Acceptance of CPAP Therapy for Sleep Apnea

Acceptance of CPAP Therapy for Sleep Apnea

Acceptance of CPAP Therapy for Sleep Apnea* Helmuth Rauscher M. D.; Wolfgang Popp, M. D.; Theodor Wanke, M. D.; and Hartmut Zwick M.D., F.C.C.R Althou...

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Acceptance of CPAP Therapy for Sleep Apnea* Helmuth Rauscher M. D.; Wolfgang Popp, M. D.; Theodor Wanke, M. D.; and Hartmut Zwick M.D., F.C.C.R Although NCPAP is the most efficient nonsurgical treatment for patients with OSA, many patients do not accept sleeping with a nose mask. To determine the factors inOuencing acceptance, treatment with NCPAP was offered to 95 patients with an AHI greater than 15. After the 6rst night on NCPAP, 47 of 65 patients decided to have NCPAP as a home therapy. Excessive daytime sleepiness was more frequently reported by acceptors than re£USers. The frequency of complaints about psychomental symptoms such as poor mental performance and bad memory, was not different between the two groups. There was a close correlation between the rate of acceptance and the AHI as

continuous positive airway pressure was first Nasaldescribed as a treatment for OSA in 1981. 1Since

then, NCPAP has become the first-line therapy for patients with OSA because of effectiveness2.3 and lack of serious side effects. 4 Although technical modifications of the devices have made NCPAP more convenient for patients, 5 acceptance still is the major problem with this therapy;6 even in sleep apnea patients exhibiting daytime sleepiness, cardiopulmonary consequences of OSA or severe nocturnal hypoxemia. Moreover, several studies have shown that even snoring without apneas may be associated with increased morbidity7-10 and daytime sleepiness. l1 Thus, it could be reasonable to prescribe NCPAP also for patients with relatively mild sleep-disordered breathing. Whereas long-term compliance with NCPAP has been extensively studied in patients with full-blown sleep apnea syndrome,12-15 there is little known about the percentage of these patients refusing NCPAP a priori or after the first night and there is even less knowledge about acceptance of NCPAP in patients with rather mild disease. To define the main factors influencing acceptance of NCPA~ we offered this treatment to 95 consecutive patients with an AHI greater than 15 regardless of their clinical symptoms and complaints. METHODS

Of 203 consecutive patients referred to our sleep lab because of suspected OSA, 95 (78 male and 17 female) exhibited an AHI greater than 15 and were included in this study. Subjective complaints and symptoms were recorded by a ques-

·From the Pulmonary Department, Krankenhaus Lainz, Vienna, Austria. Manuscript received November 26; revision accepted February 20. !feptint requests: Dr. Rauscher, Pulmonary Department KrankenhaW LAinz, Wolkersbergenstr 1, Vienna, Austria All30

well as the number of positive answers to questions about symptoms of daytime sleepiness in a questionnaire, which correlated with the number and length of apneas. Acceptance of NCPAP was found to be dependent on the subjective feeling of impairment by hypersomnolence due (Chest 1991; 100:1019-23) to OSA. AHI = apnea plus hypopnea index; A max = longest apnea period; EDS = excessive daytime sleepiness; NCPAP = nasal continuous positive airway pressure; REM rapid eye movement; SaO.m = mean nocturnal SaO.; SaO.m 30= mean oftbe 30 lowest SaO. values during sleep; SaO. min lowest SaO. during sleep; TST = total sleep time

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tionnaire. Questions about EDS were: 1. Do you feel extremely tired during daytime? 2. Do you fall asleep during the day against your will? 3. Do you frequently fall asleep when watching W? 4. Do you frequently fall asleep when reading books or newspapers? 5. Did you ever fall asleep while driving a car? 6. Did you ever fall asleep when talking with others? To determine psychomental impairment we asked: 1. Did your irritability increase during the recent past? 2. Did you notice a decrease in your mental performance? 3. Has your memory worsened? 4. Has it become difficult for you to concentrate on a certain task? 5. Did you experience troubles in comprehension of things you usually understood immediately? 6. Have your reactions to dangerous traffic situations become slower? All patients underwent whole night polysomnographic examination including continuous registration of EEG, EOG, submental EMG, ECG, airflow at the nose and mouth (thermistors), movements of rib cage and abdomen (Respitrace, Ambulatory monitoring, Ardsley, NY) and Sa02 from the ear (Novametrix 505). Sleep staging was done according to standard criteria. 16 Apneas were defined as cessation ofairflow at the nose and mouth for longer than 10 s. Hypopneas were defined as a reduction in rib cage and abdominal movements to 50 percent or less compared with the preceding five breaths for longer than 10 s accompanied by a fall in Sa02 to 92 percent or lower if baseline was equal to or above 94 percent or a fall in Sa02 of 3 percent or more if baseline was 93 percent or lower. The total number of apneas and hypopneas per hour of sleep represented the AHI. After the diagnostic study night, all patients with an AHI greater than 15 were informed by the same physician in the same manner about the nature and consequences ofOSA. The NCPAP was offered as the most efficient mode of treatment for their disease. Although the counselling physician was not blinded to the results of the study night, he tried to present necessity and value of treatment without taldng into account the results of the polysomnographic study by explaining the same written text to each patient. Alternative forms of treatment were offered only if the patient refused to try NCPAP after solely looking at the device or fixing the mask for the first time. If the patients agreed to try NCPA~ treatment was initiated during a further night of polysomnography. The NCPAP device used was the Sleep Easy II (Respironics, Inc). Until sleep onset, mask pressure was set to 3 cm H 20. With the occurrence ofapneas, this pressure was increased in steps of 1 em HIO every 10 min until CHEST I 100 I 4 I OCTOBER, 1991

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Table 1-Poly.omnographic Beaulta from 47 OSA Ibtienta Accepeing and 48 OSA Ebtienta Rsju.mg NCPAP (Median:t SEM) Probability

Polysomnographic Results

Acceptors

Refusers

TST(h) Awakenings REM (%TSlj NREM 3+4 (% TSlj AHI A max (s) SaOlm (%) SaOlmin (%) Sa01m3O (%)

6.2 ± 0.5 (2.8-8.1) 3.1 ±0.2 (2-11) 10.5±2.6 (4.2-16) 3.9 ± 1.6 (1.4-9.9) 52.5±7.5 (17.6-86.5) 50±4.3 (12-140) 9O.7±0.8 (79-96.9) 62 ± 4.9 (34-88) 72.6 ± 2.6 (48.5-91.6)

6.1±0.7 (3-7.5) 3.5±0.4 (1-9) 14.3±3.2 (3.5-17.8) 4.7 ± 1.8 (1.8-8.6) 27.7± 1.3 (15.6-76.6) 3O±2.9 (10-75) 92.5 ± 0.6 (72-98.1) 78± 1.2 (36-93) 84.3± 1.2 (46.2-95.6)

obstructive apneas as well as snoring disappeared. Patients not sure about accepting NCPAP as a home therapy after the first night were offered up to three further nights to become accustomed to the device. Patients accepting NCPAP after the first night continued treatment at home. Results are given as medians and standard error of the median. To determine statistical differences between acceptors and refusers, the Kolmogoroff-Smirnoff test and contingency table analysis were used. Correlations between polysomnographic parameters and results from the questionnaire were calculated by Spearman·s rank test. A probability value less than 0.05 was considered statistically significant. RESULTS

Out of 95 consecutive patients with an AHI greater than 15 events per hour of sleep, 65 agreed to have a night of trial on NCPAP (68 percent). Of the 30 refusers who did not even try NCPA~ 13 underwent uvulopalatopharyngoplas~ the others decided to reduce body weight or to have no treatment at all. The 13 refusers undergoing uvulopalatopharyngoplasty reported heavy snoring as their main complaint and only four of them reported falling asleep involuntaril~ However, 8 of the remaining 17 refusers who decided to not even have a night of trial on NCPAP nor any other therapy aside weight loss reported this symptom. After the first night on NCPA~ 47 of the 65 patients accepted this treatment for home therapy (72 percent). The remaining 18 patients tried NCPAP for one to three further nights, but none of them decided to continue treatment at home. Thus, an acceptance rate of50 percent was found when offering NCPAP therapy to unselected patients with an AHI greater than 15. Reasons for noncompliance after the first night of usage were difficulties in falling asleep with NCPAP on (15 of 18 [83 percent]), frequent nocturnal awakenings (7 of 18 [39 percent]) and discomfort caused by the mask (5 of 18 [28 percent]). Acceptors (n = 47) and refusers (n = 48) did not differ in age (51.6±2.4 years; range, 33 to 69.1 years vs 5O.1±1.4 years; range, 29.6 to 67.9 years; NS), sex distribution (40 male, 7 female vs 38 male, 10 female; NS) and daytime POi corrected according to Mays'17 diagram (72.7 ± 1.8 mm Hg; range, 54.7 to 91 mm Hg vs 72± 1.6 mm Hg; range, 44.4 to 92.1 mm Hg; NS). There was also no difference in body weight between 1020

Value

NS NS p
the two groups, the Broca index (= weight in kilograms X 100lheight in centimeters - 100) being I32'.8±7.8 (range, 101 to 210) for the acceptors and 129.4 ± 9.8 (range, 85 to 259) for the refusers. Acceptors had more and longer apneas and hypopneas per hour of sleep, lower mean nocturnal Sa02 values and more pronounced desaturations (Table 1). There was no difference in TST and the number of awakenings during the first study night between acceptors and refusers, but the latter had slightly less disturbed sleep architecture. Analysis of symptoms reported in the questionnaire revealed more complaints about EDS in acceptors than in refusers (Table 2). However, the subjective impression of sleep disturbance as well as difficulties in concentration, comprehension and memory were not different between the two groups. There was a close correlation between the rate of acceptance and the AHI (Fig 1). Similarl~ the rate of acceptance increased with the number of positive answers to questions about symptoms of EDS in the questionnaire (Fig 2). Acceptance was not influenced Table I-Subjective Complainta in Ibtienta with OSA Accepting NCPAP (n=47) and Ibtienta &fuaing NCPAP (n = 48)

Subjective Complaints Feeling tired Falling asleep involuntarily Falling asleep while Watching1V

Reading Driving

11illdng

Increased irritability Poor mental perfonnance Bad memory Difficulties in concentration Difficulties in comprehension Slow reactions when driving

Refusers (%)

Probability Value

39 (83)

23 (48) 22 (46)

p
41 33 16 12 17 28 24 19

(87) (70) (34) (26) (36) (60) (51) (40)

30 24 6 5 21 25 24 23

p
2

(4)

Acceptors (If,)

35 (75)

5 (11)

(63) (50) (13) (10) (44) (52) (50) (48)

8 (17)

NS

(6)

NS

3

CPAP Therapy for Sleep Apnea (Rauscher et 81)

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APNEA PLUS HVPOPNEA INDEX

FIGURE 1. In8uence of the AUI on the acceptance rate of NCPAP therapy in 95 unselected OSA patients.

by the number of positive answers to questions about psychomental symptoms (Fig 3). The number of positive answers to questions about EDS was positively correlated with the number (r=0.218; p
This study shows that acceptance of NCPAP therapy parallels severity of OSA. On the one hand, the rate of acceptance was higher the more and longer apneas occurred during sleep. On the other hand, acceptance increased with the degree that the subject felt impaired by EDS. Obstructive sleep apnea is associated with increased morbidity and mortalityl8-23 due to cardiovascular diseases and accidents,24.25 and even snoring has been 188

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FIGURE 3. Correlation between the number of positive answers to questions about psychomental symptoms ofOSAand the acceptance rate of NCPAP therapy.

suggested as a risk factor for arterial hypertension and cardiac disorders. 7' lo Therefore, the logical consequence would be to recommend NCPAP also in OSA patients with rather mild disease. However, as shown in this study, such a therapeutic approach would result in a high rate of refusers to NCPAP. Out of 40 patients with an AHI between 15 and 30, only 11 (28 percent) accepted this treatment, and of the 29 refusers in this group, 22 did not even try it (76 percent). This points out the therapeutic dilemma with "silent" sleep apnea, ie, with patients referred to a sleep lab by their bed partners because ofloud snoring and witnessed apneas, but being themselves unaware of the disease due to the lack of symptoms. On the other end of the scale are patients undergoing a sleep study because of daytime sleepiness. Ofthe 19 patients with the highest number of positive answers to questions about EDS in the questionnaire, 16 (84 percent) accepted NCPAP. Only for patients with severe OSA, the AHI appeared to be a predictor of acceptance, since 19 out of 21 patients (95 percent) with an AHI greater than 60 agreed to use NCPAP at home. The high rate of acceptance in sleepy patients can be explained by the rapid disappearance of EDS with NCPAP therapy. 12.26 Since sleepiness recurs after short periods of noncompliance with treatment, patients accepting NCPAP once show a high rate of long-tenn compliance. I 3-15.27 However, it has been shown that long-tenn compliance with NCPAP correlates only with the degree of subjective improvement. 26 Thus, the possible benefit from achieving primary acceptance of NCPAP in asymptomatic patients-if at all possible-remains to be established. The main reasons for noncompliance with NCPAP after the first night of treatment were difficulties initiating and maintaining sleep with NCPAP on, even in patients with daytime hypersomnolence. This hapCHEST I 100 I .. I OCTOBER. 1991

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pened despite the fact that the pressure applied until sleep onset was very low and was increased very slowly with the appearance of apneas. Since most patients who did not accept NCPAP after the first night had difficulties falling asleep with the pressure necessary to abolish apneas, they also refused to accept this treatment after additional nights oftrial. Initiation of NCPAP therapy was re-tried in five of the refusers 8 to 14 months after the first study: Although the AHI for these patients was between 21 and 52, they still did not feel impaired by hypersomnolence and none of them accepted NCPAP therapy after this further night of trial. In accordance with the finding that the degree of EDS mainly depends on nocturnal sleep structure and not on oxygenation during sleep,29 the number of positive answers to questions about symptoms of EDS in the questionnaire correlated only with the number and length of apneas and hypopneas, but not with polysomnographic parameters indicating nocturnal oxygenation. Since we did not perform objective measurements of alertness, eg, multiple sleep latency tests, we are unable to say that the acceptors were really sleepier than the refusers, but can only say that they felt sleepier. Surprisingl~ complaints about psychomental symptoms due to OSA were found to be of no influence on the rate of acceptance of NCPAE Although our method of correlating acceptance only with the number of positive answers in the questionnaire does not permit a description of the objective differences in impairment due to OSA between acceptors and refusers, this approach seems to reHect the true reasons for the patients· decision for or against NCPA~ which obviously is based on the subjective impression of impairment and not on' the results of tests. We cannot exclude the fact that the lower rate of acceptance in patients with less severe sleep apnea might have been caused by some subtle bias due to the counselling physician's presentation ofthe need for treatment being less urgent in those patients. However, every attempt was made to control for such an inHuence. Expense as a reason for refusing NCPAP was of no influence because according to the health care system in our country the patients were only charged for the study nights at a fee of about $5.00 a night and the cost for the NCPAP device in case of acceptance were entirely refunded by the patient's health insurance. In summary, acceptance of NCPAP was found to be dependent on the degree of subjective impairment by daytime sleepiness due to OSA. Since the number and length of respiratory events during sleep correlated positively with acceptance, initiating NCPAP in patients with rather mild sleep-disordered breathing was very seldom successful. Furthermore, from our 1022

results further nights of trial in patients who do not tolerate NCPAP during the first night appear to be useless. REFERENCES 1 Sullivan CE, Berthon-Jones M, Issa FG, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1981; 1:862-65 2 Sanders MH, Moore SE, Eveslage J. CPAP via nasal mask: a treatment for obstructive sleep apnea. Chest 1983; 83:144-45 3 Berry RB, Block AJ. Positive nasal airway pressure eliminates snoring as well as sleep apnea. Chest 1984; 85:15-20 4 Nino-Murcia G, Crowe-McCann C, Bliwise DL, Guilleminault C, Dement WC. Compliance and side effects in sleep apnea patients tested with nasal continuous positive airway pressure. West J Moo 1989; 150:165-69 5 Crowe-McCann C, Nino-Murcia G, Guilleminault C. Nasal CPAP: The Stanford experience. In: Guilleminault C, Partinen M, eds. Obstructive sleep apnea syndrome: clinical research and treatment. New York: Raven Press, 1990; 119-27 6 Wagner DR, Pollack C~ Weitzman ED. Nocturnal nasal-airway pressure for sleep apnea. N Eng} J Med 1983; 308:461-62 7 Koskenvuo M, Kaprio J, Partinen M, Langinvainio H, Sarna S, Heikkila K. Snoring as a risk factor for hypertension and angina pectoris. Lancet 1985; 1:893-95 8 Norton PG, Dunn E~ Snoring as a risk factor for disease: an epidemiological survey. Br Med J 1985; 291:630-32 9 Koskenvuo M, Kaprio J, Telakivi T, Partinen M, Heikkila K, Sarna S. Snoring as a risk factor for ischemic heart disease and stroke in men. Br Med J 1987; 294:16-19 10 Gislason T, Aberg H, Taube A. Snoring and systemic hypertension-an epidemiological stud~ Acta Med Scand 1987; 222: 415-21 11 Gould GA, Whyte KF, Rhind GB, Airlie MA, Catterall JR, Shapiro CM, et ale The sleep hypopnea syndrome. Am Rev Respir Dis 1988; 137:895-98 12 Sullivan CE, Issa FG, Berthon-Jones M, McCauley JB, Costas L~ Home treatment of obstructive apnoea with continuous positive pressure applied through a nosemask. Bull Eur Physiopathol Respir 1984; 20:49-54 13 McEvoy RD, Thornton AT. Treatment ofobstructive sleep apnea syndrome with nasal continuous positive airway pressure. Sleep 1984; 7:313-25 14 Frith RW Severe obstructive sleep apnoea treated with long term nasal continuous positive airway pressure. Thorax 1985; 40:45-50 15 Sanders MH, Gruendl CA, Rogers RM. Patient compliance with nasal CPAP therapy for sleep apnea. Chest 1986; 90:330-33 16 RechtschafFen A, Kales A. A manual ofstandardized terminology techniques and scoring systems for sleep stages of human subjects. Washington, DC: National Institute of Health, 1968, publication no. 204 17 Mays EE. An arterial blood gas diagram for clinical use. Chest 1973; 63:793-800 18 Fletcher EC, DeBehnke RD, Lovoi MS, Gorin AG. Undiagnosed sleep apnea in patients with essential hypertension. Ann Intern Moo 1985; 103:190-95 19 WilliamsAJ, Houston D, FinbergS, LamC, KinneyJL, Santiago S. Sleep apnea syndrome and essential hypertension. Am J Cardioll985; 55:1019-22 20 Gonzalez-Rothi RJ, Foresman GE, Block AJ. Do patients with sleep apnea die in their sleep? Chest 1988; 94:531-38 21 Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients. Chest 1988; 94: 1200-04 22 He J, Kryger MH, Zorick FJ, Conway ~ Roth T. Mortality and CPAP Therapy for Sleep Apnea (Rauscher st 81)

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apnea index in obstructive sleep apnea: experience in 385 male patients. Chest 1988; 94:9-14 Partinen M, Guilleminault C. Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest 1990; 97:27-32 George C, Nickerson ~ Hanly ~ Millar T, Kryger M. Sleep apnea patients have more automobile accidents (Letter). Lancet 1987; 1(8556):447 Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988; 138:337-40 Rajagopal KR, Bennett LL, Dillard TA, Tellis CJ, Tenholder

MF. Overnight nasal CPAP improves hypersomnolence in sleep apnea. Chest 1986; 90:172-76 27 Krieger J, Kurtz D. Objective measurement ofcompliance with nasalCPAP treatment for obstructive sleep apnea syndrome. Eur Respir J 1988; 1:436-38 28 Fletcher JG, Luckett RM, Fletcher EC, Hine M. Reinforcement of compliance with nasal CPAP in obstructive sleep apnea. Eur Respir J 1989; 2:782s 29 Guilleminatilt C, Partinen M, Quera-Salva MA, Hayes B, Dement WC, Nino-Murcia G. Determinants of daytime sleepiness in obstructive sleep apnea. Chest 1988; 94:32-37

Plan to Attend ACCP's

57th Annual Scientific Assembly San Francisco November 4-8, 1991

CHEST I 100 I 4 I OCTOBER, 1991

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