Learning Center

Oxygen Concentrator
An oxygen concentrator is a device providing oxygen therapy to a patient at minimally to substantially higher concentrations than available in ambient air. They are used as a safer, less expensive, and more convenient alternative to tanks of compressed oxygen.

How oxygen concentrators work
An oxygen concentrator has two cylinders filled with zeolite materials that selectively adsorbs thenitrogen in the air. In each cycle, air flows through one cylinder at a pressure of around 20 pounds per square inch (gauge), where this is the gauge pressure of 1.36 atmospheres (138 kilopascal) at which the nitrogen molecules are captured by the zeolite, while the contents of the other cylinder are vented away at atmospheric pressure to dissipate the captured nitrogen.

The following applies to stationary oxygen concentrators and not to the newer portable devices. The older oxygen concentrators cycled with a period of about 20 seconds, and they provided a continuous supply of oxygen at a flow rate of about five liters or less per minute at oxygen concentrations selectable from about 25 percent to 95 percent. This process is called pressure swing adsorption (PSA). Since about 1999, oxygen concentrators providing up to 10 liters per minute have been available for patients requiring higher flows of oxygen. These devices come in sizes that are not much larger or heavier than the devices that yield five liters per minute.

Portable oxygen concentrators
Since the year 2000, a number of companies have produced portable oxygen concentrators. Typically, these devices produce less than one liter per minute of oxygen, and they use some version of pulse flow or "demand flow" to deliver oxygen only when the patient is inhaling. However, there are a few portable oxygen concentrators that produce three liters per minute of oxygen continuously. Also, they can provide pulses of oxygen either to provide higher intermittant flows or to reduce the power consumption.

These portable concentrators typically plug into an electrical outlet like the larger, heavier stationary oxygen concentrators.

Portable oxygen concentrators usually can also be plugged into the DC outlet of a vehicle, and most of these devices have the ability to run from electric batteries, also, for ambulatory use. Concerning for airline travel, The Federal Aviation Adminstration (FAA) of the United Stateshas approved the use of portable oxygen concentrators on commercial airlines. However, users of these devices should check in advance as to whether a particular brand or model is permitted on a particular airline.

Usually, "demand" or pulse-flow oxygen concentrators have not been used by patients while sleeping. There have been problems with the oxygen concentrators not being able to detect when the sleeping patient is inhaling.

In both clinical and emergency-care situations, oxygen concentrators have the advantage of not being as dangerous as oxygen cylinders, which can, if ruptured or leaking, greatly increase the combustion rate of a fire. As such, oxygen concentrators are particularly advantageous in military or disaster situations, where oxygen tanks may be dangerous or infeasible.

Oxygen concentrators are considered sufficiently foolproof to be leased to individual patients as a prescription item for use in their homes. Typically they are used as an adjunct to CPAP treatment of severe sleep apnea. There also are other medical uses for oxygen concentrators, including emphysema and other respiratory diseases.

Sleep apnea
Classification and external resources

Sleep apnea is a sleep disorder characterized by abnormal pauses in breathing or instances of abnormally low breathing, during sleep. Each pause in breathing, called an apnea, can last from a few seconds to minutes, and may occur 5 to 30 times or more an hour. Similarly, each abnormally low breathing event is called a hypopnea. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram, or "sleep study".

There are three forms of sleep apnea: central (CSA), obstructive (OSA), and complex or mixed sleep apnea (i.e., a combination of central and obstructive) constituting 0.4%, 84% and 15% of cases respectively. In CSA, breathing is interrupted by a lack of respiratory effort; in OSA, breathing is interrupted by a physical block to airflow despite respiratory effort, and snoring is common.

Regardless of type, an individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years (or even decades) without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.

Signs and symptoms
Sleep apnea affects not only adults but some children as well . As stated by El-Ad, "patients complain about excessive daytime sleepiness (EDS) and impaired alertness." In other words, common effects of sleep apnea include daytime fatigue, a slower reaction time, and vision problems . Moreover, patients are examined using "standard test batteries" in order to further identify parts of the brain that are affected by sleep apnea . Tests have shown that certain parts of the brain cause different effects. The "executive functioning" part of the brain affects the way the patient plans and initiates tasks . Second, the part of the brain that deals with attention causes difficulty in paying attention, working effectively and processing information when in a waking state . Thirdly, the part of the brain that uses memory and learning is also affected . Due to the disruption in daytime cognitive state, behavioral effects are also present . This includes moodiness, belligerence, as well as a decrease in attentiveness and drive . These effects become very difficult to deal with, thus the development of depression may transpire . Finally, because there are many factors that could lead to some of the effects previously listed, some patients are not aware that they suffer from sleep apnea and are either misdiagnosed, or just ignore the symptoms altogether .

The diagnosis of sleep apnea is based on the conjoint evaluation of clinical symptoms (e.g. excessive daytime sleepiness and fatigue) and of the results of a formal sleep study (polysomnography, or reduced channels home based test). The latter aims at establishing an "objective" diagnosis indicator linked to the quantity of apneic events per hour of sleep (Apnea Hypopnea Index(AHI), or Respiratory Disturbance Index (RDI)), associated to a formal threshold, above which a patient is considered as suffering from sleep apnea, and the severity of his sleep apnea can be then quantified.

Nevertheless, due to the number and variability in the actual symptoms and nature of apneic events (e.g., hypopnea vs apnea, central vs obstructive), the variability of patients' physiologies, and the intrinsic imperfections of the experimental setups and methods, this field is opened to debate.Within this context, the definition of an apneic event depends on several factors (e.g. patient's age) and account for this variability through a multi-criteria decision rule described in several, sometimes conflicting, guidelines.One example of a commonly adopted definition of an apnea (for an adult) includes a minimum 10 second interval between breaths, with either a neurological arousal (a 3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2) or a blood oxygen desaturation of 3-4% or greater, or both arousal and desaturation.

Oximetry, which may be performed overnight in a patient's home, is an easier alternative to formal sleep study (polysomnography). In one study, normal overnight oximetry was very sensitive and so if normal, sleep apnea was unlikely.In addition, home oximetry may be equally effective in guiding prescription for automatically self-adjusting continuous positive airway pressure.[19]

Obstructive sleep apnea
Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The muscle tone of the body ordinarily relaxes during sleep, and at the level of the throat the human airway is composed of collapsible walls of soft tissue which can obstruct breathing during sleep. Mild occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be important, but chronic severe obstructive sleep apnea requires treatment to prevent low blood oxygen (hypoxemia), sleep deprivation, and other complications.

Individuals with low muscle tone and soft tissue around the airway (e.g., because of obesity) and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. The elderly are more likely to have OSA than young people. Men are more likely to suffer sleep apnea than women and children are, though it is not uncommon in the last two population groups.[20]

The risk of OSA rises with increasing body weight, active smoking and age. In addition, patients with diabetes or "borderline" diabetes have up to three times the risk of having OSA.

Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry orpolysomnography in a sleep clinic.

Some treatments involve lifestyle changes, such as avoiding alcohol or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30-degree elevation of the upper body[21] or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Lateral positions (sleeping on a side), as opposed to supine positions (sleeping on the back), are also recommended as a treatment for sleep apnea,[22][23][24] largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances to keep the airway open during sleep. Continuous positive airway pressure (CPAP) is the most effective treatment for obstructive sleep apnea.[25] There are also surgical procedures to remove and tighten tissue and widen the airway.

As already mentioned, snoring is a common finding in people with this syndrome. Snoring is the turbulent sound of air moving through the back of the mouth, nose, and throat. Although not everyone who snores is experiencing difficulty breathing, snoring in combination with other conditions such as overweight and obesity has been found to be highly predictive of OSA risk.[26] The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs when snoring stops.

Other indicators include (but are not limited to): hypersomnolence, obesity BMI >30, large neck circumference (16 in (410 mm) in women, 17 in (430 mm) in men), enlarged tonsils and large tongue volume, micrognathia, morning headaches, irritability/mood-swings/depression, learning and/or memory difficulties, and sexual dysfunction.

The term "sleep-disordered breathing" is commonly used in the U.S. to describe the full range of breathing problems during sleep in which not enough air reaches the lungs (hypopnea and apnea). Sleep-disordered breathing is associated with an increased risk of cardiovascular disease, stroke, high blood pressure, arrhythmias, diabetes, and sleep deprived driving accidents.[27][28][29][30] When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping.[31] Stroke is associated with obstructive sleep apnea.

In the June 27, 2008, edition of the journal Neuroscience Letters, researchers revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss. Using magnetic resonance imaging (MRI), the scientists discovered that sleep apnea patients' mammillary bodies were nearly 20 percent smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.[34]

Central sleep apnea
In pure central sleep apnea or Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors them, do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.

While sleeping, a normal individual is "at rest" as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe.

In central sleep apnea, the basic neurological controls for breathing rate malfunction and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (hypoxaemia) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live, and if the level of blood oxygen goes low enough for long enough, the consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is and on the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.

In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs owing to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brain's mandate for the body to breathe.

Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gases with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. Oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx(so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and diaphragm. These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it.

Physiologic effects of central apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures, even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications[verification needed]. In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may cause an increase in carbon dioxide levels that can change the pH of the blood enough to cause a metabolic acidosis.

Mixed apnea and complex sleep apnea
Some people with sleep apnea have a combination of both types. When obstructive sleep apnea syndrome is severe and longstanding, episodes of central apnea sometimes develop. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most commonly related to acid-base and CO2 feedback malfunctions stemming from heart failure. There is a constellation of diseases and symptoms relating to body mass, cardiovascular, respiratory, and occasionally, neurological dysfunction that have a synergistic effect in sleep-disordered breathing. In some cases, a side effect from the lack of sleep is a mild case of Excessive Daytime Sleepiness (EDS) where the subject has had minimal sleep and this extreme fatigue over time takes its toll on the subject. The presence of central sleep apnea without an obstructive component is a common result of chronic opiate use (or abuse) owing to the characteristic respiratory depression caused by large doses of narcotics.

Complex sleep apnea has recently been described by researchers as a novel presentation of sleep apnea.Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy after the obstructive component has been eliminated. This has long been seen in sleep laboratories and has historically been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation (ASV) modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating Cheyne-Stokes breathing; however, no longitudinal studies have yet been published, nor have any results been generated that suggest any differential outcomes versus standard CPAP therapy. At the AARC 2006 in Las Vegas, NV, researchers reported successful treatment of hundreds of patients on ASV therapy; however, these results have not been reported in peer-reviewed publications as of July 2007.

An important finding by Dernaika et al. suggests that transient central apnea produced during CPAP titration (the so-called "complex sleep apnea") is "transient and self-limited."[35] The central apneas may in fact be secondary to sleep fragmentation during the titration process. As of July 2007, there has been no alternate convincing evidence produced that these central sleep apnea events associated with CPAP therapy for obstructive sleep apnea are of any significant pathophysiologic importance.[dated info]

Research is ongoing, however, at the Harvard Medical School, including adding dead space to positive airway pressure for treatment of complex sleep-disordered breathing.[36]

Treatment often starts with behavioral therapy. For mild cases of sleep apnea, physicians often recommend sleeping on one's side, which can prevent the tongue and palate from falling backwards in the throat and blocking the airway. Many patients are told to avoid alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night.[37]

For moderate to severe sleep apnea, the most common treatment is the use of a continuous positive airway pressure (CPAP) or Automatic Positive Airway Pressure (APAP) device,[37] which 'splints' the patient's airway open during sleep by means of a flow of pressurized air into the throat. The patient typically wears a plastic facial mask, which is connected by a flexible tube to a small bedside CPAP machine. The CPAP machine generates the required air pressure to keep the patient's airways open during sleep. Advanced models may warm or humidify the air and monitor the patient's breathing to ensure proper treatment. CPAP therapy is extremely effective in reducing apneas and less expensive than other treatments,

Surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat, procedures done at either a doctor's office or a hospital. Small shots or other treatments, sometimes in a series, are used for shrinkage, while the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues.[37]

Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction, swelling may negate some of the effects in the immediate postoperative period. Once the swelling resolves and the palate becomes tightened by postoperative scarring,

CPAP is the most consistently safe and effective treatment for obstructive sleep apnea