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Discussion Starter · #1 ·
Was wondering if yall could help me with what I feel is a lack of grasp of something fundamental

I'm trying to reconcile the following (all from FA, except obstruction causing tachypnea but google confirms that kind of)
1 airway obstruction -> hypoxemia [w/ tachypnea to compensate, at least I'm assuming] -> respiratory acidosis
2 neonatal RDS -> hypoxemia [w/ tachypnea to compensate] -> metabolic acidosis
3 pulmonary embolism -> hypoxemia [w/ tachypnea to compensate] -> respiratory alkalosis

For 1, I'm confused why compensatory tachypnea doesn't lead to alkalosis. Is it because you'd increase ventilation to poorly perfused areas? But wouldn't hypoxic vasoconstriction ensure the poorly perfused areas were shut off? Or would the resulting increased PVR be too much for the tachypnea to compensate for, thus having a net result of hypoventilation still? Wiki says "Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation" - which to be honest confuses me more (I haven't learned of a mechanism for "decreased responsiveness" or I forgot it, and I thought obstruction = shunt, not dead space)

For 2, I'm not sure why tachypnea would lead to metabolic acidosis and not alkalosis. Is it because the compensatory tachypnea isn't enough to overcome the physiological barriers? And why don't they call it respiratory acidosis? I know lactic acid is also involved, but I feel like I've been taught/been assuming that respiratory issue-caused acid-base disturbance was labeled respiratory acidosis

For 3, it makes sense that tachypnea would compensate and cause respiratory alkalosis. It's just the other 2 above don't make sense to me if this makes sense - so I feel like I'm missing huge chunks of the bigger picture

Any help would be majorly appreciated
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