Obesity hypoventilation syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Despite many studies, it is still unclear why some obese people develop hypoventilation and others do not. Impairment of lung expansion by adipose tissue means that one need to breathe faster and deeper to still absorb sufficient amounts of oxygen and remove adequate amounts of carbon dioxide. It appears that the respiratory center (an area in the brain stem that regulates breathing) becomes relatively insensitive to normal stimuli, leading to a decreased response to low oxygen levels. While this may be the result of obstructive sleep apnea, it does not explain why some people with OHS have no features of obstruction. Recent studies postulate that there is a vicious cycle in which low oxygen levels make the respiratory center progressively more insensitive to hypoxia, impairing normal compensatory mechanisms normally in place to prevent hypercapnia. It appears that insensitivity to the hormone leptin, which is elevated in obesity, plays a role in this process, but there is no conclusive evidence that this is the case.
Low oxygen levels lead to hypoxic pulmonary vasoconstriction, the tightening of small blood vessels in the lung to create an optimal distribution of blood through the lung. Persistently low oxygen levels causing chronic vasoconstriction leads to increased pressure on the pulmonary artery (pulmonary hypertension), which in turn puts strain on the right ventricle, the part of the heart that pumps blood to the lungs. The right ventricle undergoes remodeling, becomes distended and is less able to remove blood from the veins. When this is the case, raised hydrostatic pressure leads to accumulation of fluid in the skin (edema), and in more severe cases the liver and the abdominal cavity. The dysfunction of the right ventricle improves with treatment.[1]
References
- ↑ Nahmias J, Lao R, Karetzky M (1996). "Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure" (PDF). Eur. Respir. J. 9 (5): 945–51. PMID 8793456.