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Nephro critical care said:
I had a guy on APRV pulling TV 358. Started becoming hypercarbic pH 7.1, pCO2 100. I tried PC RR 28 I:E 1:2. He immediately desated to 80%. How would you play with APRV to ensure better ventilation ?
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FFP said:
Decrease sedation to allow better spontaneous breathing, increase P-high, increase T-low. (I'm not an APRV expert.)
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Initial settings for me will often be 30/0 with a release rate of 16-18, tL of 0.8 tweaked to match reinflation when you hit 75% of the PEF. Similar to Hibashi's recs from Maryland.

Unfortunately with APRV anything you do to increase your VE is going to decrease your oxygenation benefit (other than increasing your Phigh)

Depending on your patients physiology, if you're dealing with ok compliance and you're not as worried about losing recruitment then increasing your TLow should be ok, would be hesitant to go past 65% of your PEF (disclaimer: arbitrary number)

Also not an expert on APRV, used by a variety of colleagues in my shop so have gotten used to troubleshooting
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Nephro critical care said:
I had a guy on APRV pulling TV 358. Started becoming hypercarbic pH 7.1, pCO2 100. I tried PC RR 28 I:E 1:2. He immediately desated to 80%. How would you play with APRV to ensure better ventilation ?
Click to expand...

Decrease the T-high first. This is like increasing the respiratory rate. If they are doing any spontaneous breathing increase their pressure support. If they are paralyzed stop it. If they are very sedated, lighten it.

I've had a few folks do fine totally awake on APRV - though these were people with the normal lung compliance hypoxia
 
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MoMoGesiologist said:
If u r paralyzing on APRV, I don’t think you are doing it right...
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People use "APRV" interchangeably with "bilevel" and to mean "bilevel" all the time, but yes, the whole point of the actual vent mode APRV is that patient spontaneously breath and it sounds fantastic on paper. The big problem with it is there is no good way to determine plateau pressures or transpulmonary pressures in a way that is arguably accurate, which is one reason I sort of despise its use in "normal" ARDS. But I wont tell you I haven't used it in ARDS (with crpapy compliance) anyway, because, I have, as the big good thing about it is the increase in mean airway pressures and glorious beautiful SpO2 you almost always get with it. It's a nice enough mode for COVID19. At least the normal lung compliance hypoxemics. But then . . . why even use APRV when they really seem to need the PEEP. Just healthy CPAP and PS, especially if awake.
 
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For some reason, our RTs freak out when you ask for PSV: “but the pt is gonna get tired!”

Wtf. You breathe every single second of every single day of your life. Y would u get tired putting in some effort into your breathing? Then they try to tell me pt is on “VC+” or some other fancy vent mode and the vent is working them out and tbh I just kinda stop listening...
 
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MoMoGesiologist said:
For some reason, our RTs freak out when you ask for PSV: “but the pt is gonna get tired!”

Wtf. You breathe every single second of every single day of your life. Y would u get tired putting in some effort into your breathing? Then they try to tell me pt is on “VC+” or some other fancy vent mode and the vent is working them out and tbh I just kinda stop listening...
Click to expand...

Not all RT's are created equal. Sounds like you may work with a few chuckleheads. My RT's would never say something so stupid. I work with a great group.
 
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jdh71 said:
People use "APRV" interchangeably with "bilevel" and to mean "bilevel" all the time, but yes, the whole point of the actual vent mode APRV is that patient spontaneously breath and it sounds fantastic on paper. The big problem with it is there is no good way to determine plateau pressures or transpulmonary pressures in a way that is arguably accurate, which is one reason I sort of despise its use in "normal" ARDS. But I wont tell you I haven't used it in ARDS (with crpapy compliance) anyway, because, I have, as the big good thing about it is the increase in mean airway pressures and glorious beautiful SpO2 you almost always get with it. It's a nice enough mode for COVID19. At least the normal lung compliance hypoxemics. But then . . . why even use APRV when they really seem to need the PEEP. Just healthy CPAP and PS, especially if awake.
Click to expand...

Two questions:
1) Why do you care about the plateau pressure if you're using APRV. As long as you keep the Phigh </= 30 shouldn't you be good?
2) Isn't part of the value of aprv in poorly compliant lungs the fact that Tlow can be so short, b/c there is rapid expiration?

For the low elastance covid patients, I would cpap is as good as aprv...
 
turkeyjerky said:
Two questions:
1) Why do you care about the plateau pressure if you're using APRV. As long as you keep the Phigh </= 30 shouldn't you be good?
2) Isn't part of the value of aprv in poorly compliant lungs the fact that Tlow can be so short, b/c there is rapid expiration?

For the low elastance covid patients, I would cpap is as good as aprv...
Click to expand...

1) In APRV the patient breathes spontaneously over the high pressure. You can know what the peak pressure is during those breathes but you have no idea what the plateau is. None. You can drop an esophageal balloon and get a sense of transpulmonary pressure enough that you feel ok enough with it all but that wasn’t what was studied or described in ARDSnet. Without a plateau pressure you also can’t come any conclusion about driving pressure and that may be where the real devil is in the ARDS details.

2) I’m not sure I understand your second question because uniformly regardless of your prior conventional vent settings APRV is going to worsening your effective minute ventilation and decrease more normal CO2 exchange and worse hypercapnia and resp acidosis. It’s basically like an inverse ratio A/C mode. The lungs being stiff don’t really make much difference here. You hope the release gives you enough ventilation to keep your hypercapnia to tolerable levels.
 
jdh71 said:
1) In APRV the patient breathes spontaneously over the high pressure. You can know what the peak pressure is during those breathes but you have no idea what the plateau is. None. You can drop an esophageal balloon and get a sense of transpulmonary pressure enough that you feel ok enough with it all but that wasn’t what was studied or described in ARDSnet. Without a plateau pressure you also can’t come any conclusion about driving pressure and that may be where the real devil is in the ARDS details.

2) I’m not sure I understand your second question because uniformly regardless of your prior conventional vent settings APRV is going to worsening your effective minute ventilation and decrease more normal CO2 exchange and worse hypercapnia and resp acidosis. It’s basically like an inverse ratio A/C mode. The lungs being stiff don’t really make much difference here. You hope the release gives you enough ventilation to keep your hypercapnia to tolerable levels.
Click to expand...

Thanks for the reply. During the spont breaths, isn't the pressure always lower than the set Phigh (I guess unless you have PS added...)?

With my second question, I was responding to your note 'It's a nice enough mode for COVID19. At least the normal lung compliance hypoxemics. But then . . . why even use APRV when they really seem to need the PEEP. '
 
turkeyjerky said:
Thanks for the reply. During the spont breaths, isn't the pressure always lower than the set Phigh (I guess unless you have PS added...)?

With my second question, I was responding to your note 'It's a nice enough mode for COVID19. At least the normal lung compliance hypoxemics. But then . . . why even use APRV when they really seem to need the PEEP. '
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Well. I guess if you don’t have any pressure added then the negative thoracic pressure of the spontaneous breaths would mean that whatever plateau was present would be less than 30cmh2o. But patients with sick lungs don’t get good breaths then at 0 of pressure support and then they HATE APRV. The only way to make them “like” it is to sedate them highly or paralyze them but then it’s not really APRV any longer and just bilevel.

You use APRV or as I like to CPAP/PS in the Covid19 folks with good mechanics because 1) patients seems to like it and 2) your “A/C types of usual modes” will be causing high shifts in the differences between pressures which is much more pro inflammatory. There is a difference between keeping the lung open with spontaneous breaths (+/- some PS) and using high prep plus a dialed in volume at 6cc/kg.
 
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jdh71 said:
Well. I guess if you don’t have any pressure added then the negative thoracic pressure of the spontaneous breaths would mean that whatever plateau was present would be less than 30cmh2o. But patients with sick lungs don’t get good breaths then at 0 of pressure support and then they HATE APRV. The only way to make them “like” it is to sedate them highly or paralyze them but then it’s not really APRV any longer and just bilevel.

You use APRV or as I like to CPAP/PS in the Covid19 folks with good mechanics because 1) patients seems to like it and 2) your “A/C types of usual modes” will be causing high shifts in the differences between pressures which is much more pro inflammatory. There is a difference between keeping the lung open with spontaneous breaths (+/- some PS) and using high prep plus a dialed in volume at 6cc/kg.
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gotcah, I think we're on the same page.
 
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I'm sure you guys have all seen this JAMA review of hospitalized patients in NY (Clinical Characteristics, Comorbidities, and Outcomes Among Patients With COVID-19 Hospitalized in the NYC Area).

One thing that's striking to me is that out of all the hospitalized patients in NYC who were discharged/deceased, only 9 of those under the age of 50 with Charlson index of 0 died. This gives us a mortality of 2% for hospitalized patients in that group, and a CFR that is probably 20-50x less.

Does this match up with what you guys are seeing? I remember several ICU docs and nurses initially reporting that they had a flux of young healthy patients who were being tubed/died, but this doesn't appear to be true. Granted, the limitation is that maybe there are a bunch of them whose outcomes could not be reported because they are surviving longer on the vent.
 
teacher2md said:
I'm sure you guys have all seen this JAMA review of hospitalized patients in NY (Clinical Characteristics, Comorbidities, and Outcomes Among Patients With COVID-19 Hospitalized in the NYC Area).

One thing that's striking to me is that out of all the hospitalized patients in NYC who were discharged/deceased, only 9 of those under the age of 50 with Charlson index of 0 died. This gives us a mortality of 2% for hospitalized patients in that group, and a CFR that is probably 20-50x less.

Does this match up with what you guys are seeing? I remember several ICU docs and nurses initially reporting that they had a flux of young healthy patients who were being tubed/died, but this doesn't appear to be true. Granted, the limitation is that maybe there are a bunch of them whose outcomes could not be reported because they are surviving longer on the vent.
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everyone has those stories of young and sick because they stand out more. It’s the shark attack phenomenon a few years ago where it was all in the news but turns out attacks were actually down. in my current experience it’s been the under 50 that have made it off a vent and home predictably enough. It’s The the older than 65 who die or who have been on the vent for like three weeks. If you are diabetic or obese between those age groups your course is more like the older folks and if otherwise you are in pretty decent shape shape you will usual recover albeit slower assuming you don’t have a secondary complication like big PE, renal failure, and or acute cardiomyopathy.

Interestingly enough I’ve not yet seen a bronchospastic asthmatic with this virus.

My anecdotes.
 
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We've had our fair share of 65+ who've died, many due to prolonged course and family withdrawal. The younger one's I've been involved with (35-60ish) have done fairly well, two gentlemen in their 50s who started circling that we just couldn't stabilize (one with sig LV dysfunction, other refractory hypoxemia).

Wife's colleague in the ED, 37yo asthmatic ended up tubed for a couple days, seems to have bounced back fairly well, will see if there's any longer term sequelae.

Noticing a strong correlation of an excess of knuckle tattoos and poor outcomes, considering writing up a case series...
 
chocomorsel said:
What comorbidities did the 20's year old have?
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I had a 22 year old with asthma but no bronchospasm. And a 27 year old with obesity. Both made it though. But both were sick AF for a minute or two. Got both through it with CPAP and in the case of the obese some intermittent prone positioning.
 
jdh71 said:
I had a 22 year old with asthma but no bronchospasm. And a 27 year old with obesity. Both made it though. But both were sick AF for a minute or two. Got both through it with CPAP and in the case of the obese some intermittent prone positioning.
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I was wondering about the one that died.
 
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emcrit.org

PulmCrit- First placebo-controlled RCT on remdesivir for COVID-19

Remdesivir is being promoted as an anti-viral agent for the treatment of COVID-19. The first randomized, blinded, placebo-controlled trial of
emcrit.org emcrit.org
  • Wang et al. is the first placebo-controlled, double-blinded, multi-center RCT of remdesivir. The study was stopped early due to poor recruitment after including 237 patients, but otherwise appears well designed.
  • Remdesivir had no effect on any clinical or biological endpoint (including viral load).
  • Lack of an observable effect could theoretically relate to delayed administration of remdesivir or underpowering of the study. However, this is a thoroughly neutral study that shouldn’t be mischaracterized as showing promise.
  • Further RCTs will clarify what role remdesivir has in COVID-19, if any. This study suggests that remdesivir probably doesn’t confer major clinical benefits.
 
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FFP said:
Translation, please.
Click to expand...

Basically I’m not convinced the blunt instrument of ARDSnet style ventilation or even prone positioning in every patient with COVID19 meeting Berlin criteria is the right thing to do. I think it’s the thoughtless thing to do in too many cases, and worsening inflammation in the lungs unnecessarily in too many cases. What cases inflammation in ARDS? Or even with mechanical ventilation? Barotrauma? Volutrauma? Atelectrauma? Increased driving pressure? It all does. Proven in pigs many many many times in fellowship. We need to approach these patients, especially in the context of the dreaded “cytokines storm” but using strategies when possible to decrease . . . CYTOKINE production. When you have patients that definitely have the stiff lungs we usually see in “classic” ARDS, you need to use what has the best scientific backing. But to insist that the patients who have a different phenotypic presentation of disease and only really need strategies to increase their mean airway pressures +/- additional FiO2 not applying the same blunt instrument. It’s crazy making to me and shows a lack of curiosity, physiologic thinking, and fear leading to potentially hiding behind wrong strategies.
 
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jdh71 said:
Basically I’m not convinced the blunt instrument of ARDSnet style ventilation or even prone positioning in every patient with COVID19 meeting Berlin criteria is the right thing to do. I think it’s the thoughtless thing to do in too many cases, and worsening inflammation in the lungs unnecessarily in too many cases. What cases inflammation in ARDS? Or even with mechanical ventilation? Barotrauma? Volutrauma? Atelectrauma? Increased driving pressure? It all does. Proven in pigs many many many times in fellowship. We need to approach these patients, especially in the context of the dreaded “cytokines storm” but using strategies when possible to decrease . . . CYTOKINE production. When you have patients that definitely have the stiff lungs we usually see in “classic” ARDS, you need to use what has the best scientific backing. But to insist that the patients who have a different phenotypic presentation of disease and only really need strategies to increase their mean airway pressures +/- additional FiO2 not applying the same blunt instrument. It’s crazy making to me and shows a lack of curiosity, physiologic thinking, and fear leading to potentially hiding behind wrong strategies.
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It seems that the main therapeutic mechanism here may have been lung recruitment (almost all patients increased their P/F ratios significantly in the first 24 hours).

I am with you when about individualizing treatment. My feeling is that Farkas was bothered by the high tidal volumes recommended by Gatinoni (7-9 ml/kg) with a low PEEP (under 10), and he's arguing against those, especially since he's not convinced that the high-compliance phenotype actually exists.

What has your experience been?

Boston must have been doing something right, because their mortality was only 16.7%, which is amazing to me. They discharged from the ICU 75% of the patients, 62% extubated (the rest with trach, I assume).

Btw, this is what Gatinoni thinks (for those of us who don't want to dig through this saga):
ccforum.biomedcentral.com

COVID-19 pneumonia: ARDS or not? - Critical Care

ccforum.biomedcentral.com ccforum.biomedcentral.com
jamanetwork.com

Ventilator Management of Patients With COVID-19

This JAMA Insights Clinical Update discusses the pathophysiology of SARS-CoV-2–related respiratory failure, distinguishing unique L and H phenotypes and their implications for ventilator strategies and settings.
jamanetwork.com jamanetwork.com
 
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FFP said:
It seems that the main therapeutic mechanism here may have been lung recruitment (almost all patients increased their P/F ratios significantly in the first 24 hours).

I am with you when about individualizing treatment. My feeling is that Farkas was bothered by the high tidal volumes recommended by Gatinoni (7-9 ml/kg) with a low PEEP (under 10), and he's arguing against those, especially since he's not convinced that the high-compliance phenotype actually exists.

What has your experience been?

Boston must have been doing something right, because their mortality was only 16.7%, which is amazing to me. They discharged from the ICU 75% of the patients, 62% extubated (the rest with trach, I assume).

Btw, this is what Gatinoni thinks (for those of us who don't want to dig through this saga):
ccforum.biomedcentral.com

COVID-19 pneumonia: ARDS or not? - Critical Care

ccforum.biomedcentral.com ccforum.biomedcentral.com
jamanetwork.com

Ventilator Management of Patients With COVID-19

This JAMA Insights Clinical Update discusses the pathophysiology of SARS-CoV-2–related respiratory failure, distinguishing unique L and H phenotypes and their implications for ventilator strategies and settings.
jamanetwork.com jamanetwork.com
Click to expand...

Gatinoni is a lightning rod at the best of times. And all these top vent guys love to hate each other’s asses. But that isn’t the point. Just kind of amusing.

Anyway, I won’t pretend Ive seen 100s. Our group has taken care of around 30. We have had a weekly meeting to discuss what seems to work and what doesn’t. Current cases have dropped to very low. And we’ve gotten most people off a vent. Though while I haven’t crunched numbers I think our mortality rate is probably closer to 20-25%. Though until you really crunch the data I’m not convinced it’s because we’ve done anything “wrong” per se. it’s just a hell of a disease. Anyway we treat those clearly with classic ards physiology with ARDSnet settings. We aren’t recreating the wheel here and these folks do seem to obviously have the sicker lungs. Those who only seem to need CPAP (or PEEP) to recruit and increase mean airway pressure seem to do really well and I think we’ve extubated all of these folks.
 
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Multiple interesting thoughts in that series, not just about ARDS:
litfl.com

Is COVID-19 ARDS? What about lung compliance?

Part 3 of the "COVID-19: Keeping the baby in the bath" series discussing whether COVID-19 is part of acute respiratory distress syndrome (ARDS) and the importance of lung compliance.
litfl.com litfl.com
 
MoMoGesiologist said:
For some reason, our RTs freak out when you ask for PSV: “but the pt is gonna get tired!”

Wtf. You breathe every single second of every single day of your life. Y would u get tired putting in some effort into your breathing? Then they try to tell me pt is on “VC+” or some other fancy vent mode and the vent is working them out and tbh I just kinda stop listening...
Click to expand...
To counter your point, you don't normally breathe every single day of your life with an abnormally high respiratory load coupled likely with worse respiratory muscle function (due to critical illness neuropathy/myopathy etc). Or are you arguing there's no role for pressure controlled assist-control ventilation in spontaneously breathing patients?
 
leviathan said:
To counter your point, you don't normally breathe every single day of your life with an abnormally high respiratory load coupled likely with worse respiratory muscle function (due to critical illness neuropathy/myopathy etc). Or are you arguing there's no role for pressure controlled assist-control ventilation in spontaneously breathing patients?
Click to expand...
Agreed. But we do not “rest” a kidney with dialysis, for example to improve AKI. We try to use the GI tract if we can and it helps prevent enterocyte decay. We give pts PT/OT so they aren’t a limp noodle by the end of their hospital stay. Same way we should engage and exercise the lungs with PSV rather than 100% vent support to prevent diaphragm atrophy.

Quick google search:
PSV leads to less diaphragm atrophy: Mechanical Ventilation and Diaphragmatic Atrophy in Critically Ill Patients: An Ultrasound Study. - PubMed - NCBI
Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study
 
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The beauty of having them attached to a vent is, when they get tired and start struggling you put them back on a controlled mode. In the meantime, they exercise their diaphragm.
 
If you leave a patient only partially supported until the point of diaphragmatic failure, it takes days for muscle function to recover and will set back your weaning process.
diaphragm.jpg


This may be partially why RCTs support that daily SBTs are better than PSV weaning (or there may be other reasons that we can all guess as to why, e.g. if you have RTs that only adjust PSV settings once a shift and under-recognize readiness for extubation).

However I agree if a patient can continue on PSV and use their diaphragm, they will have less atrophy. There is a balance you have to strike for sure..
 
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leviathan said:
If you leave a patient only partially supported until the point of diaphragmatic failure, it takes days for muscle function to recover and will set back your weaning process.
View attachment 306313

This may be partially why RCTs support that daily SBTs are better than PSV weaning (or there may be other reasons that we can all guess as to why, e.g. if you have RTs that only adjust PSV settings once a shift and under-recognize readiness for extubation).

However I agree if a patient can continue on PSV and use their diaphragm, they will have less atrophy. There is a balance you have to strike for sure..
Click to expand...
Yup, agree. My pet peeve is RTs who place pts on their SBT for only a couple minutes then flip back to full support without trying to go up on PSV or adjust sedation or telling an MD pt is failing so we can figure out what to optimize. They then get a shocked face when I ask for another SBT later in the day, like it’s sacrilege to make more than one vent change a day.
 
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MoMoGesiologist said:
Yup, agree. My pet peeve is RTs who place pts on their SBT for only a couple minutes then flip back to full support without trying to go up on PSV or adjust sedation or telling an MD pt is failing so we can figure out what to optimize. They then get a shocked face when I ask for another SBT later in the day, like it’s sacrilege to make more than one vent change a day.
Click to expand...

You have ****ty RTs.
 
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MoMoGesiologist said:
Yup, agree. My pet peeve is RTs who place pts on their SBT for only a couple minutes then flip back to full support without trying to go up on PSV or adjust sedation or telling an MD pt is failing so we can figure out what to optimize. They then get a shocked face when I ask for another SBT later in the day, like it’s sacrilege to make more than one vent change a day.
Click to expand...
Also my pet peeve hahaa.
 
jdh71 said:
I wonder if the Vet C was high enough for the cramping and osmotic diarrhea you can get taking too much oral vit C
Click to expand...
Didn't know this. Interesting.
One of our pharmacists asked me to D/C the IV Vit C because the patient had been on it for weeks and wasn't improving. No surprise there, it is Covid. However, she told me each bag was hundreds of dollars and this patient was receiving it Q8. I promptly complied. What a waste of money.
 
chocomorsel said:
Didn't know this. Interesting.
One of our pharmacists asked me to D/C the IV Vit C because the patient had been on it for weeks and wasn't improving. No surprise there, it is Covid. However, she told me each bag was hundreds of dollars and this patient was receiving it Q8. I promptly complied. What a waste of money.
Click to expand...
How is IV vitamins hundreds of dollars!?
 
MoMoGesiologist said:
How is IV vitamins hundreds of dollars!?
Click to expand...
Same reason insulin and Eli is hundreds of dollars. I don’t know. I doubt she was lying.
Probably because there is not a bunch of it laying around and companies were probably not making a bunch of it and then Covid came and demand shot up.
I don’t know.
When was the last time you ordered some IV Vitamin C?
 
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