.jpg)
Win an iPod
Obstructive Sleep Apnea
| Article Date: 5/31/2007 |
Obstructive sleep apnea is one of the most common disorders in medicine; twenty-four percent of working middle-aged men and 9% of working middle-aged women have at least mild obstructive sleep apnea and the prevalence of obstructive sleep apnea in clinical populations is much higher. For example, 50% of middle-aged men hospitalized with myocardial infarction have obstructive sleep apnea. Sleep disorders literally permeate the practice of medicine, yet most health care providers are woefully under-prepared to diagnose and treat patients with sleep disorders. The vast majority of patients with obstructive apnea are not aware that they have a significant problem and they are suffering real consequences. Yet, obstructive sleep apnea is actually very easy to diagnose and very easy to treat; the most common treatment of obstructive sleep apnea is effective , relatively inexpensive (when compared to other medical therapies for other illnesses), and virtually devoid of serious side-effects.
Untreated Obstructive Sleep Apnea is associated with numerous significant long-term adverse health problems including: hypertension, increased risk of myocardial infarction, probable increased risk of stroke, mood abnormalities, neurocognitive dysfunction, and very importantly a marked increase risk of nonfatal and fatal automobile accidents. Patients with untreated Obstructive Sleep Apnea also consume excessive medical resources. With treatment, blood pressure may become easier to control, the risk of myocardial infarction may decline, mood typically improves, neurocognitive function improves and the risk of automobile accidents falls. Utilization of medical resources by the patient with OSA declines with treatment.
Obstructive sleep apnea is a relatively new medical disorder which was really first recognized in the medical literature in the 1970’s; in fact clinical sleep medicine, in general, is a very new medical specialty which has been growing for the last 20 years or so. As a result, the medical literature on sleep disorders is not as developed nor as complete as the literature on other medical disorders such as diabetes, heart disease, hypertension, asthma, cancer, and other disorders. Very little time is spent on sleep disorders in most medical school curricula (several surveys suggest less than 2 hours is spent formally on sleep disorders in medical school) and thus most health care providers are undereducated. Yet, when one looks at prevalence rates, one can predict that the average primary care physician who cares for 1500 patients will have 120 with diabetes, 450 with hypertension, less than 100 with heart failure, and 150-500 with obstructive sleep apnea. Whereas the vast majority of patients with diabetes, hypertension and heart failure will be diagnosed and treated, the same can’t be said for those with obstructive sleep apnea.
There are three conditions which underlie the physiologic basis of obstructive sleep apnea: 1) the anatomy of the posterior oropharynx which tends to be “small” and crowded in patients with obstructive sleep apnea; 2) most of the tissues supporting the posterior oropharynx are muscular; and 3) the fact that muscle relaxation occurs during sleep. During wakefulness, all skeletal muscles have significant tone – even the small, crowded posterior oropharynx is relatively non-collapsible during wakefulness because of this muscle tone. However, when sleep occurs, muscle tone decreases and there is a general collapse of the posterior oropharynx. Most individuals have a sufficiently large posterior oropharynx such that even with sleep related muscle relaxation and posterior oropharyngeal collapse, there is no compromise of airflow into the trachea. However, in patients with obstructive sleep apnea, the collapsible posterior oropharynx in sleep collapses in such a way that the airflow intake to the trachea is partially or completely obstructed. It is this partial and sometimes complete collapse that is the basis for the pathophysiologic effects and adverse clinical consequences of Obstructive Sleep Apnea (which could just as well be termed “Sleep Suffocation Syndrome”).
When the “tube” from the nose/mouth to the trachea is sufficiently open, airflow is laminar and thus quiet. However, when obstruction to the flow of air occurs, the diaphragm will reflexively generate more negative thoracic pressure “forcing” air through the partial obstruction. As the airflow then gets “funneled” through the posterior oropharynx, flow becomes turbulent and generates sound. Additionally, the soft tissues of the posterior oropharynx are collapsible and relaxed and as a result they vibrate when airflow becomes turbulent. This physiology generates the most common symptom of obstructive sleep apnea: SNORING. Snoring can ONLY occur if airflow is turbulent; airflow turbulence can only result if the airway diameter is insufficient (partially obstructed); thus snoring only occurs if airway obstruction is present.
There are several pathophysiologic mechanisms that occur as a result of posterior airway obstruction. The tital volume may decrease such that oxygen saturation may fall. It is not uncommon to see oxygen saturations under 50% in patients with severe obstructive sleep apnea. Chronically low oxygen saturation may induce significant (and in experimental animals irreversible) brain damage and may lead to activation of inflammatory mechanisms which have the potential to increase atherogenesis.
Moreover, the negative intrathoracic pressure changes which occur during partial/complete obstruction have physiologic consequences of its own (Mueller Maneuver). As intrathoracic pressures become more negative, venous blood return increases and tends to accumulate in the right heart and pulmonary circulation. This can result, in susceptible hearts, to a decreased blood return to the left atrium which can result in a decrease in left ventricular ejection fraction by up to 25%. Additionally, as the right atrium distends as a result of increasingly negative intrathoracic pressures and increased systemic venous blood return, stretch receptors are activated which lead to the production of atrial natiuretic peptide which ultimately results in increased urine production (nocturia is a very common manifestation of OSA). As right atrial pressures increase, a right to left shunt may occur through a patent foramen ovale (which is present in 30% of people) allowing the possibility of small paradoxical emboli to occur.
During the obstructive process, vagal influences predominate which causes a slight fall in blood pressure and heart rate. All of these abnormalities eventually lead to an arousal from sleep. During the arousal, sympathetic discharge predominates causing the blood pressure to suddenly rise and the heart rate to increase. If the obstruction has resulted in significant oxygen desaturation, it may take several heart beats before saturation returns to normal. This combination of vagal alternating with sympathetic discharge and hypoxemia can be very arrhythmogenic in hearts with significant coronary artery disease. As the brain arouses, normal breathing is restored. As normal breathing is restored, sleep occurs and the whole process is repeated. Thus, sleep is spent with repetitive airflow obstruction and arousals; sleep becomes very fragmented.
The sleep fragmentation of obstructive sleep apnea can then lead to neurocognitive dysfunction which is typically associated with sleep deprivation (depressed mood, decreased reaction time, decreased attention, frank sleepiness, etc).
These pathophysiologic mechanisms also seem to activate the inflammatory system (increased levels of c-reactive protein, increased lipid peroxidation) as well as affecting various hormones (ghrelin, leptin, insulin) in ways that contribute to obesity and diabetes.
Thus the mechanisms of physiologic dysfunction caused by OSA can be attributed to 1) oxygen desaturation; 2) sleep fragmentation; 3) repetitive Meuller maneuver during sleep; 4) increased inflammatory system activation; and 5) hormonal changes. The degree to which the dysfunctions occasioned by these mechanisms are reversible isn’t entirely known. Presumably, the earlier the diagnosis is made and the earlier treatment is offered, the more reversible/preventable these adverse outcomes will be.
Diagnosis of OSA is rather straightforward and involves the demonstration, during sleep, of repetitive obstruction to the flow of air. At a basic minimum the following data must be obtained during sleep: airflow, pulmonary effort, and oxygen saturation. Obstructive apnea can be diagnosed when there is decreased airflow in the face of thoracic effort. Screening studies using only limited physiologic measurements such as airflow, effort, and oxygen saturation can accurately diagnose OSA – but they cannot reliably “exclude” clinically significant obstructive apnea. Thus a “positive” home “screening” study can be used to diagnose OSA, but it can’t be used to exclude OSA. To exclude OSA a formal polysomnogram (airflow, effort, oxygen saturation, EEG sleep staging, and other channels) is required.
Treatment of OSA involves either bypassing the obstruction to the flow of air (tracheostomy) or of mechanically opening the posterior oropharynx. There are multiple ways to increase the posterior airway during sleep including: 1) positional therapy (in some patients sleeping in non-supine positions increases posterior airway diameter – the base of the tongue is less likely to obstruct); 2) weight loss (by decreasing fat deposits in neck); 3) “dental devices” (which either advance lower jaw or tongue); 4) Positive Airway Pressure; and 5) Surgical therapy. To date, there are no medications which appear effective.
The application of positive airway pressure during sleep is the first line therapy for obstructive sleep apnea for three reasons: 1) it will eliminate respiratory disturbances and significantly lower the Apnea Hypopnea Index (the number of breathing abnormalities per hour of sleep) when compared to placebo (“sham”-Positive Airway Pressure), conservative management, or positional therapy; 2) compared to other treatment modalities (dental devices, surgery), it is modestly priced; and 3) it is virtually without dangerous risk. Positive airway pressure is applied through nasal mask, nasal pillows, or a full face mask attached to a pressure generating device. By applying positive airway pressure during sleep, the posterior oropharynx is “splinted” during sleep such that collapse does not occur when the muscle relaxation of sleep occurs. Individual patient requirements for Positive Airway Pressure differ and accordingly each patient must be “titrated” to that patient’s optimal pressure.
Determining the optimal pressure for an individual patient can be done in fundamentally three ways: 1) full attended polysomnographically guided PAP titration (done in a sleep center); 2) home “autotitrating” study (using autotitrating PAP machines for a period of time and then averaging the pressures used to prescribe “fixed” PAP); 3) based on various formulas (using such variables as BMI, Neck circumference). Additionally, clinical autotitrating PAP is available.
Long-term compliance with CPAP therapy is quite variable from study to study but typically is in the 46%-85% range; the variability is in part attributed to different study definitions of “compliance/adherence”. Nevertheless, it is quite clear that PAP therapy is well tolerated by most, but not all, patients. In general compliance is better for patients with more severe OSA and in patients who derive significant clinical benefit from therapy with either improved night-time sleep or improved daytime functioning. The use of heated humidification also seems to significantly improve PAP compliance. Because patients who do not comply well with treatment do so within the first few weeks of therapy, close follow-up during the first few weeks appears to improve compliance. Durable medical goods companies can be used very effectively during these first few weeks to assure that patients have a quiet and comfortable PAP machine, the machine/face interface (nasal mask, nasal pillows, full face mask) is properly fitted and comfortable, and that heated humidity is appropriately provided. For some patients, formal desensitization protocols may be useful. And there are some patients who are intolerant of PAP because they may have other co-existing sleep disorders which require attention, such as circadian rhythm disorders (shift work, delayed sleep phase syndrome), Restless Legs Syndrome, or primary insomnia.
For patients intolerant of PAP who have significant OSA, other treatment options should be pursued and in such patients a sleep consultation will likely be required.
Primary care providers are asked to do a lot and they aren’t well-reimbursed for the work they do; many just don’t want to hear about yet another disease or another issue that to which they must respond. Most primary care providers are already over-worked, underpaid, and don’t have as much time as they would like to spend with each individual patient; the pressure to see a large number of patients is great. Sleep disordered patients do take time and they can be challenging. And patients with Obstructive Apnea can be challenging.
But sleep disordered patients can’t be ignored. And patients with obstructive apnea can’t be ignored; the consequences (increased risk of myocardial infarction, hypertension, possibly stroke, car accidents, and neurocognitive dysfunction) of ignored OSA are just too great. The average primary care provider has literally hundreds of patients with OSA – those patients MUST be identified and treated.
I would suggest to all primary care providers that each patient be asked about snoring. If a patient snores, and in particular if the snoring is loud and nightly, some type of sleep study should be performed. The vast majority of those patients will in fact have obstructive sleep apnea.
Whether the diagnosis is made with an unattended home study or a full attended-polysomnogram depends on the experience of the clinician and on local insurance regulations. For primary care providers who don’t have much experience, all patients who snore loudly and consistently should be referred for a formal sleep consultation. PATIENTS WHO SNORE LOUDLY AND REGULARLY need to be evaluated for OSA. End of story.
Suggested Reading:
Peter Gay MD; Terri Weaver RN, CS, FAAN; Daniel Loube MD; Conrad Iber MD. “Evaluation of Positive Airway Pressure Treatment for Sleep Related Breathing Disorders in Adults”. Sleep 2006;29:381-401
Lee K Brown MD. “Mild Obstructive Sleep Apnea Syndrome Should Be Treated”. Journal of Clinical Sleep Medicine 2007;3:259-262
Michael R. Littner MD. “Mild Obstructive Sleep Apnea Syndrome Should Not Be Treated”. Journal of Clinical Sleep Medicine 2007;3:263-264.
Ball EM, Simon RD, Tall AA, Banks MB, Nino-Murcia G, Dement WC. Diagnosis and Treatment of Sleep Apnea within the Community: The Walla Walla Project. Arch Intern Med 1997;157:419-424.
Kushida CA, Nichols DA, Simon RD, Young T, Grauke JH, Britzmann JB, Hyde PR, Dement WC. Symptom-Based Prevalence of Sleep Disorders in an Adult Primary Care Population. Sleep and Breathing.2000;4:11-16.
Untreated Obstructive Sleep Apnea is associated with numerous significant long-term adverse health problems including: hypertension, increased risk of myocardial infarction, probable increased risk of stroke, mood abnormalities, neurocognitive dysfunction, and very importantly a marked increase risk of nonfatal and fatal automobile accidents. Patients with untreated Obstructive Sleep Apnea also consume excessive medical resources. With treatment, blood pressure may become easier to control, the risk of myocardial infarction may decline, mood typically improves, neurocognitive function improves and the risk of automobile accidents falls. Utilization of medical resources by the patient with OSA declines with treatment.
Obstructive sleep apnea is a relatively new medical disorder which was really first recognized in the medical literature in the 1970’s; in fact clinical sleep medicine, in general, is a very new medical specialty which has been growing for the last 20 years or so. As a result, the medical literature on sleep disorders is not as developed nor as complete as the literature on other medical disorders such as diabetes, heart disease, hypertension, asthma, cancer, and other disorders. Very little time is spent on sleep disorders in most medical school curricula (several surveys suggest less than 2 hours is spent formally on sleep disorders in medical school) and thus most health care providers are undereducated. Yet, when one looks at prevalence rates, one can predict that the average primary care physician who cares for 1500 patients will have 120 with diabetes, 450 with hypertension, less than 100 with heart failure, and 150-500 with obstructive sleep apnea. Whereas the vast majority of patients with diabetes, hypertension and heart failure will be diagnosed and treated, the same can’t be said for those with obstructive sleep apnea.
There are three conditions which underlie the physiologic basis of obstructive sleep apnea: 1) the anatomy of the posterior oropharynx which tends to be “small” and crowded in patients with obstructive sleep apnea; 2) most of the tissues supporting the posterior oropharynx are muscular; and 3) the fact that muscle relaxation occurs during sleep. During wakefulness, all skeletal muscles have significant tone – even the small, crowded posterior oropharynx is relatively non-collapsible during wakefulness because of this muscle tone. However, when sleep occurs, muscle tone decreases and there is a general collapse of the posterior oropharynx. Most individuals have a sufficiently large posterior oropharynx such that even with sleep related muscle relaxation and posterior oropharyngeal collapse, there is no compromise of airflow into the trachea. However, in patients with obstructive sleep apnea, the collapsible posterior oropharynx in sleep collapses in such a way that the airflow intake to the trachea is partially or completely obstructed. It is this partial and sometimes complete collapse that is the basis for the pathophysiologic effects and adverse clinical consequences of Obstructive Sleep Apnea (which could just as well be termed “Sleep Suffocation Syndrome”).
When the “tube” from the nose/mouth to the trachea is sufficiently open, airflow is laminar and thus quiet. However, when obstruction to the flow of air occurs, the diaphragm will reflexively generate more negative thoracic pressure “forcing” air through the partial obstruction. As the airflow then gets “funneled” through the posterior oropharynx, flow becomes turbulent and generates sound. Additionally, the soft tissues of the posterior oropharynx are collapsible and relaxed and as a result they vibrate when airflow becomes turbulent. This physiology generates the most common symptom of obstructive sleep apnea: SNORING. Snoring can ONLY occur if airflow is turbulent; airflow turbulence can only result if the airway diameter is insufficient (partially obstructed); thus snoring only occurs if airway obstruction is present.
There are several pathophysiologic mechanisms that occur as a result of posterior airway obstruction. The tital volume may decrease such that oxygen saturation may fall. It is not uncommon to see oxygen saturations under 50% in patients with severe obstructive sleep apnea. Chronically low oxygen saturation may induce significant (and in experimental animals irreversible) brain damage and may lead to activation of inflammatory mechanisms which have the potential to increase atherogenesis.
Moreover, the negative intrathoracic pressure changes which occur during partial/complete obstruction have physiologic consequences of its own (Mueller Maneuver). As intrathoracic pressures become more negative, venous blood return increases and tends to accumulate in the right heart and pulmonary circulation. This can result, in susceptible hearts, to a decreased blood return to the left atrium which can result in a decrease in left ventricular ejection fraction by up to 25%. Additionally, as the right atrium distends as a result of increasingly negative intrathoracic pressures and increased systemic venous blood return, stretch receptors are activated which lead to the production of atrial natiuretic peptide which ultimately results in increased urine production (nocturia is a very common manifestation of OSA). As right atrial pressures increase, a right to left shunt may occur through a patent foramen ovale (which is present in 30% of people) allowing the possibility of small paradoxical emboli to occur.
During the obstructive process, vagal influences predominate which causes a slight fall in blood pressure and heart rate. All of these abnormalities eventually lead to an arousal from sleep. During the arousal, sympathetic discharge predominates causing the blood pressure to suddenly rise and the heart rate to increase. If the obstruction has resulted in significant oxygen desaturation, it may take several heart beats before saturation returns to normal. This combination of vagal alternating with sympathetic discharge and hypoxemia can be very arrhythmogenic in hearts with significant coronary artery disease. As the brain arouses, normal breathing is restored. As normal breathing is restored, sleep occurs and the whole process is repeated. Thus, sleep is spent with repetitive airflow obstruction and arousals; sleep becomes very fragmented.
The sleep fragmentation of obstructive sleep apnea can then lead to neurocognitive dysfunction which is typically associated with sleep deprivation (depressed mood, decreased reaction time, decreased attention, frank sleepiness, etc).
These pathophysiologic mechanisms also seem to activate the inflammatory system (increased levels of c-reactive protein, increased lipid peroxidation) as well as affecting various hormones (ghrelin, leptin, insulin) in ways that contribute to obesity and diabetes.
Thus the mechanisms of physiologic dysfunction caused by OSA can be attributed to 1) oxygen desaturation; 2) sleep fragmentation; 3) repetitive Meuller maneuver during sleep; 4) increased inflammatory system activation; and 5) hormonal changes. The degree to which the dysfunctions occasioned by these mechanisms are reversible isn’t entirely known. Presumably, the earlier the diagnosis is made and the earlier treatment is offered, the more reversible/preventable these adverse outcomes will be.
Diagnosis of OSA is rather straightforward and involves the demonstration, during sleep, of repetitive obstruction to the flow of air. At a basic minimum the following data must be obtained during sleep: airflow, pulmonary effort, and oxygen saturation. Obstructive apnea can be diagnosed when there is decreased airflow in the face of thoracic effort. Screening studies using only limited physiologic measurements such as airflow, effort, and oxygen saturation can accurately diagnose OSA – but they cannot reliably “exclude” clinically significant obstructive apnea. Thus a “positive” home “screening” study can be used to diagnose OSA, but it can’t be used to exclude OSA. To exclude OSA a formal polysomnogram (airflow, effort, oxygen saturation, EEG sleep staging, and other channels) is required.
Treatment of OSA involves either bypassing the obstruction to the flow of air (tracheostomy) or of mechanically opening the posterior oropharynx. There are multiple ways to increase the posterior airway during sleep including: 1) positional therapy (in some patients sleeping in non-supine positions increases posterior airway diameter – the base of the tongue is less likely to obstruct); 2) weight loss (by decreasing fat deposits in neck); 3) “dental devices” (which either advance lower jaw or tongue); 4) Positive Airway Pressure; and 5) Surgical therapy. To date, there are no medications which appear effective.
The application of positive airway pressure during sleep is the first line therapy for obstructive sleep apnea for three reasons: 1) it will eliminate respiratory disturbances and significantly lower the Apnea Hypopnea Index (the number of breathing abnormalities per hour of sleep) when compared to placebo (“sham”-Positive Airway Pressure), conservative management, or positional therapy; 2) compared to other treatment modalities (dental devices, surgery), it is modestly priced; and 3) it is virtually without dangerous risk. Positive airway pressure is applied through nasal mask, nasal pillows, or a full face mask attached to a pressure generating device. By applying positive airway pressure during sleep, the posterior oropharynx is “splinted” during sleep such that collapse does not occur when the muscle relaxation of sleep occurs. Individual patient requirements for Positive Airway Pressure differ and accordingly each patient must be “titrated” to that patient’s optimal pressure.
Determining the optimal pressure for an individual patient can be done in fundamentally three ways: 1) full attended polysomnographically guided PAP titration (done in a sleep center); 2) home “autotitrating” study (using autotitrating PAP machines for a period of time and then averaging the pressures used to prescribe “fixed” PAP); 3) based on various formulas (using such variables as BMI, Neck circumference). Additionally, clinical autotitrating PAP is available.
Long-term compliance with CPAP therapy is quite variable from study to study but typically is in the 46%-85% range; the variability is in part attributed to different study definitions of “compliance/adherence”. Nevertheless, it is quite clear that PAP therapy is well tolerated by most, but not all, patients. In general compliance is better for patients with more severe OSA and in patients who derive significant clinical benefit from therapy with either improved night-time sleep or improved daytime functioning. The use of heated humidification also seems to significantly improve PAP compliance. Because patients who do not comply well with treatment do so within the first few weeks of therapy, close follow-up during the first few weeks appears to improve compliance. Durable medical goods companies can be used very effectively during these first few weeks to assure that patients have a quiet and comfortable PAP machine, the machine/face interface (nasal mask, nasal pillows, full face mask) is properly fitted and comfortable, and that heated humidity is appropriately provided. For some patients, formal desensitization protocols may be useful. And there are some patients who are intolerant of PAP because they may have other co-existing sleep disorders which require attention, such as circadian rhythm disorders (shift work, delayed sleep phase syndrome), Restless Legs Syndrome, or primary insomnia.
For patients intolerant of PAP who have significant OSA, other treatment options should be pursued and in such patients a sleep consultation will likely be required.
Primary care providers are asked to do a lot and they aren’t well-reimbursed for the work they do; many just don’t want to hear about yet another disease or another issue that to which they must respond. Most primary care providers are already over-worked, underpaid, and don’t have as much time as they would like to spend with each individual patient; the pressure to see a large number of patients is great. Sleep disordered patients do take time and they can be challenging. And patients with Obstructive Apnea can be challenging.
But sleep disordered patients can’t be ignored. And patients with obstructive apnea can’t be ignored; the consequences (increased risk of myocardial infarction, hypertension, possibly stroke, car accidents, and neurocognitive dysfunction) of ignored OSA are just too great. The average primary care provider has literally hundreds of patients with OSA – those patients MUST be identified and treated.
I would suggest to all primary care providers that each patient be asked about snoring. If a patient snores, and in particular if the snoring is loud and nightly, some type of sleep study should be performed. The vast majority of those patients will in fact have obstructive sleep apnea.
Whether the diagnosis is made with an unattended home study or a full attended-polysomnogram depends on the experience of the clinician and on local insurance regulations. For primary care providers who don’t have much experience, all patients who snore loudly and consistently should be referred for a formal sleep consultation. PATIENTS WHO SNORE LOUDLY AND REGULARLY need to be evaluated for OSA. End of story.
Suggested Reading:
Peter Gay MD; Terri Weaver RN, CS, FAAN; Daniel Loube MD; Conrad Iber MD. “Evaluation of Positive Airway Pressure Treatment for Sleep Related Breathing Disorders in Adults”. Sleep 2006;29:381-401
Lee K Brown MD. “Mild Obstructive Sleep Apnea Syndrome Should Be Treated”. Journal of Clinical Sleep Medicine 2007;3:259-262
Michael R. Littner MD. “Mild Obstructive Sleep Apnea Syndrome Should Not Be Treated”. Journal of Clinical Sleep Medicine 2007;3:263-264.
Ball EM, Simon RD, Tall AA, Banks MB, Nino-Murcia G, Dement WC. Diagnosis and Treatment of Sleep Apnea within the Community: The Walla Walla Project. Arch Intern Med 1997;157:419-424.
Kushida CA, Nichols DA, Simon RD, Young T, Grauke JH, Britzmann JB, Hyde PR, Dement WC. Symptom-Based Prevalence of Sleep Disorders in an Adult Primary Care Population. Sleep and Breathing.2000;4:11-16.