Hypoxia is most important feature of acute pulmonary embolism.
It occurs due to variety of mechanisms
- Ventilation perfusion mismatch is the major mechanism ( Normal ventilation /Reduced perfusion)
- Atelectasis of lung ( Left to right shunt)
- Loss of lung volume due to pulmonary infarct contribute later
- Low mixed venous Oxygen saturation (Tissue hypoxia -more extraction )
- One more important cause is right to left shunting across PFO due to sudden elevation of right atrial mean pressure reflected from RVEDP .
Can acute pulmonary embolism be diagnosed with out Hypoxia ?
Surprisingly many standard text books mention hypoxia is a soft sign . In fact , Braunwald’s text book of cardiology do mention about it .
Significant acute pulmonary embolism can not occur without affecting o2 saturation .
However , it is possible sub acute pulmonary embolism could occur with normal oxygen saturation.
Final message
Hypoxia is indeed a hard sign for most events of major pulmonary embolism . It can even be termed as an essential criteria .A hypoxic , tachypenic patient in sinus tachycardia with echo evidence of new onset RA or RV dilatation is almost 100 % specific for acute pulmonary embolism . ( This becomes 200 % if he or she has DVT as well !)
Dr.S.Venkatesan MD 
So you list the paths by which hypoxia is PLAUSIBLE in pulmonary edema, but fail to cite any evidence supporting the claim that “significant acute pulmonary embolism cannot occur without affecting o2 saturation.” To the contrary, my understanding is that PEs kill primarily through RV strain and “SPO2 < 98%" is a convenient red flag but by no means a marker we should be hanging our hat on. I think it's a terrifying scenario when medics or ER docs are crossing "acute PE" off their differential if the patient is satting fine…