bulgethetwine

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AAF, bib EMS unresponsive. Missed dialysis yesterday, and has a nice midline CABG scar. Now in the resus bay, unresponsive, JUST started wide complex tach on the monitor. Vitals: HR 210 BP 175/90 T' 36.8 Sat% 97ra Just converted from agonal resps to apnea.

Intubated without drugs or gag reflex. BS equal bilaterally, ventilated. Pulses palpable at carotid, radial, femoral.

Suspecting hyperkalemia, give calcium and bicarb. Now waiting for insulin to arrive. Still wide complex tach on the monitor, rate > 200. This has been going on for 60s, now, and although the pressure is still holding, you wonder how long the pressure will stay there with the HR going 200.

Do you:

a) Shock! It's wide complex after all, and although you're suspecting hyperkalemia, the calcium hasn't worked yet and she does have that CABG scar. Besides, what harm will the shock have?

b) Shock!?! Are you crazy?? This is hyperkalemia -- she missed dialysis yesterday for God sake!

c) Give amiodarone. She still has pressure afterall (although she's unresponsive). This buys you time for the insulin to arrive, calcium to work, etc.

d) Something else to suggest. I would .... "_________________...."


Let me hear your thoughts. I'll let you know what happened.
 
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dynx

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With a one lead reading I'd make sure the reading was kosher, push amio and have the pads ready. She's got pulses and a good pressure, she was LOC before the rhythm its not a unstable tach. causing her AMS.
 
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I'm with DocB - for wide-complex tachycardia, altered LOC/unconscious, hypotensive, chest pain, or rales make it unstable, and electricity is the way to go. ABC's, then ACLS. After all, you think you know what's going on, and there are two heavy players (the hyperK and the intrinsic cardiac history, as gleaned by the zipper), and, what's the worst that happens? She's already circling the drain, and, with the calcium on board, if it IS hyperkalemia, you should be seeing something.

And, like DocB says - it's hard to not shock it. It's one thing if it's transient, but, for 60s - if you don't shock, you gots some 'splainin' to do.
 

Hard24Get

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AAF, bib EMS unresponsive. Missed dialysis yesterday, and has a nice midline CABG scar. Now in the resus bay, unresponsive, JUST started wide complex tach on the monitor. Vitals: HR 210 BP 175/90 T' 36.8 Sat% 97ra Just converted from agonal resps to apnea.

Intubated without drugs or gag reflex. BS equal bilaterally, ventilated. Pulses palpable at carotid, radial, femoral.

Suspecting hyperkalemia, give calcium and bicarb. Now waiting for insulin to arrive. Still wide complex tach on the monitor, rate > 200. This has been going on for 60s, now, and although the pressure is still holding, you wonder how long the pressure will stay there with the HR going 200.

Do you:

a) Shock! It's wide complex after all, and although you're suspecting hyperkalemia, the calcium hasn't worked yet and she does have that CABG scar. Besides, what harm will the shock have?

b) Shock!?! Are you crazy?? This is hyperkalemia -- she missed dialysis yesterday for God sake!

c) Give amiodarone. She still has pressure afterall (although she's unresponsive). This buys you time for the insulin to arrive, calcium to work, etc.

d) Something else to suggest. I would .... "_________________...."


Let me hear your thoughts. I'll let you know what happened.

Doing a Cardiology elective now, so I will take a stab:

- I would take her deteriorating mental status as an invitation to shock her. If she was responsive with a pulse and a good BP, I would give it a bit, but not an unresponsive pt

- Not sure if the sternotomy scar is KNOWN to be from CABG or how old it is, but certainly there is the suggestion of cardiologic compromise, she may not be able to tolerate VT for long without an ischemic event if she is not already having one.

- would use amiodarone for refractory VT, though may not work for hyperK
-Missing dialysis by one day should not put her at a supremely dangerous potassium level and may not be the cause of her sx, though someone could glance at the pre-tach EKG to look for potential tell-tale signs. Either way, not sure it would change my management....

Look forward to more senior thoughts on this case, thanks!
 

BKN

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"Arrhythmias due to hyperkalemia are very difficult to treat with defibrillation, epinephrine, or antiarrhythmic drugs without emergently lowering the serum potassium level." . . .from an emedicine article.

That's been my experience too. You've got a great pressure, and reasonable perfusion. I think if you shock this patient your resulting rhythm is likely to be asystole. On the other hand, rapid narrowing of the QRS is the usual rule with bicarb, Ca, glucose and Insulin.

If the pressure drops, you can shock her then.
 
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"Arrhythmias due to hyperkalemia are very difficult to treat with defibrillation, epinephrine, or antiarrhythmic drugs without emergently lowering the serum potassium level." . . .from an emedicine article.

That's been my experience too. You've got a great pressure, and reasonable perfusion. I think if you shock this patient your resulting rhythm is likely to be asystole. On the other hand, rapid narrowing of the QRS is the usual rule with bicarb, Ca, glucose and Insulin.

If the pressure drops, you can shock her then.

However, look at the OP - the calcium and bicarb are on board, but the complexes have not changed - this leans against it being an electrolyte disturbance and towards a primary rhythm disturbance. When I had it happen last year, the sine wave EKG changed in a matter of seconds to a RSR, nice and narrow. It's directly a function of chemistry.

I still stand by the juice.
 

dgmedic

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"Arrhythmias due to hyperkalemia are very difficult to treat with defibrillation, epinephrine, or antiarrhythmic drugs without emergently lowering the serum potassium level." . . .from an emedicine article.

That's been my experience too. You've got a great pressure, and reasonable perfusion. I think if you shock this patient your resulting rhythm is likely to be asystole. On the other hand, rapid narrowing of the QRS is the usual rule with bicarb, Ca, glucose and Insulin.

If the pressure drops, you can shock her then.
Right off the bat, I would agree with no shock, no antiarhythmics. Anymore info from the medics? Look at their 12-lead or grab one of your own to see the axis to rule on ventricular nature. If extreme, zap her.

Any bedside labs? How frequently is she dialyzed? Surely her sugar was checked by EMS? (knock out the embarrasing misses quickly for M&M insurance, right?)

The other thing concerning is that she was able to be intubated without being sequenced!! CVA? Did she miss dialysis because she has been stroking (unless EMS can give a better scene picture)?

Oh yeah...if waiting on insulin and you have her tubed...you might as well start bagging in a neb treatment to help along the K+ shift.

.....just a paramedics view....

Interested to hear the case follow-up and other's thoughts as well.

-dg

::Edit:: noticed that the original post noted "JUST started...wide complex..." I may have to change my answer above. The wide complex is typically a progressive issue with hyperK, right? What did it look like right before it JUST went wide? ......hhhhmmmmmm, I probably would go ahead and hang a drip of amiodarone. I am still concerned with the neuro status. Folks in VT with that pressure typically (in my experience) just have horrid chest pain....not completely unresponsive.
 

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Are you not able to do a blood gas to get the answer to your K+ question straight away? (If not, why not?)

I'd be prepping to shock while waiting for the gas result, which would tell me the K+ level. If for whatever reason the resus gas machine was bust, then I'd probably go for shock now, for the reasons stated above.
 

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Are you not able to do a blood gas to get the answer to your K+ question straight away? (If not, why not?)
Costs too much and results in a huge political fight between respiratory and lab every time it comes up. It's a similar fight to the one that has resulted in all stool guiac cards being sent to lab to be developed, seriously (actually that's more of a JCAHO debacle but the result is the same).
 

bulgethetwine

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Right off the bat, I would agree with no shock, no antiarhythmics. Anymore info from the medics? Look at their 12-lead or grab one of your own to see the axis to rule on ventricular nature. If extreme, zap her.

Any bedside labs? How frequently is she dialyzed? Surely her sugar was checked by EMS? (knock out the embarrasing misses quickly for M&M insurance, right?)

The other thing concerning is that she was able to be intubated without being sequenced!! CVA? Did she miss dialysis because she has been stroking (unless EMS can give a better scene picture)?

Oh yeah...if waiting on insulin and you have her tubed...you might as well start bagging in a neb treatment to help along the K+ shift.

.....just a paramedics view....

Interested to hear the case follow-up and other's thoughts as well.

-dg

::Edit:: noticed that the original post noted "JUST started...wide complex..." I may have to change my answer above. The wide complex is typically a progressive issue with hyperK, right? What did it look like right before it JUST went wide? ......hhhhmmmmmm, I probably would go ahead and hang a drip of amiodarone. I am still concerned with the neuro status. Folks in VT with that pressure typically (in my experience) just have horrid chest pain....not completely unresponsive.

Wow, great responses. Here's what happened:

While waiting for the insulin to arrive (turns out it was in a central part of the ED with new nurses scrambling to find it) we decided to shock the rhythm. Into sinus she goes.

So now she's had two amps of calcium chloride, two amps of bicarb. Glucose was low normal, so she was given glucose immediately, and then once the insulin arrived, we gave her another amp along with the 10u of regular.

We're now 3-4 minutes into things, she's now got the insulin and the complex reverts to rapid V tach. I shocked her again. Keep in mind we're trying to get an EKG, trying to track down an old one since we know she's got a cardiac history anyway, AND I've hung amiodarone since the 2nd shock put her into sinus again and I'm calling it refractory.

EKG gets printed -- looks like there is LVH, ischemia in the lateral leads, but half the ekg is v tach again... is it elevated ST or the V Tach? Tough to interpret the EKG given the change in rhythm, the lack of a previous one to compare, the chaos, and the general "what the hell are we missing".

By the time the shock panel has come back, I've shocked her FIVE times, each time she stays in sinus for about 30-45 seconds.

At minute 8, she still in normal sinus rhythm since the last shock, and her shock panel comes back. This is what we got:

K+ - 11.4
pH - 7.07
PCO2 - 52
PO2 - >200 (can't remember exactly, but she was on FiO2 100%)

A: Intubated with RSI, on FiO2
B: bs equal bilaterally
C: Now in narrow complex, pressure maintained at SBP 150

Therapies she has received:

two amps of calcium chloride
two amps of bicarb
two amps of glucose
10 units of insulin
150 amiodarone push


-----------------------------------

Get renal involved, call the MICU. Patient remains in ED for 20 minutes intubated but unresponsive (sedated with propofol and fentanyl now), vitals stable in narrow complex rhythm, albeit peak Ts. Still showing ST depresion in I and aVL and inverted Ts in V2-V6.

Repeat shock panel, K+ down to 7.2.

Patient went to MICU, emergent dialysis, turn of propofol....

And she comes out of it 100% intact.

Alert and oriented and comfortable on the vent 1/2 way through dialysis. Once dialysis finishes, she was successfully extubated, and is now in the general medical floor, headed home tomorrow to live independetly again. Her enzymes bumped, but we don't know if it was demand, or primary cardiac (cards had no interest in cathing).

One of my most interesting cases. A few points I thought of:


1. The idea about giving nebs through the ET tube would probably have been a good idea.

2. I am no longer 100% wed to the rule of 'don't shock V tach in hyperkalemia' because you can never be sure it is ONLY hyperkalemia.

3. Is this one of those cases where, for whatever reason, there really was NO WRONG ANSWER and the patient would have pulled through even if we hadn't shocked? What was the definitive therapy in this lady -- the shocks? Likely not, but maybe it helped. The amiodarone? Maybe. The calcium, etc? Probably, but who's to tell?
 
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dgmedic

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Thanks for the follow up....interesting case. I will have to post a case soon that was extremely odd!!! You all can play the role of on-line medical control to a medic between hospitals with a TRAIN-WRECK overdose.

-dg
 

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Great case bulgethewine....

I'm curious if others would have advocated shocking so many times in such a short period of time (5 shocks in 8 minutes). Even in full cardiac arrest, ACLS only suggests 1 defibrillation every 3 minutes.

I probably would have bolused Amio first, started a gtt, and rechecked the pressure... and at the first sign of deterioration, shocked. But I could just as easily see myself doing it the other way too. I just worry about iatrogenic myocardial damage from such frequent delivery of shocks with a good pressure, and no deterioration in BP or pulse.

If I had my money on it, I was going to say 50% chance hyperkalemia and 50% chance ICH (AMS, Severe HTN, ST changes with Arrhythmia). I would have liked to make a mad dash to the CT scanner, but nobody in their right mind would do that with an unstable wide complex tachycardia!

Excellent case!
 

Hard24Get

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I am no longer 100% wed to the rule of 'don't shock V tach in hyperkalemia' because you can never be sure it is ONLY hyperkalemia.

Yeah, I actually ended up asking my electrophysiology attending about this case and she felt that even in a known hyperk+, you should give hyperK+ treatment, but not hesitate to additionally shock these guys if hemodynamic or MS compromise.

I thought this article was interesting:

Regional hyperkalemia increases ventricular defibrillation energy requirements: role of electrical heterogeneity in defibrillation.

Sims JJ,
Miller AW,
Ujhelyi MR.
University of Georgia College of Pharmacy, Medical College of Georgia School of Medicine, and Augusta VA Medical Center, USA.
INTRODUCTION: Increased spatial electrical heterogeneity has been associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity. METHODS AND RESULTS: We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo in the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P < 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient. CONCLUSION: Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.
 

MasterintuBater

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I'd shock it. This is an unstable, wide complex tachycardia, unstable based on the pateint's ALOC. It may be hyper K but it's hard not to shock an unstable Vtach, even a pulsatile one.

Why not push amio first? You've got time. Shock her if her pressure bottoms out. I would lean that this is more stable than unstable, and that you can correct the underlying problem (i.e. K+) without shocking. I don't think the pt's ALOC necessarily put's her V-tach in the "unstable" category. I'd look more at the baseline hemodynamics.

I agree with the other poster...lots of Bicarb, lots of calcium (if she's alive you can fix her hypercalcemia later), and Amio.
 

BKN

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Why not push amio first? You've got time. Shock her if her pressure bottoms out. I would lean that this is more stable than unstable, and that you can correct the underlying problem (i.e. K+) without shocking. I don't think the pt's ALOC necessarily put's her V-tach in the "unstable" category. I'd look more at the baseline hemodynamics.

I agree with the other poster...lots of Bicarb, lots of calcium (if she's alive you can fix her hypercalcemia later), and Amio.

Master, I hate to argue with somebody who's 90% on my page, but here are my thoughts about amiodarone for this patient. The experience over the last 50 years with antiarrhythmics is that they are all poisons. . .sometimes useful poisons. It's always been a race between the rhythm benefits and cardiodepressant cost. Lidocaine, quinidine, dig, aprindine, norpace, encainide, flecanide, phenytoin . . . I can't even remember all the drugs that have come and gone in my lifetime. The only drug that was cardiotonic was bretyllium and that didn't work either. That's why today it's all about treating ischemia, AICDs and radioablation.

So at this point for V tach we have procainamide, amiodarone and electricity. I think procainamide is usually good, because before you get finished loading, you'll surely drop the pressure and then feel better about Senor Paddles. :D But in this case, as we have seen, electricity ain't gonna do it until you correct the underlying conditions.

Amio, like all the rest is a cardiodepressant. It may be a little safer and effective than the others, but the evidence isn't that strong. My gut feeling is that amiodarone will not fix the problem and may make the patient unstable. I could be wrong, since we're out in poorly charted territory, but I'll still go with Ca, Bicarb, Glucose, insulin and call the dialysis team. If they are going to be slow or the patient must be transfer, some kayexalate. If the pressure drops, amiodarone and electricity.

Cheers.
 

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Great case bulgethewine....

I'm curious if others would have advocated shocking so many times in such a short period of time (5 shocks in 8 minutes). Even in full cardiac arrest, ACLS only suggests 1 defibrillation every 3 minutes.

I probably would have bolused Amio first, started a gtt, and rechecked the pressure... and at the first sign of deterioration, shocked. But I could just as easily see myself doing it the other way too. I just worry about iatrogenic myocardial damage from such frequent delivery of shocks with a good pressure, and no deterioration in BP or pulse.

If I had my money on it, I was going to say 50% chance hyperkalemia and 50% chance ICH (AMS, Severe HTN, ST changes with Arrhythmia). I would have liked to make a mad dash to the CT scanner, but nobody in their right mind would do that with an unstable wide complex tachycardia!

Excellent case!


Yeah, if I was gonna do the case again, I would have resisted the temptation to shock so many times so quickly. But with the hyperK+ treatments having (seemingly) little effect, it was awful enticing -- especially since each time we shocked, she seemed to convert to narrow complex at least temporarily.

I should add, too, in full disclosure, that our "5" shocks was actually a round of stacked shocks (200-300-360) followed by two more 360s.
 

bulgethetwine

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Why not push amio first? You've got time. Shock her if her pressure bottoms out. I would lean that this is more stable than unstable, and that you can correct the underlying problem (i.e. K+) without shocking. I don't think the pt's ALOC necessarily put's her V-tach in the "unstable" category. I'd look more at the baseline hemodynamics.

I agree with the other poster...lots of Bicarb, lots of calcium (if she's alive you can fix her hypercalcemia later), and Amio.

Well, we gave amio fairly rapidly in the overall time line. But also, amio can take up to 15 minutes to work. And she was getting bicarb and calcium. Perhaps we could have given more of the same.

I hasten to add that even among all of us on this board we seem to have trouble deciding if this person is unstable/stable... I just can't help but come back to the fact that this lady basically became apneic as she was wheeled in, just prior to us intubating her. Pressure or not on the monitor, this was a lady who became apneic, and had wide complex tach to the rate of 200+. I just can't in good conscience call her anything but "unstable" regardless of what the damn pressure says, you know?
 

bulgethetwine

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Master, I hate to argue with somebody who's 90% on my page, but here are my thoughts about amiodarone for this patient. The experience over the last 50 years with antiarrhythmics is that they are all poisons. . .sometimes useful poisons. It's always been a race between the rhythm benefits and cardiodepressant cost. Lidocaine, quinidine, dig, aprindine, norpace, encainide, flecanide, phenytoin . . . I can't even remember all the drugs that have come and gone in my lifetime. The only drug that was cardiotonic was bretyllium and that didn't work either. That's why today it's all about treating ischemia, AICDs and radioablation.

So at this point for V tach we have procainamide, amiodarone and electricity. I think procainamide is usually good, because before you get finished loading, you'll surely drop the pressure and then feel better about Senor Paddles. :D But in this case, as we have seen, electricity ain't gonna do it until you correct the underlying conditions.

Amio, like all the rest is a cardiodepressant. It may be a little safer and effective than the others, but the evidence isn't that strong. My gut feeling is that amiodarone will not fix the problem and may make the patient unstable. I could be wrong, since we're out in poorly charted territory, but I'll still go with Ca, Bicarb, Glucose, insulin and call the dialysis team. If they are going to be slow or the patient must be transfer, some kayexalate. If the pressure drops, amiodarone and electricity.

Cheers.

BKN - and I ask this as a resident approaching an attending, not as an anonymous poster trying to defend what I did in this case -- should I consider the patient stable so long as the pressure is there on the monitor? I mean, in the context of obtundation, apnea, etc?

It isn't lost on me that the patient may have had the seemingly positive outcome that she did if I had just stopped short of shocking her, and let some more time lapse for the usual hyperK+ treatments to act.
 

BKN

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BKN - and I ask this as a resident approaching an attending, not as an anonymous poster trying to defend what I did in this case -- should I consider the patient stable so long as the pressure is there on the monitor? I mean, in the context of obtundation, apnea, etc?

It isn't lost on me that the patient may have had the seemingly positive outcome that she did if I had just stopped short of shocking her, and let some more time lapse for the usual hyperK+ treatments to act.

Never thought you were being defensive. These are good questions. You were well out beyond the protocols in judgement territory. And all I'm giving is the judgement of someone who practiced in an era in which we had to treat V tach far more often with possibly lesser tools. All I'm saying is that you treat obtundation and apnea with ventilation and airway protection, you treat hyperkalemia with drugs and dialysis and that you treat v tach with cardioversion. But in some situations (hyperkalemia, hypothermia, hypovolemia) you may need to treat the underlying problem before cardioversion works. And fairly often in a wide complex tachydardia with an acceptable pressure,antidysrhythmics make things worse because if they don't convert, they certainly will depress your myocardium.

Oh yes, and a lot of shocks may depress myocardium as well and give you at least temporary myocardial depression.

In short, everything we do in a crisis has both benefits and complications. You do the best you can. And by the way, congrats on saving this lady, you did good.

cheers.
 

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A then B. Electrical then pharm cardioversion with amiodarone. Hard to differentiate unstable VT or SVT with single lead, but given her status I'm with docB. Stabilize and transfer to MICU.
 
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