- OHS characterised by
- Obesity
- Daytime hypercapnia (>45mmHg PaCO2)
- Difference between OHS and obstructive sleep anpea is that OHS has
- Longer and more continuous episodes of hypoventilation overnight (± upper airway obstruction)
- Daytime hypercapnia
Pathophysiology
- ↑work of breathing as fat restricts movement of chest muscles
- Makes chest wall less compliant – so diaphragm moves less effectively
- Therefore, patients need to expend more energy to breathe efficiently
- Leads to sleep disordered breathing
- Inadequate removal of CO2 → hypercapnia → acidosis
- Under normal circumstances, brainstem chemoreceptors detect acidity and respond by increasing respiration rate
- In OHS this ventilator response is blunted due to ↑leptin levels in obese people
- ↓O2 levels → pulmonary vasoconstriction → pulmonary hypertension → RV strain → RV hypertrophy and remodelling → peripheral edema (pitting edema)
- Chronic hypoxemia → ↑erythropoietin → polycythemia
Clinical features
- Features of sleep apnea
- Chronic mouth breathing
- Daytime sleepiness
- Morning headaches
- Typical patient is obese, with fat deposition around chin and abdomen
- Diagnostic criteria
- BMI >30
- Daytime PaCO2 >45mmHg
- Associated sleep-related breathing disorder e.g. OSA
- Absence of other causes of hypoventilation
Diagnosis
- ABG
- Nocturnal oximetry
- CXR – to see signs of heart failure
- Echo – RVH
- FBC – for polycythemia
Treatment
- Advise pt to lose weight
- CPAP/assisted ventilation
- Treat concomitant OSA/asthma/COPD