ECMO for Prone Ventilation

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chrisv

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21 y/o with the (nasty) flu, otherwise healthy, being ventilated in prone position, on ARDS protocol settings (high RR, small TV, 100% fio2 at this point), brought to the OR on ICU ventilator, saturating 94%...surgeon plans on placing patient on VV ecmo via right IJ. Any thoughts on how to prevent impending de-saturation? He doesn't have a swan, but I was thinking he's likely has a pulm htn component to his hypoxia so could potentially benefit from iNO or iv flolan?
 
IMO, that's the role of ECMO in this case, to improve oxygenation. Don't touch the vent, do it as TIVA.

The patient most likely has bad V/Q mismatch. Flolan might buy some time, but only if that sat drops much lower. Why wasn't this done at bedside?
 
Keep him on the ICU ventilator. Consider iNO. Tell the surgeon to work fast.

A saturation in the 80s while ECMO is being established won't kill him. How low does he desat while supine?



Or you can just tell the surgeon to climb under the bed, lie on his back, and get to work...they are just overpaid mechanics anyway! 😉
 
FFP said:
IMO, that's the role of ECMO in this case, to improve oxygenation. Don't touch the vent, do it as TIVA.

Why would a 21 y/o have pulmonary HTN? You are confusing V/Q mismatch with PHTN. And why wasn't this done at bedside?
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Haha I had similar thoughts when I first read it...I think he is scared about flipping him back over from the prone position. Most patients don't stay prone 100% of the time anyway though so not sure why he's worrying about it.
 
Urzuz said:
Haha I had similar thoughts when I first read it...I think he is scared about flipping him back over from the prone position. Most patients don't stay prone 100% of the time anyway though so not sure why he's worrying about it.
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OP, when they flip the patient, the sat might go down to the 80s. I wouldn't sweat it, if the surgeon is fast.

If all hell breaks loose, see if adding more PEEP (up to 20+) helps, and make sure that the I:E ratio is 1 or higher. Just watch the BP. If the person is big, ignore the plateau pressure alarms, because probably the abdominal pressure itself is 20+, so you can aim for a plateau in the 40's (transpulmonary pressure still under 30, hence no risk for alveolar damage). If the person is small, keep the plateau under 30; ask for an RT to stay with the ICU ventilator in the room to do the adjustments and pressure checks for you, and have them bring Flolan, just in case.
 
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Thank you guys!!!

So this was my resident colleague's case, I stopped by for moral support. We flipped the patient, saturations in low 80s (expected as that's where he was before prone ventilation was started), and the surgeon worked fast and we quickly benefited established of ECMO.

I've also heard other people say mid/low 80s won't kill a patient (done a couple of OLV with slow surgeons with sat in low/mid 80s, patient woke up great the next day, I went to Vegas the day after).

Surgeon didn't want to do it in the ICU because he didn't have "his team" and didn't have "all my cannulas" and is used to having us on standby for these cases.

Maintained TIVA to avoid touching the vent setting and to avoid use of inhaled which would inhibiting HPV. The echo didn't show any pulm htn (and I realize he likely still had severe PHtn), so could pulmonary vasodilators (flolan or iNO) make the situation worse by vasodilating all pulm vasculature and thus diverting flow from well ventilated alveoli to poorly ventilated alveoli (similar to what the inhalation would do by inhibiting HPV)?

FFP--thanks for your guidance on vent setting, was already on PEEP of 18, TV 380 mL, RR 32, PIP 37, normal BMI. I:E was 1:1. Probably could've tried a higher I:E ratio and accepted higher plateau pressure. Should've grabbed an RT (and an anesthesia attending).
 
Arch Guillotti said:
😵😵😵
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+1.

@chrisv, you have to realize the pathophysiology of ARDS/severe PNA. There is a huge territory with either V/Q mismatch or downright shunt. If it's shunt, inhaled Flolan won't do crap, because it just won't get absorbed. But if it's V/Q mismatch, what will happen? 😉

Also, you can have all the HPV in the world, and that still won't fix hypoxia if too few alveoli are both properly ventilated and perfused. How many alveoli do you think are still properly ventilated and perfused in a massive pneumonia/ARDS/inflammation, without significant V/Q mismatch? (The estimate for ARDS is 1/3 - baby lung concept.) You need to recruit lung (PEEP) and you need to improve the perfusion of those few ventilated alveoli (inhaled vasodilators).
 
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We do a lot of these at my hospital (i'm pulm/ccm). The IJ avalon usually goes in pretty smoothly but not always - sometimes it requires a lot of position adjustments to work well and we've found it very beneficial to have TEE and good fluoro (not bedside fluoro). We do almost all of these in the OR. If the patient is going to be unstable when flipped over we will do femoral VV ecmo canulation in the unit and covert to an avalon in a day or two.

Agree that iNO or flolan not likely to help much. Sometimes doing a recruitment maneuver with a higher PEEP for 30-60 sec will buy you some time.
 
Paralyze for sure if not already done. Could try aprv. Would go up on PEEP if it buys you a increase in plat of less than the increase in PEEP. Flolan will buy you a better PO2.

Plus, I wouldn't lose any sleep about a sat above 80 or so if you're in the act of transitioning to ECMO.

Thankfully, our surgeons would put the patient on in the ICU.
 
Arch Guillotti said:
😵😵😵
Click to expand...

I say because I've seen many TTEs being as patient having not pulm htn (minimal TR jet or doppler not correctly aligned) yet seen higher numbers on cardiac caths and during swan placement. Of course, with patients this sick, everything is a dynamic process. In his case, TTE was 48 hours old, so with I had to keep a high degree of suspicion.
 
FFP said:
+1.

@chrisv, you have to realize the pathophysiology of ARDS/severe PNA. There is a huge territory with either V/Q mismatch or downright shunt. If it's shunt, inhaled Flolan won't do crap, because it just won't get absorbed. But if it's V/Q mismatch, what will happen? 😉

Also, you can have all the HPV in the world, and that still won't fix hypoxia if too few alveoli are both properly ventilated and perfused. How many alveoli do you think are still properly ventilated and perfused in a massive pneumonia/ARDS/inflammation, without significant V/Q mismatch? (The estimate for ARDS is 1/3 - baby lung concept.) You need to recruit lung (PEEP) and you need to improve the perfusion of those few ventilated alveoli (inhaled vasodilators).
Click to expand...

Thanks for your insight.

@bigtuna--yes, it was the avalon cannula that he was interested in placing, wanted fluoro. Good to know that we could've bridged with femoral cannulation.
 
VV ECMO is not a great choice for severe pulmonary HTN with ARDS. VA ECMO is a better choice. TEE is key here.

But say you do VV ECMO via RIJ and Right femoral cannulation and sats don't improve.

What's the usual cause for this?
 
This definitely could've been done in the unit. Use TIVA with TEE for Avalon placement, no need for fluoro (though our surgeons like fluoro as well).

And @chrisv, the pHTN if present is a red herring, if there was true mod-severe pHTN or right heart dysfunction he's getting put on VA (though no good data for VA in ARDS other than a specialty center benefit most likely), and TTE/TEE will only ever underestimate pHTN (unless you really screw up on the simple math part of it). Lastly, as an academic question, how would you manage the ventilation in this patient post-VV ecmo initiation?
 
sevoflurane said:
VV ECMO is not a great choice for severe pulmonary HTN with ARDS. VA ECMO is a better choice. TEE is key here.

But say you do VV ECMO via RIJ and Right femoral cannulation and sats don't improve.

What's the usual cause for this?
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ECMO flow:CO mismatch. Slow down their rate and/or decrease VO2.
 
Robotic Wis-Hipple said:
This definitely could've been done in the unit. Use TIVA with TEE for Avalon placement, no need for fluoro (though our surgeons like fluoro as well).

And @chrisv, the pHTN if present is a red herring, if there was true mod-severe pHTN or right heart dysfunction he's getting put on VA (though no good data for VA in ARDS other than a specialty center benefit most likely), and TTE/TEE will only ever underestimate pHTN (unless you really screw up on the simple math part of it). Lastly, as an academic question, how would you manage the ventilation in this patient post-VV ecmo initiation?
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My point with the pHTN was that even if there was mild pHTN and perhaps if it was untreated, it would give us an opportunity to treat that and perhaps gain a few points on the saturations.
 
chrisv said:
My point with the pHTN was that even if there was mild pHTN and perhaps if it was untreated, it would give us an opportunity to treat that and perhaps gain a few points on the saturations.
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Maybe. Or, as FFP implied you may create more shunt if you didn't increase ventilation to the lung units perfused by these newly vasodilated vascular beds. Your concern with pHTN is mainly on the R heart, reducing PVR reduces RV afterload and all of the benefits that brings. But throwing pulmonary vasodilators at a severe ARDS pt with V/Q mismatch in the absence of pHTN and R heart dysfunction may in fact worsen your shunt and in doing so decrease your PaO2. Of course, things are rarely as black and white or dichotomous as this and usually you'd have a mix of R heart dysfunction and V/Q mismatch, not to mention the varying degree of vasodilatory response in different vascular beds if you saw response at all.
 
@chrisv, things are rarely crystal clear with ARDS so, when in doubt, just give the Flolan its therapeutic trial. Worst case scenario it won't work, and you waste a couple of hours to get on it and wean it off. And get used to looking at the heart with a TTE; all the Swan will give you is numbers, some to interpret as shapes in coffee (PCWP, CVP), some important (especially in this case) and real, such as the pulmonary arterial pressures and the cardiac output.

Also, when considering increased pulmonary pressures, especially in the context of anesthesia/sedation, don't forget pain/stress and catecholamines as possible causes.
 
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Robotic Wis-Hipple said:
This definitely could've been done in the unit. Use TIVA with TEE for Avalon placement, no need for fluoro (though our surgeons like fluoro as well).

And @chrisv, the pHTN if present is a red herring, if there was true mod-severe pHTN or right heart dysfunction he's getting put on VA (though no good data for VA in ARDS other than a specialty center benefit most likely), and TTE/TEE will only ever underestimate pHTN (unless you really screw up on the simple math part of it). Lastly, as an academic question, how would you manage the ventilation in this patient post-VV ecmo initiation?
Click to expand...


Things that I understand: (please do correct if i'm misunderstood):
VV echo is beneficial in purported Pul HTN from ARDS as the shunt and HPV aspects improve with better oxygenation and normocarbia restoration , improvement in acidosis . Would one trial on VV ecmo before throwing in an additional A cannula to switch it to VA configuration?

Ventilatory strategies: Although no one is proven to be better , overall tenets would be Reduce TV to 3-4 ml/kg, reduce fio2 to about 30-40%, maintain PEEP of 10-15 cm H2o to avoid atelectasis and derecruitemnt , Low RR 10-15/min, keeping Plat <25 cm H20. This is assuming patient has no esophageal pressure monitoring for estimating Transpulmonary pressures (aim to keep TPP between 0-15 )
 
sevodex1 said:
Things that I understand: (please do correct if i'm misunderstood):
VV echo is beneficial in purported Pul HTN from ARDS as the shunt and HPV aspects improve with better oxygenation and normocarbia restoration , improvement in acidosis . Would one trial on VV ecmo before throwing in an additional A cannula to switch it to VA configuration?

Ventilatory strategies: Although no one is proven to be better , overall tenets would be Reduce TV to 3-4 ml/kg, reduce fio2 to about 30-40%, maintain PEEP of 10-15 cm H2o to avoid atelectasis and derecruitemnt , Low RR 10-15/min, keeping Plat <25 cm H20. This is assuming patient has no esophageal pressure monitoring for estimating Transpulmonary pressures (aim to keep TPP between 0-15 )
Click to expand...

You don't need a low RR.
 
Off topic here, but have any of you cats used the new right-sided Impellas yet? We got them maybe a month or so ago but I haven't had occasion to use one yet. Just wondering what pitfalls or pearls anyone may have.

Very glad to have this tool in our toolbox finally.
 
Hawaiian Bruin said:
Off topic here, but have any of you cats used the new right-sided Impellas yet? We got them maybe a month or so ago but I haven't had occasion to use one yet. Just wondering what pitfalls or pearls anyone may have.

Very glad to have this tool in our toolbox finally.
Click to expand...

No but have you had much success with the left sided impellas?
 
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nimbus said:
No but have you had much success with the left sided inpellas?
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Yes. I'm a fan. We've had a few successful salvage scenarios with them, and have used them as a bridge to transplant or bridge to bridge to transplant.
 
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