Defined by the presence of a pathologic number of episodes of cessation or reduction of respiratory flow during sleep usually associated with arterial desaturation, sleep disruption, severe snoring and excessive daytime sleepiness.
The prevalence of OSA estimated to between 73-82% in individuals with resistant hypertension, 76-85% of patients with atrial fibrillation, 65-85% of patients with type two diabetes, 71% in individuals with stroke, and 71-77% of patients undergoing bariatric surgery.
It is characterized by recurrent episodes of partial or complete collapse of the upper airway during sleep resulting in reduced or absent airflow lasting for at least 10 seconds and associated with either cortical arousal or a fall in blood oxygen saturation.
Episodic sleep state-dependent collapse of the upper airway, resulting in periodic reductions or cessations in ventilation, with consequent hypoxia, hypercapnia, or arousals from sleep.
The involvement of the hyoid bone is demonstrated to have an inferior position that is strongly associated with the presence and severity of the obstructive sleep apnea.
Contraction of upper airway dilator muscles is necessary to maintain airway patency during inspiration.
The prevalence of obstructive sleep apnea is conservatively estimated to be 3% among women and 10% among men 30 to 49 years of age and 9% among women and 17% among men 50 to 70 years of age, including an estimated 24 million persons in the United States who have not received a diagnosis.
The estimated prevalence mean of at least mild OSA plus symptoms of daytime sleepiness among adults age 30 to 70 years is 14% for men and 5% for women, and the estimated prevalence of moderate to severe OSA is 13% for men and 6% for women.
OSA increases with age and is approximately twice is common in men as in women.
Severe OSA is associated with increased all cause mortality and other health outcomes include cardiovascular disease cerebrovascular events, type two diabetes, cognitive impairment, and decreased quality of life and motor vehicle crashes.
Associated with hypertension, type two diabetes, atrial fibrillation, heart failure, coronary heart disease, stroke, and death.
Obstructive sleep apnea is an independent risk factor for motor vehicle accidents and cardiovascular disease.
Patients treated with percutaneous coronary intervention experience a high prevalence of obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep.
Characterized by repeated collapse of the upper airway during the night causing intermittent hypoxemia, sleep disruption and increased risk for neurocognitive and cardiovascular morbidity.
Characterized by recurring cessations or reductions in respiratory flow due to upper airway collapse during sleep.
Associated with recurrent episodes of nocturnal hypercnea, nocturnal hypoxemia, and endothelial dysfunction, hypercoagulability, and sympathetic overactivity.
Associated with a higher risk of cardiovascular complications such as hypertension, myocardial ischemia, heart failure, arrhythmias, stroke, and sudden cardiac death.
Black men and higher risk for sleep happier mortality.
The use of general anesthetics, sedatives and postoperative analgesics or respiratory depressants that relax the upper airway dilator muscles and impair ventilatory responses to hypoxemia and hypercapnia and may predispose patients to postoperative cardiovascular complications.
Prevalence of 22% in men and 17% in women.
Affects about 14% of adult men and 5% of adult women.
The majority of cases remain undiagnosed.
Among patients undergoing major non-cardiac surgery the presence of severe OSA is significantly associated with 30 day cardiovascular complications.
Prevalence estimated to be 3% among women and 10% among men 30-49 years of age and 9% among women and 17% among men 50-70 years of age.
Estimated 24 million persons in the US.
Many patients are unaware that their breathing is affected.
Due to narrowing of the pharynx causing gas exchange abnormalities with impairment of sleep and secondary neurobehavioral and cardiovascular changes.Risk factors are related to conditions that reduce the size of the resting pharynx or increase airway collapsibility.
The most important risk factor for obstructive sleep apnea, is obesity, as increased adipose tissue within the tongue and pharynx compromises upper-airway dimensions and makes the airway more prone to collapse during sleep.
Sleep causes narrowing of the upper airway behind the uvula and soft palate or at the base of the tongue, or at both sites associated a result of anatomical or neuromuscular dysfunction preventing the patency of the airway.
Protective reflexes in the pharyngeal airway maintains patency during wakefulness, but with sleep there is a loss of these reflexes reducing the activity of the pharyngeal dilator muscle, causing collapse of a susceptible airway.
Often manifested by snoring which occurs when turbulent airflow through a narrowed upper airway causes vibration of pharyngeal structures.
Before diagnosis, patients have higher rates of healthcare utilization, more frequent and longer hospital stays, and greater healthcare costs then after diagnosis.
Associated with intermittent oxyhemoglobin desaturation and sympathetic activation.
Moderate to severe obstructive sleep apnea is defined as an apnea-hypopnea index (AHI) score a 15 or more apnea or hypopnea events per hour.
Obstructive apneas are defined as near-complete, that is > 90% cessations in airflow for more than 10 seconds in sleep, despite ventilatory effort, and hypopneas are generally defined as reductions in airflow by more than 30% with concurrent reductions in oxyhemoglobin saturation by at least 3% or arousals from sleep.
Obstructive apneas and hypopneas result in large changes in intrathoracic pressure, intermittent hypoxemia and arousal from sleep.
OSA sleep arousals generally did not wake the patient, but sleep fragmentation is the primary cause of excessive sleepiness in individuals.
Moderate to severe obstructive sleep is an independent risk factor for insulin resistance, dyslipidemia, vascular disease, and death.
Results from narrowing or closure of airways from any point from the nose to the larynx.
Increased androgen levels with the use of androgen supplementation and polycystic ovarian disease, may increase muscle mass in the tongue and worsen obstructive sleep apnea.
The prevalence of obstructive sleep apnea is increased among persons with hypothyroidism or acromegaly.
Increased tonsillar and adenoid tissue and certain craniofacial abnormalities may also confer a predisposition to obstructive sleep apnea.
Results from an obstruction of the upper airway during sleep with inadequate motor tone of the tongue and or airway dilator muscles.
A reduction in the activity of the dilator muscles of the pharynx may contribute to the problem.
Leads to brain arousal, intermittent hypoxemia, impared quality of life and metabolic disturbances.
Associated with cardiovascular morbidity, insulin resistance, accelerated mortality and neural injury.
Occurs most commonly when the patient is in rapid eye movement sleep and when relaxation of pharyngeal muscles occur leading to collapse of the upper airway.
Refers to cessation of breathing during sleep for 10 seconds in adults and for two or more consecutive breaths in children.
Healthy adults have up to 4.9 cessation of breathing events per hour.
Weight loss is effective reducing obstructive sleep apnea.
It is estimated that roughly one in every 15 Americans is affected by at least a moderate degree of sleep apnea.
Causes hemoglobin desaturation, blood pressure fluctuations, cortical arousal and sleep fragmentation.
Airway obstruction during obstructive sleep apnea is associated with pulsatile and crescendo-decrescendo activity in respiratory muscles and often in supplemental muscles to increase respiratory effort, and to reposition the patient.
Muscles involved include the diaphragm and muscles of the thorax, neck, and head.
Muscle activity in the arms and legs, abdominal wall become involved in each contraction of skeletal muscles resulting in mechanical coupling activation of muscle afferent receptors with transmission within nerves of the muscle to the brain with potential to arouse the brain and hinder normal sleep.
Daytime somnolence, obesity, snoring, lower-extremity edema, morning headaches and nocturia suggest the diagnosis.
Chronic morning headache is twice as common in patients will always say than in the general population.
Difficulty falling asleep is unlikely to be caused by obstructive sleep apnea.
OSA should be considered an old patient to report sleepiness.
Obesity is the most important risk factor.
OSA reported to be present in more than 40% of patients with a BMI of more than 30 and 60% of persons with metabolic syndrome.
Male gender is an important risk factor.
It is suspected that progesterone stimulation of upper airway muscles and ventilation in females may contribute to the lower prevalence among premenopausal women than among older women,
whereas higher androgen levels in some women may increase muscle mass in the tongue and worsen obstructive sleep apnea.
Increased adipose tissue within the tongue and pharynx compromise the airway dimensions and makes the airway more prone to collapse during sleep.
The prevalence of OSA is increased among persons with hypothyroidism or acromegaly.
Increased tonsillar and adenoid tissue and various cranial facial abnormalities may increase the predisposition to OSA.
Solriamfetol (Sunosi) to improve wakefulness in adults with excessive daytime sleepiness associated with narcolepsy or obstructive sleep apnea.
May occur in up to 50% of patients with obstructive sleep apnea, and is due to increased atrial natriuretic factor (ANF).
CPAP treatment has a 70% chance of reducing obstructive sleep apnea associated
Treatment is guided by the severity of disease, symptoms, coexisting conditions, and the presence of exacerbating factors.
Should be considered in all patients who report sleepiness.
Treatment for OSA is recommended for all patients with an AHI of 15 or more events per hour, as well as for persons with an AHI of 5 to 14 events per hour with symptoms of sleepiness, impaired cognition, mood disturbance, or insomnia or with coexisting conditions such as hypertension, ischemic heart disease, or a history of stroke.
Positive airway pressure (PAP) is applied with a tight seal to the nose or mouth, or both, serving to open the upper airway.
Continuous positive airway pressure (CPAP) provides a constant level of positive pressure across inspiration and expiration.
Positive airway pressure is highly effective in reducing the AHI to <5 events per hour in most patients.
Cognitive behavioral therapy or short-term use of a hypnotic drug at positive airway pressure initiation may increase its nightly use.
CPAP is more effective than a mandibular-advancement splint in reducing AHI, but adherence is greater with the oral appliance.
Mandibular-advancement splints are recommended for patients with mild-to-moderate obstructive sleep apnea who are unable to use CPAP.
A substantial proportion of patients refuse to do not tolerate CPAP.
Uvulopharyngopalatoplasty may be beneficial in patients with mild or moderate obstructive sleep apnea and favorable anatomy.
Hypoglossal-nerve stimulation during sleep to move the tongue forward and open the airway shows sustained effectiveness, with clinically relevant improvement with AHI of <20 events per hour and >50% reduction in the AHI in 75% of the patients.
Electrical stimulation to improve tongue muscle function helps reduce snoring in mild obstructive sleep apnea: the device eXciteOSA.
Weight loss is recommended to all overweight or obese patients with obstructive sleep apnea.
Weight loss of more than 10 kg may resolve obstructive sleep apnea in more than 50% of persons with mild disease and improve cardiometabolic health.
Bariatric surgery is associated with improvement of OSA.
Medications and substances that relax muscles or suppress respiratory drive (e.g.,
Alcohol, benzodiazepines, and opioids may exacerbate obstructive sleep apnea by relaxing muscles or suppressing respiratory drive.
Effective CPAP markedly improved self-perception of health and vitality,
fatigue and daytime sleepiness.
CPAP treatment of obstructive sleep apnea was associated with a substantial reduction in the risk of motor vehicle accidents.
Elevated ANF levels from right atrial stretching from either negative intrathoracic pressure, hypoxia induced pulmonary vasoconstriction or both.
Many patients undergoing sinonasal surgery have undiagnosed OSA.
High incidence of sleep apnea in COPD patients.
Craniofacial and upper airway structure may play important role in the occurrence of obstructive sleep apnea, and these may be significant in Asians.
Patients with skeletal or soft tissue abnormalities including mandibular or maxillary size, or position changes, and nasal narrowing, tonsillar hypertrophy may play a role in the development of sleep apnea.
A formal sleep study is usually needed for diagnosis.
Diagnosis usually requires overnight polysomnography to detect frequency of apneic and hypopneic events are.
Sleep studies determine sleep time, sleep stages, respiratory effort, air flow, cardiac rhythm, oximetry and limb movements.
The frequency of apnea and hypopnea events per hour of sleep, referred to as the apnea-hypopnea index (AHI), is determined by polysomnography which is a continuous overnight recording of sleep, breathing and cardiac parameters.
Hypoxemia in patients with obstructive sleep apnea probably drives parasympathetic activation and bradyarrhythmias.
Hypoxemia is a predictor of cardiovascular outcomes, including sudden cardiac death.
OSA with an AHI of 20 or more events per hour has been associated with an increase in an adjusted risk of stroke by a factor of four in men and a factor of two in women.
OSA is associated with an increased risk of diabetes, increased levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides and decreased levels of high-density lipoprotein cholesterol.
Polysomnography involves a minimum of 12 channels of recordings that include electroencephalogram, electrooculogram, oronasal airflow, electromyogram, chest wall effort, body position, snore microphone, electrocardiogramand oxyhemoglobin saturation level.
Polysomnography measures an anterior tibial electromyogram, body position, nasal pressure and nasal oral airflow, a throat microphone, and chest / abdominal movement.
Polysomnography should last at least 6 hours to evaluate the different stages of sleep.
Polysomnography over 1 night has a sensitivity of 75-88% to detect mild OSA with a apnea-hypopnea index of 5 or greater.
OSA syndrome defined by an AHI of five or greater with associated symptoms.
The number of apneas and hypopneas per hour of sleep is termed the apnea–hypopnea index (AHI), in which the presence of obstructive sleep apnea is defined as an AHI of 5 or more events per hour.
With an AHI of 5 to 15, 16 to 30, or more than 30 events per hour are considered to have mild, moderate, or severe obstructive sleep apnea, respectively.
Obstructive sleep apnea is also associated with an increased risk of cardiovascular disease: more likely to have histories of hypertension, stroke, coronary artery disease, or heart failure, even after adjustment for BMI and other cardiovascular risk factors.
Patients with obstructive sleep apnea with an AHI of more than 30 events per hour, are at increased risk for sleep-related dysrhythmias, such as sinus bradycardia and atrioventricular block. and nonsustained ventricular tachycardia.
The AHI is influenced by weight, sleeping position, age, alcohol and medications, and fluid balance..
As AHI varies over time and even on consecutive nights, there are limits to the value of using the AHI calculated from one night of sleep to categorize disease severity and long-term risks.
Measures of oxygen desaturation, and the lowest value of oxyhemoglobin saturation during sleep, may provide additional information.
An apnea is defined as no airflow for 10 seconds or more and hypopnea as a 30% or greater reduction in airflow for 10 seconds or more with a corresponding 4% oxygen desaturation.
OSA defined as near complete, greater than 90%, cessations in airflow for more than 10 seconds in sleep, despite ventilatory effort, and hypopneas are general defined as reductions in airflow by more than 30% with concurrent reduction in oxyhemoglobin saturation by at least 3% or arousals from sleep.
Apnea-hypopnea index 5, 15, and 30 indicate mild, moderate and severe disease, respectively.
AHI may be lowered in some patients by weight loss.
Home sleep apnea tests, do not measure sleep and cannot determine the AHI, but they measure the respiratory-event index (REI).
Respiratory-event index (REI) is calculated as the frequency of breathing events with oxyhemoglobin desaturation of ≥4% for the entire recording time with exclusion of events scored because of arousal.
Patients with chronic snoring and untreated sleep apnea have a higher risk of stroke and cardiovascular disease, and most of these patients have a higher BMI, low level of activity and hypertension.
Patients with moderate-to-severe OSA are three times more likely to die from cancer and 2.5 times likelier to develop cancer.
Apnea-hypopnea index greater than 5 may be associated with excessive daytime sleepiness.
May be associated with recent weight gain.
Diabetes mellitus is an independent predictor of OSA during REM sleep
OSA during the REM sleep cycle is associated with intense hypoxemic insult and cardiovascular instability.
Obesity can worsen sleep apnea and lead to progression and the severity of both processes.
Long term sleep disturbance may contribute to hypertension, right sided heart failure and death.
Sleep apnea associated with multiple metabolic derangements including elevated blood glucose, blood pressure, and triglycerides, higher evening cortisone levels, reduced serum leptin secretion, and increases inflammatory cytokines.
May contribute to poor control of hypertension, and a very high percentage, that is greater than 70% of resistant hypertension patients have OSA..
Risk factors include male gender, obesity, increased neck circumference cranio-facial abnormalities and acromegaly.
According to the CDC is estimated that one in four men and one in 10 women have obstructive sleep apnea.
Obstructive sleep apnea may increase the risk of perioperative complications.
Associated with endothelial dysfunction which is related to the pathogenesis of cardiovascular complications.
Associated with decreased levels of nitrous oxide released by endothelial cells.
Obstructive sleep apnea is more prevalent among candidates for surgery than the general population.
Estimated that the prevalence of obstructive sleep apnea is 25% among candidates for elective surgery and may be as high as 80% in high-risk populations such as those who undergo bariatric surgery.
Obstructive sleep apnea remains undiagnosed in 80% of patients at the time of surgery.
Male:female 8:1.
Prevalence of 2% in women and 4% in men aged 30 to 60 years.
Prevalence in the US estimated to be 3-7% in men and 2-5% in women.
Among individuals with a BMI of greater than 28 it is present and 41%.
In the morbidly obese the prevalence may be as high as 78% of patients presenting for bariatric surgery.
Up to 93% of women and 82% of men have under diagnosed moderate to severe OSA (Young T et al).
Approximately 1 of 5 adults have mild disease and 1 in 15 adults have moderate or more severe obstructive sleep disease.
Estimated 17% of US adults affected.
Prevalence up to 10% in children.
The Berlin Questionnaire is a 10 items questionnaire focusing on BMI, sleepiness, blood pressure and consist of 3 categories related to the risk of having sleep apnea.
The Berlin Questionnaire classifies patients into high risk or low risk based on responses and there overall scores in the symptom categories.
Childhood obstructive sleep apnea is associated with adverse health outcomes including cognitive and behavioral deficits.
The most common risk factor for childhood obstructive sleep apnea syndrome is adenotonsillar hypertrophy.
Risk among relatives of patients is almost twice that of controls.
Patients have 2-7 times increased risk of having a traffic accident.
An AHI of more than 15 events per hour is associated with a decrement in psychomotor speed equivalent to 5 years of aging.
Patients with untreated obstructive sleep apnea have three times the risk of motor vehicle accidents as the general population.
Patients with untreated obstructive sleep apnea have three times the risk of motor vehicle accidents as the general population.
Accidents related to this process may cost 1400 lives annually.
Treatment reductions in the number of episodes of apnea and hypopnea have reduced the rate of motor vehicle accidents among persons with this syndrome.
Increased morbidity and mortality probably related to increased ventilatory and sympathetic responses to hypoxia, impaired cerebral perfusion, and increased coagulability.
Cross sectional data indicates associated with increased cardiovascular, cerebrovascular disease and insulin resistance.
Untreated male patients have a greater risk of fatal and non fatal cardiovascular events of 2.8 and 3.1, respectively.
Associated with higher incidence of cerebrovascular events.
Untreated patients with OSA living at low altitude of less than 800m above sea level experience pronounced hypoxemia and exacerbation of sleep-related breathing problems with frequent central apneas/hypopneas during a stay at moderate altitude for a few days (Nussbaumer-Ochsner Y et al).
Untreated patients with obstructive sleep apnea at altitude to have elevated blood pressures and more frequent cardiac arrhythmias.
Cardiac arrhythmias, including sinus arrest, AV blocks, premature atrial and ventricular contractions, supraventricular and ventricular tachy arrhythmias, have been reported to occur in 30 to 50% of patients with obstructive sleep apnea.
There is an increase prevalence of brady arrhythmias and heart block in patients with obstructive sleep apnea attributed to chemoreflexes induced by hypoxemia, as well as to decreases in intrathoracic pressure.
Patients with obstructive sleep apnea spending three days at moderately elevated altitude, combination of acetazolamide and auto CPAP therapy compared to auto CPAP alone resulted in improved nocturnal oxygen saturation and apnea/hypopnea index ( Latshang TD et al).
Treatment results in improved blood pressure, reduction in baroreceptor sensitivity, nitric oxide derivative production, reduction in cardiac arrhythmias and sympathetic nervous system activation.
Patients with CHF and obstructive sleep apnea have improved cardiac function, sympathetic activity with CPAP treatment.
Nasal continuous positive airway pressure (CPAP) is the treatment of choice.
CPAP acts as a pneumatic splint of the upper airway during sleep and corrects the obstruction.
CPAP can reduce blood pressure in OSA.
CPAP is the good standard of OSA treatment and ranges from 4cm -20cm water pressure.
CPAP treatment can improve insulin responsiveness without a significant change in obesity.
CPAP reduces sleep related myocardial ischemia in patients with severe sleep apnea syndrome.
CPAP decreases OSA associated arrhythmias.
CPAP increases levels of nitrous oxide, and decreases lepton levels.
Observation studies suggest CPAP management in OSA reduces fatal and nonfatal CV events in moderate and severe OSA (Marin JM et al, Buchner NJ et al).
Continuous positive airway pressure (CPAP) is considered first-line therapy for symptomatic or moderate-to-severe obstructive sleep apnea.
Lifestyle modifications suggested include weight-loss in overweight and obese patients, avoiding medications and substances that promote relaxation of the upper airway,and increasing awareness of and providing countermeasures for the risk of drowsy driving.
CPAP provides no benefit in patients with obstructive sleep apnea and a respiratory disturbance index greater than 30 episodes/h but no self-reported sleepiness.
CPAP associated with a 2 mm reduction in BP.
Recent randomized studies, however, reveal CPAP provides no benefits in nonsleepy OSA.
Indication for CPAP treatment in nonsleepy patients with OSA is not clear.
Obstructive sleep apnea is an independent risk factor for motor vehicle accidents and cardiovascular disease.
In a randomized study in patients with OSA without sleepiness, CPAP compared with usuall care does not decrease incidence of hypertension or CV events: post hoc analysis suggests that CPAP treatment for 4 h/night or longer may may reduce the incidence of hypertension or CV disease. (Barbe F et al).
Patients compliance with nasal CPAP ranges between 65-80%.
Patients with obstructive sleep apnea due primarily to velopharyngeal compromise may have a good response to palate surgery.
Radio frequency volume reduction of the tongue helps to manage and prevent collapse of the upper airway behind the palate and tongue.
The Inspire® Upper Airway Stimulation (IUAS) device is used to treat patients with moderate to severe sleep apnea who are unable to use CPAP.
Patients with unstable ventilatory control may improve with oxygen or acetazolamide which can stabilize the breathing pattern.
Less than 10% of clinically significant cases are diagnosed.
Prevalence in patients with chronic renal failure 50-70%.
At least half of patients with obstructive sleep apnea have hypertension.
Associated with an increased mortality.
2-3 greater risk of automobile crashes related the excessive day time sleepiness.
Increased risk of cardiovascular disease including hypertension, coronary artery disease and stroke.
Data indicate obstructive sleep apnea in the pathogenesis of risk factors associated with stroke such as hypertension, coronary heart disease, diabetes, and atrial fibrillation which are believed to be mediated by adverse physiologic responses to recurrent periods of pharyngeal occlusion and oxyhemoglobin desaturation-resaturation.
The above responses result in the generation of free radicals, release of pro-inflammatory and prothrombotic mediators, endothelial dysfunction, increased sympathetic nervous system and increased blood pressure along with cerebrovascular alteration in autoregulation.
Obstructive sleep apnea increases the risk of stroke and prevalence in patients after a stroke.
Common in patients with congestive heart failure and treatment in such patients improves survival rates and left ventricular ejection fractions.
Severe syndrome increases the incidence of fatal and nonfatal cardiovascular events.
OSA associated with oxygen desaturation so and arousals from sleep, which can lead to increases in blood pressure and cardiovascular risk.
Some data suggest poorer survival in female patients.
Prevalence increases with age with a 2-3 increase in patients older than 65 years compared to those 30-64 years of age.
Prevalence increasing due to increasing prevalence of obesity.
Prevalence plateaus of about 65 years of age.
Graded increase in prevalence with increasing body mass index, neck circumference, and waist-hip-ratio.
May be common in non obese individuals.
10% increase in weight associated with a 6 fold increase in the risk of developing obstructive sleep apnea.
In obese patients with obstructive sleep apnea a reduction in weight results in substantial decrease in severity of disease.
Obstructive sleep apnea estimated prevalence in obese adults varies from 42-48% of men and 8-38% in women (Young T et al).
For obstructive sleep apnea greater weight loss provided by surgical bypass did not translate into better effect compared to conventional weight loss therapy: Bariatric surgery did not result in statistical greater reduction in apnea-hypopnea index (AHI) of 20 events/hour or more (Dixon JB et all).
Prevalence in stroke patients exceeds 60%.
The Childhood Adenotonsillectomy Trial (CHAT) demonstrated that compared to watchful waiting, surgical treatment for the obstructive sleep apnea syndrome on school age children did not significantly improve attention or executive function, but did reduce symptoms, improve secondary outcomes of behavior, quality-of-life, and polysomnographic findings (Marcus CL et al).
The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits in harms of screening for obstructive sleep apnea in the general adult population.