Hypoxia in Pulmonary Embolus

24 Sep

mechanism hypoxia featured

Hypoxia is almost ubiquitous in PE (In the comments Liam suggests otherwise. I honestly can’t find a clear answer. in PEITHO, a trial of submassive PE, 85% were receiving oxygen suggesting hypoxia. Certainly in the tiny PEs, lots of people don’t have hypoxia. If you have a better answer let us know in the comments). Yet it is not immediately clear why. You might think you know but certainly when I start to think about it too much it all becomes very muddy. This is mainly due to my poor understanding of respiratory physiology no doubt. I’ve tried to correct that somewhat with this post.

My basic thinking has always been. A PE is a big clot in the lung, this means part of the lung doesn’t work right, ipso facto then there must be hypoxia. That gets you through day to day existence in emergency medicine but it’s hardly a detailed description of the problem.

The terminology doesn’t really help here as V/Q mismatch technically seems to mean that there is an imbalance ventilation to perfusion. In the context of PE people state that the hypoxia is due to V/Q mismatch but don’t clearly state if it’s a high or low V/Q state.

The terms shunt and venous admixture are also used with some frequency which has a tendency to confuse the anatomist in me where the I can tell where the superior oblique is and what direction it runs in purely from the name…

I started with Rosen’s 8th Edition. The PE chapter is written of course by Jeff Kline.

A lodged clot can redistribute blood flow to areas of the lung with already high perfusion relative to ventilation and therefore cause more blue blood to pass through the lung without being fully oxygenated. This venous admixture is probably the primary cause of hypoxemia with PE and the increased alveolar-arterial oxygen difference

This actually is a pretty decent explanation of what seems to be happening. PE causes redistribution and instead of the left lung getting 50% of the cardiac output it suddenly gets 80% and the ventilation isn’t sufficient to oxygenate the blood.

But  figured I’d do a bit of further reading just to see what else is out there.

Paper #1

Huet Y, Lemaire F, Brun-Buisson C. Hypoxemia in acute pulmonary embolism. Chest. 88(6):829-36. 1985. [pubmed]


These guys studied a whopping 7 people,  all 1-9 days post PE, but 2 hrs post their formal angio that was used to diagnose it. Most had greater than 50% pulmonary vascular occlusion and most had some CXR changes too (something we don’t see very commonly). They all had Swan-Ganz catheters placed hence all the lovely data they got to play with.

They were all on heparin and were given urokinase after their “gas exchange test”. This involved infusing a bunch of inert gases dissolved in dextrose and measuring lots of things.

They suggest that the hypoxia had different causes depending on the patient and interestingly could be related to their CXR changes.

  • if they had atelectasis on CXR then there hypoxia was from shunt.
  • if the CXR was normal it was due to perfusion of lung units with low V/Q ratios (ie overperfusing a lung unit with no increase in ventilation)


In PE there is a degree of shifting of ventilation away from and around the underperfused lung, this presumably, is the lung autoregulating itself. This shifting is not particularly well done and after a while atelectasis occurs and as a result of that you now have shunt as an additional cause of hypoxia.

They conclude from their data that initial hypoxia is due to V/Q mismatch (in particular ,perfusion of lung units with low V/Q ratios) and later in the disease course it is likely shunting.

Paper #2

Burton GH, Seed WA, Vernon P. Observations on the mechanism of hypoxaemia in acute minor pulmonary embolism. British medical journal (Clinical research ed.). 289(6440):276-9. 1984. [pubmed]

These were probable PEs, all diagnosed on V/Q scans. All were tachy and breathless with normal CXRs and patients were identified through chart review. Mostly post op. They describe them as minor PE but I suspect they were all quite impressive and may well be termed “submassive” in these days of right heart strain and trops…

Most were a week post symptoms and the ABG was taken just after the diagnostic V/Q scan.

They garnered a huge 11 pts. The V/Q all showed reduced perfusion in areas well ventilated (which seems to be the definition of PE on a V/Q scan) and lots of other distal areas that were overperfused comared to how well ventilated they were. The more severe the V/Q scan changes the more severe the ABG abnormalities.

One of the big issues here is that they assume the cardiac output was normal or raised i their calculations but they don;t actually measure it. The prior study did measure CO in their patients and that it was reduced in all patients.

This doesn’t really help much in working out what’s going on to be honest

Paper #3

D’Alonzo GE, Bower JS, DeHart P, Dantzker DR. The mechanisms of abnormal gas exchange in acute massive pulmonary embolism. The American review of respiratory disease. 128(1):170-2. 1983. [pubmed]

I had to work off the abstract here as I couldn’t get full access. They studied two patients here, both with “massive PE” (they don’t provide a definition in the abstract) using the inert gas method and found that shunt was the main issue, not V/Q mismatch . They state that 20% and 39% of blood flow was through unventilated lung. They conclude that shunt is the main issue.

Paper #4

D’Angelo E. Lung mechanics and gas exchange in pulmonary embolism. Haematologica. 82(3):371-4. 1997. [pubmed]

This a review article written by one of the authots above. It’s the best I’ve found and is open access too. Bottom line: shunt and V/Q mismatch are the main causes of hypoxia. (are there any other options???)

It does try and explain why V/Q mismatch causes low O2 – apparently due to the sigmoidal shape of the O2 curve increases in ventilation cannot keep pace with either increased or decreased perfusion. Note this does not apply to CO2 as its curve is linear. This did ring a bell from my ICU reading years ago…

It highlights that some reports have noted bronchoconstriction and airway narrowing is part of PE – though perhaps this is clinically silent for most patients as I can’t say I’ve heard a great deal of wheezing in there.

The atelectasis that occurs (with resulting shunt) could be down to pneumoconstriction from low CO2 or it could be down to humoral mediators from the platelets in the clot surrounding it.



Both shunt (perfusing a totally unventialted lung segment) and V/Q mismatch (poor matching of ventilation to perfusion) are important causes of hypoxia in PE. The shunt is probably the important take away point as we commonly see patients with pleuritic pain for a week with what looks like consolidation/atelectasis on a CXR and we don’t entertain the diagnosis of PE as most of us were brought up believing that we should think of PE in patients with SOB and a clear CXR.

In my search I did find some great videos on basic mechanisms of hypoxia in all conditions which I’ve embedded below.

Any questions, comments, corrections are always welcome.

UPDATE: Martin on twitter noted that shunt is really just V/Q mismatch in the extreme. In particular shunt refers to perfusion of a completely unventilated lung segment. If the segment is perfused and partially ventilated then it is just an area of high V/Q (numerator bigger than the denominator). I hope this doesn’t confuse matters.

Update Dec 2015:

When looking into this originally I’d wondered just how many patients had PE (see note from Liam in the text). Jeff Kline on twitter had suggested this paper from PIOPED II. They had 74 pts with PE with ABGs on room air and 32% of these had a PaO2 >80mmHg (>10kpa) so as expected hypoxia isn’t that great a sign as a rule out.

Image source: https://commons.wikimedia.org/wiki/File:Saddle_thromboembolus.jpg

6 thoughts on “Hypoxia in Pulmonary Embolus

  1. I would add that hypoxia is actually relatively uncommon in PE. In the US, of course, we scan everybody, so we pick up many small segmental and subsegmental PEs, and they are rarely hypoxic. When we get the big central ones, they are sometimes hypoxic, but certainly not always, but I would venture that not even most of the time are they hypoxic.

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  3. Thanks for a good topic and public pondering.
    Interesting that a shunt would be it. I have always figured that it was a V/Q mismatch but on the other end of the spectrum, Increased Dead Space that is. Thinking that you have ventilation to segments where there is no circulation, leaving the rest of the lungs to manage oxygenation. Otherwise healthy individuals can saturate themselves fine with even one lung which then could explain the rare Hypoxia.
    But then again, the overperfusion theory sound convincing as well although usually the lung is very capable of handle large increases in CO (e.g. running -- CO increase by maybe +300%) without any desat. Hence a full left sided pulmonary artery occlusion would deliver a 100 % increase in blood flow to the right lung -- which in turn the right lung should handle quite well, if respiratory Minute Volume increased properly (e.g. Tachypnea). This tachypnea could in turn explain why you often get normal/low pO2 but low pCO2 since there is no significant rise in CO2-production and CO2 much more easily diffuse between the alveolae and the lungcapillarys.

    Honestly I don´t have a clue. I´m just thinking with my keyboard here but it is difficult to comprehend all facets of this. Confused on a higher level?

    • Hi Greyman -- your thoughts echo mine exactly. I had thought that the right lung should be able to oxygenate fine if the left pulm artery were occluded but it seems it’s more complex than that. The papers i looked at aren’t wonderful and it’s such a niche area I doubt there’s that much interest in studying it further

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