Here's a physiology case that *everyone* who touches a ventilator needs to understand:
A 60 yo woman is intubated for hypoxemia from multifocal pneumonia.
She has a SpO2 of 89% on PEEP +12 and 100% FiO2.
PEEP is increased to +16 & her SpO2 drops to 80%!
What happened?
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Before we get into the answer, let's make it interesting with some multiple choice.
Which mechanism(s) could cause worsening hypoxemia with increasing PEEP?
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Wow! 6000 votes! Im amazed by how many people share my love for 🫁 physiology!
I’ll post the answer tomorrow. If you can’t wait there’s a complete explanation on #MedMastodon.
So we understand why PEEP can help, but why can it be *harmful*?
We need to understand the relationship between lung volumes & blood flow.
Let's take a closer look. With an electron microscope we can see that alveoli are surrounded by a dense network of blood vessels. 6/
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).
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PVR is lowest at Functional residual capacity (where normal tidal breathing occurs). PVR increases with both lower or higher lung volumes.
(btw, this is an important fact to remember when managing RV failure & PA hypertension too)
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Excessive PEEP overdistends alveoli & decreases blood flow through the intra-alveolar vessels responsible for gas exchange.
It also increases blood flow in the extra-alveolar blood vessels that don't participate in gas exchange.
This causes intra-pulmonary shunt & hypoxemia! 8/
Another factor to consider is that PEEP may be uniform, especially if different areas have different compliance.
Areas of the lung affected by pneumonia may not be recruitable, but normal areas may be overdistended by too much PEEP. This too worsens intra-pulmonary shunt. 9/
Now that we understand how PEEP effects the lungs, we also must 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 matters! 10/
One study found that the two biggest predictors of right to left shunt through a PFO were the degree of RV dilation & higher plateau pressures. Excessive PEEP can increase both! ncbi.nlm.nih.gov/pmc/articles/P…
Be suspicious if a small change in PEEP causes a big drop in SpO2. 11/
Finally, let's consider the effects of PEEP on cardiac output.
PEEP decreases venous return because of increased intrathoracic pressure. Depending on volume status a decrease in preload *usually* decreases CO.
Decreasing CO has many effects (hypotension, reflex tachycardia, decreased UOP, etc).
But why can low CO worsen hypoxemia?
Recall that low CO drops SvO2. If your SvO2 drops enough it will worsen hypoxemia. This is the SIXTH cause of hypoxemia.
See my ICU OnePager for more 13/
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:
1️⃣ alveolar recruitment
2️⃣ higher mean airway pressure (Henry's law)
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And 3 mxns where PEEP can worsen hypoxemia:
1️⃣ intra-pulmonary shunt (overdistension of alveoli & shunt into extra-alveolar vessels)
2️⃣ intra-cardiac shunt (via a PFO; in the 25-30% of people who have one)
3️⃣ decreased CO (particularly in people with low CO at baseline)
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The best (and fastest) way to evaluate for 2️⃣ & 3️⃣ 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. Remember to r/o PTX too!
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It's very helpful to compare measurements at different PEEP values to help find the "sweet spot" for oxygenation, compliance, and cardiac output. Something like this (though maybe with a column for LVOT VTI):
To learn more about this important topic, including a really nice deep dive into the physiology, I *highly* recommend this paper by @basakcoruhUW & Andy Luks.
Important ICU teaching case:
A woman with AL amyloidosis presents with hemorrhagic shock from a GI bleed. HR 130, BP 80s/40s, Hb 4.5. She’s been receiving CyBorD-Dara chemotherapy up until 1 month ago.
What crucial fact do you need to remember when ordering blood transfusions?
The answer is that daratumumab (an anti-CD38 monoclonal) interferes with antibody screening & crossmatch!
In order to understand *why* this occurs we need to step back and review how blood is tested for compatibility.
Buckle up for a🧵! Let’s get our Coombs on, indirectly. 2/
To safely transfuse blood, we test for:
-major antigens (ABO, Rh)
-minor antigens (everything else)
Testing patient ABO & Rh is called “typing”
Testing for antibodies against minor antigens is called “screening”
Mixing donor blood w/ recipient serum is “cross matching”
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During my undergrad @BrownUniversity I remember when researchers did this in *humans*: A man with quadriplegia controlled a computer or robotic limb using a brain-machine interface. It was on the cover of @Nature. That was in 2006.
More hilarious is in a “groundbreaking paper” ostensibly written by Elon & published in the Journal of Internet Medical Research, they claim it’s “plausible a person may someday control a digital mouse” w/ this technology.
Ignoring the fact that it was accomplished >15 yrs ago!
Here’s a fun ICU puzzle: what is causing this crazy spiking pattern on the ECG waveform of both an intra-aortic balloon pump & ICU monitor?
A #MedEd 🧵 on an important clinical artifact & the triboelectric effect that we’ll need to go back in time 2500 years to understand!
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Before we get to the cool physics behind this important clinical artifact, what device could attached to the patient that’s causing these crazy spikes on the EKG?
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The answer is: CRRT machine
In fact, any machine that uses a *roller pump* can cause this artifact.
A roller pump squeezes tubing to generate flow. Here’s the roller pump on the CRRT machine that was causing this weird EKG artifact 👇