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What do you use to guage CPR adequacy?


Jwade

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Its interesting that I read this thread tonight after just working a code a few hours ago. My answer to the original question, in terms of the average prehospital ground ambulance, would be purely observational. That is to say, watch the person performing chest compressions. If you can observe the person doing compressions using their shoulders, causing the pts chest to depress an adequate depth and then recoil, I'd say the compressions are probably being done properly.

On today's call the end tidal C02 probe wasn't working, luckily we had a bunch of big strong fire fighters on scene and they were able to perform what looked to me like high quality compressions. In retrospect, I gauged the CPR by observing the compressions, watching the ECG waveform in lead II- a wide, regular pattern, and also by asessing femoral pulse. With respect to the OP, the 2 times I did attempt to assess femoral pulse I felt nothing at all.

However, when it comes to CPR, why not just stick to the basics? If compressions are being performed the way we were taught- hard and fast- then we really don't need to worry about a lot else. I will agree that end tidal C02 is a fantastic tool, and should be used on all cardiac arrest and intubated pts.

If the femoral pulse checks are useless, as the posted study would suggest, then yes, I agree we shouldn't be wasting our time doing them. But, if someone does have a audacity to check one during compressions, I fail to see what harm it does to the overall delivery of CPR.

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  • 3 weeks later...

In the prehospital field, I've seen and personally felt for a femoral pulse during compressions and also looked on the monitor in lead 2 primarily and looked for continious wide complexes in sync with the compressions. Complying with the standards of hard and fast and allowing adequate recoil of the chest between compressions was the standards taught and the evidence presented in the AHA guidelines as well as the training given. We dont have the Autopulse devices etc HOWEVER..... most of the ambulances in NZ are now going MRX with QCPR so be interesting to see what that does to perhaps the CPR we have done for ages thinking was adequate. ETCO2 is also used if the patient is LMA'd or intubated.

In Hospital as a CCU RN, the monitors, femoral pulse, ETCO2 and maybe them fighting us off of them is signs we are getting good compressions/resus in. I do think though that CCU is one of the harder areas to assess as we get a defib in within about 10 seconds roughly or at least a Pthump and all of the staff are trained in manual defib with paddles to get the shock in faster.

It is interesting though reading the femoral pulse debate. Through any of my training it was standardly taught to feel the groin..... wait that sounds wrong....

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What is the MRX and QCPR? I'm not familiar with those terms.

MRX is the philips heartstart manual defibrillator which when combined with the QCPR sensor, gives feedback on compression effectiveness. This pad sits in the middle of the chest where you perform compressions and gives feedback in real time to the Monitor to advise CPR changes *push harder, faster, slower...... wait sounds like a night out with the wife.... anyway back to the topic*

Only downside to QCPR, not compatable with the MRX units with Paddles as it requires the pads to collaborate the resus information as the pads sense the recoil etc.

More information can be found on the philips health care site.

Scotty

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  • 3 weeks later...

In answer to your question on how to gauge effective CPR, it was stated in a threat "Although end-tidal CO2 serves as an indicator of cardiac output produced by chest compressions". More specifically End Tidal CO2 serves and indicator of cellular metabolism, excretion and ventilation that momentarily may or may not have any bearing on cardiac output. However. The Blood pressure cuff and "Rate" function in the Pulsoximeter is the only device that I know, we carry, that is dependant on "cardiac output" in order to function.

This brings us to a bigger problem, on of which I have been is discussion with Physio over the past year. It would be logical that during a cardiac arrest we would have the Life Pak hooked up monitoring the end tidal on the tube and the pulsox taped to the finger forehead or toe. If the rate function of the pulsox picks up a rate at the finger tips we know we have a B/P that approximates 80 systolic at what ever rate it indicates. If the pulsox is on the toe and reads, the B/P would be something higher.

Understand that if we have a reading indicated by the pulsox, we have a fact, and can confirm cardiac output and its “effective rate”. Remember the rate on the pulsox may differ from the rate you are doing compressions, however the rate indicated on the pulsox is the “effective rate” at wherever the sensor is placed. If we don’t have a reading we can neither confirm or deny the presence of cardiac output. Further, it would be irresponsible and one should not “chase the pulsox” as increasing the rate or depth of compressions ,to get a pulsox reading, beyond the specific norms recommended by the AHA is bad and wrong on many levels. Pulsoximetry actually measure the expansion of a pulsing vessel with no regard to electrical activity and is definitive.

I grew up on and started with the Life Pak 3. I am an ardent supporter of the Physio and as such was very disappointed. I don’t know if anyone has noticed that although the life Pak 12 has a rate function built in to the pulsox as soon as you hook up the EKG cables the “RATE” indicator on the display defaults to the Electronic Rate as read by the amount of electrical complexes on the screen or more simply the “heart rate and not the pulse rate”. When you unplug the leads it reverts back to the pulse rate providing you have the pulsox hooked up. As we in the field are primarily concerned with the pulse rate this is obviously and error and I have approached Physio on this and they have no answer yet. In addition the competition (who will remain nameless) has on their monitor 2 separate and distinct displays one for heart rate and one for pulse rate. This duel display is also helpful in detecting blocks or a brady with non perusing escape beats.

In answer to the question, if one of the 3 displays on my Life Pak is tuned to Pulsox wave form and if a waveform is present and the sensor itself is motionless on the fingertip and I have no intrinsic EKG complex I can say my CPR compressions have a cardiac output with a blood pressure approx at least 80 +/- systolic. The NIBP is also effective in this manner as well. If the NIBP detects a B/P on the calf or arm during CPR it is what is it.

Lastly the term effective needs to be clarified. Is the objective to be performing according the numbers in the AHA guidelines? Or to meet a consistent numeric pressure blood pressure value and pulse rate? If so what is min rate and more important the B/P to be effective?

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Please read your question

Now this quote is one of the first lines in RED you posted.

Seems like you posted this to stroke your own ego.

You specifically asked how WE assess proper CPR, then after the very 1st post, you slam the guy stating there is NO proper assessment backed up by evidence.

Duhhh......

He wanted evidence based assessment. Meaning, he wants numbers. He was asking for statistics of where the patient started at during a code, and where they ended up at and everything in between. This, is why CPR guidelines change. People do the leg work like John here to see how effective CPR actually is or isn't. You CANNOT say how good/bad CPR is just by saying they had no pulse, gave CPR, and now they have a pulse. This, is what he was asking for, he wanted documentation of how and why the patient regained a pulse. Effectiveness of CPR, o2 profusion and how the patient comes out.

He didn't want a war story. He gave an example of what he was looking for, and didn't get it.

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In answer to your question on how to gauge effective CPR, it was stated in a threat "Although end-tidal CO2 serves as an indicator of cardiac output produced by chest compressions". More specifically End Tidal CO2 serves and indicator of cellular metabolism, excretion and ventilation that momentarily may or may not have any bearing on cardiac output. However. The Blood pressure cuff and "Rate" function in the Pulsoximeter is the only device that I know, we carry, that is dependant on "cardiac output" in order to function.

This brings us to a bigger problem, on of which I have been is discussion with Physio over the past year. It would be logical that during a cardiac arrest we would have the Life Pak hooked up monitoring the end tidal on the tube and the pulsox taped to the finger forehead or toe. If the rate function of the pulsox picks up a rate at the finger tips we know we have a B/P that approximates 80 systolic at what ever rate it indicates. If the pulsox is on the toe and reads, the B/P would be something higher.

Understand that if we have a reading indicated by the pulsox, we have a fact, and can confirm cardiac output and its “effective rate”. Remember the rate on the pulsox may differ from the rate you are doing compressions, however the rate indicated on the pulsox is the “effective rate” at wherever the sensor is placed. If we don’t have a reading we can neither confirm or deny the presence of cardiac output. Further, it would be irresponsible and one should not “chase the pulsox” as increasing the rate or depth of compressions ,to get a pulsox reading, beyond the specific norms recommended by the AHA is bad and wrong on many levels. Pulsoximetry actually measure the expansion of a pulsing vessel with no regard to electrical activity and is definitive.

I grew up on and started with the Life Pak 3. I am an ardent supporter of the Physio and as such was very disappointed. I don’t know if anyone has noticed that although the life Pak 12 has a rate function built in to the pulsox as soon as you hook up the EKG cables the “RATE” indicator on the display defaults to the Electronic Rate as read by the amount of electrical complexes on the screen or more simply the “heart rate and not the pulse rate”. When you unplug the leads it reverts back to the pulse rate providing you have the pulsox hooked up. As we in the field are primarily concerned with the pulse rate this is obviously and error and I have approached Physio on this and they have no answer yet. In addition the competition (who will remain nameless) has on their monitor 2 separate and distinct displays one for heart rate and one for pulse rate. This duel display is also helpful in detecting blocks or a brady with non perusing escape beats.

In answer to the question, if one of the 3 displays on my Life Pak is tuned to Pulsox wave form and if a waveform is present and the sensor itself is motionless on the fingertip and I have no intrinsic EKG complex I can say my CPR compressions have a cardiac output with a blood pressure approx at least 80 +/- systolic. The NIBP is also effective in this manner as well. If the NIBP detects a B/P on the calf or arm during CPR it is what is it.

Lastly the term effective needs to be clarified. Is the objective to be performing according the numbers in the AHA guidelines? Or to meet a consistent numeric pressure blood pressure value and pulse rate? If so what is min rate and more important the B/P to be effective?

I have to take issue with the RED highlighted portion.....This is the problem with so many field providers......

Lets review some basic pathophys...

BLOOD PRESSURE = BRAIN PERFUSION

Normal CPP ( Cerebral Perfusion Pressure) Adult = 70 NEO / PED = 40 - 60

CPP CALCULATION CPP = MAP - ICP

A reliable estimate of ICP in a NON-Head injured patient is 10% of your MAP

MAP = Systolic + 2 * Diastolic / 3

Lets say you have a HR of 76 and a BP of 60/40 after a ROSC ......Do the simple math

MAP ( Mean Arterial Pressure ) = 46.6

ICP ( Inter-cranial Pressure ) = 4.6

46.6 - 4.6 = CPP 42 This is NOT perfusing the BRAIN! No brain perfusion = DEAD

Remember, the Coronary Arteries fill during DIASTOLE.....So, if your diastolic is 40, you have some issues....

ALL one can do is the proper rate of 100 min with adequate depth and chest recoil......

Respectfully,

JW

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MRX is the philips heartstart manual defibrillator which when combined with the QCPR sensor, gives feedback on compression effectiveness. This pad sits in the middle of the chest where you perform compressions and gives feedback in real time to the Monitor to advise CPR changes *push harder, faster, slower...... wait sounds like a night out with the wife.... anyway back to the topic*

Only downside to QCPR, not compatable with the MRX units with Paddles as it requires the pads to collaborate the resus information as the pads sense the recoil etc.

More information can be found on the philips health care site.

Scotty

They do have a Mrx that can opperate with the pads. They have a doohicky that is commonly nicknamed the hockey puck that sticks to the chest with adhesives so to monitor compression depth, rate, and recoil. I like the phillips monitors myself.

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I have to take issue with the RED highlighted portion.....This is the problem with so many field providers......

Lets review some basic pathophys...

BLOOD PRESSURE = BRAIN PERFUSION

Normal CPP ( Cerebral Perfusion Pressure) Adult = 70 NEO / PED = 40 - 60

CPP CALCULATION CPP = MAP - ICP

A reliable estimate of ICP in a NON-Head injured patient is 10% of your MAP

MAP = Systolic + 2 * Diastolic / 3

Lets say you have a HR of 76 and a BP of 60/40 after a ROSC ......Do the simple math

MAP ( Mean Arterial Pressure ) = 46.6

ICP ( Inter-cranial Pressure ) = 4.6

46.6 - 4.6 = CPP 42 This is NOT perfusing the BRAIN! No brain perfusion = DEAD

Remember, the Coronary Arteries fill during DIASTOLE.....So, if your diastolic is 40, you have some issues....

ALL one can do is the proper rate of 100 min with adequate depth and chest recoil......

Respectfully,

JW

John, I think you took my comments out of context. I meant to convey the primary concern of the pre-hospital provider is the actual pulsing beat of a heart and secondarily the electronic wave form that pulse produces of which the Life Pak defaults to. ACLS 101 "any beat beats no beat" if you disagree with this then I think we have the beginnings of a whole new topic. Further more I was very clear that one should not chase the pulsox and follow the AHA guidelines of 100 beats per min. In support of my point you point out that regardless of the rate the efficacy of CPR is judged on the ability to maintain MAP in order to support cerebral perfusion. Although the Life Pak does have the ability of invasive blood pressure monitoring our does not. Since you point out and I agree the only thing that matters is to maintain the MAP, do you disagree with the premise that the most common tools we currently carry pre-hospital to estimate or map and therefore the efficacy of CPR is the pulsox and or the blood pressure cuff?

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'kohlerrf'

In answer to your question on how to gauge effective CPR, it was stated in a threat "Although end-tidal CO2 serves as an indicator of cardiac output produced by chest compressions". More specifically End Tidal CO2 serves and indicator of cellular metabolism, excretion and ventilation that momentarily may or may not have any bearing on cardiac output. However. The Blood pressure cuff and "Rate" function in the Pulsoximeter is the only device that I know, we carry, that is dependant on "cardiac output" in order to function.

Agreed generally but if you have ANY detection of ETCO2 production this is a very positive indicator of actual efficacy of forward blood flow/ CPR/ ie some effective perfusion.

This brings us to a bigger problem, on of which I have been is discussion with Physio over the past year. It would be logical that during a cardiac arrest we would have the Life Pak hooked up monitoring the end tidal on the tube and the pulsox taped to the finger forehead or toe. If the rate function of the pulsox picks up a rate at the finger tips we know we have a B/P that approximates 80 systolic at what ever rate it indicates. If the pulsox is on the toe and reads, the B/P would be something higher.

Maybe I am reading this incorrectly ... the assumption that pulse ox applied distally during an arrest or that you have a BP of 80 is something I cant get my head around or understand your point, one cannot assume in low perfusion states that the pulse ox is anywhere near reliable and if your using LP 12 do you have C- Lock ON or OFF in default setup ?

Understand that if we have a reading indicated by the pulsox, we have a fact, and can confirm cardiac output and its “effective rate”. Remember the rate on the pulsox may differ from the rate you are doing compressions, however the rate indicated on the pulsox is the “effective rate” at wherever the sensor is placed. If we don’t have a reading we can neither confirm or deny the presence of cardiac output. Further, it would be irresponsible and one should not “chase the pulsox” as increasing the rate or depth of compressions ,to get a pulsox reading, beyond the specific norms recommended by the AHA is bad and wrong on many levels. Pulsoximetry actually measure the expansion of a pulsing vessel with no regard to electrical activity and is definitive.

Relying on efficacy of change in chest impedance is folly IMHO.

Better explanation may be it measures pulsatile capillary flow, then compares both readings of red vs infrared and calculates, if it hits and sticks on 85 (the cross over on the algorithmic program on the machine) it could be it is one of the artifact result being sunlight contamination, or any other reading could be a direct result of motion artifact, that said if you get a correlated reading best stop compressions and check pulses.

Have you heard of the new inter nasal septal pulse ox probe ? an interesting device as this would be measuring a more central blood flow ... mind you I don't think most awake patients would tolerate a cloths pin in their noses.

I grew up on and started with the Life Pak 3. I am an ardent supporter of the Physio and as such was very disappointed. I don’t know if anyone has noticed that although the life Pak 12 has a rate function built in to the pulsox as soon as you hook up the EKG cables the “RATE” indicator on the display defaults to the Electronic Rate as read by the amount of electrical complexes on the screen or more simply the “heart rate and not the pulse rate”. When you unplug the leads it reverts back to the pulse rate providing you have the pulsox hooked up. As we in the field are primarily concerned with the pulse rate this is obviously and error and I have approached Physio on this and they have no answer yet. In addition the competition (who will remain nameless) has on their monitor 2 separate and distinct displays one for heart rate and one for pulse rate. This duel display is also helpful in detecting blocks or a brady with non perusing escape beats.

Ok first off MAN your OLD LP 3, I loved my LP 4 although it was about 30 kgs but I was young and good looking in those days strong like bull, smart like refrigerator too.

Yea and Physio is playing catch up .... have you seen the new improved LP 15 ?

The ECG pulse rate is dependent on "R" wave within its set algorithm, again try increasing or decreasing ECG size ... Any repeat I repeat any irregular rhythm best check pulse because my rep for Physio has stated clearly it is not to be trusted, as in "extras ventricular complexes" they may or may not be counted, better question are the extras perfusing.

In answer to the question, if one of the 3 displays on my Life Pak is tuned to Pulsox wave form and if a waveform is present and the sensor itself is motionless on the fingertip and I have no intrinsic EKG complex I can say my CPR compressions have a cardiac output with a blood pressure approx at least 80 +/- systolic. The NIBP is also effective in this manner as well. If the NIBP detects a B/P on the calf or arm during CPR it is what is it
.

Perhaps motion artifact ? again check C- Lock too.

Lastly the term effective needs to be clarified. Is the objective to be performing according the numbers in the AHA guidelines? Or to meet a consistent numeric pressure blood pressure value and pulse rate? If so what is min rate and more important the B/P to be effective?

Indications of End Organ perfusion quite simply stated and the NIBP is only a machine too in fact I did a test the other day personally my BP diastolic is 20 mmgs lower from a trained ear to NIBP, so in hypoperfusion states I have lost all respect for that plastic brain ... Seriously to answer you question one would need an in site Art Line and callibrated before an arrest occured (I know putting art lines in an arrest that just ain't going to happen in my lifetime)

cheers

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