Synopsis
Detect obesity-related awake ventilatory failure, separate it from uncomplicated sleep apnoea and other causes, and select CPAP, NIV, oxygen and weight care safely.
- OHS is obesity with awake alveolar hypoventilation after excluding another primary cause; it is not synonymous with obesity plus snoring.
- Most people with OHS also have OSAHS, but some have predominantly non-obstructive sleep hypoventilation and need a different positive-pressure strategy.
- Clues include morning headache, hypersomnolence, dyspnoea, oedema, hypoxaemia, raised serum bicarbonate and unexplained secondary polycythaemia or pulmonary hypertension.
- Measure awake PaCO2 with arterial or arterialised capillary gas when OHS is suspected; venous bicarbonate is a useful screen in lower-probability settings but does not establish the diagnosis.
- Exclude COPD, neuromuscular weakness, severe chest-wall restriction, hypothyroidism, sedative or opioid effects and other causes of chronic hypoventilation.
- Use respiratory polygraphy with overnight carbon dioxide assessment to determine whether severe OSAHS or sustained hypoventilation predominates.
- NICE recommends CPAP first line for OHS with severe OSAHS when acute ventilatory failure is absent.
- Use NIV when OSAHS is not severe, CPAP is ineffective or poorly tolerated despite optimisation, or ventilatory failure requires direct pressure support.
- Add supplemental oxygen only if hypoxaemia persists despite optimised CPAP or NIV, with monitoring for carbon dioxide deterioration.
- Positive-pressure therapy stabilises physiology but does not replace respectful, evidence-based weight management and cardiovascular risk care.
Key red flags
Infection, fluid overload, sedatives or uncontrolled oxygen can precipitate drowsiness, worsening hypercapnia and acidaemia; absence of dramatic wheeze does not make this less urgent.
Peripheral oedema, loud pulmonary component, raised JVP, polycythaemia or exertional syncope may reflect pulmonary hypertension and right-heart strain requiring prompt specialist evaluation.
Investigation priorities
Confirm daytime hypercapnia and quantify acute or chronic compensation.
Management branches
Obesity coexists with low saturation, raised bicarbonate, sleepiness or morning headache.
- Assess symptoms, respiratory rate, oedema, OSAHS features, medicines, alcohol and prior gases, treating acute decompensation before elective work-up.
- Measure awake arterial or arterialised capillary gas and document oxygen exposure; use bicarbonate only as a screening bridge, not the final diagnosis.
- Exclude COPD, neuromuscular or chest-wall disease, hypothyroidism and medicine-related respiratory depression with targeted testing.
- Arrange respiratory polygraphy and overnight carbon dioxide monitoring to define obstructive versus sustained hypoventilation physiology.
OHS is confirmed outside acute ventilatory failure.
- If severe OSAHS predominates, offer CPAP first line and provide early mask, humidification, adherence and pressure troubleshooting.
- Offer NIV when severe OSAHS is absent, CPAP is not tolerated despite support, or hypercapnia and symptoms fail to improve adequately.
- Add oxygen only for persistent hypoxaemia after positive-pressure treatment is optimised, checking carbon dioxide response and device connection.
- Refer to NICE-aligned weight-management care and treat cardiovascular, metabolic and mobility needs without making weight loss a condition of ventilation.
Key medicines
CPAP for OHS with severe OSAHSUse the sleep-service-titrated fixed or auto-adjusting pressure throughout sleep as first-line stable treatment when severe obstructive events predominate.Do not use CPAP as sole treatment of acute respiratory acidosis. Check adherence, leak and residual carbon dioxide; persistent hypercapnia despite competent optimisation requires specialist consideration of NIV.
Bilevel non-invasive ventilationUse the specialist-selected interface, inspiratory and expiratory pressures and backup rate nightly, with daytime support added only when clinically prescribed.Monitor aspiration and secretion risk, mask pressure, leak and synchrony. Acute initiation needs trained monitoring and an escalation plan; home settings should not be changed without the responsible ventilation service.