# ROSC after giving D50 in cardiac arrest?



## KellyBracket (Feb 4, 2014)

It is no longer an official "reversible cause" per ACLS, but many folks are still checking the finger stick in cardiac arrest, and giving D50 for hypoglycemia.

Has anyone actually had a "save" that they believe was because of the dextrose?

I'm preparing a talk, and I'd love to hear any experiences people have had with this.


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## STXmedic (Feb 4, 2014)

Strangely enough, no. I make hypoglycemics in the toilet once or twice a shift, yet very rarely do I make a cardiac arrest that has been hypoglycemic. On the very rare occasion one has been, I don't remember D50 making a difference (I don't recall those getting ROSC).


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## mycrofft (Feb 4, 2014)

Worked inpatient diabetes six years, saw seizures ended and levels of consciousness improve with sugar (D-10 or D-50), never saw a code "caused" by a hypoglycemic etiology.

 If I did, it would probably be due to hypoxia and exhaustion from a seizure; sugar would help keep that from happening again, but I'm not sure what role sugar might play directly on the brainstem's cardiac and respiratory centers. I suppose it needs sugar too, but a prolonged seizure and low intracellular blood sugar overall will probably carry you off faster due to hypoxia=>arrest.


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## medicdan (Feb 4, 2014)

KellyBracket said:


> It is no longer an official "reversible cause" per ACLS, but many folks are still checking the finger stick in cardiac arrest, and giving D50 for hypoglycemia.
> 
> Has anyone actually had a "save" that they believe was because of the dextrose?
> 
> I'm preparing a talk, and I'd love to hear any experiences people have had with this.



Are finger sticks really reliable in a patient in extremis or in cardiac arrest? Is a venous blood sugar any better? I doubt there are studies on it....

If we know there's no pathophysiology for hypoglycemia causing CA, why are you looking for anecdote of Dextrose helping?


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## TomB (Feb 4, 2014)

No, but I've checked a BGL that read "high" and gave calcium because I suspected a potassium shift. It was an unwitnessed asystolic arrest and we did get ROSC. Turned out the patient was hypothermic (we figured that out en route to the hospital) and when the labs came back in the ED it did turn out that she was hyperkalemic. The family decided "she wouldn't want all that" and life support was discontinued. You know, the same family that watched us work the code for 30 minutes.


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## KellyBracket (Feb 4, 2014)

medicdan said:


> Are finger sticks really reliable in a patient in extremis or in cardiac arrest? Is a venous blood sugar any better? I doubt there are studies on it....
> 
> If we know there's no pathophysiology for hypoglycemia causing CA, why are you looking for anecdote of Dextrose helping?



There is at least one study looking at finger sticks in cardiac arrest, using the venous blood sugar as the comparison. The capillary level was neither sensitive nor specific for hypoglycemia.

Since hypoglycemia was labeled as one of the "5 Hs" in ACLS back in 2005 (but then mysteriously removed in 2010), I wondered if anyone ever had success with addressing this "reversible cause." My guess is no, but if anyone had a good story, perhaps I could add it to my talk.

OTOH, there is some consistent data that hypoglycemia causing prolonged QTc and other ECG changes, which may account for the so-called "dead in bed" syndrome.



mycrofft said:


> Worked inpatient diabetes six years, saw seizures ended and levels of consciousness improve with sugar (D-10 or D-50), never saw a code "caused" by a hypoglycemic etiology.
> 
> If I did, it would probably be due to hypoxia and exhaustion from a seizure; sugar would help keep that from happening again, but I'm not sure what role sugar might play directly on the brainstem's cardiac and respiratory centers. I suppose it needs sugar too, but a prolonged seizure and low intracellular blood sugar overall will probably carry you off faster due to hypoxia=>arrest.



Other studies show changes on the EEG in type 1 diabetics during episodes of nighttime hypoglycemia, at the same time as the ECG changes. No idea if these EEG changes could lead to a seizure.



TomB said:


> No, but I've checked a BGL that read "high" and gave calcium because I suspected a potassium shift. It was an unwitnessed asystolic arrest and we did get ROSC. Turned out the patient was hypothermic (we figured that out en route to the hospital) and when the labs came back in the ED it did turn out that she was hyperkalemic. ..



Great catch! I like the reasoning - very plausible.

I wrote a brief review of this topic last year. It has links to the studies I mentioned, as well as some weak attempts at humor! *Using Dextrose in Cardiac Arrest*


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## mycrofft (Feb 4, 2014)

mycrofft said:


> Worked inpatient diabetes six years, saw seizures ended and levels of consciousness improve with sugar (D-10 or D-50), never saw a code "caused" by a hypoglycemic etiology.
> 
> If I did, it would probably be due to hypoxia and exhaustion from a seizure; sugar would help keep that from happening again, but I'm not sure what role sugar might play directly on the brainstem's cardiac and respiratory centers. I suppose it needs sugar too, but a prolonged seizure and low intracellular blood sugar overall will probably carry you off faster due to hypoxia=>arrest.



So, the missing ingredient I wasn't seeing was electrolyte disorder. 
I was, again, seeing these guys at least BID as in-pts, so their disorders wasn't allowed to get that far.

The one person I saw down from hyperglyc in the field, was before fingerstick glucometry  and we were EMT-Ambulance ("B" nowadays) so it was O2, transport, and change the sheets.


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## mycrofft (Feb 4, 2014)

KellyBracket said:


> There is at least one study looking at finger sticks in cardiac arrest, using the venous blood sugar as the comparison. The capillary level was neither sensitive nor specific for hypoglycemia.
> 
> Since hypoglycemia was labeled as one of the "5 Hs" in ACLS back in 2005 (but then mysteriously removed in 2010), I wondered if anyone ever had success with addressing this "reversible cause." My guess is no, but if anyone had a good story, perhaps I could add it to my talk.
> 
> ...



Thanks Doc!
Link didn't open for me. Awaiting a good one, want to see it!

I know one thing about fingerstick glucometry, in the heat of an emergency; any weakness in the tech is amplified by the user's over-squeezing ("milking") the digit for blood (yielding a suboptimal sample) because when you most need it RIGHT NOW, it isn't as easy to get…and time gets sort of whacky when you're in "STAT-RESCUE" mode.

We had fast spot tests for electrolytes at the doc on a box I worked in '86-87 (Kodak "Ektachem" system), just needed about 1/4 cc clean serum, the slide and the reader, and about two minutes if I recall. Too bad a similar device isn't available for field work, including maybe a cellular filter to fudge a serum sample without a centrifuge and that attendant time lag. (Not so bad if you're in Mooseheiner, Minn. heading for Rochester, though).


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## Fire51 (Feb 4, 2014)

I couldn't get the article to open either.


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## KellyBracket (Feb 4, 2014)

Dang myself. 

Fixed it in the post ( *Using Dextrose in Cardiac Arrest* )

Mycroftt, I'm not sure if they attempted to control for technique in that one CPR study. On the other hand, the results were similar to those seen in a study of critically-ill patients, so I imagine it isn't just technique (although that likely plays a significant role). BTW, there are fairly accurate, portable devices like the *i-Stat* that use a venous sample to quickly determine chemistries, a hemoglobin, and a troponin if you want that as well. A bit pricey for routine EMS, but I read a study where National Park rangers were using these in the Grand Canyon to identify exertional hyponatremia, etc.


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## Fire51 (Feb 4, 2014)

There we go now it's working!


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## VA Transport EMT (Feb 5, 2014)

Are there any sources? Common sense says It would be the most easily reversible if it is the epidemiology
Edit: no smack,found it


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## mycrofft (Feb 5, 2014)

The more I come to know (sort of) humans, the more I see the mechanisms at work in "high places" (especially with protocols) which I have seen at work with PTA bake sales.

It's in…it's out…it's in… where's the science? A quincennial should give a protocol aspect like glucose a fair shake.

One trouble, as with all medical science, is that while you can often prove something tends to cause bad outcomes (sometimes with a tendency of 100%, i.e., "certainty"), it is danged hard to prove one factor caused a cure.

And don't get me started on distractors in diagnosis (even if it is post-mortem). "Dead in bed" is a phenomenon also seen in middle aged Asian males having undergone recent horrific emotional loss or disgrace, seemingly healthy infants of many types and kinds, and detractors of the new Russia.


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## onrope (Feb 5, 2014)

Had a code last week, 40 something male call came in as a seizure, full arrest upon arrival initially in asystole. Line, tube, 2 rounds of epi before a bgl check which read low. Amp of d50 given along with bicarb along with 3rd round of epi. About 2 minutes later during rhythm check pt in course v-fib one shock back into nsr, did not re arrest that we know of in er. Cooling measures taken place in er, hr around 60 bp 120/80 with no pressors running. We always check bgl in seizures and cardiac arrest, can't say for sure it made a difference but my feeble mind would think without energy (sugar) there is no chance of ROSC. Great topic


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## mycrofft (Feb 5, 2014)

onrope said:


> Had a code last week, 40 something male call came in as a seizure, full arrest upon arrival initially in asystole. Line, tube, 2 rounds of epi before a bgl check which read low. Amp of d50 given along with bicarb along with 3rd round of epi. About 2 minutes later during rhythm check pt in course v-fib one shock back into nsr, did not re arrest that we know of in er. Cooling measures taken place in er, hr around 60 bp 120/80 with no pressors running. We always check bgl in seizures and cardiac arrest, can't say for sure it made a difference but my feeble mind would think without energy (sugar) there is no chance of ROSC. Great topic



1. Many types of calls come in as "a seizure". But could have been.
2. Was "asystole" by palp, aus, or EKG? If EKG, what sort of activity? Flatline, burbles, v-tach or fib, or ???

Congrats on a save by the way.


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## onrope (Feb 5, 2014)

mycrofft said:


> 1. Many types of calls come in as "a seizure". But could have been.
> 2. Was "asystole" by palp, aus, or EKG? If EKG, what sort of activity? Flatline, burbles, v-tach or fib, or ???
> 
> Congrats on a save by the way.



We use proQA emd and yes I know that the dispatched complaint is rarely correct. Family stated hx of diabetes and seizures, unknown downtime.

2. Pulseless and apneic, palped on carotid. Monitor showed aystole, burbles. 

Thanks, feels good to give someone a chance every now and then. Especially when the doc feels they are a candidate for post ROSC cooling measures. I just wish there was a better way to follow up on these PT's to see if they actually made some recovery of if they are a cardiac cripple.


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## mycrofft (Feb 5, 2014)

:beerchug:


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## TheLocalMedic (Feb 6, 2014)

Typically when I work a code the BG check typically occurs later on.  On a few occasions I've given dextrose, but it's getting delivered around the same time I'm considering bicarb, which is pretty far in.  I have had ROSC after delivering it, but I'm pretty sure it was the epi talking rather than the sugar, and those have all universally had poor outcomes.  

I'm curious if anyone out there checks a BG right off the bat on codes?


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## KellyBracket (Feb 8, 2014)

This is pretty much what I expected to hear. No miraculous recoveries after giving just dextrose.


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## TomB (Feb 9, 2014)

onrope said:


> We use proQA emd and yes I know that the dispatched complaint is rarely correct.



That's why dispatchers should be specifically trained to consider any adult who suddenly collapses a cardiac arrest until proven otherwise (only exception is the patient who is reported to be breathing NORMALLY). 

This will result in a lot of over-triage but will catch many of the sudden cardiac arrest calls that are reported as seizures or faintings (which is a lot of them). But, those are the witnessed collapse calls, so they are really important!


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## NomadicMedic (Feb 9, 2014)

I can't tell you how many fall/seizure calls we have that are upgraded to Cardiac Arrest one the all taker digs in a little more. Luckily, those calls AE usually dispatched as delta calls, so medics are enroute anyway.


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## mycrofft (Feb 9, 2014)

Roger the two above.


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## zzyzx (Feb 12, 2014)

I don't see how you can get an answer to your questions since no one is ever going administer only dextrose on a cardiac arrest. Good topic though. Would love to read your lecture.


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## KellyBracket (Feb 12, 2014)

zzyzx said:


> ... Good topic though. Would love to read your lecture.



If it works out, it will be a 2.5 minute rant on a #FOAMED podcast - I'll update this thread with a link when it comes out!


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## Merck (Feb 12, 2014)

It seems unlikely that a cardiac arrest would have a solely hypoglycemic etiology, even given the possibility presented of a prolonged QT.  I wonder if some of the anecdotal effect of D50W administration might not be due not to the sugary-goodness but rather to what is essentially a fluid bolus in patients amenable to such therapy in cardiac arrest (i.e. ROSC from a PEA with an element of hypovolemia).  The osmolarity of D50W is on the extreme side (around 2,600, I believe).  This likely causes some decent fluid shift and possibly a temporary bump in intravascular volume before the sugar is taken up by cells - a process likely delayed in arrest or low-flow states.  Just a thought.


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## onrope (Feb 12, 2014)

Merck said:


> It seems unlikely that a cardiac arrest would have a solely hypoglycemic etiology, even given the possibility presented of a prolonged QT.  I wonder if some of the anecdotal effect of D50W administration might not be due not to the sugary-goodness but rather to what is essentially a fluid bolus in patients amenable to such therapy in cardiac arrest (i.e. ROSC from a PEA with an element of hypovolemia).  The osmolarity of D50W is on the extreme side (around 2,600, I believe).  This likely causes some decent fluid shift and possibly a temporary bump in intravascular volume before the sugar is taken up by cells - a process likely delayed in arrest or low-flow states.  Just a thought.



Not sure what your protocols are but take a gander at mine:
http://www.sbcounty.gov/icema/main/ViewFile.aspx?DocID=1522

300cc fluid challenge is frontline in PEA/asystole arrest. I am not sure what everyone elses protocols look like in regards to fluid bolus in cardiac arrest. Down the "list" is BGL analysis and opiate od consideration. Then again lidocaine is also on there after 2 cycles of cpr for v-fib/tach


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## Merck (Feb 13, 2014)

I understand that most PEA protocols would have a bolus of some volume to account for the possibility that the issue is one of preload/straight-up hypovolemia.  I'm just saying that if D50W is given, the benefit may be derived from the osmotic pull and subsequent repletion of intravascular volume rather than the sugar itself.


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## Carlos Danger (Feb 13, 2014)

Merck said:


> I understand that most PEA protocols would have a bolus of some volume to account for the possibility that the issue is one of preload/straight-up hypovolemia.  I'm just saying that if D50W is given, the benefit may be derived from the osmotic pull and subsequent repletion of intravascular volume rather than the sugar itself.



That is an interesting and plausible hypothesis.


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