Thread by @IM_Crit_

ICU stories: COVID(+), sick > 4 wks, with tracheostomy just 1 day ago. 1st encounter with pt, I didn't know his "behavior" and I found him on ACV, ARDSnet protocol on 100%-peep 12, sedated-paralyzed, with sat 75%, crashing... No time to "study the chart". What would you do?

Well, I made sure pt was well sedated/paralyzed, tube-vent in place, and did POCUS (sorry for the clips' quality). Things that had to be ruled out and could kill fast: pneumothorax + PE. I saw bil lung sliding and felt quite confident that there was no PTX. Let's look at the 🧡:

PLAX with decent LV size and function:

Subcostal view with "full" IVC ( I measured it 2.4 cm in the transverse view) but patient was on the vent with peep 12 etc, so hard to interpret:

Interesting 4ch view. Do you see anything?

I thought the RV was not huge but had "some dilatation" and was contracting "less than well". I thought there was McConnell's sign... The septum also was moving in a "funny" way... Let's see if PSAX helped:

PSAX at the aortic valve level. Useless. No, wait... Is the inter-atrial septum bouncing towards the L side? This indicated increased R-sided pressures. Let's keep scanning:

My goal was to get PSAX at the papillary muscles' level but was not easy and I was "cutting" the LV a bit higher, closer to the mitral valve...🤦‍♂️Was this a D-sign or I was subconsciously trying to make the case for PE by over-reading the clips? Poor technique can create "ghosts"!

OK, let's summarize: I have a crashing patient with bad COVID-19 ARDS

... and in the POCUS that I could not show/discuss with anybody I thought there was evidence of RV strain. Should I thrombolyze empirically? Is there anything else that POCUS can help with? Of course. I did lower ext US; no evidence of clots. I could not still make the case of PE

Would you give empirically t-PA? I was looking for more data. What about Doppler? May be not a POCUS skill but frequently helpful in the ICU. This was the TV velocity signal. Not as clean as I would like but 3-4 m/sec + dilated IVC suggest pulmonary hypertension...

Would you give empirically t-PA? I was looking for more data. PSAX not easy but I tried to get a PA Doppler signal. Voila:

🤦‍♂️There was a PA Doppler signal notching... Now what? In patients with suspected PE, PA systolic notching pattern is considered sensitive/specific for a submassive or massive PE. @msiuba @ThinkingCC @MDBeni @khaycock2 @iceman_ex @TaotePOCUS

Would you do anything else? And with all the information I gave you, would you give t-PA?
@msiuba @ThinkingCC @MDBeni @khaycock2 @iceman_ex @TaotePOCUS @NephroP @vaszochios

So, the votes are almost split in half regarding the management of this patient.
I don’t know if I did the right thing for the pt and PLEASE don’t accept what I did as the recommended approach in similar scenarios. Even though I thought a lot (in the few minutes I had to decide!)

about thrombolysis, I never gave t-PA. If I had found a lower extremity DVT, I might have been more eager to give t-PA. As suggested, I did a bubble study and did not find R->L shunt. I had no way to give inhaled NO/prostacyclin/milrinone...

The patient was proned "stat", ventilator adjusted and heparin drip was started. Patient made it through the night and next day, when more stable, he had a chest CT. For what it was worth, it did not show a large central PE but - to keep things murky - ...

the report mentioned that “evaluation of small/distal segmental/subsegmental PA branches was limited due to lung disease and motion”. 🤦‍♂️

Life in the ICU is complicated, isn’t it? Would u change your mind if I told u that ICU has no intensivist at night and only chance to give t-PA was during day-shift, so the decision was on me to pull the trigger? What would I say if the patient had a PEA arrest later that night?

My rationale was that with acute PE, I MIGHT have seen "more" RV dysfunction. I tried to resist the temptation of accepting the McConnell’s sign and the PA systolic notching as proof of PE.

I thought that acute cor pulmonale (ACP) from COVID / ARDS / ventilation might be enough explanation for my POCUS findings. We know from the fantastic French group (DOI 10.1007/s00134-015-4141-2) that PNA as ARDS cause, driving pressure >18, PF ratio < 150 and PaCO2 > 48 are ...

the four independent factors associated with ACP. In the presence of all 4 factors (like in my patient!), the prevalence of ACP is 75%.

We should not ignore basic physiology. Remember the O2 saturation curve? If the patient lives on the edge of the cliff, a small drop of the pO2 for whatever reason (atelectasis, loss of recruitment after suctioning, asynchrony) can easily bring the sat down from 90 to 80%

I think if a patient has an already dysfunctional RV and high PA pressures, whatever “event" may further decrease PaO2, increase PaCO2, move him/her away from the FRC, could lead to a "PE picture" in POCUS.

Take-home messages:
1. McConnell’s sign and systolic notching of the RVOT Doppler signal are not specific for PE
2. Acute cor pulmonale is very common in severe ARDS
3. POCUS is an amazing tool. What to do with POCUS findings is a whole different story

4.Daniel Kahneman showed (en.wikipedia.org/wiki/Thinking,…) that our brain functions with 2 operating systems. System 1 is effortless and uses easy shortcuts (McConnell’s sign = acute PE). System 2 requires deliberate and conscious integration of all data points. You need both in the ICU!

Many thanks to everybody that read the case, voted and shared thoughts and experiences with me.

Thank you!