What is Sleep Apnea? Apnea is defined as the stopping or pausing of breathing. Sleep apnea is a common condition in which a person stops breathing intermittently during sleep. This occur a few times during one session of sleep or hundreds of times per hour. There are three kinds of sleep apnea:        Obstructive Sleep Apnea (OSA)        Central Sleep Apnea        Mixed Sleep Apnea Obstructive sleep apnea occurs when the upper airway is blocked multiple times throughout sleep, resulting in less or no airflow. Sleep apnea can also occur when the brain does not send signals to the muscles responsible for controlling breathing (central sleep apnea). Mixed sleep apnea is when both conditions occur. In some cases, when OSA is being treated, symptoms of central sleep apnea will occur. Obstructive sleep apnea OSA occurs when the airway either completely or partially collapses resulting in reduced oxygen saturation or the person waking up. The upshot is interrupted, non-restorative sleep. The upper airway muscles The pharynx is the cavity behind the nose and mouth that connects the nose and mouth to the esophagus. This region consists of over 20 muscles that contribute to both breathing and non-breathing related functions. A group of muscles called the upper airway dilator muscles stabilize the airway during breathing.

What are the symptoms of OSA? Common symptoms include:        Fatigue        Non-restorative sleep        Nocturnal polyuria (Excessive urination at night)        Morning headaches        Irritability        Memory loss        Loud, disruptive snoring        Gasping during sleep        Choking during sleep        Apneas (cessation of breathing) during sleep        Excessive daytime sleepiness Excessive daytime sleepiness is the most common symptom of OSA. Improvements to daytime sleepiness is the most significantly affected symptom following treatment. About 23% of women and 16% of men experience daytime sleepiness. However, it is difficult to link daytime sleepiness to apneic events since several factors can contribute to it. Health problems that can arise from OSA Long-term untreated OSA can increase the risk of several other medical conditions including: Cardiovascular conditions        High blood pressure There is evidence supporting a link between OSA and high blood pressure. Both conditions are common among the middle-aged and elderly. Animal models of OSA have shown a temporary increase in nighttime blood pressure is OSA animals that developed into chronic daytime high blood pressure. Temporary stabilization of blood pressure has also been shown to reduce episodes of sleep apnea in animals with high blood pressure. Studies in humans have also found that nearly half of individuals with OSA have high blood pressure, while 30% of individuals with high blood pressure have OSA.

Epidemiology: What is the incidence of OSA? OSA is a common sleep disorder. It occurs along with daytime sleepiness in approximately 3% to 7% of adult men and 2% to 5% of adult women. There are some people that are more likely to experience OSA including individuals that are:        Overweight        Obese        Minorities        Older Prevalence is similar among most continents, suggesting that it is similar in both developed and developing countries. Patients with OSA have a higher risk of mortality than those without OSA. Mortality rate also increases with the severity of the OSA. However, this risk can be reduced with treatment. Pathophysiology: How are physiological processes altered in OSA? OSA pathophysiology can be divided into two categories:        Non-anatomical contributors        Anatomical contributors Anatomical contributors include:        A pharyngeal airway susceptible to closure during sleep o    Narrow pharyngeal airway o    Increased airway length o    Unusual pharyngeal lumen shapes o    Large neck circumference (>17 inches in males and >16 inches in females) o    Specific craniofacial morphology o    Specific positions of the hyoid bone o    Tongue scalloping (tongues with rippled edges) o    Tongue fat Non-anatomical contributors include:        Impaired pharyngeal dilator muscle function        Premature awakening        Mild airway narrowing        Unstable control of breathing While a combination of non-anatomical and anatomical contributors may lead to OSA, the leading causes are anatomical resulting in one or multiple areas of upper airway collapse.

What are the risk factors for OSA? Common risk factors or signs of OSA include:        Increased daytime sleepiness        Cognitive difficulties due to fatigue        High blood pressure        Narrowing of the nasopharynx (upper part of the throat behind the nose)        Pulmonary hypertension (high blood pressure affecting arteries in the heart and lungs)        Specific positions of the hyoid bone        Tongue scalloping (tongues with rippled edges)        Tongue fat        Airway edema Accumulation of fluid can increase the size of upper airway soft tissue is individuals with OSA and individuals that snore.        Airway surface tension Surface tension in the fluid lining the mucosa of the upper airway can also have an effect on its collapsibility. Individuals with OSA have been found to have higher surface tension in the upper airway walls. In turn, surfactant treatments have been shown to significantly reduce airway collapsibility and reduce AHI by up to 30% in individuals with OSA.        Age (middle age) As individuals age, they naturally experience more difficulties when sleeping. More than half of adults over the age of 65 years experience a chronic sleep-related issue. Sleep becomes more irregular impart due to OSA. Approximately 70% of men and 56% of women between 65 and 99 years of age have mild OSA.

How is OSA diagnosed? Unfortunately, many people with OSA are not aware they have it and thus go untreated. Polysomnography The primary method to diagnosis sleep-disordered breathing is polysomnography or PSG. PSG is a multi-parametric test.  A PSG records physiological changes that occur during sleep such as electrical activity in the brain measured by electroencephalography (EEG), eye movement measured by Electrooculography (EOG), muscle activity and/or skeletal muscle activation measured by electromyography (EMG), and heart rhythm determined by electrocardiography (ECG). Most importantly respiratory airflow, respiratory effort and oxygen saturation are also examined. A PSG involves recording at least 12 channels using at least 22 wires connected to the patient while sleeping. Snoring may also be recorded using a sound probe placed across the neck. Apnea–Hypopnea Index While there are several outcomes to these tests, diagnosis primarily depends on the Apnea–Hypopnea Index or Apnoea–Hypopnoea Index (AHI). The level of severity is determined by the AIH. The AHI index is a number determined from the number of apnea (cessations in breathing lasting at least 10 sec accompanied by decreased blood flow) and/or hypopnea (Shallow breathing) events that occur during sleep, and the decrease in oxygen saturation.  AHI is determined by dividing the number of apnea events that occur during sleep by the number of hours slept.