Thanks to Dr. Lo Cascio for today’s Morning Report!
Case: 70 F BIBA with transcutaneous pacing pads on being paced at 80 bpm. Pt is unresponsive with SBP 170s. Pt is normothermic with FS 170. Pt has PMH of HTN, DM, ESRD (no missed dialysis). Pt took ibuprofen at home yesterday for aches and pains, less responsive today, and found bradycardic and hypotensive by EMS. EMS gave atropine with no improvement and they started transcutaneous pacing.
What do you do?
- As always ABC, IV/O2/monitor!
- Dialysis pt + unstable bradycardia (or really any arrhythmia) = calcium
- This is a time to give a calcium chloride push, not a slow calcium gluconate piggy back.
- You push 1 g calcium chloride with no result.
What next?
Differential diagnosis of sinus bradycardia:
Toxins – beta blocker, calcium channel blocker, digoxin
Electrolytes – potassium, calcium
Hypothermia
Endocrine – hypoglycemia, hypothyroid
What medications other than calcium could you give at this point?
If beta blocker toxicity is a possibility you can give 5 mg glucagon.
While you are pondering all of this you notice your patient has lost a pulse, you start CPR and get ROSC after 1 epi.
Maybe it’s time to consider an airway?
Probably a good idea to use a paralytic other than succinylcholine!
Your patient is now intubated, still being transcutaneously paced with SBP 90s. You have 2 choices to buy time while you figure out the underlying cause of the bradycardia and definitive treatment.
Option 1: pressors, dopamine (2-10 mcg/kg/min) or epi (2-10 mcg/min)
Option 2: transvenous pacer
You choose option #2 and place a transvenous pacer. I’m not going to go over how to do this today but you should know how to do it.
The pacer goes in beautifully, and the patient is stable for the moment.
Labs start to trickle back and the potassium is mildly elevated so you treat medically with insulin, D50 and albuterol.
What do EM docs love more than ABCs? Dispo! So you call cardiology for CCU admission and while you are waiting for them to come see the patient her nephrologist arrives. He happens to mention that she also has a history of hypothyroidism and he isn’t sure when her TFTs were checked last. You add on TFTs and admit the patient to the CCU. You run into the cardiology fellow a few days later who tells you the TSH came back through the roof and after her hypothyroidism was treated the patient returned to baseline and the pacer was removed.
Moral of the story…always remember the thyroid!
A few quick myxedema coma pearls:
- most often seen in elderly women with long standing disease with added stress of infection, systemic disease, medication and cold environment
- because of decreased metabolism medication overdoses can occur and precipitate myxedema crisis
- mental status, cardiac contractility, GI motility and renal function are all depressed
- high mortality rate! early recognition and treatment very important so maintain high index of suspicion and get help from endocrine
- T3 works faster than T4 but higher risk of complications
- send cortisol level and give stress dose steroids
For more reading (and asynchronous credit):
http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=195
Jay Khadpe MD
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