One-liner#

OSA management centers on CPAP therapy for moderate-severe disease (AHI ≥15), weight loss (10% loss reduces AHI by ~26%), and aggressive cardiovascular risk management given the strong association with resistant hypertension, atrial fibrillation, and heart failure.

Quick nav#

• Definition and epidemiology
• Pathophysiology
• Clinical presentation
• Diagnostic workup
• Treatment
• Patient education
• Prognosis and monitoring
• Special populations
• When to refer
• Smartphrase snippets
• Related pages

Definition and epidemiology#

Diagnostic criteria#

OSA is defined by ≥5 obstructive respiratory events (apneas, hypopneas, or respiratory effort-related arousals) per hour of sleep (Apnea-Hypopnea Index, AHI ≥5) with associated symptoms OR AHI ≥15 regardless of symptoms.

Severity Classification (by AHI):

• Mild: AHI 5-14 events/hour
• Moderate: AHI 15-29 events/hour
• Severe: AHI ≥30 events/hour

Key definitions:

• Apnea: ≥90% reduction in airflow for ≥10 seconds
• Hypopnea: ≥30% reduction in airflow for ≥10 seconds with ≥3% oxygen desaturation or arousal
• Oxygen Desaturation Index (ODI): number of ≥3% desaturations per hour

Epidemiology#

Prevalence is approximately 10-30% of adults, with significant underdiagnosis (80-90% undiagnosed). More common in men (2:1 ratio), though gap narrows after menopause. Prevalence increases with age, peaking at 55-65 years. Major risk factors include obesity (BMI >30 increases risk 10-14x), neck circumference >17 inches (men) or >16 inches (women), craniofacial abnormalities (retrognathia, micrognathia), and family history. Strong associations with hypertension (30-50% of HTN patients have OSA), atrial fibrillation (OSA in 40-50% of AF patients), heart failure (50-75% prevalence), and type 2 diabetes.

Pathophysiology#

Mechanism (clinical understanding)#

OSA results from repetitive upper airway collapse during sleep, driven by the interplay of anatomical and neuromuscular factors:

Anatomical factors (structural narrowing):

• Obesity: fat deposition in pharyngeal tissues and tongue, reduced lung volumes
• Craniofacial structure: retrognathia, micrognathia, macroglossia
• Soft tissue: tonsillar/adenoid hypertrophy, elongated soft palate
• Nasal obstruction: deviated septum, turbinate hypertrophy

Neuromuscular factors:

• Sleep reduces pharyngeal dilator muscle tone (especially genioglossus)
• Negative inspiratory pressure during inhalation collapses the narrowed airway
• Arousal terminates apnea but fragments sleep

Downstream consequences:

• Intermittent hypoxemia → oxidative stress, sympathetic activation, endothelial dysfunction
• Intrathoracic pressure swings → increased cardiac afterload, atrial stretch (promotes AF)
• Sleep fragmentation → daytime sleepiness, cognitive impairment, increased accident risk
• Chronic sympathetic activation → sustained hypertension, insulin resistance, inflammation

Why OSA causes cardiovascular disease:

• Resistant hypertension: nocturnal sympathetic surges prevent normal BP dipping; 80% of resistant HTN patients have OSA
• Atrial fibrillation: atrial stretch, hypoxemia, and autonomic dysfunction promote AF; OSA increases AF recurrence after cardioversion/ablation
• Heart failure: increased afterload, hypoxemia, and neurohormonal activation worsen both HFrEF and HFpEF
• Stroke: hypercoagulability, endothelial dysfunction, and paradoxical embolism (patent foramen ovale)

How to explain to patients#

When you sleep, the muscles in your throat relax. In sleep apnea, your throat closes off repeatedly during the night, blocking your breathing. Your brain wakes you up just enough to start breathing again, but you don’t remember these awakenings.

Think of it like trying to breathe through a straw that keeps getting pinched shut. Each time it closes, your oxygen drops and your body has to work hard to open it back up. This happens dozens or even hundreds of times per night.

This constant struggle puts stress on your heart and blood vessels. That’s why sleep apnea is linked to high blood pressure, heart problems, and stroke. The good news is that treating sleep apnea with a CPAP machine keeps your airway open and protects your heart.

Clinical presentation#

Characteristic symptoms#

Nocturnal symptoms:

• Snoring: loud, often with witnessed apneas or gasping/choking
• Witnessed apneas: bed partner reports breathing stops
• Gasping or choking awakenings
• Nocturia: 2+ times per night (from atrial natriuretic peptide release)
• Restless sleep, frequent position changes
• Night sweats (from respiratory effort)

Daytime symptoms:

• Excessive daytime sleepiness (EDS): falling asleep during passive activities (watching TV, reading) or active activities (driving, conversations)
• Morning headaches: typically frontal, resolve within hours (from nocturnal hypercapnia)
• Cognitive impairment: poor concentration, memory problems
• Mood changes: irritability, depression
• Decreased libido, erectile dysfunction

Quantify sleepiness with Epworth Sleepiness Scale (ESS):

• Score 0-24; ≥10 indicates excessive daytime sleepiness
• Ask about likelihood of dozing in 8 situations (sitting, reading, watching TV, passenger in car, lying down, talking, after lunch, in traffic)

Physical exam findings#

Obesity markers:

• BMI ≥30 (present in 60-70% of OSA patients)
• Neck circumference: >17 inches (43 cm) in men, >16 inches (41 cm) in women
• Waist circumference: >40 inches (men), >35 inches (women)

Upper airway examination:

• Mallampati score III-IV (only soft palate visible, or only hard palate visible)
• Tonsillar hypertrophy (grade 3-4)
• Macroglossia (tongue indentations from teeth)
• Elongated or edematous uvula
• High-arched or narrow hard palate
• Retrognathia or micrognathia

Nasal examination:

• Deviated septum
• Turbinate hypertrophy
• Nasal polyps

Cardiovascular findings:

• Hypertension (especially if resistant or non-dipping pattern)
• Signs of right heart failure in severe cases (JVD, edema)
• Atrial fibrillation (irregular pulse)

Red flags#

Require urgent evaluation or expedited sleep study:

• Commercial driver or safety-sensitive occupation with high clinical suspicion
• Severe daytime sleepiness with near-miss or actual motor vehicle accident
• Unstable cardiovascular disease (recent MI, decompensated HF, uncontrolled arrhythmia)
• Severe nocturnal hypoxemia reported by home pulse oximetry (SpO2 <80%)
• Obesity hypoventilation syndrome suspected (daytime hypercapnia, BMI >40)
• Pregnancy with suspected OSA (increased maternal and fetal risk)

Diagnostic workup#

Initial evaluation#

Screening questionnaires:

STOP-BANG Questionnaire (preferred screening tool):

• S: Snoring loudly?
• T: Tired/sleepy during day?
• O: Observed apneas?
• P: Pressure (high blood pressure)?
• B: BMI >35?
• A: Age >50?
• N: Neck circumference >17" (M) or >16" (F)?
• G: Gender male?
• Score: 0-2 = low risk; 3-4 = intermediate risk; 5-8 = high risk
• Sensitivity 90% for moderate-severe OSA at score ≥3

Epworth Sleepiness Scale (ESS):

• Quantifies daytime sleepiness (0-24)
• ≥10 = excessive daytime sleepiness
• Does NOT diagnose OSA but supports clinical suspicion

Basic labs:

• TSH: hypothyroidism can worsen OSA and cause similar symptoms
• CBC: polycythemia suggests chronic hypoxemia
• BMP: baseline if considering diuretics for comorbid HTN/HF
• HbA1c or fasting glucose: screen for diabetes (high comorbidity)

Overnight pulse oximetry (limited role):

• Can support diagnosis if shows repetitive desaturations
• ODI ≥15 with high pretest probability may support diagnosis
• Cannot rule out OSA (many patients have minimal desaturations)
• Not a substitute for sleep study

Confirmatory testing#

Polysomnography (PSG) — Gold standard:

• In-lab overnight study with EEG, EOG, EMG, airflow, respiratory effort, SpO2, ECG, body position
• Provides AHI, oxygen nadir, sleep architecture, arrhythmia detection
• Required for: suspected central sleep apnea, significant cardiopulmonary disease, prior negative HSAT with high suspicion, CPAP titration
• Turnaround: 2-6 weeks depending on lab availability

Home Sleep Apnea Testing (HSAT):

• Portable device measuring airflow, respiratory effort, SpO2 (minimum)
• Appropriate for: uncomplicated patients with high pretest probability, no significant cardiopulmonary disease
• Advantages: lower cost ($300-500 vs $1500-3000 for PSG), faster access, patient convenience
• Limitations: underestimates AHI (no EEG to measure sleep time), misses central apneas, higher failure rate
• If HSAT negative but clinical suspicion high → proceed to in-lab PSG

Interpreting results:

Additional findings to note:

• Oxygen nadir: <80% indicates severe desaturations
• Time SpO2 <90%: >10% of sleep time is significant
• REM-predominant OSA: worse in REM sleep (common in women, milder obesity)
• Positional OSA: AHI ≥2x higher supine vs non-supine (may respond to positional therapy)

When to refer for specialist workup#

Sleep medicine referral (routine, 2-4 weeks):

• Positive HSAT requiring CPAP titration
• CPAP intolerance or failure after troubleshooting
• Suspected central sleep apnea or complex sleep apnea
• Persistent symptoms despite adequate CPAP use
• Consideration for oral appliance or surgery

Sleep medicine referral (urgent, within 1-2 weeks):

• Commercial driver or safety-sensitive occupation
• Severe symptoms with safety concerns
• Significant cardiovascular comorbidity (recent MI, decompensated HF, uncontrolled AF)
• Suspected obesity hypoventilation syndrome

ENT referral:

• Significant nasal obstruction affecting CPAP tolerance
• Tonsillar hypertrophy (grade 3-4)
• Consideration for surgical intervention (UPPP, hypoglossal nerve stimulator)

What NOT to order#

• Routine imaging (CT, MRI of airway): clinical exam sufficient; imaging rarely changes management
• Arterial blood gas in stable patients: pulse oximetry sufficient; ABG only if OHS suspected
• Multiple sleep latency test (MSLT): for narcolepsy evaluation, not routine OSA
• Drug-induced sleep endoscopy (DISE): specialist procedure for surgical planning only
• Repeat sleep studies routinely: only if significant weight change (>10%), symptom recurrence, or treatment failure

Treatment#

Goals of therapy#

1. Eliminate apneas and hypopneas: target AHI <5 on therapy
2. Resolve symptoms: ESS <10, improved energy and cognitive function
3. Reduce cardiovascular risk: improve BP control, reduce AF burden
4. Improve quality of life: better sleep, daytime function, mood
5. Reduce accident risk: eliminate drowsy driving, improve occupational safety

Targets:

• AHI <5 events/hour on CPAP (residual AHI on machine download)
• CPAP usage ≥4 hours/night on ≥70% of nights (Medicare compliance definition)
• ESS <10 (resolution of excessive sleepiness)
• BP improvement (expect 2-3 mmHg reduction with CPAP)

Non-pharmacologic management#

Weight loss (CRITICAL for overweight/obese patients):

• 10% weight loss reduces AHI by approximately 26% (Sleep Heart Health Study)
• May achieve OSA remission in mild-moderate disease
• Bariatric surgery: consider if BMI ≥40 or BMI ≥35 with comorbidities; 75-80% achieve significant AHI reduction
• Weight loss does NOT replace CPAP in severe OSA but is essential adjunct
• Counsel: “Losing weight can significantly improve your sleep apnea and may reduce how much you need the CPAP machine”

Positional therapy (for positional OSA):

• Indicated if AHI ≥2x higher supine vs non-supine
• Options: tennis ball sewn into back of shirt, positional therapy devices, wedge pillows
• Effectiveness: reduces AHI by 50% in appropriate patients
• Limitations: poor long-term adherence, not effective for severe OSA

Sleep hygiene and behavioral measures:

• Avoid alcohol within 3 hours of bedtime (relaxes pharyngeal muscles, worsens OSA)
• Avoid sedatives/hypnotics when possible (worsen airway collapse)
• Maintain regular sleep schedule
• Elevate head of bed 30-60 degrees (reduces AHI modestly)
• Treat nasal congestion (improves CPAP tolerance)

Avoid exacerbating factors:

• Alcohol: increases apnea frequency and duration
• Sedative-hypnotics: benzodiazepines, opioids worsen OSA
• Smoking: increases upper airway inflammation
• Sleep deprivation: worsens OSA severity

Pharmacologic management#

Note: No medications are FDA-approved for OSA treatment. Pharmacotherapy is adjunctive only.

Medications to AVOID in OSA:

• Benzodiazepines: worsen airway collapse, increase apnea duration
• Opioids: suppress respiratory drive, worsen OSA
• Muscle relaxants: may worsen pharyngeal collapse
• Alcohol: relaxes upper airway muscles

CPAP and device therapy#

Continuous Positive Airway Pressure (CPAP) — First-line treatment:

CPAP initiation:

• Can start empirically with auto-CPAP (pressure range 4-20 cm H2O) OR
• In-lab CPAP titration study to determine fixed pressure
• Most patients start with auto-CPAP; switch to fixed if issues arise

CPAP adherence strategies:

• Proper mask fitting: try multiple mask types (nasal pillows, nasal mask, full face)
• Heated humidification: reduces nasal dryness and congestion
• Ramp feature: starts at low pressure, gradually increases
• Pressure relief (EPR/C-Flex): reduces expiratory pressure for comfort
• Chin strap: for mouth breathing with nasal mask
• Address side effects promptly: mask leak, aerophagia, claustrophobia

Oral appliances (Mandibular Advancement Devices):

• Custom-fitted by dentist trained in sleep medicine
• Advances mandible forward, increasing airway space
• Indicated for: mild-moderate OSA, CPAP intolerance, patient preference
• Efficacy: reduces AHI by 50% on average; less effective than CPAP for severe OSA
• Cost: $1500-3000 for custom device
• Side effects: jaw pain, tooth movement, TMJ discomfort

Surgical options (specialist-initiated):

• Uvulopalatopharyngoplasty (UPPP): removes excess tissue; 40-50% success rate; significant morbidity
• Hypoglossal nerve stimulator (Inspire): for moderate-severe OSA, CPAP failure, BMI <35; 70% response rate
• Maxillomandibular advancement: most effective surgery; reserved for severe cases
• Bariatric surgery: for morbid obesity with OSA

Patient counseling points#

For CPAP therapy:

• “The CPAP machine keeps your airway open by blowing a gentle stream of air. It’s like a splint for your throat.”
• “It takes time to get used to—most people need 2-4 weeks. Don’t give up after a few nights.”
• “Use it every night, all night. Even naps. The more you use it, the better you’ll feel.”
• “If the mask is uncomfortable or leaking, call us. There are many different masks, and we can find one that works for you.”
• “Clean your mask and tubing weekly with mild soap and water. Replace the mask every 3-6 months.”

For weight loss:

• “Losing weight is one of the most effective things you can do for your sleep apnea. Even 10% weight loss can make a big difference.”
• “Weight loss may not cure your sleep apnea, but it can make it milder and make the CPAP work better.”

For cardiovascular risk:

• “Sleep apnea puts extra stress on your heart. Treating it helps protect your heart and blood vessels.”
• “If you have high blood pressure that’s hard to control, treating your sleep apnea may help lower it.”

Monitoring and follow-up#

Initial follow-up (2-4 weeks after CPAP initiation):

• Review CPAP download: usage hours, AHI on therapy, mask leak
• Assess symptom improvement (ESS)
• Address side effects and adherence barriers
• Adjust mask, pressure, or settings as needed

Ongoing monitoring:

When to repeat sleep study:

• Significant weight change (gain or loss >10%)
• Recurrence of symptoms despite good CPAP adherence
• Persistent elevated residual AHI on CPAP
• Before discontinuing CPAP after major weight loss

Patient education#

What is this condition?#

Sleep apnea means your breathing stops and starts many times while you sleep. The most common type is called obstructive sleep apnea. It happens when the muscles in your throat relax too much and block your airway.

When your airway gets blocked, you stop breathing for a few seconds. Your brain wakes you up just enough to start breathing again. This can happen dozens or even hundreds of times each night. You usually don’t remember waking up, but it keeps you from getting good sleep.

Sleep apnea is very common. It affects about 1 in 4 adults. It is more common if you are overweight, have a large neck, or are male. It runs in families.

What you can do#

Use your CPAP machine every night, all night long. It may feel strange at first, but most people get used to it within a few weeks. The more you use it, the better you will feel.

Lose weight if you are overweight. Even losing 10 pounds can help. Weight loss is one of the best things you can do for your sleep apnea.

Avoid alcohol for at least 3 hours before bed. Alcohol relaxes your throat muscles and makes sleep apnea worse.

Sleep on your side instead of your back. Sleeping on your back makes it easier for your airway to collapse.

Keep your CPAP equipment clean. Wash your mask with mild soap and water every week. Replace your mask and tubing when they get worn out.

When to seek care#

Call your doctor if you are still very sleepy during the day even though you are using your CPAP machine. Call if your CPAP machine is not working right or if your mask does not fit well.

Call if you are having trouble using your CPAP machine. There are many different masks and settings. We can help find what works for you.

Go to the emergency room if you have chest pain, severe shortness of breath, or if you pass out.

Tell your doctor before any surgery. Sleep apnea can affect anesthesia and recovery.

Questions to ask your doctor#

How severe is my sleep apnea? What is my AHI number? Am I using my CPAP machine enough? Is my sleep apnea under control? Should I lose weight? Do I need to see a sleep specialist? Can I ever stop using the CPAP machine?

Prognosis and monitoring#

Expected course#

With treatment (CPAP adherence ≥4 hours/night):

• Symptoms improve within days to weeks (sleepiness, energy, mood)
• Snoring eliminated
• Cardiovascular risk reduced (BP improves 2-3 mmHg on average)
• AF recurrence reduced after cardioversion/ablation
• Quality of life significantly improved
• Motor vehicle accident risk returns to baseline

Without treatment:

• Progressive worsening with weight gain
• Increased cardiovascular morbidity: 2-3x risk of HTN, 4x risk of AF, increased stroke risk
• Increased motor vehicle accidents (2-7x risk)
• Cognitive decline, depression
• Increased mortality in severe untreated OSA (HR 1.5-3.0)

With weight loss:

• 10% weight loss → ~26% reduction in AHI
• Bariatric surgery: 75-80% achieve significant improvement; some achieve remission
• Weight regain leads to OSA recurrence

Monitoring parameters#

Complications to watch for#

Cardiovascular complications:

• Resistant hypertension: screen all patients with resistant HTN for OSA
• Atrial fibrillation: OSA increases AF recurrence; ensure CPAP adherence before/after cardioversion
• Heart failure: OSA worsens HF; HF worsens OSA (fluid redistribution); treat both aggressively
• Stroke: increased risk with untreated OSA; CPAP may reduce risk

Metabolic complications:

• Type 2 diabetes: OSA worsens insulin resistance; treatment may improve glycemic control
• Metabolic syndrome: OSA is independent risk factor

Neurocognitive complications:

• Cognitive impairment: memory, attention, executive function affected
• Depression: screen and treat; improves with OSA treatment
• Drowsy driving: assess at every visit; report to DMV if required by state law

Treatment-related complications:

• CPAP intolerance: 30-50% of patients struggle with adherence; address proactively
• Aerophagia (air swallowing): reduce pressure, try BiPAP
• Mask-related skin breakdown: adjust fit, try different mask type
• Dry mouth/nose: add heated humidification, consider chin strap

Special populations#

Elderly/geriatric#

Prevalence and presentation:

• OSA prevalence increases with age (up to 50% in adults >65)
• Symptoms may be atypical: nocturia, cognitive impairment, falls may be presenting features
• Sleepiness may be attributed to “normal aging”—maintain high suspicion

Treatment considerations:

• CPAP remains first-line; efficacy similar to younger adults
• May need lower pressures (reduced airway collapsibility)
• Cognitive impairment may affect CPAP adherence—involve caregivers
• Dexterity issues: consider masks that are easier to apply
• Polypharmacy: review medications that worsen OSA (sedatives, opioids, muscle relaxants)

Beers criteria considerations:

• Avoid benzodiazepines and non-benzodiazepine hypnotics (worsen OSA, increase fall risk)
• Avoid sedating antihistamines (diphenhydramine)
• Use caution with opioids (respiratory depression)

Goals may differ:

• Focus on symptom improvement and quality of life
• Cardiovascular risk reduction still important
• Adherence thresholds may be more flexible if cognitive impairment limits use

Chronic kidney disease#

Prevalence:

• OSA highly prevalent in CKD (50-70%) and ESRD (up to 80%)
• Fluid overload contributes to upper airway edema and OSA severity
• OSA may accelerate CKD progression

Treatment considerations:

• CPAP effective and safe in CKD
• Fluid management (diuretics, dialysis timing) may reduce OSA severity
• Nocturnal hemodialysis may improve OSA more than conventional HD
• No dose adjustments needed for CPAP

Medication adjustments:

Other populations#

Heart failure:

• OSA present in 50-75% of HF patients
• Central sleep apnea (CSA) also common in HF—different treatment
• CPAP improves symptoms and may improve EF in HFrEF
• Treat fluid overload aggressively—reduces OSA severity
• Adaptive servo-ventilation (ASV) contraindicated in HFrEF with EF <45% (increased mortality in SERVE-HF trial)

Atrial fibrillation:

• Screen all AF patients for OSA (40-50% prevalence)
• Untreated OSA increases AF recurrence after cardioversion and ablation
• CPAP adherence improves AF outcomes
• Ensure OSA treated before elective cardioversion/ablation

Pregnancy:

• OSA increases risk of gestational HTN, preeclampsia, gestational diabetes
• CPAP safe in pregnancy
• May need pressure adjustments as pregnancy progresses
• Refer to high-risk OB and sleep medicine

Commercial drivers:

• Federal Motor Carrier Safety Administration (FMCSA) guidelines apply
• Must demonstrate CPAP adherence (≥4 hours/night) for medical certification
• Annual recertification required
• Untreated moderate-severe OSA disqualifies from commercial driving

Polypharmacy considerations:

• Review all sedating medications: benzodiazepines, opioids, muscle relaxants, antihistamines
• Drug interactions with wake-promoting agents: modafinil induces CYP3A4 (reduces efficacy of hormonal contraceptives, some statins)
• Multiple antihypertensives may indicate resistant HTN—screen for OSA

When to refer#

Specialist referral criteria#

Sleep medicine referral (routine, 2-4 weeks):

• Positive screening (STOP-BANG ≥3) for sleep study
• HSAT interpretation and CPAP initiation
• CPAP intolerance after initial troubleshooting
• Consideration for oral appliance therapy
• Persistent symptoms despite adequate CPAP use
• Complex sleep apnea (central apneas emerging on CPAP)

Sleep medicine referral (urgent, within 1-2 weeks):

• Commercial driver or safety-sensitive occupation with high suspicion
• Severe daytime sleepiness with safety concerns (near-miss accidents)
• Significant cardiovascular comorbidity (recent MI, decompensated HF, uncontrolled AF)
• Suspected obesity hypoventilation syndrome (daytime hypercapnia)
• Pregnancy with suspected OSA

ENT referral:

• Significant nasal obstruction affecting CPAP tolerance
• Tonsillar hypertrophy (grade 3-4) in adults
• Consideration for surgical intervention
• Evaluation for hypoglossal nerve stimulator candidacy

Cardiology referral:

• Resistant hypertension (on ≥3 agents including diuretic)
• New or poorly controlled atrial fibrillation
• Heart failure with suspected sleep-disordered breathing
• Pulmonary hypertension

Bariatric surgery referral:

• BMI ≥40, or BMI ≥35 with OSA and other comorbidities
• Failed medical weight loss attempts
• Motivated patient who understands lifelong commitment

Urgency levels#

Smartphrase snippets#

OSA, stable on CPAP: OSA on CPAP [X] cm H2O with good adherence ([X] hours/night), residual AHI [X], ESS [X]. Weight stable, no mask issues, continue current therapy with f/u 6-12 months.

OSA, CPAP non-adherent: OSA with suboptimal CPAP adherence ([X] hours/night); barriers include [mask discomfort/claustrophobia/aerophagia]. Adjusted [mask type/pressure/humidification], reinforced importance of nightly use, recheck in 4 weeks.

OSA, new diagnosis: New diagnosis OSA (AHI [X], [severity]) based on [HSAT/PSG]; initiated auto-CPAP with [mask type]. Counseled on weight loss (BMI [X]), avoiding alcohol before bed; f/u 2-4 weeks for adherence check.

OSA screening, high risk: High risk for OSA (STOP-BANG [X]/8, ESS [X]) with [snoring/witnessed apneas/EDS]. Ordering [HSAT/PSG referral], counseled on positional therapy and alcohol avoidance.

Related pages#

• Dyspnea - Chronic (complaint) — OSA can present with exertional dyspnea; consider in differential
• COPD (problem) — overlap syndrome (COPD + OSA) requires treatment of both conditions
• Asthma (problem) — OSA worsens asthma control; treat both
• Hypertension (problem) — OSA is leading cause of resistant hypertension; screen all resistant HTN patients
• Atrial Fibrillation (problem) — OSA present in 40-50% of AF patients; treatment improves AF outcomes
• Heart Failure (problem) — high OSA prevalence in HF; CPAP may improve symptoms and EF