Bicarb in ketoacidosis

[migm]

I don't personally use bicarb for metabolic acidosis from dka or aka... but the intensivists and culture at my hospital is to do it for just about any acidosis. Thoughts? Case example: Had a pt with AKA with pH 6.9 pCO2 30 something +kussmaul respirations.. I pushed D5LR as she had a metabolic and respiratory acidosis I didn't feel comfortable giving bicarb. Obviously when she arrived to the ICU it was immediately given without a second thought.

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[TheSingularity]

Could be wrong but I think literature supports bicarb drip for pH less than 7?

I don't personally use bicarb for metabolic acidosis from dka or aka... but the intensivists and culture at my hospital is to do it for just about any acidosis. Thoughts? Case example: Had a pt with AKA with pH 6.9 pCO2 30 something +kussmaul respirations.. I pushed D5LR as she had a metabolic and respiratory acidosis I didn't feel comfortable giving bicarb. Obviously when she arrived to the ICU it was immediately given without a second thought.

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[migm]

Could be wrong but I think literature supports bicarb drip for pH less than 7?

the expert level recommendation without any good evidence suggests bicarb for pH <6.9 (ADA). There are no good studies suggesting this actually does anything patient oriented and there is a significant chance of harm imo.

 

[TheSingularity]

For my own education the harms are:

1) hypokalemia
2) worsening acidosis if the patient cannot keep up sufficient respiratory rate to breathe off the resultant CO2

What else?

the expert level recommendation without any good evidence suggests bicarb for pH QUOTE]

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[TheSingularity]

EM has a pretty active FOAM community that's able to dispell a lot of commonly practiced dogmas. Unfortunately most of our colleagues haven't opened a book in ten years

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[migm]

No patient care oriented outcomes showing improvement in mortality, length of stay, insulin requirement or hemodynamic stability with bicarb. additionally, paradoxical CSF acidosis, possible cerebral edema (kids), lack of benefit for anyone with pH >7 so they changed to 6.9 because there's no great data at that point

edit: i am not talking about the crashing DKA pt who is peri-arrest because their heart is not tolerating a pH 6.9. I'm talking about someone who was sick but talking to me holding their own and was going to improve with the usual regimen without what I suspect are at least significant risks incurred with bicarb therapy.

 

[Apollyon]

EM has a pretty active FOAM community that's able to dispell a lot of commonly practiced dogmas. Unfortunately most of our colleagues haven't opened a book in ten years

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My whatever and whatever is still in its plastic. That is from 2003.

 

[shookwell]

I don't give bicarb. The ICU is 50/50, some of the newer attendings don't believe in it either but the old school guys will start it as soon as they get the patient.

 

[RustedFox]

I don't give bicarb and regularly endure insults from our ICU staff.

 

[deleted547339]

Could be wrong but I think literature supports bicarb drip for pH less than 7?

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You are wrong. No literature supports its use.

 

[deleted547339]

I don't personally use bicarb for metabolic acidosis from dka or aka... but the intensivists and culture at my hospital is to do it for just about any acidosis. Thoughts? Case example: Had a pt with AKA with pH 6.9 pCO2 30 something +kussmaul respirations.. I pushed D5LR as she had a metabolic and respiratory acidosis I didn't feel comfortable giving bicarb. Obviously when she arrived to the ICU it was immediately given without a second thought.

On behalf of <good> icu doctors everywhere, my apologizes.
That patient needed a dextrose source and probably some thiamine, not hco3-

 

[migm]

yeah thiamine and dextrose is what I did. oh well

 

[DrGasPasser]

I don't personally use bicarb for metabolic acidosis from dka or aka... but the intensivists and culture at my hospital is to do it for just about any acidosis. Thoughts? Case example: Had a pt with AKA with pH 6.9 pCO2 30 something +kussmaul respirations.. I pushed D5LR as she had a metabolic and respiratory acidosis I didn't feel comfortable giving bicarb. Obviously when she arrived to the ICU it was immediately given without a second thought.

I suspect that your intensivists are misapplying the results of the BICAR-ICU trial. This methodologically flawed study provided some evidence that hypertonic bicarbonate infusions may help select patients avoid dialysis (uremic AG acidosis). It should not be applied to every patient with an AG acidosis. Like TimesNewRoman, I would have shut of their ketosis with dextrose plus the traditional mix of vitamins for alcoholics.

Having said that, this patient appears to be sicker than your average bear with AKA based on their exceptionally low pH and incomplete respiratory compensation; patients with AKA usually stay above 7.1. I’d watch’em like a hawk and have a low threshold for intubating them if the mental status began to decline or if it looked like they were starting to fatigue.

 

[DrGasPasser]

yeah thiamine and dextrose is what I did. oh well

Don’t let differences in management strategy make you question your decision making. Medicine is a broad canvas; some paint in pale pastels, others in bold colors. Many of us like to keep it simple and finger paint.

 

[Jabbed]

**Evidence-free zone**

I try to avoid bicarbonate pushes outside of peri-arrest/arrest situations.

If not peri-arrest, I prefer isotonic bicarb blouses (3 amps/150 mEq HCO3 in 1 L sterile water/D5) as it obviates the concerns of worsening intracellular acidosis/hyperkalemia due to hypertonicity of bicarb pushes.

Paul Farkas (EMCrit) has great discussion of this topic. Interesting to note is that it can be totally appropriate in DKA as most times they have an AG and NAG acidosis.

PulmCrit: pH-guided fluid resuscitation & BICAR-ICU

The use of bicarbonate is a source of eternal disagreement. Bicarbonate has a shameful history of being abused in situations where it’s unhelpful (e.g. cardiac arrest). This has impugned its reputation, giving it an aura of ignorance and failure. Consequently, bicarbonate is underutilized in...

emcrit.org

 

[deleted547339]

I suspect that your intensivists are misapplying the results of the BICAR-ICU trial. This methodologically flawed study provided some evidence that hypertonic bicarbonate infusions may help select patients avoid dialysis (uremic AG acidosis). It should not be applied to every patient with an AG acidosis. Like TimesNewRoman, I would have shut of their ketosis with dextrose plus the traditional mix of vitamins for alcoholics.

Having said that, this patient appears to be sicker than your average bear with AKA based on their exceptionally low pH and incomplete respiratory compensation; patients with AKA usually stay above 7.1. I’d watch’em like a hawk and have a low threshold for intubating them if the mental status began to decline or if it looked like they were starting to fatigue.

Nah, dawg. You tube that guy and you’re f’ed. Throw some bipap on and resuscitate.

 

[thegenius]

I don't personally use bicarb for metabolic acidosis from dka or aka... but the intensivists and culture at my hospital is to do it for just about any acidosis. Thoughts? Case example: Had a pt with AKA with pH 6.9 pCO2 30 something +kussmaul respirations.. I pushed D5LR as she had a metabolic and respiratory acidosis I didn't feel comfortable giving bicarb. Obviously when she arrived to the ICU it was immediately given without a second thought.

You are correct but there are some who support (whether there is good evidence or not) using bicarb for severe acidosis like < 7.0 or 6.9.

If there was a bad outcome for that DKA pt of yours and I was called in as an expert witness to review your chart, and you didn't give bicarb but did everything else OK, I would give you a THUMBS UP and say you met standard of care.

I consider doing it for pH 6.9 or less regardless of the cause. You just gotta make sure they can ventilate because that HCO3- will turn right into CO2.

 

[thegenius]

EM has a pretty active FOAM community that's able to dispell a lot of commonly practiced dogmas. Unfortunately most of our colleagues haven't opened a book in ten years

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It's a real problem in all aspects of medicine. I feel like doctors generally stop learning once they finish residency.

 

[thegenius]

No patient care oriented outcomes showing improvement in mortality, length of stay, insulin requirement or hemodynamic stability with bicarb. additionally, paradoxical CSF acidosis, possible cerebral edema (kids), lack of benefit for anyone with pH >7 so they changed to 6.9 because there's no great data at that point

edit: i am not talking about the crashing DKA pt who is peri-arrest because their heart is not tolerating a pH 6.9. I'm talking about someone who was sick but talking to me holding their own and was going to improve with the usual regimen without what I suspect are at least significant risks incurred with bicarb therapy.

Dude we all agree. When I have these patients, I don't start bicarb. If the intensivist of hospitalist asks me to, I say there is no good evidence for it and I won't start it in the ED. There is some grumbling and they start it on the floor.

Whatevs

 

[thegenius]

I suspect that your intensivists are misapplying the results of the BICAR-ICU trial. This methodologically flawed study provided some evidence that hypertonic bicarbonate infusions may help select patients avoid dialysis (uremic AG acidosis). It should not be applied to every patient with an AG acidosis. Like TimesNewRoman, I would have shut of their ketosis with dextrose plus the traditional mix of vitamins for alcoholics.

I suspect the majority of the community ICU doctors practicing more than 7 years couldn't quote anything about that trial, give bicarb because that's what they always do, and move to the next patient in the ICU.

 

[DrGasPasser]

Nah, dawg. You tube that guy and you’re f’ed. Throw some bipap on and resuscitate.

I hear you and I don’t like tubing severe metabolic acidosis and trying to match their minute ventilation. However, some people poop out and force your hand.

 

[thegenius]

I hear you and I don’t like tubing severe metabolic acidosis and trying to match their minute ventilation. However, some people poop out and force your hand.

Sounds like there are a couple of ICU guys on here. Maybe someone can help me understand this more.

Suppose a very sick person is breathing 40 and they have a severe metabolic acidosis and their pH is 7.0. (I'm purposely trying to avoid describing specific pathology here). Their minute ventilation is 'x' L/min

Is there some reason why a ventilator cannot be set (setting RR, PEEP, etc) to achieve the same minute ventilation?

I am fully aware that the process of getting to mechanical ventilation is frought with danger, especially if you plan on paralyzing the patient prior to intubation. That's why, for instance, for severe aspirin overdoses, we give like 5 amps of NaHCO3 right before you tube to buy you some time.

However once you reach steady state...can't a ventilator achieve similar minute ventilations? If not does it have something to do with positive pressure vs negative pressure, how a tidal volume is delivered by the ventilator, etc.

 

[southerndoc]

By the time a book comes out of press, it's pretty much out of date.

Curious what the EMCritter (Scott Weingart) would say about this. He always has some passionate opinions. He may have already commented on it.

 

[Groove]

In general, I don't give bicarb. Occasionally, I will give it for the severe acidotic pt's with pH < 7 and I will freely admit that I'm just treating a number at that point. It's nothing more than difficulty breaking muscle memory from training and lack of any overwhelming evidence to prove that I'm harming the pt though I will readily admit that proving benefit is just as difficult. Here's a few links to related discussions. Our ICU guys seem to give a lot of bicarb. In fact, most ICUs where I've worked seem to give bicarb. Old and young attendings alike. In spite of the paucity of data supporting it's routine use, the habit seems to be alive and well.

Bicarbonate Therapy in Severe Metabolic Acidosis : Journal of the American Society of Nephrology

r diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The...

jasn.asnjournals.org

BICAR-ICU – The Bottom Line

www.thebottomline.org.uk

down with the Bicarb

bicarb is not all bad

 

[Jabbed]

Sounds like there are a couple of ICU guys on here. Maybe someone can help me understand this more.

Suppose a very sick person is breathing 40 and they have a severe metabolic acidosis and their pH is 7.0. (I'm purposely trying to avoid describing specific pathology here). Their minute ventilation is 'x' L/min

Is there some reason why a ventilator cannot be set (setting RR, PEEP, etc) to achieve the same minute ventilation?

I am fully aware that the process of getting to mechanical ventilation is frought with danger, especially if you plan on paralyzing the patient prior to intubation. That's why, for instance, for severe aspirin overdoses, we give like 5 amps of NaHCO3 right before you tube to buy you some time.

However once you reach steady state...can't a ventilator achieve similar minute ventilations? If not does it have something to do with positive pressure vs negative pressure, how a tidal volume is delivered by the ventilator, etc.

Spontaneous ventilation will virtually always exceed mechanical, until they tire out. The resistance of your circuit and ET tube is a hard limit on your flow rate. This is the same reason why you DON'T want to intubate massive hemoptysis unless absolutely necessary.

In the era of "lung protective" ventilation, there's also the issue of buy-in from your institution and RTs on setting TVs of 1200

Regarding RSIng hypotensive, acidotic patients.. Peri-intubation cardiovascular collapse is real, albeit uncommon. Awake fiberoptic is imo, criminally underutilized in the ED setting and significantly safer.

 

[Fox800]

Spontaneous ventilation will virtually always exceed mechanical, until they tire out. The resistance of your circuit and ET tube is a hard limit on your flow rate. This is the same reason why you DON'T want to intubate massive hemoptysis unless absolutely necessary.

In the era of "lung protective" ventilation, there's also the issue of buy-in from your institution and RTs on setting TVs of 1200

Regarding RSIng hypotensive, acidotic patients.. Peri-intubation cardiovascular collapse is real, albeit uncommon. Awake fiberoptic is imo, criminally underutilized in the ED setting and significantly safer.

There's a lot to debate here.

Early intubation of massive hemoptysis is important because you can asphyxiate by filling your lungs with just 300 mL of blood. Waiting until absolutely necessary is, imho, dangerous. Waiting too long means your patient dies. I favor early airway control.

The large minute volumes are driven by the respiratory rate, not a ridiculous tidal volume like 1,200. You use the same lung protective tidal volumes (on the higher end). If your intensivists and RTs can't understand the importance of maintaining minute volume, I can't help you. Obviously we don't take the decision to intubate these people lightly. I have had to prompt multiple RTs to yes, actually set the ventilator rate to 30 until we get the post-intubation blood gas back. Even when I explained this pre-intubation, they still don't want to do it.

 

[deleted547339]

Spontaneous ventilation will virtually always exceed mechanical, until they tire out. The resistance of your circuit and ET tube is a hard limit on your flow rate. This is the same reason why you DON'T want to intubate massive hemoptysis unless absolutely necessary.

In the era of "lung protective" ventilation, there's also the issue of buy-in from your institution and RTs on setting TVs of 1200

Regarding RSIng hypotensive, acidotic patients.. Peri-intubation cardiovascular collapse is real, albeit uncommon. Awake fiberoptic is imo, criminally underutilized in the ED setting and significantly safer.

I respectfully disagree on several points.

You’re obviously right about the increased resistance intrinsic to the ETT being the driving factor for not being able to match a MV of 40 lpm.

I strongly disagree with your statement about hemoptysis. Being a frequent night-time icu doc and cross covering for colleagues patients who decided to wait and watch their hemoptysis, when these things open up, its an S show. Take the airway early, put the bad side down and get IR there now.

I also disagree on awake FOI being “criminally” underutilized in the ED. How many bronchs have you done? Hundreds, right? You know how many most ER docs have done outside of training? 0. I think the push towards this is dangerous. Taking a critically ill patient and doing a rarely performed procedure when you have an equally efficacious one thatyou’re comfortable with, that’s crazy and dangerous. Do a modified RSI and bag the hell out of them. Peri-intubation hypotension is a sign of a bad doctor. Resuscitate and prophylacticly start pressors. It’s not that hard.

Lastly, why do you have quotes around lung protective ventilation. ARDS has a mortality if ~50% in the sickest cohorts and that’s probably the most effective treatment. It’s also been show to decrease progression to ARDS in patients with normal lungs. Are there compelling reasons not to use low tidal volumes and limit your Pplats? Sure. But maybe we should talk about “antibiotics” and “surgery” and “nutrition” while we’re at it.

 

[DrGasPasser]

Sounds like there are a couple of ICU guys on here. Maybe someone can help me understand this more.

Suppose a very sick person is breathing 40 and they have a severe metabolic acidosis and their pH is 7.0. (I'm purposely trying to avoid describing specific pathology here). Their minute ventilation is 'x' L/min

Is there some reason why a ventilator cannot be set (setting RR, PEEP, etc) to achieve the same minute ventilation?

I am fully aware that the process of getting to mechanical ventilation is frought with danger, especially if you plan on paralyzing the patient prior to intubation. That's why, for instance, for severe aspirin overdoses, we give like 5 amps of NaHCO3 right before you tube to buy you some time.

However once you reach steady state...can't a ventilator achieve similar minute ventilations? If not does it have something to do with positive pressure vs negative pressure, how a tidal volume is delivered by the ventilator, etc.

I think that Jabbed, TimesNewRoman, and Fox800 are hitting the nail on the head. The key is preventing your patient’s minute ventilation from falling with pressure support (BiPAP), or at least being atune to it early when it happens. Patients who are starting to fatigue may appear to be breathing fast but the minute ventilation is falling due to shallow tidal volumes resulting in increases VD/VT. While an ABG will give you the numbers when it happens, waiting on a gas is not cool as this is usually very clinically apparent. You can actually see this in patients on BiPAP if you pay attention to the delivered tidal volumes. Those tidal volumes also give you a rough baseline that must be met when transitioning to invasive ventilation. As an aside, an early lessen for me as an intensivist was learning that BiPAP gives you a lot of useful information outside of IPAP and EPAP setting.

The problems come when the patient is not a great candidate for NIPPV due to persistent altered mental status or hemodynamic instability. I personally have a pretty low threshold for intubating those if things are not turning around quick. I also do modified RSI with plenty of bagging during induction; the PreVent trial has shown us this is probably safe in select patients. For me, awake fiber optic intubation takes to long and becomes a cluster in altered or unstable patients.

Once intubated, you will need to pay careful attention to your vent settings and plateau pressures. The concern is dynamic hyperinflation with these faster rates. Patients who do not have time to exhale have a host of problems related to volutrauma. In most patients with severe metabolic acidosis, I’ll start with ACV rate of 30, VT 8-10 cc/kg PBW, PEEP 5, and pretty high flow rates to keep I:E at least 2. However, your mileage may very with these settings. I get a gas within an hour and adjust my VT down a little if we are making progress.

Where you can kill a patient is by putting them on a rate of 20-24 BPM with a 6cc/kg lung protective ventilation strategy in that first hour when their pH is less than 7 (bring down the VT if the plateau pressures are >30 or after your first gas). You really must stay on top of your RT and make them understand the importance.

 

[Siggy]

I don't give bicarb and regularly endure insults from our ICU staff.

I routinely get DKA patients from the ED and any pH <7.3 gets at least one amp of bicarb from the emergency physicians. We're lucky if they even ordered an insulin infusion. ::shrugs::

 

[DrGasPasser]

I routinely get DKA patients from the ED and any pH <7.3 gets at least one amp of bicarb from the emergency physicians. We're lucky if they even ordered an insulin infusion. ::shrugs::

It sounds like your hospital needs to fire the group managing your ED.

 

[alpinism]

I respectfully disagree on several points.

You’re obviously right about the increased resistance intrinsic to the ETT being the driving factor for not being able to match a MV of 40 lpm.

I strongly disagree with your statement about hemoptysis. Being a frequent night-time icu doc and cross covering for colleagues patients who decided to wait and watch their hemoptysis, when these things open up, its an S show. Take the airway early, put the bad side down and get IR there now.

I also disagree on awake FOI being “criminally” underutilized in the ED. How many bronchs have you done? Hundreds, right? You know how many most ER docs have done outside of training? 0. I think the push towards this is dangerous. Taking a critically ill patient and doing a rarely performed procedure when you have an equally efficacious one thatyou’re comfortable with, that’s crazy and dangerous. Do a modified RSI and bag the hell out of them. Peri-intubation hypotension is a sign of a bad doctor. Resuscitate and prophylacticly start pressors. It’s not that hard.

Lastly, why do you have quotes around lung protective ventilation. ARDS has a mortality if ~50% in the sickest cohorts and that’s probably the most effective treatment. It’s also been show to decrease progression to ARDS in patients with normal lungs. Are there compelling reasons not to use low tidal volumes and limit your Pplats? Sure. But maybe we should talk about “antibiotics” and “surgery” and “nutrition” while we’re at it.

Most of the lung protective ventilation studies are garbage and compare 6cc/kg vs 12cc/kg tidal volumes.

 

[Jabbed]

I respectfully disagree on several points.

You’re obviously right about the increased resistance intrinsic to the ETT being the driving factor for not being able to match a MV of 40 lpm.

I strongly disagree with your statement about hemoptysis. Being a frequent night-time icu doc and cross covering for colleagues patients who decided to wait and watch their hemoptysis, when these things open up, its an S show. Take the airway early, put the bad side down and get IR there now.

I also disagree on awake FOI being “criminally” underutilized in the ED. How many bronchs have you done? Hundreds, right? You know how many most ER docs have done outside of training? 0. I think the push towards this is dangerous. Taking a critically ill patient and doing a rarely performed procedure when you have an equally efficacious one thatyou’re comfortable with, that’s crazy and dangerous. Do a modified RSI and bag the hell out of them. Peri-intubation hypotension is a sign of a bad doctor. Resuscitate and prophylacticly start pressors. It’s not that hard.

Lastly, why do you have quotes around lung protective ventilation. ARDS has a mortality if ~50% in the sickest cohorts and that’s probably the most effective treatment. It’s also been show to decrease progression to ARDS in patients with normal lungs. Are there compelling reasons not to use low tidal volumes and limit your Pplats? Sure. But maybe we should talk about “antibiotics” and “surgery” and “nutrition” while we’re at it.

I'll take a step back, I've only had two true massive hemoptysis patients. My thoughts are that it was difficult to localize bleeding on CXR, ET tubes were continually clogged, and that they were able to expectorate significantly more than I could suction.

Re: intubating acidotic patients. They routinely pull >6-8 mL/kg while on BiPAP, until they don't. "Lung protective" is in quotes as I feel that there's more physiologic harm than benefit with low TV ventilation in these patients.

 

[thegenius]

I was simply asking for clarification on why it's difficult for a machine to match a patients minute ventilation. I guess it has everything to do with the tubing and trying to overcome the resistance of that tubing.

Perhaps I'm looking at this naively. If I have a long garden hose and I turn it on and a little bit of water comes out, if I want to overcome the resistance to flow from the hose, I just turn the spigot more. Maybe there is a maximum flow rate of the garden hose. With mechanical ventilation, i guess it sounds like there are theoretical, or perhaps actual, maximums on flow rates through ET tubes and ventilator circuits.

I also though it had something to do with human respiratory mechanics too. For instance I can easily blow out air in my lungs (forcing air out) but if I'm paralyzed and a machine is breathing for me, exhaling is more complicated.

 

[DrGasPasser]

I was simply asking for clarification on why it's difficult for a machine to match a patients minute ventilation. I guess it has everything to do with the tubing and trying to overcome the resistance of that tubing.

Perhaps I'm looking at this naively. If I have a long garden hose and I turn it on and a little bit of water comes out, if I want to overcome the resistance to flow from the hose, I just turn the spigot more. Maybe there is a maximum flow rate of the garden hose. With mechanical ventilation, i guess it sounds like there are theoretical, or perhaps actual, maximums on flow rates through ET tubes and ventilator circuits.

I also though it had something to do with human respiratory mechanics too. For instance I can easily blow out air in my lungs (forcing air out) but if I'm paralyzed and a machine is breathing for me, exhaling is more complicated.

With the caveat that I’m still early in my CCM training, the issue for me is not so much inspiratory flow rates, but sufficient expiration time at very high respiratory rates. While it is true that inspiratory flow governs inspiratory time, you eventually reach a point where there is insufficient time for full exhalation no matter how fast you deliver that breath.

Generally, patients will not initially be paralyzed on controlled mechanical ventilation after intubation. I typically put them on assist controlled with a background rate of 30 with a severe metabolic acidosis. That means that any patient effort that meets a certain threshold that I set will trigger the vent to deliver a full tidal volume breath. Patients (especially with with obstructive lung disease or ARDS) can run into problems when they are triggering the vent to deliver 40 or 50 BPM because they can’t exhale completely before another full tidal volume comes rushing in causing dynamic hyperinflation. Pretty soon the vent is alarming. Fortunately, I’ve not run into that scenario with a severe metabolic acidosis, but my first instinct would be to get the flow rate up and VT down to 6cc/kg to max E time, and then try a period of SIMV if that didn’t work with the understand that I’m giving up ground on work of breathing.

I’m curious to hear how some of the intensivist who are out of fellowship would handle a patient with bad COPD and 7.0/30/80/10.

 

[thegenius]

I wonder if one could set up a vent to "suction" air out of the lungs during exhalation. Air normally leaves the lung as air travels from high pressure to low pressure. What about a vent that also actively "sucks" air out during exhalation? Literally like a vacuum that is on for maybe 0.5 seconds during exhalation. This might help prevent air trapping and deliver consistent TV breaths.

(I bet someone has tried this on animals and it didn't work.)

 

[deleted547339]

Most of the lung protective ventilation studies are garbage and compare 6cc/kg vs 12cc/kg tidal volumes.

Fair. But there’s a lot of retrospective stuff looking at this as well. The lower the TV and driving pressure, the less lung damage. Not that surprising.

 

[deleted547339]

I'll take a step back, I've only had two true massive hemoptysis patients. My thoughts are that it was difficult to localize bleeding on CXR, ET tubes were continually clogged, and that they were able to expectorate significantly more than I could suction.

Re: intubating acidotic patients. They routinely pull >6-8 mL/kg while on BiPAP, until they don't. "Lung protective" is in quotes as I feel that there's more physiologic harm than benefit with low TV ventilation in these patients.

6-8 ml/kg isn’t what I’m talking about. It’s the 12+ ml/kg patient were talking about. And they rarely just stop breathing. Set your alarms appropriately and you’re fine.

 

[thegenius]

I’m curious to hear how some of the intensivist who are out of fellowship would handle a patient with bad COPD and 7.0/30/80/10.

I bet my ICU docs would intubate that patient and start them on a bicarb drip to treat whatever is causing the metabolic acidosis
LMAO

 

[deleted547339]

With the caveat that I’m still early in my CCM training, the issue for me is not so much inspiratory flow rates, but sufficient expiration time at very high respiratory rates. While it is true that inspiratory flow governs inspiratory time, you eventually reach a point where there is insufficient time for full exhalation no matter how fast you deliver that breath.

Generally, patients will not initially be paralyzed on controlled mechanical ventilation after intubation. I typically put them on assist controlled with a background rate of 30 with a severe metabolic acidosis. That means that any patient effort that meets a certain threshold that I set will trigger the vent to deliver a full tidal volume breath. Patients (especially with with obstructive lung disease or ARDS) can run into problems when they are triggering the vent to deliver 40 or 50 BPM because they can’t exhale completely before another full tidal volume comes rushing in causing dynamic hyperinflation. Pretty soon the vent is alarming. Fortunately, I’ve not run into that scenario with a severe metabolic acidosis, but my first instinct would be to get the flow rate up and VT down to 6cc/kg to max E time, and then try a period of SIMV if that didn’t work with the understand that I’m giving up ground on work of breathing.

I’m curious to hear how some of the intensivist who are out of fellowship would handle a patient with bad COPD and 7.0/30/80/10.

First, I’d want to know the anion gap. I’d also say this is likely not a bad COPD’er based on the gas. But let’s assume you did have a bad metabolic acidosis and copd, I’d go heavy bicarb gtt if nagma. If agap, I’d resuscitate like hell and use bipap if mental status isn’t shot. I’d go IPAP of ~20, set min RR ~20, want a MV> 20lpm.

If mental status sucked, would do an RSI and bag aggressively during induction. I’d go TV like 800-1000cc on ACVC, probably start with a RR of 14. Id turn the flows up as high as possible and turn the peak pressure and MV alarms off. I’d stay at bedside. If any dynamic hyperinflation, I’d paralyze. Potentially square wave form. I’d titrate the RR to maximize MV without causing auto-peep.

 

[DrGasPasser]

First, I’d want to know the anion gap. I’d also say this is likely not a bad COPD’er based on the gas. But let’s assume you did have a bad metabolic acidosis and copd, I’d go heavy bicarb gtt if nagma. If agap, I’d resuscitate like hell and use bipap if mental status isn’t shot. I’d go IPAP of ~20, set min RR ~20, want a MV> 20lpm.

If mental status sucked, would do an RSI and bag aggressively during induction. I’d go TV like 800-1000cc on ACVC, probably start with a RR of 14. Id turn the flows up as high as possible and turn the peak pressure and MV alarms off. I’d stay at bedside. If any dynamic hyperinflation, I’d paralyze. Potentially square wave form. I’d titrate the RR to maximize MV without causing auto-peep.

Cool. I think we are not too far apart. You used a lower set RR than me in ACV, but in the end our final rates will be pretty similar after accounting for patient-initiated breaths. Your initial TVs were probably a little more aggressive than my 8-10 ml/kg but not by much.

Thanks for the reply. I learned something and appreciate it.

 

[deleted547339]

Cool. I think we are not too far apart. You used a lower set RR than me in ACV, but in the end our final rates will be pretty similar after accounting for patient-initiated breaths. Your initial TVs were probably a little more aggressive than my 8-10 ml/kg but not by much.

Thanks for the reply. I learned something and appreciate it.

If you have a truly bad COPDer in exacerbation, you probably can’t go much higher and probably won’t even be able to get away with 14-16. I usually start at a RR of like 6-8 if it’s truly bad COPD and tolerate any pH > 7. This is different because you have to do something to compensate for the metabolic component.

 

[DrGasPasser]

If you have a truly bad COPDer in exacerbation, you probably can’t go much higher and probably won’t even be able to get away with 14-16. I usually start at a RR of like 6-8 if it’s truly bad COPD and tolerate any pH > 7. This is different because you have to do something to compensate for the metabolic component.

By COPDer, I was thinking along the lines of someone who was prone to auto PEEP at higher RR and not adequately compensating for their primary metabolic acidosis. Sorry, I should have been more specific that I wasn’t referring to a severe exacerbation.

I gew up in EM mostly using AC ventilation and it is used almost exclusively in our MICU. However, our surgeons use a lot of SIMV in the surgical ICUs. Thus, I’m still feeling out when to use various modes in different patient populations that goes beyond simply what floor of the hospital they happen to be on.

 

[deleted547339]

However, our surgeons use a lot of SIMV in the surgical ICUs.

I know they’re surgeons, but they can read, right?