Skip to content Skip to sidebar Skip to footer
Home / Can You Have Sleep Apnea and Not Snore

Can You Have Sleep Apnea and Not Snore

Post a Comment

Disorder involving pauses in breathing during sleep

Medical condition

Sleep apnea
Other names Slumber apnoea, slumber apnea syndrome
Obstruction ventilation apnée sommeil.svg
Obstructive sleep apnea
Pronunciation
  • ,
Specialty Otorhinolaryngology, sleep medicine
Symptoms Pauses breathing or periods of shallow breathing during sleep, snoring, tired during the day[1] [two]
Complications Middle set on, stroke, diabetes, middle failure, irregular heartbeat, obesity, motor vehicle collisions,[1] Alzheimer's affliction,[three] [4] and premature death[5]
Usual onset Varies; fifty% of women age 20-70[6]
Types Obstructive sleep apnea (OSA), central sleep apnea (CSA), mixed sleep apnea[1]
Risk factors Overweight, family unit history, allergies, enlarged tonsils[vii]
Diagnostic method Overnight sleep study[viii]
Handling Lifestyle changes, mouthpieces, animate devices, surgery[1]
Frequency ~ 1 in every 10 people,[4] [9] 2:i ratio of men to women, crumbling and obesity higher risk [half-dozen]

Sleep apnea, also spelled sleep apnoea, is a sleep disorder in which pauses in breathing or periods of shallow breathing during sleep occur more than often than normal.[1] Each pause can last for a few seconds to a few minutes and they happen many times a nighttime.[1] In the most common form, this follows loud snoring.[2] In that location may exist a choking or snorting sound as animate resumes.[1] Because the disorder disrupts normal sleep, those affected may experience sleepiness or feel tired during the twenty-four hour period.[one] In children, it may cause hyperactivity or issues in school.[ii]

Sleep apnea may be either obstructive slumber apnea (OSA), in which breathing is interrupted by a blockage of air flow, fundamental sleep apnea (CSA), in which regular unconscious jiff simply stops, or a combination of the ii.[1] OSA is the most common form.[1] OSA has 4 key contributors; these include "anatomical compromises" like a narrow, crowded, or collapsible upper airway. Or "non-anatomical" ones similar an ineffective pharyngeal dilator muscle function during sleep, airway narrowing during sleep, or unstable control of breathing (high loop gain).[x] Other risk factors include being overweight, a family history of the condition, allergies, and enlarged tonsils.[7] Some people with sleep apnea are unaware they have the condition.[1] In many cases it is showtime observed by a family unit fellow member.[1] Sleep apnea is oftentimes diagnosed with an overnight sleep written report.[8] For a diagnosis of slumber apnea, more 5 episodes per hour must occur.[11]

In central sleep apnea (CSA), the basic neurological controls for breathing rate malfunction and fail to give the signal to inhale, causing the individual to miss one or more than cycles of breathing. If the pause in animate is long plenty, 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).[12] In turn, these conditions of hypoxia and hypercapnia volition trigger additional effects on the body. Encephalon cells need constant oxygen to alive, and if the level of blood oxygen goes low plenty for long enough, the consequences of brain damage and even death volition occur. Yet, central sleep apnea is more often a chronic condition that causes much milder effects than sudden decease. The exact furnishings of the condition will depend on how severe the apnea is and on the individual characteristics of the person having the apnea.

Treatment may include lifestyle changes, mouthpieces, breathing devices, and surgery.[1] Effective lifestyle changes may include avoiding alcohol, losing weight, stopping smoking, and sleeping on one's side.[13] Animate devices include the utilize of a CPAP motorcar.[14] With proper utilise, CPAP improves outcomes.[fifteen] Evidence suggests that CPAP may meliorate sensitivity to insulin, claret pressure, and sleepiness.[16] [17] [eighteen] Long term compliance, however, is an issue with more half of people not appropriately using the device.[15] [19] In 2017, merely 15% of potential patients in developed countries used CPAP machines, while in developing countries well under 1% of potential patients used CPAP.[20] Without treatment, slumber apnea may increase the gamble of heart attack, stroke, diabetes, heart failure, irregular heartbeat, obesity, and motor vehicle collisions.[one]

Alzheimer'southward Disease and severe obstructive sleep apnea are connected[three] because in that location is an increase in the protein beta-amyloid as well as white-affair harm. These are the main indicators of Alzheimer'due south, which in this instance comes from the lack of proper rest or poorer slumber efficiency resulting in neurodegeneration.[4] Having sleep apnea in mid-life brings a college likelihood of developing Alzheimer'due south in older age, and if 1 has Alzheimer's then 1 is also more likely to take slumber apnea.[ix] This is demonstrated past cases of slumber apnea even being misdiagnosed as dementia.[21] With the use of handling through CPAP, there is a reversible risk factor in terms of the amyloid proteins. This usually restores brain structure and cognitive impairment.[22] [23]

OSA is a mutual sleep disorder. A large analysis in 2022 of the estimated prevalence of OSA found that OSA affects 936 million—1 billion people between the ages of 30-69 globally, or roughly every one in 10 people, and up to xxx% of the elderly.[24] Sleep apnea is somewhat more mutual in men than women, roughly a 2:1 ratio of men to women, and in general more people are probable to have it with older age and obesity.[vi]

Signs and symptoms [edit]

People with sleep apnea have problems with excessive daytime sleepiness (EDS) and impaired alacrity.[25] OSA may increase run a risk for driving accidents and work-related accidents. If OSA is not treated, people are at increased risk of other health issues, such as diabetes.

Due to the disruption in daytime cerebral state, behavioral effects may exist present. These can include moodiness, belligerence, equally well equally a decrease in attentiveness and energy.[26] These effects may become intractable, leading to low.[27]

In that location is evidence that the risk of diabetes amid those with moderate or severe slumber apnea is higher.[28] Finally, considering there are many factors that could lead to some of the effects previously listed, some people are non enlightened that they have sleep apnea and are either misdiagnosed or ignore the symptoms altogether.[25]

Adventure factors [edit]

Sleep apnea can affect people regardless of sex, race, or historic period. However, risk factors include:

  • being male
  • obesity
  • age over 40
  • large neck circumference (greater than 16–17 inches)
  • enlarged tonsils or tongue
  • narrow upper jaw
  • nasal congestion
  • allergies
  • receding chin
  • gastroesophageal reflux
  • a family history of slumber apnea

Alcohol, sedatives and tranquilizers may also promote sleep apnea past relaxing throat muscles. People who fume tobacco accept slumber apnea at 3 times the rate of people who take never done so.[29]

Primal slumber apnea is more often associated with whatever of the following take a chance factors:

  • being male person
  • an age higher up 65
  • having centre disorders such every bit atrial fibrillation or atrial septal defects such as PFO
  • stroke

High blood pressure level is very common in people with sleep apnea.[30]

Mechanism [edit]

When breathing is paused, carbon dioxide builds up in the bloodstream. Chemoreceptors in the bloodstream note the high carbon dioxide levels. The encephalon is signaled to awaken the person, which clears the airway and allows animate to resume. Breathing ordinarily will restore oxygen levels and the person will autumn comatose once more.[31] This carbon dioxide build-up may be due to the subtract of output of the brainstem regulating the chest wall or pharyngeal muscles, which causes the pharynx to collapse.[32] People with slumber apnea experience reduced or no tedious-wave slumber and spend less time in REM slumber.[32]

Diagnosis [edit]

Despite this[ which? ] medical consensus, the variety of apneic events (e.g., hypopnea vs apnea, cardinal vs obstructive), the variability of patients' physiologies, and the inherent shortcomings and variability of equipment and methods, this field is field of study to debate.[33] Within this context, the definition of an event depends on several factors (east.grand., patient's age) and account for this variability through a multi-criteria decision rule described in several, sometimes conflicting, guidelines.[34] [35]

Oximetry [edit]

Oximetry, which may exist performed over one or several nights in a person's home, is a simpler, only less reliable alternative to a polysomnography. The exam is recommended only when requested by a physician and should not be used to test those without symptoms.[36] Dwelling oximetry may be effective in guiding prescription for automatically self-adjusting continuous positive airway pressure level.[37] [38]

Classification [edit]

There are three types of sleep apnea. OSA accounts for 84%, CSA for 0.9%, and 15% of cases are mixed.[39]

Obstructive slumber apnea [edit]

Screenshot of a PSG arrangement showing an obstructive apnea.

No airway obstruction during sleep.

Airway obstruction during sleep.

Obstructive sleep apnea (OSA) is the nearly common category of sleep-disordered breathing. The musculus tone of the trunk ordinarily relaxes during sleep, and at the level of the throat, the man airway is equanimous of collapsible walls of soft tissue that can obstruct breathing. Mild occasional slumber apnea, such every bit many people experience during an upper respiratory infection, may non exist meaning, but chronic severe obstructive sleep apnea requires handling to forbid depression claret oxygen (hypoxemia), sleep deprivation, and other complications.

Individuals with low muscle-tone and soft tissue around the airway (east.g., considering of obesity) and structural features that give rise to a narrowed airway are at loftier adventure 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.[forty]

The risk of OSA rises with increasing torso weight, active smoking and historic period. In addition, patients with diabetes or "deadline" diabetes accept upward 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 or polysomnography in a sleep clinic.

Some treatments involve lifestyle changes, such as avoiding booze or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30-degree top of the upper body[41] or higher, equally if in a recliner. Doing so helps preclude 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 handling for sleep apnea,[42] [43] [44] largely considering the gravitational component is smaller in the lateral position. Some people do good from various kinds of oral appliances such as the Mandibular advancement splint to keep the airway open during slumber. Continuous positive airway pressure (CPAP) is the most effective handling for severe obstructive sleep apnea, simply oral appliances are considered a first-line approach equal to CPAP for mild to moderate slumber apnea, according to the AASM parameters of care.[45] At that place are as well surgical procedures to remove and tighten tissue and widen the airway.

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 pharynx. Although non everyone who snores is experiencing difficulty breathing, snoring in combination with other risk factors has been found to exist highly predictive of OSA.[46] The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, at that place may not be enough air movement to brand much sound. Even the loudest snoring does not hateful that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs when snoring stops.

Up to 78% of genes associated with habitual snoring also increment the risk for OSA.[47]

Other indicators include (just are not limited to): hypersomnolence, obesity (BMI ≥ 30), large cervix 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/low, learning and/or retentiveness difficulties, and sexual dysfunction.

The term "sleep-disordered breathing" is normally used in the U.S. to depict the full range of animate issues during slumber in which not enough air reaches the lungs (hypopnea and apnea). Sleep-disordered animate is associated with an increased risk of cardiovascular disease, stroke, loftier blood pressure, arrhythmias, diabetes, and sleep deprived driving accidents.[48] [49] [fifty] [51] When high blood pressure is caused by OSA, it is distinctive in that, unlike virtually cases of loftier blood pressure (and so-called essential hypertension), the readings practise not drib significantly when the individual is sleeping.[52] Stroke is associated with obstructive slumber apnea.[53]

Obstructive sleep apnea is associated with problems in daytime functioning, such every bit daytime sleepiness, motor vehicle crashes, psychological problems, decreased cognitive functioning, and reduced quality of life.[54] Other associated bug include cerebrovascular diseases (hypertension, coronary artery affliction, and stroke) and diabetes.[54] These problems could be, at least in part, caused by risk factors of OSA.[54]

Cardinal slumber apnea [edit]

Screenshot of a PSG system showing a primal apnea.

In pure central sleep apnea or Cheyne–Stokes respiration, the encephalon'south respiratory control centers are imbalanced during sleep.[55] 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 organization cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops animate and so starts over again. There is no effort fabricated to breathe during the break in breathing: in that location 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 product gases and absorb more than oxygen.

While sleeping, a normal private 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 abiding. Any sudden driblet in oxygen or backlog of carbon dioxide (even if tiny) strongly stimulates the encephalon's respiratory centers to exhale.

In any person, hypoxia and hypercapnia have certain mutual furnishings on the body.[56] The eye charge per unit will increment, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase incommunicable. The more than translucent areas of the body will evidence a blue or dusky bandage from cyanosis, which is the change in hue that occurs owing to lack of oxygen in the blood ("turning blueish"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill past damping the action of the encephalon's respiratory control centers. In primal slumber apnea, the effects of sleep alone can remove the brain'south 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 congenital-upwardly carbon dioxide. Oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) ship nerve impulses to the encephalon, which and so signals reflex opening of the larynx (so that the opening betwixt 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 make full it.
  • Physiologic effects of cardinal apnea: During fundamental apneas, the central respiratory bulldoze is absent, and the brain does not reply to changing blood levels of the respiratory gases. No jiff is taken despite the normal signals to inhale. The immediate effects of key sleep apnea on the trunk depend on how long the failure to breathe endures. At worst, key slumber apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures, fifty-fifty in the absence of epilepsy. In people with epilepsy, the hypoxia acquired by apnea may trigger seizures that had previously been well controlled by medications.[57] In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery illness, a severe driblet in claret oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may crusade an increase in carbon dioxide levels that can alter the pH of the blood enough to crusade a respiratory acidosis.

Mixed apnea [edit]

Some people with sleep apnea accept a combination of both types; its prevalence ranges from 0.56% to 18%. The condition is generally detected when obstructive slumber apnea is treated with CPAP and central slumber apnea emerges. The verbal mechanism of the loss of cardinal respiratory drive during sleep in OSA is unknown but is near likely related to incorrect settings of the CPAP treatment and other medical conditions the person has.[58]

Management [edit]

The treatment of obstructive sleep apnea is different than that of central sleep apnea. Treatment frequently starts with behavioral therapy. Many people are told to avert alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night.[59]

Continuous positive airway force per unit area [edit]

Person using a CPAP mask, covering merely the nose

CPAP car with two models of masks

For moderate to severe slumber apnea, the most mutual handling is the utilize of a continuous positive airway pressure (CPAP) or automatic positive airway pressure (APAP) device.[59] [threescore] These splint the person'south airway open during sleep past means of pressurized air. The person typically wears a plastic facial mask, which is connected past a flexible tube to a small bedside CPAP machine.[59]

Although CPAP therapy is effective in reducing apneas and less expensive than other treatments, some people notice it uncomfortable. Some mutter of feeling trapped, having chest discomfort, and skin or nose irritation. Other side furnishings may include dry rima oris, dry nose, nosebleeds, sore lips and gums.[61]

Whether or not it decreases the gamble of death or heart illness is controversial with some reviews finding benefit and others not.[15] [62] This variation across studies might exist driven by low rates of compliance—analyses of those who apply CPAP for at least iv hours a night suggests a decrease in cardiovascular events.[63]

Weight loss [edit]

Excess torso weight is thought to be an important cause of sleep apnea.[64] People who are overweight have more than tissues in the back of their throat which can restrict the airway, especially when sleeping.[65] In weight loss studies of overweight individuals, those who lose weight show reduced apnea frequencies and improved Apnoea–Hypopnoea Alphabetize (AHI).[64] [66] Weight loss constructive enough to salvage obesity hypoventilation syndrome (OHS) must be 25–30% of body weight. For some obese people, it can be difficult to reach and maintain this issue without bariatric surgery.[67]

Rapid Palatal Expansion [edit]

In children, orthodontic handling to aggrandize the volume of the nasal airway, such as nonsurgical Rapid Palatal expansion is mutual. The procedure has been institute to significantly decrease the AHI and lead to long-term resolution of clinical symptoms.[68] [69]

Since the palatal suture is fused in adults, regular RPE using tooth-borne expanders cannot be performed. Mini-implant assisted rapid palatal expansion (MARPE) has been recently adult as a non-surgical option for the transverse expansion of the maxilla in adults. This method increases the volume of the nasal cavity and nasopharynx, leading to increased airflow and reduced respiratory arousals during sleep.[70] [71] Changes are permanent with minimal complications.

Palatal expansion is a unique handling in that it is minimally invasive, has lasting changes and requires minimal patient compliance for treatment success.

Surgery [edit]

Analogy of surgery on the mouth and throat.

Several surgical procedures (slumber surgery) are used to treat sleep apnea, although they are commonly a third line of treatment for those who reject or are non helped past CPAP handling or dental appliances.[15] Surgical handling for obstructive sleep apnea needs to be individualized to address all anatomical areas of obstruction.

Nasal obstruction [edit]

Often, correction of the nasal passages needs to be performed in addition to correction of the oropharynx passage. Septoplasty and turbinate surgery may improve the nasal airway,[72] merely has been institute to be ineffective at reducing respiratory arousals during slumber.[73]

Pharyngeal obstacle [edit]

Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) are bachelor to address pharyngeal obstruction.

Uvulopalatopharyngoplasty. A) pre-operative, B) original UPPP, C) modified UPPP, and D) minimal UPPP.

The "Pillar" device is a treatment for snoring and obstructive sleep apnea; information technology is sparse, narrow strips of polyester. Three strips are inserted into the roof of the oral fissure (the soft palate) using a modified syringe and local coldhearted, in order to stiffen the soft palate. This process addresses one of the most common causes of snoring and slumber apnea — vibration or collapse of the soft palate. It was approved by the FDA for snoring in 2002 and for obstructive sleep apnea in 2004. A 2022 meta-analysis plant that "the Pillar implant has a moderate issue on snoring and mild-to-moderate obstructive sleep apnea" and that more studies with high level of evidence were needed to go far at a definite decision; it also found that the polyester strips work their way out of the soft palate in near x% of the people in whom they are implanted.[74]

Hypopharyngeal or base of tongue obstruction [edit]

Base of operations-of-tongue advocacy by means of advancing the genial tubercle of the mandible, natural language suspension, or hyoid suspension (aka hyoid myotomy and pause or hyoid advancement) may help with the lower throat.

Other surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat, procedures done at either a doctor'southward 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 potent plastic is used in the case of surgery whose goal is to stiffen tissues.[59]

Multi-level surgery [edit]

Maxillomandibular advancement (MMA) is considered the nigh effective surgery for people with sleep apnea, because it increases the posterior airway space (PAS).[75] However, health professionals are often unsure as to who should be referred for surgery and when to do so: some factors in referral may include failed apply of CPAP or device utilise; anatomy which favors rather than impedes surgery; or significant craniofacial abnormalities which hinder device use.[76]

Potential complications [edit]

Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to save pain and to depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to crusade life-threatening irregularities in breathing or collapses in a patient'south airways.[77] Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.

Surgery on the oral fissure and throat, too as dental surgery and procedures, can result in postoperative swelling of the lining of the oral fissure and other areas that affect the airway. Even when the surgical procedure is designed to amend the airway, such every bit tonsillectomy and adenoidectomy or tongue reduction, swelling may negate some of the furnishings in the immediate postoperative period. In one case the swelling resolves and the palate becomes tightened by postoperative scarring, however, the full do good of the surgery may exist noticed.

A person with slumber apnea undergoing any medical treatment must make certain their doctor and anesthetist are informed most the sleep apnea. Culling and emergency procedures may be necessary to maintain the airway of sleep apnea patients.[78]

Other [edit]

Neurostimulation [edit]

Diaphragm pacing, which involves the rhythmic application of electric impulses to the diaphragm, has been used to treat central sleep apnea.[79] [80]

In April 2014, the U.S. Food and Drug Administration granted pre-market approval for use of an upper airway stimulation system in people who cannot utilize a continuous positive airway pressure device. The Inspire Upper Airway Stimulation system senses respiration and applies mild electrical stimulation during inspiration, which pushes the natural language slightly forwards to open the airway.[81]

Medications [edit]

There is currently insufficient evidence to recommend any medication for OSA.[82] In that location is limited testify for medication, but acetazolamide "may exist considered" for the handling of central slumber apnea; it[ clarification needed ] besides found that zolpidem and triazolam may exist considered for the treatment of fundamental sleep apnea, but "only if the patient does not have underlying adventure factors for respiratory depression".[82] [60] Low doses of oxygen are also used equally a treatment for hypoxia but are discouraged due to side furnishings.[83] [84] [85]

Oral appliances [edit]

An oral appliance, often referred to equally a mandibular advancement splint, is a custom-made mouthpiece that shifts the lower jaw frontward and opens the bite slightly, opening upwards the airway. These devices tin can be fabricated by a general dentist. Oral apparatus therapy (OAT) is usually successful in patients with balmy to moderate obstructive slumber apnea.[86] [87] While CPAP is more effective for sleep apnea than oral appliances, oral appliances do ameliorate sleepiness and quality of life and are often improve tolerated than CPAP.[87]

Nasal EPAP [edit]

Nasal EPAP is a bandage-similar device placed over the nostrils that uses a person'due south own animate to create positive airway pressure to prevent obstructed animate.[88]

Oral pressure therapy [edit]

Oral pressure therapy uses a device that creates a vacuum in the rima oris, pulling the soft palate tissue forward. It has been found useful in about 25 to 37% of people.[89] [90]

Prognosis [edit]

Death could occur from untreated OSA due to lack of oxygen to the body.[61]

There is increasing show that slumber apnea may atomic number 82 to liver part impairment, particularly fatty liver diseases (meet steatosis).[26] [91] [92] [93]

Information technology has been revealed that people with OSA show tissue loss in encephalon regions that aid store memory, thus linking OSA with retentiveness loss.[94] Using magnetic resonance imaging (MRI), the scientists discovered that people with slumber apnea have mammillary bodies that are almost xx% smaller, particularly on the left side. 1 of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.[95]

The firsthand effects of cardinal sleep apnea on the body depend on how long the failure to exhale endures. At worst, central sleep apnea may crusade sudden death. Brusk of expiry, 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.[57] In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drib in blood oxygen level tin can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may cause an increment in carbon dioxide levels that can change the pH of the blood enough to crusade a respiratory acidosis.

Epidemiology [edit]

The Wisconsin Sleep Accomplice Study estimated in 1993 that roughly 1 in every 15 Americans was afflicted by at least moderate sleep apnea.[96] [97] It as well estimated that in centre-age equally many every bit ix% of women and 24% of men were affected, undiagnosed and untreated.[64] [96] [97]

The costs of untreated slumber apnea reach further than just health issues. It is estimated that in the U.South., the average untreated sleep apnea patient's annual health care costs $ane,336 more than an individual without sleep apnea. This may cause $three.iv billion/year in additional medical costs. Whether medical toll savings occur with treatment of sleep apnea remains to exist adamant.[98]

History [edit]

A type of CSA was described in the High german myth of Ondine's curse where the person when asleep would forget to breathe.[99] The clinical picture of this condition has long been recognized as a character trait, without an understanding of the illness process. The term "Pickwickian syndrome" that is sometimes used for the syndrome was coined by the famous early 20th-century physician William Osler, who must have been a reader of Charles Dickens. The description of Joe, "the fatty boy" in Dickens's novel The Pickwick Papers, is an authentic clinical motion picture of an adult with obstructive sleep apnea syndrome.[100]

The early reports of obstructive sleep apnea in the medical literature described individuals who were very severely affected, often presenting with severe hypoxemia, hypercapnia and congestive heart failure.

Treatment [edit]

The management of obstructive sleep apnea was improved with the introduction of continuous positive airway pressure (CPAP), first described in 1981 past Colin Sullivan and associates in Sydney, Commonwealth of australia.[101] The start models were beefy and noisy, only the design was rapidly improved and by the late 1980s, CPAP was widely adopted. The availability of an constructive treatment stimulated an aggressive search for afflicted individuals and led to the establishment of hundreds of specialized clinics dedicated to the diagnosis and treatment of sleep disorders. Though many types of sleep problems are recognized, the vast majority of patients attention these centers have sleep-disordered animate. Sleep apnea awareness day is April 18 in recognition of Colin Sullivan.[102]

Come across likewise [edit]

  • Built fundamental hypoventilation syndrome
  • Modes of mechanical ventilation
  • Periodic breathing
  • Obesity hypoventilation syndrome
  • Respiratory disturbance index (RDI)
  • Upper airway resistance syndrome

References [edit]

  1. ^ a b c d e f m h i j k fifty m n "Sleep Apnea: What Is Sleep Apnea?". NHLBI: Health Information for the Public. U.S. Section of Health and Man Services. July 10, 2012. Archived from the original on August xix, 2016. Retrieved 2016-08-18 .
  2. ^ a b c "What Are the Signs and Symptoms of Sleep Apnea?". NHLBI. July x, 2012. Archived from the original on 26 Baronial 2016. Retrieved 18 August 2016.
  3. ^ a b Andrade, A.; Bubu, O. M.; Varga, A. Westward.; Osorio, R. Due south. (2018). "The relationship between Obstructive Slumber Apnea and Alzheimer's Disease". Journal of Alzheimer'south Disease. 64 (Suppl i): S255–S270. doi:10.3233/JAD-179936. PMC6542637. PMID 29782319.
  4. ^ a b c Jackson, Melinda L.; Cavuoto, Marina; Schembri, Rachel; Doré, Vincent; Villemagne, Victor L.; Barnes, Maree; O'Donoghue, Fergal J.; Rowe, Christopher C.; Robinson, Stephen R. (10 November 2020). "Astringent Obstructive Sleep Apnea Is Associated with Higher Brain Amyloid Burden: A Preliminary PET Imaging Study". Periodical of Alzheimer's Illness. 78 (2): 611–617. doi:x.3233/JAD-200571. PMID 33016907. S2CID 222145149. Lay summary.
  5. ^ Young, Terry; Finn, Laurel; Peppard, Paul E.; Szklo-Coxe, Mariana; Austin, Diane; Nieto, F. Javier; Stubbs, Robin; Hla, Chiliad. Mae (1 August 2008). "Sleep Disordered Breathing and Mortality: Eighteen-Twelvemonth Follow-up of the Wisconsin Slumber Cohort". Sleep. 31 (8): 1071–1078. PMC2542952. PMID 18714778. Lay summary.
  6. ^ a b c Franklin, K. A.; Lindberg, E. (2015). "Obstructive sleep apnea is a common disorder in the population—a review on the epidemiology of sleep apnea". Journal of Thoracic Disease. vii (eight): 1311–1322. doi:ten.3978/j.issn.2072-1439.2015.06.xi. PMC4561280. PMID 26380759.
  7. ^ a b "Who Is at Gamble for Sleep Apnea?". NHLBI. July 10, 2012. Archived from the original on 26 Baronial 2016. Retrieved 18 Baronial 2016.
  8. ^ a b "How Is Sleep Apnea Diagnosed?". NHLBI. July x, 2012. Archived from the original on 11 Baronial 2016. Retrieved eighteen August 2016.
  9. ^ a b Owen, Jessica East; Benediktsdottir, Bryndis; Cook, Elizabeth; Olafsson, Isleifur; Gislason, Thorarinn; Robinson, Stephen R (21 September 2020). "Alzheimer's illness neuropathology in the hippocampus and brainstem of people with obstructive sleep apnea". Slumber. 44 (3): zsaa195. doi:10.1093/slumber/zsaa195. PMID 32954401. Lay summary.
  10. ^ Osman, A. Grand.; Carter, S. Thousand.; Carberry, J. C.; Eckert, D. J. (2018). "Obstructive sleep apnea: Current perspectives". Nature and Science of Sleep. 10: 21–34. doi:x.2147/NSS.S124657. PMC5789079. PMID 29416383.
  11. ^ De Backer Due west (June 2013). "Obstructive sleep apnea/hypopnea syndrome". Panminerva Medica. 55 (two): 191–5. PMID 23676959.
  12. ^ Majmundar, Sapan H.; Patel, Shivani (2018-x-27). Physiology, Carbon Dioxide Retentivity. StatPearls Publishing. PMID 29494063.
  13. ^ Gottlieb, D. J., & Punjabi, N. M. (2020). Diagnosis and management of obstructive slumber apnea. JAMA, 323(14), 1389. https://doi.org/10.1001/jama.2020.3514
  14. ^ "How Is Sleep Apnea Treated?". NHLBI. July 10, 2012. Archived from the original on 27 August 2016. Retrieved 18 August 2016.
  15. ^ a b c d Spicuzza L, Caruso D, Di Maria G (September 2015). "Obstructive sleep apnoea syndrome and its direction". Therapeutic Advances in Chronic Affliction. 6 (v): 273–85. doi:ten.1177/2040622315590318. PMC4549693. PMID 26336596.
  16. ^ Iftikhar IH, Khan MF, Das A, Magalang UJ (Apr 2013). "Meta-assay: continuous positive airway pressure improves insulin resistance in patients with sleep apnea without diabetes". Annals of the American Thoracic Society. 10 (2): 115–twenty. doi:10.1513/annalsats.201209-081oc. PMC3960898. PMID 23607839.
  17. ^ Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe Grand, Dupont A, Velkeniers B (April 2007). "The impact of continuous positive airway pressure on blood pressure in patients with obstructive slumber apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials". Archives of Internal Medicine. 167 (8): 757–64. doi:10.1001/archinte.167.8.757. PMID 17452537.
  18. ^ Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT (March 2003). "Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive slumber apnea: results of a meta-analysis". Archives of Internal Medicine. 163 (v): 565–71. doi:10.1001/archinte.163.5.565. PMID 12622603.
  19. ^ Hsu AA, Lo C (December 2003). "Continuous positive airway pressure therapy in sleep apnoea". Respirology. eight (four): 447–54. doi:ten.1046/j.1440-1843.2003.00494.10. PMID 14708553.
  20. ^ "iii Top Medical Device Stocks to Buy Now". 18 Nov 2017.
  21. ^ "When Sleep Apnea Masquerades every bit Dementia". 6 October 2010.
  22. ^ Liguori, Claudio; Chiaravalloti, Agostino; Izzi, Francesca; Nuccetelli, Marzia; Bernardini, Sergio; Schillaci, Orazio; Mercuri, Nicola Biagio; Placidi, Fabio (1 December 2017). "Slumber apnoeas may represent a reversible take a chance factor for amyloid-β pathology". Brain. 140 (12): e75. doi:10.1093/brain/awx281. PMID 29077794.
  23. ^ Castronovo, Vincenza; Scifo, Paola; Castellano, Antonella; Aloia, Mark S.; Iadanza, Antonella; Marelli, Sara; Cappa, Stefano F.; Strambi, Luigi Ferini; Falini, Andrea (one September 2014). "White Thing Integrity in Obstructive Sleep Apnea before and after Treatment". Sleep. 37 (ix): 1465–1475. doi:10.5665/sleep.3994. PMC4153061. PMID 25142557. Lay summary.
  24. ^ Franklin, Karl A.; Lindberg, Eva (August 2015). "Obstructive slumber apnea is a common disorder in the population—a review on the epidemiology of sleep apnea". Journal of Thoracic Disease. seven (eight): 1311–1322. doi:10.3978/j.issn.2072-1439.2015.06.11. ISSN 2072-1439. PMC4561280. PMID 26380759.
  25. ^ a b El-Advert B, Lavie P (August 2005). "Effect of sleep apnea on knowledge and mood". International Review of Psychiatry. 17 (4): 277–82. doi:10.1080/09540260500104508. PMID 16194800. S2CID 7527654.
  26. ^ a b Aloia MS, Sweet LH, Jerskey BA, Zimmerman Grand, Arnedt JT, Millman RP (December 2009). "Treatment effects on brain activity during a working memory task in obstructive sleep apnea". Journal of Sleep Research. 18 (iv): 404–ten. doi:10.1111/j.1365-2869.2009.00755.x. hdl:2027.42/73986. PMID 19765205. S2CID 15806274.
  27. ^ Sculthorpe LD, Douglass AB (July 2010). "Sleep pathologies in depression and the clinical utility of polysomnography". Canadian Journal of Psychiatry. 55 (7): 413–21. doi:10.1177/070674371005500704. PMID 20704768.
  28. ^ Morgenstern M, Wang J, Beatty N, Batemarco T, Sica AL, Greenberg H (March 2014). "Obstructive sleep apnea: an unexpected cause of insulin resistance and diabetes". Endocrinology and Metabolism Clinics of North America. 43 (1): 187–204. doi:10.1016/j.ecl.2013.09.002. PMID 24582098.
  29. ^ Mayo Clinic. "Sleep apnea". Mayo Clinic. Archived from the original on 2014-04-30.
  30. ^ "What Is Sleep Apnea?". Nhlbi health. Archived from the original on 2015-08-twenty.
  31. ^ Green, Simon (8 February 2011). Biological Rhythms, Sleep and Hyponosis. England: Palgrave Macmillan. p. 85. ISBN978-0-230-25265-3.
  32. ^ a b Purves, Dale (2018-07-04). Neuroscience (Sixth ed.). New York. ISBN978-1-60535-380-7. OCLC 990257568. [ page needed ]
  33. ^ Redline S, Budhiraja R, Kapur V, Marcus CL, Mateika JH, Mehra R, Parthasarthy Southward, Somers VK, Strohl KP, Sulit LG, Gozal D, Wise MS, Quan SF (March 2007). "The scoring of respiratory events in sleep: reliability and validity". Journal of Clinical Sleep Medicine. 3 (2): 169–200. doi:10.5664/jcsm.26818. PMID 17557426.
  34. ^ AASM Task Strength (August 1999). "Sleep-related animate disorders in adults: recommendations for syndrome definition and measurement techniques in clinical enquiry. The Study of an American Academy of Sleep Medicine Task Strength". Slumber. 22 (five): 667–89. doi:ten.1093/slumber/22.five.667. PMID 10450601.
  35. ^ Ruehland WR, Rochford PD, O'Donoghue FJ, Pierce RJ, Singh P, Thornton AT (February 2009). "The new AASM criteria for scoring hypopneas: touch on the apnea hypopnea index". Slumber. 32 (2): 150–7. doi:10.1093/slumber/32.2.150. PMC2635578. PMID 19238801.
  36. ^ "AASM releases position statement on abode sleep apnea testing – American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers". aasm.org. 2017-ten-xiii. Retrieved 18 October 2017.
  37. ^ Whitelaw, William A.; Brant, Rollin F.; Flemons, W. Ward (15 January 2005). "Clinical Usefulness of Dwelling house Oximetry Compared with Polysomnography for Assessment of Sleep Apnea". American Journal of Respiratory and Critical Intendance Medicine. 171 (2): 188–193. doi:10.1164/rccm.200310-1360OC. PMID 15486338. S2CID 26015566.
  38. ^ Caples SM (2005). "The accuracy of physicians in predicting successful handling response in suspected obstructive sleep apnea did non differ between abode monitoring and polysomnography". ACP Journal Lodge. 143 (ane): 21. PMID 15989309.
  39. ^ Morgenthaler, Timothy I.; Kagramanov, Vadim; Hanak, Viktor; Decker, Paul A. (September 2006). "Complex Slumber Apnea Syndrome: Is It a Unique Clinical Syndrome?". Sleep. 29 (9): 1203–1209. doi:10.1093/sleep/29.9.1203. PMID 17040008. Lay summary.
  40. ^ "Slumber Apnea: Who Is At Chance for Sleep Apnea?". NHLBI: Health Information for the Public. U.South. Department of Health and Human Services. Archived from the original on 2010-07-21.
  41. ^ Neill AM, Angus SM, Sajkov D, McEvoy RD (January 1997). "Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea". American Journal of Respiratory and Critical Intendance Medicine. 155 (1): 199–204. doi:x.1164/ajrccm.155.one.9001312. PMID 9001312.
  42. ^ Xiheng, Guo; Chen, Wang; Hongyu, Zhang; Weimin, Kong; Li, An; Li, Liu; Xinzhi, Weng (2003). "The Study Of The Influence Of Sleep Position On Slumber Apnea". Cardinal Health. Archived from the original on 2014-06-26.
  43. ^ Loord H, Hultcrantz E (August 2007). "Positioner--a method for preventing sleep apnea". Acta Oto-Laryngologica. 127 (eight): 861–8. doi:10.1080/00016480601089390. PMID 17762999. S2CID 323418.
  44. ^ Szollosi, Irene; Roebuck, Teanau; Thompson, Bruce; Naughton, Matthew T (August 2006). "Lateral Sleeping Position Reduces Severity of Central Slumber Apnea / Cheyne-Stokes Respiration". Sleep. 29 (8): 1045–1051. doi:10.1093/sleep/29.8.1045. PMID 16944673.
  45. ^ Vennelle Chiliad, White S, Riha RL, Mackay TW, Engleman HM, Douglas NJ (February 2010). "Randomized controlled trial of variable-force per unit area versus stock-still-pressure continuous positive airway force per unit area (CPAP) treatment for patients with obstructive slumber apnea/hypopnea syndrome (OSAHS)". Sleep. 33 (2): 267–71. doi:10.1093/sleep/33.ii.267. PMC2817914. PMID 20175411.
  46. ^ Morris LG, Kleinberger A, Lee KC, Liberatore LA, Burschtin O (November 2008). "Rapid chance stratification for obstructive sleep apnea, based on snoring severity and body mass index". Otolaryngology–Head and Neck Surgery. 139 (v): 615–8. doi:x.1016/j.otohns.2008.08.026. PMID 18984252. S2CID 5851919.
  47. ^ Campos, Adrián I.; García-Marín, Luis 1000.; Byrne, Enda Yard.; Martin, Nicholas K.; Cuéllar-Partida, Gabriel; Rentería, Miguel E. (December 2020). "Insights into the aetiology of snoring from observational and genetic investigations in the Great britain Biobank". Nature Communications. 11 (1): 817. Bibcode:2020NatCo..11..817C. doi:10.1038/s41467-020-14625-1. PMC7021827. PMID 32060260.
  48. ^ Yan-fang S, Yu-ping Due west (August 2009). "Slumber-matted breathing: impact on functional outcome of ischemic stroke patients". Slumber Medicine. x (7): 717–9. doi:ten.1016/j.slumber.2008.08.006. PMID 19168390.
  49. ^ Bixler EO, Vgontzas AN, Lin HM, Liao D, Calhoun S, Fedok F, Vlasic V, Graff One thousand (November 2008). "Blood pressure associated with sleep-disordered breathing in a population sample of children". Hypertension. 52 (5): 841–6. doi:10.1161/HYPERTENSIONAHA.108.116756. PMC3597109. PMID 18838624.
  50. ^ Leung RS (2009). "Sleep-matted breathing: autonomic mechanisms and arrhythmias". Progress in Cardiovascular Diseases. 51 (4): 324–38. doi:x.1016/j.pcad.2008.06.002. PMID 19110134.
  51. ^ Silverberg DS, Iaina A, Oksenberg A (Jan 2002). "Treating obstructive sleep apnea improves essential hypertension and quality of life". American Family unit Doc. 65 (2): 229–36. PMID 11820487. Archived from the original on 2008-05-13.
  52. ^ Grigg-Damberger M (Feb 2006). "Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack". Journal of Clinical Neurophysiology. 23 (1): 21–38. doi:x.1097/01.wnp.0000201077.44102.80. PMID 16514349. S2CID 19626174.
  53. ^ Yaggi, H. Klar; Concato, John; Kernan, Walter N.; Lichtman, Judith H.; Contumely, Lawrence M.; Mohsenin, Vahid (10 November 2005). "Obstructive Sleep Apnea as a Risk Cistron for Stroke and Death". New England Journal of Medicine. 353 (19): 2034–2041. doi:10.1056/NEJMoa043104. PMID 16282178. S2CID 23360654.
  54. ^ a b c Young, Terry (28 April 2004). "Adventure Factors for Obstructive Sleep Apnea in Adults". JAMA. 291 (16): 2013–half-dozen. doi:10.1001/jama.291.sixteen.2013. PMID 15113821.
  55. ^ Yumino D, Bradley TD (February 2008). "Cardinal slumber apnea and Cheyne-Stokes respiration". Proceedings of the American Thoracic Society. v (ii): 226–36. doi:10.1513/pats.200708-129MG. PMID 18250216.
  56. ^ Sicard KM, Duong TQ (April 2005). "Furnishings of hypoxia, hyperoxia, and hypercapnia on baseline and stimulus-evoked Assuming, CBF, and CMRO2 in spontaneously breathing animals". NeuroImage. 25 (iii): 850–8. doi:10.1016/j.neuroimage.2004.12.010. PMC2962945. PMID 15808985.
  57. ^ a b Devinsky O, Ehrenberg B, Barthlen GM, Abramson HS, Luciano D (November 1994). "Epilepsy and sleep apnea syndrome". Neurology. 44 (xi): 2060–4. doi:10.1212/WNL.44.11.2060. PMID 7969960. S2CID 2165184.
  58. ^ Khan MT, Franco RA (2014). "Circuitous sleep apnea syndrome". Slumber Disorders. 2014: 1–6. doi:ten.1155/2014/798487. PMC3945285. PMID 24693440.
  59. ^ a b c d "How Is Sleep Apnea Treated?". National Heart, Lung, and Blood Establish. Archived from the original on 2007-10-13.
  60. ^ a b Aurora RN, Chowdhuri South, Ramar G, Bista SR, Casey KR, Lamm CI, Kristo DA, Mallea JM, Rowley JA, Zak RS, Tracy SL (January 2012). "The treatment of central sleep apnea syndromes in adults: exercise parameters with an evidence-based literature review and meta-analyses". Slumber. 35 (1): 17–40. doi:ten.5665/sleep.1580. PMC3242685. PMID 22215916.
  61. ^ a b "Diagnosis and Treatment of Obstructive Sleep Apnea in Adults". AHRQ Effective Health Care Program. August 8, 2011. Archived from the original on December 31, 2016. . A 2022 surveillance update Archived 2017-01-25 at the Wayback Machine found no significant data to update.
  62. ^ Yu J, Zhou Z, McEvoy RD, Anderson CS, Rodgers A, Perkovic V, Neal B (July 2017). "Association of Positive Airway Pressure With Cardiovascular Events and Expiry in Adults With Slumber Apnea: A Systematic Review and Meta-analysis". JAMA. 318 (two): 156–166. doi:10.1001/jama.2017.7967. PMC5541330. PMID 28697252.
  63. ^ Gottlieb DJ (July 2017). "Does Obstructive Slumber Apnea Handling Reduce Cardiovascular Risk?: It Is Far Too Soon to Say". JAMA. 318 (ii): 128–130. doi:10.1001/jama.2017.7966. PMID 28697240.
  64. ^ a b c Young, Terry; Peppard, Paul E.; Gottlieb, Daniel J. (May 2002). "Epidemiology of Obstructive Slumber Apnea: A Population Health Perspective". American Journal of Respiratory and Disquisitional Care Medicine. 165 (ix): 1217–1239. doi:ten.1164/rccm.2109080. PMID 11991871. S2CID 23784058.
  65. ^ Watson, Stephanie (2 October 2013). "Weight loss, breathing devices still best for treating obstructive sleep apnea". Harvard Health Blog.
  66. ^ Tuomilehto HP, Seppä JM, Partinen MM, Peltonen K, Gylling H, Tuomilehto JO, Vanninen EJ, Kokkarinen J, Sahlman JK, Martikainen T, Soini EJ, Randell J, Tukiainen H, Uusitupa M (Feb 2009). "Lifestyle intervention with weight reduction: offset-line treatment in mild obstructive slumber apnea". American Journal of Respiratory and Disquisitional Care Medicine. 179 (4): 320–7. doi:10.1164/rccm.200805-669OC. PMID 19011153.
  67. ^ Mokhlesi, Babak; Masa, Juan Fernando; Brozek, Jan L.; Gurubhagavatula, Indira; Murphy, Patrick B.; Piper, Amanda J.; Tulaimat, Aiman; Afshar, Majid; Balachandran, Jay S.; Dweik, Raed A.; Grunstein, Ronald R.; Hart, Nicholas; Kaw, Roop; Lorenzi-Filho, Geraldo; Pamidi, Sushmita; Patel, Bhakti K.; Patil, Susheel P.; Pépin, Jean Louis; Soghier, Israa; Tamae Kakazu, Maximiliano; Teodorescu, Mihaela (1 August 2019). "Evaluation and Direction of Obesity Hypoventilation Syndrome. An Official American Thoracic Gild Clinical Practice Guideline". American Journal of Respiratory and Disquisitional Care Medicine. 200 (3): e6–e24. doi:ten.1164/rccm.201905-1071ST. PMC6680300. PMID 31368798.
  68. ^ Villa, Maria Pia; Rizzoli, Alessandra; Miano, Silvia; Malagola, Caterina (1 May 2011). "Efficacy of rapid maxillary expansion in children with obstructive sleep apnea syndrome: 36 months of follow-upward". Sleep and Breathing. xv (2): 179–184. doi:10.1007/s11325-011-0505-ane. PMID 21437777. S2CID 4505051.
  69. ^ Machado-Júnior, Almiro-José; Zancanella, Edilson; Crespo, Agrício-Nubiato (2016). "Rapid maxillary expansion and obstructive sleep apnea: A review and meta-analysis". Medicina Oral, Patología Oral y Cirugía Bucal. 21 (four): e465–e469. doi:ten.4317/medoral.21073. PMC4920460. PMID 27031063.
  70. ^ Li, Qiming; Tang, Hongyi; Liu, Xueye; Luo, Qing; Jiang, Zhe; Martin, Domingo; Guo, Jing (1 May 2020). "Comparison of dimensions and volume of upper airway before and afterward mini-implant assisted rapid maxillary expansion". The Angle Orthodontist. 90 (3): 432–441. doi:10.2319/080919-522.i. PMC8032299. PMID 33378437.
  71. ^ Abdullatif, Jose; Certal, Victor; Zaghi, Soroush; Vocal, Sungjin A.; Chang, Edward T.; Gillespie, M. Boyd; Camacho, Macario (1 May 2016). "Maxillary expansion and maxillomandibular expansion for adult OSA: A systematic review and meta-assay". Journal of Cranio-Maxillofacial Surgery. 44 (5): 574–578. doi:10.1016/j.jcms.2016.02.001. PMID 26948172.
  72. ^ Sundaram, Supriya; Lim, Jerome; Lasserson, Toby J; Lasserson, TJ (nineteen Oct 2005). "Surgery for obstructive sleep apnoea in adults". Cochrane Database of Systematic Reviews (4): CD001004. doi:10.1002/14651858.CD001004.pub2. PMID 16235277.
  73. ^ Li, Hsueh-Yu; Wang, Pa-Chun; Chen, Yu-Pin; Lee, Li-Ang; Fang, Tuan-Jen; Lin, Hsin-Ching (January 2011). "Critical Appraisal and Meta-Assay of Nasal Surgery for Obstructive Sleep Apnea". American Journal of Rhinology & Allergy. 25 (1): 45–49. doi:10.2500/ajra.2011.25.3558. PMID 21711978. S2CID 35117004.
  74. ^ Choi JH, Kim SN, Cho JH (Jan 2013). "Efficacy of the Pillar implant in the handling of snoring and mild-to-moderate obstructive sleep apnea: a meta-analysis". The Laryngoscope. 123 (one): 269–76. doi:10.1002/lary.23470. PMID 22865236. S2CID 25875843.
  75. ^ Prinsell JR (November 2002). "Maxillomandibular advancement surgery for obstructive sleep apnea syndrome". Journal of the American Dental Clan. 133 (11): 1489–97, quiz 1539–40. doi:10.14219/jada.archive.2002.0079. PMID 12462692.
  76. ^ MacKay, Stuart (June 2011). "Treatments for snoring in adults". Australian Prescriber. 34 (34): 77–79. doi:10.18773/austprescr.2011.048.
  77. ^ Johnson, T. Scott; Broughton, William A.; Halberstadt, Jerry (2003). Slumber Apnea – The Phantom of the Dark: Overcome Sleep Apnea Syndrome and Win Your Subconscious Struggle to Breathe, Sleep, and Live . New Engineering Publishing. ISBN978-1-882431-05-2. [ folio needed ]
  78. ^ "What is Slumber Apnea?". National Heart, Lung, and Blood Constitute. National Institutes of Health. 2012. Archived from the original on 28 August 2011. Retrieved 15 February 2013.
  79. ^ Diaphragm Pacing at eMedicine
  80. ^ Yun AJ, Lee PY, Doux JD (May 2007). "Negative pressure ventilation via diaphragmatic pacing: a potential gateway for treating systemic dysfunctions". Expert Review of Medical Devices. 4 (3): 315–9. doi:ten.1586/17434440.4.3.315. PMID 17488226. S2CID 30419488.
  81. ^ "Inspire Upper Airway Stimulation – P130008". FDA.gov. Nutrient and Drug Administration. 11 January 2016. Archived from the original on 11 March 2016. Retrieved 9 March 2016.
  82. ^ a b Gaisl, Thomas; Haile, Sarah R.; Thiel, Sira; Osswald, Martin; Kohler, Malcolm (August 2019). "Efficacy of pharmacotherapy for OSA in adults: A systematic review and network meta-assay". Sleep Medicine Reviews. 46: 74–86. doi:x.1016/j.smrv.2019.04.009. PMID 31075665. S2CID 149455430.
  83. ^ "Sleep Apnea". Diagnosis Lexicon. Psychology Today. Archived from the original on 2013-04-08.
  84. ^ Mayos, Chiliad.; Hernández Plaza, L.; Farré, A.; Mota, S.; Sanchis, J. (January 2001). "Efecto de la oxigenoterapia nocturna en el paciente con síndrome de apnea-hipopnea del sueño y limitación crónica al flujo aéreo" [The issue of nocturnal oxygen therapy in patients with sleep apnea syndrome and chronic airflow limitation]. Archivos de Bronconeumología (in Spanish). 37 (two): 65–68. doi:10.1016/s0300-2896(01)75016-8. PMID 11181239.
  85. ^ Breitenbücher A, Keller-Wossidlo H, Keller R (November 1989). "Transtracheale Sauerstofftherapie beim obstruktiven Schlafapnoe-Syndrom" [Transtracheal oxygen therapy in obstructive sleep apnea syndrome]. Schweizerische Medizinische Wochenschrift (in German language). 119 (46): 1638–1641. OCLC 119157195. PMID 2609134.
  86. ^ Machado MA, Juliano 50, Taga Chiliad, de Carvalho LB, do Prado LB, do Prado GF (December 2007). "Titratable mandibular repositioner appliances for obstructive sleep apnea syndrome: are they an choice?". Sleep & Animate = Schlaf & Atmung. 11 (four): 225–31. doi:10.1007/s11325-007-0109-y. PMID 17440760. S2CID 24535360.
  87. ^ a b Chen H, Lowe AA (May 2013). "Updates in oral apparatus therapy for snoring and obstructive slumber apnea". Sleep & Breathing = Schlaf & Atmung. 17 (2): 473–86. doi:x.1007/s11325-012-0712-4. PMID 22562263. S2CID 21267378.
  88. ^ Riaz M, Certal Five, Nigam G, Abdullatif J, Zaghi Southward, Kushida CA, Camacho Thou (2015). "Nasal Expiratory Positive Airway Force per unit area Devices (Provent) for OSA: A Systematic Review and Meta-Analysis". Slumber Disorders. 2015: 734798. doi:10.1155/2015/734798. PMC4699057. PMID 26798519.
  89. ^ Nigam G, Pathak C, Riaz M (May 2016). "Effectiveness of oral pressure level therapy in obstructive sleep apnea: a systematic analysis". Sleep & Breathing = Schlaf & Atmung. xx (2): 663–71. doi:x.1007/s11325-015-1270-3. PMID 26483265. S2CID 29755875.
  90. ^ Colrain IM, Black J, Siegel LC, Bogan RK, Becker PM, Farid-Moayer M, Goldberg R, Lankford DA, Goldberg AN, Malhotra A (September 2013). "A multicenter evaluation of oral force per unit area therapy for the treatment of obstructive sleep apnea". Sleep Medicine. fourteen (9): 830–7. doi:x.1016/j.sleep.2013.05.009. PMC3932027. PMID 23871259.
  91. ^ Ahmed MH, Byrne CD (September 2010). "Obstructive sleep apnea syndrome and fat liver: clan or causal link?". World Journal of Gastroenterology. 16 (34): 4243–52. doi:10.3748/wjg.v16.i34.4243. PMC2937104. PMID 20818807.
  92. ^ Singh H, Pollock R, Uhanova J, Kryger M, Hawkins One thousand, Minuk GY (December 2005). "Symptoms of obstructive slumber apnea in patients with nonalcoholic fatty liver affliction". Digestive Diseases and Sciences. l (12): 2338–43. doi:10.1007/s10620-005-3058-y. PMID 16416185. S2CID 21852391.
  93. ^ Tanné F, Gagnadoux F, Chazouillères O, Fleury B, Wendum D, Lasnier E, Lebeau B, Poupon R, Serfaty L (June 2005). "Chronic liver injury during obstructive sleep apnea". Hepatology. 41 (vi): 1290–6. doi:10.1002/hep.20725. PMID 15915459.
  94. ^ Kumar R, Birrer BV, Macey PM, Woo MA, Gupta RK, Yan-Go FL, Harper RM (June 2008). "Reduced mammillary torso book in patients with obstructive sleep apnea". Neuroscience Letters. 438 (three): 330–4. doi:10.1016/j.neulet.2008.04.071. PMID 18486338. S2CID 207126691.
  95. ^ Kumar R, Birrer BV, Macey PM, Woo MA, Gupta RK, Yan-Go FL, Harper RM (June 2008). "Reduced mammillary torso book in patients with obstructive sleep apnea". Neuroscience Letters. 438 (3): 330–iv. doi:10.1016/j.neulet.2008.04.071. PMID 18486338. S2CID 207126691. Lay summary – Newswise (June 6, 2008).
  96. ^ a b Immature, Terry; Palta, Mari; Dempsey, Jerome; Skatrud, James; Weber, Steven; Badr, Safwan (29 April 1993). "The Occurrence of Sleep-Disordered Animate amidst Eye-Aged Adults". New England Periodical of Medicine. 328 (17): 1230–1235. doi:ten.1056/NEJM199304293281704. PMID 8464434. S2CID 9183654.
  97. ^ a b Lee W, Nagubadi S, Kryger MH, Mokhlesi B (June 2008). "Epidemiology of Obstructive Slumber Apnea: a Population-based Perspective". Skilful Review of Respiratory Medicine. ii (3): 349–364. doi:10.1586/17476348.2.3.349. PMC2727690. PMID 19690624.
  98. ^ Kapur, Vishesh; Blough, David Yard.; Sandblom, Robert E.; Hert, Richard; de Maine, James B.; Sullivan, Sean D.; Psaty, Bruce M. (September 1999). "The Medical Price of Undiagnosed Slumber Apnea". Sleep. 22 (half dozen): 749–755. doi:10.1093/sleep/22.six.749. PMID 10505820.
  99. ^ Yentis, Steven Thousand.; Hirsch, Nicholas P.; Ip, James (2013). Amazement and Intensive Intendance A-Z: An Encyclopedia of Principles and Practice. Elsevier Wellness Sciences. p. 428. ISBN978-0-7020-5375-7.
  100. ^ Kryger MH (December 1985). "Fat, sleep, and Charles Dickens: literary and medical contributions to the understanding of sleep apnea". Clinics in Chest Medicine. 6 (four): 555–62. doi:10.1016/S0272-5231(21)00394-4. PMID 3910333.
  101. ^ Sullivan CE, Issa FG, Berthon-Jones One thousand, Eves L (Apr 1981). "Reversal of obstructive sleep apnoea past continuous positive airway pressure applied through the nares". Lancet. 1 (8225): 862–v. doi:x.1016/S0140-6736(81)92140-one. PMID 6112294. S2CID 25219388.
  102. ^ Sichtermann, Lori. "Industry Recognizes Sleep Apnea Sensation Mean solar day 2014". Slumber Review. Archived from the original on 30 April 2014. Retrieved 30 April 2014.

External links [edit]

farquharyesectood.blogspot.com

Source: https://en.wikipedia.org/wiki/Sleep_apnea

You may like these posts

Post a Comment for "Can You Have Sleep Apnea and Not Snore"