32. Large neck circumference only 3. BMI and allergies Walter is a 42 year old male complaining of daytime fatigue and depression. What additional risk factors should you consider for a diagnosis of sleep apnea?1. BMI only2. Large neck circumference only3. BMI and allergiesBMI and respiratory diseaseBMI, Respiratory disease and large neck circumferenceDO NOT DISPLAY CORRECT ANSWER OR RESULTS
4Hypertension Asthma Erectile Dysfunction Insulin resistance Fred, a 56 year old Asian man, has been diagnosed with diabetes and obstructive sleep apnea. All of the following co-morbidities are likely affected by Fred’s sleep apnea EXCEPT:HypertensionAsthmaErectile DysfunctionInsulin resistanceHeart FailureDO NOT DISPLAY CORRECT ANSWER OR RESULTS
5Mild cough and frequent headaches Restlessness and depression Jesse is a 52 year old executive who presents with fatigue. His wife has been complaining of his snoring over the past two years. He has been a two-pack a day smoker for 28 years. He weighs 260# and is sedentary. What symptoms would you ask Jesse about to make an initial diagnosis of obstructive sleep apnea?Mild cough and frequent headachesRestlessness and depressionSore throat and difficulty swallowingDry eyes and shortness of breathDO NOT DISPLAY CORRECT ANSWER OR RESULTS
6The Epworth Sleepiness Scale (ESS) Polysomnography Nighttime Oximetry You confirm that Jesse has met the conditions for a diagnosis of OSA. What test would most likely confirm this diagnosis?The Epworth Sleepiness Scale (ESS)PolysomnographyNighttime OximetryNone of the aboveDO NOT DISPLAY CORRECT ANSWER OR RESULTS
7A beer or other alcoholic beverage at bed time CPAP Jesse’s test confirms OSA. He says he is motivated to lose weight. What other treatment regimens do you prescribe?A beer or other alcoholic beverage at bed timeCPAPPrescription sleeping aids and CPAPSmoking cessation and CPAPDO NOT DISPLAY CORRECT ANSWER OR RESULTS
8Understanding, Recognizing and Managing Obstructive Sleep Apnea Federico Cerrone, MD,FCCP,DASSMDirector, Center for Sleep DisordersOverlook Hospital, Summit, NJ
9Sleep Disorders - Socioeconomic Consequences 40 million Americans suffer from chronic disorders of sleep and wakefulness.95% of these remain unidentified and undiagnosed.The annual direct cost of sleep-related problems is $16 billion, with an additional $50-$100 billion in indirect costs (accidents, litigation, property destruction, hospitalization, and death).
10Sleep ApneaRecently, a primary care physician working in an urgent care setting evaluated a 35-year-old woman complaining of ear pain. She was diagnosed with otitis externa from trauma. She stated that she wore ear plugs each night because of her husband’s snoring.Additional questioning revealed that her husband snored loudly with frequent pauses and gasps, which frightened her. Her husband was seen and examined by his primary care physician. He weighed over 250 pounds and had a shirt collar size of 18. A diagnosis of probable sleep apnea was made and the husband was referred for a polysomnogram.Primary care physicians are commonly the first healthcare professional to have the opportunity to see patients with sleep apnea and their spouses. The informed physician can dramatically improve the patient’s quality of life. This talk will help you better understand the nature of the disorder, how it presents, and how to treat it.
11Patient # 1 52 year old male with history of borderline hypertension Wife complains of his snoringHis weight has increased 10 pounds over the last yearFeels tired, but states he is very busy with work and the kids
12Sleep Apnea is: Common Dangerous Easily recognized Treatable The important message to take home from this talk is that sleep apnea is a common disorder; it is dangerous for the patient and others; and it is easily recognizable and is treatable.We will first define what sleep apnea is, then describe the physiological consequences of the disorder and how these lead to the presenting features. This will be followed by a discussion of clinical features and risk factors suggestive of the presence of sleep apnea and methods for making the diagnosis. Finally, we will discuss the treatment options available for patients with sleep apnea.
13Sleep Apnea Definition Pathophysiology Clinical Features Risk Factors Methods of DiagnosisTreatment
15Question 1 What is the definition of obstructive sleep apnea? Patient makes no effort to breathe?Patient’s oxygen levels and carbon dioxide levels decrease with sleep?There is a reduction in airflow, but patient still makes effort to breathe?Patient has an inability to fall asleep, stay asleep or has early morning awakenings?Answer: 3 - There is a reduction in airflow, but patient still makes effort to breathe?; display results and correct answer
16Types of Sleep Disordered Breathing ApneaCessation of airflow > 10 secondsHypopneaAt least 30% reduction airflow > 10 seconds associated with:ArousalOxyhemoglobin desaturationWhen abnormal breathing patterns disrupt sleep, this is called sleep-disordered breathing. There are different types which can occur in one of several patterns. An apnea is defined as the cessation of airflow for 10 or more seconds.1 Controversy exists about the definition of hypopnea. Because of the relationship of sleep fragmentation and daytime sleepiness, many investigators consider a decrease in airflow for > 10 seconds accompanied by an arousal as a significant disordered breathing (hypopnea) event without requiring a specific level of desaturation.2Recently, the presence of apneas and hypopneas has been associated with an increased prevalence of cardiovascular disease.3 In this study, hypopnea was defined as an event lasting at least 10 seconds with a greater than 30% reduction in thorocoabdominal movement or airflow, and with at least a 4% oxygen desaturation. When a 4% desaturation criteria is applied to the definition of hypopnea significant cardiovascular co-morbidity has been detected at an AHI => 5 per hour.For this talk, hypopnea will be broadly defined as those obstructive events, lasting > 10 seconds, accompanied by either oxyhemoglobin desaturation or an arousal.1. American Thoracic Society. Indications and standards for the use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. Am J Respir Crit Care Med 1994;150(6 Pt 1):2. American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. SLEEP 1999;22(5):3. Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier Nieto F, O’Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163(1):19-25.
17Apnea Patterns Obstructive Mixed Central Airflow Respiratory effort There are three characteristic patterns of apnea.An obstructive apnea is defined by the absence of airflow despite persistent ventilatory efforts, demonstrated by contraction of respiratory muscles such as the diaphragm.A central apnea, in contrast, is the absence of airflow due to the lack of ventilatory effort. Since no effort is made to breathe, no airflow occurs.A mixed apnea includes both central and obstructive components, usually with an initial central component followed by the obstructive component.The clinical and pathological consequences of, and treatment for, mixed and obstructive apneas and hypopneas are the same, so we will refer to them together as sleep apnea. Clinically significant central apneas are less common and will not be discussed further in this presentation.
18Upper Airway Resistance Syndrome EEGArousalAirflowEffort(Rib Cage)Effort(Abdomen)Slide 18Level 2Effort(Pes)There is a group of patients who present with daytime sleepiness due to narrowing of their upper airway without apneas or hypopneas. This condition is called the Upper Airway Resistance Syndrome (UARS). These patients have repetitive, short arousals caused by the increased work of breathing required to overcome the increased resistance of a narrowed airway. With sleep onset, the airway narrows, thereby increasing resistance to airflow. Airflow is maintained due to increased ventilatory effort, shown by the decrease in esophageal pressure. When the work of breathing increases past a threshold level, an arousal occurs, fragmenting sleep. This fragmentation of sleep results in the symptom of daytime sleepiness.SaO210 sec4. Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest 1993;104(3):
19Measures of Sleep Apnea Frequency Apnea Index# apneas per hour of sleepApnea / Hypopnea Index (AHI)# apneas + hypopneas per hour of sleepThese are the terms most commonly used to describe the frequency of sleep apnea. The Apnea Index is defined as the number of apneas per hour of sleep. The Apnea/Hypopnea Index, or AHI, represents the total number of apneas and hypopneas per hour of sleep. This has also been called the Respiratory Disturbance Index or RDI.An AHI < 5 is considered normal.5 What frequency above this level requires therapy or leads to adverse clinical consequences is controversial. The sleep apnea syndrome, or clinical sleep apnea, is defined as recurrent apneas or hypopneas that are associated with clinical impairment, such as daytime sleepiness, motor vehicle accidents or cardiovascular disease.15. National Center on Sleep Disorders Research. Sleep apnea: is your patient at risk? Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute, NIH Publication No , September 1995.1. American Thoracic Society. Indications and standards for the use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. Am J Respir Crit Care Med 1994;150:
20Severity Criteria Mild: 5-15 events per hour Moderate: events per hourSevere: more than 30 events per hour
21Limitations to Criteria Does not incorporate severity of oxygen desaturationDoes not consider non-apneic respiratory events
23Question 2Which of the following statements regarding prevalence of obstructive sleep apnea is true?24% of men and 9% of women have OSAS?4% of men and 2% of women had an AHI≥5 according to the first major US population-based prevalence study?Prevalence of OSAS will continue to increase as prevalence of obesity continues to rise?Sleep apnea occurs equally in men and women?3 - Prevalence of OSAS will continue to increase as prevalence of obesity continues to rise?; display results and correct answer
24Prevalence of Sleep Apnea 30-60 year oldsPercent ofPopulationSleep apnea is a common disorder. On this slide is information from a study which examined the prevalence of sleep apnea in the year old population.6 A random sample of 602 men and women were studied in the sleep laboratory using standard polysomnography. Using a cut-off of AHI > 5 per hour, there was a high prevalence of sleep-disordered breathing in both men and women. An elevated AHI was found in 24% of men and 9% of women. When the AHI is combined with symptoms of sleep apnea, a minimum prevalence of the sleep apnea syndrome was determined to be 4% in men and 2% in women. For comparison, the prevalence of asthma, another common disorder, is 4.5% of the United States population.7Adapted from Young T et al. N Engl J Med 1993;328.6. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328(17):7. National Heart, Lung, and Blood Institute. Fact book: Fiscal year U.S. Department of Health and Human Services, U.S. Public Health Service, National Institutes of Health, February 1994.
25Patient # 1Patient tells you that a couple of drinks increases the snoringHe also grinds his teeth per his dentist
27Question 3Which of the following best characterizes the pathogenesis of OSA?Increased genioglossus activity while awake?Reduced tensor palatini activity while awake?Not enough skeletal support of upper airway?Decreased genioglossus activity while awake?1 - Increased genioglossus activity while awake?; display results and correct answer
28The Upper Airway219364857This is a sagittal section through the pharyngeal airway of a normal human. To orient you, here is the nose, (1) maxilla, (2) mandible, (3) hard palate, (4) soft palate and (5) uvula. The body of the tongue is the (6) genioglossus muscle. Pharyngeal collapse in apneic patients occurs somewhere between the (7) choane and the (8) epiglottis, usually behind the uvula and soft palate, behind the tongue, or some combination of these sites.It is important to understand that this portion of the airway (between the choane and the epiglottis), in humans, has little or no bony or rigid support and is therefore dependent on the activity of muscles, such as the genioglossus, to maintain airway patency. As a result, humans are uniquely vulnerable to the development of sleep apnea. This may be a consequence of the evolutionary changes which accompanied the development of speech. Phonation requires an airway which can change shape and size. This was accomplished by freeing the (9) hyoid bone from rigid fixation, leaving the airway muscles in control of the patency of the airway. Therefore any event, such as sleep, which could affect the activity of these muscles, could influence airway patency.The principal problem of the sleep apnea patient is an anatomically small pharyngeal airway between the choane and epiglottis. The airway may be small due to fat deposition (obesity); a small, posteriorly placed mandible (retrognathia or micrognathia); tonsillar hypertrophy; or many other causes.Anything which narrows the airway or decreases muscle tone can cause sleep apnea.
29Anatomical Factors Collapsible tube Changes in upper airway anatomy There are increased parapharyngeal fat padsObesity can reduce lung volumesDilator muscles
30Control of Dilator Muscles Effects On Pharyngeal Muscle ActivityAwakeNREMGenioglosus EMGNormal SubjectTensor Palatini EMGAirflowGenioglosus EMGSlide 30Level 2OSA PatientTensor Palatini EMGThis slide shows how the airway dilator muscles work in normal subjects and in people with sleep apnea. Different muscles are affected differently by the onset of sleep. The activity of two representative dilator muscles – the geniglossus, which controls the tongue, and the tensor palatini, which controls the palate – is shown here. The activity of the muscles, as measured by electromyogram (EMG), is depicted during wakefulness and sleep. Both muscles act to combat the tendency of the airway to collapse as negative pressure is generated during inspiration.Both muscles function during wakefulness. In normal subjects, the onset of sleep leads to a drop in the activity of the tensor palatini, resulting in a small amount of airway narrowing, and a small but normal decrease in airflow.The situation is different in patients with sleep apnea. Their airway is narrowed to begin with. As a result, even during wakefulness the dilator muscles have to work harder to maintain a patent airway. Here you can see the augmented dilator muscle activity, which represents neuromuscular compensation for the anatomically small airway.8During sleep, this neuromuscular compensation is lost and muscle activity returns to the same level as seen in normals. The combination of the anatomically small airway and loss of neuromuscular compensation results in collapse of the airway and the cessation of airflow shown here in the bottom figure. This is an apnea.Airflow8. Mezzanote WS, Tangel DJ, White DP. Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). J Clin Invest 1992;89(5):
31Pathophysiology of Apnea This slide shows the effect of sleep on the upper airway in a sleep apnea patient. In the figure on the left, the patient is awake and the airway is narrowed but patent. The upper airway dilator muscles are responsible for maintaining the patency of the airway despite the reduced size of the airway, which may be due to fat deposition from obesity or structural abnormalities such as retrognathia. Note that collapse, shown on the right, may occur anywhere along the upper airway, from the retropalatal space to the hypopharynx, and often occurs in multiple places.
32Pathophysiology of Sleep Apnea Awake: Small airway + neuromuscular compensationSleep OnsetLoss of neuromuscular compensation+Decreased pharyngeal muscle activityHyperventilate: connect hypoxia & hypercapniaAirway opensPharyngeal muscle activity restoredAirway collapsesApneaArousal from sleepThis figure depicts the repetitive pathophysiologic events which occur during sleep apnea. The primary problem in the sleep apnea patient is the presence of an anatomically small pharyngeal airway. To prevent airway collapse during wakefulness, the action of the airway dilator muscles is augmented – a neuromuscular compensation for the small airway. With sleep onset, there is a loss of the upper airway reflex which drives this neuromuscular compensation. As a result, dilator muscle activity falls, the pharynx closes and the apnea begins. During the apnea, hypoxia and hypercapnia develop, leading to increasing ventilatory effort. Once this effort reaches a threshold level, the patient arouses. Pharyngeal muscle activity is restored, and the airway opens. The patient then hyperventilates to correct the blood gas derangements, returns to sleep, and the cycle begins again.As a result, sleep can be severely disrupted by the repetitive arousals needed to end the apneas, and episodes of cyclic hypoxia and hypercapnia occur. These events lead to the observed clinical consequences.Hypoxia & HypercapniaIncreased ventilatory effort
33Patient # 1The patient upon further questioning does get tired when driving more than one hourHe is on medication for depressionSleep study reveals AHI=55 with lowest oxygen saturation of 80%
34Clinical Consequences Sleep ApneaSleep FragmentationHypoxia/ HypercapniaExcessive Daytime SleepinessCardiovascular ComplicationsAs we proceed to detail the many clinical consequences of sleep apnea, it will be helpful to recall that all these adverse effects are the result of the two fundamental abnormalities which characterize sleep apnea.First, the patient cycles from apnea to arousal many times each night which leads to severe sleep fragmentation.Second, most apneic episodes are accompanied by hypoxemia and hypercapnia, which repeatedly stress the patient’s cardiovascular system.The many ill-effects which result from these two abnormalities can be broadly grouped into two categories: excessive daytime sleepiness and cardiovascular dysfunction.The end result of all these adverse effects is a substantial increase in both morbidity and mortality among sleep apnea patients.MorbidityMortality
35Consequences: Excessive Daytime Sleepiness Increased motor vehicle crashesIncreased work-related accidentsPoor job performanceDepressionFamily discordDecreased quality of lifeThe repetitive arousals which terminate the apneic episodes cause multiple awakenings each night. The patients are usually not aware of these events because they are brief. However, they cause disruption of the restorative effect of sleep. As a result, patients often wake up unrefreshed and sleepy. They complain of sleepiness during the day despite what should be adequate (and sometimes excessive) amounts of time in bed. This daytime sleepiness can have significant consequences.It has been shown that patients with sleep apnea have an increased incidence of motor vehicle crashes9 and work related accidents, poor job performance, depression, family discord, and overall decreased quality of life.10,119. Findley LU, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138(2):10. Roth T, Roehrs TA, Conway WA. Behavioral morbidity of apnea. Sem Respir Med 1998;9:11. Strohl KP, Redline S. Recognition of obstructive sleep apnea. Am J Respir Crit Care Med 1996;154(2 Pt 1):
36Consequences: Automobile Accidents Accident / driver / 5 yrsSlide 36Level 2Shown here is data comparing the automobile accident rate in sleep apnea patients with matched controls and with all Virginia drivers. The accident incidence was seven-fold greater in patients with sleep apnea than in matched controls without the disorder. The percentage of individuals with one or more crashes was also greater in the patients with apnea (13%) than in the controls (6%). The automobile crash rate for sleep apnea patients was 2.6 times the crash rate of all licensed drivers in Virginia.9 The risk of automobile accidents is related to severity of disease, with the highest rates seen in patients with severe apnea.12Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.9. Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138(2):12. Findley L, Fabrizo M, Thommi G, Suratt PM. Severity of sleep apnea and automobile crashes. N Engl J Med 1989;320(13):
37Consequences: Automobile Accidents Risk of Traffic Accident: OSA + ETOH12108Odds Ratio64Slide 37Level 22The risk of motor vehicle accidents is elevated in sleep apnea patients. This risk is further increased by the consumption of alcohol. Teran-Santos et al13 conducted a case-control study to evaluate the risk of traffic accidents in those with sleep apnea. They found a six-fold increase in the risk of having a traffic accident in those with an AHI > 10/hour compared to those without sleep apnea. This risk was potentiated with concurrent alcohol use. As shown above, among subjects with an AHI > 10 the risk of having an accident was much higher in those who had consumed alcohol on the day of the accident compared to those who had not.13. Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. N Engl J Med 1999;340(11):NO ETOH+ ETOHETOH On Day of AccidentAdapted from Teran-Santos J et al.N Engl J Med 1999;340.
38Consequences: Cardiovascular Systemic hypertensionCardiac arrhythmiasMyocardial ischemiaCerebrovascular diseasePulmonary hypertension / cor pulmonaleThe second major category of morbidity from sleep apnea is that caused by cardiovascular dysfunction. Systemic hypertension has been reported in up to 50% of patients with sleep apnea.14 This is in part related to the common risk factor for both disorders of upper body obesity. With apneic events, there are cyclical increases in systemic blood pressure associated with increased sympathetic tone.15 In some patients, the elevation in sympathetic tone persists into the daytime. Mean morning blood pressure has been shown to increase almost linearly with increasing apneic activity in both obese and non-obese patients.16 Cardiac arrhythmias have also been associated with sleep apnea.17 Typically one observes bradycardiac arrhythmias, though ventricular tachycaradia may be noted with severe hypoxemia. In patients with underlying coronary artery disease, myocardial ischemia and perhaps infarction may be triggered by the hypoxemia, reduction in heart rate, and rise in blood pressure seen during severe apneic events.18 Case control studies have shown an increased risk of stroke in patients with symptoms of snoring, daytime sleepiness and a history of observed apneas, independent of heart disease, hypertension and alcohol use.19 A small subset of patients with severe sleep apnea go on to develop the Pickwickian syndrome, which is characterized by daytime hypercapnia and hypoxemia, pulmonary hypertension, polycythemia and cor pulmonale in obese patients.2014. Fletcher EC. The relationship between systemic hypertension and obstructive sleep apnea: facts and theory. Am J Med 1995;98(2):15. Shepard JW Jr. Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992;13(3):16. Strohl KP, Novak RD, Singer W, et al. Insulin levels, blood pressure and sleep apnea. SLEEP 1994;17(7):17. Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52(5):18. Hung J, Whitford EG, Parsons RW, Hillman DR. Association of sleep apnoea with myocardial infarction in men. Lancet 1990;336(8710):19. Palomäki H. Snoring and the risk of ischemic brain infarction. Stroke 1991;22(8):20. Rapoport DM, Garay SM, Epstein H, Goldring RM. Hypercapnia in the obstructive sleep apnea syndrome. A reevaluation of the “Pickwickian Syndrome.” Chest 1986;89(5):
39Consequences: Mortality Effect of Al on MortalityAI < 20AI > 20Cumulative SurvivalSeveral reports have shown an increased mortality for patients with sleep apnea. This slide shows the impact on mortality of severity of disease from a retrospective study of sleep apnea patients.21 Patients with an apnea index greater than 20 per hour, who elected to forgo treatment, were found to have reduced survival when compared to patients with an apnea index less than 20. This is most likely due to the cardiovascular consequences previously discussed.Interval (Years)(Untreated, age<50)He J et al. Chest 1988;94.21. He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988;94(1):9-14.
41Back to our patient in Case 1: Question 4Back to our patient in Case 1:Which of the following is correct regarding the relationship between OSA and hypertension?Prospective observational cohort studies have not demonstrated an increased risk of htn associated with OSASystemic htn is not on the causal pathway between OSA and stroke?Blinded RCT have shown that CPAP reduces blood pressure in htn patients with sleep apnea?Answer: 3 - Blinded RCT have shown that CPAP reduces blood pressure in htn patients with sleep apnea?; display correct answer and results
42Consequences: Hypertension Slide 42Level 2This slide shows the cyclical elevations in systemic blood pressure which accompany apneic events. Note that peak pressures occur after apnea termination, indicated by the resumption of airflow in the thermistor channel.15Shepard JW Jr. Med Clin North Am 1985;69.15. Shepard JW Jr. Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992;13(3):
43Cardiovascular Consequences: Hypertension Prospective Study of Association Between OSA and Hypertension32.52Adjustedfor age, sex, BMI, neck circ., cigs., ETOH, baseline HtnOdds Ratio1.510.5There is increasing evidence for a causal role of sleep-disordered breathing in the development of hypertension. Shown here are data from the longitudinal Wisconsin Sleep Cohort Study in which over 700 patients were evaluated at baseline and four years later with full polysomnography.22 Hypertension status and blood pressure were also monitored. The investigators found that baseline elevations of AHI were associated with blood pressure elevation at follow-up. This relationship persisted even after correcting for confounding variables (age, sex, measures of obesity such as neck circumference and body mass index, alcohol and cigarette use and the presence of hypertension at baseline). There was a dose response relationship – those with the highest AHI at baseline had the greatest odds ratio of having hypertension four years later. Those with an AHI > 15 were nearly three times as likely to have hypertension at follow-up than those without sleep-disordered breathing. 22. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342(19):> 15Apnea / Hypopnea Index (AHI)Adapted from Peppard PE et al. N Engl J Med 2000;342.
44Consequences: Arrhythmias EEGLOCEMGCHINEKGSAO2FLOWPNTEFFRCSlide 44Level 2EFFABDSUMThe most common arrhythmia occurring during sleep apnea is bradycardia.15 The extent of cardiac slowing increases in proportion to the severity of hypoxemia.23 On this slide the apnea – shown here by the absence of airflow despite continued respiratory effort – leads to bradycardia. The heart rate progressively slows to an eventual 4 second pause. The bradycardia ends with the termination of the apnea by arousal.Shepard JW Jr. Clin Chest Med 1992;12.15. Shepard JW Jr. Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992;13(3):23. Zwillich C, Devlin T, White D, Douglas N, Weil J, Martin R. Bradycardia during sleep apnea. Characteristics and mechanism. J Clin Invest 1982;69(6):
45Atrial FibrillationDecrease in oxygen saturation may be the best predictor of riskGami,JACC,2007
46StrokeIncreased severity of obstructive sleep apnea increases risk of strokeYaggi et al: NEJM 2005
47Consequences: Cardiovascular Disease Cross Sectional Study of Association Between OSA and CVD2.52AHIOdds Ratio1.51> 11.00.5The previous slides demonstrate the unfavorable effects of sleep apnea on cardiovascular physiology and the relationship between sleep-disordered breathing and the development of hypertension. Sleep apnea has also been implicated in the development of other manifestations of cardiovascular disease (CVD). The Sleep Heart Health Study is a community-based multicenter study of the relationship of sleep-disordered breathing to CVD in 6,424 free-living individuals.3 Participants underwent overnight, unattended, polysomnography at home and an interview to evaluate for self-reported cardiovascular disease. Cross sectional analysis results are shown above. The population was divided into quartiles according to apnea severity (AHI). The Odds Ratio for the presence of any cardiovascular disease was significantly elevated for the third and fourth quartiles. The relative odds for individual disorders, coronary artery disease (CAD), heart failure (HF), and stroke (CVA) are shown on this slide. The increased risk persisted even when corrected for age, sex, race, obesity (body mass index – BMI), the presence of hypertension or hypercholesterolemia and cigarette use. These findings are consistent with a modest to moderate effect of sleep-disordered breathing on multiple manifestations of cardiovascular disease. Of note, this increased risk of CVD occurred at ranges of AHI that are considered normal or only mildly elevated.3. Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier Nieto F, O’Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163(1):19-25.CADHFCVAAdjusted for age, sex, race, BMI, Htn, cigs., chol.Adapted from Shahar E et al. Am J Respir Crit Care Med 2001;163.
48Metabolic Consequences OSA is linked to glucose intolerance and increased leptin levelsLeptin mediates appetite suppressionObese patients have increased leptin levels but are resistant to the appetite suppressant effectsOSA patients have higher leptin levels than similarly obese pts without OSACPAP reduces leptin levels and improves glucose toleranceBarkoukis: Review of Sleep Medicine,2007
49Patient # 2 55 year old female post-menopause complains of insomnia Extreme fatigue during the dayInterrupted sleep at nightNormal blood pressureBMI 24 (normal)Moderate overbiteSleep study with AHI=8, RDI=30, oxygen saturation low 94%
51Question 5 Which one of the following is a known risk factor of OSA? Decreased neck circumferenceThe Premenopausal statusPresence of RetronagthiaLonger thyromental distance3 - Presence of Retronagthia; display results and correct answer
52Sleep Apnea Risk Factors- Patient # 1 ObesityIncreasing ageMale genderAnatomic abnormalities of upper airwayFamily historyAlcohol or sedative useSmokingAssociated conditionsA number of factors which put people at higher risk for developing sleep apnea are listed on this slide. The most common risk factor is the presence of obesity, specifically measures of central obesity. Upper body fat distribution is one of the major contributing factors to the development of sleep apnea. In both sexes the syndrome is more prevalent with increasing age,6 reaching very high rates in patients over 65 years.24 Males appear to have a higher rate of sleep apnea than women, with a ratio of 2:1 to 10:1, depending on the study.11 Any condition resulting in an anatomic abnormality which narrows the posterior airspace can predispose to the development of sleep apnea. This includes nasal obstruction, retro- or micrognathia, tonsillar hypertrophy and macroglossia. Several studies have demonstrated a higher risk for development of sleep apnea if there is a family history of the disorder, with increasing risk with increasing number of affected relatives.25 Use of alcohol or sedative medication can contribute to the development of sleep apnea through their relaxant effect on the upper airway muscles.26 A longitudinal epidemiological study showed that smokers are at an increased risk for developing sleep apnea, with current smokers at greater risk than nonsmokers, and heavy smokers having the greatest risk.27 Cessation of smoking resulted in the elimination of the increased risk. Associated conditions: Hypothyroidism can contribute to the development of sleep apnea through the development of macroglossia or obesity, and through its effect on upper airway muscle function. Other conditions in which sleep apnea has been reported – due to their effects on upper airway anatomy or muscle function – include acromegaly, amyloidosis, vocal cord paralysis, post-polio syndrome, neuromuscular disorders, Marfan syndrome and Down syndrome.116. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328(17):24. Ancoli-Israel S, Klauber MR, Kripke DF, Parker L, Cobarrubias M. Sleep apnea in female patients in a nursing home. Increased risk of mortality. Chest 1989;96(5):11. Strohl KP, Redline S. Recognition of obstructive sleep apnea. Am J Respir Crit Care Med 1996;154(2 Pt 1):25. Redline S, Tishler PV, Tosteson TD, et al. The familial aggregation of obstructive sleep apnea. Am J Respir Crit Care Med 1995:151(3 Pt 1):26. Issa FG, Sullivan CD. Alcohol, snoring and sleep apnea. J Neurol Neruosurg Psychiatry 1982;45(4):27. Wetter DW, Young BT, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154(19):
53Risk Factor: Obesity >4% Arterial saturation dipa h-1 This slide shows the association between the severity of sleep apnea, indicated by frequency of oxyhemoglobin desaturation, and neck size, which is a measure of central obesity. After passing a threshold neck circumference, the severity of apnea increases linearly with increasing neck size.Several studies have shown that most patients with sleep apnea are obese with thick necks. It has been postulated that excessive fat deposition in the neck would tend to narrow the pharyngeal cross-sectional area and increase pharyngeal collapsibility during sleep.% Predicted normal neck circumferenceDavies RJ et al. Eur Respir J 1990;3.28. Davies RJ, Stradling JR. The relationship between neck circumference, radiographic pharyngeal anatomy, and the obstructive sleep apnoea syndrome. Eur Respir J 1990;3(5):
54Risk Factor: Age % with AHI > 5 Slide 54 Level 2 The risk of developing sleep apnea increases with increasing age. This slide shows the results of a study which evaluated the prevalence of sleep-disordered breathing in a general middle aged adult population.6 The percentage of subjects with 5 or more apneas and hypopneas per hour of sleep increases with increasing age in both men and women.Adapted from Young T et al. N Engl J Med 1993;328.6. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;32(17):
55Age Prevalence plateaus after age 65 Is sleep apnea different in older people?Young; 2002 Arch Intern Med
56Risk Factor: Gender Slide 56 Apnea/Hypopnea Index Skinfold Sum (mm) MaleFemaleSlide 56Level 2Male patients have more severe sleep apnea than women, even when corrected for degree of obesity. This could partly be due to the greater degree of upper body obesity seen in men. In addition, men have more severe sleep apnea than female patients with the same degree of upper body obesity, as shown in the graph above.29 Note that for each level of obesity, indicated by skinfold sum, the AHI is greater in men than in women. This implies that there are gender differences in the mechanical properties of the pharynx.Skinfold Sum (mm)Millman RP et al. Chest 1995;107.29. Millman RP, Carlisle CC, McGarvey ST, Eveloff SE, Levinson PD. Body fat distribution and sleep apnea severity in women. Chest 1995;107(2):
57Risk Factor: Anatomic Abnormality 756485Apneas & Hypopneas per hour of sleep3721Slide 57Level 2Any anatomic abnormality which results in narrowing of the upper airway can predispose to the development of sleep apnea. This slide demonstrates the effect of nasal obstruction. Occlusion of the nose has been shown in several studies to lead to an increase in obstructive apneas and hypopneas, even in normal subjects.30 Nasal obstruction results in a change in the pressure gradient across the oropharynx, promoting its collapse. The nose is the preferred pathway for breathing during sleep in adults since it is a low-resistance pathway. Mouth-breathing secondary to nasal occlusion leads to an increase in pharyngeal resistance. Overcoming the increased resistance requires increased work of breathing, which creates more negative intrathoracic pressure and an increased oropharyngeal pressure gradient. This pressure gradient increases inward forces on the phargyneal tissues, promoting collapse of the airway.Suratt PM et al. Chest 1986;90.30. Suratt PM, Turner BL, Wilhoit SC. Effect of intranasal obstruction on breathing during sleep. Chest 1986;90(3):
58Risk Factor: Family History Likelihood of Sleep Apnea as Function of Family PrevalenceOdds Ratio(Adjusted for age, race, sex,BMI)Slide 58Level 2A family history of sleep apnea increases an individual’s risk of developing sleep apnea. This study shows that the risk of developing sleep apnea increases as the number of family members with sleep apnea increases, to an almost four-fold greater risk if three other relatives have sleep apnea.25This familial aggregation is not explained entirely by familial similarities in Body Mass Index (BMI) or neck circumference, suggesting other familial factors are important in increasing susceptibility to the disorder. However, this risk factor is not strong enough to warrant screening asymptomatic family members with sleep studies.Relative Relatives RelativesAdapted from Redline S et al. Am J Resp Crit Care Med 1995;151.25. Redline S, Tishler PV, Tosteson TD, et al. The familial aggregation of obstructive sleep apnea. Am J Respir Crit Care Med 1995:151(3 Pt 1):
59Risk Factor: Sedatives 150Phrenic Nerve100Peak Integrated activity(% control)Hypoglossal Nerve50Diazepam InjectionSlide 59Level 2Sedatives such as benzodiazepines have been shown to worsen sleep apnea in patients with pre-existing disease and to induce sleep apnea in individuals previously without the disorder.31,32 These agents work by selectively reducing hypoglossal nerve output to the genioglossus muscle, one of the pharyngeal dilator muscles.This slide shows the effect of injected diazepam on the output of the phrenic and hypoglossal nerves in a cat.33 There is a selective reduction in the hypoglosssal nerve activity over time, while the phrenic nerve is spared. This reduction in neural output to the dilator muscle promotes collapse of the pharyngeal airspace. Sedatives may also increase the arousal threshold, prolonging apneas.34Minutes after injectionSanders MH. In: Principles and Practice of Sleep Medicine. Philadelphia: W.B. Saunders Company, 1994.31. Dolly FR, Block AJ. Effect of flurazepam on sleep-disordered breathing and nocturnal oxygen desaturation in asymptomatic subjects. Am J Med 1982;73(2):32. Mendelson WB, Garnett D, Gillin JC. Flurazepam-induced sleep apnea syndrome in a patient with insomnia and mild sleep-related respiratory changes. J Nerv Ment Dis 1981;169(4):33. Bonora M, St. John WM, Bledsoe TA. Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity. Am Rev Respir Dis 1985;131(1):41-45.34. Sanders MH. Medical therapy for sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994;
62Risk Factor: Associated Conditions HypothyriodismAcromegalyAmyloidosisVocal cord paralysisMarfan syndromeDown syndromeNeuromuscular disordersSlide 62Level 2Patients with hypothyroidism are at increased risk for developing sleep apnea. The weight gain and macroglossia which can accompany the disease may narrow the upper airway, and the function of the upper airway muscles can be compromised.34 Thyroid hormone replacement therapy can reduce the degree of sleep apnea, independent of weight change.35 Other disorders which increase the risk of developing sleep apnea by causing narrowing of the upper airway include acromegaly,36 amyloidosis and vocal cord dysfunction,37 Marfan syndrome,38 and Down syndrome.39 Neuromuscular disorders such as post-polio syndrome, muscular dystrophy, and kyphoscoliosis increase the risk of sleep apnea through their effects on upper airway muscle activity.4034. Sanders MH. Medical therapy for sleep apnea. In Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine, 2nd edition. Philadelphia: WB Saunders, 1994:35. Rajagopal KR, Abbrecht P, Derderian SS et al. Obstructive sleep apnea in hypothyroidism. Ann Intern Med 1984;101(4):36. Partinen M, Telakivi T. Epidemiology of obstructive sleep apnea syndrome. SLEEP 1992;15(6 Suppl):S1-4.37. Kales A, Bela-bueno A, Kales JD. Sleep disorders: sleep apnea and narcolepsy. Ann Intern Med 1987;106(3):38. Cistulli P, Sullivan CE. Sleep-disordered breathing in Marfan’s syndrome. Am Rev Respir Dis 1993;147(3):39. Redline S, Tishler PV. Familian influences on sleep apnea. In: Lenfant C, Saunders N, eds. Lung Biology in Health and Disease: Sleep Related Breathing Disorder. New York: Marcel-Dekker, 1994:40. Guilleminault C. Clinical features and evaluation of obstructive sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994:
63Patient # 3 42 year old male weight lifter Girlfriend states he holds his breath during sleepHe is not aware of thisNo complaints of tirednessEpworth Sleepiness Scale 11
64Diagnosis: History Snoring (loud, chronic) Nocturnal gasping and chokingAsk bed partner (witnessed apneas)Automobile or work related accidentsPersonality changes or cognitive problemsRisk factorsExcessive daytime sleepinessThe first step in making a diagnosis of sleep apnea is taking a thorough history of the patient’s sleep schedule and sleep apnea symptoms. The responses shown on this slide indicate an increased probability of obstructive sleep apnea.5 Patients with loud, long-standing snoring are at an increased risk of having sleep apnea,41 especially if paired with gasping or choking episodes during sleep. These episodes may represent apneic events. It is very important that an attempt be made to elicit information from the patient’s bed partner. The patient is often unaware of what occurs during sleep and may not be aware of symptoms such as snoring. A bed partner’s description of witnessed apneas is highly suggestive of the presence of sleep apnea.42 A history of multiple automobile or work-related accidents, especially when associated with tiredness or fatigue, should prompt an investigation for sleep apnea.43 Information concerning risk factors – such as family history, alcohol or sedative use, predisposing medical conditions or cigarette smoking – should be elicited from anyone suspected of having sleep apnea. Most patients with sleep apnea are objectively sleepy, although daytime sleepiness is frequently underreported. As a result, it is important to know how to assess daytime sleepiness.Sleep Apnea: Is Your Patient at Risk? NIH Publication, No5. National Center on Sleep Disorders Research. Sleep apnea: Is your patient at risk? Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute, NIH Publication No , September 1995.41. Stradling JR, Crosby JH. Predictors and prevalence of obstructive sleep apnoea and snoring in 1001 middle aged men. Thorax 1991;46(2):85-90.42. Kump K, Whalen C, Tishler PV, Browner I, Ferrette V, Strohl KP, Rosenberg C, Redline S. Assessment of the validity and utility of a sleep-symptom questionnaire. Am J Respir Crit Care Med 1994;150(3):43. American Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med 1994;150(5 Pt 1):
65Diagnosis: Assessing Daytime Sleepiness Often unrecognized by patientAsk family membersMust ask specific questionsFatigue vs. sleepinessAuto crashes or near missesSleep in inappropriate settingsWorkSocial situationsPatients need to be specifically asked about the presence of daytime sleepiness. They often don’t recognize they are sleepy since the problem has been present for a prolonged period of time and they have changed their lifestyles gradually to compensate for it. By asking specific questions, the presence and degree of sleepiness can be elicited. Family members can provide valuable information.First, it is important to differentiate between sleepiness – falling asleep – and terms such as fatigue or tiredness, which can be due to other problems such as depression, anemia or heart failure.Once sleepiness is established, information about severity can be obtained by asking about situations in which the patient is falling asleep. Patients with sleep apnea have a higher rate of motor vehicle accidents,9 and a history of accidents related to falling asleep at the wheel may be a marker of more severe sleep apnea.43 Questions should be asked about falling asleep in inappropriate settings. The greater the degree of sleepiness, the more likely it is that a person will fall asleep in inappropriate settings such as while performing tasks at work, or while out at a restaurant or dinner party.9. Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138(2):43. American Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med 1994;150(5 Pt 1):
66Epworth Sleepiness Scale 0 = would never doze or sleep. 1 = slight chance of dozing or sleeping 2 = moderate chance of dozing or sleeping 3 = high chance of dozing or sleepingEpworth Sleepiness ScaleSituationChance of Dozing or SleepingSitting and reading____Watching TVSitting inactive in a public placeBeing a passenger in a motor vehicle for an hour or moreLying down in the afternoonSitting and talking to someoneSitting quietly after lunch (no alcohol)Stopped for a few minutes in traffic while drivingTotal score (add the scores up) (This is your Epworth score)
67Patient # 3 Blood pressure 140/85 His neck size is 18 inches Tonsils are 4+Rest of exam unremarkableSleep study with AHI of 25Lowest oxygen saturation 92%
68Diagnosis: Physical Examination Upper body obesity / thick neck> 17” males> 16” femalesHypertensionObvious airway abnormalityThe presence of these physical characteristics on physical examination should raise the physicians’ suspicion about the presence of sleep apnea.Obesity, particularly upper body obesity, is associated with the presence and severity of sleep apnea.29 In general, men with a neck circumference of 17 inches or greater and women with a neck circumference of 16 inches or greater are at a higher risk for sleep apnea.28Systemic hypertension is common in sleep apnea patients.44The presence of any obvious airway abnormality – such as a crowded oropharynx, tonsillar hypertrophy, retrognathia or nasal obstruction – puts the patient at risk for the development of sleep apnea.4529. Millman RP, Carlisle CC, McGarvey ST, Eveloff SE, Levinson PD. Body fat distribution and sleep apnea severity in women. Chest 1995;107(2):28. Davies RJ, Stradling JE. The relationship between neck circumference, radiographic pharyngeal anatomy, and the obstructive sleep apnoea syndrome. Eur Respir J (Denmark) 1990;3(5):44. Hla KM, Young TB, Bidwell T, Palta M, Skatrud JB, Dempsey J. Sleep apnea and hypertension. A population-based study. Ann Intern Med 1994;120(5):45. Shepard JW Jr., Gefter WB, Guilleminault C, et al. Evaluation of the upper airway in patients with obstructive sleep apnea. SLEEP 1991;14(4):
69Exam: Tonsillar Hypertrophy Oropharynx With Tonsillar HypertrophyNormal OropharynxThis slide shows a comparison of a normal oropharynx with one narrowed by tonsillar hypertrophy.Shepard JW Jr et al. Mayo Clin Proc 1990;65.46. Shepard JW Jr, Olsen KD. Uvulopalatopharygoplasty for treatment of obstructive sleep apnea. Mayo Clin Proc 1990;65(9):
70Patient With the Crowded Oropharynx Exam: OropharynxPatient With the Crowded OropharynxSlide 70Level 2This picture demonstrates a common finding in sleep apnea patients, the crowded oropharynx. The soft palate hangs low, the uvula is slightly enlarged and there is crowding by the lateral tonsillar pillars. The palatine tonsils are not visualized.46. Shepard JW Jr, Olsen KD. Uvulopalatopharygoplasty for treatment of obstructive sleep apnea. Mayo Clin Proc 1990;65(9):
71Structural Abnormalities Physical ExaminationStructural AbnormalitiesThis patient demonstrates structural abnormalities which can lead to airway narrowing and sleep apnea. Note the presence of a thick neck and retrognathia.47Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.47. Coccagna G, et al. The bird-like face syndrome (acquired micrognathia, hypersomnia, and sleep apnea). In: Guilleminault C, Dement WC, eds. Sleep apnea syndromes. New York: Alan R Liss, 1978:
72Practice Recommendation The risk for obstructive sleep apnea correlates on a continuum with obesity, large neck circumference, and hypertension. Combinations of these factors increase the risk for OSAHS in a non-linear manner.Evidence-Based Source:Institute for Clinical Systems ImprovementWeb Site of Supporting Evidence:Strength of Evidence:Class A: Randomized, controlled trial; Class B: Cohort study; Class C: Non-randomized trial with concurrent or historical controls, Case-control study, Study of sensitivity and specificity of a diagnostic test, Population-based descriptive study; Class D: Cross-sectional study, Case series, Case report; Class R: Consensus statement, Consensus report, Narrative review
73Diagnosis: Pediatric Apnea PresentationBehavioral problems / irritabilityPoor school performanceEnuresisSnoringCauseAdenotonsillar hypertrophyCraniofacial abnormalityFrequently not obeseSleep apnea can also occur in children. However, the presentation may be different from that seen in adults. The child may demonstrate behavioral problems, irritability, worsening school performance or recurrence of enuresis.48 The sleep study may show obstructive hypoventilation rather than classic apneas.49 Snoring or labored breathing is still observed during sleep.The most common cause of sleep apnea in children is tonsillar hypertrophy but sleep apnea can be seen with other craniofacial abnormalities which narrow the upper airway.50 Obesity is not a frequent cause of sleep apnea in children.48. Rosen CL, D’andrea L, Haddad GG. Adult criteria for obstructive sleep apnea do not identify children with serious obstruction. Am Rev Respir Dis 1992;146(5 pt I):49. Carrol JL, Laughlin GM. Obstructive sleep apnea syndrome in infants and children: diagnosis and management. In: Ferber R, Kryger MH, eds. Principles and practice of sleep medicine in the child. Philadelphia: WB Saunders, 1995:50. American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996;153(2):
74Child’s Enlarged Palatine & Adenoidal Tonsils Pediatric Sleep ApneaChild’s Enlarged Palatine & Adenoidal TonsilsChild with Sleep ApneaSlide 74Level 2Here is a picture of a typical child with sleep apnea. Note she is thin and is breathing through her mouth because of an occluded nasopharynx. This slide shows the reason: enlarged palatine and adenoidal tonsils blocking the air passageway.
76Question 6 What is the Gold Standard for diagnosing OSA? Overnight home oximetry?History from a bed partner?Overnight sleep study?Physical exam with obesity, increased neck size and history of daytime sleepiness?Answer: 3 - Overnight sleep study?; display results and correct answer
77Why Get a Sleep Study?Signs and symptoms poorly predict disease severityAppropriate therapy dependent on severityFailure to treat leads to:Increased morbidityMotor vehicle crashesMortalityOther causes of daytime sleepinessA sleep study is performed to confirm the presence of sleep apnea and to assess the level of severity of the disorder. Although identification of patients at risk for sleep apnea can be made through the history and physical, the signs and symptoms in any particular patient are poor indicators of the level of disease severity.51 The severity of illness determines the type and urgency of treatment.Delay in confirming the diagnosis and determining the severity of sleep apnea can lead to delay in initiating treatment. This can lead to increased morbidity from the cardiovascular consequences, increased risk of motor vehicle accidents and, as a result, increased mortality.Before initiating treatment, it is also important to confirm the diagnosis and rule out other possible causes of excessive daytime sleepiness such as periodic limb movements of sleep, narcolepsy or insufficient amounts of sleep. Because sleepiness is a nonspecific symptom that can be caused by other disorders, and snoring is common even in people without sleep apnea, it is necessary to confirm the presence of sleep apnea. A sleep study will provide this information.51. Viner S, Szalai JP, Hoffstein V. Are history and physical examination a good screening test for sleep apnea? Ann Intern Med 1991;115(5):
78What Test Should be Used? In-laboratory full night polysomnographySplit night studiesHome diagnostic systemsOximetry to full polysomnographyPhysiologic monitoring is required to make the diagnosis of sleep apnea. The options are listed on this slide.In-laboratory full-night polysomnography is the current gold standard and involves the measurement of multiple physiologic parameters while the patient sleeps in the sleep laboratory.A variant of this, the split-night study, incorporates two to four hours of diagnostic time and three to four hours of treatment time into a single night.Another option is to use a variety of home diagnostic systems. These range from quite simple approaches such as oximetry, which measures only one physiologic parameter, to more complex ones such as full polysomnography in the home.The availability of resources and the population to be studied will frequently dictate the optimal approach to testing.
79PolysomnographyThis slide shows the setup of equipment on a patient undergoing overnight polysomnography. Note the multiple EEG, EOG, EMG and respiratory electrodes required for full physiologic monitoring.
80Polysomnography in OSA PolysomnogramPolysomnography in OSASlide 80Level 2This figure demonstrates a page from a standard multi-channel all-night polysomnogram. Sleep stage is determined using the electroencephalogram (EEG), the electrooculogram (EOG), and the electromyogram (EMG). The lower series of channels measures respiratory parameters and are used to detect sleep apnea. They represent nasal-oral airflow, chest and abdominal wall motion, and arterial oxygen saturation. Additional parameters measured can include the electrocardiogram (EKG) and leg movement. Such a recording allows for a careful assessment of all desired variables over the course of an entire night, providing a relatively complete picture of the events occurring during sleep.52. American Thoracic Society. Indications and standards for cardiopulmonary sleep studies. Am Rev Respir Dis 1989;139(2):
81Full-Night In-Laboratory Polysomnography ProFull set of variables obtainedEquipment problems can be repairedTechnician can address patient problemsConCostAccessibilityPatient sleeps away from homeSlide 81Level 2There are both pros and cons to the use of a full-night in-laboratory polysomnogram. The pros include the fact that a full data set with all desired variables can be obtained. Thus, there is a complete picture of the night. Patient movement often necessitates transducer adjustment and changing EEG electrode leads. The observing technician can correct any problems, guaranteeing that quality signals are obtained all night. Finally, the technician can interact with the patient to insure comfort and address problems the patient might have.On the negative side, there are also potential problems. In-laboratory polysomnography is generally expensive, although direct comparisons to other approaches have not been undertaken. The patient may potentially be uncomfortable with all the monitoring equipment in the laboratory. Finally the patient must sleep away from home and the natural environment, which may yield less ideal sleep.
82Split-Night In-Laboratory Polysomnography ProReduced costPatient may be studied only onceReduces time to treatment initiationConDiagnostic time may be inadequateTreatment time limitedDifficult decisions required of techniciansSlide 82Level 2A split-night study involves both an early diagnostic portion, the same as with full night polysomnography, followed by a therapeutic trial later in the same night if apnea is present. During the therapeutic portion, continuous positive airway pressure (CPAP) is introduced. There are positives and negatives to this approach.The positives include reduced cost and the fact that the patient has to spend only one night in the sleep laboratory. By avoiding a second study, treatment can be started sooner.The negatives include potentially inadequate diagnostic time, such that apnea frequency is not adequately quantified and other diagnoses are potentially missed. Also, an incorrect CPAP pressure may be chosen due to time constraints as the night progresses. Finally, this approach may place difficult decisions in the hands of the night technician. This individual must decide whether a level of apnea severity appropriate to initiate CPAP has been reached, which is sometimes not completely clear.
83CasesSome cases can be misleading and you can miss serious cases if you just use oximetryIt is important to conduct the proper study
84Oximetry Pro Con Inexpensive Simple to perform Little patient discomfortWidely availableConInterpretation not standardPoor sensitivity – missed diagnosisSpecificity controversialSlide 84Level 2The advantage of overnight oximetry is that it is inexpensive, simple to perform, can be done in the patient’s home with little discomfort, and is widely available.The disadvantage of this method is that it is often difficult to interpret the results. The most appropriate way to interpret the test has not been standardized and results vary depending on the method used. As a result, sensitivity of the test can be poor, which can lead to missed diagnoses. Specificity is dependent on the method of interpretation used and may lead to increased testing.5454. Yamashiro Y, Kryger MH. Nocturnal oximetry: is it a screening tool for sleep disorders? SLEEP 1995;18(3):
85Home Study Tracing Slide 85 Level 2 Redline S et al. Chest 1991;100. Shown is a typical tracing from one of the other currently available home diagnostic units. This unit measures four physiologic parameters: heart rate, airflow, respiratory effort and oxyhemoglobin saturation. These areas where airflow stops, effort continues and saturation drops represent apneas.A large variety of units is available, each measuring from four to sixteen channels. A few have been carefully evaluated scientifically, but most have never been studied. As a result, generic statements about their utility are difficult.Redline S et al. Chest 1991;100.55. Redline S, Toreson T, Boucher MA, Millman RP. Measurement of sleep-related breathing disturbances in epidemiologic studies. Assessment of the validity and reproducibility of a portable monitoring device. Chest 1991;100(5):
86Home Study Pro Potentially less expensive Patient sleeps at home Con Generally fewer signals are recordedEquipment cannot be adjustedTechnician cannot assist patientSlide 86Level 2Despite the limitation of our knowledge about home study devices, several general pros and cons can be considered.On the pro side, the home studies are potentially less expensive, although careful cost comparisons have not been made. The home systems are likely more comfortable, with less monitoring equipment, and the patient can sleep at home in his or her own bed.On the con side, generally fewer signals are recorded and therefore less information is obtained. In addition, poor signal quality or loss of a signal may not be recognized or repaired. Finally, the technician cannot interact with the patient to address any problems. As a result, the appropriate use of these systems remains quite controversial.
87Diagnosis of Sleep Apnea In-laboratory polysomnographyGold standardAssess severityInitiate treatmentSlide 87Level 2In-laboratory polysomnography is the gold standard for the initial diagnosis, determination of severity, and treatment of sleep apnea.56. Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the use of portable recording in the assessment of obstructive sleep apnea. SLEEP 1994;17(4):
88Diagnostic Conclusions Signs and symptomsExcessive daytime sleepinessHypertension and other cardiovascular sequelaeSleep study resultsApnea / hypopnea frequencySleep fragmentationOxyhemoglobin desaturationIn interpreting the sleep study and making decisions regarding therapy, the signs and symptoms of the patient should be considered first. In particular, these include waking hypersomnolence and signs of cardiovascular sequelae.Next, the results of the sleep study should be reviewed with particular attention to apnea and hypopnea frequency, sleep disruption, arterial oxygen desaturation, and arrhythmias.Once all these are considered, therapy can be individualized to the needs of the patient.
89Treatment Objectives Reduce mortality and morbidity Decrease cardiovascular consequencesReduce sleepinessImprove quality of lifeThe goal of treatment for patients with sleep apnea should be the reduction of morbidity and mortality and improvement of their quality of life. This can be accomplished by preventing the cardiovascular consequences of sleep apnea and reducing the complications of daytime sleepiness.
90Therapeutic Approach Risk counseling Motor vehicle crashes Job-related hazardsJudgment impairmentApnea and comorbidity treatmentBehavioralMedicalSurgicalAs part of the therapeutic approach to sleep apnea, all patients should be counseled regarding their increased risk of motor vehicle crashes, job related injuries and impairment of judgement.43The treatment of sleep apnea and existing or consequent comorbidities can include behavioral, medical or surgical interventions.5743. American Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med 1994;150(5 Pt 1):57. Strollo PJ Jr., Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334(2):
91The High-Risk Driver Educate patient Document warning Resolve apnea quicklyFollow-upEffectivenessCompliancePatients with sleep apnea have an increased risk for motor vehicle accidents.58 The higher risk driver can be identified by a history of a previous motor vehicle accident related to falling asleep at the wheel, or by a history of being so profoundly sleepy that a high level of concern is raised.43It is imperative that the clinician educate the patient regarding the risk of driving while sleepy and document that this counseling has occurred. The most effective way to reduce this risk is prompt treatment and resolution of sleep apnea. If treatment cannot be initiated expeditiously, reporting the patient to the local motor vehicle authorities should be considered; local statutes vary however, and it is important to learn the laws for your region. Once treatment has been initiated, follow-up is essential to determine effectiveness of, and compliance, with therapy.58. Findley LJ, Levinson MP, Bonnie RJ. Driving performance and automobile accidents in patients with sleep apneas. Clin Chest Med 1992;13(3):43. American Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care 1994;150(5 Pt 1):
92Behavioral Interventions Encourage patients to:Lose weightAvoid alcohol and sedativesAvoid sleep deprivationAvoid supine sleep positionStop smokingA variety of behavioral interventions are available to modify sleep apnea. Where appropriate, weight loss should be encouraged.59 Alcohol and sedatives should be avoided as they induce instability and promote collapsibility of the upper airway during sleep.34 Sleep deprivation also leads to upper airway instability during sleep, increasing the likelihood of collapse.60 Avoiding the supine position may modify the severity of the apnea in patients with position-dependent sleep apnea.61 Finally, smoking cessation should be encouraged since data suggests that smoking is an independent risk factor for sleep apnea.2759. Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985;103(6 PT 1):34. Sanders MH. Medical Therapy for sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine, 2nd edition. Philadelphia: WB Saunders, 1994;60. Neilly JB, Kribbs NB, Maislin G, Pack AI. Effects of selective sleep deprivation on ventilation during recovery sleep in normal humans. J Appl Physiol 1992;72(1):61. Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. SLEEP 1991;14(6):27. Wetter DW, Young DB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154(19):
93Weight Loss Should be prescribed for all obese patients Can be curative but has low success rateOther treatment is required until optimal weight loss is achievedBecause of the high correlation between sleep apnea and obesity, particularly increased upper body mass, all patients who are obese should be encouraged to lose weight. Exercise and fitness should be recommended to all patients, both to improve sleep apnea and reduce cardiovascular disease risk. Weight loss can be very effective and, in some cases, even curative.59,62 The problem that frequently occurs is that weight loss, while effective, is difficult to achieve and to maintain.63,64 In patients with significant sleep apnea, other forms of treatment should not be delayed until proper weight loss is achieved since they may continue to experience the complications of sleep apnea during the period of attempted weight loss.59. Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985;103(6 PT 1):62. Sugerman HJ, Fairman RP, Baron PL, Kwentus JA. Gastric surgery for respiratory insufficiency of obesity. Chest 1986;90(1):81-86.63. Weintraub M. Long-term weight control study: conclusions. Clin Pharmacol Ther 1992;51(5):64. National Institutes of Health. Strategy development workshop for public education on weight and obesity. U.S. Department of Health and Human Services, Public Health Service, National Heart, Lung, and Blood Institute. NIH publication No September 1992.
94Weight Loss and Sleep Apnea 6543Mean Change in AHI, Events/hr21-1-2-3-4This slide depicts the relationship between weight change and apnea severity. In this study 694 randomly selected individuals were evaluated at four year intervals for sleep-disordered breathing to determine the longitudinal association between weight change and sleep apnea. A decrease in weight reduced the severity of the sleep apnea, with a 10% weight loss predicting a 26% drop in AHI. Conversely, a 10% gain in weight predicted a 32% increase in the AHI. This indicates that even a modest degree of weight loss can have a significant impact on apnea severity and that weight control can be an effective method for managing sleep apnea.65. Peppard PE, Young T, Palta, Dempsey J, Skatrud. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000; 284(23):-20 to <-10%-10 to <-5%-5% to <+5+5 to +10%+10% to +20Change in Body WeightAdapted from Peppard PE et al. JAMA 2000;284.
95Practice Recommendation Lifestyle modifications, particularly weight loss and reduced alcohol consumption can play a significant role in the reduction of severity of sleep apneaEvidence-Based Source:Institute for Clinical Systems ImprovementWeb Site of Supporting Evidence:Strength of Evidence:Class A: Randomized, controlled trial; Class B: Cohort study; Class C: Non-randomized trial with concurrent or historical controls, Case-control study, Study of sensitivity and specificity of a diagnostic test, Population-based descriptive study; Class D: Cross-sectional study, Case series, Case report; Class R: Consensus statement, Consensus report, Narrative review
96Sleep-Position Training Lying in the supine position results in a decrease in the size of the pharynx because of the effects of gravity.66,67 As a result, some people experience sleep apnea only when sleeping on their backs, while others may experience a worsening of the severity of their apnea when supine. These patients may benefit from sleep-position training, which is designed to prevent sleeping in the supine position.61 This slide illustrates the use of a tennis ball sewn into the back of a night shirt as a means of training the patient to avoid the supine position and sleep in the lateral recumbent position.The presence of a position-dependent breathing disturbance should be demonstrated before initiating this form of treatment. Positional dependence is less common in obese patients with severe disease. Changing position may convert severe apneas to milder forms of the disease such as hypopneas without changing the degree of sleep fragmentation.68 In these settings, positional therapy may not be sufficient and should be carefully monitored for effectiveness.66. Fouke JM, Strohl KP. Effect of position and lung volume on upper airway geometry. J Appl Physiol 1987;63(1):67. Pevernagie DA, Stanson AW, Sheedy PF, Daniels BK, Shepard JW Jr. Effects of body position on the upper airway of patients with obstructive sleep apnea. Am J Respir Crit Care Med 1995;152(1):61. Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. SLEEP 1991;14(6):68. Pevernagie DA, Shepard JW Jr. Relations between sleep stage, posture and effective nasal CPAP levels in OSA. SLEEP 1992;15(2):
97Medical Interventions Positive airway pressureContinuous positive airway pressure (CPAP)Bi-level positive airway pressureOral appliancesOther (limited role)MedicationsOxygenA number of medical interventions are available for the treatment of sleep apnea. Pressure devices act as pneumatic splints to keep the airway from collapsing and include continuous positive airway pressure systems and bi-level positive airway systems. A variety of oral appliances have been developed which mechanically hold the airway open, preventing collapse.In certain circumstances medications and/or oxygen may play a limited role in treatment.57. Strollo PJ Jr., Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334(2):
99Question 7A young adult male has htn and daytime sleepiness and is diagnosed with severe OSA. He will be starting CPAP therapy. He believes all his problems will be solved.In addition to resolving his breathing events, CPAP is most likely to improve:HypertensionDaytime sleepinessDepressionMemory issuesAnswer: 2 - Daytime sleepiness
100Positive Airway Pressure This slide depicts the therapeutic effect of continuous positive airway pressure (CPAP). In the panel on the left, you can see upper airway closure in an untreated sleep apnea patient. Note that the airway closure is diffuse, involving both the palate and the base of the tongue. In the second panel, CPAP is applied and the airway is splinted open by the positive pressure.69. Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1(8225):
101Positive Airway Pressure This slide depicts a patient sleeping while using a positive airway pressure system. These devices are highly portable, fit on a nightstand, and can easily be transported outside of the home.
102Benefits of CPAP: Mortality (AI > 20, All Ages)1.0CPAP0.9**0.8******0.7Control0.6Cumulative Survival0.50.40.30.20.10.0Treatment with continuous positive airway pressure (CPAP) reduces mortality. This figure from a retrospective study by He et al shows that patients with 20 or more apneas per hour who are treated with CPAP have fewer deaths than those who did not use CPAP.Interval YearsHe J et al. Chest 1988;94.21. He J, Kryger MH, Zorick FJ, Conway WA, Roth T. Mortality and apnea index in obstructive sleep apnea. Chest 1988;94(1):9-14.
103Benefits of CPAP: Sleepiness CPAP TreatmentLatency to Sleep (min)Continuous positive airway pressure (CPAP) has been objectively shown to improve daytime sleepiness. Lamphere et al measured the recovery of alertness after treatment with CPAP in sleep apnea patients. As shown on this slide, treatment with CPAP increased the latency to sleep onset, a measure of sleepiness determined by the Multiple Sleep Latency Test (MSLT), back to the normal range. This corresponds with a decrease in the propensity to fall asleep – the less sleepy one is, the longer it takes to fall asleep. The effect could be seen after one night on CPAP, and improved with continued use, shown by increasing sleep latency after 14 and 42 nights on CPAP.Adapted from Lamphere J et al. Chest 1989;96.70. Lamphere J, Roehrs T, Wittig R, Zorick F, Conway WA, Roth T. Recovery of alertness after CPAP in apnea. Chest 1989;96(6):
104Benefits of CPAP: Performance Obstacles hit in 30 min.Slide 104Level 2Treatment with CPAP improves alertness and daytime performance. Findley and colleagues tested the effect of CPAP on driving performance. They compared the number of obstacles hit in a driving simulator before and after three to five months of CPAP treatment. As shown on this slide, there was a significant decrease in the number of obstacles hit after CPAP, to a level not statistically different from that of control subjects.(n=6) (n=6)(n=12)Adapted from Findley L et al. Clin Chest Med 1992;13.58. Findley L, Levinson MR, Bonnie RJ. Driving performance and automobile accidents in patients with sleep apnea. Clin Chest Med 1992;13(3):
105Positive Airway Pressure: Problems Mask DiscomfortPatient Acceptance Claustrophobia Aerophagia Chest DiscomfortA variety of problems may be encountered when patients are treated with positive airway pressure therapy. The most common complaints are related to discomfort with the mask71,72: the mask is too tight, it hurts the bridge of the nose, it leaves marks, or air leaks. Nasal problems account for the highest rate of adverse effects: obstruction from nasal congestion, rhinorrhea, or dry nose and throat.71,73 Approximately 10% of patients will experience claustrophobia with a nasal mask.71 Some patients complain of air in the stomach or of chest discomfort. There is also a subset of patients who discontinue therapy because they find the use of a positive pressure system via nasal interface to be inconvenient.71,7371. Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis 1992;145(4 Pt 1):72. Waldhorn RE, Herrick TW, Nguyen MC, O’Donnell AE, Sodero J, Potolicchio SJ. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 1990;97(1):33-38.73. Nino-Murcia G, Mc Cann CC, Bliwise DL, Guilleminault C, Dement WC. Compliance and side effects in sleep apnea patients treated with nasal continuous positive airway pressure. West J Med 1989;150(2):
106Positive Airway Pressure: Problems Slide 106Level 2This slide depicts one of the problems associated with the use of nasal CPAP. Mechanical trauma from a tight-fitting mask can result in skin breakdown, especially on the bridge of the nose where the skin is particularly thin. This can be treated with the application of a barrier dressing to the bridge of the nose and refitting the interface. Patients may also develop an allergic skin reaction to the silicone component of the mask.
107CPAP Compliance Patient report: 75% Objectively measured use > 4 hrs for > 5 nights / week: 46%Asthma-medicine compliance: 30%Subjective patient compliance with nasal CPAP therapy has been quite favorable, with reports of 75% or greater long-term compliance.74,71 However, objective measures of compliance have been less encouraging. Only about half the patients are regular CPAP users, defined by use of their CPAP for four or more hours at least five nights a week.75Compliance with positive pressure therapy is similar to compliance with other types of chronic medical therapy, such as use of asthma medication, which has been found to be only about 30%.7674. Sanders MH, Gruendl CA, Rogers RM. Patient compliance with nasal CPAP therapy for sleep apnea. Chest 1986;90(3):71. Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis 1992;145(4 Pt 1):75. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993;147(4):76. Dekker FW, et al. Compliance with pulmonary medication in general practice. Eur Respir J (Denmark) 1993;6(6):
108CPAP Compliance: Apnea Severity CPAP Run Hours/NightSlide 108Level 2In order to improve use of CPAP, it would be helpful to understand what factors contribute to compliance with CPAP therapy. This slide shows data from Engleman et al, investigating the relationship between apnea severity and CPAP compliance.77 On the “Y” axis is the average number of hours per night of CPAP use, measured objectively by a time meter. The severity of apnea, using the Apnea/Hypopnea Index, is shown on the “X” axis. Note the lack of a significant linear relationship between apnea severity and objective hourly compliance. Additionally, neither patient demographics, such as age, sex and weight, nor rates of adverse reactions, have been shown to differentiate between those who use or discontinue CPAP.72,73 The most consistent factor associated with improved compliance is patient and family recognition of improvement in the sensations of sleepiness and alertness.1Apneas and Hypopneas/Hr.Engleman HM et al. SLEEP 1993;16.77. Engleman HM, Douglas NJ. CPAP compliance. SLEEP 1993;16(8):S114.72. Waldhorn RE, Herrick TW, Nguyen MC, O’Donnell AE, Sodero J, Potolicchio SJ. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 1990;97(1):33-38.73. Nino-Murcia G, Mc Cann CC, Bliwise DL, Guilleminault C, Dement WC. Compliance and side effects in sleep apnea patients treated with nasal continuous positive airway pressure. West J Med 1989;150(2):1. American Thoracic Society. Indications and standards for use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. Am J Respir Crit Care Med 1994;150(6 Pt 1):
109Practice Recommendation Polysomnography is the accepted standard test for the diagnosis of obstructive sleep apnea syndrome. The benefit of using attended polysomnography for diagnosis is the ability to establish a diagnosis and ascertain an effective CPAP treatment pressure.Evidence-Based Source:Institute for Clinical Systems ImprovementWeb Site of Supporting Evidence:Strength of Evidence:Class C: Non-randomized trial with concurrent or historical controls, Case-control study, Study of sensitivity and specificity of a diagnostic test, Population-based descriptive study; Class D: Cross-sectional study, Case series, Case report; Class M: Meta-analysis, Systematic review, Decision analysis, Cost-effectiveness analysis; Class R: Consensus statement, Consensus report, Narrative review
111Question 8A 50 yo male with OSA is started on CPAP at 12 cm H2O at home. He returns 2 weeks later and is having trouble tolerating CPAP.Which of following has been shown to help compliance?Zolpidem 5 mg at bedtimeAdd ramp systemHeated humidificationAdd chinstrapAnswer: 3 – heated humidification; display results and correct answer
112Strategies to Improve Compliance Machine-patient interfacesMasksNasal pillowsChin strapsHumidifiersRampDesensitizationBi-level pressureA variety of interventions may be utilized to improve compliance with CPAP. If machine-patient interface problems are present, changing the type of mask to improve comfort and decrease leaks may be efficacious. Nasal pillows may be helpful for people who find the mask too uncomfortable or who complain of claustrophobia. If significant mouth leaks are present, the application of a chin strap may be useful.Nasal congestion and airway dryness due to leak or high pressures may respond to the addition of a humidifier.Patients who have problems falling asleep due to high pressures may benefit from use of a ramp feature. With this feature, the CPAP pressure is gradually increased to the treatment pressure over a defined period of time, allowing the patient to fall asleep before maximal pressure is achieved.For patients having difficulty tolerating CPAP because of initial claustrophobic or anxiety response, desensitization or gradual habituation can sometimes be helpful. This can be performed at home or in the laboratory.If patients complain of difficulty exhaling against a high expiratory pressure, switching from CPAP to a bi-level device may improve acceptance of therapy.78. Strollo PJ Jr., Sanders MH, Stiller RA. Continuous and bi-level positive airway pressure therapy in sleep disordered breathing. COMS 1995;7:
113CPAP MasksSlide 113Level 2On the left is an illustration of a patient wearing an oral-nasal mask. In patients who have difficulty breathing by the nasal route, or in patients who have significant mouth leakage despite a chin strap, an oral-nasal mask may allow adequate pressurization of the airway. Caution should be used when utilizing in patients who experience trouble removing a mask.On the right is an illustration of a patient wearing nasal pillows. As you can see, the interface covers a smaller portion of the nose than the nasal mask. For certain patients, especially those who are claustrophobic, this may be more comfortable.
114Bi-level Positive Airway Pressure Positive Pressure TherapyCPAPBi-level1510Pressure5Slide 114Level 2InspFlowBi-level positive airway pressure may improve acceptability of therapy to patients requiring high pressure levels or those who complain of difficulty exhaling against the positive pressure. Bi-level devices allow the application of different pressure levels during inspiration and expiration. This slide shows the difference in the way positive pressure is delivered by the two modalities.With CPAP, positive pressure is delivered at the same level during inspiration and expiration. Bi-level therapy takes advantage of the differences in pressure in the upper airway during phases of respiration. During inspiration, negative intrathoracic pressure creates a pressure gradient which causes the pressure in the upper airway to be negative, promoting collapse of the airway.During expiration, the gradient reverses, pressure in the upper airway increases, and the forces promoting airway collapse are reduced. As a result, less pressure is required to keep the airway open during expiration than during inspiration. Bi-level devices allow independent adjustment of pressure levels during respiration, permitting the patient to breathe out against a lower positive pressure .Exp80. Sanders MH, Kern N. Obstructive sleep apnea treated by independently adjusted inspiratory and expiratory positive airway pressures via nasal mask. Physiologic and clinical implications. Chest 1990;98(2):
116Oral Appliances Indications Efficacy Side effects Snoring and apnea (not severe)EfficacyVariableSide effectsTMJ discomfort, dental misalignment, and salivationOral appliances may be efficacious in the treatment of sleep apnea. They appear to be particularly effective in patients with simple snoring and mild to moderate sleep apnea. Individual response to treatment is varied. Oral appliance therapy eliminates apnea in approximately 50% of patients.82A variety of side effects may be encountered, which include temporomandibular joint (TMJ) discomfort, dental misalignment and complaints of increased salivation.82. Schmidt-Nowara W, Lowe A, Wiegand L, Cartwright R, Perez-Guerra F, Menn S. Oral appliances for the treatment of snoring and obstructive sleep apnea: a review. SLEEP 1995;18(6):
117Oral Appliance: Mechanics There are several types of oral appliances available for the treatment of sleep apnea. This slide depicts a mandibular repositioning device. The oral appliance causes the mandible to move forward and the bite to open slightly. The effect of this mandibular repositioning is to enlarge the airway, reduce airway collapsibility and decrease airway resistance.82The device also anchors the mandible so that contraction of the genioglossus muscle moves the hyoid bone forward rather than just opening the mouth.Another proposed mechanism is the activation of upper airway muscles, although this has not been proven conclusively. In some patients, oral appliances are an effective treatment for sleep apnea.82. Schmidt-Nowara W, Lowe A, Wiegand L, Cartwright R, Perez-Guerra F, Menn S. Oral appliances for the treatment of snoring and obstructive sleep apnea: a review. SLEEP 1995;18(6):
118Supplemental Oxygen Not a primary treatment for sleep apnea Does not improve daytime sleepinessMay prolong apneasReduces oxygen desaturation during apneasReduces arrhythmiasSupplemental oxygen is not a first-line therapy for sleep apnea, but may be useful in patients who will not accept more definitive therapy but have severe nocturnal desaturation. Because collapse of the airway continues to occur, use of oxygen alone does not prevent the fragmentation of sleep caused by the recurrent sleep apnea events. As a result, there is no improvement in the symptoms of daytime sleepiness. Oxygen therapy may prolong apnea duration by increasing oxygen stores prior to the apneas, delaying one of the signals of arousal. The depth of oxyhemoglobin desaturation during the apneic events, however, may be decreased. The use of oxygen may reduce the frequency of dysrhythmias in patients who have dysrhythmias that are related to hypoxemia but should be used with caution in patients with obstructive lung disease and CO2 retention.83. Fletcher EC, Munafo DA. Role of nocturnal oxygen therapy in obstructive sleep apneas. When should it be used? Chest 1990;98(6):
119Pharmacologic Treatment Limited RoleProtriptyline or fluoxetineDecongestantsNasal steroidsAntihistaminesOtherSlide 119Level 2A variety of pharmacologic agents have been investigated as potential therapeutic options but they have been found to play only a limited role in the treatment of sleep apnea.57Protriptyline or fluoxetine may reduce the number of apneas in some patients, however, the overall effect is not a robust one.84 Treatment with these agents is also limited by a high rate of side effects.Nasal decongestants, nasal steroids, and antihistamines are helpful in decreasing nasal symptoms, particularly when related to the use of positive pressure devices, but are not efficacious as sole agents for treating sleep apnea.Other agents which have been investigated, such as theophylline, acetazolamide and progesterone, are not recommended.3457. Strollo PJ, Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334(2):84. Hanzel DA, Proia NG, Hudgel DW. Response of obstructive sleep apnea to fluoxetine and protriptyline. Chest 1991;100(2):34. Sanders MH. Medical therapy for sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994:
120Surgical Alternatives Reconstruct upper airwayUvulopalatopharyngoplasty (UPPP)Laser-assisted uvulopalatopharyngoplasty (LAUP)Radiofrequency tissue volume reductionGenioglossal advancementNasal reconstructionTonsillectomyBypass upper airwayTracheostomySeveral surgical alternatives have been developed for the treatment of sleep apnea. These treatments fall in two basic categories: upper airway reconstruction or bypassing of the upper airway. At present time tracheostomy, which bypasses the entire upper airway, is used only in life threatening situations or when all other therapies have failed.85Treatments which involve upper airway reconstruction include:uvulopalatopharyngoplasty (UPPP)laser-assisted uvulopalatopharyngoplasty (LAUP)radiofrequency tissue volume reduction (also called somnoplasty)genioglossal advancement (GA)maxillomandibular advancement (MMA)nasal surgerytonsillectomyThese are site-specific surgeries, attempts to surgically correct the site of airway collapse.8685. Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the treatment of obstructive sleep apnea in adults: efficacy of surgical modifications of the upper airway. SLEEP 1996;19(2):86. Powell NB, Guilleminault C, Riley RW. Surgical therapy of obstructive sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994:
121Sites of Airway Narrowing 18%82%Slide 121Level 2Airway closure during sleep is usually a diffuse process which limits the effectiveness of site-specific surgery. Morrison and colleagues used sleep endoscopy to show that only 18% of the patients in their study had airway closure limited to the palate alone. The rest of the patients demonstrated multiple sites of airway collapse. As a result, a single surgery may not be sufficient to eliminate sleep apnea.Adapted from Morrison DL et al. Am Rev Respir Dis 1993;148.87. Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in the patients with obstructive sleep apnea. Am Rev Respir Dis 1993;148(3):
122Uvulopalatopharyngoplasty (UPPP) Usually eliminates snoring41% chance of achieving AHI < 20No accurate method to predict surgical successFollow-up sleep study requiredUvulopalatopharyngoplasty (UPPP) has been the most common upper airway surgery performed on patients with sleep apnea. While it is usually effective in eliminating snoring, it frequently does not result in satisfactory treatment of sleep apnea. A meta-analysis by Sher et al demonstrated that there was only a 41% response rate, defined as reducing the apnea-hypopnea index to less than 20 following surgery.88 The more severe the apnea, the lower the likelihood of achieving a surgical cure utilizing this procedure.There is currently no way to accurately predict which patients are likely to achieve a surgical success. If uvulopalatopharyngoplasty is utilized as a treatment option, a follow-up sleep study should be performed to insure that the sleep apnea has been adequately treated.8588. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. SLEEP 1996;19(2):85. Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the treatment of obstructive sleep apnea in adults: efficacy of surgical modifications of the upper airway. SLEEP 1996;19(2):
123Uvulopalatopharyngoplasty (UPPP) This slide depicts the uvulopalatopharyngoplasty (UPPP) surgical technique.The panel on the left depicts the preoperative upper airway, demonstrating a long soft palate and the presence of palatine tonsils. The incision site is marked with the dotted line.The panel on the right depicts the postoperative oropharynx, with amputation of the uvula, bilateral palatine tonsillectomy, and trimming and suturing together of the anterior and posterior tonsillar pillars.89. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981;89(6):
124Radiofrequency Tissue Volume Reduction Radiofrequency energy delivered to palate or tongueCauses tissue scarring / retractionRelatively painlessOffice vs O.R. procedureFDA approved for snoring and sleep apneaRole unclear - limited efficacy dataThe most recently introduced method for changing the shape of the upper airway is Radiofrequency Tissue Volume Reduction, known as Somnoplasty®. A generator delivers pulses of radiofrequency energy through a needle electrode to the midline soft palate or the base of the tongue. The procedure causes tissue necrosis and fibrosis/scarring that leads to tissue retraction. Compared to other surgical and laser procedures, somonoplasty is relatively painless. The procedure can be performed as an office procedure or in an operating room, according to the surgeon’s evaluation of possible complications. Somnoplasty was approved by the FDA as a treatment for snoring and sleep apnea. Several studies have demonstrated significant improvement in snoring following the procedure.92,93 However, efficacy data for use of somnoplasty to treat sleep apnea is limited, suggesting only modest improvement.94 The true role of somnoplasty in the treatment of sleep apnea is unclear.92. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Radiofrequency volumetric reduction of the palate: an extended follow-up study. Otolaryngol Head Neck Surg 2000;122(3):93. Boudewyns A, Van De Heyning P. Temperature-controlled radiofrequency tissue volume reduction of the soft palate (somnoplasty) in the treatment of habitual snoring: results of a European multicenter trial. Acta Otolaryngol 2000;120(8):94. Powell NB, Riley RW, Guilleminault C. Radiofrequency tongue base reduction in sleep-disordered breathing: a pilot study. Otolaryngol Head Neck Surg 1999;120(5):
125Staged Surgical Procedures Additional maxillofacial surgeries have been developed to address the multiple sites of the upper airway collapse. They can be used alone or in conjunction with the uvulopalatopharyngoplasty. The procedure shown on the left is a genioglossal advancement, designed to correct obstruction in the hypopharynx by anteriorly advancing the base of the tongue.95Maxillomandibular advancement surgery is designed to enlarge the entire airway and is shown in the figure on the right. The maxilla and mandible are anteriorly advanced, moving the palate, tongue and hypopharynx.9695. Riley RW, Powell NB, Guilleminault C. Inferior sagittal osteotomy of the mandible with hyoid myotomy-suspension: a new procedure for obstructive sleep apnea. Otolaryngol Head Neck Surg 1986;94(5):96. Riley RW, Powell NB, Guilleminault C, Nino-Murcia G. Maxillary, mandibular, and hyoid advancement: an alternative to tracheostomy in obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 1986;94(5):
126Primary Care Management Risk counselingBehavior modificationMonitor symptoms and complianceMonitor weight and blood pressureAsk about recurrence of symptomsEvaluate CPAP use and side effectsA variety of issues should be addressed by the primary care clinician5:1. Risk counseling should be provided for all patients with sleep apnea.2. Initiation of appropriate behavioral modification treatments such as weight loss and smoking cessation.3. Patients undergoing treatment require monitoring for efficacy of and compliance with treatment and resolution of symptoms. Weight loss and changes in blood pressure should be monitored. Patients should be periodically re-evaluated for recurrence of symptoms after successful treatment. CPAP equipment should be checked periodically for proper functioning. Finally, objective compliance with CPAP should be documented, using hour meters currently available on most machines, and side effects or troubles with use detected and resolved.Sleep Apnea: Is Your Patient at Risk? NIH Publication No5. National Center on Sleep Disorders Research. Sleep Apnea: Is Your Patient at Risk? U.S. Department of Health and Human Services, National Institutes of Health, National Heart, Lung and Blood Institute, NIH Publication No , September 1995.
127Primary Care Management Reasons for lack of improvementNoncomplianceAlcohol and sedative useDepressionPoor sleep habitsNonapneic sleep disorderPersistent or recurrent symptomsConsider referral to sleep specialistThere are a number of reasons why patients do not improve despite appropriate treatment. The most likely reason is noncompliance. Alcohol and sedative effects on the upper airway muscles can negate the beneficial effects of treatment. Concomitant depression can present as sleep disturbances and should be excluded. Poor sleep habits which lead to sleep deprivation should be explored and, if present, corrected. If none of the above are apparent, other sleep disorders which are not related to apnea should be investigated.For individuals with persistent or recurrent symptoms, referral to a sleep specialist should be considered.
128Sleep Apnea Common Dangerous Easily recognized Treatable CONCLUSION Sleep apnea is a common disorder. It is dangerous for the patient and those around him or her. It is easily recognized and treated.
1322. Large neck circumference only 3. BMI and allergies Walter is a 42 year old male complaining of daytime fatigue and depression. What additional risk factors should you consider for a diagnosis of sleep apnea?1. BMI only2. Large neck circumference only3. BMI and allergiesBMI and respiratory diseaseBMI, Respiratory disease and large neck circumferenceAnswer 5 - BMI, Respiratory disease and large neck circumference. Display pre and post test results and correct answer.
133Fred, a 56 year old Asian man, has been diagnosed with diabetes and obstructive sleep apnea. All of the following co-morbidities are likely affected by Fred’s sleep apnea EXCEPT:HypertensionAsthmaErectile DysfunctionInsulin resistanceHeart FailureAnswer: 2 – Asthma; Display pre and post test results and correct answer.
134Mild cough and frequent headaches Restlessness and depression Jesse is a 52 year old executive who presents with fatigue. His wife has been complaining of his snoring over the past two years. He has been a two-pack a day smoker for 28 years. He weighs 260# and is sedentary. What symptoms would you ask Jesse about to make an initial diagnosis of obstructive sleep apnea?Mild cough and frequent headachesRestlessness and depressionSore throat and difficulty swallowingDry eyes and shortness of breathAnswer: 2 - Restlessness and depression; Display pre and post test results and correct answer.
135The Epworth Sleepiness Scale (ESS) Polysomnography Nighttime Oximetry You confirm that Jesse has met the conditions for a diagnosis of OSA. What test would most likely confirm this diagnosis?The Epworth Sleepiness Scale (ESS)PolysomnographyNighttime OximetryNone of the aboveAnswer: 2 – Polysomnography; Display pre and post test results and correct answer.
136A beer or other alcoholic beverage at bed time CPAP Jesse’s test confirms OSA. He says he is motivated to lose weight. What other treatment regimens do you prescribe?A beer or other alcoholic beverage at bed timeCPAPPrescription sleeping aids and CPAPSmoking cessation and CPAPAnswer: 4 - Smoking cessation and CPAP; Display pre and post test results and correct answer.