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Long-term compliance to continuous positive airway pressure (CPAP) therapy


 

Table of Contents
  Learning Objectives
What is Continuous Positive Airway Pressure (CPAP)?
Obstructive Sleep Apnea-Hypopnea Syndrome
Long-term Compliance Rates to CPAP in Obstructive Sleep Apnea
Patient Compliance
Compliance with CPAP therapy in older men with obstructive sleep apnea
Effects of Augmented CPAP Education and Support on Compliance and Outcome in a Chinese Population
Can patients with OSA titrate their own continuous positive airway pressure?
Taking a Bite Out of SDB
The Results of CPAP therapy under two adherence schedules
Long-term compliance rates to CPAP in OSA: a population-based study
Compliance with CPAP therapy: assessing and improving treatment outcomes
Determinants of compliance with nasal CPAP treatment applied in a community setting
Glossary of Sleep-Related Terms
Post-Test

 


Learning Objectives

Upon successful completion of this course, you will be able to:

  • Define and discuss CPAP
  • Explain what is meant by "compliance" in the context of CPAP treatment
  • Discuss why compliance is so important
  • List and discuss the factors that affect compliance rates
  • Identify the actions that caregivers can take to increase patient compliance

This course presents you with a variety of readings from a variety of viewpoints regarding the issues associated with patient compliance with their CPAP instructions.

 


What is Continuous Positive Airway Pressure (CPAP)?

Snoring Problems

Forty-five percent of normal adults snore at least occasionally, and 25 percent are habitual snorers. Problem snoring is more frequent in males and overweight persons and it usually grows worse with age. Snoring sounds are caused when there is an obstruction to the free flow of air through the passages at the back of the mouth and nose.

Only recently have the adverse medical effects of snoring and its association with Obstructive Sleep Apnea (OSA) and Upper Airway Resistance Syndrome (UARS) been recognized. Various methods are used to alleviate snoring and/or OSA. They include behavior modification, sleep positioning, Continuous Positive Airway Pressure (CPAP), Uvulopalatopharyngoplasty (UPPP), and Laser Assisted Uvula Palatoplasty (LAUP), and jaw adjustment techniques.

What Is Continuous Positive Airway Pressure (CPAP)?

Nasal CPAP delivers air into your airway through a specially designed nasal mask or pillows. The mask does not breathe for you; the flow of air creates enough pressure when you inhale to keep your airway open. CPAP is considered the most effective nonsurgical treatment for the alleviation of snoring and obstructive sleep apnea.

If your otolaryngologist determines that the CPAP treatment is right for you, you will be required to wear the nasal mask every night. During this treatment, you may have to undertake a significant change in lifestyle. That change could consist of losing weight, quitting smoking, or adopting a new exercise regimen.

Before the invention of the nasal CPAP, a recommended course of action for a patient with sleep apnea or habitual snoring was a tracheostomy, or creating a temporary opening in the windpipe. The CPAP treatment has been found to be nearly 100 percent effective in eliminating sleep apnea and snoring when used correctly and will eliminate the necessity of a surgical procedure.

So, If I Use A Nasal CPAP I Will Never Need Surgery?

With the exception of some patients with severe nasal obstruction, CPAP has been found to be nearly 100 percent effective, although it does not cure the problem. However, studies have shown that long-term compliance in wearing the nasal CPAP is about 70 percent.

Some people have found the device to be claustrophobic or have difficulty using it when traveling. If you find that you cannot wear a nasal CPAP each night, a surgical solution might be necessary. Your otolaryngologist will advise you of the best course of action.

Should You Consider CPAP?

If you have significant sleep apnea, you may be a prime for CPAP. Your otolaryngologist will evaluate you and ask the following questions:

  • Do you snore loudly and disturb your family and friends?
  • Do you have daytime sleepiness?
  • Do you wake up frequently in the middle of the night?
  • Do you have frequent episodes of obstructed breathing during sleep?
  • Do you have morning headaches or tiredness?

Suitability for CPAP use is determined after a review of your medical history, lifestyle factors (alcohol and tobacco intake as well as exercise), cardiovascular condition, and current medications. You will also receive a physical and otorhinolaryngological (ear, nose, and throat) examination to evaluate your airway.

Before receiving the nasal mask, you would need to have the proper CPAP pressure set during a "sleep study." This will complete the evaluation necessary for prescribing the appropriate treatment for your needs.

What is compliance anyway? And Why is CPAP Compliance Important?

Compliance simply means that a patient is carrying out a prescribed treatment plan exactly as directed. In most cases, this will mean that their condition, disorder or disease is cured, or under control. The treatment plan can be as simple as taking medications or as complicated as doing physical therapy. In the case of OSA (Obstructive Sleep Apnea), it means proper use of a CPAP machine on a regular basis.

When patients don't comply with treatment, the consequences can be very negative for the patient. The patient continues suffering from the complex of OSA symptoms and complications that can include fatigue, confusion, falling asleep at inappropriate times and decreased productivity. Many fatal and non-fatal victims of stroke and heart attack may have avoided death or disability, if their OSA had been diagnosed and treated prior to the occurrence of the catastrophic event. Furthermore, individuals with OSA at the moderate to severe level are 4.5 times as likely to have coronary heart disease, myocardial infarction, and angina as are those without sleep apnea. On the other hand, we have seen patients whose hypertension and Congestive Heart Failure (CHF) were completely reversed by successful treatment of their severe OSA.

Multiple factors influence compliance

We are convinced beyond the shadow of a doubt from our experience that treatment compliance and its associated benefits rise dramatically with high quality patient training, education, communication and follow up. A great example from a different area of medicine is diabetes. It has been repeatedly demonstrated that when well educated, informed patients comply with treatment, and proactively manage their condition, the incidence of secondary complications is dramatically reduced or eliminated. This results in higher quality of life for the patient, less visits to the physician over time, and reduced cost to treat these patients.

While CPAP compliance is difficult to track, several studies indicate that it is influenced by a variety of factors. These include; severity of the disease, quality of patient training and education, initial success/problems, participation in a support group, mask-related comfort and claustrophobia, follow-up and monitoring by health care professionals, patient motivation, use of humidification, treatment reactions, and patient age. One of the reasons for SleepQuest's successful compliance rate is that our high-quality training, education, and long term monitoring identify these problem early and address them immediately, before they have a chance to affect the patients' motivation and treatment success.

A little knowledge goes a long way

There are some simple yet effective guidelines that can help you achieve high compliance and treatment success. 1) Be proactive and learn as much as you can about OSA and your particular machine. 2) Follow your doctor's instructions exactly and use the machine on a regular basis. Often, the difference between using the CPAP occasionally and on a regular basis is dramatic. 3) If you encounter any problems at any time in your treatment, work with your doctor or CPAP health care specialist to resolve them.

CPAP compliance works!

The bottom line is that when patients use their machines on a regular basis, their condition is managed, they get the sleep that they need which means they're not suffering from daytime fatigue, and worrying about work performance. You can get back to doing what is really important - getting on with your life.

 


Obstructive Sleep Apnea-Hypopnea Syndrome

ERIC J. OLSON, MD; WENDY R. MOORE, RN; TIMOTHY I. MORGENTHALER, MD; PETER C. GAY, MD; BRUCE A. STAATS, MDFrom the Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine and Internal Medicine, Mayo Clinic, Rochester, Minn.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repetitive episodes of airflow reduction (hypopnea) or cessation (apnea) due to upper airway collapse during sleep. Increasing recognition and a greater understanding of the scope of this condition have substantially affected the practices of many clinicians. This review provides practical information for physicians assessing patients with OSAHS. It discusses complications, clinical recognition, the polysomnographic report, and treatment of OSAHS, including strategies for troubleshooting problems associated with continuous positive airway pressure therapy.

AASM = American Academy of Sleep Medicine; AHI = apnea-hypopnea index; BMI = body mass index; CMS = Centers for Medicare and Medicaid Services; CPAP = continuous positive airway pressure; NREM = non-rapid eye movement; OSAHS = obstructive sleep apnea-hypopnea syndrome; REM = rapid eye movement; RERA = respiratory effort-related arousal; UARS = upper airway resistance syndrome

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repetitive episodes of airflow reduction due to pharyngeal narrowing, leading to acute gas exchange abnormalities and sleep fragmentation and resulting in neurobehavioral and cardiovascular consequences. During sleep, critical narrowing of the upper airway occurs behind the uvula and soft palate, at the base of the tongue, or at both sites; it develops because of a dysfunctional interplay of anatomical factors and compensatory neuromuscular mechanisms insufficient to maintain airway patency. Obstructive sleep apnea-hypopnea syndrome may be considered part of a spectrum of sleep-related breathing disorders that includes the upper airway resistance syndrome (UARS) and primary snoring. Upper airway resistance syndrome is characterized by hypersomnolence caused by recurrent respiratory effort–related arousals (RERAs)1 without overt apneas or hypopneas. Snoring is the sound of pharyngeal vibration triggered by airflow turbulence across a narrowed upper airway and when present without affecting respiration or the patient’s sleep quality is termed primary snoring.

Because of a greater appreciation of the ramifications of OSAHS, clinicians are more aware of this syndrome, and the demand for sleep medicine services has accelerated. During the past decade, the number of sleep centers accredited by the American Academy of Sleep Medicine (AASM) and the number of sleep specialists credentialed by the American Board of Sleep Medicine have increased by approximately 300%. Despite such growth in the sleep medicine enterprise, waiting lists at sleep disorders centers are long, and the vast majority of patients remain undiagnosed.2 The increasing prevalence of obesity3 and a better understanding of the link between OSAHS and cardiovascular disease4 will substantially affect the health care delivery system.

CONSEQUENCES OF OSAHS

Neurobehavioral and Social

Excessive daytime sleepiness, impaired vigilance, mood disturbances, and cognitive dysfunction are features of OSAHS. Accordingly, pretreatment personal and public health ramifications include increased risk for motor vehicle crashes, occupational injuries, and decreased quality of life.5 Performance deficits during neuropsychological testing can be documented with even mild OSAHS. With a frequency of 15 apneas-hypopneas per hour of sleep, the decrement is equivalent to that associated with 5 years of aging.6 Vulnerability to sleepiness resulting from OSAHS varies considerably among patients. Partners of patients with OSAHS experience poor sleep,7 and often it is the partner who prompts the sleep evaluation, seeking relief from loud snoring and disturbing apneas.

Cardiovascular

An OSAHS-hypertension link has been suspected for years because of clinical observations and biologic plausibility. The intermittent hypoxia, negative intrathoracic pressure variations, and arousals characteristic of apneas and hypopneas lead to acute increases in blood pressure at the termination of disordered breathing events, evolving into sustained hypertension via chronically heightened sympathetic nervous system activity and arterial baroreceptor dysfunction.4 The strongest evidentiary association comes from the Wisconsin Sleep Cohort Study, an ongoing study of state employees undergoing serial in-laboratory polysomnography, which has shown a dose-dependent link between apnea-hypopnea frequency at baseline and the development of hypertension at follow-up.8 For a baseline apnea-hypopnea frequency of 15/h, the odds ratio for hypertension at 4 years was 2.89 (95% confidence interval, 1.46-5.64) vs zero events per hour, after adjusting for known confounding variables. Hypertension in the setting of OSAHS may be more difficult to treat. Sleep apnea is listed first in the table of identifiable causes of hypertension in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.9 Data on the effect of OSAHS treatment on blood pressure are mixed; some intervention studies show a positive effect.5

TABLE 1. DIFFERENTIAL DIAGNOSIS OF THE SLEEPY PATIENT

Too little time in bed  
Insufficient sleep syndrome  
Impaired sleep quality  
Obstructive sleep apnea-hypopnea syndrome  
Upper airway resistance syndrome  
Central sleep apnea syndrome  
Restless legs syndrome-periodic movement disorder  
Intrinsic sleepiness  
Narcolepsy  
Idiopathic hypersomnia  
Recurrent hypersomnia  
Irregular timing of sleep-wake pattern  
Shift work sleep disorder  
Delayed-advanced sleep phase syndrome  
Time zone change (jet lag) syndrome  
Medical-psychiatric comorbidity  
Cardiopulmonary disease  
Mood disorders  
Alcoholism  
Medications  

Large population-based studies have associated OSAHS with cardiovascular and cerebrovascular disease, and retrospective data indicate untreated OSAHS is associated with increased mortality. The Sleep Heart Health Study has shown cross-sectional, dose-dependent associations between OSAHS and vascular disease.10 More than 6000 subjects from multiple longitudinal cardiovascular cohorts were studied with in-home polysomnography. For those in the highest quartile of apnea-hypopnea frequency (=11/h), the multivariable adjusted odds of self-reported cardiovascular disease was 1.42 (95% confidence interval, 1.13-1.78) with the strongest links to heart failure and stroke.10 Although a skeptical person might conclude that the association of OSAHS with cardiovascular disease is modest, it is seen within a range of apnea-hypopnea frequencies (5-15 events per hour) that occur in 1 of every 15 adults.5 Prospective data indicating that OSAHS treatment positively affects cardiovascular morbidity or mortality are minimal; however, a recent study showed that optimal treatment of heart failure could not be achieved until OSAHS was eliminated.11

Perioperative and Postoperative

Patients with OSAHS may have an increased perioperative risk, but data quantifying the risk are limited. In such patients, endotracheal intubation may be more difficult, and forced supine sleep positioning and analgesics can result in upper airway narrowing postoperatively. A retrospective study of 101 patients who underwent hip or knee replacement and who had or were later found to have OSAHS vs 101 age-, sex-, and operation-matched controls found that the percentage of patients with complications was higher (39% in the OSAHS group vs 18% in the control group) and hospital stay was longer (6.8±2.8 vs 5.1±4.1 days) in the OSAHS group.12 Only 12 of 33 patients who were using continuous positive airway pressure (CPAP) therapy at home preoperatively were prescribed CPAP therapy in the hospital postoperatively and before the development of complications, and only 3 patients had planned to use CPAP therapy in the postanesthesia recovery area.

RECOGNITION OF OSAHS

History and Physical Examination

The history focuses on breathing disturbances during sleep, unsatisfactory sleep quality, daytime dysfunction, and OSAHS risk factors. A collateral history should be obtained from the patient’s bed partner. Reports of habitual, socially disruptive snoring and witnessed apneas terminated by snorts or gasps increase diagnostic accuracy. Sleepiness lacks diagnostic sensitivity and specificity (Table 1). The onset of sleepiness may be so insidious that the patient is unaware of its development, and the symptom is more commonly due to chronic insufficient time in bed in the general population. Obstructive sleep apnea-hypopnea syndrome is 2 to 3 times more prevalent in men.13 This sex-protective effect is diminished in premenopausal overweight women (body mass index [BMI] =32 kg/m2), menopausal women not receiving hormone replacement therapy, and overweight women receiving hormone replacement therapy.13 Prevalence appears to plateau after age 65 years.14 Other risk factors may include smoking, alcohol, and nasal congestion.5

The physical examination focuses on craniofacial and soft tissue conditions associated with increased upper airway resistance, such as retrognathia, deviated nasal septum, low-lying soft palate, enlarged uvula, and base of tongue. The preponderance of evidence suggests a causal role for obesity (BMI >28 kg/m2) in OSAHS.5 Neck circumference of 43 cm or greater tends to make the retropharyngeal space shallow and has been highly correlated with OSAHS.15 After controlling for BMI and neck circumference, tonsillar enlargement (defined as lateral impingement >50% of the posterior pharyngeal airspace) and narrowing of the airway by the lateral pharyngeal walls (defined as impingement >25% of the pharyngeal space by peritonsillar tissues, excluding the tonsils) are also predictive of OSAHS.15 Because OSAHS is not considered capable of causing severe increases in right heart pressures without a comorbid condition producing persistent hypoxemia,16 severe pulmonary hypertension should prompt investigation for coexisting disorders.

Prediction Models

The cardinal features of OSAHS—namely, snoring and excessive sleepiness—are highly prevalent in the general population. Nearly 40% of outpatients in a survey of urban primary care practices reported clinical characteristics (BMI >30 kg/m2, hypertension, snoring, sleepiness, and tiredness) that suggested OSAHS17; however, the estimated prevalence of undiagnosed OSAHS is 5% in the middle-aged population.5 Prediction models based on various combinations of symptoms, demographics, and anthropometric parameters have been proposed to help clinicians determine the probability of OSAHS. Four clinical prediction models applied prospectively to a large group of patients referred for OSAHS evaluation performed equivalently and without distinction (sensitivities, >75%; specificities, <55%; positive predictive values, 69%-77%).18 There is no consensus on the optimal prediction formula, and such models have not been widely used in clinical practice.

Pulse Oximetry

Obstructive apneas and hypopneas result in repetitive “sawtooth” oscillations in the oxyhemoglobin saturation on a time-compressed profile. Published sensitivities and sensitivities vary widely because of nonstandardized oximetry data sampling and study populations. For diagnosing OSAHS, pulse oximetry is not considered a singularly sufficient alternative to polysomnography. The utility of pulse oximetry may lie at the extremes of the OSAHS spectrum.19 If clinical suspicion for OSAHS is high, pulse oximetry may help triage the timing of polysomnography when entry to a sleep center is delayed. If clinical suspicion is low, normal study findings effectively exclude OSAHS. However, RERAs are not detectable by pulse oximetry because arousals occur before ventilation or oxyhemoglobin saturation is compromised. Therefore, sleepy patients with normal findings on oximetry require further evaluation.

LABORATORY DIAGNOSIS OF OSAHS

The diagnosis of OSAHS is based on an integration of clinical information and laboratory testing. The recommended diagnostic test for sleep-related breathing disorders is polysomnography.20 The standard polysomnogram is a laboratory-based, technician-attended multimodality recording of sleep architecture by electroencephalography, electro-oculography, and electromyography; respiratory activity by nasal and oral airflow or pressure, thoracoabdominal inductance plethysmography, and oximetry; electrocardiography; limb movements by lower extremity electromyography; and body position. Adjunctive measures may include a sound meter to detect snoring, endtidal carbon dioxide determination when OSAHS is being investigated in children, and, rarely, esophageal pressure monitoring if RERAs or central sleep apnea is suspected.

Definitions of Disordered-Breathing Events

Obstructive apneas and hypopneas are characterized by repetitive periods of complete (apnea) or partial (hypopnea) airflow reduction. The event must be at least 10 seconds in duration in association with respiratory efforts, and it usually ends with arousal from sleep.1 Identification of hypopnea also requires an accompanying decrease in oxyhemoglobin saturation. The requisite desaturation is controversial, although hypopnea criteria from both the Clinical Practice Review Committee of the AASM21 and the Centers for Medicare and Medicaid Services (CMS) stipulate a decrease in oxyhemoglobin saturation of 4% or greater. An RERA is a series of breaths occurring for at least 10 seconds associated with an ever-increasing respiratory effort against a narrowed upper airway that terminates with arousal from sleep before criteria for a true apnea or hypopnea event are met.1 With esophageal pressure monitoring, RERAs are marked by progressively negative esophageal pressure deflections (reflecting increasing work of breathing) during the breaths immediately preceding an arousal. Upper airway resistance syndrome is the condition of excessive sleepiness associated with 10 or more RERAs per hour.22

Reviewing the Polysomnographic Results

The principal factor for the clinician to note is the apnea-hypopnea index (AHI), defined as the number of apneas and hypopneas per hour of sleep. A similar but not necessarily equivalent term is the respiratory disturbance index. The respiratory disturbance index may be used to report the number of apneas and hypopneas per hour of recording in limited study montages that do not measure sleep. Furthermore, the respiratory disturbance index may be used by some sleep laboratories to report the number of apneas, hypopneas, and RERAs per hour of sleep. By consensus, OSAHS is defined by an AHI of 5 or greater with evidence of unsatisfying or disturbed sleep, daytime sleepiness, or other daytime symptoms or when the AHI is 15 or higher. The AHI specific for sleep position (lateral decubitus vs supine) and sleep stage (non–rapid eye movement [NREM] vs rapid eye movement [REM]) may be reported separately because of potential therapeutic implications. An AASM expert panel has recommended that, at least for purposes of standardizing research methodology, mild OSAHS be defined by an AHI of 5 to 14, moderate by an AHI of 15 to 30, and severe by an AHI greater than 30.1

Other polysomnographic factors help reveal the extent of physiologic perturbations caused by OSAHS. The arousal index, defined as the number of arousals per hour of sleep (normal, <20/h), is increased by apneas, hypopneas, and/or RERAs. Sleep architecture figures often reveal increases in stage 1 NREM (normal, 5% of sleep) and decreases in stage 3/4 NREM (normal, 15%-20% in young adults; decreases with age) and REM (normal, 20%). The depth of desaturation by oximetry depends on the duration of the apneas-hypopneas and the underlying lung function. Pronounced ventricular ectopy in patients with OSAHS is uncommon unless oxyhemoglobin desaturation is severe or underlying heart disease is present.23

Other Diagnostic Test Strategies

Numerous efforts have been made to modify standard polysomnography because it is cumbersome for patients, labor intensive, and difficult to access in many laboratories. One strategy that has been validated is split night polysomnography—the initial diagnostic portion is followed on the same night by CPAP titration.20 A variety of more limited diagnostic monitoring systems, some designed for unattended home use, are being used. The role for these systems remains uncertain. The CMS mandates that, for CPAP reimbursement purposes, the diagnosis of OSAHS must be established by a facility-based (not in the home or mobile facility) polysomnogram and that the AHI be based on at least 120 minutes of sleep. Nonetheless, technological advances and access pressures predict further efforts to tailor the extent of diagnostic testing to the pretest probability of OSAHS.

TREATMENT OF OSAHS

Obstructive sleep apnea-hypopnea syndrome is a chronic disease that requires patient education, alleviation of upper airway obstruction, and ongoing follow-up with adjustment of treatment strategies to ensure efficacy. Because many patients with OSAHS are overweight or have comorbid cardiovascular risk factors or diseases, they must be informed of the interaction of OSAHS and overall health. Prospective data on the cardiovascular and perioperative benefits of OSAHS treatment are emerging, but the current, most widely accepted patient and physician treatment target is hypersomnolence.24

Conservative Maneuvers

In many patients, lifestyle modifications will decrease both the symptoms of OSAHS and the comorbid conditions.25 Lifestyle changes include weight loss, alcohol-sedative avoidance, smoking cessation, avoidance of sleep deprivation, and, if appropriate, sleep position restriction. Longitudinal data from the Wisconsin Sleep Cohort Study indicate that a 10% weight loss predicts a 26% decrease in the AHI.26
Continuous Positive Airway Pressure

The decision to treat OSAHS usually means a trial use of CPAP, a device that pneumatically splints the upper airway during inspiration and expiration. A placebo-controlled, randomized trial24 showed that CPAP decreases sleepiness and increases quality of life. During polysomnography, CPAP is titrated to a level that eliminates snoring, RERAs, and apneas-hypopneas and is then most often prescribed at a “fixed” level, typically at the pressure necessary to maintain airway patency during conditions of greatest vulnerability (REM sleep while supine). For most patients, the prescribed pressure is in the 7- to 11-cm H2O range. CPAP systems consist of a blower connected to a nasal interface by a flexible 180-cm hose, all weighing approximately 2.2 kg and transportable in a soft-sided case. Criteria from CMS for reimbursement for CPAP are an AHI of 15 or greater or an AHI of 5 to 14 with documented symptoms of excessive sleepiness, impaired cognition, mood disorders, or insomnia; or documented hypertension or ischemic heart disease; or history of stroke.

Monitoring and Optimizing the CPAP Experience

Follow-up of a patient should occur shortly after initiation of CPAP therapy and annually thereafter.27 The following 5 questions, posed annually or at times of change in health status, should enable clinicians to assess their patients using CPAP.

  1. What interferes with your use of CPAP?
  2. Are you sleepy during the day?
  3. Does your bed partner observe snoring or breathing pauses when you use CPAP?
  4. How has your weight changed since CPAP therapy was initially prescribed or last adjusted?
  5. When was the last time your CPAP equipment was assessed?

Usage patterns and problems with CPAP vary among patients. The minimum effective CPAP use time is unknown, but improvements in objective daytime sleepiness have been shown when average use is less than 4 hours per night.28 Nightly vs intermittent (suboptimal compliance) CPAP use patterns may be established within the first several weeks to a month,29 highlighting the importance of early support. An important component is patient education.30 The patient (and partner) must understand the importance of treating OSAHS, how CPAP works and why it was chosen, and the specific features of the CPAP equipment. Patient characteristics that consistently predict CPAP compliance have not been identified. Only a few comprehensive, long-term compliance studies have been published,31,32 and they indicate that continuing CPAP use generally correlates with AHI severity, average nightly use of fewer than 2 hours at 3 months predicts failure, and ongoing use at 5 years is 65% to 90%. Many units now have downloadable compliance monitoring capability.

The most commonly encountered problems with CPAP therapy and suggested interventions, admittedly more experience based than evidence based, are listed in Table 2. Tolerating the prescribed pressure is a common hurdle at the outset. Clinicians can remind their patients to use the CPAP ramp, a feature on all new machines that allows a gradual increase in the pressure from a base of 3 to 4 cm H2O to the prescribed level at 5 to 45 minutes. This can be reset at any time.

Autotitrating CPAP devices can be recommended; they are perhaps most useful for patients with marked differences in pressure requirements due to body position or sleep stage. The proprietary systems within these units allow dynamic variations in delivered pressure in response to changes in pharyngeal pressure, airflow, or vibration; therefore, the lowest appropriate pressure can be administered for the given circumstance. These systems provide equivalent positive effects on sleep and breathing factors at lower mean pressures compared with standard CPAP systems and have been shown in some, but not all, studies to produce modest increases in compliance.33 Use of unattended autotitrating devices in CPAP-naive patients to determine a fixed CPAP or to initiate therapy without polysomnography is not currently recommended.34 Conventional35 and novel36 bilevel systems capable of independent adjustment of inspiratory and expiratory pressures are an option but have not been shown in randomized trials to improve compliance.

The basic patient interfaces are nasal masks, oronasal masks, and nasal pillows (Figure 1). Many variations in mask configurations, headgears, and cushioning materials are available. Patients struggling with tightness of masks can be reassured that CPAP blowers will compensate for air leaks if the mask is loosened slightly. Nasal irritation (congestion, dripping, dryness, sneezing) is the most common problem after initial acclimatization to CPAP therapy. Patients can be advised to obtain a heated humidifier or activate one already integrated into many of the newer blowers. Heated humidification has been shown to improve CPAP compliance compared with no added humidity.37 The humidifier reservoir must be emptied and air dried daily, then refilled with fresh distilled water at bedtime.

TABLE 2. TROUBLESHOOTING GUIDE FOR COMMON CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP)-RELATED PROBLEMS

Challenge Solutions  
Difficulty tolerating pressure Have sleep center or vendor evaluate blower to ensure pressure as prescribed
Activate CPAP ramp feature
Wear CPAP device while awake (daily practice)
Lower pressure by 1 to 2 cm H2O*
Return to sleep center for consideration of autoadjusting CPAP or bilevel positive airway pressure therapy

 
Intolerance of interface Loosen mask slightly
Ensure that mask or pillows are situated properly
Rule out interface modification by patient
Return to sleep center or vendor for resizing
Use barrier, such as moleskin or bandage, for bridge of nose irritation
Inspect interface; replace if deteriorated

 
Nasal irritation Use nasal saline spray before bed
Use heated CPAP humidifier
Use nasal corticosteroid spray
Use ipratropium bromide nasal spray if rhinorrhea is present
Ensure that patient is cleaning and air drying CPAP humidifier reservoir daily

 
Claustrophobic response Have sleep center or vendor fit patient with nasal pillows or sleeker mask
Wear CPAP device while awake (daily practice)
Telephone sleep center for support or desensitization plan

 
Difficulty initiating sleep with CPAP Wear CPAP device while awake (daily practice)
Reinforce good sleep hygiene (warm bath before bed, exercise program, decrease caffeine and alcohol use, limit time in bed to 8 h)
Delay bedtime until very sleepy
Prescribe brief sedative-hypnotic trial

 
Dry mouth Add chin strap
Have sleep center or vendor fit patient for oronasal mask
Add CPAP-heated humidifier

 
Removal of CPAP device unintentionally during sleep Reasure patient that this is normal
Assess all other headgear-nasal interface problems, especially nasal congestion
Add humidification
Add chin strap
Lower pressure alarm on blower unit
For severe cases: set alarm at night for patients to check headgear; progressively set alarm later with improvement
 

*Empirical reductions in the level of CPAP to enhance adherence to therapy must be made cautiously because too much of a reduction in pressure may result in reemergence of sleep-disordered breathing events.

Symptoms that persist despite optimal CPAP compliance should prompt reappraisal of the patient. The caregiver should also be ready to investigate the possible presence of a concurrent sleep disorder (Table 1). The differential diagnosis for persistent sleepiness during CPAP therapy includes technical problems (incorrect use of mask, pressure incorrectly set by vendor or improperly altered by patient); pressure not accurately determined during the initial sleep study; prescribed pressure invalidated by patient weight gain or increases in alcohol, sedative, or narcotic use; or a concurrent sleep disorder.

If breakthrough snoring is reported, upper airway obstruction is not fully relieved, and the CPAP level needs upward adjustment, the nasal interface needs replacement or the interface may not be situated properly during sleep. The blower should be assessed at least annually, and the nasal interface should be evaluated and/or replaced every 6 months.

Changes in the patient’s weight or medical condition may require alteration of the treatment plan. Management options in response to weight gain include overnight oximetry with referral to a sleep disorders center if findings are abnormal or an empirical increase of 1 to 2 cm H2O if symptoms of OSAHS have reemerged or oximetry findings are abnormal. Conversely, clinical experience suggests that a 10% weight loss may allow an empirical reduction in pressure by 1 to 2 cm H2O; greater weight loss requires formal reevaluation.

Other Options

Oral appliances have been developed for mechanically enlarging or stabilizing the upper airway by advancing the mandible or tongue. The mandible is usually set forward 5 to 11 mm (50%-75% of maximal protrusion). Subjective improvements in snoring are reported in most case series with oral appliances; approximately 50% of patients achieve an AHI lower than 10, and long-term compliance rates are 50% to 100%.38 Randomized crossover comparisons reveal that CPAP devices are more effective at lowering the AHI39 than oral appliances, which are most appropriate for patients with mild to moderate OSAHS.

Uvulopalatopharyngoplasty, an operation that modifies the retropalatal airway by excision of the uvula, a portion of the soft palate, and tonsils (if present), produces mixed results. Although snoring is usually subjectively improved, objective improvements have not been well documented. Furthermore, less than 50% of patients achieve an apnea index lower than 10 and at least a 50% reduction in apneas.40 Laser-assisted uvulopalatoplasty is not currently recommended for the treatment of OSAHS.41 Radiofrequency ablation techniques can be applied focally to reduce the size of the palate and base of tongue, but efficacy data are limited. Other surgical options include tracheostomy (used rarely) and oral maxillofacial procedures.

CONCLUSION

Even mild OSAHS can be associated with pronounced behavioral, social, and cardiovascular morbidity. Thus, it is not surprising that patients with untreated OSAHS have higher health care utilization rates and incur greater medical costs.42 Further data are needed to define the specific cardiovascular risks of untreated OSAHS and to determine the extent of the impact of treatment. Clinicians should suspect OSAHS in patients with habitually loud snoring; witnessed apneas, choking, or gasping during sleep; hypertension; neck circumferences of 43 cm or greater; obesity; and laterally narrowed oropharynxes. The threshold for initiating a sleep center referral should be lower when 1 or more clinical features are severe, serious comorbidities are present, major surgery is being planned, and/or additional risk factors for OSAHS are identified. Referral efforts should be more vigilant when patient or public safety issues arise, such as with commercial motor vehicle or airplane operation.

The patient with suspected primary snoring should also be considered for further evaluation if careful questioning suggests excessive daytime sleepiness (raising the possibility of UARS) or when occult OSAHS might complicate management of a comorbidity, such as hypertension. Overnight oximetry has little additive diagnostic value in the patient with suspected classic OSAHS. Polysomnography is the recommended approach to assessing patients for apneas, hypopneas, and RERAs and for titrating CPAP. Our understanding of what constitutes a sufficient diagnostic method continues to evolve. The AHI is the traditional marker for OSAHS but may not convey the full physiologic impact of sleep-disordered breathing. CPAP is the treatment of choice for most patients with OSAHS. Heated humidification helps decrease CPAP-associated nasal irritation and is a recommended accessory for most patients in whom CPAP therapy is being initiated. Early follow-up is necessary because use patterns are established within the first month.

Self-Test Questions About OSAHS

  1. Which one of the following is not independently associated with untreated OSAHS?
    a. Systemic hypertension
    b. Stroke
    c. Motor vehicle crash
    d. Excessive daytime sleepiness
    e. Fibromyalgia

  2. Which one of the following statements is false regarding recognition of OSAHS?
    a. Prevalence of OSAHS rises inevitably each year after age 65 years
    b. Snoring and sleepiness are not specific for OSAHS
    c. OSAHS is an underappreciated component of the preoperative evaluation
    d. Neck circumference of 43 cm or greater correlates with OSAHS
    e. Male sex confers a higher risk for OSAHS

  3. Which one of the following statements regarding the diagnosis of sleep-disordered breathing is false?
    a. Polysomnography is the recommended diagnostic test
    b. A sleepy snorer with normal findings on overnight oximetry does not have sleep-disordered breathing
    c. OSAHS is defined by an AHI of 5 or more plus daytime symptoms
    d. RERAs are arousals from sleep due to an ever-increasing breathing effort against a narrowed airway before apnea or hypopnea occurs
    e. UARS is associated with 10 or more RERAs per hour of sleep

  4. Which one of the following statements regarding treatment of OSAHS is false?
    a. CPAP pneumatically splints the upper airway during sleep
    b. CPAP can be administered via nasal masks, nasal prongs, or oronasal masks
    c. Oral appliances are generally less effective in lowering the AHI when compared directly to CPAP devices
    d. The AASM currently recommends laser-assisted uvuloplasty as a treatment option for OSAHS
    e. A 10% weight reduction may translate into a 26% AHI reduction

  5. Which one of the following statements about CPAP is true?
    a. CPAP blowers and masks need to be checked every 2 years
    b. Long-term compliance rates are less than 40%
    c. Heated humidification improves compliance
    d. Autotitrating CPAP devices consistently produce substantially higher increases in patient compliance compared to standard CPAP devices
    e. Standard CPAP devices automatically compensate for changes in patient weight

Correct answers: 1. e, 2. a, 3. b, 4. d, 5. c

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Long-term Compliance Rates to Continuous Positive Airway Pressure in Obstructive Sleep Apnea*

A Population-Based Study

Don D. Sin, MD; Irvin Mayers, MD, FCCP; Godfrey C. W. Man, MBBS, FCCP and Larry Pawluk, MD * From the Departments of Pulmonary Medicine (Drs. Sin, Mayers, and Man) and Psychiatry (Dr. Pawluk), University of Alberta, Edmonton, AB, Canada.

Abstract

Study objectives: To determine long-term compliance rates to continuous positive airway pressure (CPAP) therapy in patients with obstructive sleep apnea enrolled in a comprehensive CPAP program in the community.

Design: Prospective cohort longitudinal study.

Setting: University sleep disorders center.

Patients: Two hundred ninety-six patients with an apnea-hypopnea index (AHI) 20/h on polysomnography.

Interventions: A CPAP device equipped with a monitoring chip was supplied. Within the first week, daily telephone contacts were made. Patients were seen at 2 weeks, 4 weeks, 3 months, and 6 months.

Results: Of the 296 subjects enrolled, 81.1% were males. Mean ± SD AHI was 64.4 ± 34.2/h of sleep; age, 51 ± 11.7 years; and body mass index, 35.2 ± 7.9 kg/m2. The mean duration of CPAP use was 5.7 h/d at 2 weeks, 5.7 h/d at 4 weeks, 5.9 h/d at 3 months, and 5.8 h/d at 6 months. The percentage of patients using CPAP 3.5 h/d was 89.0% at 2 weeks, 86.6% at 4 weeks, 88.6% at 3 months, and 88.5% at 6 months. There was a decrease in the Epworth Sleepiness Scale (ESS) score of 44% by 2 weeks of therapy. The patients continue to improve over the follow-up period, with the lowest mean ESS score observed at 6 months. With multiple regression analysis, three variables were found to be significantly correlated with increased CPAP use: female gender, increasing age, and reduction in ESS score.

Conclusion: A population-based CPAP program consisting of consistent follow-up, "troubleshooting," and regular feedback to both patients and physicians can achieve CPAP compliance rates of > 85% over 6 months.

Key Words: compliance rate • continuous positive airway pressure • obstructive sleep apnea

Introduction

Obstructive sleep apnea (OSA) is a common condition affecting 2% of adult female and 4% of adult male populations,1 and close to 20% of the elderly population.2 OSA results in excess daytime sleepiness and decreased health-related quality of life.3

Continuous positive airway pressure (CPAP) is an effective therapy for OSA, significantly reducing OSA symptoms in a vast majority of cases.4 Successful application of CPAP can dramatically improve the health-related quality of life of patients and transform somnolent individuals into energetic and more productive people.5 Moreover, the use of CPAP can decrease systemic BP and improve cardiovascular performance, thereby decreasing cardiovascular morbidity and mortality associated with OSA.5

However, CPAP therapy is often difficult to tolerate and patients frequently stop using it because of discomfort. The nasal mask interface may cause pressure sores, persistent air leakage, claustrophobia, nasal congestion, and other side effects that may lead to suboptimal compliance.6 One study7 suggests that CPAP compliance might be improved with intensive CPAP support, where these problems can be addressed through a multidisciplinary team approach. However, as these results were produced in a clinical trial setting, it remains uncertain whether high CPAP compliance rates can also be achieved in the community using a similar CPAP program.

Using data from a comprehensive CPAP program implemented in Northern Alberta (population 1.3 million persons) beginning in July of 1999, the aims of this study were to determine:
(1) short-term and long-term CPAP compliance rates in the community,
(2) baseline predictors for long-term CPAP compliance, and
(3) whether CPAP use is associated with sustained improvements in daytime sleepiness in OSA patients with moderate-to-severe disease.

Methods and Materials

General Program Description

This study was conducted at the University of Alberta Hospital (UAH) Sleep Disorders Laboratory, in Edmonton, AB, which is the only accredited sleep facility to conduct supervised polysomnography in Northern Alberta. Funding for the CPAP devices were provided by the Alberta Aids to Daily Living, a government agency that oversees the provision of Respiratory Health Services and respiratory equipment to the citizens of Alberta. Funding was also provided for hiring a dedicated CPAP clinic nurse with the specific role of educating and following these patients on a regular basis.

Recruitment and Consent

Between July 1999 and March 2000, all patients undergoing diagnostic polysomnography at the UAH Sleep Disorders Laboratory were considered as potential recruits for this study. All patients were referred for clinical evaluation of possible sleep disorders.

Patients with an AHI 20/h were considered to be eligible candidates to receive a CPAP device provided by Alberta Aids to Daily Living without any cost to the patient. Some subjects with an AHI < 20/h also received CPAP therapy if there were significant clinical indications for CPAP therapy. All patients receiving CPAP devices were asked to sign a consent form indicating their willingness to comply with CPAP therapy, and their explicit understanding that the CPAP device must be returned if their compliance was deemed unsatisfactory, as measured through a pressure-sensing chip included in each CPAP unit.

Polysomnography

The diagnostic polysomnographic studies were performed at the UAH Sleep Disorders Laboratory. Recordings were performed overnight with continuous monitoring of EEG, electro-oculogram, chin electromyogram, oronasal airflow (by thermistor), chest and abdominal respiratory movements, oximetry, anterior tibialis electromyogram, body position sensor, and snoring noise sensor. Digitized signals were stored on optical disk and analyzed using software (Sandman Elite Version 5.0; Nellcor Puritan Bennett [Melville] Ltd., Ottawa, ON, Canada). Manual scoring was done by trained, certified technologist to verify the automated scoring system in every case. All sleep recordings were verified by American Board of Sleep Medicine-certified sleep specialists who provided descriptive diagnostic interpretation of the polysomnographic studies.

Scoring of sleep staging was done using published criteria.8 An apnea episode was defined as a cessation of oronasal airflow for > 10 s. An hypopnea episode was defined as a diminution of the amplitude of respiratory signals by > 50% for > 10 s, with or without desaturation. An obstructive respiratory event was scored when there was evidence of paradoxical chest and abdomen movement. A central respiratory event was scored when both the chest and abdominal respiratory movements were diminished.

Follow-up Protocol

All CPAP subjects underwent an educational session prior to commencement of CPAP therapy, which included a 26-min video presentation (produced locally by the Sleep Apnea Society of Alberta) and a one-on-one discussion session with a qualified CPAP clinic nurse. The videotape presented information on OSA, including symptoms, health consequences, and pathophysiology, and a detailed explanation on the use of the CPAP device. The key concepts from this videotape was subsequently reinforced by a CPAP nurse who had prior training and experience in polysomnographic studies and in basic respiratory therapy principles relevant to the care of the CPAP devices. Reading materials were given to each subject, with a pamphlet on OSA, CPAP devices, suggestions for troubleshooting and remedies, as well as a follow-up schedule.

Subjects were instructed to contact the CPAP clinic nurse da