Sure, the over-inflation can weaken the elastic recoil of the alveoli, resulting in air trapping, hypoxia, and vasoconstriction. Relevant info, but I don't understand why dead space increases. Something else the article notes is that over-enthusiastic PEEP (tx for ARDS) can further increase dead space. My perspective is that the hyaline membranes (and later in the disease, interstitial fibrosis) impair gas exchange, resulting in hypoxic vasoconstriction.
Which I assume results in upstream vasoconstriction (due to endothelin or something)? Look at the bullet points under Clinical Significance: Įven the article seems a little unsure, but it says that it's due to "disturbances in the pulmonary microvasculature".
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