APRV TCAV can be really complicated for ongoing management of a respiratory failure patient. But when your patient is failing conventional ventilator modes, EVERY resus and crit care doc should know how to crash a patient on to APRV. EMCrit Team member and EMNerd, Rory Spiegel, has recently published a how-to guide on doing exactly that.
Rory's Paper
Update–Phil Rola just Published Another Great TCAV Paper
APRV on Different Vents
Rory feels older Puritan Bennetts and Servo vents are dangerous with APRV once a patient starts spont. breathing as they do not maintain the Tlow
Settings Diagram
Additional New Information
- Habashi's Group Published a Myth Busting Paper –TCAV Myths Corrected
- Habashi Review on TCAV
- Have Caution with the Use of APRV until More Studies
More on EMCrit
- EMCrit Wee – The Philosophy of APRV – TCAV with Nader Habashi
- IBCC chapter: Guide to APRV for COVID-19
- APRV Guideline
- EMCrit – Ghali Grills 1 – When to Use APRV
- EMCrit Wee – Follow-Up to the Ghali Grills Episode on APRV
Additional Resources
- Phil Rola's Paper of APRV TCAV during Covid
- TCAV as a Recruitment Maneuver
- EMCrit 373 – Mike Weinstock with another Critical Care Bounceback: “Asymptomatic Hypertension” - April 18, 2024
- EMCrit Wee – Ross Prager on 10 Heuristics for the New ICU Attending - April 13, 2024
- EMCrit 372 – FoundStab Intubation SOP - April 5, 2024
I believe you’ll have better luck with EMNerd_ with the underscore score 🙂 although the other may be interesting as well lol
Great simplification Rory!!! Thx!!!
It’s because you recruit significantly more lung with APRV compared to PC. The mean airway pressure is significantly higher in APRV.
Higher mean airway pressure means more lung recruitment means bigger TV.
This was a great conversation, thanks so much!
I had a question about single lung shunts hating PEEP. (I guess I’m in the category of people Rory mentioned that still don’t know about this!) I’ve been unable to find much literature (besides papers specifically on OLV) on the rationale for why this might be, and why turning the PEEP down to 2 cmH2O will help resolve the worsening hypoxemia.
I’d be very grateful to be pointed in the right direction!
conversation was on SINGLE LUNG pathology shunts. In this case increasing PEEP just ruins the bad lung and makes things worse
Is the reason that single lung shunts are so sensitive to PEEP because overdistending/increasing PVR in the good lung simply shunts blood to the nondependent lung? Or are we missing something deleterious that happens to the bad lung as well?
In the podcast Rory commented “P low minus trapping pressure is your driving pressure”. I think he meant P high minus trapping pressure is the driving pressure in APRV? thanks!
absolutely!