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Here's a #physiology teaching case that *everyone* who touches a ventilator needs to understand:
A 60 yo woman is intubated for hypoxemia from pneumonia. She has a SpO2 of 88% on PEEP +12 and 100% FiO2. PEEP is increased to +16 & her SpO2 drops to 80%.
What happened?
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Let's start with a little multiple choice. Which mechanism(s) could contribute to hypoxemia in this patient?
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The answer is ALL of the above!
But why? To answer, we need to understand what PEEP is and what effects it has on the lung.
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Positive end expiratory pressure (PEEP) is the pressure above atmospheric that is applied in between breaths while on a mechanical ventilator.
PEEP is beneficial for two reasons:
PEEP recruits collapsed lung (see video)
greater alveolar pressure drives more O2 into the blood (Henry's law)
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As an aside, it's worth noting that the benefits of PEEP in ARDS were discovered *accidentally*.
In 1967, two doctors caring for a patient on a ventilatory spotted a knob labeled "expiratory retard" and - not knowing what it did - decided to give it a try. It worked!
Nowadays we call that knob PEEP and it's an indispensable part of mechanical ventilation.
https://pubmed.ncbi.nlm.nih.gov/28731363/
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Ok so we understand why PEEP can help, but why can PEEP be *harmful*?
We need to understand the relationship between lung volumes & pulmonary blood flow.
Let's take a closer look at the alveoli. With the help of an electron microscope we can see that alveoli are surrounded by a dense interconnected network of blood vessels.
(btw, if you were wondering, they obtain these amazing images by injecting the vessels with a polymer, dissolving the remaining tissue, then taking SEM micrographs)
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There's a dynamic relationship between alveoli inflation & blood flow.
As the alveoli become more inflated, blood flow through these dense intra-alveolar vessels decreases. This increases the pulmonary vascular resistance (PVR).
PVR is lowest at Functional residual capacity (where normal tidal breathing occurs). PVR increases with both lower or higher lung volumes.
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Adding too much PEEP can overdistend the alveoli and decrease blood flow through the intra-alveolar vessels responsible for gas exchange.
It also increases blood flow through the extra-alveolar blood vessels, which do not participate in gas exchange.
This causes intra-pulmonary shunt and causes hypoxemia!
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Another factor to consider is that the effects of PEEP aren't uniform, especially if different areas have different compliance.
Areas of the lung that are affected by pneumonia may not be recruitable, but normal areas may become overdistended with too much PEEP. This too can worsen intra-pulmonary shunt & cause hypoxemia.
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Now that we understand how PEEP effects the lungs, we also need to consider how PEEP effects the heart.
We've already talked about how larger volumes can increase PVR. This increases RV afterload & right sided pressures.
For the 25% of the population with a PFO, this rise in right sided pressures may cause R-->L shunt, causing hypoxemia due to an intra-cardiac shunt.
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The two biggest predictors of right to left shunt through a PFO, were the degree of RV dilation & higher plateau pressures.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654438/
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Finally, we need to consider the effects of PEEP on cardiac output.
Applying PEEP decreases venous return because of increased intrathoracic pressure (which reduces venous filling).
Depending on the patients volume status a decrease in preload *usually* decreases cardiac output.
(btw check out the great explanation at https://derangedphysiology.com/main/home )
@nick@med-mastodon.comDecreasing cardiac output has many physiologic effects (hypotension, reflex tachycardia, decreased UOP, etc). But why does low CO worsen hypoxemia?
Recall that low CO drops the mixed venous O2 sat due to stagnant blood flow. If your SvO2 drops low enough it will worsen hypoxemia. This is the SIXTH cause of hypoxemia (which is often overlooked).
See my ICU OnePager on hypoxemia for more on this.
https://onepagericu.com/hypoxia
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So now that you're experts in the physiology of PEEP, let's put this all together.
There are 2 mechanisms where PEEP can improve oxygenation: alveolar recruitment higher mean airway pressure (Henry's law)
And 3 mechanisms where PEEP can worsen hypoxemia: intra-pulmonary shunt (overdistension of alveoli and shunt into extra-alveolar vessels) intra-cardiac shunt (via a PFO; in the 25-30% of people who have one)
decreased CO (particularly in people with low CO at baseline)
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The best (and fastest) way to evaluate for & is with point of care ultrasound.
Looking for bubbles in the LA after agitated saline can help spot a PFO. Measuring LVOT VTI at different PEEPs can be very helpful in titrating.
It's also worth remembering that anyone who worsens on mechanical ventilation, could have developed a pneumothorax. Yet another good reason to use POCUS in your workup of someone with worsening hypoxemia!
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I hope you've enjoyed this thread.
To learn more about this important topic, including a really nice deep dive into the physiology, I highly recommend this paper:
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@nick they asked for teaching today and I conveniently maneuvered it into this 
The missing point in this thread is that higher PEEP may improve oxygenation by decreasing cardiac output, and therefore a paradoxical decrease in oxygen delivery
Better SpO2 or PaO2 doesn’t equal improvement
@nick nice discussion, although I think “stagnant” blood flow is a strange way to describe low CO leading to low mixed venous sats. I like to describe it as a lower supply of oxygen delivered with a fixed demand, meaning tissues extract a larger percentage of the oxygen they see, meaning a lower percentage returns.