Aug 24, 2026 · 1 hr 9 min · 11 segments
Ryan Coleman, MD is an Associate Professor of Pediatrics at Baylor College of Medicine with dual appointments in Critical Care Medicine and Pulmonary Medicine at Texas Children’s Hospital in Houston…
Zach HodgesHost
Alice ShanklinHostYou know, another thing that I think, at least from my personal experience as a fellow, right, you hear people talk about VQ mismatch.
What does that mean, right? Like, is it actually that big of a deal? But in these diseases, right, this is where it becomes the big deal.
Because with PEs, right, you get impaired pulmonary blood flow, right? So you're trying to oxygenate potentially an area of the lung where there's just no flow, right? And so these kids get hypoxemic.
You get progressive VQ mismatch worsening, which then pretends more hypoxemia.
You get hypoxic vasoconstriction, again, trying to maximize the VQ matching where you can.
But that only contributes to further increases in your PBR over time, especially if you've got a big PE that's taking out a good portion of the lung.
And so, again, you get into this vicious spiral of more hypoxemia begets more hypoxemia.
you know, and the thing people reach for, right, is turn up the high flow, right? Give them more high flow, high flow, high flow, high flow.
But there's no blood flow, right? So you can have all the high flow in the world you want, but if there's no blood flow, it doesn't matter.
Again, you get into the hemodynamic worsening with the increased metabolic demand on top of the hypoxemia, right? Here comes your lactate.
Here comes kind of all the bad things that happen in this state but again as you guys mentioned right it's not more fluid and turn up the high flow in this particular circumstance like if you're needing more high flow you have a huge problem on your hands and you better get moving

This really gets at what's the mechanism of hypoxia in your patient in front of you.

If that question comes up on rounds, it's probably VQ mismatch because there's so many different types.

But this is a situation where these kids are tachypneic and they usually have excessive amount of ventilation, but there's going to be a very low perfusion, especially if a lot of the pulmonary arteries are occluded by a thrombus.

Thinking more about the hemodynamic assessment of these patients, you've already mentioned lactate.

What comes to mind as the essentials of what you would want the emergency department to start or would be your immediate priorities when they land in your unit?
you know, that sometimes the labs actually look relatively normal depending on where you are in the course of the PE, right? Like if they've had time to start bumping a troponin or they're, you know, so things like troponin, BNP or NT pro BNP, depending on your institution and whatever your flavor of BNP is, a blood gas with a lactate.
And one where people will say, oh, well, there was a tourniquet on it, so that lactate's probably not real.
You know, another thing that I think, at least from my personal experience as a fellow, right, you hear people talk about VQ mismatch.
What does that mean, right? Like, is it actually that big of a deal? But in these diseases, right, this is where it becomes the big deal.
Because with PEs, right, you get impaired pulmonary blood flow, right? So you're trying to oxygenate potentially an area of the lung where there's just no flow, right? And so these kids get hypoxemic.
You get progressive VQ mismatch worsening, which then pretends more hypoxemia.
You get hypoxic vasoconstriction, again, trying to maximize the VQ matching where you can.
But that only contributes to further increases in your PBR over time, especially if you've got a big PE that's taking out a good portion of the lung.
And so, again, you get into this vicious spiral of more hypoxemia begets more hypoxemia.
you know, and the thing people reach for, right, is turn up the high flow, right? Give them more high flow, high flow, high flow, high flow.
But there's no blood flow, right? So you can have all the high flow in the world you want, but if there's no blood flow, it doesn't matter.
Again, you get into the hemodynamic worsening with the increased metabolic demand on top of the hypoxemia, right? Here comes your lactate.
Here comes kind of all the bad things that happen in this state but again as you guys mentioned right it's not more fluid and turn up the high flow in this particular circumstance like if you're needing more high flow you have a huge problem on your hands and you better get moving

This really gets at what's the mechanism of hypoxia in your patient in front of you.

If that question comes up on rounds, it's probably VQ mismatch because there's so many different types.

But this is a situation where these kids are tachypneic and they usually have excessive amount of ventilation, but there's going to be a very low perfusion, especially if a lot of the pulmonary arteries are occluded by a thrombus.

Thinking more about the hemodynamic assessment of these patients, you've already mentioned lactate.

What comes to mind as the essentials of what you would want the emergency department to start or would be your immediate priorities when they land in your unit?
you know, that sometimes the labs actually look relatively normal depending on where you are in the course of the PE, right? Like if they've had time to start bumping a troponin or they're, you know, so things like troponin, BNP or NT pro BNP, depending on your institution and whatever your flavor of BNP is, a blood gas with a lactate.
And one where people will say, oh, well, there was a tourniquet on it, so that lactate's probably not real.
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