# CPR in infants and children



## HMartinho (Nov 25, 2011)

I learned 15 compressions and 2 ventilations, but there are some pediatricians who defend 30 compressions by 2 ventilations, as in the adults.

What ratio do you use?


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## Shishkabob (Nov 25, 2011)

The primary cause of arrest in most kids is an airway / oxygenation issue, and not a cardiac issue, therefor you fix it with oxygen and not cardiac therapy.  Kids get more ventilations than adults.



Per AHA, 1 rescuer is 30:2, 2-rescuer is 15:2

http://circ.ahajournals.org/content/122/18_suppl_3/S862.full


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## TheGodfather (Nov 25, 2011)

if you are CERTAIN that the arrest is cardiac in origin, then yes, 30:2 would be more beneficial. However, as linuss stated: most pediatric arrests are respiratory in nature, therefore more effective PPV with 100% oxygen will usually fix the problem (15:2)..

In neonatal resus, it goes even farther than that: If you are required to perform CPR on a neo (HR<60), AAP calls for 3:1 ratio with 2 rescuers. Again, with that, if there is a CERTAIN/KNOWN cardiac defect then 15:2 would be more beneficial.


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## Brandon O (Nov 25, 2011)

TheGodfather said:


> if you are CERTAIN that the arrest is cardiac in origin, then yes, 30:2 would be more beneficial. However, as linuss stated: most pediatric arrests are respiratory in nature, therefore more effective PPV with 100% oxygen will usually fix the problem (15:2)..
> 
> In neonatal resus, it goes even farther than that: If you are required to perform CPR on a neo (HR<60), AAP calls for 3:1 ratio with 2 rescuers. Again, with that, if there is a CERTAIN/KNOWN cardiac defect then 15:2 would be more beneficial.



Interesting statement. Neonatal resus is considered such a specialized scenario that it's rarely taught seriously in standard BLS curricula. 3:1 is the standard but I agree that this likely assumes multiple rescuers, given the rare probability of working a solo neonatal arrest. However I don't think this has been stated explicitly. Attempting 3:1 with one person would certainly require fast movement and I doubt would work well, even though  neonatal resuscitation is almost all about oxygenation and general TLC.


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## TheGodfather (Nov 25, 2011)

Brandon Oto said:


> Interesting statement. Neonatal resus is considered such a specialized scenario that it's rarely taught seriously in standard BLS curricula. 3:1 is the standard but I agree that this likely assumes multiple rescuers, given the rare probability of working a solo neonatal arrest. However I don't think this has been stated explicitly. Attempting 3:1 with one person would certainly require fast movement and I doubt would work well, even though  neonatal resuscitation is almost all about oxygenation and general TLC.



Like anything, everything looks good on paper. i think they say the percentage of live births that even make it to the steps of CPR, are 1%. the percentage that need PPV is around 8-10% (if my memory serves me correctly) and those usually will improve with just the PPV alone. With that said, it really can be done correctly with 2 rescuers. (typically) the only drug u will be pushing is epi. the standard epi 1:10,000 pre-filled syringe should last you an entire code (with some left over at the end) so not much time is spent drawing up/prepping meds. Your fluid challenges can be pushed using pre-filled NS syringes (typically 30cc's is more than enough for initial fluid challenge). So really, once intubated, one rescuer should be able to maintain ventilations/compressions while the other manages medications (assuming that the second person rechecks tube placement often, or you have continuous capnography monitoring capabilities).

forgot to add: AAP standards state that before compressions are even started, or IO access is obtained, ET tube placement should be performed. So when performing standard BVM by mask ventilations, there should always be 2 rescuers (in a perfect setting)


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## WTEngel (Nov 25, 2011)

Agressive oxygenation of the full term newborn infant has fallen out of style in recent years.

The target goals for pre-ductal %SPO2 in the full term neonate are:

1 minute post partum - 60-65%
2 minutes                 - 65-70%
3 minutes                 - 70-75%
4 minutes                 - 75-80%
5 minutes                 - 80-85%
10 minutes                - 85-95%

Aggressively oxygenating to levels above this does not demonstrate better patient outcomes and can actually harm the vital organs.

There is a considerable amount of patho that changes in the fetal circulation in the first hour after birth, and continues to change for the next 48-72 hours generally. The administration of high concentration oxygen can negatively impact these processes.

There have been a few randomized studies that indicate higher survival rates in neonates resuscitated with room air as opposed to brief exposure to high concentration oxygen.

In regards to the OP, for BLS resuscitation of pediatric patients greater than 30 days old until the onset of secondary sexual characteristics, we use 30:2 for one rescuer, and 15:2 for 2 rescuer, and titrate supplementary oxygen to a %SPO2 of 94 - 99.

Hope that helps.


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## WTEngel (Nov 25, 2011)

I also wanted to point out that it is somewhat of an over-simplification to say we give pediatric patients more breaths than adults solely because we have a high suspicion of hypoxic etiology of arrest. 

We administer more breaths in pediatric patients because it easier to match ventilation to perfusion in the pediatric patient population, due to more compliant rib cages, the strength of the provider giving compressions compared to the amount of energy necessary to get coronary perfusion pressure up, etc. 

Simply put, we can not effectively do CPR well enough on adults to match a compression to ventilation rate of 15:2. When we do not match ventilation to perfusion (typically over ventilating), we get a shift of the oxyhemoglobin dissociation curve, ultimately causing hypoxia and ischemia, despite the 100% saturation.

I just wanted to point that out, because it is important to understand the concept of matching ventilation to perfusion, as many of the AHA resuscitation changes have been made with v/q matching in mind. What everyone is saying about giving more breaths because of hypoxic etiology is not necessarily wrong, but it glosses over some important concepts.


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## Brandon O (Nov 25, 2011)

Well said as always Engel. I didn't mean to imply that high FiO2 is the goal in neonates; merely that circulatory dysfunction is typically resolved by respiratory support rather than primarily cardiac interventions (unless congenital). Warming, stimulation, PPV, O2, etc as appropriate is far more common.

I agree that the relative ease of the bottom half of the V/Q is likely part of the reason for the CPR ratios in peds; however I haven't seen this noted explicitly in the guidelines. Are you basing this on personal correspondence?

Also am curious and hope you can elaborate on V/Q mismatch shifting oxyhemoglobin dissociation curve -- I assume you mean a true shift of the curve and not mere motion along it. Do you mean leftward shift? If so why?

Sent via my Droid


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## WTEngel (Nov 25, 2011)

My emphasis on matching ventilation to perfusion is gleaned from extensive personal experience, and being well read on the 2010 AHA guidelines.

The guidelines do not say in so many words "match ventilation to perfusion," but when read in detail, they include in their rationale for many treatments, sentences like the following, taken from pg S878 of Circulation published on 2 November, 2010:

"Remember that adequate oxygen delivery requires not only adequate arterial oxyhemoglobin saturation but also adequate hemoglobin concentration and cardiac output."

Like everyone has said, and I fully agree, oxygen delivery is the key treatment in correcting the precipitating cause of the majority of pediatric arrest scenarios.

That is just one example of the AHA reminding folks that ventilation is one component of high quality resuscitation. I don't fault many people for not going through the Circulation journal ad nauseam, but I teach PALS, ACLS, and BLS to incoming residents, med students, attending physicians, among many other well educated disciplines, so they keep me on my game. These students are what we call "sharp shooters." That is to say, they ask the questions that 95% of instructors can not answer, and they do it because they know this!

Regarding the oxyhemoglobin dissociation curve, there are a few factors at play. You are correct that we are talking about a left shift of the entire curve, not left movement along the curve. This happens for a few reasons.

During resuscitation, if we have increased ventilation in the presence of decreased perfusion, we see arterial pH begin to rise. This causes a left shift and increased affinity (decrease release) of oxygen that is bound to hemoglobin. While we do see acidosis when we look at venous lab results, some studies have suggested that this is not necessarily the best representation of metabolic state, and the arterial delivery of oxygen is what will perfuse organs.

Also, CO2 retention is increased during arrest, which leads to a left shift. While increased ventilation can assist in removing exhaled CO2, if our perfusion/circulation is poor, we are not effectively removing systemic CO2 no matter how much we increase ventilation rate. Again, match ventilation to perfusion, in this case, optimize perfusion.

Last, and probably most significant, neonates are born with an already left shifted curve. This is because fetal hemoglobin has a higher affinity for oxygen (the presence of 2,3-DPG does not effect fetal Hb) so it can bind at lower partial pressures. This assists in facilitating gas exchange across the placenta. The high concentration of 2,3-DPG at the placenta causes increase 2,3-DPG binding to adult Hb, allowing it release oxygen more readily. 2,3-DPG does not have this effect on fetal Hb, thus allowing binding at lower partial pressures, ultimately allowing for effective oxygenation of the fetus.

Ultimately, it is easier to match ventilation to perfusion than vice versa. Compressions will very likely never be so effective as to surpass the currently accepted standards for ventilation rate during arrest, so the focus is on the most effective compressions, understanding that we will most likely have to decrease ventilation to match the output achieved.

I am by no means an expert on these things, and if anyone has anything to add to, correct, expand upon, etc. please do so. I really know just enough to make me think very carefully about certain decisions I make during resuscitation.


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## TheGodfather (Nov 25, 2011)

WTEngel said:


> " I am by no means an expert on these things, "



coulda fooled me! good info.:beerchug:


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## Brandon O (Nov 25, 2011)

Excellent stuff, thank you. My peds is very weak; I didn't realize that about fetal 2,3-DPG. Does this effect begin to reverse at birth, or does it persist for some time into infancy?

If a leftward shift is typical in neonates, however, it seems like our response to this be to deemphasize ventilation in favor of compressions, not the other way around. If neonates have a very high affinity for oxygen, then we won't need to ventilate very aggressively to keep saturation high; however, we're behind the 8-ball on actually delivering O2 to the tissue, so the more circulation the better.

In general I suppose I agree about the role of V/Q in resuscitation; however, I take a different approach to it. In cardiac arrest we know that positive pressure ventilation has major negative effects on preload, thoracic impedance, compression fraction, training complexity and willingness of bystander intervention, and so on. We should therefore view it as a treatment with substantial downsides, and our goal as therefore to use as little of it as possible to achieve the necessary gas exchange. Since circulation is minimal in arrest anyway and so is metabolism, little ventilation will be needed to match perfusion. (This is assuming that interrupting our much-needed circulation to give ANY breaths is helpful, which is far from obvious, but even the most gas-happy critic will surely agree it doesn't take much.) So in that sense, the goal is really to maximize circulation of adequately (not overly) oxygenated blood, and that requires lots of compressions, but not much ventilation.

Which I suppose is another way of saying what you did! But the point is that there's nothing magical about a well-matched V/Q; it's just that too much V is clearly detrimental to circulation, and circulation is usually what we need to focus on.


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## WTEngel (Nov 26, 2011)

Adult Hb production commences at birth and between 18 and 24 weeks it is the predominant Hb found in the blood. Between 1-2 years most if not all of the fetal Hb will be gone from the blood. If you poke around on google you can look at some really interesting sickle cell anemia treatment modalities being developed around fetal Hb. 

While reducing the emphasis on ventilation makes sense in the adults because of decreased perfusion, in neonates and peds we see higher coronary perfusion and cardiac output during compressions because of higher chest wall compliance and the rescuers ability to more effectively attain adequate depth of compression, making it easier to match a higher rate of ventilation to perfusion.

I completely agree about the profound effects positive pressure ventilation has on patients who are peri-arrest or in full arrest. All things being equal, I would have to side with you on the fact that overly aggressive positive pressure ventilation and its effects on cardiac output, venous return, etc. have more relevance to field personnel than the metabolic effects of v/q mismatch.

It is really ironic that this is in the BLS discussion thread, because this happens to be one of the most high minded discussions about resuscitation on the forum. The bottom line is we are both talking about some extremely in depth science that is great to know for advanced providers, but will have little effect on field practice. I still enjoy talking about it though!

Ultimately, just as you said, we are arriving at the same conclusion. It is great to have these round table discussions though. I always enjoy your posts Brandon.


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## systemet (Nov 26, 2011)

TheGodfather said:


> forgot to add: AAP standards state that before compressions are even started, or IO access is obtained, ET tube placement should be performed.



In immediate post-delivery resuscitation?  Or are you talking abut a different situation?


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## systemet (Nov 26, 2011)

WTEngel said:


> Also, CO2 retention is increased during arrest, which leads to a left shift.



This is a great post, but I think you misspoke here.  CO2 retention should right shift the curve, via (i) Haldane effect: i.e. CO2 binding to form carbaminohemoglobin decreases O2 affinity, and (ii) Bohr effect: CO2 dissolves to form carbonic acid, and favouring acidosis, which also reduces oxygen affinity. Or maybe I misunderstood what you were trying to say.


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## Brandon O (Nov 26, 2011)

WTEngel said:


> Adult Hb production commences at birth and between 18 and 24 weeks it is the predominant Hb found in the blood. Between 1-2 years most if not all of the fetal Hb will be gone from the blood. If you poke around on google you can look at some really interesting sickle cell anemia treatment modalities being developed around fetal Hb.



Yup -- my girlfriend's a first year med student and she mentioned this to me. Very cool stuff. Adult Hb aren't working? Switch back to your baby ones... might have a goofy affinity for O2, but better than what you had going on.



> The bottom line is we are both talking about some extremely in depth science that is great to know for advanced providers, but will have little effect on field practice.



True enough. But I like to think that BLS describes a scope of practice, not a level of understanding, and that we all can -- and perhaps should -- be able to provide "BLS" care with an extremely strong grounding in assessment, pathophysiology, and treatment modalities. In fact, everyone from the Basic to the EM intensivist should ideally be doing BLS in that sense, because it's foundational skills, not just starting points. I'm always surprised at how the most esoteric information can -- when thrown into the pot with a million other things -- end up influencing the decisions we make... because the human body is complicated, and working in the field adds a lot of chaos and challenges, and understanding how things work and how important it is ends up determining what the best course of action will be.



> Ultimately, just as you said, we are arriving at the same conclusion. It is great to have these round table discussions though. I always enjoy your posts Brandon.



Likewise, sir. Fly safe.


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## WTEngel (Nov 27, 2011)

systemet said:


> This is a great post, but I think you misspoke here.  CO2 retention should right shift the curve, via (i) Haldane effect: i.e. CO2 binding to form carbaminohemoglobin decreases O2 affinity, and (ii) Bohr effect: CO2 dissolves to form carbonic acid, and favouring acidosis, which also reduces oxygen affinity. Or maybe I misunderstood what you were trying to say.



You are correct, and thank you for pointing that out. While CO2 retention will cause carbamino levels to increase, which would cause a left shift, in theory, the fact that only around 10% of the CO2 in the blood is in the form of carbamino compounds allows the prevailing effect of CO2 retention to actually be a rightward shift.

I saw an interesting research article that pointed out the difference between venous pH values and arterial pH values during resuscitation in pigs. They found that while venous pH had a tendency to be acidic (7.2 or so) arterial pH had been found to show mild alkalosis (7.5 or above.) 

They mentioned the difference in pvO2 and paO2 also, along with lactate production during and after arrest. These values are routinely examined after arrest, but there has not been a lot of research of these processes DURING arrest.

They also noted that the arterial values returned to normal quite rapidly after resuscitation given appropriate ventilation strategies, which is why the findings may not be as clear when drawing gases in the patient who has been resuscitated. The exact meaning of this and its effect on practice hasn't been fully explored yet.

Thanks again for the correction.


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## Handsome Robb (Nov 27, 2011)

WTEngel said:


> They mentioned the difference in pvO2 and paO2 also, along with lactate production during and after arrest. These values are routinely examined after arrest, but there has not been a lot of research of these processes DURING arrest.



Quick semi on topic question since we are doing PALS and NRP right now and I'm a bit confused on this one. When measuring Pv02 it has been mentioned that the value will differ depending on where it is measured from ie superior/inferior vena cava. Knowing that blood supplying cerebral functions tends to be more oxygen depleted where are you supposed to measure it? I know in the prehospital environment this doesn't come into play but it peaked my curiosity. I am leaning towards measuring superior venous values would be ideal along with a good physical exam of the periphery for SxS of hypoperfusion however the text isn't very clear on it.


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## WTEngel (Nov 27, 2011)

You are correct about IVC vO2 values being higher than SVC vO2 values. I have not seen these values vary more than 5-10% typically, so the difference is not profound. 

I don't have any personal experience with specifically drawing a lab from the IVC or SVC, and I can't think of a specific instance where one would be better than the other, although I am sure one exists. 

In kids who are post cardio thoracic surgery, typically we monitor vO2 values from a central line, so we end up getting a mixed sample. We measure cerebral oxygen saturation with a probe on the scalp, and we measure renal oxygen saturation with a probe across the abdomen. These probes are basically identical to the SPO2 monitors used on a patient's finger, but they lie in those specific areas so we can look at perfusion to vital organs. The general idea is that in the presence of adequate MAP and appropriate oxygen saturation values in these areas, we can be reasonably safe in saying that systemic perfusion is adequate.

So my perception would be, in almost any instance, any VBG you draw will be a relatively accurate indicator of overall oxygenation and consumption. 

In the newborn-72 hour range you do have to take the sample site into account when evaluating the arterial gas. Understanding that pre ductal values should be higher and are the important indicator for cerebral oxygenation will help you evaluate patient condition. Alternatively, a seemingly alarming gas drawn in the post ductal vasculature may not be as alarming as it looks, when taking into account that the DA should still be patent.


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## systemet (Nov 28, 2011)

WTEngel said:


> I saw an interesting research article that pointed out the difference between venous pH values and arterial pH values during resuscitation in pigs. They found that while venous pH had a tendency to be acidic (7.2 or so) arterial pH had been found to show mild alkalosis (7.5 or above.)



You don't happen to have the citation handy, do you?  I wouldn't mind reading this.  I'm a little surprised that the values are actually so high.  I would have expected them to be lower.  But I guess this also varies with the pathology.



> They mentioned the difference in pvO2 and paO2 also, along with lactate production during and after arrest. These values are routinely examined after arrest, but there has not been a lot of research of these processes DURING arrest.



It would be interesting to know what happens.  I'm a little weak on cardiac arrest physiology.




> Thanks again for the correction.



No problem, thanks for the awesome and insightful posts.  I hope I didn't come across as nitpicking.


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