Obesity Hypoventilation Syndrome

Obesity hypoventilation syndrome (OHS) is defined by obesity (BMI 30 kg/m2 or more), daytime hypercapnia (PaCO2 over 45 mmHg) and sleep disordered breathing, in the absence of other causes of hypoventilation.

Prevalence 10 to 20% of obese patients with sleep apnoea and about 0.4% of the general population; rising with the obesity epidemic.

About 90% have obstructive sleep apnoea; 10% have sleep hypoventilation only.

Pathophysiology: obesity related restrictive load, blunted ventilatory response to CO2, leptin resistance, upper airway collapse, bicarbonate retention.

Complications: pulmonary hypertension, right heart failure, polycythaemia, acute on chronic respiratory failure, arrhythmia, diabetes, increased mortality (23% at 18 months untreated vs 9% with treatment).

• Excessive daytime sleepiness, morning headaches, loud snoring, witnessed apnoea, fatigue, dyspnoea, cognitive impairment, nocturia.
• Plethora, cyanosis, peripheral oedema, signs of cor pulmonale (raised JVP, loud P2).
• Often discovered during acute hypercapnic respiratory failure.

• Arterial blood gas: PaCO2 over 45 mmHg awake, elevated serum bicarbonate (over 27 mmol/L) as a screen.
• Polysomnography with CO2 monitoring (transcutaneous or end tidal): obstructive apnoea and sustained hypoventilation (PaCO2 rise 10 mmHg or more, or over 50 mmHg for 10 minutes).
• Exclude other causes of hypercapnia: COPD, neuromuscular disease, chest wall disease, hypothyroidism, medications; spirometry (FEV1/FVC normal, restrictive), chest radiograph, TSH.
• Haemoglobin, echocardiography for pulmonary hypertension.

• Positive airway pressure therapy is first line:
  • CPAP (initial pressure 10 to 15 cmH2O) if OSA predominant and normalises ventilation.
  • Bilevel positive pressure (NIV, IPAP 18 to 25, EPAP 8 to 12, backup rate) when hypoventilation persists, in acute hypercapnic failure, or CPAP fails after 3 months. Volume assured pressure support (AVAPS) improves ventilation.
• Supplemental oxygen only after adequate ventilation established (add to PAP bleed-in if persistent hypoxaemia).
• Weight loss: structured lifestyle programmes, GLP 1 receptor agonists (semaglutide 2.4 mg weekly, tirzepatide), bariatric surgery (sleeve gastrectomy or gastric bypass) giving sustained improvement; weight loss of 10 to 15% or more improves hypoventilation.
• Avoid sedatives, opioids and alcohol.
• Acute hypercapnic respiratory failure: NIV first line, titrate oxygen to SpO2 88 to 92%.
• Respiratory stimulants (acetazolamide 250 to 500 mg, medroxyprogesterone) have limited evidence.
• Tracheostomy rarely for refractory cases.
• Treat comorbidities: diabetes, hypertension, heart failure, pulmonary hypertension.
• Follow up in sleep clinic at 1 to 3 months with download data (adherence 4 hours or more nightly), repeat blood gas, bicarbonate.
• Perioperative planning: preoperative PAP, regional anaesthesia, postoperative monitoring.