Obstructive Sleep Apnea inthe Hospital ized Patient

Peter G. Kallas, MD

KEYWORDS

� Obstructive sleep apnea � Positive airway pressure � Continuous pulse oximetry�

Berlin Questionnaire

HOSPITAL MEDICINE CLINICS CHECKLIST

1. Incorporate sleep apnea questioning into a routine review of systems, and pos-itive airway pressure (PAP) machines into themedication reconciliation process.

2. Continue the patient’s home PAP device while the patient is hospitalized usingeither the patient’s own device or a hospital device set at the patient’s homesettings.

3. Consider continuous pulse oximetry in sleep apnea patients who are chal-lenged medically or surgically:a. Patients undergoing major surgery, especially airway surgeryb. Patients receiving general anesthesia or deep sedationc. Patients requiring high-dose narcoticsd. Patients with a respiratory illness such as pneumonia, congestive heart fail-

ure, or chronic obstructive pulmonary disease exacerbatione. Patients with altered mental status, such as those with delirium or an insult to

the brainf. Patients with altered neuromuscular function, such as poststroke patients or

those with multiple sclerosis exacerbations4. Organize a discharge management plan for those patients who are new to

continuous PAP and do not carry a formal diagnosis.

DEFINITIONS

What is obstructive sleep apnea and how does it differ from central sleep apnea?

Obstructive sleep apnea (OSA) is the pathologic closure of the posterior pharynx duringsleep. Officially it can only be diagnosed using an in-laboratory sleep study called poly-somnography (PSG) or a home sleep study. An apneic episode is defined as a greater

Preoperative Clinic and Inpatient Perioperative Medicine Consult Service, Northwestern Memo-rial Hospital, Northwestern University Feinberg School of Medicine, Northwestern Medical Fac-ulty Foundation, 259 E. Erie, 17th Floor, Chicago, IL 60611, USAE-mail address: pkallas@nmh.org

Hosp Med Clin 4 (2015) 12–22http://dx.doi.org/10.1016/j.ehmc.2014.09.0092211-5943/15/$ – see front matter � 2015 Elsevier Inc. All rights reserved.

Obstructive Sleep Apnea 13

than 90% cessation of air flow for 10 seconds, whereas a hypopneic episode is definedas a 30% decrease in air flow lasting at least 10 seconds and associated with a 4% ox-ygen desaturation.1 The PSG will document vigorous chest wall movement during anapneic episode in OSA, whereas in central sleep apnea a patient will show a completeabsence of any inspiratory effort during an entire period of absent air flow, and iscommonly associated with a pathologic neurologic disorder such as stroke.The severity of OSA is measured using the apnea-hypopnea index (AHI), which re-

flects the number of apneas and hypopneas per hour during the sleep study (Table 1).One qualifies for the diagnosis of OSA if he or she has an AHI of 5 or more, with mildOSA defined as an AHI of 5 to 14, moderate OSA as 15 to 30, and severe OSA greaterthan 30 apneas/hypopneas per hour.

EPIDEMIOLOGY

What is the incidence of OSA in hospitalized patients?

The incidence of OSA in the general population has been estimated to be 2% inwomen and 4% in men.2 However, the hospitalized patient population representsan older, less healthy population, which makes the incidence much higher. Studieshave found the incidence to be as high as 24% to 33%3,4 in the preoperative popula-tion and 60% to 96%5,6 in the acute stroke population. Among 513 consecutive pa-tients screened for OSA on one inpatient cardiology service, 44.1% screened ashigh risk.7 Although most OSA patients remain undiagnosed, with increased aware-ness in the medical community and the general public more patients are arriving athospitals with the diagnosis of OSA who are routinely using continuous positive airwaypressure (CPAP) at home. Despite improved awareness and diagnosis, hospitalsremain ill-equipped to manage what has classically been seen as an outpatient dis-ease. A look at the 2004 National Hospital Discharge Survey found that only 5.8%of patients who carried the diagnosis of OSA were given CPAP while in hospital.8

Much of this is a consequence of an educational gap among the hospital staff, andantiquated hospital policies that inappropriately view home CPAP resumption asacute respiratory failure requiring intensive care monitoring.

HISTORY AND EXAMINATION

What are common symptoms of OSA?

The loud snoring that is generated in OSA patients is produced by the floppy, partiallyobstructed posterior orophayrnx, and tends to reach higher decibels than that pro-duced by the nasopharynx. A study during which the oropharynx of OSA patientswas compared with normal patients, all of whom had general anesthesia and a para-lytic administered, showed that the posterior oropharynx of OSA patients was signif-icantly more narrow and/or collapsible.9 Daytime drowsiness is another common

Table 1Apnea-hypopnea index (AHI)

AHI Degree of OSA

5–14 Mild

15–30 Moderate

>30 Severe

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symptom, and often indicates more severe disease. If either loud snoring and/or day-time drowsiness occur together or in combination with hypertension or obesity(defined as a body mass index [BMI] >30 kg/m2), the likelihood of the patient havingOSA is very high. The Berlin Questionnaire, created in 1996 and validated severaltimes in the outpatient setting and preoperatively, combines these 4 indicators (loudsnoring, daytime drowsiness, hypertension, obesity) into a simple, patient-drivenscreening tool that can even be used in hospitalized patients (Appendix 1).4,10

What are common physical findings in patients with OSA?

OSA patients tend to have what is commonly described as a crowded airway. In theanesthesia literature theairway isclassified intoMallampati classes,11 asshown inFig.1.The neck circumference tends to be larger in OSA patients than in the average pop-

ulation, typically larger than 40 cm. Although BMI plays a critical role in OSA pathol-ogy, the disease is not limited to the obese. Airway structure (eg, large tongue,receded jaw) and age are independent issues that also predispose patients to OSA.OSA patients will often be drowsy during the physician interview and can even fallasleep during questioning, a clear indication of severe disease. Lastly, resistant hyper-tension has been linked to OSA through mechanisms stemming from elevated adren-ergic tone and endothelin activation from repeated hypoxic episodes.12

DIAGNOSIS

What is the role for inpatient sleep study evaluation?

Sleep studies have classically been an outpatient test performed in sleep laboratoriesstaffed by sleep specialists who are trained in sleep disorders after pulmonary,

Fig. 1. Mallampati classification. (Courtesy of Christine Gralapp, MA, CMI, San Francisco, CA.)

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neurology, or psychiatry training. Although portable sleep studies are now availableand are recognized by the Center for Medicare Services, only rarely are sleep studiesperformed in the hospital setting. A continuous pulse oximeter can be used to docu-ment sleeping desaturations in the hospital; if there is correction on waking, one canfeel relatively confident that a patient has sleep apnea13 but cannot differentiate be-tween central and OSA in this manner (Fig. 2).Unfortunately, if CPAP is introduced to a patient for the first time during a hospital-

ization, it is often difficult to continue CPAP at home without a formal sleep study,because of insurance and Medicare rules. Often, however, companies that providedurable medical equipment are willing to loan CPAP machines to patients ondischarge while they wait for a formal sleep study to be performed. Unfortunately,this remains a dangerous gap in the clinical care of these patients.

COMPLICATIONS

What are the major respiratory complications in hospitalized patients with OSA?

Much of the literature pertaining to inpatient complications related to OSA comes fromthe postoperative arena, although it is logical to assume that patients on the medicalwards face similar challenges. Respiratory failure is the most feared complication inthese patients, but the incidence of death is low. A retrospective look at one institu-tion’s medical records over a 6-year span (87,650 anesthesia cases) found 32(0.038%) incidents of postoperative inpatients with sudden, life-threatening respira-tory events while receiving high-dose analgesia14; 37.5% carried the diagnosis ofOSA and 2 of the 4 who died had OSA. Compared with a matched cohort, the patientswith severe respiratory compromise required fewer narcotics, and the events were notassociated with a narcotic bolus or dose stacking. In a small perioperative study at aninstitution that routinely follows a strict postoperative narcotic protocol, 22 childrenunderwent home pulse oximetry before a surgical procedure.15 The study foundthat those children desaturating to less than 85% while sleeping at home required

Fig. 2. Example of pulse oximeter tracing. (From Auckland District Health Board. Starshipchildren’s health clinical guideline. Oximetry. Available at: http://www.adhb.govt.nz/starshipclinicalguidelines/Oximetry.htm. Accessed September 10, 2014.)

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half the amount of morphine postoperatively in comparison with the children who satu-rated normally. Theoretically, repeated desaturations may sensitize the pain pathwaysto the effects of narcotics. In the postoperative period, the physician must also worryabout the lingering effects of anesthesia compromising pharyngeal muscular tone,tidal volume, and the body’s response to carbon dioxide. One can look at the periop-erative period as the perfect storm for OSA patients, as this setting often combines theelements of anesthesia, temporary paralysis, high-dose analgesia, and supine posi-tioning, all within a 24-hour period. The perioperative risk, however, often lingersinto postoperative days 2 and 3 owing to a phenomenon termed rapid eye movement(REM) rebound, whereby patients compensate for lack of REM sleep on postoperativeday zero by experiencing more REM sleep in the subsequent nights. As seen in a studyof 202 postoperative OSA patients, all of whom underwent daily sleep studies, theseverity of OSA or AHI worsened from day 1 to day 3 (Table 2).16

Which nonrespiratory complications have been associated with OSA in hospitalizedpatients?

In a prospective observational study by Hwang and colleagues,17 172 preoperativepatients underwent home pulse oximetry during which 98 had an oxygen desaturationindex (number of oxygen desaturations from baseline per hour) greater than 4%. Ashome desaturation deepened, so did the number of postoperative complications,from 2.7% in the normal population to 17.5% in the group that dropped their oxygensaturations 20% or more from baseline. Most complications were nonrespiratory andincluded bleeding, pulmonary embolism, and cardiac complications. An analysis ofthe Nationwide Inpatient Sample of 16,680 patients undergoing joint arthroplastyrevision with an ICD-9 code for OSA found that, compared with a matched cohort,the OSA patients had twice the inpatient mortality (odds ratio of 0.4% vs 0.2% in thenon-OSApopulation).18 Aftermultivariate analysis that includedBMI, pulmonary embo-lism was independently linked to OSA and accounted for most of the excess mortality.

MANAGEMENT

Do hospitalized OSA patients require special monitoring?

A standard policy that spans all hospitals and hospital settings typically states thatprocedures (including obtaining vital signs) cannot be performed on a patient whowould otherwise be conscious without first waking the patient. Hence, intermittentpulse oximetry as part of standard vital-sign measurements will typically miss apneicepisodes that tend to be most severe during REM sleep. A study that blinded themanaging staff to continuous pulse oximetry and arterial blood gas results in the first24 hours after bariatric surgery found that every patient, whether or not they had OSAand were on oxygen versus CPAP, desaturated to below 90% for an average of165 minutes.19 It is likely that challenges such as anesthesia, high-dose narcotics,

Table 2Progression of OSA severity

Postoperative day 1 2 3

AHI 19 29 37

Data from Gross JB, Apfelbaum JL, Caplan RA, et al. Practice guidelines for the perioperative man-agement of patients with obstructive sleep apnea: an updated report. Anesthesiology2014;120(2):268–86.

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and decompensated congestive heart failure (CHF) put OSA patients at particularlyhigh risk for dangerous desaturations even if the patient’s home CPAP settingswere continued while hospitalized. In 2006 the American Society of AnesthesiologistsTask Force devised a simple, nonvalidated OSA tool that triages perioperative pa-tients based on multiple risk factors into different levels of monitoring (Fig. 3).16

A key caveat to the appropriate monitoring of these patients is access to centralizedpulse oximetry. Often a patient must occupy an intensive care or step-down unit bedbecause the noncentralized pulse oximeters commonly deployed on the generalwards are not considered safe for this function. Centralized pulse oximetry boxes,much like telemetry boxes, are gaining in popularity and appear to be an ideal fit forthis patient population.

To what extent do positive airway pressure (PAP) devices lower the risk of in-hospitalcomplications in OSA patients?

Treatment of OSA with PAP improves oxygenation, endothelial function, sympatheticnerve activity, and afterload. In a study of outpatients with coronary artery disease andsleep apnea, continuous electrocardiogram monitoring before and after initiation of

Fig. 3. Scoring tool for perioperative patients based on risk factors. AHI, apnea-hypopneaindex; BIPAP, biphasic positive airway pressure; CPAP, continuous positive airway pressure;cwp, centimeters of water pressure; mEq/L, milliequivalents per liter; mm Hg, millimeterof mercury; PaCO2, partial pressure of carbon dioxide in arterial blood; PACU, postanesthesiacare unit. (Adapted from Gross JB, Apfelbaum JL, Caplan RA, et al. Practice guidelines forthe perioperative management of patients with obstructive sleep apnea: an updated report.Anesthesiology 2014;120(2):279; with permission.)

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CPAP showed a significant decrease in both the frequency and duration of night-timeischemic episodes in addition to improving OSA parameters (Fig. 4).20

In a study of 1116 women referred for an outpatient sleep study, those with un-treated mild-to-moderate or severe OSA had 3 and 12 times the risk, respectively,for cardiovascular death at 4 years compared with controls. Those with similar diseaseseverity who recorded at least 4 hours of CPAP use per night resolved their risk forcardiovascular death to that of the controls (Fig. 5).21

Finally, in a study of 355 patients undergoing bariatric surgery at one institution, pa-tients were screened for OSA, given a PSG if screened positive, and titrated with PAP,as appropriate; 93% of those who tested positive for OSA successfully used PAP peri-operatively.22 In this aggressively managed cohort, no difference was found betweenthe OSA and control groups in regard to total complications, respiratory complica-tions, or surgery complications. Hence, even with the challenges of surgery, anes-thesia, and narcotics, the patients’ home settings seemed to be adequate inpreventing complications postoperatively.

PERFORMANCE IMPROVEMENT

How does one identify and triage patients who are most at risk for OSA-relatedinpatient complications? What barriers exist to improve inpatient treatment of OSApatients?

Most hospitals do not have the proper infrastructure to handle inpatient OSA issues,23

andmany still have antiquated respiratory care policies that treat home CPAP initiationin the hospital as acute respiratory failure. Many house staff and nurses are not trainedto manage inpatient OSA, and continue to use intermittent pulse oximetry and oxygenalone to manage these patients. Given the added factors of the growing obesityepidemic in America and the rising incidence of OSA, one can see the challenge ofimproving performance in the care of these patients.Process improvement depends on the participation of multiple specialties and

administrative departments. Before addressing a screening process for undiagnosedOSA, management of known OSA patients should be the starting point for improve-ment. Initial evaluations by nurses or hospitalists that routinely address the diagnosisof OSA and inquire about the home use of PAP machines is essential. Resuming PAPjust as one would home medication after surgery or on admission to the medicalward is the next step. These 2 steps often involve changing hospital policies and the

Fig. 4. Ischemic minutes before and during CPAP treatment (9 patients) (P<.01, pairedt test). CPAP, continuous positive airway pressure. (From Peled N, Abinader EG, Pillar G,et al. Nocturnal ischemic events in patients with obstructive sleep apnea syndrome andischemic heart disease. J Am Coll Cardiol 1999;34(6):1748; with permission.)

Fig. 5. Kaplan-Meierplotof cardiovascular cumulativemortality. *means comparedwith con-trol group. (From Campos-Rodriguez F, Martinez-GarciaMA, de la Cruz-Moron I, et al. Cardio-vascularmortality inwomenwithobstructive sleepapneawithorwithout continuous positiveairway pressure treatment. Ann Int Med 2012;156:119; with permission.)

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relatively simple training of respiratory care therapists and nursing staff. Identifyingthose patients who are at particularly high risk for complications and safeguardingthemwith continuous, centralized pulse oximetry is the final, more difficult step. Nonva-lidated tools exist for the perioperative risk assessment and management of these pa-tients, but are lacking for the nonsurgical inpatient population. Some suggestions forclassifying an OSA patient as high risk for inpatient OSA-related complications include:

1. Patients undergoing major surgery, especially airway surgery2. Patients receiving general anesthesia or deep sedation3. Patients requiring high-dose narcotics4. Patients with a respiratory illness such as:

a. Pneumoniab. CHFc. Asthma exacerbationd. Chronic obstructive pulmonary disease exacerbation

5. Patients with altered mental status, such as those with delirium or an insult to thebrain

6. Patients with altered neuromuscular function, such as poststroke patients or thosewith exacerbations of multiple sclerosis

Many companies that manufacture pulse oximetry units now have remote moni-toring capabilities that serve to safely centralize these systems. Hence, patients are

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allowed to stay on their respective specialty wards while the hospital avoids overbur-dening intensive care and step-down units with this population.Finally, discharge management can be standardized by implementing triage tools in

the recovery rooms to easily identify and manage postoperative outpatients. The timeof discharge from the hospital, however, has not been standardized and remains prob-lematic, especially for those patients without a formal PSG diagnosis of OSA whorequire CPAP initiation in the hospital. Until this gap is addressed at a national level,hospitalists must navigate this issue on a case-by-case basis.

CLINICAL GUIDELINES

Practice guidelines for the perioperative management of patients with obstructivesleep apnea. Anesthesiology 2006;104:1081–93.

REFERENCES

1. Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events insleep: update of the 2007 AASM manual for the scoring sleep and associatedevents. Deliberations of the sleep apnea definitions task force of the AmericanAcademy of Sleep Medicine. J Clin Sleep Med 2012;8:597–619.

2. Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breath-ing among middle-aged adults. N Engl J Med 1993;328:1230–5.

3. Finkel KJ, Searleman AC, Tymkew H, et al. Prevalence of obstructive sleep apneaamong adult surgical patients in an academic medical center. Sleep Med 2009;10(7):753–8.

4. Chung F, Yegneswaran B, Liao P, et al. Validation of the Berlin questionnaire andAmerican Society of Anesthesiologists checklist as screening tools for obstructivesleep apnea in surgical patients. Anesthesiology 2008;108(5):822–30.

5. Mohsenin C, Valor R. Sleep apnea in patients with hemispheric stroke. Arch PhysMed Rehabil 1995;76(1):71–6.

6. Ironza A, Santamaria J, Berengeur J, et al. Prevalence and clinical importance ofsleep apnea in the first night after cerebral infarction. Neurology 2002;58(6):911–6.

7. LooG,Hein T, Tai BC, et al. Screening of hospitalizedpatients at high risk of obstruc-tive sleep apnea in general cardiology service. Int J Cardiol 2013;164:368–77.

8. Spurr KF, Graven MA, Gilbert RW. Prevalence of unspecified sleep apnea and theuse of continuous positive airway pressure in hospitalized patients, 2004 nationalhospital discharge survey. Sleep Breath 2008;12:229–34.

9. Isono S, Remmers JE, Tanaka A, et al. Anatomy of pharynx in patients with obstruc-tive sleep apnea and in normal subjects. J Appl Physiol (1985) 1997;82(4):1319–26.

10. Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identifypatients at risk for the sleep apnea syndrome. Ann Intern Med 1999;131(7):485–91.

11. Mallampati SR, Gatt SP, Gugino LD, et al. A clinical sign to predict difficulttracheal intubation: a prospective study. Can Anaesth Soc J 1985;32(4):429–34.

12. Marcs JA, Pothineni A, Marcus CZ, et al. The role of obesity and obstructive sleepapnea in the pathogenesis and treatment of resistant hypertension. Curr Hyper-tens Rep 2014;16(1):411.

13. Bohning N, Schmittendorf E, Schultheiss B. Analysis of nocturnal pulse oximetryin sleep medicine. Biomed Tech (Berl) 2011;56(4):215–22.

14. Ramachandran SK, Haider N, Saran KA, et al. Life-threatening critical respiratoryevents: a retrospective study of postoperative patients found unresponsive dur-ing analgesic therapy. J Clin Anesth 2011;23:207–13.

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15. Brown KA, Laferriere A, Lakheeram I, et al. Recurrent hypoxemia in children isassociated with increased analgesic sensitivity to opiates. Anesthesiology2006;105(4):665–9.

16. Gross JB, Apfelbaum JL, Caplan RA, et al. Practice guidelines for the perioper-ative management of patients with obstructive sleep apnea: an updated report.Anesthesiology 2014;120(2):268–86.

17. Hwang D, Shakir N, Liman B, et al. Association of sleep-disordered breathingwith postoperative complications. Chest 2008;133(5):1128–34.

18. D’Appuzo MR, Browne JA. Obstructive sleep apnea as a risk factor for postopera-tive complications after revision joint arthroplasty. J Arthroplasty 2012;27(8 Suppl):95–8.

19. Gallagher SF, Haines KL, Osterlund LG, et al. Postoperative hypoxemia: com-mon, undetected, and unsuspected after bariatric surgery. J Surg Res 2010;159:622–6.

20. Peled N, Abinader EG, Pillar G, et al. Nocturnal ischemic events in patients withobstructive sleep apnea syndrome and ischemic heart disease. J Am Coll Cardiol1999;34(6):1744–9.

21. Campos-Rodriguez F, Martinez-Garcia MA, de la Cruz-Moron I, et al. Cardiovas-cular mortality in women with obstructive sleep apnea with or without continuouspositive airway pressure treatment. Ann Intern Med 2012;156:115–22.

22. Weingarten TN, Flores AS, McKenzie JA, et al. Obstructive sleep apnoea and peri-operative complications in bariatric patients. Br J Anaesth 2011;106(1):131–9.

23. Patil D, Patil YJ. Perioperative management of obstructive sleep apnea: a survey ofVeterans Affairs health care providers. Otolaryngol Head Neck Surg 2012;146(1):156–61.

APPENDIX 1: BERLIN QUESTIONNAIRE FOR SLEEP APNEA

Berlin Questionnaire scoringThe questionnaire consists of 3 categories related to the risk of having sleep apnea.Patients can be classified into high risk or low risk based on their responses to the individual

items and their overall scores in the symptom categories.

Categories and scoring:Category 1: items 1, 2, 3, 4, 5Item 1: if ‘Yes’, assign 1 pointItem 2: if ‘c’ or ‘d’ is the response, assign 1 pointItem 3: if ‘a’ or ‘b’ is the response, assign 1 pointItem 4: if ‘a’ is the response, assign 1 pointItem 5: if ‘a’ or ‘b’ is the response, assign 2 points

Add points. Category 1 is positive if the total score is 2 or more pointsCategory 2: items 6, 7, 8 (item 9 should be noted separately)Item 6: if ‘a’ or ‘b’ is the response, assign 1 pointItem 7: if ‘a’ or ‘b’ is the response, assign 1 pointItem 8: if ‘a’ is the response, assign 1 point

Add points. Category 2 is positive if the total score is 2 or more pointsCategory 3 is positive if the answer to item 10 is ‘Yes’ OR if the BMI of the patient is >30 kg/m2

(BMI must be calculated, defined as weight (kg) divided by height (m) squared, ie, kg/m2)

High Risk: if there are 2 or more Categories where the score is positiveLow Risk: if there is only 1 or no Categories where the score is positiveAdditional question: item 9 should be noted separately.

BERLIN QUESTIONNAIRE

Height (m) ________ Weight (kg)________ Age______ Male / Female Please choose the correct response to each question.

CATEGORY 11. Do you snore? _ a. Yes _ b. No _ c. Don’t know

If you snore: 2. Your snoring is: _ a. Slightly louder than breathing _ b. As loud as talking _ c. Louder than talking _ d. Very loud – can be heard in adjacent rooms

3. How often do you snore _ a. Nearly every day _ b. 3-4 times a week _ c. 1-2 times a week _ d. 1-2 times a month _ e. Never or nearly never

4. Has your snoring ever bothered other people? _ a. Yes _ b. No _ c. Don’t Know 5. Has anyone noticed that you quit breathing during your sleep?

_ a. Nearly every day _ b. 3-4 times a week _ c. 1-2 times a week _ d. 1-2 times a month _ e. Never or nearly never

CATEGORY 26. How often do you feel tired or fatigued after your sleep? _ a. Nearly every day _ b. 3-4 times a week _ c. 1-2 times a week _ d. 1-2 times a month _ e. Never or nearly never

7. During your waking time, do you feel tired, fatigued or not up to par? _ a. Nearly every day _ b. 3-4 times a week _ c. 1-2 times a week _ d. 1-2 times a month _ e. Never or nearly never

8. Have you ever nodded off or fallen asleep while driving a vehicle? _ a. Yes _ b. No

If yes: 9. How often does this occur? _ a. Nearly every day _ b. 3-4 times a week _ c. 1-2 times a week _ d. 1-2 times a month _ e. Never or nearly never

CATEGORY 310. Do you have high blood pressure? _ Yes_ No_ Don’t know

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Adapted from Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaireto identify patients at risk for the sleep apnea syndrome. Ann Intern Med1999;131(7):485–91.