APRV in pediatrics, any experience?
I want some other lung nerds to help me understand the pulmonary mechanics behind what I experienced with a patient recently. We never use APRV in our peds populations. I have a lot of experience with it in adults though.
The patient was a five month old with a history of reactive airway/multiple bronchiolitis infections, intubated for RSV/work of breathing and transferred to us. Outside facility said they had a tough time ventilating him. We had the same problem, and started continuous albuterol at 12ml/hr and this helped initially, but only lasted about an hour before we started having difficulting ventilating again (asynchrony, beaked waveforms, low tidal volumes, persistent hypercapnia). We paralyzed him, we tried several different positioning techniques, we tried every mode, I:E manipulation, high rate low VTs , low rate high VTs, higher peeps, and nothing worked. End tidal was consistently reading 70’s-80’s. VBGs were worsening at one point 7.00 with a CO2 of 97. He was starting to brady/desat frequently and we had three events where he required bagging to recover. We were very close to needing to place him on an oscillator and transfer. Our doc asked me to try APRV before oscillator because “we had nothing to lose”.
I was always told APRV is not a good mode for obstructive diseases, so I was very apprehensive and afraid to cause hyperinflation/alveolar sheering. And I had never used it on a patient that small. I always thought APRV was more for oxygenation because in the adult world we actually target permissive hypercapnia to improve p/f ratio. But we did some research and tried some settings that had been trialed in a few NICUs. Phigh 25, thigh 2 seconds, p low 0, tlow 0.8. Pt end tidal immediately went from 90 to 70, and kept dropping by 10 every 20 minutes or so. Heart rate improved from 90 to 130’s, we were able to wean from 80% Fio2 to 50% and he didn’t have a single brady/desat for the rest of the shift. Repeat vbg two hours after APRV went from 7.00/97 to 7.25 and a CO2 of 52. His breath sounds improved from moving almost no air to just some crackles in his bases. The doc and I were amazed. But I still don’t understand what actually happened physiologically. Was he just so derecruited we couldn’t ventilate?
I really want to understand this to try to pinpoint where I need to advocate for it in the future!