Sleep-related breathing abnormalities are frequently accompanied by repetitive oxygen desaturations [12] that can be used to identify and characterize abnormal respiratory events during polysomnographic studies [13]. Home measurement of nighttime oxygen saturation levels using oximetry recording has been considered to be unreliable [14], because even 20 to 30 seconds of apnea can result in minimal SaO₂ changes [15] and because it does not effectively exclude substantial sleep apnea [16, 17]. These findings were based on the decrease in the SaO₂ level, and the number of times the SaO₂ level decreased below a fixed threshold; however, evidence exists that depth of the decreases in nocturnal SaO₂ levels do not always parallel the presence of sleep-induced breathing disorders [18]. The amount of apnea-related desaturation depends on several factors including the baseline SaO₂ level; the expiratory reserve volume; the total apnea time; and the different apnea types [19, 20]. Therefore, an apnea of a fixed duration will result in a wide range of decreases in SaO₂ levels from one patient to another and from one apnea event to the other, in the same patient. Further, the definition of apnea is based on the absence of airflow and not on the presence of desaturation. Therefore, considering only a fixed decrease in SaO₂ levels or a decrease below the SaO₂ threshold as suggestive criteria of respiratory abnormalities may lead to a misinterpretation of nocturnal oximetry test results. Thus, we reasoned that the interpretation of the SaO₂ recording based on the presence of repetitive fluctuations in the SaO₂ signal without rigid criteria for the amplitude of the SaO₂ decline should improve its accuracy as a test for detecting SAHS. Because a valid nocturnal home oximetry test would greatly decrease the costs of diagnosing these patients, we evaluated its utility for diagnosing SAHS using these criteria.

Methods

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Patients

A total of 240 consecutive outpatients referred to our sleep clinic (216 men, 24 women; ages 24 to 68 years; body mass index, 31.7 ± 0.8 kg/m² [mean ± SE]) were included in our study. They were clinically suspected of having SAHS because of loud snoring; nocturnal choking and awakenings or apneic events or all three reported by a bedmate; bad sleep quality; and daytime hypersomnolence. None had previously been investigated by home or sleep laboratory recordings. The review board on human studies in our institution approved the experimental protocol, and each patient gave his or her informed consent to participate in the study.

Protocol

Patients were prospectively evaluated by a single night nocturnal home oximetry test followed by a conventional polysomnographic study. Patients were asked to avoid alcohol consumption for at least 12 hours before the different studies. The ambulatory SaO₂ recording was done with a Biox IVA oximeter (Ohmeda, Louisville, Colorado) with a finger probe at a 0.5 Hz sampling frequency. The patients were instructed in the use of the oximeter by the sleep laboratory technician. They were told to install the finger probe, to check that the SaO₂ and pulse rate values appeared on the screen, and to begin the recording by pressing the key corresponding to the high-frequency sampling mode when they turned off the lights. They interrupted the recording if they awoke during the night and stopped it when they awoke in the morning. The home recording was done twice in 18 patients who did not sleep well during the first home recording. No treatment was initiated between home oximetry and the polysomnographic sleep study, and the patients weights remained unchanged. The sleep study was done within 1 month of the home SaO₂ monitoring (range, 1 to 4 weeks).

Sleep studies included the determination of sleep stages (electroencephalogram, C₄A₁ and C₃A_–1; electroculogram; submental electromyogram); nasal and mouth airflow with thermocouples (Grass Instruments, Quincy, Massachusetts); SaO₂ with a Criticare 504 ear oximeter (CSI, Waukesha, Wisconsin); electrocardiogram; and thoracoabdominal movements by respiratory inductive plethysmography (Respitrace, Ambulatory Monitoring, Ardsley, New York) calibrated by the isovolume method [21]. Intrathoracic pressures were recorded with an esophageal balloon in 105 patients. All measurements were recorded on a 16-channel polygraph (Model 78; Grass Instruments) running at 10 mm/s. Sleep stages were defined in 30-second periods according to standard criteria [22]. An apneic event was defined as a cessation of the oronasal flow for at least 10 seconds, and hypopnea was defined as a 50% decrease in the sum signal of the Respitrace associated with a desaturation greater than 4% [23]. An arousal was defined by the simultaneous transition to a lighter sleep stage with eye movements and an increase in electromyographic activity of less than 15 seconds [24].

Data Analysis and Statistical Analysis

Polysomnographic recordings were manually interpreted by trained technicians who were unaware of the results of the oximetry (these recordings were interpreted before the sleep study). Home oximetry was classified as abnormal (suspicion of sleep-related breathing abnormalities) in the presence of repetitive episodes [mean for the whole night greater than 10/h] of transient desaturation followed by a rapid return to the baseline SaO₂ level using no minimum decrease in SaO₂ levels and no threshold. Figure 1 illustrates typical examples of abnormal oximetry recordings that were considered compatible with sleep-induced respiratory disorders. Abnormalities of the oximetry recording were of two types: deep repetitive desaturation episodes Figure 1, top) or low-amplitude periodic SaO₂ fluctuations Figure 1, bottom). The diagnosis of SAHS was confirmed when the apnea plus hypopnea index obtained by the sleep study was greater than 10. The individual baseline SaO₂ values obtained during home oximetry and polysomnographic study were compared by a Student paired t-test. The accuracy of home oximetry was evaluated by a contingency analysis with a two-tail Fisher exact test.

View larger version (50K): [in this window] [in a new window]   Figure 1. Typical examples of abnormal, nocturnal arterial oxyhemoglobin saturation tracings.Top. Repetitive episodes of periodic deep desaturation are accompanied by cyclic variations in the pulse rate (PR). Bottom. Small-amplitude periodic fluctuations in the arterial oxyhemoglobin saturation (SaO2) signal that were considered as abnormal even if the decreases in the SaO2 level were less than 4% or did not reach 90% or both.

Results

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Almost all patients reported normal sleep quality and duration of sleep during the home oximetry recording. The diagnosis of SAHS was confirmed in 110 of the 240 patients studied. In this group, the apnea plus hypopnea index and the arousal index were 38.1 ± 2.5/h and 36.8 ± 2.7/h (mean ± SE), respectively. The mean total apnea time (percentage of total sleep time spent in apnea) was 13.1% (CI, 10.8% to 15.4%), and obstructive apnea represented 72.4% of total apnea time (CI, 66.7% to 78.1%). The baseline Sa (_o)₂ value was 95.2% ± 0.1% during home recording and was 95.7% ± 0.1% during the polysomnographic study (P > 0.05). Oximetry was abnormal in 176 patients, which included all but 2 of those with SAHS. In the SAHS group, 41 oximetry tests were interpreted as abnormal despite decreases in SaO₂ levels of less than 4% that did not reach 90% (see Figure 1, bottom). Nocturnal home oximetry was normal (absence of SaO₂ fluctuations, Figure 2 in all 62 patients who had no sleep disordered breathing.

View larger version (27K): [in this window] [in a new window]   Figure 2. Typical example of a normal home oximetry recording. The arterial oxyhemoglobin saturation (SaO2) tracing was stable and no periodic fluctuations occurred. PR = pulse rate.

The overall results of the home oximetry and polysomnographic testing are detailed in Figure 3. Based on a cutoff point of 10/h, home oximetry testing had a sensitivity of 108/110 or 98.2% (CI, 93.6% to 99.8%) and a specificity of 62/130 or 47.7% (CI, 38.8% to 56.6%). Given that 110 of 240 (46%) patients had sleep apnea, the likelihood of sleep apnea increased to 61.4% with a positive test and decreased to 3.1% with a negative test. The main characteristics of the patients with true and false results are reported in Table 1. The two patients who had a false-negative home oximetry recording (using a cutoff point of 10/h) had an apnea hypopnea index of 16.1/h and 14/h, respectively, and a body mass index of 27.1 kg/m² and 32.5 kg/m², respectively.

View larger version (8K): [in this window] [in a new window]   Figure 3. Contingency Tables Comparing the Results of the Home Oximetry and Polysomnographic Recordings Using Two Different Diagnosis Thresholds of the Apnea-Plus-Hypopnea Index (AHI).

To specify the influence of the abnormal apnea-plus-hypopnea index threshold on these results, we analyzed our data using a different cutoff point of 20/h [4]. Using this cutoff point, 176 patients had an abnormal home oximetry test, and the diagnosis of SAHS was confirmed in 75 of them. Home oximetry test results were normal in the 64 patients without SAHS with no false-negative results (see Figure 3). Therefore, we used these SAHS diagnostic criteria, a sensitivity for nocturnal home oximetry testing of 100%; a specificity of 38.8%; a positive predictive value of 42.6%; and a negative predictive value of 100% Figure 3 [P < 10^–4]. The reproducibility of our interpretation criteria was verified in 60 randomly selected home oximetry recordings interpreted blindly by two physicians. The concordance between the two interpretations was 95%.

Discussion

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Our results show that a qualitative analysis of the SaO₂ tracing can help in excluding SAHS. These results differ from those of previous studies that examined the accuracy of nocturnal oximetry for case finding in patients clinically suspected of having the sleep apnea syndrome. Although some of this difference can be explained by differences in the population size, most of it is probably related to several methodologic differences between ours and previous studies. First, the characteristics of the signal sampling were different. Our sampling frequency was higher than that reported in other studies [16, 25, 26] and provided a more precise Sa (_o)₂ tracing and a more accurate analysis of the recording. Second, hypopnea was included in the sleep-related breathing abnormalities. Therefore, in contrast to Williams and colleagues [16], our study took into account the sleep hypopnea syndrome that is clinically similar to the sleep apnea syndrome [27]. Finally, our interpretation of home nocturnal oximetry was not based on the occurrence of a minimal decrease in the SaO₂ level or having a value below a fixed threshold. If the 4% decrease in the SaO₂ level and the 90% threshold had been used in our population, the sensitivity would have been 60.9% and the negative predictive value would have been 65.0%.

Home oximetry testing, as used here, failed to identify sleep-related breathing abnormalities in only two patients. These negative results probably reflect the fact that the factors determining the severity of nocturnal desaturation (weight excess, low baseline SaO₂ value, predominance of obstructive apneas) [19, 20, 28] were not present in these patients. However, because their apnea-plus-hypopnea index was low and because the night-to-night variability of apnea frequency is increased in patients with low apnea indices [29], it is possible that the negative result was related to spontaneous variations in the nocturnal breathing disorders. Nevertheless, our results show that nocturnal SaO₂ recording accurately selects most patients clinically suspected of having SAHS.

We are aware that different values for decreased SaO₂ levels can be used in the definition of hypopneic events and that a normal apnea-plus-hypopnea index does not rule out the presence of breathing abnormalities, such as the sleep fragmentation observed in snorers with periodic increases in respiratory efforts and repeated arousals (the upper-airway resistance syndrome) [18]. Therefore, we looked at the results of home oximetry recording in non-SAHS patients with such sleep-related disordered breathing. Because upper-airway resistance was not measured in our study, the diagnosis of this syndrome was considered established when the arousal index was more than 10/h. Home oximetry was abnormal in 19 of the 25 patients who had an abnormal arousal index. This illustrates that nonapneic or hypopneic changes in ventilation are usually followed by small-amplitude fluctuations of the SaO₂ tracing, confirming that periodic increases in upper-airway resistance are frequently associated with small but regular desaturations [18].

To our knowledge, this is the first study that documents the diagnostic value of home oximetry as a case finding test for SAHS using unfixed SaO₂ criteria. This method of interpretation is simple and practical because it does not require sophisticated and costly apparatus. We did not consider any desaturation index as indicative of the frequency of the sleep-induced respiratory disturbances because the usefulness of such an index is limited by the variability of the decrease in the SaO₂ level induced by respiratory abnormalities and because the clinical diagnosis of SAHS requires polysomnographic recording. Therefore, our study was designed to examine the accuracy of home oximetry testing for selecting patients who would then have a conventional sleep study. Our results show that the interpretation of the home oximetry recordings with our measurements was useful because its use can obviate the need for a whole night of monitoring and several hours of interpretation by a technician (with its related costs) in 62 of our 240 patients. However, because of its low specificity and consequent low positive predictive value, positive home oximetry must be followed by complete polysomnographic monitoring to confirm or rule out the diagnosis of SAHS.