests to: F. S6ri~s
282
F. S6ri~s et al.
Key words: Desaturation curve--Apnea length--Oxygen stores, Lung volu m e - S l e e p apnea.
Introduction
Repetitive nocturnal desaturations are frequently observed in sleep apnea patients [23]. The severity of these transient decreases in SaO2 depends on the preapneic SaO2 level, the percentage of the total sleep time spent in apnea, and the supine value of the expiratory reserve volume [4]. Continuous positive airway pressure (CPAP) is commonly used in the treatment of sleep apnea; it is accompanied by a dramatic decrease in the number of apneic events [22], with resumption of a normal sleep architecture, and an improvement in the mean SaO 2 during sleep [12, 16, 22, 26]. This improvement is mainly due to the disappearance of apneic events, but it is generally observed that the apnearelated desaturations of the remaining apneas are less severe during CPAP therapy. Since lung volume is an important determinant of apnea-related desaturations [1, 13, 20], the CPAP-induced increase in lung volume can theoretically account for this improvement. However, CPAP can also modify the apnea length [1, 16], the preapneic SaO 2 level [17], and the composition of the apnea time within the different apnea types (obstructive, central, mixed) [l 1]. Since these different factors are known to determine the severity of apnea-related desaturations [4, 18], they may be involved in this CPAP effect, but their respective influence has not been determined. We have recently described a method of analyzing the sleep apnea-related desaturations that characterizes the postapneic SaO 2 level, taking the duration of each apnea, the apnea type, and the preapneic SaO 2 value into account [18]. The aims of the present study were to characterize the changes in apnea-related SaO 2 fall induced by CPAP independently of the variations in apnea lengths, apnea types, and preapneic SaO2 values. Methods
Subjects: Fifteen sleep apnea patients (12 male, 3 female) were included in the study. The diagnosis of sleep apnea syndrome (SAS) was based on clinical findings and on the results of polysomnographic studies (apnea index > 5, and/or apnea-hypopnea index > 10). To be included in the study, the baseline SaO2 value (stable pre- and postapneic SaO 2value) had to be greater than 90%. Due to the restriction criteria imposed to characterize the apnea-related desaturations, a minimum number of apneas had to be collected during the sleep studies (see below); therefore the persistence of apneas despite maximum tolerated CPAP was required for a patient to be included in the study. No patient had bronchopulmonary or cardiac disease, and none was treated for sleep apnea or had already received CPAP prior to the study.
Pulmonary Function Measurements of lung volume, expiratory flow, and arterial blood gases were done in the sitting
CPAP and Postapneic Desaturation
283
position. Lung volumes were measured by body plethysmography. Normal values were those of Grimby [9].
Polysomnographic Studies Baseline and CPAP sleep studies included the determination of sleep stages (electroencephalogram [EEG], electro-oculogram [EOG], electromyogram [EMG]), the recording of nasal and mouth flows with 3 thermistors (1 below each nostril, and 1 in front of the mouth), SaO 2 with an ear oximeter (Criticare 504, CSI), thoracoabdominal movements with an inductance vest (Respitrace, ambulatory monitoring), calibrated by the least-square method [5]. During the baseline (diagnostic) sleep recording, intrathoracic pressures were measured with an esophageal balloon. These signals were continuously displayed on a polygraph (Grass instruments 78 D, Quincy, MA) at a paper speed of 10 mm/sec. Sleep stages and respiratory abnormalities were scored according to standard criteria [14, 15]. The length of apneas was measured from the end of an expiration to the beginning of the next inspiration. During the CPAP study, apneas' duration was determined according to the absence of flow on the thermistors and Sum Respitrace signals. Apneas were defined as obstructive in type (OA) if there were persistent inspiratory efforts and/or thoracoabdominal paradoxes during the apnea. The nasal CPAP study was done the night immediately following the initial diagnostic sleep study. Positive airway pressure was applied via a Healthdyne Tranquility CPAP nasal system. The study was initiated at a 5 cmH20 pressure. This pressure was progressively increased up to 15 cmH20 until apnea was no longer observed, or the patient complained of discomfort. The pressure level was determined within the first hour, and was then kept constant for the rest of the night. During the sleep study, the stability of the positive pressure level was verified with a Bird manometer.
Characterization of Apnea-Related SaO 2 Fall Postapneic desaturations were quantified as previously described [18]. For each subject the apnearelated desaturations were characterized by determining an individual desaturation curve. This was obtained by collecting the value of the lowest SaO2 following an apnea and the length of this apnea throughout the night recordings. The desaturation curve was obtained by a regression model between these two variables (see section on statistical analysis). This curve included all the apneic events in which the preapneic SaO2 was constant and equal to the baseline SaO2 value (by definition > 90%) and within 2% of the baseline value during the CPAP study, and the lowest SaO 2 value was -> 60%. Data were analyzed separately for the different apnea types and sleep stages during the baseline and the CPAP sleep studies. During the CPAP night, we only analyzed respiratory events that occurred after the stable level of CPAP had been reached. For the different sleep stages (stage I-II: non-REM and REM sleep) a minimum of 10 OA meeting the above restriction criteria had to be retained for a desaturation curve to be determined. This was done with a second-degree polynomial regression model passing through the origin. Since differences in the apnea lengths between baseline and CPAP studies could influence the characteristics of the desaturation curve, the curve was determined only up to the maximal apnea duration reached during both studies. From the equation of the desaturation curve obtained in each apnea category, we determined a desaturation area, defined as the area under the curve between 10 sec and the individual's upper time limit of the desaturation curve. The desaturation area was expressed in % SaO2/sec of apnea.
Statistical Analysis Since minimum SaO 2 decreased curvilinearily with increasing apnea duration, the correlation between these 2 variables was analyzed with a second-degree polynomial regression model passing through the origin. There was always a significant relationship between the postapneic SaO 2 value and the apnea length. The individual baseline values of the desaturation areas obtained for non-
284
F. S~ri6s et al.
Table 1. Anthropometric characteristics and results of the pulmonary function tests of the 15 patients studied. Age (yr) Body mass index (Kg/m2) FEV 1(L) (% predicted) FVC (L) (% predicted) TLC (L) (% predicted) FRC (L) (% predicted) ERV (L) (% predicted) PaO2 (mmHg) PaCO2 (mmHg)
55 _+3 47.0 -+ 3.6 2.7 -+ 0.2 (82.7 -+ 3.8) 3.6 -+ 0.2 (81.8 -+ 3.0) 5.7 _+0.4 (100.2 + 4.2) 2.7 -+ 0.1 (102 _+4.7) 0.4 -+ 0.05 (77.8 + 3.0) 84.1 + 1.4 41.4 -+ 1.0
FEV I, forced expiratory volume in 1 sec; FVC, forced vital capacity; TLC, total lung capacity; FRC, functional residual capacity; ERV, expiratory reserve volume (mean -+ SEM)
REM OA and REM OA were paired compared to the respective values measured during the CPAP study. Since our data were not normally distributed, the results of the 2 polysomnographicstudies were compared by the Wilcoxon signed-rank test.
Results The anthropometric characteristics of our subjects and the results of the pulmonary function tests are given in Table I. The mean effective C P A P level applied was 9 c m H 2 0 (range, 5-15 cmH20). There was no difference between the baseline and C P A P total sleep time values (6.7 -+ 0.3 hr and 6.4 - 0.4 hr, respectively; mean -+ SEM). As illustrated in Table 2, the frequency of the sleep-related breathing abnormalities and the percentage of total sleep time spent in apnea significantly decreased with CPAP. There was no significant difference in the composition of the total apnea time within the different apnea types between the baseline and C P A P sleep studies. The mean apnea duration was 22.9 -+ 1.5 sec at baseline and 16.8 -+ 0.5 sec with C P A P (p = 0.001). The severity of the nocturnal desaturations was estimated by the cumulative SaO 2 curve representing the percentage o f total sleep time (TST) spent at each 5% SaO 2 value (Fig. 1). The curve obtained during CPAP was shifted d o w n w a r d and to the right, the difference being significant for SaO 2 values greater than 75% (Fig. 1). There was a highly significant relationship between the postapneic SaO2 value and the apnea length during both baseline (r range, 0.61-0.94; mean r, 0.8; p = 0.0001) and C P A P studies (r range, 0.68-0.90; mean r, 0.79; p = 0.0001). As illustrated in Fig. 2 for a typical subject, the desaturation area obtained during C P A P was less than that measured at baseline. The individual values of the preapneic SaO2 and the desaturation area obtained without and with C P A P are reported in Table 3. There was no significant difference in the preapneic SaO 2 value between these 2 conditions. The improvement in the apnea-related desaturation observed with nasal CPAP seemed to be greater
285
CPAP and Postapneic Desaturation Table 2. Characteristics of the sleep-related breathing abnormalities observed during the baseline and CPAP sleep studies.
Apnea index (n/hr) Apnea ÷ hypopnea index (n/h) Total apnea-time (% TST) Obstructive apnea time (% TAT)
Baseline
CPAP
37.5 63.8 24.4 67.7
14.3 19.6 7.2 59.4
_+ 6.5 + 8.3 + 4.6 + 7.7
+ 3.7* -+ 4.4* +- 1.9" -+ 6.9
The total apnea-time (TAT) is the percentage of the total sleep time (TST) spent in apnea. The apnea and apnea + hypopnea indices and the total apnea time improved significantly with CPAP Mean + SEM, *p - 0.001
during non-REM than during REM sleep. For the whole group, the desaturation area measured with CPAP was significantly lower than at baseline.
Discussion
Our results demonstrate that the improvement in sleep apnea-related desaturations observed with nasal CPAP is independent of apnea duration and of an observed difference in the preapneic S a O 2. The postapneic changes in SaO2 were measured with an individual desaturation curve that characterizes the overnight apnea-related desaturation of each category of apnea. To reduce the influence of the differences in the preapneic S a O 2 value between the baseline and the CPAP studies, the apneas included in the regression model were very similar in term of preapneic SaO2 value. It can be argued that the small increase in the baseline S a O 2 value observed with CPAP may have contributed to the improvement in the apnea-related desaturation, as suggested by the significant increase in the preapneic PaO 2 values (estimated from the oxyhemoglobin dissociation curve by assuming a normal P50) with CPAP (79 -+ 2 mmHg) compared to baseline (75 -+ 2 mmHg, p < 0.05). However, the improvement in the apnea-related desaturation was observed even in the 8 patients whose preapneic SaO2 value did not change with CPAP (Table 3). Therefore, even if the CPAP-induced increase in the oxygen partial pressure had helped to improve desaturation, this parameter cannot entirely account for our results. Since the apnea-desaturation relationship is curvilinear, the decrease of apneas' length observed with CPAP could, theoretically, by itself improve the severity of apnea-induced desaturation. However, our study design controlled for this variable by including only the apneas within the time range seen under both conditions (baseline and CPAP); therefore, this parameter cannot account for the difference observed. The selection criteria for an apnea to be included in the analysis and for a desaturation curve to be determined reduced the categories of apnea that could
286
F. S6ri6s et al.
% Total sleep time
I
=
I --o---
Baseline CPAP
40 35 30 25 20 15 10 5 0
* ~C -
