sleep-disordered breathing

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definitions

obstructive sleep apnoea (OSA)

• Recurrent partial or complete upper airway collapse during sleep despite ongoing respiratory effort
• Apnoea: absent airflow ≥ 10 s; hypopnoea: reduced airflow ≥ 10 s with ≥ 3% desaturation or arousal
• Diagnosis: AHI ≥ 5/hr with symptoms (daytime sleepiness, witnessed apnoeas, nocturnal gasping) or AHI ≥ 15 regardless of symptoms
• Severity: mild (AHI 5–14), moderate (AHI 15–29), severe (AHI ≥ 30)
• Present in > 40% of patients with BMI > 30 and ~60% with metabolic syndrome

obesity hypoventilation syndrome (OHS)

• Triad: BMI ≥ 30 + daytime PaCO₂ ≥ 45 mmHg (sea level) + SDB, after excluding other hypoventilation causes (neuromuscular, mechanical, metabolic)
• ~90% have coexistent OSA; ~70% have severe OSA (AHI ≥ 30)
• More severe hypersomnolence, morning headaches, and signs of right heart failure / pulmonary hypertension compared to OSA alone

central sleep apnoea (CSA)

• Recurrent cessation or reduction of airflow due to absent or diminished respiratory effort
• ≥ 5 central apnoeas or hypopnoeas/hr with central events > 50% of total
• Pathophysiology: PaCO₂ oscillates around apnoeic threshold → ventilatory control instability
• Most common context: heart failure (Cheyne-Stokes respiration — crescendo-decrescendo tidal volumes with central apnoeas)
• Other causes: stroke, opioid use, high altitude, treatment-emergent CSA (appears during CPAP titration for OSA)

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cardiovascular consequences of OSA

Intermittent hypoxaemia → sympathetic activation, oxidative stress, systemic inflammation, endothelial dysfunction

Complication	Association
Hypertension	OSA is the most common secondary cause; dose-response with AHI
Atrial fibrillation	2–4× increased risk; untreated OSA increases AF recurrence post-cardioversion/ablation
Heart failure	Both cause and consequence; CSA common in HFrEF
Stroke	Independent risk factor; also worsens post-stroke outcomes
Coronary artery disease	Associated but CPAP has not demonstrated mortality benefit in RCTs
Pulmonary hypertension	Mild PH in 20–30% of OSA; rarely the sole cause

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screening and diagnosis

screening

STOP-Bang questionnaire — most validated screening tool:

• Snoring, Tiredness, Observed apnoea, blood Pressure, BMI > 35, Age > 50, Neck > 40 cm, Gender (male)
• Score ≥ 3: high risk (sensitivity ≥ 93% for moderate–severe OSA)
• Negative predictive value: 77% to exclude moderate OSA, 91% to exclude severe OSA

diagnostic pathway

Clinical scenario	Test	Rationale
High pretest probability, uncomplicated	HSAT (type III)	Acceptable first-line; cheaper, faster
Negative/inconclusive HSAT with persistent suspicion	In-lab PSG	AASM strongly recommends escalation
Suspected OHS, CSA, complex SDB	In-lab PSG	HSAT cannot detect hypoventilation or distinguish central from obstructive events
Significant cardiopulmonary comorbidity, neuromuscular disease, chronic opioid use	In-lab PSG	HSAT unreliable in these populations

OHS screening shortcut

• Serum bicarbonate < 27 mmol/L has high negative predictive value to exclude OHS in obese patients with OSA
• If HCO₃⁻ ≥ 27 mmol/L → obtain ABG to assess for daytime hypercapnia

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management

OSA

CPAP — first-line for:

• AHI ≥ 15 (all patients)
• AHI 5–14 with symptoms or comorbidities (hypertension, ischaemic heart disease, stroke, atrial fibrillation)

Key evidence:

• Improves blood pressure, subjective sleepiness, quality of life
• No RCT has demonstrated mortality benefit — SAVE (2016) (n=2687) found no reduction in CV events with CPAP vs usual care in patients with moderate–severe OSA and established CVD, though adherence averaged only 3.3 hr/night
• 10% weight loss reduces AHI by ~26%
• Tirzepatide — SURMOUNT-OSA (2024): reduced AHI by ~30 events/hr (≈63% reduction) vs placebo in patients with moderate–severe OSA and obesity; also improved weight, hypoxaemic burden, and sleepiness — may reshape the treatment landscape for OSA with obesity

Alternatives:

• Mandibular advancement device — mild–moderate OSA or CPAP intolerance; similar sleepiness improvement despite less AHI reduction
• Hypoglossal nerve stimulation — moderate–severe OSA (AHI 20–65), BMI < 35, failed CPAP, < 25% central apnoeas
• Pharmacotherapy (solriamfetol, modafinil) — persistent excessive daytime sleepiness despite optimal PAP only; not monotherapy

OHS

Phenotype	First-line	Escalation
OHS + severe OSA (AHI ≥ 30)	CPAP	NIV (BiPAP-ST) if persistent hypoventilation after 6–8 weeks adequate CPAP
OHS without severe OSA	NIV with backup rate (BiPAP-ST)	—
Acute-on-chronic respiratory failure	NIV (BiPAP-ST)	—

• Weight loss targeting 25–30% of body weight (bariatric surgery most likely to achieve this)
• Pickwick (2019): CPAP and NIV equivalent outcomes in OHS with severe OSA

CSA

1. Optimise underlying condition — GDMT for heart failure, opioid reduction, stroke rehabilitation
2. CPAP — may be trialled first-line for CSA associated with heart failure
3. Adaptive servo-ventilation (ASV) — most effective for central event control

ASV indications (after CPAP failure):

• Treatment-emergent CSA
• Opioid-induced CSA
• Post-stroke CSA
• Idiopathic CSA
• May be considered in HFpEF or LVEF 30–45% in expert centres

Other CSA therapies: low-flow supplemental O₂, acetazolamide, transvenous phrenic nerve stimulation (refractory cases)

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adherence

• Early adherence predicts long-term use — close follow-up in initial weeks is critical
• Review objective device data (patients overestimate usage)
• Behavioural interventions (CBT, motivational interviewing): +1.31 hr/night CPAP use (Cochrane; 95% CI 0.95–1.66), NNT 8 for ≥ 4 hr/night adherence
• Supportive interventions (telemonitoring, scheduled follow-up): +0.70 hr/night
• Heated humidification, nasal mask preference, and treating nasal symptoms improve comfort

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follow-up

Timing	Indication
4–8 weeks	All new PAP starts; OHS after discharge
2–3 months	OHS outpatient titration; reassess treatment-emergent CSA
6–8 weeks	Switch CPAP → NIV in OHS if persistent hypoventilation
Annually	Stable, adherent patients

Repeat sleep study indicated for: recurrent/persistent symptoms despite good adherence, clinically significant weight change, new/worsening cardiovascular disease, unexplained device data, post-surgical intervention

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referral criteria

when to refer to respirology / sleep medicine

Condition	Refer when	Red flags for urgent referral
OSA	STOP-Bang ≥ 3 with symptoms; positive HSAT needing treatment; diagnostic uncertainty	Severe sleepiness with accident risk (drowsy driving); hypoventilation signs; cardiorespiratory disease; CPAP failure/intolerance; suspected CSA/complex SDB
OHS	All suspected cases; obesity + unexplained HCO₃⁻ ≥ 27 or PaCO₂ > 45 mmHg	Right heart failure; polycythaemia; pulmonary hypertension
CSA	All suspected or confirmed cases	Heart failure with Cheyne-Stokes; neurological disease; opioid-related CSA; treatment-emergent central apnoeas; LVEF assessment needed before ASV

Additional populations warranting referral: neuromuscular disease, chronic opioid use, pregnancy with high-risk features (BMI > 30, hypertension, diabetes)

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Ontario VEP access

The Ontario Ventilator Equipment Pool (VEP) provides publicly funded CPAP and NIV devices.

CPAP eligibility

• Sleep study (PSG or HSAT) documenting AHI ≥ 15, or AHI ≥ 5 with significant symptoms/comorbidities
• Required documentation: sleep study report, CPAP prescription with pressure settings, signed VEP application form

NIV (BiPAP-ST) eligibility

More stringent criteria — reserved for OHS, CSA, neuromuscular/thoracic restrictive disorders:

• ABG confirming daytime PaCO₂ > 45 mmHg
• Evidence of nocturnal hypoventilation (sustained SpO₂ < 88% for > 5 min or elevated TcCO₂)
• Evidence of failed CPAP therapy
• Formal NIV prescription (device type, mode, settings)
• Patient and caregiver education/competency documentation

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key trials and evidence

Trial / Source	Year	Key finding
SERVE-HF	2015	ASV increased CV mortality in HFrEF (LVEF ≤ 45%) with predominant CSA
ADVENT-HF	2024	Newer ASV algorithm — no mortality increase, but underpowered (stopped early)
Pickwick	2019	CPAP ≈ NIV for OHS with severe OSA; both superior to lifestyle alone
Askland, Cochrane	2020	Behavioural interventions increase CPAP use +1.31 hr/night; NNT 8 for ≥ 4 hr
Figard, EClinicalMedicine	2025	Umbrella review: CPAP improves BP and sleepiness; no mortality benefit in RCTs
Mokhlesi, ATS CPG	2019	OHS management guideline: CPAP first for OHS + severe OSA; weight loss 25–30%
SAVE	2016	CPAP did not reduce CV events in OSA + established CVD (n=2687; mean adherence 3.3 hr/night)
SURMOUNT-OSA	2024	Tirzepatide reduced AHI ~63% vs placebo in moderate–severe OSA with obesity
Badr, AASM	2025	CSA treatment guideline: optimise HF first; CPAP trial; ASV with LVEF caveat

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what NOT to do

• Do not start ASV without confirming LVEF — contraindicated if ≤ 45% with predominant CSA
• Do not use HSAT when OHS, CSA, or neuromuscular disease is suspected — PSG required
• Do not accept a negative HSAT as definitive when clinical suspicion remains high — escalate to PSG
• Do not use solriamfetol or modafinil as monotherapy for OSA
• Do not delay OHS evaluation in obese patients with unexplained hypercapnia or HCO₃⁻ ≥ 27 mmol/L
• Do not forget to reassess treatment-emergent CSA after ≥ 3 months of PAP (may resolve spontaneously)