"elective intubation" to decrease cardiac output s/p massive MI

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VentdependenT

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Got a consult today in the CCU for an elective/pre-emptive intubation in a patient who suffered a massive MI. She was on high dose dopamine and on a balloon pump. She was speaking full sentences, breathing at 20/minute, sats 95% on 50% ventimask. Puked up blood a few times from the heparin GGT.

So I says, whats the deal people.

They said that they wanted us to intubate her so that they could decrease her Vo2 and thereby give her heart less work to do. OK says I. Get a full consent from her for intubation and mechanical ventilation. She's mentating fine and she consents.

Ok. Fentanyl/versed/roc tube in. BP's didn't budge. Grade 3 view per the CA-2 who nailed it after the CA-1 missed it x1.

The question: Was this appropriate?

I did a perfunctory google search on "cardiac output and work of breathing." Didn't yeild much.

Found this paper which is way nerdy but something that an anesthesiologist could get off on: http://www.cja-jca.org/cgi/reprint/32/3/236.pdf

I mean if we're gonna do that why not cool her off to 96degrees, put some ice on her noggin, snow her with STP, and do some other wacky crap to decrease her Vo2.

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Got a consult today in the CCU for an elective/pre-emptive intubation in a patient who suffered a massive MI. She was on high dose dopamine and on a balloon pump. She was speaking full sentences, breathing at 20/minute, sats 95% on 50% ventimask. Puked up blood a few times from the heparin GGT.

So I says, whats the deal people.

They said that they wanted us to intubate her so that they could decrease her Vo2 and thereby give her heart less work to do. OK says I. Get a full consent from her for intubation and mechanical ventilation. She's mentating fine and she consents.

Ok. Fentanyl/versed/roc tube in. BP's didn't budge. Grade 3 view per the CA-2 who nailed it after the CA-1 missed it x1.

The question: Was this appropriate?

I did a perfunctory google search on "cardiac output and work of breathing." Didn't yeild much.

Found this paper which is way nerdy but something that an anesthesiologist could get off on: http://www.cja-jca.org/cgi/reprint/32/3/236.pdf

I mean if we're gonna do that why not cool her off to 96degrees, put some ice on her noggin, snow her with STP, and do some other wacky crap to decrease her Vo2.
A general rule in medicine:
It's never better to replace something natural with something artificial.
So, they want you to intubate the patient and put her on mechanical positive pressure ventilation because this will give her heart a break!
There is few issues:
PPV is going to decrease cardiac output further, it's going to alter the pulmonary physiology, and being on a vent is going to give this poor woman a very good chance to develop pneumonia with some weird bacteria.
Being intubated is going to require some form of sedation with a drug that is going to further complicate the hemodynamics.
If we don't want the sedation to affect the hemodynamics too much then we might give too little sedation and the result would be stress and possibly a new heart attack.
These are some reasons why intubating someone who doesn't need intubation is never a good idea.
 
A general rule in medicine:
It's never better to replace something natural with something artificial.
So, they want you to intubate the patient and put her on mechanical positive pressure ventilation because this will give her heart a break!
There is few issues:
PPV is going to decrease cardiac output further, it's going to alter the pulmonary physiology, and being on a vent is going to give this poor woman a very good chance to develop pneumonia with some weird bacteria.
Being intubated is going to require some form of sedation with a drug that is going to further complicate the hemodynamics.
If we don't want the sedation to affect the hemodynamics too much then we might give too little sedation and the result would be stress and possibly a new heart attack.
These are some reasons why intubating someone who doesn't need intubation is never a good idea.

Thats why I had the team get a full consent. The attending cards guy wanted it. The patients son is an interventional cardiologist and he ok'd the consent as well.

Shes gonna be on a nimbex and versed drip man. Brutal. Hope she turns out ok.
 
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Last i checked Myocardial oxygen demand is dependent on HR, Volume and pressure work. ie beta-blockers and afterload reduction. But since we are in a cardiogenic shock picture(max dopamine and IABP) Sounds like we have clinical conundrum, Wait until she gets worse and then intubate or do it when she is semi stable. Where was she in the course of her MI? If she is getting worse (decreasing CO) just put the tube in as she will be in pulm edema shortly or if she is in stable shock :cool: then you could hold off. VAP and PPV effects on CO are real issues.

If she was already intubated nl resp parameters but on Max dopamine and IABP at 1:1 would you extubate?
 
1) dopamine sucks

2) they are idiots

3) as soon as there is any increase in PEEP there is going to be a decrease in CO... and you know they are going to do that as soon as she starts backing up some fluid into those lungs

4) when i was a resident we'd get these requests every 2 or 3 months... I usually told them that their attending had to discuss it with my ICU attending --- the ICU attending would usually ask for data to support their request... then they would shut up for 2 more months

5) i'd like her ABG first if they argue it is because of oxygenation...
 
I'm not sure I agree with all the naysayers. It's not uncommon to use non-invasive positive pressure ventilation (CPAP or BiPAP) to deliberately decrease preload in a patient with CHF in order to reduce wall stress (which is a major determinant of myocardial oxygen consumption). Furthermore, I believe the sepsis/septic shock literature supports mechanical ventilation in its various forms to, as my fellow once put it, "decrease the component of the cardiac output necessary to support ventilation."

Of course, I have nothing to support this contention other than what a few of our CCM guys have said, but they're usually pretty smart...

I'll be interested to see how this unfolds...
 
Got a consult today in the CCU for an elective/pre-emptive intubation in a patient who suffered a massive MI. She was on high dose dopamine and on a balloon pump. She was speaking full sentences, breathing at 20/minute, sats 95% on 50% ventimask. Puked up blood a few times from the heparin GGT.....

I've done this a few times in patients with severe sepsis who still had a low ScVO2 despite achieving their goals. The ScVO2 does go up when you take away the work of breath, which consumes a fair component of the cardiac output (River's quotes something like 20-25% but I don't have anything to back that up). This is actually part of the protocol (if you read the fine print) in the EGDT paper.
 
I'm not sure I agree with all the naysayers. It's not uncommon to use non-invasive positive pressure ventilation (CPAP or BiPAP) to deliberately decrease preload in a patient with CHF in order to reduce wall stress .

Yes, but if the Cardiac output is so bad that you need high dose Dopamine and an IABP, PPV is going to only decrease the cardiac output further.
and remember that ETT is not the same as non invasive ventilation, you can't tolerate an ETT without sedation and any sedation will make the patient more unstable.
Furthermore, I believe the sepsis/septic shock literature supports mechanical ventilation in its various forms to, as my fellow once put it, "decrease the component of the cardiac output necessary to support ventilation."
In septic shock you need to ventilate patients mechanically because if you don't they will indeed be working hard to compensate for the metabolic acidosis and they won't be breathing 20/min like this patient, these patients would be breathing 40-50 /min and really working hard.
 
The question: Was this appropriate?
.

Yep.

Marino says if you're even thinking the patient needs to be intubated, LETTEM' BREATHE THROUGH PLASTIC.

Or something like that.

SpO2 95% on 50% FiO2 aint the greatest.

Sounds like shes gonna need it eventually anyway, so I'll side with the critical care guru's opinion that you breathe plastic sooner than later.

Snorkel her, Venty. Go back to da rack for some RACK TIME.

Next question.
 
Yep.

Marino says if you're even thinking the patient needs to be intubated, LETTEM' BREATHE THROUGH PLASTIC.

Or something like that.

SpO2 95% on 50% FiO2 aint the greatest.

Sounds like shes gonna need it eventually anyway, so I'll side with the critical care guru's opinion that you breathe plastic sooner than later.

Next question.

If Marino says it, I believe it. I love his book. I haven't read the new edition. That reminds me of another anesthsia myth (see other thread) but since I am here, I'll post it here. According to Marino, trendelenberg worsens cardiac output and cerebral blood flow. It does increase bp however so when we do t berg and see the bp rise, we think we r doing great. Not so, according to him. (at least in the previos edition)
 
If I may be so bold as to pipe in here for a bit ...

Positive pressure ventilation can have variable effects on your cardiac output. It'll decrease your preload and therefore venous return (thanks to increased intrathoracic pressure). But it can also increase your ejection fraction (thanks to decreased ventricular transmural pressure gradient). This latter phenomenon is akin to squeezing the air (i.e. blood) out of a balloon (the ventricle).

And thus, mechanical ventilation does help an ailing heart, as does non-invasive positive pressure ventilation as alluded to above: (1) by decreasing preload, and thus decreasing wall tension and therefore myocardial oxygen demand (remember LaPlace?). And (2), augmenting LV output. Not to mention the other benefits of mechanical ventilation: able to keeps sats at 100% and therefore maximize oxygen carrying capacity of blood, keeping a patient sedated and therefore not moving and therefore not extracting so much oxygen from blood, leaving more for the heart ...

I'll stop here ... I can see some of you guys are already snoozing.
 
4) when i was a resident we'd get these requests every 2 or 3 months... I usually told them that their attending had to discuss it with my ICU attending --- the ICU attending would usually ask for data to support their request... then they would shut up for 2 more months

...


Is your ICU attending also waiting for data that shows parachutes work?

For some reason, I doubt anyone would be willing to allow themselves to be randomized into a double-blind, placebo-controlled trial that tests the hypothesis that parachutes decrease mortality.
 
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If I may be so bold as to pipe in here for a bit ...

Positive pressure ventilation can have variable effects on your cardiac output. It'll decrease your preload and therefore venous return (thanks to increased intrathoracic pressure). But it can also increase your ejection fraction (thanks to decreased ventricular transmural pressure gradient). This latter phenomenon is akin to squeezing the air (i.e. blood) out of a balloon (the ventricle).

And thus, mechanical ventilation does help an ailing heart, as does non-invasive positive pressure ventilation as alluded to above: (1) by decreasing preload, and thus decreasing wall tension and therefore myocardial oxygen demand (remember LaPlace?). And (2), augmenting LV output. Not to mention the other benefits of mechanical ventilation: able to keeps sats at 100% and therefore maximize oxygen carrying capacity of blood, keeping a patient sedated and therefore not moving and therefore not extracting so much oxygen from blood, leaving more for the heart ...

I'll stop here ... I can see some of you guys are already snoozing.
Oh, I didn't know that mechanical ventilation had so many great benefits, I think we should start offering mechanical ventilation holidays to people who can afford it, here is how the ad in the news paper would look like:
Are you tired, depressed, or just need to relax?
Come visit us at the Best Hospital On Earth, we offer state of the art intubation and mechanical ventilation, we do the breathing work for you so you can concentrate on the more important things in your life.
We offer flexible financing and take major credit cards.
se habla espanol.
 
If Marino says it, I believe it. I love his book. I haven't read the new edition. That reminds me of another anesthsia myth (see other thread) but since I am here, I'll post it here. According to Marino, trendelenberg worsens cardiac output and cerebral blood flow. It does increase bp however so when we do t berg and see the bp rise, we think we r doing great. Not so, according to him. (at least in the previos edition)

The new edition is great. Very easy to read and digest the concepts. He spends several paragraphs debunking the use of the trendelenberg position for hypotension, but try to explain that physiology to the nurses when a patient tanks.

TIVA, nice summary of the effects of PPV. Those effects are often dependent on fluid status. For those pts. that are dry, the effects of increased intrathoracic pressure/decreased preload usually predominate. However, in pts. that are euvolemic/hypervolemic such as our failing heart, the decreased afterload/pump augmentation usually predominates and we can see improvement in forward flow.

I don't have the experience or insight that everybody else has and there are a lot of risks/benefits to weigh, but I do think an elective intubation is justifiable if everyone is on board.
 
At rest....with EVERYTHING normal...lungs, heart, etc.....5% of oxygen consumption goes to the work of breathing....

You do the math.....

Therapeutic REST is something still advocated by some to improve survival in patients with severe COPD.

The CONCEPT is sound....application is a different story.

Whether this lady needed it or not is something we (ie doctors who AREN"T there) can not decide on the internet.

Just because something is NOT within your experience doesn't mean that it is stupid or useless or wrong.....

I've learned that over and over again during my fellowship in CCM and over and over again while in practice with a mulidisciplnary team in the ICU.....

Too many people only practice with physicians who are similarly trained....and that leads to ...close minded ness.
 
At rest....with EVERYTHING normal...lungs, heart, etc.....5% of oxygen consumption goes to the work of breathing....

You do the math.....

Therapeutic REST is something still advocated by some to improve survival in patients with severe COPD.

The CONCEPT is sound....application is a different story.

Whether this lady needed it or not is something we (ie doctors who AREN"T there) can not decide on the internet.

Just because something is NOT within your experience doesn't mean that it is stupid or useless or wrong.....

I've learned that over and over again during my fellowship in CCM and over and over again while in practice with a mulidisciplnary team in the ICU.....

Too many people only practice with physicians who are similarly trained....and that leads to ...close minded ness.
I am really tempted to respond to your words of wisdom but I will let you slide this time.
 
Whether this lady needed it or not is something we (ie doctors who AREN"T there) can not decide on the internet. .

i agree. I dont know how many times i have been described a patient over the phone or in the chart only to see the patient and come out with a totally different perspective.
 
If I may be so bold as to pipe in here for a bit ...

Positive pressure ventilation can have variable effects on your cardiac output. It'll decrease your preload and therefore venous return (thanks to increased intrathoracic pressure). But it can also increase your ejection fraction (thanks to decreased ventricular transmural pressure gradient). This latter phenomenon is akin to squeezing the air (i.e. blood) out of a balloon (the ventricle).

And thus, mechanical ventilation does help an ailing heart, as does non-invasive positive pressure ventilation as alluded to above: (1) by decreasing preload, and thus decreasing wall tension and therefore myocardial oxygen demand (remember LaPlace?). And (2), augmenting LV output. Not to mention the other benefits of mechanical ventilation: able to keeps sats at 100% and therefore maximize oxygen carrying capacity of blood, keeping a patient sedated and therefore not moving and therefore not extracting so much oxygen from blood, leaving more for the heart ...

I'll stop here ... I can see some of you guys are already snoozing.

Not sure if a tube is the best thing for the patient, but let's keep our physiology straight here folks. Positive pressure's effects on CO are dependent upon the ventricle in question. In a failing ventricle, TIVA is absolutely right. This is the basis for looking at systolic pressure variation or pulse-pressure variation on PPV.

If we're pulling out all the stops, why not try NI-PPV prior to the tube? She may not tolerate it, or she might enjoy the PEEP.
 
Not sure if a tube is the best thing for the patient, but let's keep our physiology straight here folks. Positive pressure's effects on CO are dependent upon the ventricle in question. In a failing ventricle, TIVA is absolutely right. This is the basis for looking at systolic pressure variation or pulse-pressure variation on PPV.

If we're pulling out all the stops, why not try NI-PPV prior to the tube? She may not tolerate it, or she might enjoy the PEEP.

In a failing ventricle, SPV will be less than 10. SPV tells us fluid responsiveness of the ventricle, or in other words, tells us if hemodynamic parameters will improve with fluid.

Actually, I should say that isn't 100% true. There is some thought after measuring systolic pressure at end expiration, then delta down correlates with ventricular function, and delta up correlates with a measure of central venous status. I don't know the normal delta numbers.
 
looking back at the last few responses validates my comments on working only with people who are similarly trained.

There seems to be a focus on mech vent and it's effect on CO.

I'll tell you right now, those attendings who are asking for the mech vent don't give a rat's as s on what the CO is or what mech vent will do to it.

BECAUSE it doesn't matter....her CO is enough right now....and will be ENOUGH after mech vent.

The overall desired effect is that she will require LESS CO AFTER mech vent is instituted.
 
Therapeutic REST is something still advocated by some to improve survival in patients with severe COPD.

Yeah, it works great... until you want to pull the tube out.

Same phenomenon with the Lil' Buddy (and other versions) of mobility chairs. People feel better and can get around more, but they die faster.

Exercise is good. Unless you have stunned myocardium you're trying to rest, there's no role for elective intubation (gosh, maybe if I keep trying and trying, someday I can be Marino with his often-untested-and-unsubstantiated opinions).

-copro
 
Yeah, it works great... until you want to pull the tube out.

Same phenomenon with the Lil' Buddy (and other versions) of mobility chairs. People feel better and can get around more, but they die faster.

Exercise is good. Unless you have stunned myocardium you're trying to rest, there's no role for elective intubation (gosh, maybe if I keep trying and trying, someday I can be Marino with his often-untested-and-unsubstantiated opinions).

-copro

In the opening post, Vent also said that she is coughing up blood 2/2 the heparin gtt. The effects on CO previously discussed aside, do we need to worry about the risk of aspiration and need to control the airway?
 
Marino's book has too much opinion in it, for me, to be an objective ICU text.
 
Marino's book has too much opinion in it, for me, to be an objective ICU text.

Which text(s) do you prefer? militarymd, any suggestions?

I'm working some extra ICU time into my CA-3 year, and am looking for something meaty vs going through Marino and the usual articles again.
 
Which text(s) do you prefer? militarymd, any suggestions?

I'm working some extra ICU time into my CA-3 year, and am looking for something meaty vs going through Marino and the usual articles again.

you're at Portsmouth....there should be a thick folder of stuff left over from me and rich bosco on icu stuff....

dean giacobee should also have a thick folder of stuff for you guys.
 
(gosh, maybe if I keep trying and trying, someday I can be Marino with his often-untested-and-unsubstantiated opinions).

-copro

Marino's book has too much opinion in it, for me, to be an objective ICU text.

Examples? If you are referring to my comment about trendelenburg causing decrease in cardiac output, I will say that it is more than opinion. He as data to support his statement (and references them in his text.) There is no data contrary to what he says (that I am aware of.)
 
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