Sleep apnea: causes and treatment

Sleep apnea is a sleep-disordered breathing disorder characterized by repeated pauses in breathing (apneas) or significant reductions in airflow (hypopneas). The most common form is obstructive sleep apnea: the upper airway narrows or collapses during sleep, despite efforts to breathe. The result is intermittent hypoxemia, sleep fragmentation, increased daytime sleepiness, fatigue, decreased concentration, and decreased quality of life. [1]

Obstructive sleep apnea is dangerous not only because of its unpleasant symptoms. It is associated with an increased risk of hypertension, atrial fibrillation, heart failure, coronary events and stroke, as well as road traffic and industrial accidents. These associations have been confirmed by major reviews and statements from cardiology societies. [2]

Today, clinical approaches are standardized: the gold standard for diagnosis is nocturnal polysomnography, and for uncomplicated adult patients, home sleep apnea testing (HSAT) with appropriate equipment and subsequent interpretation by a sleep medicine specialist is acceptable. Treatment is based on continuous positive airway pressure (CPAP/PAP), oral appliances, weight loss, positional therapy, and surgery for specific indications. New options have also emerged: hypoglossal nerve stimulation and the first approved drug (tirzepatide) for obese patients. [3]

It is important to distinguish obstructive apnea from central apnea, which is caused by instability of respiratory control and manifests as pauses without respiratory effort. This influences the choice of diagnosis and treatment and requires a different approach. [4]

Epidemiology

A global study estimates that nearly 1 billion adults aged 30–69 years worldwide may have obstructive sleep apnea, with prevalence reaching very high levels in some countries. This highlights the scale of the problem for healthcare systems. [5]

In countries with high obesity rates and aging populations, the disease burden is increasing. Projections for the United States, for example, estimate that by 2050, the number of adults with OSA will increase to approximately 76-77 million, a 35% increase over the 2020 estimate. Economic costs include direct medical expenses and significant indirect losses—labor productivity, accidents, and related illnesses. [6]

European estimates of annual costs per patient range from approximately €1,700 to €5,000, while in the US the total annual burden (undetected cases, productivity, accidents) is estimated at tens and hundreds of billions of dollars. [7]

Recent research highlights the influence of climate and environment: rising temperatures may be associated with increased prevalence of OSA and quality-adjusted life years lost, in addition to traditional risk factors. [8]

Table 1. Burden of obstructive sleep apnea

Indicator	Rating/Conclusion	Source
Globally affected	~1 billion adults aged 30-69	[9]
Forecast for the United States by 2050	~76-77 million adults	[10]
Annual costs (Europe, per patient)	~€1,700-5,000	[11]
Total spending in the US	Very high (tens to hundreds of billions of dollars/year)	[12]

Reasons

OSA is caused by mechanical narrowing/collapse of the upper airway during sleep: weakened pharyngeal muscle tone, anatomical narrowing (enlarged soft tissue, tonsils, micrognathia), accumulation of fat around the pharynx, and neuromuscular influences. These factors make the airway susceptible to collapse when tone decreases during sleep. [13]

Obesity is the leading modifiable cause: deposition of adipose tissue in the neck and tongue, increased abdominal pressure, and decreased functional residual capacity of the lungs increase the likelihood of obstruction. Weight loss dose-dependently reduces the severity of apnea. [14]

In some patients, craniofacial factors predominate: retrognathia, narrow jaw, high palatal vault. For such phenotypes, surgical techniques (e.g., bimaxillary advancement) may be more effective than standard approaches. [15]

In addition, hormonal and inflammatory mechanisms associated with metabolic disorders, as well as alcohol and sedatives that relax the muscles of the pharynx, and chronic nasal congestion contribute. [16]

Risk factors

Unchangeable factors: male gender, age (especially after 50 years), menopause in women, and genetically determined craniofacial features. Many of these are related to the anatomy and regulation of the tone of the upper respiratory tract. [17]

Modifiable factors: obesity (body mass index and neck circumference), evening alcohol consumption, smoking, sedatives/opioids, chronic nasal congestion, hypothyroidism. Their correction is part of prevention and treatment. [18]

Comorbid conditions increase the risk and severity: resistant hypertension, diabetes mellitus, chronic heart failure, as well as "overlap syndrome" (a combination of COPD and OSA) and obesity-hypoventilation syndrome. The latter require special tactics (for example, in the case of obesity-hypoventilation - blood bicarbonate screening, selection of ventilation mode). [19]

Finally, pregnancy and some endocrine disorders (acromegaly, hypothyroidism), as well as anatomical ENT causes (tonsillar hypertrophy) increase the likelihood of OSA in certain groups. [20]

Table 2. Risk factors for OSA (with examples of correction)

Category	Examples	Comment
Unchangeable	Age, gender, jaw anatomy	Determine the baseline risk
Modifiable	Obesity, alcohol, smoking, sedatives	Goals of behavioral and medical correction
Comorbid	COPD (overlap syndrome), obesity-hypoventilation	Special diagnostic and treatment algorithms are needed
ENT factors	Hypertrophy of the tonsils/palate, nasal obstruction	Role in some patients

[21]

Pathogenesis

During sleep, the activity of the pharyngeal dilator muscles (including the tongue) decreases, and in predisposing anatomy, the lumen collapses. Apnea or hypopnea occurs with a drop in oxygen saturation and micro-arousals. Repeated tens or hundreds of times per night, these events cause sleep fragmentation and daytime sleepiness. [22]

Intermittent hypoxia and intrathoracic pressure fluctuations activate the sympathoadrenal system, promoting inflammation and oxidative stress, endothelial dysfunction, and hypertension. Over time, this increases the risk of cardiovascular events. [23]

Different mechanisms predominate in different patients: "soft" collapse due to increased tissue compliance, low arousal threshold, instability of respiratory control (high "loop gain"), and an increased tendency of the tongue/palate to retroposition. This explains the different responses to various treatment methods. [24]

In central sleep apnea, breathing pauses are associated with a neuroregulatory disorder rather than mechanical obstruction, which requires a different diagnosis and often different ventilation support. [25]

Symptoms

The classic triad: loud snoring, episodes of respiratory arrest (according to the observer), and pronounced daytime sleepiness. Often accompanied by morning headaches, a feeling of not getting enough sleep, decreased libido, and cognitive impairment (attention, memory). [26]

Some patients experience predominantly "silent" symptoms: resistant hypertension, atrial fibrillation, nocturnal polyuria, depressive symptoms, and decreased performance. This is a reason for underdiagnosis: people rarely associate these complaints with sleep. [27]

Nighttime symptoms include frequent awakenings, a feeling of suffocation, and excessive sweating. Daytime symptoms include falling asleep in passive situations (while driving, in meetings), irritability, and decreased motivation. Questionnaires (STOP-Bang, Berlin) are used to screen for primary risk, but they do not provide a diagnosis. [28]

It is important to distinguish the obstructive nature of complaints from central breathing disorders, chronic insomnia, restless legs syndrome and other causes of daytime sleepiness - this influences the choice of test and treatment. [29]

Table 3. Common symptoms and tips for the doctor

Symptom	What's alarming	The next step
Snoring + pauses in breathing	According to the partner	Referral for polysomnography/HSAT
Daytime sleepiness	Falling asleep while driving	Urgent risk assessment, temporary driving restrictions
Resistant hypertension	Multiple drugs	Search for OSA, correction of therapy
Migraine morning pain	Regularly, +/- snoring	Diagnosis of sleep-disordered breathing

[30]

Forms and stages

Obstructive, central, and mixed sleep apnea are distinguished. In everyday practice, obstructive sleep apnea predominates. Mixed sleep apnea combines features of both. Central sleep apnea is less common and has a different pathogenesis and treatment. [31]

The severity of OSA in adults is determined by the apnea-hypopnea index (AHI) per hour of sleep: 5-14 is mild, 15-29 is moderate, and ≥30 is severe. An analog for home testing is the respiratory event index (REI). Additional severity metrics (hypoxic load, time SpO₂<90%, etc.) are increasingly being discussed. [32]

From a clinical point of view, phenotypes can be distinguished: “position-dependent” apnea (worse on the back), “craniofacial” phenotype, “metabolic” (obesity, insulin resistance), “low arousal threshold”. This helps to personalize therapy. [33]

In some patients, with correction of factors (weight loss, alcohol abstinence, nasal treatment), the severity is significantly reduced, while in others it requires constant hardware support or surgery. [34]

Table 4. Severity criteria for OSA in adults

Degree	AHI (events/hour)	Comment
Norm	<5	The diagnosis of OSA is not confirmed.
Light	5-14	Symptoms/risks determine the tactics
Moderate	15-29	More often, active treatment is required
Heavy	≥30	High risks, treatment is indicated

[35]

Complications and consequences

Untreated OSA increases the risk of hypertension, atrial fibrillation, coronary heart disease, heart failure, and stroke; the risks of all-cause mortality and major cardiovascular events are increased. The mechanisms are related to hypoxia, sympathetic activation, inflammation, and endothelial dysfunction. [36]

Neurocognitive functions, including attention, memory, and information processing speed, are often affected. The risk of road accidents and workplace errors increases, and productivity decreases. These effects have significant economic consequences for society. [37]

In patients with COPD, the combination with OSA (overlap syndrome) leads to more pronounced nocturnal desaturation, a high frequency of exacerbations and hospitalizations, and a greater cardiovascular risk than with each pathology separately. [38]

In obesity-hypoventilation, the risks of respiratory failure and cardiovascular complications are even higher; specific approaches to ventilation support and gas exchange control are required. [39]

Diagnostics

The "gold standard" is overnight polysomnography in a sleep lab with recording of respiratory flow, effort, oxygen saturation, electroencephalogram, etc. For uncomplicated adult patients with a high probability of OSA, home sleep testing (HSAT) with a technically appropriate device, prescribed and interpreted by a physician, is acceptable. If the HSAT is negative/questionable, proceed to polysomnography. [40]

Questionnaires (STOP-Bang, Berlin) help identify risk groups (especially in surgery and primary care), but do not replace objective sleep testing. The STOP-Bang, with a threshold of ≥3-4, shows high sensitivity to moderate-severe OSA, which is useful as a "rule of exclusion" for severe cases. [41]

Laboratory tests do not diagnose OSA, but are useful for identifying associated conditions: glycemia/lipid profile, TSH, and, if obesity-hypoventilation is suspected, blood bicarbonate levels and/or blood gas composition. In complex cases and atypical clinical presentations, a more in-depth examination is performed for central apnea and other disorders. [42]

PAP titration (pressure selection) can be performed in the laboratory or with an automated (APAP) mode in selected patients. Follow-up, training in use, and monitoring for tolerance and leaks are important. [43]

Table 5. Diagnostic algorithm for an adult with suspected OSA

Step	Action	Comment/reason
1	Complaint and risk assessment (STOP-Bang, etc.)	Screening, not diagnosis
2	Polysomnography or HSAT (as indicated)	HSAT only in "uncomplicated" adults
3	AHI/REI interpretation, severity assessment	AHI 5-14/15-29/≥30
4	Choice of therapy and monitoring plan	RAP, OA, weight loss, etc.

[44]

Differential diagnosis

The main "masks" are primary snoring without apnea, central sleep apnea, insomnia, restless legs syndrome, narcolepsy, depression, and chronic fatigue. To differentiate them, objective sleep data and clinical context are needed. [45]

In central apnea, breathing pauses occur without inspiratory attempts; there are often cardiovascular/neurological causes or high altitude, which requires different therapy (e.g., adaptive servoventilation for certain indications). [46]

COPD overlap syndrome results in marked desaturation, hypercapnia, and special risks; obesity-hypoventilation syndrome results in persistent awake hypercapnia and high bicarbonates, which will guide treatment. [47]

In patients with tonsillar hypertrophy and isolated snoring, the indications for surgery and prognosis differ from typical OSA - this is taken into account when choosing a path. [48]

Table 6. Differential diagnosis of "drowsiness + snoring"

State	Key feature	What confirms
OAS	Effortful apnea/hypopnea	Polysomnography/HSAT
Central apnea	Effortless pauses	Polysomnography, clinic
Primary snoring	No apnea	Sleep study, ENT evaluation
Overlap (COPD+OSA)	Desaturations, hypercapnia	Spirometry, gas analysis, PSG

[49]

Treatment

1) PAP therapy (CPAP/APAP/BiPAP). PAP is the basic method with the best effect on AHI and drowsiness. AASM recommendations: in uncomplicated adults, you can start with the automatic mode (APAP) or adjust the pressure in the laboratory; in cases of concomitant cardiorespiratory pathology, suspected hypoventilation, or neuromuscular diseases, laboratory titration and/or bilevel ventilation are preferable. The key to success is education, mask selection, humidification, and adherence monitoring. [50]

2) Oral (mandibular) appliances. Joint AASM/AADSM guidelines recommend custom-fit adjustable appliances for patients who prefer an alternative or who cannot tolerate RAPs. They are superior to no treatment and, for a range of phenotypes (mild-moderate OSA, retrognathia), can provide clinically significant improvement. Titration and follow-up with a qualified dentist are essential. [51]

3) Weight loss and metabolic therapy. Weight loss improves OSA dose-dependently; ≥5-10% body weight loss significantly reduces severity. Bariatric surgery leads to a significant reduction in AHI and often remission of OSA (according to meta-analyses, approximately 60-65% in the short- to medium-term), although OSA persists in some patients. In December 2024, the FDA approved the first drug for the treatment of moderate-to-severe OSA in obese adults - tirzepatide (Zepbound) in combination with diet and physical activity; this reflects the role of obesity pharmacotherapy in the treatment of OSA. [52]

4) Positional therapy. For position-dependent pain (worse on the back), "smart" positioning devices and training methods are used. The effectiveness is lower than that of PAP, but higher than no treatment; the method is appropriate for those intolerant to PAP and as part of a combined approach. [53]

5) Hypoglossal nerve stimulation. Implantable systems stimulate the tongue muscle synchronously with inspiration and reduce pharyngeal collapse in carefully selected patients (usually those intolerant of PAP, without complete obstruction at the level of the soft palate as a result of drug-induced sleep). Indications and coverage criteria are described by insurers and societies; the method is not first-line, but has a growing evidence base. [54]

6) Upper airway surgery. Options include uvulopalatopharyngoplasty (with variations), tonsillectomy when indicated, multilevel surgery, and maxillomandibular advancement (MMA), which has shown high efficacy in appropriately selected patients, including those with obesity and severe craniofacial abnormalities. The choice depends on the obstructive phenotype and sleep endoscopy results. [55]

7) Complementary/New Approaches. Myofunctional (orofacial) therapy—tongue and oropharyngeal muscle training—is gaining evidence as an adjunct to mainstream interventions: meta-analyses from 2024–2025 report reductions in AHI and symptoms, especially with daily sessions of ≥30 minutes. These techniques should be considered as an adjuvant in motivated patients. [56]

Table 7. Comparison of the main treatment methods

Method	Effect on AHI	Pros	Cons/Limitations	Who is it suitable for?
RAR	Maximum	Fast effect, proven benefits	Requires adherence, mask	Most patients
Oral appliance	Moderately expressed	Alternative to PAP, portability	Not effective for everyone, check with your dentist	Mild-moderate OSA, PAP intolerance
Weight loss/bariatrics	Dose-dependent, sometimes remission	Benefits for metabolism	Not instantly, not enough for everyone	Patients with obesity
Positional therapy	Expressed in positional OAS	Simplicity, adjuvant	Below the RAP effect	Positional OAS
Stimulation of the hypoglossus	Significant in the selected	No mask, night comfort	Invasiveness, selection	PAP intolerance, suitable phenotype
Surgery (MMA/UPPP/etc.)	Moderate to high	Potentially long-lasting effect	Operational risks, selection	Anatomical phenotype

[57]

Prevention

Primary prevention involves weight control, adequate physical activity, limiting alcohol consumption before bed, quitting smoking, and promptly treating nasal obstruction and allergic rhinitis. This reduces upper airway compliance and reduces the likelihood of snoring and apnea. [58]

Secondary prevention is aimed at early detection among risk groups (obesity, resistant hypertension, atrial fibrillation, daytime sleepiness, and intermittent snoring). It is important to remember that universal screening of asymptomatic adults in the general population is not yet recommended due to a lack of evidence, but questionnaires are appropriate in clinics and before surgery. [59]

Forecast

With proper diagnosis and appropriate therapy, the prognosis is favorable: daytime sleepiness is reduced, cognitive function and quality of life indicators improve, and the risk of cardiovascular events and accidents is reduced. The best results are achieved with a combined approach (PAP + weight management + factor correction). [60]

Without treatment, cardiovascular and metabolic burden increases, and the risk of hospitalization and complications increases, especially when combined with COPD and obesity-hypoventilation. Early diagnosis and personalized treatment fundamentally change long-term outcomes. [61]

FAQ

• Should everyone be tested?

No. Our current position is that universal screening of asymptomatic adults is not recommended—the evidence is insufficient. However, if you snore, have pauses in breathing, are sleepy, or have resistant hypertension, screening is indicated. [62]

• What to choose: a “home” test or polysomnography?

A home test is suitable for uncomplicated adults with a high probability of OSA; in case of doubt, a negative result, or complex concomitant diseases, a full polysomnography in a laboratory is preferable. [63]

• Is it possible to cure OSA without a device?

Sometimes, yes: with moderate overweight and position-dependent apnea, weight loss, positional devices, and oral appliances can help. But for moderate to severe forms, RAP remains the most effective and safe method with a rapid effect. [64]

• Are there any new drugs?

Yes. In December 2024, the FDA first approved tirzepatide for the treatment of moderate-to-severe OSA in obese adults—as an adjunct to calorie restriction and physical activity. This does not replace PAP, but expands the options for combination treatment. [65]

Additional tables for practice

Table 8. When HSAT is not appropriate (polysomnography is better)

Situation	Why
Suspected central apnea/hypoventilation	Advanced monitoring is needed
Severe cardiorespiratory diseases, history of stroke	Risk of errors and complications
Chronic opioid/sedative use	Change in breathing pattern
Severe insomnia, alternating sleep schedule	Low information content of HSAT

[66]

Table 9. Questionnaires for primary screening (not for diagnosis)

Tool	Strengths	Restrictions
STOP-Bang	High sensitivity, simplicity	Low specificity at low thresholds
Berlin	Used in primary health care, validated in Spanish-speaking	Variable accuracy, especially outside primary care
ESS (sleepiness)	Assesses the symptom, not the OSA	Not a screening test for OSA

[67]

Table 10. Selection of treatment method by phenotype

Phenotype	Basic tactics	Alternatives/adjuvants
Metabolic (obesity)	RAP + weight loss	Bariatrics, tirzepatide
Positional	RAP or positioning devices	Oral appliance
Craniofacial	RAR	MMA surgery, oral appliance
Intolerance to PAP	Oral appliance	Neurostimulation of the hypoglossus

[68]

Table 11. Key innovations of recent years

Direction	What's new	Comment
Pharmacotherapy	Tirzepatide approved by the FDA (adults with obesity and moderate-to-severe OSA)	A lifestyle supplement, not a replacement for PAP
Technologies	Smart positioning devices, remote monitoring of RAP	Improves commitment
Surgery	Clear criteria for selection for neurostimulation and MMA	Based on obstructive phenotype

[69]

Table 12. Mini-reminder for the patient

Step	What to do
1	Discuss symptoms and risks (including STOP-Bang) with your doctor.
2	Take the recommended sleep study
3	Initiate a line of therapy (PAP/alternative), follow the training
4	Plan for weight loss and risk factor management
5	Performance monitoring and adjustments every 1-3 months

[70]