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Case #51 "i Feel Cold"


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#81 TexRNmedic

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Posted 21 March 2010 - 01:24 AM

he doesn't have one [a pressure]. would you like to revise your assumption and tx? ;-)


So to update. The dude is intubated and vented. Now in what sounds like an idioventricular rhythm.

TX: Back to the basics-ABC's. Check a central pulse. Glance at the monitor (pulse ox and ETCO2 #'s). Is my airway truly secured and am I ventilating with adequate 02 delivery? Bilateral breaths sounds still OK? Other than the lytes issues next mostly like cause of a slow PEA in this guy is probably hypoxemia. Since we already have the defib/pacer on this guy I'll start pacing. Might end up needing some chest compressions to reprime the pump and reoxygenate the myocardium. Turn off the Lido drip for now. Short ETA. Going to call the ED and get them ready for us.
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Wes Seale
Houston , TX

#82 SerendepitySaki

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Posted 21 March 2010 - 10:56 PM

zero central pulses... pulse ox trailing off to non-pulsatile, EtCO2 no immediate appreciable change....

yes. airway secured

yes. O2 delivery to LUNGS appears to be adequate.

yes. BBS good (excellent differential, cause you KNOW i would've dropped a lung if someone didn't specify that they listened....)

pacer fails to capture - someone please specify initial and potentially adjusted settings, as well as pros/cons and rationales...

lido off. 2nd round of Mag going in, if I haven't already given it to you.....

you holler thru the cab window to your partner who calls the ED and begins TXing your PEA with diesel....

how about guys.... do we want to start compressions or attempt another round of pacing?

questions to be added for final round up:

what does alkalosis do to seizure threshold? how did you guys prevent that? should we then consider empiric benzos with this presentation?

if we haven't already discussed it, be thinking about the multiple players in myocardial contraction....

talk further about renal mechanism for refractory hypokalemia in presence of hypomagnesemia... will the alkalosis tie in here as well? if so, how?

So to update. The dude is intubated and vented. Now in what sounds like an idioventricular rhythm.

TX: Back to the basics-ABC's. Check a central pulse. Glance at the monitor (pulse ox and ETCO2 #'s). Is my airway truly secured and am I ventilating with adequate 02 delivery? Bilateral breaths sounds still OK? Other than the lytes issues next mostly like cause of a slow PEA in this guy is probably hypoxemia. Since we already have the defib/pacer on this guy I'll start pacing. Might end up needing some chest compressions to reprime the pump and reoxygenate the myocardium. Turn off the Lido drip for now. Short ETA. Going to call the ED and get them ready for us.


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Sean G. Smith, RN-Alphabet Soup

#83 SerendepitySaki

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Posted 22 March 2010 - 12:33 AM

as you turn back to your pt after shouting to your partner, you see EtCO2 dropping, trailing....

how about it guys.... do we want to start compressions, push some drugs, or attempt another round of pacing?


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Sean G. Smith, RN-Alphabet Soup

#84 amydayre

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Posted 22 March 2010 - 03:46 AM

as you turn back to your pt after shouting to your partner, you see EtCO2 dropping, trailing....

how about it guys.... do we want to start compressions, push some drugs, or attempt another round of pacing?


Ok, I haven't played in a looooong time, but here goes. Alkalosis drops the seizure threshhold, which we treated with ativan/versed, whichever was finally given.
This guy is hypokalemic and hypomagnesemic (sp?) which are probably the direct result of him lying in bed with his bottle and his vicoden since d/c from the hospital.I am positive he hasn't been drinking enough water, which also contributes to low mag levels. I don't think we are going to emergently correct these lytes, but I would like to crank the NS with kcl gtt up to wide open. And we turned the lido off, right?
I know you said he is being ventilated but obviously is not being oxygenated, otherwise he wouldn't be asystolic at this point. We have some sort of obstruction somewhere, so let's start compressions.
How far out are we?
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#85 Speed

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Posted 22 March 2010 - 09:56 PM

This case is still going.... just kidding. The last rhythm I saw looks shockable, unless it self resolved into what looked like an IVR rhythm? Without pulses, I'd say start CPR, maybe some epi. I'm assuming he hasn't or doesn't take Dig? I see that your not capturing on your pacer, yeah I'd be playing with that some more. Overall he sounds like a run-of-the-mill malnourished ETOH abuser with the whole renal or hepato-renal thing(thought I saw a BUN/Crea WNL earlier from the I-stat). His screwed up lytes would play a role in failure to capture. Did you ever get an accuarte temp?
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Mike Williams CCEMT-P/FP-C

#86 SerendepitySaki

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Posted 22 March 2010 - 10:22 PM

check the comments on your profile page...Posted Image

This case is still going.... just kidding. The last rhythm I saw looks shockable, unless it self resolved into what looked like an IVR rhythm? Without pulses, I'd say start CPR, maybe some epi. I'm assuming he hasn't or doesn't take Dig? I see that your not capturing on your pacer, yeah I'd be playing with that some more. Overall he sounds like a run-of-the-mill malnourished ETOH abuser with the whole renal or hepato-renal thing(thought I saw a BUN/Crea WNL earlier from the I-stat). His screwed up lytes would play a role in failure to capture. Did you ever get an accuarte temp?


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Sean G. Smith, RN-Alphabet Soup

#87 STPEMTP

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Posted 23 March 2010 - 01:05 AM

You start the normal ACLS routine. Upon arrival at receiving facility, still no success in resuscitation. They work him for a brief time before getting lucky and restore a pulse.

Pt admitted to ICU for multiple electrolyte abnormalities, cardiac rhythm abnormalities, and resuscitated cardiac arrest.

Resolution of case:
Pt sent to the ICU, where he continued to have issues with runs of VT and torsades despite maximal therapy. Pt sent to cath lab for eval to r/o other causes. Cath showed no vessels requiring treatment. Transvenous pacer placed. PT sent back to the ICU. After approx 24 hours, pt's cardiac rhythm finally stabilizes. Pt remains in the ICU intubated for 18 days. After day 21 pt is d/c to a inpatient chemical dependancy center.

SerendepitySaki will be following up with a few more points in the next couple of days. Thank you to everyone who participated.

I would like to extend my sincerest gratitude to SerendepitySaki for his assistance with this case. Thank you again for all the assistance.
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#88 Ectopy

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Posted 23 March 2010 - 01:17 AM

I'm going to bite the bullet and say to start compressions. At least do five founds, 1mg epinephrine, 1mg atropine. Lets not forget that the AHA guidelines are still the standard. The guidelines EXPLICITLY state that compressions should never be withheld in order to pace. The overwhelming body of research states that pacing is detrimental to long term survival in a PEA cardiac arrest situation (which is essentially what we have here). Withholding compressions in (my opinion) a futile attempt to capture is forcing the cerebellum and myocardial tissue to go longer without oxygen.

HOWEVER, I am new and always open to being proven wrong if anyone can provide empirical evidence contrary.

I'm also going to want to slam in another 500ml bolus in case he all of a sudden vasodilated more and it's a preload issue. I know this might be controversial, but if I am suspecting a preload issue I'd like to start a dopamine drip at 5mcg/kg/min and titrate upwards.

Thoughts?
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Matthew George - NREMT-P, FP-C, CCP, Instructor

#89 Speed

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Posted 23 March 2010 - 09:34 PM

The overwhelming body of research states that pacing is detrimental to long term survival in a PEA cardiac arrest situation (which is essentially what we have here).


In PEA sure, if you can salvage PEA is usually direct mechanism resolution. Now you're refractory VF/VT arrest, the long ones that make you start to wonder, well, I've saved (in my mind) a few too many to completely write off pacing during arrest situations. I think it really depends on how fresh of an arrested patient you have of course, but like this situation body temp, lytes, etc. all come into play. I really actually think if you could make a machine that would immediately deliver a short trial of pacing with "generalized settings" immediately after a defibrillation attempt, let's say after 1 or 2 unsuccessful standard defibrillation attempts you would see a little increase in survival. The act of defibrillation basically stamps out the activity to restore organized activity from the electrical potential by a stand-back and hope that it works routine. It becomes quickly apparent when hoping and luck aren't cutting it as the electrical potential returns in the form of something not generated from a node, I say add a little direction after that shock by organizing the potential instead of hoping that it does it itself, help it out a little. That flat line you see immediately after a shock is really just staring back at you waiting for instruction, it's usually only a few seconds of opportunity. Some monitors are easier to do this than others. I think the LP12 is the easiest because you can be in defib mode and it retains your pacer settings and you can kick it on immediately after a shock (w/ CPR still going). Some monitors dump your pacer settings when you're in defib mode and it's an act of congress to get it going again, by then the victim is usually back into VF/VT. Not protocol, not AHA approved, but hey...it works. It's easy to get wrapped up into the scripted choreograph of ACLS and lose the science of what's going on inside, research is obviously a must, but I would always keep an open mind.
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Mike Williams CCEMT-P/FP-C

#90 SerendepitySaki

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Posted 23 March 2010 - 10:21 PM

matt,
you're right....speed's bringing up great stuff....but right now, this guy's in wide complex PEA...
this guy needs compressions, + all of the above... right, in PEA, we identify and tx underlying causes.... problem here is this guy's screwed seven ways from sundown..... he's probably swirled too far down the toilet to be able to pace out of it right this second...maybe, maybe not.... but that's why i asked the question about tell me what your pacer settings are and why.... we might have thrown someone a bone if they had dialed it up slightly, but that's debatable... yeah, he's got a little mag and k on board now, maybe some calcium, i don't remember, and we definitley can't fix his alkalosis in the back of the box.... he's pretty far gone.... compressions, IVFB, EPI/Atropine, leave em dead or Dopa gtt were the "most correct" answer at this stage in my book.... dude's dryer than last summer's doggie bone.... need to PRAY there's no significant cardiac comorbities, prime that pump, spray some carb cleaner in, run high octane, manually cycle that mutha a few hundred times or so and see if she'll kick over....I DEFINITELY would have let you pace him out IF someone had chimed in after your post.....

for the AHA Buffs in the crowd.....
http://circ.ahajourn...2/suppl_1/I-136

"End of Algorithm Notes
Other observed pulseless cardiac arrest arrhythmias are those in which the electrical activity (QRS complex) is wide versus narrow and fast versus slow. Most clinical studies have observed poor survival rates from PEA that is wide-complex and slow. These rhythms often indicate malfunction of the myocardium or the cardiac conduction system, such as occurs with massive AMI. These rhythms can represent the last electrical activity of a dying myocardium, or they may indicate specific critical rhythm disturbances. For example, severe hyperkalemia, hypothermia, hypoxia, preexisting acidosis, and a large variety of drug overdoses can be wide-complex PEAs. Overdoses of tricyclic antidepressants, -blockers, calcium channel blockers, and digitalis will produce a slow, wide-complex PEA.

In contrast, a fast, narrow-complex PEA indicates a relatively normal heart responding exactly as it should for severe hypovolemia, infections, pulmonary emboli, or cardiac tamponade. These conditions have specific interventions.

The major action to take for a cardiac arrest victim in PEA is to search for possible causes. These rhythms are often a response to a specific condition, and helpful clues can appear if one simply looks at the electrical activity width and rate.

Hypovolemia is the most common cause of electrical activity without measurable blood pressure. Through prompt recognition and appropriate therapy, the many causes of hypovolemia can often be corrected, including hypovolemia from hemorrhage or from anaphylaxis-induced vasodilation. Other causes of PEA are cardiac tamponade, tension pneumothorax, and massive pulmonary embolism.

Nonspecific therapeutic interventions for PEA include epinephrine and (if the rate is slow) atropine, administered as presented in Figure 4Posted Image. In addition, personnel should provide proper airway management and aggressive hyperventilation because hypoventilation and hypoxemia are frequent causes of PEA. Clinicians can give a fluid challenge because the PEA may be due to hypovolemia.

Immediate assessment of blood flow by Doppler ultrasound may reveal an actively contracting heart and significant blood flow. The blood pressure and flow, however, may fall below the threshold of detection by simple arterial palpation. Any PEA patient with a Doppler-detectable blood flow should be aggressively treated. These patients need volume expansion, norepinephrine, dopamine, or some combination of the three. They might benefit from early transcutaneous pacing because a healthy myocardium exists and only a temporarily disturbed cardiac conduction system stands between survival and death. Although in general PEA has poor outcomes, reversible causes should always be targeted and never missed when present."


but hey...it works. ......I would always keep an open mind.


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Sean G. Smith, RN-Alphabet Soup

#91 SerendepitySaki

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Posted 27 March 2010 - 03:49 PM

hey folks:

will try circle the wagons on the "20 questions" on Tuesday, if anyone wants to chime in before then.

also, if anyone is holding off on sharing a case study because of the workload/lack of labs, strips, follow-up, whatever... please contact me if you'd like to split the workload as STP and I have done here...
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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#92 TexRNmedic

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Posted 05 April 2010 - 02:04 PM

hey folks:

will try circle the wagons on the "20 questions" on Tuesday, if anyone wants to chime in before then.

also, if anyone is holding off on sharing a case study because of the workload/lack of labs, strips, follow-up, whatever... please contact me if you'd like to split the workload as STP and I have done here...


Where did you go Sean? I was looking forward to your wrap up.
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Wes Seale
Houston , TX

#93 SerendepitySaki

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Posted 07 April 2010 - 03:12 AM

like the arhnold.... i'll be back! unexpectedly running and gunning last week... hope to wrap her this week and you and i can get the next one kicked off!



Where did you go Sean? I was looking forward to your wrap up.


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#94 TexRNmedic

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Posted 08 April 2010 - 02:23 AM

like the arhnold.... i'll be back! unexpectedly running and gunning last week... hope to wrap her this week and you and i can get the next one kicked off!


Sounds good man. Look forward to the wrap up. Sent you an email about future case study.
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Wes Seale
Houston , TX

#95 medic675

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Posted 18 April 2010 - 04:58 PM

This is awsome that the cases are back, you guys rock. As for the patient, I got lost in the labs. I am still learning them so its ok. Couple of questions:

1- Early on, before we had an EKG some said they wanted to pace, why?
2- Why didnt we just put the IO in his humerus? Avoid the legs all together.
3- Where did the fentnyl patches come from? What do his pupils look like? Narcan anyone?
4- I thought this pt was bed confined or ridden since d/c. How did he find energy to strat getting up off stretcher for his Jack? Did I miss something?

Look forward to the next one.
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Brian Nolan
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#96 SerendepitySaki

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Posted 18 April 2010 - 05:07 PM

brian- will answer all these and more in the long overdue wrap-up... should be a new case posted shortly and i am lining up the one after that.... will get to the #51 wrap up asap....

weigh in early and often on the next one and get your friends to play...!

quickly:
pacing discussion buried in thread.
could have also gone sternal... don't believe we threw in any contraindications one way or the other IO placement
fent was D/C to home post op pain mgt
as for #4, well, people surprise you sometimes.... and he was 5 weeks post op... however, the main reason for #4 was that i felt i did not do a good job conveying the pt's etOH hx and needed to clue you guys in ASAP... pt presentation was well characterized off-line, but when i typed it up, i left stuff out...d'oh!

This is awsome that the cases are back, you guys rock. As for the patient, I got lost in the labs. I am still learning them so its ok. Couple of questions:

1- Early on, before we had an EKG some said they wanted to pace, why?
2- Why didnt we just put the IO in his humerus? Avoid the legs all together.
3- Where did the fentnyl patches come from? What do his pupils look like? Narcan anyone?
4- I thought this pt was bed confined or ridden since d/c. How did he find energy to strat getting up off stretcher for his Jack? Did I miss something?

Look forward to the next one.


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#97 medic675

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Posted 19 April 2010 - 02:01 AM

Sean- thanks, cant wait for more cases. these are great to read, even about half of the stuff makes sense to me. Thanks again.
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Brian Nolan
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#98 TexRNmedic

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Posted 19 April 2010 - 06:35 PM

brian- will answer all these and more in the long overdue wrap-up... should be a new case posted shortly and i am lining up the one after that.... will get to the #51 wrap up asap....

weigh in early and often on the next one and get your friends to play...!

quickly:
pacing discussion buried in thread.
could have also gone sternal... don't believe we threw in any contraindications one way or the other IO placement
fent was D/C to home post op pain mgt
as for #4, well, people surprise you sometimes.... and he was 5 weeks post op... however, the main reason for #4 was that i felt i did not do a good job conveying the pt's etOH hx and needed to clue you guys in ASAP... pt presentation was well characterized off-line, but when i typed it up, i left stuff out...d'oh!



I'm looking forward to your wrap up dude. Especially the electrolyte review. Our next case study is ready to go, just waiting on the Mods to bless it. Good luck on your pharm exam.
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Wes Seale
Houston , TX