Obstructive Sleep Apnea (OSA) is a common chronic disease affecting at least 2 to 4% of the adult population; there are about 15 to 20 million American adults that are believed to have obstructive sleep apnea (OSA), which makes its prevalence comparable to other chronic diseases such as diabetes mellitus type 2. OSA represents an important medical condition with potential devastating consequences. Sleep deprivation with consequent daytime somnolence has been linked to motor vehicle and workplace-related accidents and there is recognition of OSA as a mediator of cardiovascular disease. There is abundant information in the medical literature implicating OSA in cardiovascular diseases such as atrial fibrillation (AF), stroke, myocardial infarction, and sudden cardiac death.
In a very simple description, OSA occurs when airflow is either partly (hypopnea) or completely (apnea) occluded or impeded during sleep. The combination of sleep-disordered breathing with daytime sleepiness is referred to as the OSA syndrome. The upper airway is a muscular and compliant structure susceptible to inspiratory collapse because of negative airway pressures generated during inspiration. Neural activation of pharyngeal dilator muscles is important in maintaining upper airway patency. It is well known that during sleep, neural activation of dilator muscles is attenuated, thus predisposing to airway collapse leading to OSA.
The signs and symptoms of OSA are considered to be a result of the multiple physiologic derangements that occur from repetitive collapse of the upper airway. There are well documented consequences of such repetitive collapse that include and are not limited to: sleep discontinuity and fragmentation, hypoxemia, hypercapnia, changes in intrathoracic pressure, and increase in sympathetic activity.
Under scientific agreement an obstructive apnea occurs when there is complete cessation of airflow for at least 10 seconds. On the other hand, an obstructive hypopnea occurs when there is evidence in decrease but not complete cessation of flow but resulting in a fall in oxygen saturation or arousal from sleep. Respiratory effort related arousals (RERAs) occurs when airflow decreases, without complete cessation but resulting in arousal from sleep without documented oxygen desaturation.
Clinically, OSA is defined as the coexistence of daytime sleepiness, snoring, witnessed pauses in breathing during sleep, or awakenings due to gasping or choking in the presence of at least 5 obstructive respiratory events (apneas, hypopneas, or respiratory effort related arousals) per hour of sleep. The presence of 15 or more obstructive respiratory event per hour of sleep in the absence of sleep related symptoms is also sufficient for the diagnosis of OSA.
The severity of OSA must be established in order to make appropriate treatment decisions. The standard accepted and objective method for diagnosis of OSA constitutes the in-laboratory polysomnogram (PSG). During a PSG, OSA is quantified on the basis of the apnea-hypopnea index (AHI), which refers to the number of apneas and hypopneas occurring per hour of sleep. OSA is presumed to be significant at an AHI of more than 5 events per hour. Although the AHI is an accepted measure for defining OSA severity, it is not clear that it is primarily or exclusively the number of events per hour of sleep that elicits daytime sleepiness and cardiovascular damage.
Definitive thresholds for treating OSA are not yet established. Current practice is based on the severity of the AHI, and many patients are treated at an AHI> 15/h. Patients with lower AHIs may require treatment if they have comorbidities associated with OSA or if they have significant daytime somnolence.
General treatment recommendations for patients with OSA are weight loss, avoidance of alcohol and upper airway mucosal irritants, and avoidance of sleeping in the supine position; but the main treatment of OSA is nasal Continuous Positive Airway Pressure (CPAP), which helps maintain patency of the upper airway and usually enables complete or almost complete resolution of apnea. Other less successful options include mechanical devices directed at altering the configuration or compliance of the upper airway, by surgical procedures like tonsillectomy or uvulopalatopharyngoplasty or by orthodontic devices or tongue-retaining appliances. Rarely, tracheostomy can be considered for intractable and life-threatening OSA.
Our mission at Central Florida Sleep Centers is to set the community standard in providing expert evaluation of sleep disorders, state of the art testing, as well as patient education and support for those suffering a sleep disorder, most particularly patients suffering with Obstructive Sleep Apnea.
Jose A. Urdaneta, MD, FCCP, FAASM earned his medical degree in Maracaibo, Venezuela and obtained his Internal Medicine Internship and Residency at Mount Sinai Medical Center in Miami Beach, FL. He then completed his Pulmonary/Critical Care Medicine at Tulane University a in New Orleans, LA which was followed a Sleep Medicine Fellowship at UT Southwestern University/Parkland in Dallas, TX. He has been in Private Practice for 3 years and currently is a practicing physician at Pulmonary Disease Specialists, PA and Central Florida Sleep Centers.
Jose A. Urdaneta, MD, FCCP, FAASM is a practicing physician at Pulmonary Disease Specialists, PA and Central Florida Sleep Centers.
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