Kasi

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I am an MPH person with a question about cardiac arrest. So, this is basically a lay person with a little bit of a health background asking. Also, this question is not related to a specific incident, it is more of a general question.

So, if a person arrives in an emergency room in cardiac arrest are blood tests for cardiac enzymes and an ECG routinely done? Or, is this only done when an MI is suspected? Are the medical staff more concerned with basic life support during a cardiac arrest than determining if it is an MI or not? So, would an ECG and blood tests not necessarily be done in such a case? I guess the real question is, in what cases are an ECG and blood tests performed and in which cases are they not performed?

Thanks for any help!
 

Apollyon

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The cardiac monitor is applied to follow the rhythm in real time - maintenance of respiration and perfusion is prime, so a 12 lead EKG is not feasible; likewise, compressions would make it useless.

Blood may be drawn, but, by the time results come back, the patient has either been resuscitated or is dead. Likewise, if there have been chest compressions, the cardiac markers may falsely be elevated.

The labs that are germane are a "shock panel" or "iStat" or whatever it's called where you're at, mostly to determine acid/base, potassium, and calcium levels - all of which can be treated/fixed.

The resuscitation comes first; then, or during, considering why the person arrested is assessed, which may assist the resuscitation (like the Ca2+, K+, and acid/base). Blood drawn can be (and often is) sent off; if the patient lives, the numbers can be evaluated, and, if the patient is pronounced dead, it's a moot point.
 
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Kasi

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Thanks for the response. I appreciate the information. I didn't realize that chest compressions could affect the blood enzymes and didn't think about them affecting the ECG. Good point!
 
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southerndoc

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How many people draw ABG's during codes? It's almost routinely asked for by the medicine people during codes on the floor, but I almost never get them during codes in the ED. Maybe I'm wrong by predicting acidosis and giving bicarb with prolonged down times.

I would be curious to hear what everyone thinks of ABG's during codes. Personally I think they're a waste of time and exposes providers to a possible needle stick. As far as I remember, they have never been a part of the ACLS algorithms.
 

Apollyon

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southerndoc said:
As far as I remember, they have never been a part of the ACLS algorithms.
So you DON'T consider it in your PEA patients (4T's and 4H's)? That would seem to me to be part of the ACLS algorithm - after all, how are you going to determine some of those components?

I mean, don't you consider it in the renal/dialysis players that come in in arrest (or arrest in the department)?

Each case is different, but most fit into one category or another. Because your practice style doesn't support it does NOT make it wrong. I don't ABG every code (V-fib-->asystole ping-pong - which is most common - doesn't get it from me), but, if it's a PEA arrest, certainly.

Of course, you could shotgun the PEA code - ET tube, consider bilateral needle decompression, epi, atropine (if the rate is slow), pericardiocentesis, fluids wide open, amp of bicarb, amp of calcium, check a core temp (if you suspect hypothermia), and consider thrombolytics - and you're done, no thinking involved.
 

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Apollyon said:
So you DON'T consider it in your PEA patients (4T's and 4H's)? That would seem to me to be part of the ACLS algorithm - after all, how are you going to determine some of those components?

I mean, don't you consider it in the renal/dialysis players that come in in arrest (or arrest in the department)?

Each case is different, but most fit into one category or another. Because your practice style doesn't support it does NOT make it wrong. I don't ABG every code (V-fib-->asystole ping-pong - which is most common - doesn't get it from me), but, if it's a PEA arrest, certainly.

Of course, you could shotgun the PEA code - ET tube, consider bilateral needle decompression, epi, atropine (if the rate is slow), pericardiocentesis, fluids wide open, amp of bicarb, amp of calcium, check a core temp (if you suspect hypothermia), and consider thrombolytics - and you're done, no thinking involved.
I don't send labs unless I get a pulse back. I wouldn't jump to thrombolytics unless I had more than a small suspicion. I haven't done a blind pericardiocentesis in awhile because I usually look for effusion when I look for cardiac motion on the U/S. I usually don't needle decompress medical arrests unless there's something suspicious. I will routinely needle decompress trauma arrests and do bilateral chest tubes if they're at least in PEA even if they have bilateral BS, etc.

mike
 

Apollyon

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Last pericardiocentesis I did was in the radiology suite (no U/S available) in a PEA arrest in a guy with metastatic Ca.

I mentioned the needle decompression mostly because it's part of the trauma arrest, and the thrombolytics are, indeed, almost never indicated (as Tintinalli says, to paraphrase: "A teenager on the way to the vascular radiology suite that arrests") - these things, though, are part of the "shotgun" approach - the kitchen sink.
 

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Apollyon said:
So you DON'T consider it in your PEA patients (4T's and 4H's)? That would seem to me to be part of the ACLS algorithm - after all, how are you going to determine some of those components?

I mean, don't you consider it in the renal/dialysis players that come in in arrest (or arrest in the department)?
Maybe I'm practicing poor medicine, but I usually give the bicarb anyhow after prolonged down time. No, I do not get ABG's on renal/dialysis patients. What benefit would it provide me? I can assume that they are acidotic and not alkalemic, and our lab does not run K's off an ABG, so it's not a great tool for diagnosis.

Quite frankly my PEA algorithm consists of airway, IV, CPR, ultrasound. No cardiac activity -> pronounce. If there is cardiac activity, then I work it.
 

Apollyon

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southerndoc said:
Maybe I'm practicing poor medicine, but I usually give the bicarb anyhow after prolonged down time. No, I do not get ABG's on renal/dialysis patients. What benefit would it provide me? I can assume that they are acidotic and not alkalemic, and our lab does not run K's off an ABG, so it's not a great tool for diagnosis.

Quite frankly my PEA algorithm consists of airway, IV, CPR, ultrasound. No cardiac activity -> pronounce. If there is cardiac activity, then I work it.
That's why I mentioned the shock panel/iStat/whatever it's called at your place.

I mean, I know what you're saying - most of the codes brought in by EMS get called pretty quickly. What I'm saying is that, sometimes, the data helps.
 

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southerndoc said:
Quite frankly my PEA algorithm consists of airway, IV, CPR, ultrasound. No cardiac activity -> pronounce. If there is cardiac activity, then I work it.
Not to question your methods, but you dont give at least a first round of epi before pronouncing? I realise that outcomes are deep into the single digits at this point but the drug is cheap and easy, right?
 

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Apollyon said:
That's why I mentioned the shock panel/iStat/whatever it's called at your place.

I mean, I know what you're saying - most of the codes brought in by EMS get called pretty quickly. What I'm saying is that, sometimes, the data helps.
I'd like to do something about that....namely help to reduce the number of codes brought in by EMS. :thumbup:
 

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fiznat said:
Not to question your methods, but you dont give at least a first round of epi before pronouncing? I realise that outcomes are deep into the single digits at this point but the drug is cheap and easy, right?
The case of end-tidal CO2 <20mmHg in an intubated patient and no cardiac movement on ultrasound in a normothermic patient is 100% ethical to cease resuscitation efforts.

In my paramedic days, we had protocols for asystole as follows: intubate patient, get IV access, 1 epi, 1 atropine, reassess rhythm. If no response, we could stop resuscitation. If any of those steps were missed, or there was any indication that it should go on, the resuscitation continued.
 

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bstone said:
I completed EMT-Intermediate training in New Hampshire in May 06 and this is our protocol as well. Well, we don't pronounce in the field but we can max out on meds. If I recall it.s 0.04mg/kg for Atropine. I don't think 1:10,000 epi has one (at least they never told me if there is one...is there?).
You're right for the atropine, and, yes, there is no limit to epi.

You have to use your head on the atropine - people who say it's "3mg max" are using the "70kg person" model. If you have someone 100kg (220lbs), they can get 4mg, and so on (150kg - 330lbs - 6mg).

This is different than that for the organophosphate poisoning dose.
 

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Apollyon said:
That's why I mentioned the shock panel/iStat/whatever it's called at your place.

I mean, I know what you're saying - most of the codes brought in by EMS get called pretty quickly. What I'm saying is that, sometimes, the data helps.
I also don't routinely send off labs in the arrest with the exception of a Hb (hemaQ in our ed) and Accucheck. We don't have Istat or a shock panel so we wouldn't get the labs back anyway for 20 minutes to whenever (this is a city hospital after all). I just treat based on rythym/clinical situation.
 

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fiznat said:
Not to question your methods, but you dont give at least a first round of epi before pronouncing? I realise that outcomes are deep into the single digits at this point but the drug is cheap and easy, right?
If it's witnessed, yes. If not, then no.

The likelihood of getting a PEA arrest back with no cardiac activity on ultrasound is abysmal.
 

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southerndoc said:
How many people draw ABG's during codes? It's almost routinely asked for by the medicine people during codes on the floor, but I almost never get them during codes in the ED. Maybe I'm wrong by predicting acidosis and giving bicarb with prolonged down times.
Why is it that according to ACLS protocol, we aren't supposed to give bicarb unless it was a case of a pre-existing acidosis that caused the arrest? It sounds like you're giving it anyways in any patient who obviously has acidosis as a result of a prolonged arrest, and to me it always made sense that we should do that anyhow.
 

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leviathan said:
Why is it that according to ACLS protocol, we aren't supposed to give bicarb unless it was a case of a pre-existing acidosis that caused the arrest? It sounds like you're giving it anyways in any patient who obviously has acidosis as a result of a prolonged arrest, and to me it always made sense that we should do that anyhow.
We've been aroung and around on this for the last 30 years. Major reasons it has been discarded are:
1. No human evidence of value
2. Little animal evidence of value
3. Concerns over risks of:
a.paradoxical central nervous system acidosis,
b.Na load inducing fluid overload,
c.if patient is resucitated he is likely to be alkalotic later. alkalemia is much more arrthymogenic than acidosis.
d. other theoretical issues that escape me now.

Main issue is that no medication (including epi) has ever been shown to change the outcome from cardiac arrest.

kinda depressing, when I started all these years ago, I thought I was gonna save all these people who were coding. the only way to save a coding patient is to get there before the event and prevent it. See the MI chapter of ACLS
 

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BKN said:
We've been aroung and around on this for the last 30 years. Major reasons it has been discarded are:
1. No human evidence of value
2. Little animal evidence of value
3. Concerns over risks of:
a.paradoxical central nervous system acidosis,
b.Na load inducing fluid overload,
c.if patient is resucitated he is likely to be alkalotic later. alkalemia is much more arrthymogenic than acidosis.
d. other theoretical issues that escape me now.

Main issue is that no medication (including epi) has ever been shown to change the outcome from cardiac arrest.

kinda depressing, when I started all these years ago, I thought I was gonna save all these people who were coding. the only way to save a coding patient is to get there before the event and prevent it. See the MI chapter of ACLS
Well, I read that defibrillation is the ONLY intervention that increases the rate of patient survival to hospital discharge. I might be wrong, but I think another reason for not overloading with bicarb that you could add is that making the blood more alkalotic would decrease tissue oxygen perfusion (because of the Bohr effect on hemoglobin).
 
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