Case Scenario - Severe COPD

[k12balla]

First time poster, CA-2, would greatly appreciate your insight as to how you would've managed this patient, and the situation....

I walk into a room at 8pm to take over for an AA, 2 hours into a 4 hour corneal transplant. As I walk in, I notice her aggressively manually bagging the pt...I take a quick glimpse of my surroundings as I was trained to do: TV 125, ETCO2 68, Fio2 30% O2 Sat 86%...MAP 55, on low dose phenylephrine gtt through sole peripheral 20g. She sighs in relief to see me...I ask why she is bagging the patient, and why she is not on 100% Fio2...she says because the attending told her to do these things. Then I realize the attending is notorious for doing things "European Style" or in his own manner, which sometimes go against common practice and rationalization. As shes fumbling with checkout, I take a peek at the chart.

65 yo AA lady, 80 kg, uncontrolled HTN, uncontrolled DM, b/l LE neuropathy, uncontrolled GERD, Severe COPD with FEV <20%. I then note that the patient has an LMA in. The attending then walks into the room, and I ask if he would like an ABG, ART line, 2nd IV given our situation. He tells me I would be "too afraid" of the values from and ABG, and brushes off my suggestions. He says he's ok with a MAP above 50-55, and would like the pt to breather manually with a CPAP of 15. So the patient goes on manual mode, and they leave. For the next 30 mins, the patients TV are 150, CO2 creeps up to 78, saturating 92%. I figure I cannot stand back any longer and place the patient on pressure mode, peak 15, TV 300, CO2 65. Later on my attending finds out about this, and labels me as insubordinate and a trouble maker since I went against his wishes....Pt back on Manual mode, for duration of case. Extubate with CO2 78, RR 10, TV 150...

She received 1 gm of IV OFIRMEV (tylenol) for the case. NO opiods...She comes to the PACU, delirious, screaming in pain, muttering nonsense. Attending order 4 mg of Haldol which quiets her down...

A few days later I get more slack from this attending for my utter disregard for his authority, however, at some point patient care should take priority over fear of repercussions. So I ask you, how would you have managed this patient, or the situation in which you feel doing the right thing in your mind might get you in trouble? Thanks in advance!

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[militarymd]

What's an abg going to tell you?

 

[RxBoy]

First time poster, CA-2, would greatly appreciate your insight as to how you would've managed this patient, and the situation....

65 yo AA lady, 80 kg, uncontrolled HTN, uncontrolled DM, b/l LE neuropathy, uncontrolled GERD, Severe COPD with FEV <20%. I then note that the patient has an LMA in. The attending then walks into the room, and I ask if he would like an ABG, ART line, 2nd IV given our situation. He tells me I would be "too afraid" of the values from and ABG, and brushes off my suggestions. He says he's ok with a MAP above 50-55, and would like the pt to breather manually with a CPAP of 15. So the patient goes on manual mode, and they leave. For the next 30 mins, the patients TV are 150, CO2 creeps up to 78, saturating 92%. I figure I cannot stand back any longer and place the patient on pressure mode, peak 15, TV 300, CO2 65. Later on my attending finds out about this, and labels me as insubordinate and a trouble maker since I went against his wishes....Pt back on Manual mode, for duration of case. Extubate with CO2 78, RR 10, TV 150...

Severe COPD'ers live with chronic hypoxia/hypercarbia. Im guessing the attending didnt want the patient to lose their "hypoxic drive" with a high FiO2 (reality is lose a balanced V/Q by letting HPV go unregulated resulting in increased shunt to heavily diseased alveoli). What they did was not optimal but it works. However, I would titrate the FiO2 to SaO2>88% and leave CPAP to 5 max. At 15, diseased lungs will not be able to recoil strong enough against the positive pressure during expiration leading to smaller TVs and increased hypercarbia.

"Uncontrolled GERD" is usually an indication for tube. But if pt denies regurg while laying flat, I would of went with a LMA too. The reason is in my opinion PPV carries a greater risk for this patient. No idea what the cxray looks like but these are the people who end up with a PTX from massive blebs/bullae. Not to mention the increased post op pulm dysfunction with PPV and risk of vent autopeeping. ABG would be worthless if you didn't have a baseline ABG.

Phenylephrine drip is a total CRNA move. But thats another discussion in itself. Thanks for the post, and just so you know I am not defending your attending. Just didn't think they were totally wrong.

 

[Idiopathic]

Severe COPD'ers live with chronic hypoxia/hypercarbia. Im guessing the attending didnt want the patient to lose their "hypoxic drive" with a high FiO2 (reality is lose a balanced V/Q by letting HPV go unregulated resulting in increased shunt to heavily diseased alveoli). What they did was not optimal but it works. However, I would titrate the FiO2 to SaO2>88% and leave CPAP to 5 max. At 15, diseased lungs will not be able to recoil strong enough against the positive pressure during expiration leading to smaller TVs and increased hypercarbia.

"Uncontrolled GERD" is usually an indication for tube. But if pt denies regurg while laying flat, I would of went with a LMA too. The reason is in my opinion PPV carries a greater risk for this patient. No idea what the cxray looks like but these are the people who end up with a PTX from massive blebs/bullae. Not to mention the increased post op pulm dysfunction with PPV and risk of vent autopeeping. ABG would be worthless if you didn't have a baseline ABG.

Phenylephrine drip is a total CRNA move. But thats another discussion in itself. Thanks for the post, and just so you know I am not defending your attending. Just didn't think they were totally wrong.

could have put a tube in and maintained spontaneous ventilation, protecting from that nasty uncontrolled gerd

 

[jennyboo]

First time poster, CA-2, would greatly appreciate your insight as to how you would've managed this patient, and the situation....

I walk into a room at 8pm to take over for an AA, 2 hours into a 4 hour corneal transplant. As I walk in, I notice her aggressively manually bagging the pt...I take a quick glimpse of my surroundings as I was trained to do: TV 125, ETCO2 68, Fio2 30% O2 Sat 86%...MAP 55, on low dose phenylephrine gtt through sole peripheral 20g. She sighs in relief to see me...I ask why she is bagging the patient, and why she is not on 100% Fio2...she says because the attending told her to do these things. Then I realize the attending is notorious for doing things "European Style" or in his own manner, which sometimes go against common practice and rationalization. As shes fumbling with checkout, I take a peek at the chart.

65 yo AA lady, 80 kg, uncontrolled HTN, uncontrolled DM, b/l LE neuropathy, uncontrolled GERD, Severe COPD with FEV <20%. I then note that the patient has an LMA in. The attending then walks into the room, and I ask if he would like an ABG, ART line, 2nd IV given our situation. He tells me I would be "too afraid" of the values from and ABG, and brushes off my suggestions. He says he's ok with a MAP above 50-55, and would like the pt to breather manually with a CPAP of 15. So the patient goes on manual mode, and they leave. For the next 30 mins, the patients TV are 150, CO2 creeps up to 78, saturating 92%. I figure I cannot stand back any longer and place the patient on pressure mode, peak 15, TV 300, CO2 65. Later on my attending finds out about this, and labels me as insubordinate and a trouble maker since I went against his wishes....Pt back on Manual mode, for duration of case. Extubate with CO2 78, RR 10, TV 150...

She received 1 gm of IV OFIRMEV (tylenol) for the case. NO opiods...She comes to the PACU, delirious, screaming in pain, muttering nonsense. Attending order 4 mg of Haldol which quiets her down...

A few days later I get more slack from this attending for my utter disregard for his authority, however, at some point patient care should take priority over fear of repercussions. So I ask you, how would you have managed this patient, or the situation in which you feel doing the right thing in your mind might get you in trouble? Thanks in advance!

Something's wrong.... this description does not sound like you understand what was happening on multiple levels.

 

[cincincyreds]

First time poster, CA-2, would greatly appreciate your insight as to how you would've managed this patient, and the situation....

I walk into a room at 8pm to take over for an AA, 2 hours into a 4 hour corneal transplant. As I walk in, I notice her aggressively manually bagging the pt...I take a quick glimpse of my surroundings as I was trained to do: TV 125, ETCO2 68, Fio2 30% O2 Sat 86%...MAP 55, on low dose phenylephrine gtt through sole peripheral 20g. She sighs in relief to see me...I ask why she is bagging the patient, and why she is not on 100% Fio2...she says because the attending told her to do these things. Then I realize the attending is notorious for doing things "European Style" or in his own manner, which sometimes go against common practice and rationalization. As shes fumbling with checkout, I take a peek at the chart.

65 yo AA lady, 80 kg, uncontrolled HTN, uncontrolled DM, b/l LE neuropathy, uncontrolled GERD, Severe COPD with FEV <20%. I then note that the patient has an LMA in. The attending then walks into the room, and I ask if he would like an ABG, ART line, 2nd IV given our situation. He tells me I would be "too afraid" of the values from and ABG, and brushes off my suggestions. He says he's ok with a MAP above 50-55, and would like the pt to breather manually with a CPAP of 15. So the patient goes on manual mode, and they leave. For the next 30 mins, the patients TV are 150, CO2 creeps up to 78, saturating 92%. I figure I cannot stand back any longer and place the patient on pressure mode, peak 15, TV 300, CO2 65. Later on my attending finds out about this, and labels me as insubordinate and a trouble maker since I went against his wishes....Pt back on Manual mode, for duration of case. Extubate with CO2 78, RR 10, TV 150...

She received 1 gm of IV OFIRMEV (tylenol) for the case. NO opiods...She comes to the PACU, delirious, screaming in pain, muttering nonsense. Attending order 4 mg of Haldol which quiets her down...

A few days later I get more slack from this attending for my utter disregard for his authority, however, at some point patient care should take priority over fear of repercussions. So I ask you, how would you have managed this patient, or the situation in which you feel doing the right thing in your mind might get you in trouble? Thanks in advance!

The first rule in residency is to do what your attending wants, even if they are incompetant. But I would ask the attending why they don't want an ABG or why they don't mind and ETCO2 of 68. It is just not worth the fight. This patient is going to do lousy no matter what you do, so as long as the Sat is above 90% and the patient is reasonable HD stable, just go with the flow. The truth is the job market is really tight and making an enemy with this dousch is just not worth it. Some of these European guys are some of the most pompous people I have ever met. You probably would not have killed this patient letting them breath spontaneously with an ETCO of 68 as I don't see anything in this patient's history of pulmonary hypertension.

The LMA versus ETT is kind of a tough one, damned if you do and damned if you don't. You need to weigh the risk of the ETT crippling already crippled lungs even more versus an LMA and increased risk of aspiration due to the uncontrolled GERD. You could argue that either way.

The phenylephrine is a cRNA thing. What you need to do is look at the 5 reasons for hypotension and figure out which one it is, preload, afterload, contractility, rate, rhythm. I'm gonna assume preload.

Lastly, rather than giving Haldol, you really need to figure out why the patient is disoriented in the PACU. What was the baseline? Are there lab abnormalities, maybe the sodium is low from the patient HCTZ. Maybe there is residual drug on board. Maybe the patient had a stroke. You should probably investigate these things before putting a restraining order on the patient along with Haldol.

I've never done a corneal transplant, so I'm not sure what is the best anesthesia for it, but it may be a good thing to look into. I would have thought it could be done under a retrobulbar block, but maybe I'm wrong.

 

[sevoflurane]

As a Ca-1 or Ca-2, you have to observe, do and learn. There are a lot of different ways to skin a cat. However, there are some situations where you need to step up to the plate. Usually the mistake is obvious and in your face.

Reminds me of my own confrontation with an attending of mine during residency. Alveolar proteinosis case, DLT, 10 or so liters of washout fluid per side... 15 year old. Anywho, sats up and down from mid 60's to mid-high 80's for a couple of hours. At the end of the case the attending wants to switch over to a single lumen tube. Takes the AW, re-intubates..... No ETCO2, hypoxia, no chest raise, blue kid, etc... I told him he goosed it and he got pissed at me and refused to re-intubate. "She's hypoxic at baseline, it will come up..." sats, 60, 50, 45, pulse ox hitting the low notes.... "It will come up". Pulm attending and I are like WTF?

Long story short, I ended up grabbing the FO scope, pushing him out of the way and poceeded to go down the tube to show him some nice looking stomach ruggae. Extubated, and re-intubated with + ETCO2. She did fine.

There is a time, especially towards the end of your Ca-3 year, your experience will surpass some of the weaker attendings at some programs. The patient always comes first... but make sure you are right before you piss off some of your attendings.

These can be delicate interactions. Tough situation...

Do what's right for the patient, the rest will follow.

 

[cincincyreds]

As a Ca-1 or Ca-2, you have to observe, do and learn. There are a lot of different ways to skin a cat. However, there are some situations where you need to step up to the plate. Usually the mistake is obvious and in your face.

Reminds me of my own confrontation with an attending of mine during residency. Alveolar proteinosis case, DLT, 10 or so liters of washout fluid per side... 15 year old. Anywho, sats up and down from mid 60's to mid-high 80's for a couple of hours. At the end of the case the attending wants to switch over to a single lumen tube. Takes the AW, re-intubates..... No ETCO2, hypoxia, no chest raise, blue kid, etc... I told him he goosed it and he got pissed at me and refused to re-intubate. "She's hypoxic at baseline, it will come up..." sats, 60, 50, 45, pulse ox hitting the low notes.... "It will come up". Pulm attending and I are like WTF?

Long story short, I ended up grabbing the FO scope, pushing him out of the way and poceeded to go down the tube to show him some nice looking stomach ruggae. Extubated, and re-intubated with + ETCO2. She did fine.

There is a time, especially towards the end of your Ca-3 year, your experience will surpass some of the weaker attendings at some programs. The patient always comes first... but make sure you are right before you piss off some of your attendings.

These can be delicate interactions. Tough situation...

Do what’s right for the patient, the rest will follow.

Wow, I hope that story isn't true. What kind of program were you in with an attending like that. I agree, if you are a resident, make sure you are right, otherwise you are really jeopardizing your career.

 

[sevoflurane]

Wow, I hope that story isn't true. What kind of program were you in with an attending like that. I agree, if you are a resident, make sure you are right, otherwise you are really jeopardizing your career.

True story. Visiting attending from Germany. Great program. In a huge dpt... you are going to come across some weak links.

 

[jwk]

I've never done a corneal transplant, so I'm not sure what is the best anesthesia for it, but it may be a good thing to look into. I would have thought it could be done under a retrobulbar block, but maybe I'm wrong.

These cases can be managed fairly easily with topical anesthesia or RBB/PBB with sedation when done in a reasonable time frame. The problem here is taking four hours to do a case that's routinely done in an hour in skilled hands. Sick old patients won't lie still for four hours, so in this particular case, GA is the only option.

 

[pgg]

I notice her aggressively manually bagging the pt

Aggressively bagging a COPD'er with uncontrolled GERD and an LMA is all kinds of wrong.

She received 1 gm of IV OFIRMEV (tylenol) for the case. NO opiods...She comes to the PACU, delirious, screaming in pain, muttering nonsense. Attending order 4 mg of Haldol which quiets her down...

Something's not right there, eyeball patients shouldn't be screaming in pain in the PACU.


As for getting an ABG - what's it going to tell you that you don't already know? What indication for an a-line were you thinking of?

You said the patient had uncontrolled HTN ... how uncontrolled? How far below baseline were the 50-55 MAPs?

Nothing wrong with a phenylephrine drip, provided the drip-starter had the right diagnosis for the patient's hypotension.

A few days later I get more slack from this attending for my utter disregard for his authority,

Just let it roll off you. Walk the line of contrite respect without being obsequious. This too shall pass.

Severe COPD'ers live with chronic hypoxia/hypercarbia. Im guessing the attending didnt want the patient to lose their "hypoxic drive" with a high FiO2

The hypoxic drive myth just won't die. I couldn't tell if you thought the attending's concern was valid, or were just offering up a possible reason for the attending's decision to let the 78 CO2 ride.

You need to weigh the risk of the ETT crippling already crippled lungs even more versus an LMA and increased risk of aspiration due to the uncontrolled GERD.

I don't think there's much if any merit to ETT fears in COPD'ers (even the severe cases) coming in for elective surgery. The patient wasn't intubated for respiratory failure. (And what do we do for resp failure in COPD'ers? We intubate them.) Provided anesthesia is adequate and the vent settings are reasonable, a tube is totally reasonable.

I'll take the small risk of airway irritability in exchange for controlled ventilation just about every time. I can count the times I've regretted intubating someone on no hands. LMA regrets are another story.

 

[RxBoy]

The hypoxic drive myth just won't die. I couldn't tell if you thought the attending's concern was valid, or were just offering up a possible reason for the attending's decision to let the 78 CO2 ride.

I don't think there's much if any merit to ETT fears in COPD'ers (even the severe cases) coming in for elective surgery. The patient wasn't intubated for respiratory failure. (And what do we do for resp failure in COPD'ers? We intubate them.) Provided anesthesia is adequate and the vent settings are reasonable, a tube is totally reasonable.

I'll take the small risk of airway irritability in exchange for controlled ventilation just about every time. I can count the times I've regretted intubating someone on no hands. LMA regrets are another story.

The ETT tube itself the least of the worries. Yeah there will be airway irritabilty and maybe even higher anesthetic requirements to tolerate the tube. But the real danger is PPV, and this is what is trying to be avoided. SV with a ET tube is an option, but this addes more airway resistance to already pathologic obstruction. Another good option would be a more secure LMA (LMA supreme/proseal). Before you attack the LMA supreme, know that I already know its not an alternative to a ETT and there is no evidence that it decreases risk of aspiration. However there is no evidence that doesn't protect from aspiration either.

As for the "hypxic drive" I thought I made it clear by putting it in quotations than explaining the real reason high FiO2 is detrimental to COPDers in parenthesis immediately after.

From Big Miller:
"Many stage II or III COPD patients have an elevated Paco2 at rest. It is not possible to differentiate these "CO2 retainers" from non-retainers on the basis of history, physical examination, or spirometric pulmonary function testing. This CO2 retention seems to be more related to an inability to maintain the increased work of respiration (WResp) required to keep the Paco2 normal in patients with mechanically inefficient pulmonary function and not primarily due to an alteration of respiratory control mechanisms. It was previously thought that chronically hypoxemic/hypercapnic patients relied on a hypoxic stimulus for ventilatory drive and became insensitive to Paco2. This explained the clinical observation that COPD patients in incipient respiratory failure could be put into a hypercapnic coma by the administration of a high concentration of oxygen (Fio2). Actually, only a minor fraction of the increase in Paco2 in such patients is due to a diminished respiratory drive, because minute ventilation is basically unchanged. The Paco2 rises because a high Fio2 causes a relative decrease in alveolar ventilation and an increase in alveolar dead space and shunt by the redistribution of perfusion away from lung areas of relatively normal V/Q matching to areas of very low V/Q ratio because regional hypoxic pulmonary vasoconstriction (HPV) is decreased[31] and also due to the Haldane effect.[32] However, supplemental oxygen must be administered to these patients postoperatively to prevent the hypoxemia associated with the unavoidable fall in functional residual capacity (FRC). The attendant rise in Paco2 should be anticipated and monitored. To identify these patients preoperatively, all stage II or III COPD patients need arterial blood gas analysis."

 

[pgg]

The ETT tube itself the least of the worries. Yeah there will be airway irritabilty and maybe even higher anesthetic requirements to tolerate the tube. But the real danger is PPV, and this is what is trying to be avoided. SV with a ET tube is an option, but this addes more airway resistance to already pathologic obstruction. Another good option would be a more secure LMA (LMA supreme/proseal). Before you attack the LMA supreme, know that I already know its not an alternative to a ETT and there is no evidence that it decreases risk of aspiration. However there is no evidence that doesn't protect from aspiration either.

PPV with appropriate vent settings, ie to avoid excessive pressures, sufficient expiratory time to avoid stacking, etc is OK. SV with some pressure support alleviates the inspiratory work of breathing through a straw, and a normal sized ETT isn't really going to cause problems with expiration.

I just think that the seemingly common cultural preference of avoiding ETTs in COPD patients is unwarranted. I think LMAs are overrated as "pulmonary function protective" airway devices and tend to avoid them, especially in patients with pulmonary disease, because I want better control of resp function.

I'm a fan of the LMA supremes. IMO LMAs have a place for simplifying simple anesthetics. Trying to shoehorn them into more complex patients just seems to go badly often. I know lots of people like to use them in lateral or prone patients, or sitting shoulders, or [insert other look-what-case-I-did-with-just-a-LMA] ... but 99% of the time I'd rather just stick a tube in those patients and be done with it.

As for the "hypxic drive" I thought I made it clear by putting it in quotations than explaining the real reason high FiO2 is detrimental to COPDers in parenthesis immediately after.

Fair enough, that's what I figured.

 

[RxBoy]

The phenylephrine is a cRNA thing. What you need to do is look at the 5 reasons for hypotension and figure out which one it is, preload, afterload, contractility, rate, rhythm. I'm gonna assume preload.

I was always taught to treat the patient not the monitor. Sure use the drip to temporize dangerous hypotension while the diagnosis/treatment is established. But running it through a case is what defines the difference between a technician and a physician.

The other day was helping out in a junior room and remember setting the vent settings (RR 10) after he intubated. I came back later to give him a lunch, and the RR was 7. I asked him why did he have to go down on the RR and he said the EtCO2 was 34 but started creep down a couple hours into the case. I look over the drapes and there is 500 cc blood in the canister. I told him to put the RR back to 10, go to lunch, and by the time him comes back I will fix the EtCo2 without the vent.

I opened fluids while the vent established a new baseline EtCO2 of 31. I bolused a 250 albumin and it came back up to 33. The resident came back surprised and I explained to him how CO and EtCO2 are related. But more importantly, I explained the importance of establishing a baseline. A baseline VS/mac/vent should be obtained in 30 min and deviance from the value is far more important than the value itself. I only treat the value if its at a dangerous level.

I see the same idiocay all the time when residents are constantly turning the vapor up then down while pushing fentanyl and phenyephrine through out a case. With all the variable that are constantly changing, how does someone even know what to treat?

Well that's my 2 cents on a phenylephrine drip.

 

[k12balla]

Wow, thanks for all of your responses and insight.

While I can appreciate the benefit of allowing this type of pt to maintain spontaneous ventilation in order to avoid PPV, and possible rupture of a pleural bleb and subsequent PTX, I think at some point you have to be able to re-evaluate your management and adjust appropriately. In my situation, the pt was not adequately ventilating, as evidenced by her low TV, and increasing ETC02, thus my decision to try something different and try pressure mode as there was no pressure support mode on my vent. Which for right or wrong, I don't think I should've been reprimanded so harshly. It is difficult to times to balance subservience with autonomy, especially when there is no effort to explain one's rationalization or hear opposing thoughts.

-It would have been nice to have had a baseline ABG, however I did not start the case, and my rationalization to obtain another one was to assess whether the current mode of ventilation was adequate, or if she was growing more hypercapnic and acidoditic above and beyond her baseline and what she could metabolically compensate for. I was also hoping this might help support a decision to switch modes...Her increasing acidosis coudl've worsened her vasodilation and hypotension, as well as bring her close to arrythmias as her baseline K+ was 4.8.

-I can also appreciate possibly using an LMA in pts with precarious situations, however it appears the pt had multiple contraindications to this: uncontrolled GERD, diabetic neuroapthy and likely gastroparesis. I think the risk of gastric aspiration in a pt with poor lung functioning would outweigh the benefit of avoiding PPV, especially if it proves to be inadequate.

- I have no qualms with a phenylephrine gtt to temporize a pt, however it running through my sole small caliber peripheral IV, in a not so stable pt, leads me to think I may need another line to push drugs, or transfuse volume if need be.

-Pts baseline MAP was 85, I asked what our goal was and he said 50-55 non nonchalantly, which seems a little low going by 20% of baseline

- As far as her post op delerium, I did not support the decision to give her Haldol, as this only calmed her symptoms and not the cause. Which may have been pain or hypercapnia. It is a difficult situation, as you would try to avoid opoids and further resetting her threshold, but I guess I'm just not familiar with the use of Haldol in these situations.

.

 

[RxBoy]

Which for right or wrong, I don't think I should've been reprimanded so harshly. It is difficult to times to balance subservience with autonomy, especially when there is no effort to explain one's rationalization or hear opposing thoughts.

I agree, I think no explanation is the attending's biggest problem. The fact that he yelled at you makes him even a bigger douche.

As for tube or LMA? Operator specific. Each has pros/cons. I would LMA, others would tube. You cause a pneumo or unexptected ICU admission for difficulty to wean off vent and you'll say I wish I went with the LMA, I cause an aspiration and I'll say I wish I went with a tube. There really isn't a clear answer, but being able to weigh both sides and defend your position is whats important.

 

[Arch Guillotti]

The other day was helping out in a junior room and remember setting the vent settings (RR 10) after he intubated. I came back later to give him a lunch, and the RR was 7. I asked him why did he have to go down on the RR and he said the EtCO2 was 34 but started creep down a couple hours into the case. I look over the drapes and there is 500 cc blood in the canister. I told him to put the RR back to 10, go to lunch, and by the time him comes back I will fix the EtCo2 without the vent.

I opened fluids while the vent established a new baseline EtCO2 of 31. I bolused a 250 albumin and it came back up to 33. The resident came back surprised and I explained to him how CO and EtCO2 are related. But more importantly, I explained the importance of establishing a baseline. A baseline VS/mac/vent should be obtained in 30 min and deviance from the value is far more important than the value itself. I only treat the value if its at a dangerous level.

Can you elaborate because I think I understand what you are saying but I don't think I agree. The only time I have seen CO2 dwindle is when the patients are circling the drain. I have never observed a drop in CO2 as a surrogate for CO in a case with mild blood loss.

 

[Idiopathic]

Can you elaborate because I think I understand what you are saying but I don't think I agree. The only time I have seen CO2 dwindle is when the patients are circling the drain. I have never observed a drop in CO2 as a surrogate for CO in a case with mild blood loss.

just leave it alone

 

[RxBoy]

Can you elaborate because I think I understand what you are saying but I don't think I agree. The only time I have seen CO2 dwindle is when the patients are circling the drain. I have never observed a drop in CO2 as a surrogate for CO in a case with mild blood loss.

I'm actually surprised you asked... Never looked it up but Just did a quick pubmed seach:


"The relationship between CO and partial end-tidal CO2 pressure (PETCO2) has been known for decades [13,14], so measurement of PETCO2 has been proposed to confirm the restoration of spontaneous circulation in patients with cardiac arrest [15], but also as a quantitative indicator of hemodynamic effectiveness of precordial compression during cardiopulmonary resuscitation [16]. Moreover, since PETCO2 is mainly determined by tissue CO2 production (VCO2), alveolar ventilation and CO (that is, pulmonary blood flow) [17], when stable metabolic conditions are assumed and minute ventilation is kept constant, acute changes in PETCO2 have been shown to correlate strongly with changes in CO in experimental [18-24] and clinical [25,26] settings. Thus, PETCO2 has been suggested as a noninvasive alternative for continuous assessment of CO in different shock states [20]."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327636/?tool=pubmed

"
Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output?

Abstract

In anesthetized patients, acute decreases in cardiac output (CO) are often reflected as decreases in end-tidal CO2 tension (PETCO2), but the quantitative relationship between the changes in CO and the changes in PETCO2 is uncertain. We hypothesize that a quantitative relationship can be demonstrated if timing of the measurements in each episode of hemodynamic perturbation is standardized. In 24 patients undergoing abdominal aortic aneurysm surgery with constant ventilation, we prospectively performed 33 measurements of CO, PETCO2, and CO2 elimination (VECO2) within 10 min of hemodynamic changes. The percent decrease in PETCO2 directly correlated with the percent decrease in CO (slope = 0.33, r2 = 0.82). Also, the percent decrease in VECO2 correlated with the percent decrease in CO similarly (slope = 0.28, r2 = 0.84). The changes in PETCO2 and VECO2 following hemodynamic perturbation were parallel. This finding suggests that decreases in PETCO2 quantitatively reflect the decreases in CO2 elimination."


http://www.ncbi.nlm.nih.gov/pubmed/7978395

 

[Idiopathic]

i didnt know the OR patient was in shock

 

[Arch Guillotti]

Eh - I understand what you are saying but I just don't buy that you gave some dude a bottle of albumin and magically "fixed" his ETCO2. A routine case with mild EBL over a period of time is much different than a ruptured AAA/bad belly trauma/VAE (all of which I have seen cause an abrupt decline in ETCO2 because the patient was under maximum stress/circling the drain.

 

[RxBoy]

i didnt know the OR patient was in shock

Fine... I picked 2 random studies... here are non shock states... I am actually shocked that people don't follow EtCO2 as a surrogate for CO. Its actually very sensitive once you reach steady state.

There are a dozen other studies if you would like to look it up. For the sake of sanity, I didn't include more.

[Effects of cardiac output on PETCO2 and PaCO2 during combined inhalational-epidural anesthesia].

[Article in Japanese]
Hayashida M, Orii R, Komatsu K, Chinzei M, Nakagawa Y, Nishiyama T, Suwa K, Hanaoka K.
Source

Department of Anesthesiology, Faculty of Medicine, University of Tokyo.

Abstract

We investigated the effects of cardiac output on PETCO2 in anesthetized patients. We studied 8 adult patients undergoing long-lasting lower abdominal surgery. Anesthesia was maintained with epidural combined with inhalational anesthesia. The minute ventilation volume was kept constant at 10 ml.kg-1 x 10 cycles.min-1. PETCO2, PaCO2, and cardiac index, (CI) by thermodilution method were measured simultaneously. PaCO2 was corrected for body temperature for comparison with PETCO2. Approximate value of alveolar dead space to tidal volume ratio was calculated as VD/ VTalv = (PaCO2-PETCO2)/PaCO2. The measurements were repeated every 10 to 20 minutes under the steady body temperature. One hundred and six sets of data were obtained from these patients. PETCO2 as well as PaCO2 correlated positively with CI, while VD/VTalv did not correlate with CI. PETCO2 correlated positively with PaCO2, while it did not correlate with VD/VTa1v. When examined in individual patients, PETCO2 correlated positively with CI in 7 patients. PaCO2 correlated positively with CI in 6 patients, while VD/VTa1v correlated negatively with CI only in 2 patients, in whom CI showed a large fluctuation. PaCO2 correlated positively with PETCO2 in 8 patient, while VD/VTa1v correlated negatively with PETCO2 only in 1 patient. By multiple regression analysis, VD/VTa1v change accounted for only 20.0 +/- 15.3% of PETCO2 change, while PACO2 or PaCO2 change accounted for 79.3 +/- 16.7%. Decreased CI was associated with a decrease in oxygen uptake (VO2), and PaCO2 correlated positively with VO2. Decreased CI was also associated with an increase in VA/Q, and PaCO2 correlated negatively with VA/Q. Thus, PETCO2 decreased with decreasing cardiac output. A decrease in PACO2 explained the decrease in PETCO2 better than an increase in VD/VT did. Decreased cardiac output caused hypocapnia through decreased CO2 production and/or increased ventilation to perfusion ratio i.e. relative hyperventilation.



[Relationship between cardiac output and PETco2 as well as Paco2 during high-dose fentanyl anesthesia].

[Article in Japanese]
Hayashida M, Orii R, Komatsu K, Du HL, Sato Y, Uchida K, Nagata O, Hanaoka K.
Source

Department of Anesthesiology, Faculty of Medicine, University of Tokyo.

Abstract

We investigated the relationship between cardiac output and PETCO2 as well as blood PCO2 in 10 patients undergoing cardiac surgery of long duration under high-dose fentanyl anesthesia. After anesthetic induction, the minute ventilation was kept constant at 10 ml.kg-1 x 10 cycles.min-1 and a pulmonary artery catheter was inserted. PETCO2, PaCO2 and cardiac index (CI) were measured simultaneously. PaCO2 was corrected for body temperature, and alveolar dead space-to-tidal volume ratio was calculated as VD/VTalv = (PaCO2-PETCO2)/PaCO2. After body, temperature became stabilized, the measurements were started and repeated every 10 to 20 minutes during the prebypass period. One hundred and eight sets of data were taken from 10 patients. PETCO2 correlated positively with CI. Similarly, PaCO2 correlated positively with CI, but VD/VTalv, did not correlate with CI. PETCO2 correlated closely and positively with PaCO2, but it correlated negatively and only marginally with VD/VTalv. When examined in individual patients, PaCO2 correlated positively with PETCO2 in all patients, while VD/VTalv correlated negatively with PETCO2 only in 3 patients. By multiple regression analysis, VD/VTalv change accounted for only 22.3 +/- 15.0% of PETCO2 change, while PACO2 or PaCO2 change accounted for 77.6 +/- 15.0% of PETCO2 change. Decreased CI was associated with decreased CO2 delivery from the tissue to the lung (DCO2) and PaCO2 decreased with decreasing DCO2. Decreased CI was also associated with decreased oxygen uptake (VO2), and PaCO2 decreased with decreasing VO2. A decrease in CI resulted in an increase in VA/Q, and PaCO2 decreased when VA/Q increased. PETCO2 decreased when cardiac output decreased. A decrease in PACO2 explained the decrease in PETCO2 better than an increase in VD/VT did. Decreased cardiac output might cause hypocapnia through decreased CO2 delivery to the lung, decreased CO2 production and/or increased ventilation-to-perfusion ratio.

 

[nap$ter]

The phenylephrine is a cRNA thing. What you need to do is look at the 5 reasons for hypotension and figure out which one it is, preload, afterload, contractility, rate, rhythm. I'm gonna assume preload.
.

that's plain silly. you give an anesthetic that drops the SVR (the afterload) - you give the antidote, phenylephrine gtt. turn up the volatile and neo gtt a bit = train track hemodynamic stability.

sure, address the preload as per usual, but this lady is likely on lisinopril - are you really gonna bolus her with a couple liters of fluid to get her pressure up sans neo, then intubate her to diurese the wet stuff off her already sick lungs?

per your own advice to address the variables amongst the five reasons for hypotension you should a) replace the volume from NPO, then b) place her on a neo gtt to address the reduction in SVR from your volatile.

c'mon, dude.

 

[RxBoy]

that's plain silly. you give an anesthetic that drops the SVR (the afterload) - you give the antidote, phenylephrine gtt. turn up the volatile and gtt a bit = train track hemodynamic stability.

sure, address the preload as per usual, but this lady is likely on lisinopril - are you really gonna bolus her with a couple liters of fluid to get her pressure up sans neo, then intubate her to diurese the wet stuff off her already sick lungs?

per your own advice to address the variables amongst the five reasons for hypotension you should a) replace the volume from NPO, then b) place her on a neo gtt to address the reduction in SVR from your volatile.

c'mon, dude.

Rubbish

Lininopril: Afterload problem. True antidote is vasopressin but sure give you can give phenylephrine/ephedrine until the body couterregulates the lisinopril effects. The difference is you understand why you need to give phenylephrine.

Volatile induced hypotension: Either afterload and/or preload problem due to the unmasking effects of hypovolemia. Tx: Hydrate to normovolemia based on fluid status. If doesn't correct than afterload problem. Decrease MAC and possible supplemention with iv anesthetic without significant SVR effects. Anyone who needs to run a phenylephrine drip to maintain a high mac is criminal in my book.

Phenylephrine is not a benign drug. It causes renal and coronary vasoconstriction among other things.

 

[cincincyreds]

I was always taught to treat the patient not the monitor. Sure use the drip to temporize dangerous hypotension while the diagnosis/treatment is established. But running it through a case is what defines the difference between a technician and a physician.

The other day was helping out in a junior room and remember setting the vent settings (RR 10) after he intubated. I came back later to give him a lunch, and the RR was 7. I asked him why did he have to go down on the RR and he said the EtCO2 was 34 but started creep down a couple hours into the case. I look over the drapes and there is 500 cc blood in the canister. I told him to put the RR back to 10, go to lunch, and by the time him comes back I will fix the EtCo2 without the vent.

I opened fluids while the vent established a new baseline EtCO2 of 31. I bolused a 250 albumin and it came back up to 33. The resident came back surprised and I explained to him how CO and EtCO2 are related. But more importantly, I explained the importance of establishing a baseline. A baseline VS/mac/vent should be obtained in 30 min and deviance from the value is far more important than the value itself. I only treat the value if its at a dangerous level.

I see the same idiocay all the time when residents are constantly turning the vapor up then down while pushing fentanyl and phenyephrine through out a case. With all the variable that are constantly changing, how does someone even know what to treat?

Well that's my 2 cents on a phenylephrine drip.

There are very few third year residents at my place who know the difference between dead space and shunt. It is kind of sad.

 

[fakin' the funk]

Can you elaborate because I think I understand what you are saying but I don't think I agree. The only time I have seen CO2 dwindle is when the patients are circling the drain.

VO2, VCO2, CO, and etCO2 are related. VO2-VCO2, that's easy. VCO2-etCO2, that's easy too. The VO2-CO relationship, that's less straightforward, but I think we all are willing to accept that VO2 and CO are related linearly (except in patients who cannot augment CO from baseline, or who have very very high VO2s as in sepsis). We also all certainly accept that VO2 ~ METs ~ CO, and we all acknowledge the relationship of VO2 and CO as formulated in the Fick equation. I totally agree with RxBoy on this theoretical perspective, but...

I have never observed a drop in CO2 as a surrogate for CO in a case with mild blood loss.

Agree with you here, Arch. If you're seeing a dip in etCO2 because of blood loss...that blood loss ain't mild. We're talking Stage 2-3 hypovolemia.

 

[fakin' the funk]

Phenylephrine is not a benign drug. It causes renal and coronary vasoconstriction among other things.

It also causes augmented perfusion pressures to those vascular beds.

If the etiology of anesthetic-induced hypotension is venodilation and arteriodilation, then you should treat with a venoconstrictor and arterioconstrictor, not fluids.

I understand your bias against phenylephrine drips in that they can easily be used for the wrong reason (to mask excessive anesthetic depth, hypovolemia, or even cardiogenic shock), but I do think they have a role in "offsetting" the non-benign venodilatory and arteriodilatory effects of anesthetics.

 

[fakin' the funk]

Fine... I picked 2 random studies... here are non shock states... I am actually shocked that people don't follow EtCO2 as a surrogate for CO. Its actually very sensitive once you reach steady state.

There are a dozen other studies if you would like to look it up. For the sake of sanity, I didn't include more.

Ah, it's July, and the smell of fresh CA-3 confidence is in the air.

 

[RxBoy]

Ah, it's July, and the smell of fresh CA-3 confidence is in the air.

I can run a case by myself damn it, just watch me!!

 

[Idiopathic]

see you may be right about the CO2 correlating with CO, but the reason it happens in shock is simply because you cant perfuse the pulmonary circulation effectively, and you cant deliver enough blood to deliver CO2 back to the alveoli, all the while your PaCO2 rises. Those 18 patients you presented above seemed to have decreased PaCO2 as well, correlating with decreased ETCO2. They surmise that less CO2 is produced as well as delivered, so where is the need to artificially support CO through volume administration, especially if the clinical situation doesnt call for it? (i.e. stable hemodynamics off pressors). Id argue this is a metabolic phenomenon as much as a cardiac output phenomenon. Good discussion though.

 

[Bertelman]

I was always taught to treat the patient not the monitor. Sure use the drip to temporize dangerous hypotension while the diagnosis/treatment is established. But running it through a case is what defines the difference between a technician and a physician.

The other day was helping out in a junior room and remember setting the vent settings (RR 10) after he intubated. I came back later to give him a lunch, and the RR was 7. I asked him why did he have to go down on the RR and he said the EtCO2 was 34 but started creep down a couple hours into the case. I look over the drapes and there is 500 cc blood in the canister. I told him to put the RR back to 10, go to lunch, and by the time him comes back I will fix the EtCo2 without the vent.

I opened fluids while the vent established a new baseline EtCO2 of 31. I bolused a 250 albumin and it came back up to 33. The resident came back surprised and I explained to him how CO and EtCO2 are related. But more importantly, I explained the importance of establishing a baseline. A baseline VS/mac/vent should be obtained in 30 min and deviance from the value is far more important than the value itself. I only treat the value if its at a dangerous level.

I see the same idiocay all the time when residents are constantly turning the vapor up then down while pushing fentanyl and phenyephrine through out a case. With all the variable that are constantly changing, how does someone even know what to treat?

Well that's my 2 cents on a phenylephrine drip.

It appears to me that you treated a monitor to some extent.

 

[OB1🤙]

If you want your gas analyzer to double as a change-in-CO monitor, run low flow des.

 

[Substance]

I have nothing to add to the case.

I just want to say that out of all of the forums on SDN, this is the only one that consistently has clinical scenario discussions. For a non-anesthesiology doc, its still pretty interesting. I wonder if I should make a lateral jump.

It's also the only one that has heavy metal recommendations.

Strong work.

 

[Bertelman]

I have nothing to add to the case.

I just want to say that out of all of the forums on SDN, this is the only one that consistently has clinical scenario discussions. For a non-anesthesiology doc, its still pretty interesting. I wonder if I should make a lateral jump.

It's also the only one that has heavy metal recommendations.

Strong work.

Are you sure it would be a lateral jump? What's your specialty now?

 

[Substance]

Are you sure it would be a lateral jump? What's your specialty now?

I don't like to give away identifying information.

It was just a thought, and probably won't be followed through given that I'm out of this popsicle stand in less than a year. Another five or so years of residency is the last thing I'd really want to do - I'd be in my early forties before I started practicing, and that's just too late for me.

As for the case, like I said before, excellent discussion!

 

[nap$ter]

Rubbish

Lininopril: Afterload problem. True antidote is vasopressin but sure give you can give phenylephrine/ephedrine until the body couterregulates the lisinopril effects. The difference is you understand why you need to give phenylephrine.

Volatile induced hypotension: Either afterload and/or preload problem due to the unmasking effects of hypovolemia. Tx: Hydrate to normovolemia based on fluid status. If doesn't correct than afterload problem. Decrease MAC and possible supplemention with iv anesthetic without significant SVR effects. Anyone who needs to run a phenylephrine drip to maintain a high mac is criminal in my book.

Phenylephrine is not a benign drug. It causes renal and coronary vasoconstriction among other things.

1st paragraph - sounds like we're agreed

2nd paragraph - show me this study demonstrating the unmasking of hypovolemia? you should review the 3 studies referenced in fig 15-15 pg 402 of barash. it sounds like you basically agree with me that preload should be replaced (which btw is a pretty minimal amt for an npo pink puffer), and then correct the afterload problem (why not do both at the same time?)

so, for the case of the OP, you give her volume (marginalizing her tenuous pulmonary status), then decrease the mac. She moves (surgeon cries out "omg, she's awake!)and is still hypotensive. now you either paralyze her (putting her at risk for incomplete reversal with already marginalized pulmonary status), or start your IV sedation that doesn't effect SVR (specifically which IV sedation is that? dexmed? ketamine? pretty spendy, pretty fancy, pretty resource-consuming). meantime her BP curve looks like a six flags ride. smooth move, slim. way to stick to your theoretical guns. you're ready for an academic position, just like any R2.

or, expect the drop in SVR from your volatile, and treat it promptly. ever have a labile pt c chronic htn? I don't NEED to run a neo gtt to maintain CO, I DO IT ON PURPOSE because i understand the physio/pharm, and I like TRAIN TRACK RECORDS. eliminate the risk and work of a labile patient on purpose... replace the preload and normalize the SVR...

oh, and btw, while phenylephrine does cause coronary and renal vasoconstriction in vivo (ie if you drip neo on a strip of renal or coronary artery), phenylephrine actually increases coronary (in particular), and renal perfusion, given a normal preload (these studies were actually done in dogs long long ago).

remember, it's flow we care about, not just the resistance. coronary flow is determined by a LOT more than a small change in caliber c neo. look at the whole picture.

 

[RxBoy]

Really liking the discussion/rebuttals from the attendings. Stirring up the pot a bit reminds me why you guys have your **** on lock.
http://www.urbandictionary.com/define.php?term=**** on lock

 

[nap$ter]

Really liking the discussion/rebuttals from the attendings. Stirring up the pot a bit reminds me why you guys have your **** on lock.

nice. funny thing is if we were working together we'd likely realize we agree on most things important - something is lost in translation online...