you are the medical control doc...

[joeDO2]

The recent discussion on pressors got me thinking about a medical control case that I think might spark some interesting discussion.

Case: crew finds 70 yof complaining of severe dizziness and lethargy. hx of mild dementia and "heart problems." caretaker states pt was recently placed on 2 new "heart pills." one pill bottle is metoprolol, the other cannot be found.

Diagnostics:
Vitals: BP 70/p; P36; R26; Sp02 96%
Glucometry: 386
ECG: atrial flutter at 36, no acute st changes, normal cardiac axis

Initial treatment:
Oxygen by cannula
IV access attempt x3 with no success

Medical control is contacted for advice regarding further management. The options considered by the crew prior to consultation are:
1. Monitor patient and transport to hospital (looking at 20 min to hospital door)
2. Obtain IO access and manage with glucagon & Ca++
3. Obtain IO access and manage with pressor
4. Initiate transcutaneous pacing

What would you advise? Following some discussion I will post decision as well as the patient's hospital course.

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[Arcan57]

EM:RAP had a good discussion recently of management of this entity. The optimal therapy isn't available on the back of a rig, so I think moving through 2-4 in order would be reasonable if the prior step wasn't working.

 

[southerndoc]

IO access, initial management with glucagon. Not really a calcium candidate since he's on a beta blocker, not a calcium-channel blocker.

If that fails, then sedate and pace.

 

[Arcan57]

IO access, initial management with glucagon. Not really a calcium candidate since he's on a beta blocker, not a calcium-channel blocker.

If that fails, then sedate and pace.

It's a trick. The hyperglycemia w/o hx of DM in the setting of hypotension and bradycardia points to a Ca-channel blocker as the unnamed 2nd HTN med. Treatment in hospital will be similar, but B-blocker ODs trend towards hypoglycemia.

Of course in the real world, he's just as likely to be hyperglycemic and hypotensive from sepsis with a little over-aggressive beta-blockade as a full bore Ca-channel overdose. If the sugar is truly only from the Ca-channel blocker then he's in a world of hurt. Just stumbled across a paper that postulated degree of hyperglycemia was a better marker for Ca-channel blockerOD severity (some composite of end-point of death, temporary pacemaker implantation, and one other outcome I don't remember) than hemodynamic instability.

 

[Daiphon]

It's a trick. The hyperglycemia w/o hx of DM in the setting of hypotension and bradycardia points to a Ca-channel blocker as the unnamed 2nd HTN med. Treatment in hospital will be similar, but B-blocker ODs trend towards hypoglycemia.

Of course in the real world, he's just as likely to be hyperglycemic and hypotensive from sepsis with a little over-aggressive beta-blockade as a full bore Ca-channel overdose. If the sugar is truly only from the Ca-channel blocker then he's in a world of hurt. Just stumbled across a paper that postulated degree of hyperglycemia was a better marker for Ca-channel blockerOD severity (some composite of end-point of death, temporary pacemaker implantation, and one other outcome I don't remember) than hemodynamic instability.

Well said; I would agree with the CCB concept. The other concern I have is the underlying AFib with slow ventricular response --> ?digoxin. In which case, CaCl2 is "contraindicated" (although the concept of "stone heart" is flawed, imho).

Generally speaking, though, in the EMS realm, I'm a fan of Scoop-and-Run; yes, they can start pressors & do all sorts of amazing things in the field, but unless they're in Podunk, USA, there ought to be a hospital close by and the time spent trying to get these things going is time wasted that the patient could've been in the ED.

For this patient, follow ABCs, consider atropine for symptomatic bradycardia, and get the heck to your friendly neighborhood ED.

Just my $0.02,
-d

***edit***
Also, atropine is nebulizable, so the lack of access isn't that much of an issue; get them into the ED ASAFP. d=)

 

[joeDO2]

It's a trick. The hyperglycemia w/o hx of DM in the setting of hypotension and bradycardia points to a Ca-channel blocker as the unnamed 2nd HTN med. Treatment in hospital will be similar, but B-blocker ODs trend towards hypoglycemia.

Of course in the real world, he's just as likely to be hyperglycemic and hypotensive from sepsis with a little over-aggressive beta-blockade as a full bore Ca-channel overdose. If the sugar is truly only from the Ca-channel blocker then he's in a world of hurt. Just stumbled across a paper that postulated degree of hyperglycemia was a better marker for Ca-channel blockerOD severity (some composite of end-point of death, temporary pacemaker implantation, and one other outcome I don't remember) than hemodynamic instability.

good catch. this is why the Ca++ was considered as a treatment option at this point. caretaker saw the patient on a daily basis and denied any history of DM.

 

[ohiovolffemtp]

IO - especially the drills don't hurt much.
Atropine 0.5 mg - expect it to take ~ 1-2 min longer to take effect due to the route.
If no improvement in 5-8 min or pt's mental status worsens, pace.

Net, should see some change in ~10 min. Do the IO in the back of the unit prior to leaving the scene, rest in route. Interventions done by EMS will get to the patient faster than those done after arrival at the hospital.

 

[Groove]

These cases are kind of frustrating because there really is no clear answer and it's attempting to move clinical management into a field setting which is difficult. Sure, if you've got a decompensating patient and need advice, you need advice, but the overarching goal here should be to push the pedal to the metal and get the pt into the closest ED as quickly as possible.

That being said....

ABC's and it sounds like you need access. You've tried 3 times, put an IO in already. In fact, put one in the other leg. Hang 2 bags of NS. Hopefully pads are on in case you need to pace. Atropine if pressure doesn't respond, but by the time you push one liter in and are trying to re-assess his BP, you should be at the hospital. I don't care whether you give glucagon or not, not gonna make a difference in the truck and glucagon is a little pre-mature when we haven't even given him fluids yet to see if he responds. I would not push Calcium unless you run into a code situation and are in the ACLS pathway where it might be required.

 

[WilcoWorld]

This patient, while very ill, still has a pulse and a very broad differential diagnosis (multiple toxidromes, inferior MI, sepsis, DKA (caretakers can be wrong)). Sure, go for an IO and start some fluids, but get 'em to the hospital before you get too fancy.

If you lose a pulse en route, then it's time to take your best guess - mine would be to pace - but for now I want to take the time to get some more data.

 

[Hamhock]

Advice: Stop wasting time asking for advice.

You are only 20 minutes to the hospital! You could be here already.

As has been said before:

IO --> IVF +/- atropine -- and get here asap.

These cases kill me when EMS arrives 45 minutes after their arrival on scene.

HH

 

[Tiger26]

Advice: Stop wasting time asking for advice.

You are only 20 minutes to the hospital! You could be here already.

As has been said before:

IO --> IVF +/- atropine -- and get here asap.

These cases kill me when EMS arrives 45 minutes after their arrival on scene.

HH

Worse yet when they arrive with "we tried to RSI 'em but couldn't secure the airway" after 6-8 tries--in all honesty, EMS just shouldn't be putting ET tubes in with an ED close by . . . .

 

[Rendar5]

Worse yet when they arrive with "we tried to RSI 'em but couldn't secure the airway" after 6-8 tries--in all honesty, EMS just shouldn't be putting ET tubes in with an ED close by . . . .

depends on the situation and the protocols, imo. The only paramedics who are allowed to RSI without permission in my county are at the highest level of training with extremely good success rates and have ambulances equipped with end-tidal monitoring. There are some other crews, in my county that I completely 100% agree with you on.

 

[southerndoc]

good catch. this is why the Ca++ was considered as a treatment option at this point. caretaker saw the patient on a daily basis and denied any history of DM.

I guess I was thinking of the rule that you shouldn't combine a beta blocker with a calcium-channel blocker (central CCB). Tunnel vision I guess. Who would've thought a PMD would actually adhere to that.

 

[Rendar5]

I'm in agreement with most of the above. I'll just summarize my thoughts, which are not unique by any means.

Here is the problem with EMS treatment:

1. If it's a CCB overdose, the doses of antidote are MUCH higher than standard doses. EMS is going to be used to giving: 5mg Glucagon minimum enough to make the patient extremely pukey, and 3-6 boluses of Calcium Gluconate Chloride, By the time that's all in, the EMS should be at the hospital anyway. And do you really want a bradycardic, hypotensive, lethargic patient with an unknown cause to start puking all over the bus and into his airway? Now I would consider starting therapy with those 2 only if this was a witnessed and confirmed CCB overdose.

2. As has been said, the differential is huge and an unknown heart pill can cause at least 5 of them, and the stress from any of them can take a non-diabetic patient into hyperglycemia, although typically only 2 of them do it. The short list for the hypotensive, bradycardic pt (nontraumatic) is:
a. Digoxin OD
b. CCB OD
c. Beta-blocker OD
d. Clonidine OD
e. Hyperkalemia
f. Inferior wall MI

For all those reasons, EMS is not in a position to start empiric treatment of a questionable CCB OD. What they are in a position to do is to transmit the EKG, establish an IO, try a dose of atropine, which may or may not help, get some fluid in the guy assuming his lungs are clear, get pacers on him, and if they want, try a dose of dopamine or calcium as a pressor, and do all this while driving to the hospital. Diagnosis and definitive treatment are best left to an ED, which can get the appropriate lab values and has access to more resources and information.

 

[thorg12]

What about high dose insulin? Or lipid emulsion? Has anyone done these

 

[joeDO2]

Ok guys, great conversation. So here's what happend... as some of you pointed out already, moving this patient was 1st priority. we deferred contacting medical control and extricated the patient asap with pacer pads in place. by the time the patient had been stair chaired out, they were now complaining of SOB and had rales on auscultation. we began pacing with immediate improvement in symptoms. the tricky part here was access for proper sedation. again, IO was considered however medical control was contacted at this point (during transport) and ordered 4mg versed was administered via nasal atomizer along with 100mcg fentanyl. the patient reported mild improvement in pain level.

now.... the patient arrives in your ED. how would you proceed from here? the patient is being paced at 70bpm with good electrical and mechanical capture although she does complain of continued discomfort from the pads. i'd like to see what you all think at this point because what actually occurred was somewhat surprising to me.

 

[deleted109597]

If pt unstable/unable to tolerate pacing? RSI, float pacer wires through introducer. Levo if I need to maintain pressure until then.
Hyperinsulinemia/Euglycemia would be my choice. You're going to use an enormous dose though, 1unit/kg bolus and then 0.5unit/kg/hr.
Glucagon would be an option if able to get it quicker than insulin/d5, but the doses are high as noted before.
If this were actual poisoning (big dose for suicide attempt) I would consider lipid emulsions. However, this is not what is happening in this case so I would save it for last.

 

[Rendar5]

Repeat ekg to look for stemi, Abg to determine Stat K level, dig level and try to track down identity of the unknown med. If the first two are normal, I would turn off pacer to assess therapeutic response to glucagon and to calcium bolus per heart rate. Each cause of the differential above has a completely separate treatment.

 

[Lawsonc]

I'm enjoying reading this. As a field provider I wanted to put my input in.

Most rigs I've worked on don't carry enough glucagon to really make a difference, so I think that option is out.

I would consider Atropine, but most likely go with IO and then pacing. From there ABCs.

There has been some talk about wasting time contacting, but every call requires contact anyways (hospital report) so I do not see this as an issue. You guys want to know whats coming, and you may recommend something on the way over.

Thanks for the read.

 

[deleted109597]

If the first two are normal, I would turn off pacer to assess therapeutic response to glucagon and to calcium bolus per heart rate.

Unfortunately, neither glucagon nor calcium have much effect in the overdose, be it on purpose or accidental. Sure, give it, but I wouldn't turn off the pacer to see how well it worked. I've lost capture by turning off and back on before. That really sucks.

 

[Rendar5]

Unfortunately, neither glucagon nor calcium have much effect in the overdose, be it on purpose or accidental. Sure, give it, but I wouldn't turn off the pacer to see how well it worked. I've lost capture by turning off and back on before. That really sucks.

ah, I wasn't considering this possibility much. thanks for the voice of experience.

 

[joeDO2]

so to conclude this case, on arrival at the ED, the staff removed the pacer immediately upon arrival. patient developed increased SOB and audible rales with a rate drop back into the high 30's. IV was placed (ultrasound guidance) ED staff administered 5mg glucagon along with Ca++. it was discovered that the patient was recently placed on both the beta blocker as well as diltiazem by her PCP which caused the bradycardic aflutter. due to memory problems she had taken multiple doses of the diltiazem, hence the clinical finding of hyperglycemia as someone already mentioned.

so this brings me to my final question.... do you have procedures in place for when ems brings a patient in that is being actively paced? do you ever remove the pacer to "take a look at the rhythm" or "see how the patient does without it"? when you do decide to continue pacing do you have any particular tricks of the trade when switching to the hospital pacer ie using the hospital pacer at a higher setting to overdrive the existing pacer? my experience with EDs has usually been that the staff takes the ems pacer off and then decides whether to continue with their own which seems risky.

 

[Apollyon]

so to conclude this case, on arrival at the ED, the staff removed the pacer immediately upon arrival. patient developed increased SOB and audible rales with a rate drop back into the high 30's. IV was placed (ultrasound guidance) ED staff administered 5mg glucagon along with Ca++.

And then what? You didn't conclude the case. Did the patient expire? Go to the ICU? CCU? Need more pacing? Improve?

 

[southerndoc]

We turn the EMS pacer off and switch monitors (our pads/wires are compatible). We determine a baseline rhythm.

 

[joeDO2]

And then what? You didn't conclude the case. Did the patient expire? Go to the ICU? CCU? Need more pacing? Improve?

followup info for ems is usually limited to ed treatment and dispo so all i know is that she was diagnosed with ca channel blocker od and admitted to icu. further treatment approach involved high dose insulin / dextrose and the patient did improve.

@southerndoc- do you ever run into the situation where you stop and can't get capture again?

 

[ohiovolffemtp]

One option is to pause the EMS applied pacer w/o removing pads. On Lifepacks (& I believe Zoll's) you can do this to quickly look at the underlying rhythm. That way, if the patient deteriorates, you can quickly begin to pace again. Keep that going while you apply the hospital's pads, etc.