# Mystery case.



## Melclin (Apr 20, 2009)

Hey guys, 
I'm interested to see how everyone would treat the following case at all the different levels of qualifications we have here and what you think the problem might be.

Called out at 3:53am, CODE 1:Severe SOB. Arrive on scene to find 19yo male unconscious. Found by parents on the floor in the living room. 
No response. 
Trismus present, but breathing.
Palpable pulse.
No haemorrage.

I'm told triple airway was affective and OPA was "partially affective". Ventilated with closed circuit 100% O2.
Pulse: 130
ResRa:<6
3 lead ECG: Atrial Fibrillation (uncontrolled) 
BP: 140/90
GCS: 3

Temp: 35.5 (tympanic)
Skin: Cool, dry cyanotic
Pupils: equal and reactive, but pinpoint.

Chest: L and R sounds clear + shallow, decreased effort, equal expansion, UA snore.

MICA (Intensive care paramedics) arrived four mins later.

etCO2: 75 mmHG, normal resp waveform.
SP02: 100 (with oxysaver).
RBG: 15.3 mmol/l

OPA swapped for NPA after, it appears, it was decided that vents were inadequate. Not sure if that was done before or after the SPO2 of 100. After affective vents, ResRa increases to 20.

IV access: 18g AC, 500ml sodium lactate TKVO

According to parents, pt has a history of depression and self harm. A veritable pharmacy of medications exists in the house. Pt. has Xanax and Effexor prescribed, but many others are available. 

No known allergies.

No evidence of narcotics, no track marks, parents adamant no illegal drugs (aren't they always).

Pt loaded into ambulance where airway is successfully suctioned. The kid then wakes up bolt upright and rips out his NP. 
Pulse:128   BP:136/88    Skin: cool, pink, dry.
GCS: 8 (E-2, V-1, M-5) ResRa: 20   Pupils: pinpoint, reactive

10 mins later the pt drops back down to GCS 4 (eyes open to pain) and pupils were no longer pinpoint. Skin noticeably hot and and Resra:20 and uncontrolled A-Fib continue. BP:136/88, etCO2: 65, at handover.

I'm fairly tired right now but I think that's everything I can remember.

So, What do we all think happened, and more interestingly how would you have treated the situation. Would you do it differently? I might add that we were about 4 mins from a mid level hospital.


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## Scott33 (Apr 20, 2009)

Melclin said:


> No evidence of narcotics...
> 
> Pupils: pinpoint / ResRa:<6



You sure about that?

First thing I would be thinking.


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## rhan101277 (Apr 20, 2009)

Scott33 said:


> You sure about that?
> 
> First thing I would be thinking.



Same pinpoint usually indicates overdose.  The patient has respiratory depression is a sign, the type of drugs he has available and his history.  Wonder why narcan wasn't considered?


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## rmellish (Apr 20, 2009)

Could have tried a bit of narcan, especially given the lack of spontaneous respirations and pinpoint pupils.

Anyone check a BGL? Doesn't seem to be the problem, but never bad to check.


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## maxwell (Apr 20, 2009)

Has to be drugs!  A-Fib for 19 year old?  You sure?  That's strange.  MAT makes more sense to me if he took weird drugs to deplete his K, Mg.  I woulda intubated with an ETT (sounds like it coulda be done w/o RSI drugs, too).  Woulda given naloxone (while avoiding romazicon).  If the QRS was wide, I would have given sodium bicarbonate (TCAs?).  Woulda checked a blood sugar.


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## redcrossemt (Apr 20, 2009)

Melclin said:


> I'm told triple airway was affective and OPA was "partially affective".
> Ventilated with closed circuit 100% O2.



What's a triple airway? What does partially effective OPA mean? What's being used? The triple or the OPA or an NPA or what? What rate are you ventilating the patient at, or are they just on O2 via mask?



Melclin said:


> Chest: L and R sounds clear + shallow, decreased effort, equal expansion, UA snore.



What is UA snore? Snoring respirations? Are you sure you had a patent airway?



Melclin said:


> ResRa:<6
> Pupils: equal and reactive, but pinpoint.



With the patient history provided, level of unconsciousness, slow respirations, and pinpoint pupils I would have been thinking narcotic or polypharmacy overdose. Definitely need a BGL, could try nalaxone, but I would focus on airway management. You mentioned that the patient needed to be suctioned. I wasn't there, but a consideration would be intubation, possibly RSI if the trismus prevents access. Whether or not you decided to intubate, positive pressure ventilations and careful monitoring/suctioning would be my first priority for this patient.


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## fma08 (Apr 20, 2009)

rmellish said:


> Could have tried a bit of narcan, especially given the lack of spontaneous respirations and pinpoint pupils.
> 
> Anyone check a BGL? Doesn't seem to be the problem, but never bad to check.



They did, 15.3 mmol/l, a bit on the higher side.


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## Juxel (Apr 20, 2009)

fma08 said:


> They did, 15.3 mmol/l, a bit on the higher side.



That's about 276mg/dl for those of us who are familiar with that format.


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## triemal04 (Apr 20, 2009)

maxwell said:


> Has to be drugs!  A-Fib for 19 year old?  You sure?  That's strange.  MAT makes more sense to me if he took weird drugs to deplete his K, Mg.  I woulda intubated with an ETT (sounds like it coulda be done w/o RSI drugs, too).  Woulda given naloxone (while avoiding romazicon).  If the QRS was wide, I would have given sodium bicarbonate (TCAs?).  Woulda checked a blood sugar.


Second the trycyclic OD with likely several others as well.  And even without a "history" of drug use also might consider this being a speedball OD.  It be more likely to see the rapid change in pt's status after the narcan but probably could also happen after the respiratory issue was fixed.  But intubation (by RSI or otherwise) would be a good choice for him and a small dose of narcan would have been good initially.


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## Melclin (Apr 20, 2009)

Not sure exactly what 'partially effective' means. It was in the first responders notes. But obviously is wasn't working. Sp02: of 100 must have been taken with the NP. I would imagine that the OP didn't work well or they had alot of trouble getting it in and 'partially effective' was the closest option to select on the Electronic Patient Care Record. 

No TCA present in the house.

I meant triple airway maneuver. To clear and view the airway. I dont quite understand how it could be affective, but then have such problems with an OPA that you then had to use an NP.

UA snore. Yeah upper airway. Sorry that should be  UA: snore .

Has anyone considered aspiration associated conditions. Do any of the symptoms point that way? Shallow, fast (with some assitance) breathing? 

I'd be interested in suggestions as to why the pt. wasn't tubed. RSI seems a bit extreme considering a good colour returned, with more basic ventilations and given the posibility of opiate and particularly benzo overdose.


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## BruceD (Apr 20, 2009)

Tricyclic overdose typically results in anticholinergic effects, which would include mydriasis, not miosis.  (Of course wouldn't want to diagnose based on that), so i'm leaning away from TCA overdose.

Xanax overdose produces CNS depression (miosis & respiratory depression), arrhythmias,  oddly...tachycardia, seizures, muscle rigidity, syncope

Effexor has the potential to cause neuroleptic malignant syndrome, characterized by autonomic instability, delirium, agitation, coma, and.. muscle rigidity. (did he have a fever?)

So, polypharmacy can't be ruled out, but I'm not going to make a guess as to the actual cause.  If it was one of the above, narcan would be ineffective (flumazenil would be the d.o.c.)


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## boingo (Apr 21, 2009)

pinpoint, unresponive, with respiratory rate of less than 6 would get narcan here.


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## vquintessence (Apr 21, 2009)

*Polypharmacy c Dystonic reaction anybody?*

Well I was toying with polypharmacy OD c dystonic reaction?  I realize he wasn't displaying any cholinergic imbalance however there seems a possible suspicion based on:  trismus, pts age, access to psych meds, how pt described as spontaneously (yet momentarily) jerked up to only collapse back down.

I agree with Bruce with xanax and/or effexor OD and their symptom profiles fitting the bill, however the chances of either one being the culprit for the trismus are very uncommon (and I cheated about xanax to learn trismus isn't listed among any adverse reactions.)  Muscle fatigue yes, muscle rigidity less so, but trismus is beyone uncommon.

Eh some worthless $0.02.  I just like the dystonic reaction theory B)
But yeah, start with some Narcan simply based on presentation, but would definately try some Benadryl h34r:


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## MSDeltaFlt (Apr 21, 2009)

Melclin said:


> Hey guys,
> I'm interested to see how everyone would treat the following case at all the different levels of qualifications we have here and what you think the problem might be.
> 
> Called out at 3:53am, CODE 1:Severe SOB. Arrive on scene to find *19yo* male unconscious. Found by parents on the floor in the living room.
> ...


 
No 19yo is supposed to have A-Fib in any condition unless it is congenital. And then they are to have meds for it. With new onset A-Fib and ALOC, odds are you have just stroked out. Add to that pinpoint pupils, you might have a Pontene Hemorrhage. With a CVA at the base of the brain you will have temp problems. I realize you said tympanic temp, but core temps are more accurate. Rectal temps are unpractical in EMS, but noticeably hot skin is not supposed to happen.

You also need to control ICP's as best you can on the prehospital level. EtCO2's in the 60's and 70's is a bit high. High end tidals mean cerebral vasodilation which further increase ICP which take away from CPP which is what is going to drive this poor kid further down the drain. If you have RSI, put him down and get those EtCO2's in the upper 30's.

Don't waste time on scene trying to get a tube. Time is brain here. If you can't get it in a couple of tries, go to your backup airway.

Until proven otherwise (CT), assume the worse.


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## Jon (Apr 21, 2009)

MSDelta... Wow. Wasn't thinking in that direction, but you make an awesome case.

Given all the drugs in the house... I'd likely max out my 2mg of Narcan by protocol, then try for a tube.


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## fma08 (Apr 21, 2009)

Diddo MSDelta, was not thinking CVA at all. Quite enlightening really.


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## BruceD (Apr 21, 2009)

If it had been pontine hemorrhage, what are the chances he would be down a while at GCS 3, then sit up in the ambulance and pull out the tubes then 10 mins later  fall back to GCS 4?

If his skin is hot to the touch as mentioned later in the post, I'm still very much leaning toward NMS possibly with other effects from polypharm.

but either way, I still believe load'n'go best treatment for this 'un.

kinda a neat case.


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## MSDeltaFlt (Apr 21, 2009)

BruceD said:


> *If it had been pontine hemorrhage, what are the chances he would be down a while at GCS 3, then sit up in the ambulance and pull out the tubes then 10 mins later fall back to GCS 4?*
> 
> If his skin is hot to the touch as mentioned later in the post, I'm still very much leaning toward NMS possibly with other effects from polypharm.
> 
> ...


 
Actually pretty good for both.  That can happen for either field diagnoses.

What I don't like is the A-Fib with ALOC.  That tells me CVA until proven otherwise.  Which is why I would be hesitant to push Narcan on this kid.

Narcan is contraindicated for resp depression not due to opioid ingestion.  Side effects include tachycardia, hypertension, N/V, seizures, even cardiac arrest.  Do you really want to cause these side effects on someone who could quite possibly be having a CVA?


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## Melclin (Apr 21, 2009)

MSDeltaFlt said:


> No 19yo is supposed to have A-Fib in any condition unless it is congenital. And then they are to have meds for it. With new onset A-Fib and ALOC, odds are you have just stroked out. Add to that pinpoint pupils, you might have a Pontene Hemorrhage. With a CVA at the base of the brain you will have temp problems. I realize you said tympanic temp, but core temps are more accurate. Rectal temps are unpractical in EMS, but noticeably hot skin is not supposed to happen.
> 
> You also need to control ICP's as best you can on the prehospital level. EtCO2's in the 60's and 70's is a bit high. High end tidals mean cerebral vasodilation which further increase ICP which take away from CPP which is what is going to drive this poor kid further down the drain. If you have RSI, put him down and get those EtCO2's in the upper 30's.
> 
> ...



That is a Dx worthy of house. Fine work MSDeltaFlight. In this case though, I'm not sure that was what was wrong. 

Here's some more info:
They took the kid to CT and he came back a few mins later and nobody seemed any the wiser, other than his lungs were 80% full of aspriated stomach matter. His liver was also full of acetaminophen. That's about all I know from the ED.


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## MSDeltaFlt (Apr 21, 2009)

Melclin said:


> That is a Dx worthy of house. Fine work MSDeltaFlight. In this case though, I'm not sure that was what was wrong.
> 
> Here's some more info:
> They took the kid to CT and he came back a few mins later and nobody seemed any the wiser, other than his lungs were 80% full of aspriated stomach matter. His liver was also full of acetaminophen. That's about all I know from the ED.


 
Just covering all bases until confirmation. Glad he got a CT to rule out anything.

However, Aspiration Pneumonia (50% mortality on top of whatever else is going on) + Liver Failure from Acetaminophen OD + possible Anoxic Brain Injury from however long his GCS was that low and hypoventilating vs possible Pontine Hemorrhage. Junior's screwed any way you look at it.


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## BruceD (Apr 22, 2009)

MSDeltaFlt said:


> Actually pretty good for both.  That can happen for either field diagnoses.
> 
> What I don't like is the A-Fib with ALOC.  That tells me CVA until proven otherwise.  Which is why I would be hesitant to push Narcan on this kid.
> 
> Narcan is contraindicated for resp depression not due to opioid ingestion.  Side effects include tachycardia, hypertension, N/V, seizures, even cardiac arrest.  Do you really want to cause these side effects on someone who could quite possibly be having a CVA?




I've not endorsed narcan on this patient, I think you are correct about not using it.  
Treating this patient with diesel would be ideal, especially when you are 4mins from a hospital. 

Effexor has been shown to cause atrial fib along with other arrhythmias -> http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2000637 and has been associated with both NMS and Serotonin Syndrome -> http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)72791-4/fulltext

The SSNRIs have been associated with increased suicidality in patients < 25 yo.  Which was directing my thoughts more toward O.D. or drug adverse event.

I leaned away from pontine hemorrhage mostly because it's usually chronic  hypertensive in origin (or AVM) and results in hyperventilation (if you go 'by the book').  There's a good quick read on them here: Basic Neurology

 Either way...this kid may have a bad outcome.  
Heaven knows I've seen enough kids end up as eating(via tube), breathing(via tube), poopin'(via diaper) bed decorations due to attempts at suicide


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## MSDeltaFlt (Apr 22, 2009)

BruceD said:


> I've not endorsed narcan on this patient, I think you are correct about not using it.
> Treating this patient with diesel would be ideal, especially when you are 4mins from a hospital.
> 
> Effexor has been shown to cause atrial fib along with other arrhythmias -> http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2000637 and has been associated with both NMS and Serotonin Syndrome -> http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)72791-4/fulltext
> ...


 
Great on the references.  I wasn't stuck on Pontine either.  Only mentioning it as a possibility with the hot skin and the pinpoint pupils.  I was merely trying to get everyone to think about something.  With this guy's prehospital presentation, his official diagnosis could have easily gone either way.  And pushing Narcan on something that wasn't opioid induced up to and including CVA could have very counterproductive results to an already negative situation.  Add to that not getting a definitive *airway*,regardless of the type, even for a 4 min trip, and you can see how he could end up in a perpetual vegetative state for decades to come.


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## Melclin (Apr 22, 2009)

Well here comes the great and uninteresting reveal. The kid was actually me...BABAH. A few years ago now. I requested the Patient Care Records from Ambulance Victoria. 

As far as what it actually was, I'm still pretty sketchy. I spent most of my time drunk in those days, so my memory, she's notta so good. Depression yeah, suicide attempt? Nope. 

I'd had about 8 beers earlier that night but was pretty close to sober come 12am when my parents went to bed. After that I can't remember, but I had a habit of purifying codeine out of paracetamol/codeine OTC pain killers (which would explain the paracetamol in my liver). May have tried that and mixed it with some Xanax. Or possibly made opium tea from poppy seeds, that was a common one too. The ICU doctor latter argued with me that it couldn't have been that because poppy seeds are inert...my previous six months of being consistently wasted off them beg to differ. It's also possible that in my general intoxication (experience has show that xanax plus alcohol makes for some decidedly odd decision making) it may have seemed like a good idea to eat a box of panadol. Like I said, I must have aspirated my stomach contents at some stage (they put chemicals in the poppy seeds to make you nauseous if u have to many to discourage stonners like my old self, so that might have something to do with it). Lost about 80% of my lung volume, and got a nasty dose of aspiration pneumonitis. I'm interested to see that the paramedics didn't make any note of being able to hear odd lung sounds. With lungs 80% full of vommit you'd have to hear something. 

Almost died, but recovered quite well with anti-biotics, spent a week in ICU (PEEP ventilation majorly sucks when you're awake) and walked out straight into a looney bin where I spent the next week or so, convincing them I didn't try to off myself.  

Anyways, I thought it was in interesting case given that none of the practitioners involved could ever really figure out what happened exactly and it had an odd presentation, easily mistakable for a straight up heroin overdose.

PS: Lets not have any "That was stupid thing to do" comments. I realise that. I realised at the time. But in the swing of what I would later know to be my first Bi-polar related depression, I didn't particularly care. I'm quite different now, with the help of a cracking shrink, and planning to enjoy paying back my debt to society while I practice some top notch paramedicine . Oh and not that I expect it, but no sympathy, I just wanted to present an interesting case and hoped to learn a little more about what happened. You've all been extremely helpful so far. Any more stunning insights or thoughts?


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## boingo (Apr 22, 2009)

What did they do to manage your A-fib?  Did it spontaneously convert, did they chemically convert you or cardiovert?  Did you have a prior hx of A-fib, WPW?  Glad to hear you are on the mend, I know I felt pretty damn invincible in my late teens early twenties too.  Good luck with your education.


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## Melclin (Apr 22, 2009)

boingo said:


> What did they do to manage your A-fib?  Did it spontaneously convert, did they chemically convert you or cardiovert?  Did you have a prior hx of A-fib, WPW?  Glad to hear you are on the mend, I know I felt pretty damn invincible in my late teens early twenties too.  Good luck with your education.



No history of A-fib or WPW. I think someone in my family has WPW so there might be something in that but I'm sure they would have noticed that in the ICU some time during the week I was there. 

I'm not entirely sure, cos I haven't gotten around to requesting my hospital records yet but they were considering sychronised cardioversion, but I think it spontaneously converted. My parents account of the night has proven to be (understandably) inaccurate. So one of these days I'll fill out the plethora of paper work to get the hospital to send me my records.

Cheers for the encouragement.


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## BruceD (Apr 22, 2009)

MSDeltaFlt said:


> Great on the references.  I wasn't stuck on Pontine either.  Only mentioning it as a possibility with the hot skin and the pinpoint pupils.  I was merely trying to get everyone to think about something.  With this guy's prehospital presentation, his official diagnosis could have easily gone either way.  And pushing Narcan on something that wasn't opioid induced up to and including CVA could have very counterproductive results to an already negative situation.  Add to that not getting a definitive *airway*,regardless of the type, even for a 4 min trip, and you can see how he could end up in a perpetual vegetative state for decades to come.



Absolutely a good point about the Narcan.

Meclin, adding etoh to a bzd opens up a whole new area of bad-ness.  Take a few and read up on it, tell us if you think it fits your profile.

tc
-B


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## triemal04 (Apr 23, 2009)

MSDeltaFlt said:


> You also need to control ICP's as best you can on the prehospital level. EtCO2's in the 60's and 70's is a bit high. High end tidals mean cerebral vasodilation which further increase ICP which take away from CPP which is what is going to drive this poor kid further down the drain. If you have RSI, put him down and get those EtCO2's in the upper 30's.


Be worth considering why the EtCO2 is that high, even after artificial ventilation.  Something beyond downtime is causing that increase, which would point more towards med OD than anything in this case.


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## VGFDEMT34 (May 4, 2009)

Primary thought is an overdose. Secondary is a diabetic emergency. What is the BGL?

If BGL within normal range: push narcan for suspected overdose. Any change in mental status?

If hypoglycemic: D-50 IV push

If hypoglycemic: bolus NaCl


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## Melclin (May 9, 2009)

triemal04 said:


> Be worth considering why the EtCO2 is that high, even after artificial ventilation.  Something beyond downtime is causing that increase, which would point more towards med OD than anything in this case.



Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all. 

Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?


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## Melclin (May 9, 2009)

VGFDEMT34 said:


> Primary thought is an overdose. Secondary is a diabetic emergency. What is the BGL?
> 
> If BGL within normal range: push narcan for suspected overdose. Any change in mental status?
> 
> ...



A Random Blood Glucose test showed it to be 15.3 mmol/L. That's a little more than twice what it should be if you're not familiar with that format. But its not even close to enough to have caused all this.


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## BruceD (May 9, 2009)

Melclin said:


> Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.
> 
> Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?



The original high CO2 is probably due to respiratory acidosis (pt isn't blowing off CO2 'cause his resps are 6).

Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?), inadequate amount of time/volume of artificial ventilation, or an ongoing metabolic process producing acid (organic acids such as EtOH, lactic acidosis, or Rhabdo), but I think Vent would be the best person to answer this question as this is beyond my realm o' knowledge.


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## bonedog (May 9, 2009)

What was the QT interval, QRS? Effexor could be causing the arrythmia.

Methamphetamine binge followed by a dose of GHB. End up with the electrolyte imbalance and the patient that goes from GCS of 3 to ripping out the ET tube and back to a 3.


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## VentMedic (May 9, 2009)

BruceD said:


> The original high CO2 is probably due to respiratory acidosis (pt isn't blowing off CO2 'cause his resps are 6).
> 
> Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?), inadequate amount of time/volume of artificial ventilation, or an ongoing metabolic process producing acid (organic acids such as EtOH, lactic acidosis, or Rhabdo), but I think Vent would be the best person to answer this question as this is beyond my realm o' knowledge.


 
You're doing a decent job explaining it.



> Originally Posted by *Melclin*
> 
> 
> _Yeah, after 20 mins or so of apparently adequate *ventilation (with SpO2: 100, or close enough*) the etCO2 had barely dropped at all. _
> ...


 
Oxygenation and ventilation are two very different concepts. You can not tell much about ventilation from an SpO2. In this case you may not even be able to tell much about oxygenation either since the *oxyhemoglobin* *dissociation* *curve* will shift in the face of acidosis. In fact, if the shortness of breath was severe to start with the SpO2 may not be an adequate indication of oxygenation if the A-a is unknown. If you are giving an FiO2 of 1.0 but only getting a PaO2 of 85 mmHg, you have a significant A-a gradient which indicates a serious problem. Normal A-a gradient increases 5-7 mmHG for every 10% increase in FiO2 due to the overcoming of hypoxic vasoconstriction opening blood flow to poorly ventilated lung areas. There is also the relationship between pulmonary vasoconstriction if it is released with an FiO2 of 1.0 and an increase in CO2 with deadspace and V/Q mismatching. For some patients, this is now a more accepted theory to hypercarbia (hypercapnia) than the "hypoxic drive".


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## fma08 (May 10, 2009)

VentMedic said:


> the *oxyhemoglobin* *dissociation* *curve* will shift in the face of acidosis.



Yet another thing I learned in college A&P and not the "A&P" we got in medic school... <_<


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## Melclin (May 10, 2009)

BruceD said:


> Remaining acidotic after artificial ventilation to me points to some barrier preventing CO2 from diffusing in the alveoli (pulmonary congestion/edema?),



Lungs full of aspirated stomach contents would fit the bill here right? Cos I sure had that. Should the persistant ^ etCO2 have been an indicator, given the setting, that aspiration was a possibility? How relevant is identifying a significant stomach contents aspiration to the initial pre-hospital treatment?     



bonedog said:


> What was the QT interval, QRS? Effexor could be causing the arrythmia.
> 
> Methamphetamine binge followed by a dose of GHB. End up with the electrolyte imbalance and the patient that goes from GCS of 3 to ripping out the ET tube and back to a 3.



Don't have the details on the ECG just that it was A-Fib. 
And I'd know if I'd been into the methamphetamines, and I would have mentioned it here already ^_^ but I assume you were throwing out ideas from a theoretical point of view, so cheers.



VentMedic said:


> *oxyhemoglobin* *dissociation* *curve* will shift in the face of acidosis.



Ahh yeah, I forgot my old A&P. Didn't see the direct relevance of that particular until bit of info at the time. Now I know better.  

Thanks guys, very illuminating. Keep it coming. Honestly, sometimes I reckon I learn more off this forum that I do off my lecturers.


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## Amack (May 10, 2009)

MSDeltaFlt said:


> Narcan is contraindicated for resp depression not due to opioid ingestion.  Side effects include tachycardia, hypertension, N/V, seizures, even cardiac arrest.  Do you really want to cause these side effects on someone who could quite possibly be having a CVA?



CONTRAINDICATIONS — Hypersensitivity to naloxone or any component of the formulation

WARNINGS / PRECAUTIONS 
Concerns related to adverse effects:

Acute opioid withdrawal: May precipitate symptoms of acute withdrawal in opioid-dependent patients, including pain, hypertension, sweating, agitation, irritability; in neonates: shrill cry, failure to feed. Carefully titrate dose to reverse hypoventilation; do not fully awaken patient or reverse analgesic effect (postoperative patient). 
Disease-related concerns:

Cardiovascular disease: Use with caution in patients with cardiovascular disease or in patients receiving medications with potential adverse cardiovascular effects (eg, hypotension, pulmonary edema or arrhythmias); pulmonary edema and cardiovascular instability, including ventricular fibrillation, have been reported in association with abrupt reversal when using narcotic antagonists. Administration of naloxone causes the release of catecholamines; may precipitate acute withdrawal or unmask pain in those who regularly take opioids. 
Seizures: Use caution in patients with history of seizures; avoid use in treatment of meperidine-induced seizures. 
Other warnings/precautions:

Opioid overdose: Recurrence of respiratory depression is possible if the opioid involved is long-acting; observe patients until there is no reasonable risk of recurrent respiratory depression. 
Postoperative reversal: Appropriate use: Excessive dosages should be avoided after use of opiates in surgery. Abrupt postoperative reversal may result in nausea, vomiting, sweating, tachycardia, hypertension, seizures, and other cardiovascular events (including pulmonary edema and arrhythmias). 

(Taken from the following references

REFERENCES


American Academy of Pediatrics Committee on, Drugs. Naloxone Dosage and Route of Administration for Infants and Children: Addendum to Emergency Drug Doses for Infants and Children. Pediatrics 1990; 86:484. 
American Heart Association Emergency Cardiovascular Care, Committee. 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC), Part 10.2: Toxicology in ECC. Circulation 2005; 112(24 Suppl):IV126. 
American Heart Association Emergency Cardiovascular Care, Committee. 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC), Part 12: Pediatric Advanced Life Support. Circulation 2005; 112(24 Suppl):IV167. 
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I didn't see anywhere about withholding naloxone dude to respiratory depression not caused by opioids...and furthermore, without proper laboratory screening, you wouldn't be able to tell if was or wasn't due to opiods unless naloxone is a administered and a + effect is noted or not.


Also, the side effects you mentioned are probably (as explained above) sympotomatic of acute withdrawal sx from the naloxone, and not from naloxone itself


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## triemal04 (May 11, 2009)

Melclin said:


> Yeah, after 20 mins or so of apparently adequate ventilation (with SpO2: 100, or close enough) the etCO2 had barely dropped at all.
> 
> Would I be correct in thinking (I'm a student so humour me) that the high etCO2 in this situation would usually be to do with metabolic acidosis from anerobic respiration from hypoxia? Surely if that were the case it would drop faster after adequate vents. You're saying that some kind of pharmacological reason is behind the ^ etCO2? Would that mean that the polypharm OD is causing acidosis separate to that from the hypoxia, or could their be another mechanism?


Pretty much.  Someone else already pointed out that with full lungs the gas-exchange is inhibited which could also have contributed to the problem.  I was leaning more towards it being a metabolic acidosis more than anything; many many drugs (including normal over the counter drugs like aspirin, tylenol and ibuprofen) will cause acidosis, sometimes due to respiratory depression and lactate build up, but often not.

And I can't humor you if you insist on using the British way of spelling.


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## Melclin (May 12, 2009)

triemal04 said:


> Pretty much.  Someone else already pointed out that with full lungs the gas-exchange is inhibited which could also have contributed to the problem.  I was leaning more towards it being a metabolic acidosis more than anything; many many drugs (including normal over the counter drugs like aspirin, tylenol and ibuprofen) will cause acidosis, sometimes due to respiratory depression and lactate build up, but often not.
> 
> And I can't humor you if you insist on using the British way of spelling.



Ah interesting. Its all kind of coming together. I'm ganna have to do some more reading about gas exchange I think. Seems an interesting business.

Damn yanks and your sensible spelling. Whoever heard of spelling a word in a way that would make phonetic sense? That's just not sporting. The queen would not approve.


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