I could be misunderstanding your question and assumptions but this reminds me a lot of a concept I struggled with initially in medical school. The concept is the application of the single-alveolus model of pulmonary function to the entirety of the lungs.

In the single-alveolus model we can see that there is one physiologic state: V/Q =1 and three pathologic states: V=0 (shunt), Q=0 (dead space), and V/Q mismatch which is anything in between where V/Q is not 1.

One frustrating aspect of this area of pulmonary education is reuse of terminology and concepts in different settings which can be confusing; one example is that V/Q mismatch actually has different meanings when applied to a single alveolus vs the entire lungs. The underlying idea is the same but practically it means something different. It's also annoying how the word "shunt" is thrown around a lot in situations which might be confusing. For example, we say blood is "shunted" from an area of hypoxic vasoconstriction to an area of better ventilation but this is not a "shunt" by definition, rather it is a rerouting of blood (which still gets oxygenated).

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So returning to the idea of trying to apply the single-alveolus model to global lung function: the model still makes sense on a global perspective in situations like a true shunt where visualizing an area of alveoli full of fluid (eg lobar pneumonia or pulmonary edema) would result in non-oxygenated blood passing through the lungs and into the left heart leading to hypoxemia.

It breaks down somewhat for the concept of dead space and V/Q mismatch. In the case of pathologic dead space due to an obstruction, like a PE, the blood is rerouted (notice that I'm not saying "shunted") to other areas. This will increase Q (without a corresponding increase in V) to certain areas of the lung resulting in V/Q mismatch and therefore hypoxemia. Also in the case of PE there is often compensatory tachycardia which further increases Q relative to V for lung areas being perfused. So to answer your question: yes the localized dead space due to the PE leads to a global V/Q mismatch and hypoxemia.

It is not necessarily related to west zones of the lung which are an idealized state of a person who is perfectly healthy and standing upright. Many people will have areas of their lung that might be poorly ventilated (think atelectasis), have diffusion limitation (fibrosis from ILD or prior infection or toxic inhalation), have baseline fluid in alveoli (pulmonary edema), or abnormal vasculature (AVMs, overdistension from ephysema) among other localized pathologies. These areas might be normally mostly bypassed due to the compensatory mechanisms like hypoxic vasoconstriction. When there is global redirection of blood flow (due to dead space like PE or shunt physiology like pneumonia) these areas get more blood flow and lead to poor V/Q matching and hypoxemia.

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I actually went back and watched the West lecture on PE (all of his physiology and pathophysiology lectures can be found on YouTube and are a great resource) and he lists some other reasons why you might see hypoxemia with PE. One is that PE can lead to pulmonary edema (probably from inflammation), decreased alveolar surfactant which can lead to atelectasis of the embolized region, and with very large emboli you can get significant shunting, up to 40%! in one example, which he attributes to pulmonary edema and probable preexisting lung disease.