![]() ![]() For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V'A/Q') heterogeneity has been the most important pathophysiological mechanism. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. Uworld says this is v/q mismatch but that gets me confused cause why wouldn't a vent defect give v/q mismatch.An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. ![]() That's why you will see a drop in PaO2 in PE(minor). So this one is tougher but: Let's assume you have a well ventilated alveoli, when there is poor oxygen content, vasculature will constrict and redistribute this blood to other alveolar however it will overwhelm the capacity of extracting oxygen into blood - so adding oxygen will help. Dead space/physiologic dead space/V/Q mismatch to inifinty. ![]() I remember total pulm shunt as if pulm art partial pressure = pulm vein partial pressure, shunted, basically just bypassed lungs. These alveolar are already extracting maximum oxygen, adding more would not help. Lets assume this kid have some alveoli that are working.
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