Well Dan, thanks for that question, I guess...! As archy the cockroach said: "it gives me to think furiously."

To begin with I do not understand why you say that increasing dead space alone should not cause hypoxia. After all, your lung capacity is finite. Convert part of it to dead space, and immediately part of your gaseous exchange resources become unavailable. You might rightly point out that things are not so simple and I would agree, but think of the limiting case: how effective would your respiratory system be if all of your lung capacity were converted to dead space?

Very well, a pulmonary embolism might not be primarily a course of major shunts, depending on where it happens to be placed of course, but it does not follow that it would not interfere with gaseous exchange in other respects.

The claim that you quote, to the effect that the hypoxia in a PE is due to a big increase in the blood flow through healthy parts of the lung, such that the gaseous exchange becomes diffusion limited, I personally find subjectively unpersuasive. Not having done any research on this subject, I cannot argue the case from a position of strength, but it would take some very well controlled quantitative research to persuade me that the point is of predominant importance.

You argue that if this is the case we all should become hypoxic when we exercise. This is a thoughtful point, though again I should like to see cogent quantitative work to evaluate it.

Your suggestion that swelling in the adjacent alveoli limits ventilation is qualitatively logical, but once again the ugly word "quantitative" stands ready to swat beautiful ideas out of the air.

As for having a better explanation, of course I do not. All I can offer is the idea that firstly, any part of the lung in which perfusion is limited or prevented, cannot contribute much to our gaseous exchange. After all, our normal pulmonary function is predicated on a number of parameters, including the mean rate of gaseous flow (in humans generally tidal of course), the area available for gaseous exchange at the boundary between air and tissue, the mean rate of blood flow through the capillaries and the corresponding amount of time that an erythrocyte has available for gaseous exchange by diffusion, and so on and on.

Now, interference with some of these factors can be mitigated by adjustment to some other factors (though of course it does not follow that damage of one sort of, such as an embolism, even if compensated for by other mechanisms, will not cause totally other classes of damage, such as scarring, but that is not immediately relevant to our current discussion). But such mitigation is not always possible and in particular is not always adequate. My own simplistic impression always had been simply that any significant embolism must necessarily reduce the area available for gaseous exchange. Unless this could adequately be compensated for, hypoxia of a corresponding degree seemed a perfectly logical consequence. If one aspect of the compensation were increased perfusion at a higher rate in neighbouring lung tissue, then gaseous exchange in that tissue might be expected to increase and to become more efficient in that the partial pressure gradients would on average become steeper. However, the period of diffusion during an erythrocyte's passage through such a region of intense perfusion would be correspondingly shorter. It is a classic example of a quantitative question, full of traps for the innumerate and the slipshod. All the same, no matter how cheerfully we might accept the mitigating effects of flexible and redundant mechanisms in our physiology, I cannot see how an embolism could do other than harm to our respiratory capacity.

I am not sure that I have said anything to assist you in clarifying your own thoughts on the matter, so please feel welcome to challenge anything I said, or to require elaboration.

Cheers,

Jon

From my understanding (I may be wrong).... During exercise there is massive dilation of the pulmonary vessels which increases the surface area for gas exchange. This mechanism does not seem to occur during an acute pulmonary embolism, in fact there may even be some vasoconstriction. In addition if the PE is large enough there will be a drop in cardiac output (due to reduced output of the right ventrical due to pulmonary hypertension) which will also reduce oxygenation.

From my understanding as a clinical medical student, only massive pulmonary embolisms result in significant hypoxia, e.g. one involving the pulmonary artery or one of its main trunks. The mechanism is through enlargement of the dead space, e.g. a lobe of the lung which is ventilated but not perfused, as rightly mentioned by the OP.

Another important contributor to hypoxia in pulmonary embolism neglected  here is the haemodynamic consequence of the embolus, namely, the stress placed on the heart. The embolus increases the pulmonary vascular resistance resulting in a heavier load placed on the right heart, evidenced by tachycardia, right heart stress, or even right heart failure. When the right heart fails, the amount of unoxygenated blood going through the pulmonary circulation would be reduced leading to inadequte oxygenation and systemic perfusion.

Furthermore, there will be an increased 'preload', or pooling of blood on the venous system that results in lowered effective systemic volume. The decrease in cardiac output further results in activation of the renin-angiotension-aldosterone system leading to systemic vasoconstriction aggravating the heart failure.

Lastly, pulmonary infarction results if the embolus does not resolve. This will lead to further aggravation of the hypoxia, e.g. by acidosis. These factors are beyond the scope of respiratory physiology and therefore may not appear in textbooks, e.g. the one by West

Hope this helps.