# Inducing Barotrauma during CPR



## MrBooger (Oct 11, 2012)

I've taken many ACLS classes and half the time it is taught that compressions and bagging should remain separate. You know 30:2, but once a patient is intubated then bagging can remain at a slow constant pace. The other half of the time it is taught that it should still remain separate at 30:2. 

I believe that it should still remain separate. Yes, we know that the air is moving directly into the lungs and not into the stomach, but if I compress the bag and force air into the lungs while someone else does a chest compression at the same time and is forcing air out of the lungs, those two opposing forces inside the lungs is enough to cause barotrauma. Also, it isn't doing anything beneficial for the patient since it is like taking a straw and me blowing in one end, and you blowing in the other end. No air movement in either direction, just a lot of pressure in the straw. 

Am I correct? Is this what you have all been taught as well?


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## NYMedic828 (Oct 11, 2012)

Any intubated patient in arrest should be ventilated at a rate of one breath every 6-8 seconds as per AHA guidelines.

Realistically, CPR no matter how careful you are will almost always cause some if not a lot of damage if done for an extended period of time. You are already breaking their ribs off the bat.

A good provider will time their ventilations between compressions.


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## Bieber (Oct 11, 2012)

The best thing to do would be to not ventilate these patients at all. We ventilate through compressions currently, where I'm at. Hopefully we'll stop ventilating at all soon.


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## Handsome Robb (Oct 11, 2012)

Bieber said:


> The best thing to do would be to not ventilate these patients at all. We ventilate through compressions currently, where I'm at. Hopefully we'll stop ventilating at all soon.



:unsure:

Last time I checked hypoxia was a reversible cause of cardiac arrest...I'm definitely open to new opinions but compressions alone are not going to provide enough change in pressure to cause adequate ventilation for any sustained period of time. 

If you are referring to cardiocerebral resuscitation (CCR) versus cardiopulmonary resuscitation (CPR) then I get what you're saying but the NRB is still a temporizing measure until an ALS airway can be placed and the pt ventilated via conventional techniques. Also it's worth noting that CCR has contraindications just like any treatment path, one of those being cardiac arrest with a suspected respiratory etiology.


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## NYMedic828 (Oct 11, 2012)

Bieber said:


> The best thing to do would be to not ventilate these patients at all. We ventilate through compressions currently, where I'm at. Hopefully we'll stop ventilating at all soon.



I would consider this improper.

Establishing an ALS airway has more purpose than solely ventilating.

Prevention of aspiration, keeping a patent airway post resuscitation and monitoring of ETCO2 are all vital aspects of CPR.

You can try to passively oxygenate through chest compressions all you want but if the airway is blocked your effort is null.


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## BLS Systems Limited (Oct 11, 2012)

Normal spontaneous breathing generates intrapulmonary pressures in a very small range (zero plus or minus 5 cmH2O).  Bagging with or without an ETT can generate pressures anywhere from 20-60+ cmH2O, which can cause barotrauma.  Trying to force air in a system with increasing intrathoracic pressures will only increase the intrapulmonary pressures.  Your efforts to introduce oxygen and blow off CO2 will be inefficient.  Many services are moving towards adult BVM's with pressure blow-offs that limit the pressures to 35-45 cmH2O (depending on the brand).

The best solution is to work together in a co-ordinated effort.


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## Bieber (Oct 11, 2012)

NVRob said:


> :unsure:Last time I checked hypoxia was a reversible cause of cardiac arrest...


Cardiac arrest secondary to hypoxia is an exceedingly rare thing. Why should we treat all cardiac arrests as due to hypoxia when the reality is that most are due to heart disease?



> I'm definitely open to new opinions but compressions alone are not going to provide enough change in pressure to cause adequate ventilation for any sustained period of time.


Dr. Gordon Ewy might disagree with you!



> If you are referring to cardiocerebral resuscitation (CCR) versus cardiopulmonary resuscitation (CPR) then I get what you're saying but the NRB is still a temporizing measure until an ALS airway can be placed and the pt ventilated via conventional techniques. Also it's worth noting that CCR has contraindications just like any treatment path, one of those being cardiac arrest with a suspected respiratory etiology.


Again, I think Dr. Ewy would disagree with you that the NRB is a "temporizing measure until an ALS airway can be placed". As for your second comment, I'll again point out that cardiac arrest due to some respiratory etiology makes up a very small percentage of all cardiac arrests.



NYMedic828 said:


> I would consider this improper.
> 
> Establishing an ALS airway has more purpose than solely ventilating.
> 
> ...


Most cardiac arrests are not due to blocked airways. And ETCO2 can be measured via a nasal cannula. Finally, if patients in cardiac arrest are aspirating or losing their airways so frequently that intubation during cardiac arrest is as vital as you claim, then why is there no evidence of increased survival in cardiac arrest patients following intubation?

There's a place for the tube (maybe), but it's not in routine cardiac arrest.

EDIT: Another thought: even in those rare cases where intubation may be beneficial to a select subset of patients in cardiac arrest, is that benefit so great as to offset the harm caused by decreasing blood return to the heart secondary to increased intrathoracic pressure with ventilations?


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## Veneficus (Oct 11, 2012)

Bieber said:


> Cardiac arrest secondary to hypoxia *in adults* is an exceedingly rare thing. Why should we treat all cardiac arrests as due to hypoxia when the reality is that most are due to heart disease?



Fixed that for you.


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## Bieber (Oct 11, 2012)

Veneficus said:


> Fixed that for you.


Gracias. I was addressing adult patients suffering from cardiac arrest in all my previous posts, for clarification.


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## mycrofft (Oct 11, 2012)

Bieber said:


> Cardiac arrest secondary to hypoxia is an exceedingly rare thing. Why should we treat all cardiac arrests as due to hypoxia when the reality is that most are due to heart disease?
> 
> 
> Dr. Gordon Ewy might disagree with you!
> ...



(Note reply above by BLS SYSTEMS citing actual scientific measurements.)

Putting aside for the moment the new findings about giving too much oxygen:

Hypoxic cardiac arrests:  drowning, drug overdose, choking assault, electrocution, mechanical asphyxiation (plastic bag). airway embarrassment (food bolus, mucus, vomitus, blood, or tongue), prolonged seizure, poisoning, hypoxic atmosphere, airway trauma, etc. _*The majority of pediatric/infant cardiac arrests are due to hypoxia.
*_

NRB could be classed as a "temporizing measure" if you are doing compression only CPR, but anyone with clearance to use a NRB at more than a fixed 6 LPM ought to be to doing more than hands-only CPR unless they are caught without equipment (say, Texas Roadhouse on a Friday evening?). 

With the aspirations I've seen due to bystander or other CPR without airway, I find it hard to believe advanced airways have _*NO*_ salutary effect on outcome if other factors are eliminated, such as severity of the pt condition leading to code, etc.

Bieber, AHA and ARC do not suggest that compression-only CPR is superior or equivalent to compressions with inflations, it is a means to empower laypersons to do CPR by allowing them to forego mouth to mouth inflations.

I have to fix supper, but someone ought to cite some sources about barotrauma with CPR. I'm not saying it isn't a factor, I'm saying a scientific citation beats three column-inches her of jackjawing back and forth.


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## Merck (Oct 11, 2012)

There is currently a study ongoing through the Rescucitation Outcomes Consortium dealing with this question of 30:2 vs. continuous.


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## triemal04 (Oct 11, 2012)

Merck said:


> There is currently a study ongoing through the Rescucitation Outcomes Consortium dealing with this question of 30:2 vs. continuous.


I thought the point of that was to assess whether or not the difference in hands off time during ventilations would make a difference.  I suppose you could try and use the data to answer the questions about barotrauma specifically, but since you could only assess survivors, that wouldn't work so well.  

It's something to be concerned about, but it still has a very simple solution: make sure the people you work with are well trained and know to only be giving small amounts of air (no fully squeezing the bag with both hands) and at a very slow rate.  Mitigate the problem as much as you can that way.

As far as using a nasal cannula ETCO2 detector during CPR...good luck with that.  I'll pretty much gaurentee that you won't get anywhere near accurate readings.  Consider:  with an ET tube and ETCO2 detector in place you often will get "bumps" in the ETCO2 waveform from compressions...but they are minimal compared to what you get during actual ventilations and at much lower levels.


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## mycrofft (Oct 11, 2012)

*Addit to my comment above:*

I'm advised that AHA _et al_, considering all arrests, find the vast, vast majority of sudden arrests are due to MI's. 

I believe that, overall, but two or three wrinkles come to mind:

1. In some subgroups (children*, electrical supply workers, suicidal people, the severely debilitated, etc etc) that is not going to be the case. 

2. How does a responder know if a pulseless person had a "sudden" demise, or something else? 

If the treatment set for "sudden MI"  mistreats another set of patients, and the treatment set for "other types of patients" (while not as elegant) do not mistreat "sudden MI" patients, then treatment set #2 is my choice.


PS: Don't know about now, but we were taught that the presenting symptom for 70% of new MI's was "sudden death". It reciprocates.

*If it's _my_ granddaughter, don't tell _me_ you aren't going to do rescue breathing , BVM, etc.


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## Bieber (Oct 11, 2012)

mycrofft said:


> Putting aside for the moment the new findings about giving too much oxygen:



Aw, let's not do that! 



> Hypoxic cardiac arrests:  drowning, drug overdose, choking assault, electrocution, mechanical asphyxiation (plastic bag). airway embarrassment (food bolus, mucus, vomitus, blood, or tongue), prolonged seizure, poisoning, hypoxic atmosphere, airway trauma, etc. _*The majority of pediatric/infant cardiac arrests are due to hypoxia.
> *_


Yes, that is an impressive variety of etiologies, however all of those together still comprise the vast minority of total cardiac arrests. What is the point you are trying to make?



> NRB could be classed as a "temporizing measure" if you are doing compression only CPR, but anyone with clearance to use a NRB at more than a fixed 6 LPM ought to be to doing more than hands-only CPR unless they are caught without equipment (say, Texas Roadhouse on a Friday evening?).


What else would you suggest doing? Besides defibrillation, I mean.



> With the aspirations I've seen due to bystander or other CPR without airway, I find it hard to believe advanced airways have _*NO*_ salutary effect on outcome if other factors are eliminated, such as severity of the pt condition leading to code, etc.


You find it one way, the studies suggest another.



> Bieber, AHA and ARC do not suggest that compression-only CPR is superior or equivalent to compressions with inflations, it is a means to empower laypersons to do CPR by allowing them to forego mouth to mouth inflations.


And?



mycrofft said:


> 2. How does a responder know if a pulseless person had a "sudden" demise, or something else?


"Did they clutch their chest and collapse? Did they simply collapse? Were they having trouble breathing before they collapsed? Do they have any respiratory diseases?"



> If the treatment set for "sudden MI"  mistreats another set of patients, and the treatment set for "other types of patients" (while not as elegant) do not mistreat "sudden MI" patients, then treatment set #2 is my choice.


Evidence that ETI or PPV increases survival to discharge neurologically intact for ANY (adult) patients in cardiac arrest? And why should we default to "special circumstances treatment" with all patients, when the vast majority of cardiac arrest patients do not fall into those "special circumstances" situations.


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## Veneficus (Oct 11, 2012)

Bieber said:


> And why should we default to "special circumstances treatment" with all patients, when the vast majority of cardiac arrest patients do not fall into those "special circumstances" situations.



I think the point being made is one I support.

You treat the patient you have, not the statistics.

I fully agree that these special circumstances are a minority, but this minority could run into 10's of thousands of people a year.

I don't think you suggest just writing them off without attempting resuscitation at all?


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## Bieber (Oct 11, 2012)

Veneficus said:


> I think the point being made is one I support.
> 
> You treat the patient you have, not the statistics.
> 
> ...


Not at all. I advocate ending this obsession with treating all cardiac arrests as if they were the same and to start treating cardiac arrests with the most appropriate care for whatever etiology can be most likely attributed to them. And if we are going to have any particular treatment as our "default", it should be the one which applies most appropriately to the most common cause of cardiac arrest, not the least common.

Like I said, I think that there is a role for ETI in EMS (again, maybe), but I don't think it's in the treatment of routine cardiac arrest.


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## Veneficus (Oct 11, 2012)

Bieber said:


> Not at all. I advocate ending this obsession with treating all cardiac arrests as if they were the same and to start treating cardiac arrests with the most appropriate care for whatever etiology can be most likely attributed to them. And if we are going to have any particular treatment as our "default", it should be the one which applies most appropriately to the most common cause of cardiac arrest, not the least common.
> 
> Like I said, I think that there is a role for ETI in EMS (again, maybe), but I don't think it's in the treatment of routine cardiac arrest.



I could get behind that.


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## mycrofft (Oct 11, 2012)

If etiology can be determined appropriately and accurately in the field, then heck yeah, and starting about ten years ago.

But sometimes we don't know for sure. If we curtail effective respiratory support for a minority who also are the sector of arrestees who will most likely recover due to field treatment because of statistics, it will be tragic.
Make a protocol, and teach, to support when there is doubt as well as obvious non-MI etiology.

We're a long way from barotrauma.


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## Bieber (Oct 11, 2012)

mycrofft said:


> If etiology can be determined appropriately and accurately in the field, then heck yeah, and starting about ten years ago.
> 
> But sometimes we don't know for sure. If we curtail effective respiratory support for a minority who also are the sector of arrestees who will most likely recover due to field treatment because of statistics, it will be tragic.
> Make a protocol, and teach, to support when there is doubt as well as obvious non-MI etiology.
> ...


Sorry, didn't mean to sidetrack the thread.

But real quick, how can you justify applying a treatment which is not beneficial and potentially harmful to the majority of patients "when in doubt", as opposed to catering to the most common etiology when the cause of the particular patient's arrest is unknown?


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## usalsfyre (Oct 11, 2012)

Bieber said:


> But real quick, how can you justify applying a treatment which is not beneficial and potentially harmful to the majority of patients "when in doubt", as opposed to catering to the most common etiology when the cause of the particular patient's arrest is unknown?



Isn't this basically what ACLS is? 

That said, I'm not sold on CCR yet. The numbers I've seen (admittedly its been a while since I've looked) are far more ambiguous than its cheerleaders make it out to be. 

I think one of the biggest thing we need to realize is if you arrest in the field your so far behind the 8-ball your mostly screwed anyway. I'd rather see more energy focused on other areas if resuscitation.


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## mycrofft (Oct 11, 2012)

We never cater.:rofl:

Good question. Balancing likelihood of harm versus likelihood of efficacy. Hasta be an app for that. (We balance likelihood of degree of harm for the particular patient versus then likelihood of etiology for that patient).
Pint taken.


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## MrBooger (Oct 12, 2012)

So back to the origional question.............Do you guys continuously bag someone when intubated, or keep a 30:2 ratio?


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## Handsome Robb (Oct 12, 2012)

MrBooger said:


> So back to the origional question.............Do you guys continuously bag someone when intubated, or keep a 30:2 ratio?



Bag, well set my vent  , at a rate of 10-12 with an advanced airway otherwise it's 30:2.


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## Brandon O (Oct 12, 2012)

MrBooger said:


> So back to the origional question.............Do you guys continuously bag someone when intubated, or keep a 30:2 ratio?



The guidelines say that once an advanced airway is in place, you should provide continuous asynchronous ventilations. Anybody teaching otherwise in a formal setting needs to be slapped with a swordfish.

The question about barotrauma is good, but we usually try to prioritize problems. There are a lot of things we used to do in arrests in order to manage theoretical adverse effects, but they interfered with the stuff that really mattered, so they keep getting cut. That's why modern resuscitation is pretty much all about terrific compressions and electricity; those address the lack of circulation, which is the bottleneck for survival. If we had a 100% rate of ROSC, yet every single patient we brought back had aspiration pneumonia, barotrauma, broken ribs, and psoriasis, I think we'd agree that's great work and much better than the alternative.

It's certainly true that fairly minimal ventilations, if any, are needed for these patients. Pulmonary perfusion is low, systemic demand is low, and we're using (nearly) 100% FiO2. Even for longer arrests I am interested in seeing how the data bears out on methods like the NRB with passive insufflation. (Although I wonder if it might be more effective with a nasal cannula at high flow... that's been shown to provide very good apneic oxygenation, whereas the NRB only introduces gas to the airway from active inhalation -- which you're providing somewhat with compressions, but still.)

I think saying that the "vast, vast majority of sudden arrests are due to MI's" may be a stretch. I've seen a range of numbers but the highest has been a modest majority, and in some cases it's a minority (usually vs. structural problems like cardiomyopathy).


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## mycrofft (Oct 13, 2012)

OK, I should have said "structural deficits including infarcts, WPWS, etc., and excluding penetrating trauma". My sourceh34r: said MI so I passed it on.
Good one.


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