Obstructive Sleep Apnea Diagnosis and Treatment - part 4 doc

47 383 0
Obstructive Sleep Apnea Diagnosis and Treatment - part 4 doc

Đang tải... (xem toàn văn)

Tài liệu hạn chế xem trước, để xem đầy đủ mời bạn chọn Tải xuống

Thông tin tài liệu

Bilevel Pressure and Adaptive Servo-Ventilation 127 is more effective in splinting the pharynx open than BPAP in patients with OSA. Another study of 10 selected patients with OSA requiring ≥ 10 cm H 2 O of CPAP failed to show optimal resolution of SDB at any level of IPAP until a critical level of EPAP was achieved indicating a clear need to select an adequate EPAP level (11). An alternative approach to BPAP titration has been to optimize all SDB events with CPAP and then to reduce both the EPAP and IPAP as allowed taking advantage of the natural hysteresis that occurs during a typical CPAP titration episode. In one study, a small but significant reduction in the optimal CPAP level occurred when a downward titration followed an initial titration procedure (12). SELECTION OF PATIENTS Severe Obesity The importance of recognizing and addressing the differences in respiratory system loading that occurs during the inspiratory phase in specific subtypes of patients has helped guide which patients might best be considered for BPAP as well. The impact of obesity on the mechanical loading of the respiratory system, neuromuscular control, and the pathogenesis of apnea and related hypoventilation has been known for many years. This issue was more precisely studied in three groups of severely obese patients, who were eucapnic obese without OSA (O), eucapnic obese with OSA (OSA), or hypercapnic obese with sleep apnea (OH), and were compared to nonobese volunteers (NO) who were subjected to abdominal mass loading (13). This was assessed with diaphragmatic electromyogram (EMGdi), a measure of muscle activation, and mouth occlusion pressure (P0.15), an assessment of mechanical drive, during CO 2 stimulation. The authors showed that P0.15 responses were decreased in OSA and OH but the EMGdi responses did not differ from the control subjects. However, when the NO control subjects were subjected to mass loading, the EMGdi and P0.15 responses increased. Their findings showed that both OSA and OH patients did not develop the expected increase in respiratory muscle response for a given level of activation and the impaired mass load compensation predisposes obese patients to develop hypercapnia. These kinds of observations may help FIGURE 2 Algorithm for adjustment of inspiratory positive airway pressure and expiratory positive airway pressure during the trial of nasal bilevel positive airway pressure (BiPAP ® ). Source: From Ref. 9. 128 Gay explain why the early BiPAP study focused on patients with a mean body mass index (BMI) of 57.4 kg/m 2 even though they were normocapnic and why severe obesity has emerged as an independent predictor of failed CPAP therapy (9,14). The unloading of inspiratory muscle activity with BPAP measured as dia- phragmatic pressure time product was studied in 18 obese subjects with a BMI ≥ 40 kg/m 2 including five healthy controls with simple obesity (SO), seven patients with OSA, and six with obesity-hypoventilation syndrome (OHS) (15). Although the overall ventilation as measured by end-tidal carbon dioxide with BPAP was not changed in SO and OSA, it was decreased in OHS, while the inspiratory muscle activity was reduced by at least 40% in all groups. The authors concluded that BPAP may be particularly effective for improving ventilation in patients with OHS by unloading the inspiratory muscles. Hypercapnia and Other Factors Other studies have specifically targeted the presence of hypercapnia in patients with severe OSA as a reason to justify short- or long-term treatment with modes enabled to deliver more aggressive ventilatory capability (13,16,17). In most cases these studies showed marked improvement in daytime PaCO 2 levels with treat- ment of accompanying nocturnal hypoventilation with BPAP, which in some cases allowed resumption of CPAP treatment alone for satisfactory response to the under- lying OSA. Patient adherence remained high in these patients (18). In order to assess the reasons why a BPAP device was provided to a group of moderate-to-severe OSA patients, a study was done to investigate the frequency of BPAP prescription when CPAP was ineffective or not tolerated during titration (19). Of 286 consecutive adult patients referred to two sleep labs, 130 patients were enrolled and 105 (84% males) completed the study. A split-night (diagnostic and therapeutic) polysomnogram (PSG) was done, followed by another PSG with BPAP if CPAP was not tolerated, or failed to correct sleep-related breathing (SRB) abnor- malities. There were 24 patients (23% overall) that received BPAP with the highest prevalence (11 of 17) in patients with OSA associated with OHS. The BPAP treated patients were more obese, hypercapnic, had severe SRB desaturations, and also had more obstruction, restriction, and hypoxia. The prevalence and mechanism of hypercapnia in morbidly obese patients were investigated in a selected group of 285 patients presented to a sleep laboratory without other significant comorbid diseases. There were 89 morbidly obese patients (31.2%) who had a BMI ≥ 40 kg/m 2 and surprisingly 59.6% were predominately females (20). This group was further divided into three subgroups who were nor- mocapnic without OSA, normocapnic with OSA, and lastly hypercapnic (PaCO 2 ≥ 45 mmHg) with OSA. Their results showed that hypercapnia was found in 27% of the morbidly obese subjects (who were predominately males) but only in 11% of the nonmorbidly obese patients (P < 0.01). Several characteristics were more common in the patients with hypercapnia and OSA than patients with or without OSA including significantly more restriction based on a mean total lung capacity (% predicted) of 63.8% ± 16.4%, a higher respiratory disturbance index of 46.3 ± 26.9 events/hour, a longer total sleep time with SpO 2 < 90% (TSTSpO 2 < 90%) of 63.4 ± 33.9 minutes, and a lower rapid eye movement (REM) sleep at 9.5 ± 1.2%. Their conclusion about important factors associated with hypercapnia and OSA allowed them to construct a predictive model for diurnal hypercapnia: PaCO 2 = −0.03 FVC %predicted − 0.05 FEV1 % predicted + 0.036 TSTSpO 2 < 90% − PaO 2 + 57.13 (r 2 = 0.44). Bilevel Pressure and Adaptive Servo-Ventilation 129 Another small study investigated whether a variety of factors were associated with failure of CPAP therapy to resolve the apnea–hypopnea index (AHI) to < 5 or mean SaO2 > 90% (14). This study of 13 patients with OSA (Group A) over a 15-month period compared to an age- and AHI-matched control group (Group B) successfully treated by CPAP used logistic regression analysis to identify factors associated with initial failure to CPAP. The Group A versus Group B patients were significantly more obese (mean BMI = 44.2 kg/m 2 vs. 31.2 kg/m 2 ; P < 0.001), hypoxic at rest (P < 0.001), and at exercise (P < 0.005). Hypercapnia at rest (P < 0.001) and worsening during exercise was also more likely, and Group A patients also spent significantly (P < 0.0001) more time with oxygen saturation < 90%, which was the only factor independently associated with the initial failure of CPAP [odds ratio (OR) 1.13; 95% confidence interval (CI) 1.0–1.2]. The patients’ awake blood gases proved that both daytime hypoxemia and hypercapnia improved significantly (P < 0.05) after three months of treatment with BPAP. ADHERENCE CPAP can produce objective and subjective improvements in patients with OSA and other types of SDB (21–23). Despite its demonstrable efficacy, many OSA patients have difficulty with long-term acceptance of CPAP (24,25). Several intervention strategies have been suggested to improve adherence to CPAP, including use of specialized education and follow-up programs (26,27) and added airway humidifi- cation (28). Others have suggested that modifications of the airflow delivery pattern, as with continuously auto-adjusting CPAP (29) or bilevel devices capable of varying inspiratory and expiratory levels (9), may also boost adherence in more difficult- to-treat OSA patients. As these earlier reports indicated, there was a general reduction in the mean effective PAP level using BPAP compared to CPAP (3,9). It was therefore thought that bilevel devices might prove to be a benefit for improvement in adherence to PAP in OSA patients. There have been two high-level evidence randomized trials that compared the use of BPAP versus CPAP for OSA patients who were first time users without complicating comorbid medical problems. The first study random- ized 83 OSA patients to receive either CPAP or BPAP with a primary endpoint of adherence based on mean machine timer hours of CPAP (30). A total of 62 patients were evaluated and followed for one year and of these, 26 received BPAP and 36 CPAP pressures. The groups did not differ for BPAP versus CPAP by age (48 ± 1 years vs. 46 ± 1 years) or BMI (40 ± 1 kg/m 2 vs. 39 ± 1 kg/m 2 ), but were different by gender (65.5% vs. 52.8% males). Over the 12-month period, the mean machine timer hours of CPAP versus bilevel therapy were not different at 5.0 ± 0.19 (SEM) versus 4.9 ± 0.23 hours per night. There was also no difference between high and low hourly users for the CPAP or BPAP pressures required during therapy. These patients had similar percentages of time that the machine was running at the pre- scribed effective pressure at 80% in the CPAP group and 82% in the BPAP users with both groups reporting an equal number of complaints with respect to mask discom- fort, machine noise, and nasal stuffiness. The second high-level evidence trial studied newly diagnosed OSA patients without coexisting daytime respiratory disease and compared CPAP with a bilevel device that also employed a prototype flow feature of the presently available Bi-Flex ® device (Respironics, Inc., Murrysville, Pennsylvania, U.S.) (31). The primary endpoint was the percentage of nights with at least four hours of use and hours of 130 Gay use per night after 30 days treatment. This was based on objective machine- determined measurement of time at effective pressure beginning after diagnosis and titration by split-night polysomnography (PSG) in a sleep laboratory. There were no significant baseline group differences for the 27 adults (22 men) in age, BMI, AHI (mean ± SD, CPAP vs. BPAP group of 46.1 ± 23.1 events/hour vs. 41.8 ± 25.8 events/hour, respectively), CPAP requirement, or scores on the Epworth sleepi- ness scale and Functional Outcomes of Sleep Questionnaire. The percentage of nights with ≥ 4 hours/night use was high in both groups but was not significantly different (CPAP vs. BPAP = 80.5 ± 24% vs. 77.6 ± 24.8%). In both of these studies, the BPAP appeared to be as effective as CPAP for the treatment of OSA but offered no advantages in patients receiving first-time therapy for OSA. A randomized controlled trial published in 2005 investigated whether BPAP with Bi-Flex could prove valuable in patients who were considered nonadherent to CPAP therapy (32). The unique design had two phases that first attempted to improve adherence to a treatment threshold of four hours per night of CPAP. There were 204 adult patients diagnosed with OSA (AHI ≥ 10) by PSG within 24 months who had been titrated to an optimal CPAP level but were not able to adhere to regular CPAP use (nonresponders) at a mean treatment time of 254 ± 333 (SD) days. Patients were questioned about various complaints and these were addressed with a systematic conventional intervention program including further education, CPAP desensitization as needed, alternative mask or resizing, and heated humidification. After two more weeks of CPAP therapy there were 24% (49 patients) who became responders (≥ 4 hours/night), 76% (155 patients) who were still nonresponders or who withdrew. The nonresponders who agreed to proceed on to phase 2 then had a full-night PSG retitration and blinded randomization to either CPAP or Bi-Flex for three months. In the 104 patients initiating the trial, there were no significant differ- ences in baseline characteristics of the Bi-Flex versus CPAP groups for age (51.9 ± 11.3 years vs. 52.5 ± 11.3 years), sex (65% vs. 72% males), BMI (33.4 ± 7.9 kg/m 2 vs. 32.5 ± 6.3 kg/m 2 ), and AHI (40.4 ± 23.4 events/hour vs. 44.0 ± 26.1 events/hour). At three months, there was a trend to a higher success rate with Bi-Flex versus CPAP treatment (49% vs. 28.3% of patients using PAP therapy > 4 hours/night; p < 0.05) but the overall success rate for either PAP treatment was low at near 40%. The authors found no strong clinical predictors to distinguish patients in either arm who become adherent (responders) after conventional intervention techniques and concluded that sleep specialists must be very aggressive at achieving initial CPAP adherence as subsequent efforts to achieve optimal adherence to PAP therapy are less fruitful but consideration could be given to repeat PSG and use of alternative modes of flow delivery to further encourage patients to use PAP treatment. COMPLEX SLEEP APNEA Central and obstructive apneas may occur in the same individual, either simultane- ously within a single breath as a mixed apnea, or as sequential breathing events (33). The majority of OSA patients can be expected to respond favorably to CPAP but CPAP often initially exaggerates central sleep apnea (CSA) and some patients identified as having OSA, develop frequent central apneas and/or Cheyne-Stokes respiratory (CSR) pattern after application of CPAP. This is an increasingly recog- nized but not new clinical problem encountered when patients with significant OSA develop CSA when exposed to CPAP (34,35). These patients that develop new or very prominent CSA during CPAP titration are now referred to as complex sleep Bilevel Pressure and Adaptive Servo-Ventilation 131 apnea (CompSA) and from a consecutive series of 133 patients referred to a sleep lab for OSA, 34 (25.6%) proved to have CompSA (36). In this study, the mean age (near 55 years) and total diagnostic AHI (near 30 events/hour) were similar between the groups but there were a few distinguishing features between the patients with OSA versus CompSA. The CompSA patients were more likely to be males (82.4% vs. 63.9%; p = 0.03) and the OSA patients tended to be slightly heavier (36 ± 10.3 kg/m 2 vs. 33 ± 5.9 kg/m 2 ; p < 0.03). By definition, CompSA patients had a significantly higher AHI during a standard CPAP titration (CompSA vs. OSA AHI on CPAP = 24.6 ± 21.6 events/hour vs. 2.1 ± 2.7 events/hour; p < 0.0001) with most or all the residual difference related to the central apneas that emerged on CPAP (19.4 ± 19.0 vs. 2.1 ± 2.7 central events/hour; p < 0.0001). In a different investigation selecting patients who were chosen to undergo BPAP for a variety of reasons, many patients showed a CompSA like response to BPAP (rarely was a backup rate added) but it was not possible to discern an incidence estimate from the data provided (37). Treatment of Complex Sleep Apnea with Bilevel Positive Airway Pressure Vs. Adaptive Servo-Ventilation BPAP and ASV have been shown to improve SDB in patients with CSA (38). The best approach for treatment of CompSA patients remains unclear but one study pursued this issue comparing the response for both BPAP and the newly approved VPAP Adapt™, Adapt Servo Ventilator or ASV (ResMed, Poway, CA) (39). This study investi- gated 21 adult patients (95% male) with CSA/CSR mixed apnea or CompSA who had previously undergone diagnostic PSG and titration with PAP in a randomized cross- over design. Patients with a diagnostic AHI = 54.7 ± 23.8 events/hour, mean age and BMI of 65 ± 12.4 (SD) years and 31.0 ± 4.9 kg/m 2 , respectively, were randomly assigned initially to either BPAP or ASV during two full-night PSG studies. Following previously attempted optimal titration with CPAP, the CompSA patients (n = 15) had a mean AHI > 30 but with either BPAP or ASV the AHI improved markedly from baseline to 6.2 ± 7.6 events/hour or 0.8 ± 2.4 events/hour, respectively. The treatment arms were different; however based on the preselected endpoints of the AHI and respiratory arousal index proving to be significantly superior for ASV (p < 0.02). The authors concluded that both BPAP and ASV seem to be effective in the acute setting for treat- ment of SDB in patients with CompSA and far more efficacious than CPAP alone but the CompSA patients seemed to respond optimally to ASV. A classic example of a CompSA patient response at baseline, treated with CPAP, and then the improvement with ASV can been seen in Figures 3 to 5, respectively. REIMBURSEMENT CRITERIA The delivery of appropriate treatment for any condition may at times become prob- lematic if coverage criteria are not met or are not well-documented for the individual patient. This is especially true in the world of SDB for Medicare patients with respect to PAP therapy. There are separate criteria specifically for BPAP or in Center for Medicare and Medicaid (CMS) vernacular, respiratory assist devices. The coverage criteria are divided into four categories but two of these related to patients with either neuromuscular or chronic obstructive lung disease are not pertinent for this chapter. The specifics can be obtained from any regional durable medical equipment regional carrier (DMERC) web site (40). The new regulations released in March 2006 and retroactive to January 1, 2006 recognize two basic pathways for BPAP treatment 132 Gay coverage. The simplest avenue to BPAP is for OSA patients who have a “facility-based” diagnostic PSG and meet criteria for CPAP treatment; yet, CPAP “has been tried and proven ineffective.” Although this is nonspecific, it can be utilized if the patient has tried CPAP and is intolerant, nonadherent to CPAP, or it does not satisfy the thera- peutic goals. A BPAP device without a backup rate (E0470) can be prescribed and covered under these circumstances. The patients with CompSA can obtain BPAP with a backup rate (E0471 and ASV is considered an equivalent device) through the same pathway as the patients with CSA. This approach also requires a diagnostic PSG and failure with CPAP titration with a primary diagnosis of CSA or CompSA which the DMERC web sites specifically define as: “Complex sleep apnea (CompSA) is a form of central apnea specifically iden- tified by the persistence or emergence of central apneas or hypopneas upon exposure to CPAP (E0601) or an E0470 device once obstructive events have disappeared. These patients have predominately obstructive or mixed apneas during the diag- nostic sleep study occurring at greater than or equal to five times per hour. With use of a CPAP or E0470, they show a pattern of apneas and hypopneas that meets the definition of CSA described earlier.” Central apnea is precisely defined as: 1. An AHI greater than five, 2. Central apneas/hypopneas greater than 50% of the total apneas/hypopneas, 3. Central apneas or hypopneas greater than or equal to 5 times per hour, and 4. Symptoms of either excessive sleepiness or disrupted sleep. FIGURE 3 A two-minute epoch during Stage 2 sleep with frequent episodes of obstructive apnea and oxygen desaturation. Incidental periodic limb movements are also noted in leg electromyogram channel. Abbreviations: ABD, abdominal plethysmogram; C4-A1, right central-left reference EEG; CZ-OZ, midline central-occipital EEG; ECG, electrocardiogram; EEG, electroencephalogram; EMG, electro- myogram; FZ-CZ, midline frontal-central EEG; HR, heart rate; LOC and ROC, left and right outer canthi (eye movements), respectively; Nasal P, nasal pressure via transducer; RC, rib cage plethysmogram; Sono, sonogram (snoring intensity); SpO 2 , oxygen saturation; Sum, plethysmogram summed signal. Bilevel Pressure and Adaptive Servo-Ventilation 133 The last complicating feature regarding reimbursement is that patients must be followed up and proven adherent with the PAP treatment at least four hours per night between 61 and 90 days after initiation. The whole process demands that formal documentation be readily available for patients and although exact follow-up guidelines are not otherwise provided in any literature, some formal and regular follow-up is generally accepted as good clinical practice (23). CONCLUSIONS This chapter reviewed the rationale for the design of BPAP to treat patients with SDB primarily due to OSA and additional clinical recommendations from evidence review and practice parameter paper were published in 2006 (23,41). Even though there have been no comparative studies to determine the optimal titration protocol, a few titration techniques were discussed above. There was no evidence found that BPAP improves efficacy or adherence to therapy in OSA patients who are first-time PAP users but studies did at least support equivalency of CPAP and BPAP. There was also no evidence available to support the practice of BPAP use at an arbitrary higher level of CPAP pressure during a routine titration of OSA patients. There may be some role for BPAP treatment in patients who have struggled with CPAP but there is limited data. Special considerations are also needed for patients with mixed apnea or CompSA who respond poorly to CPAP and it seems most appropriate to FIGURE 4 Another two-minute epoch during non-rapid eye movement stage 2 sleep now with 10 cm H 2 O of continuous positive airway pressure applied. Note the exaggerated periodic breathing with central apnea pattern now predominating. Abbreviations: ABD, abdominal plethysmogram; C4-A1, right central-left reference EEG; CZ-OZ, midline central-occipital EEG; ECG, electrocardio- gram; EEG, electroencephalogram; EMG, electromyogram; FZ-CZ, midline frontal-central EEG; HR, heart rate; LOC and ROC, left and right outer canthi (eye movements), respectively; Nasal P, nasal pressure via transducer; RC, rib cage plethysmogram; Sono, sonogram (snoring intensity); SpO 2 , oxygen saturation; Sum, plethysmogram summed signal; VEST, estimated flow from device. 134 Gay consider treatment with BPAP with a backup rate or an ASV device. It is important to know and document coverage criteria so that the information is available to enable proper reimbursement and some formal follow-up program is encouraged. Lastly, future research should be performed to pursue ways to verify the efficacy and treatment adherence benefits with BPAP or ASV in patients with CSA or CompSA especially over the long term. REFERENCES 1. Gastaut H, Tassinari A, Duron B. Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestations of the Pickwickian syndrome. Brain Res 1966; 2:167. 2. Martin RJ, Pennock BE, Orr WC, et al. Respiratory mechanics and timing during sleep in occlusive sleep apnea. J Appl Physiol 1980; 48(3):432–437. 3. Sanders MH, Moore SE. Inspiratory and expiratory partitioning of airway resistance during sleep in patients with sleep apnea. Am Rev Respir Dis 1983; 127(5):554–558. FIGURE 5 This 180-second epoch shows the patient stabilized in non-rapid eye movement stage 2 sleep now using the Adaptive Servo Ventilator (ASV) device. Note the subtle alterations in the ASV pressure (P) as the abdominal excursion is reduced or increased. The ASV P falls during increased abdominal effort and vice versa to create a more uniform breathing pattern. Abbreviations: ABD, abdominal plethysmogram; ASV P, mask pressure from ASV device; C4-A1, right central-left reference EEG; CZ-OZ, midline central-occipital EEG; ECG, electrocardiogram; EEG, electroencephalogram; EMG, electromyogram; Fpz-Cz, midline fronto-parietal-central EEG; HR, heart rate; LOC and ROC, left and right outer canthi (eye movements), respectively; Nasal P, nasal pressure via transducer; RC, rib cage plethysmogram; Sono, sonogram (snoring intensity); SaO 2 , oxygen saturation; SUM, plethysmogram summed signal; VEST, estimated flow from device. Bilevel Pressure and Adaptive Servo-Ventilation 135 4. Remmers JE, Bartlett D. Reflex control of expiratory airflow and duration. J Appl Physiol 1977; 42:80–87. 5. Malhotra A, White DP. Obstructive sleep apnoea. Lancet 2002; 360:237–245. 6. Schwab RJ, Pasirstein M, Pierson R, et al. Identification of upper airway anatomic risk factors for obstructive sleep apnea with volumetric magnetic resonance imaging. Am J Respir Crit Care Med 2003; 168(5):522–530. 7. Juhasz J, Becker H, Cassel W, et al. Proportional positive airway pressure: a new concept to treat obstructive sleep apnoea. Eur Respir J 2001; 17(3):467–473. 8. Farré R, Peslin R, Montserrat JM, et al. Flow-dependent positive airway pressure to maintain airway patency in sleep apnea–hypopnea syndrome. Am J Respir Crit Care Med 1998; 157:1855–1863. 9. Sanders MH, Kern N. Obstructive sleep apnea treated by independently adjusted inspira- tory and expiratory positive airway pressures via nasal mask. Physiologic and clinical implications. Chest 1990; 98(2):317–324. 10. Gugger M, Vock P. Effect of reduced expiratory pressure on pharyngeal size during nasal positive airway pressure in patients with sleep apnoea: evaluation by continuous com- puted tomography. Thorax 1992; 47(10):809–813. 11. Resta O, Guido P, Picca V, et al. The role of the expiratory phase in obstructive sleep apnoea. Respir Med 1999; 93(3):190–195. 12. Bureau MP, Series F. Comparison of two in-laboratory titration methods to determine effective pressure levels in patients with obstructive sleep apnoea. Thorax 2000; 55:741–745. 13. Lopata M, Onal E. Mass loading, sleep apnea, and the pathogenesis of obesity hypo- ventilation. Am Rev Respir Dis 1982; 126(4):640–645. 14. Schafer H, Ewig S, Hasper E, et al. Failure of CPAP therapy in obstructive sleep apnoea syndrome: predictive factors and treatment with bilevel-positive airway pressure. Respir Med 1998; 92(2):208–215. 15. Pankow W, Hijjeh N, Schuttler F, et al. Influence of noninvasive positive pressure ventilation on inspiratory muscle activity in obese subjects. Eur Respir J 1997; 10(12):2847–2852. 16. Piper AJ, Sullivan CE. Effects of short-term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia. Chest 1994; 105:434–440. 17. Waldhorn RE. Nocturnal nasal intermittent positive pressure ventilation with bi-level positive airway pressure (BiPAP) in respiratory failure. Chest 1992; 101:516–521. 18. Laursen SB, Dreijer B, Hemmingsen C, et al. Bi-level positive airway pressure treatment of obstructive sleep apnoea syndrome. Respiration 1998; 65:114–119. 19. Resta O, Guido P, Picca V, et al. Prescription of nCPAP and nBIPAP in obstructive sleep apnoea syndrome: Italian experience in 105 subjects. A prospective two centre study. Respir Med 1998; 92(6):820–827. 20. Resta O, Foschino-Barbaro MP, Bonfitto P, et al. Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea. Respir Med 2000; 94(3):240–246. 21. Engelman HM, Kingshott RN, Wraith PK, et al. Randomized placebo-controlled crossover trial of continuous positive airway pressure for mild sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med 1999; 159:461–467. 22. Jenkinson C, Davies RJ, Mullins R, et al. Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomized prospective parallel trial. Lancet 1999; 353:2100–2105. 23. Gay PC, Weaver T, Loube D, et al. Evaluation of positive airway pressure treatment for sleep related breathing disorders in adults. Sleep 2006; 29(3):381–401. 24. Berry RB. Improving CPAP compliance-man more than machine. Sleep Med 2000; 1:175–178. 25. Weaver TE, Kribbs NB, Pack AI, et al. Night-to-night variability in CPAP use over the first three months of treatment. Sleep 1997; 20:278–283. 26. Hoy CJ, Vennelle M, Kingshott RN, et al. Can intensive support improve continuous positive airway pressure use in patients with sleep apnea/hypopnea syndrome? Am J Respir Crit Care Med 1999; 159:1096–1100. 27. Chervin RD, Theut S, Bassetti C, et al. Compliance with nasal CPAP can be improved by simple interventions. Sleep 1997; 20:284–289. 136 Gay 28. Massie CA, Hart RW, Peralez K, et al. Effects of humidification on nasal symptoms and compliance in sleep apnea patients using continuous positive airway pressure. Chest 1999; 116:403–408. 29. Berry RB, Parish JM, Hartse KM. The use of auto-titrating continuous positive airway pressure for treatment of adult obstructive sleep apnea. An American Academy of Sleep Medicine review. Sleep 2002; 25:148–173. 30. Reeves-Hoche MK, Hudgel DW, Meck R, et al. Continuous versus bilevel positive airway pressure for obstructive sleep apnea. Am J Respir Crit Care Med 1995; 151:443–449. 31. Gay PC, Herold DL, Olson EJ. A randomized, double-blind clinical trial comparing con- tinuous positive airway pressure with a novel bilevel pressure system for treatment of obstructive sleep apnea syndrome. Sleep 2003; 26:864–869. 32. Ballard R, Gay PC, Strollo PJ. Interventions to improve compliance in sleep apnea patients previously non-compliant with continuous positive airway pressure. Accepted Chest 2007. 33. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999; 22:667–689. 34. Thomas RJ, Terzano MG, Parrino L, et al. Obstructive sleep-disordered breathing with a dominant cyclic alternating pattern—a recognizable polysomnographic variant with practical clinical implications. Sleep 2004; 27:229–234. 35. Gilmartin GS, Daly RW, Thomas RJ. Recognition and management of complex sleep-dis- ordered breathing. Curr Opin Pulm Med 2005; 11:485–493. 36. Pusalavidyasagar SS, Olson EJ, Gay PC, et al. Treatment of complex sleep apnea syndrome: a retrospective comparative review. Sleep Med 2006; 7(6):474–479. 37. Johnson KG, Johnson DC. Bilevel positive airway pressure worsens central apneas during sleep. Chest 2005; 128:2141–2150. 38. Teschler H, Dohring J, Wang YM, et al. Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med 2001; 164(4):614–619. 39. Morgenthaler TI, Gay PC, Brown LK. Adaptive servo-ventilation versus noninvasive positive pressure ventilation for central and complex sleep apnea syndromes. Sleep 2007; in press. 40. http://www.palmettogba.com/palmetto/providers.nsf/$$ViewTemplate+for+ Docs?ReadForm&Providers/DMERC/Publications/DMEPOS+Supplier+Manual/Current 41. Standards of Practice Committee of the American Academy of Sleep Medicine. Kushida CA, Littner MR, Hirshkowitz M, et al. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breath- ing disorders. Sleep 2006; 29(3):375–380. [...]... versus standard continuous positive airway pressure for the treatment of obstructive sleep apnea: results of a meta-analysis: Sleep 20 04; 27: 249 –253 34 Rolfe I, Olson LG, Sanders NA Long-term acceptance of continuous positive airway pressure in obstructive sleep apnea Am Rev Respir Dis 1991; 144 :1130–1133 35 Series F, Marc I Importance of sleep stage and body position dependence of sleep apnea in determining... Marc I, Series F Efficacy of auto-CPAP in the treatment of obstructive sleep apnea/ hypopnea syndrome Am J Respir Crit Care Med 1996; 153:7 94 798 26 Hudgel DW, Fung C A long-term randomized, cross-over comparison of auto-titrating and standard nasal continuous airway pressure Sleep 2000; 23: 645 – 648 27 Massie CA, McArdle N, Hart RW, et al Comparison between automatic and fixed positive airway pressure... for treatment of obstructive sleep apnea Sleep 1999; 22:1095–1097 14 Teschler H, Berthon-Jones M, Thompson AB, et al Automated continuous positive airway pressure titration for obstructive sleep apnea syndrome Am J Respir Crit Care Med 1996; 1 54: 7 34 740 15 Teschler H, Farhat AA, Exner V, et al AutoSet nasal CPAP titration: Constancy of pressure, compliance, and effectiveness at 8 months follow-up Eur... 116 :40 3 40 8 40 Marrone O, Resta O, Salvaggio A, Giliberti T, Stefan A, Insalaco G Preference for fixed or automatic CPAP in patients with obstructive sleep apnea Sleep Med 20 04; 5: 247 –251 41 Randerath W, Galetke W, Ruehle KH Auto-adjusting CPAP based on impedance versus bilevel pressure in difficult to treat sleep apnea syndrome: a prospective randomized crossover study Med Sci Monit 2003; 9:CR353–358 42 ... a given brand of device is essential to benefit from the stored information As with any type of PAP treatment, close follow-up of objective adherence and outcome measures such as subjective sleepiness is essential Auto-Positive Airway Pressure 149 REFERENCES 1 Berry RB, Parish JM, Hartse KM The use of auto-titrating CPAP for treatment of adults with obstructive sleep apnea Sleep 2002; 25: 148 –173 2... Unattended home diagnosis and treatment of obstructive sleep apnea without polysomnography Arch Fam Med 2000; 9:168–1 74 21 Masa JF, Jimenez A, Duran J, et al Alternative methods of titrating continuous positive airway pressure Am J Respir Crit Care Med 20 04; 170:1218–12 24 22 Miljeteig H, Hoffstein V Determinants of continuous positive airway pressure for treatment of obstructive sleep apnea Am Rev Respir... Hirshkowitz M, Davila D, et al Standards of Practice Committee of the American Academy of Sleep Medicine Practice parameters for the use of auto-titrating continuous airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome An American Academy of Sleep Medicine Report Sleep 2002; 15(25): 143 – 147 3 Teschler H, Berthon-Jones M Intelligent CPAP systems:... compliance, and acceptance Am J Respir Crit Care Med 2001; 163:652–657 31 Planès C, d’Ortho M, Foucher A, et al Efficacy and cost of home-initiated auto-nCPAP versus conventional nCPAP Sleep 2003; 26:156–160 32 Hukins C Comparative study of autotitrating and fixed-pressure CPAP in the home: a randomized, single-blind crossover trial Sleep 20 04; 27:1512–1517 33 Ayas NT, Patel SR, Malhotra A, et al Auto-titrating... with obstructive sleep apnea Am J Respir Crit Care Med 1997; 155:199–2 04 7 Farré R, Montserrat JM, Rigau J, Trepat X, Pinto P, Navajas D Response of automatic continuous positive pressure devices to different sleep breathing patterns Am J Respir Crit Care Med 2002; 166 :46 9 47 3 8 Abdenbi F, Chambille B, Escourrou P Bench testing of auto-adjusting positive airway pressure devices Eur Respir J 20 04; 24: 649 –658... difference in death and heart transplantation in the CPAP-treated group ( 64) It is important to note that 1 54 Leibowitz and Aloia although adherence with CPAP was fairly high in this trial, hours of use in the treatment group was between 3.5 and 4 hours/night and the average AHI after treatment was 19 events per hour Despite many shortcomings of this study, the results demonstrate the complexities and barriers . 1997; 10(12):2 847 –2852. 16. Piper AJ, Sullivan CE. Effects of short-term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia. Chest 19 94; 105 :43 4 44 0. 17. Waldhorn. occlusive sleep apnea. J Appl Physiol 1980; 48 (3) :43 2 43 7. 3. Sanders MH, Moore SE. Inspiratory and expiratory partitioning of airway resistance during sleep in patients with sleep apnea. Am. obesity hypo- ventilation. Am Rev Respir Dis 1982; 126 (4) : 640 – 645 . 14. Schafer H, Ewig S, Hasper E, et al. Failure of CPAP therapy in obstructive sleep apnoea syndrome: predictive factors and treatment

Ngày đăng: 10/08/2014, 18:21

Từ khóa liên quan

Tài liệu cùng người dùng

Tài liệu liên quan