What causes obesity-hypoventilation syndrome?

Updated: Jul 22, 2021
  • Author: Jazeela Fayyaz, DO; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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Patients with OHS have a higher incidence of restrictive ventilatory defects when compared with patients who are obese but do not hypoventilate. Studies have shown that patients with OHS have total lung capacities that are 20% lower and maximal voluntary ventilation that is 40% lower than patients who are obese who do not have hypoventilation. [6]

Patients with OHS demonstrate an excessive work of breathing and an increase in carbon dioxide production. Inspiratory muscle strength and resting tidal volumes also are reported to be decreased in patients with obesity hypoventilation. Pulmonary compliance is lower in patients with OHS when compared with patients who are obese who do not have hypoventilation.

Obesity increases the work of breathing because of reductions in chest wall compliance and respiratory muscle strength. An excessive demand on the respiratory muscles leads to the perception of increased breathing effort and could unmask other associated respiratory and heart diseases.

Leptin deficiency or leptin resistance may also contribute to OHS, by reducing ventilatory responsiveness and leading to carbon dioxide retention. [7]

Despite the above-mentioned physiologic abnormalities, the most important factor in the development of hypoventilation in OHS is likely a defect in the central respiratory control system. These patients have been shown to have a decreased responsiveness to carbon dioxide rebreathing, hypoxia, or both.

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