Question May 11, 2008
Posted by keepbreathing in Uncategorized.trackback
A question for my fellow RTs.
I had a patient on A/C, low volume/high rate sort of strategy. His ABGs were holding steady with a respiratory acidosis, pH around 7.3 and PaCO2 in the high 50’s no matter what we did to him. His peak pressures were rising consistently so we switched him to PCV just to see what happened.
With a high inspiratory pressure set, he was drawing smaller tidal volumes and therefore had a lower minute volume than he had had on volume control. I could not increase the respiratory rate, and the inspiratory pressure was at the maximum that I was comfortable with. I wasn’t sure this would work because of the lower minute volume, but I figured that I’d leave the patient on for half an hour and see what he did.
Despite the lower minute ventilation, my patient’s PaCO2 dropped like a rock and his acidosis corrected. It was exactly the opposite of what I had expected.
I feel like I’m missing something here. Am I just having a brain block, or is this actually kind of weird?
Just a guess, but…
…better alveolar ventilation - in the nature of stenting open some of those atelectic alveoli - and thus better gas exchange?
It does seem counterintuitive that decreasing minute volume would resolve his hypercarbia and acidosis, but that’s my guess.
I think he was probably air trapping on the low vol/high rate strategy. Even if you weren’t seeing autopeep, his gas exchange could have been crappy due to air trapping due to inadequate time allowed for exhalation…especially if this pt is a COPDer or severe long term asthmatic.
my guess is air trapping. Too many breaths without enough time for exhalation. I have seen this happen also and I don’t have a concrete explaination for it. I would also like to hear what others think.
I’m voting with Ambulance Driver…perhaps some additional recruitment taking place. Were they on an inverse ratio in PCV?
was the rate same with PC as in VC?
Same theory here, with the switch in modes, flow delivery is decelerating, so stiffer lungs are more likely to be inflated rather than “ignored” because of probable turbulent (vs. laminar) flow in volume control. Any CXR changes, do you know?
Also, remember that PC has no set minute ventilation and may vary from hour to hour so check the vent flow sheet for any drastic changes, and possible signs of lung recruitment like increased volumes, better compliances.
Also, what was the underlying condition for you to consider a low volume/high rate type of strategy.
PS., I wish we had that kind of REAL therapy provided in our facility, instead of us being knob turners. We’re just drones in our ICU. Fortunately in the ER, our practice is given full potential with regards to how we provide treatment.
After reading your post,it reaffirmed how much I love our RTs.
Hello, there.
Good question. I believe GFP was the closest to the answer.I think it had to do with the decelerating flow pattern of PCV. We used to think of PCV as “protection from barotrauma”. We know here in 2008 that “volutrauma” is the beast.
“Stenting open alveoli” is usually from beneficial end expiratory pressure, and will improve Oxygenation (PaO2 or SpO2) more than Ventilation (PaCO2 or ETCO2).
Improved alveolar ventilation is my bet, as well as AD’s. It would have to be so, as long as our patient’s CO2 production didn’t change.
(eg. hypermetabolism , high temp, seizure, etc. increasing CO2 production, and hypothermia, chemical paralysis lowering CO2 production).If CO2 production(VCO2) remained the same, PaCO2 should be liniar with Minute Ventilation (VE).
I’ve seen this phenomenon before. A ramp wave improving alveolar ventilation and lowering PaCO2 with identical VE. It’s the bulk of tidal volume being delivered early on, and flow dropping dramatically and being less turbulent /more laminar that lets the breath reach deeper through lower obstructed airways. Careful, though.
Beware the affect of ramp wave .It usually DOUBLES Inspiratory Time. More “fill time”= less “empty time” and you may create that darn “air trapping” when you don’t want it.
I usually strive for SYNCHRONY between vent and patient. That means a careful look at I Time and Pressure/Time scalars on the screen. In PCV, I find the FLOW/TIME scalar the most useful.You can see if the lungs “emptied all the way” as well as “filled all the way”.
So…Increasing I Time with someone with COPD can be bad if it impedes adequate expiratory time (empty time). But the Ramp can double that I Time, unless you increase the Flow Rate (how fast the gas pushes in) Can there be a difference between square wave and ramp wave with identical I Times?
I believe you’ve seen it as, so mentioned above, have I.
How can you tell if it will help you patient right then, right now? That’s why they call it work. Make your changes thoughtfully and carefully, and watch the results then and there.
Don’t get me going.
BTW,
The flow patterns can be very different between “Ramp” and “PCV”.
Ramp is very predictable for a shape (and thus delivery) of flow and volume.
PCV’s flow pattern peaks quickly, and then drops dramatically over the I Time. The difference, and alveolar ventilation, can be noticible.
As you’ve documented.
You reached deeper through the damaged airways to alveoli, and let the breath back out without air trapping.
Good Show!
AJC