The new protocol for the adult patient in undifferentiated shock puts a lot of tools in the hands of paramedics. To be clear, the approach changes if there is a clear etiology for the shock, but for the patient who is in shock without a clear reason why, there’s now a protocol to assist! Providers at the BLS level will initiate transport procedures while checking a blood glucose level. ALS providers will obtain vascular access and check an EKG to look for a cardiac cause of the shock, after which they will initiate a 20mL/kg crystalloid bolus. If this doesn’t resolve the shock, paramedics can either administer a repeat bolus or start a vasopressor agent – options include infusions of norepinephrine or dopamine, or push-doses of epinephrine. After choosing an agent, if crews want to switch to a different agent (or give an additional one), OLMC can be used for additional orders. OLMC also has the option of authorizing vasopressin administration as another option.
Check the attached pdf for specifics in dosing, but overall this is a great summary of what’s now available in the paramedic’s toolbox for shock. Protocol binder or www.nycremsco.org for more.
Dave
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POTD: Emergency Contraception
I wanted to touch on emergency contraception and the modalities available to emergency physicians. It’s been surprising to me that this request has not come up more often in residency. Remember, you want to initiate emergency contraception as soon as possible for higher efficacy.
What does “emergency contraception” mean?
Emergency contraception refers to the products that prevent pregnancy from occurring after an episode of unprotected intercourse or a failure of alternate forms of contraception.
Emergency contraception can be in the form of oral medications or IUDs.
Oral medications:
Technically, the FDA has only approved two forms of emergency contraception: oral levonorgestrel and oral ulipristal acetate.
Oral levonorgestrel – 1.5mg PO (one dose)
Must be initiated within 72 hours, maximum up to 5 days for moderate efficacy
Relative risk reduction (RRR) of pregnancy: 89% if initiated within 48h
Brand names: Plan B, Plan B One Step, My Way, Next Choice
Mechanism of action: progestin (aka synthetic progesterone)
prevents fertilization by inhibiting ovulation, and it thickens cervical mucus
Side effects: heavy/irregular vaginal bleeding, GI symptoms
Available OTC for ~$40 out of pocket, (or $10 with GoodRx)
Not recommended if patient’s BMI > 25
There is a long list of drug interactions
Oral ulipristal acetate – 30 mg (one dose)
Must be initiated within 5 days
May be more effective for overweight patients
Brand name: Ella
Mechanism of action: progestin
Delays or inhibits ovulation and prevents implantation by altering the endometrium
Recommended to discard breast milk x 24 hours after ingestion
Side effects: GI symptoms, headache
Available OTC for ~$50 out of pocket, (or $40 with GoodRx)
IUDs:
IUDs are the most effective forms of emergency contraception
They must be inserted within 5 days of unprotected intercourse
99+% RRR of pregnancy
No weight limit!
Traditionally, the copper IUD (e.g. ParaGard) was considered the gold standard.
However, recent literature shows that hormonal IUDs (e.g. Mirena, Liletta), are just as effective forms for emergency contraception. (See the NEJM study below.) Personally, I think this is a game changer.
Emergency contraceptive users have an incidence of ~10% of pregnancy within 1 year
Contraindicated in patients with PID or with active gonorrhea/chlamydia
Consider an OB/GYN consult if you think an IUD might be the best option for your patient.
Yuzpe Method:
Lastly, in lower-resource areas where access is a concern, you can consider the “Yuzpe” method, which is a combination estrogen/progesterone treatment.
100mcg ethinyl estradiol (aka synthetic estrogen) + 0.5 mg levonorgestrel Q12h for one day
RRR of pregnancy is ~75%
Recommended within 5 days
Should you find yourself in a pickle overseas, this Wikipedia article has information regarding EC availability by country. I thought it was interesting!
https://en.wikipedia.org/wiki/Emergency_contraceptive_availability_by_country
Resources:
https://www.nejm.org/doi/full/10.1056/NEJMoa2022141 https://www.mayoclinic.org/drugs-supplements/levonorgestrel-oral-route/before-using/drg-20074413
POTD: QTc Prolongation
POTD: QT Prolongation
Today’s POTD is thanks to Dr. Haines, who pointed out to me the weird values on the top left of our EKG’s. Namely, the QTcF vs. QTcB. Simply put, they’re just different ways of calculating the QTc.
Briefly about the QT interval.
What is it?
Time from the start of the Q wave to the end of the T wave. Represents time taken for ventricular depolarization and repolarization.
- QT interval shortens at faster heart rates
- QT interval lengthens at slower heart rates
- A quick way to estimate prolonged QT the QT should be less than half the preceding RR interval
Prolonged values are…
· > 440ms in men
· > 460ms in women
· QTc > 500 is associated with an increased risk of torsades de pointes
· QTc < 350 is short
Causes of QTc prolongation
- Medications – the list is EXHAUSTIVE. Common one’s we see.
o Antipsychotics – Haloperidol, droperidol, chlorpromazine, quetiapine, olanzapine
o Benadryl
o Zofran (ondansetron)
o Amiodarone
o Antidepressants
o Antbiotics – the -ofloxacin’s, Bactrim, macrolides (azithromycin)
o Antifungals
o Methadone
- Electrolytes – HypoK, HypoMg, Hypocalcemia
- Hypothermia
- Myocardial Ischemia
- Congenital Prolonged QT Syndrome
Torsades de Pointes (TdP) and QT prolongation
Torsades, a form of polymorphic ventricular tachycardia, is the complication that occurs with QT prolongation. The pathophysiology revolves around the delayed repolarization reflected in the QT prolongation, which can cause early after-depolarizations (can manifest as PVCs). If the PVC occurs concurrently with the T wave, known as “R on T” phenomenon, it can cause degeneration of the rhythm into TdP. Incidentally, this is also why we always use synchronized cardioversion on patients with a pulse rather than defibrillation, as shocking a patient on their T wave can also cause “R on T” phenomenon.
TdP is usually short and self-resolving, so mainstays of treatment involve prevention of recurrent TdP. With active TdP, shock. Otherwise, there are a few therapies for potentially preventing future TdP episodes.
Treatment:
- As for other ventricular tachyarrhythmias, synchronized cardioversion if unstable and defibrillation if pulseless (many times the defibrillator may not be able to sync anyways, so just shock)
- Magnesium 1-2g IV over 10-15 min, can be repeated, followed by an infusion
- Treat underlying cause – correct electrolytes, stop offending drugs, cardiac reperfusion therapy, etc.
- Lidocaine – for refractory TdP. Only non-QT prolonging agent compared with amiodarone and procainamide.
Prevention of TdP:
- Overdrive pacing – no great evidence. The idea is to increase the HR of the patient to shorten the QT interval. Transvenous is preferred. Target is typically ~100-110BPM
- Isoproterenol – also no great evidence, can use prior to pacing to medically increase the HR.
o 5mcg/min (0.1mcg/kg/min in children) target HR 100 or 30 above natural HR
o For both overdrive pacing and isoproterenol, may need to titrate HR to whatever will prevent the patient from going into TdP
Now, back to the original clinical question…
The QTc estimates the QT interval at a standard heart rate of 60 BPM. If the HR is 60 on your EKG, you can just use the QT =).
· Bazett formula: QTC = QT / √ RR
· Fridericia formula: QTC = QT / RR 1/3
· Note: The RR interval is given in seconds (RR interval = 60 / heart rate).
The Bazett formula is the most commonly used because of its simplicity. The Bazett formula overcorrects at HR > 100 and under corrects at HR < 60. If the HR is >100 or <60, the Fridericia formula should be used instead. No, I’m not savvy enough with math to explain why.
Some tips when calculating your own QTc
- Use the lead with the longest, easily measurable QT interval
- Where the maximum slope of the T wave intersects the isoelectric line determines the end of the QT interval
MDCalc has great calculators for calculating your own QTcs.
Random Questions
1) Does magnesium decrease the QTc?
A: No. Thought to stabilize the myocardium through an unknown mechanism.
2) What do I do with my asymptomatic patient’s with QTc > 500?
A: Admit them? Honestly, I have (although they were sent in by their cardiologist for elevated QT). Doesn’t appear to be a clear cut answer… likely hinges on multiple factors like ability to follow-up, comorbidities, number of QT prolonging medications, discussion with PCP, etc.
https://litfl.com/qt-interval-ecg-library/
https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdp/
https://first10em.com/torsades-de-pointes/