Authors: Ava Littlewood-Snodgrass, PharmD (Pharmacy Resident, Geisinger Wyoming Valley) and Lloyd Tannenbaum, MD (EM Attending Physician, APD, Geisinger Wyoming Valley, PA) // Reviewer: Brit Long, MD (@long_brit)
Hello and welcome back to ECG Pointers, a series designed to make you more confident in your ECG interpretations. This week, we feature a post from Dr. Tannenbaum’s ECG Teaching Cases, a free ECG resource. Please check it out. Without further ado, let’s look at some ECGs!
“CODE BLUE ROOM 1529 CODE BLUE ROOM 1529!” you hear the hospital voice boom.
You are midconversation with one of your nurses when Shannon, your charge nurse, comes running to remind you, “Doc! It’s the weekend, we respond to floor codes on the weekend! And 1529 is the med/surg ward on the opposite side of the hospital, you better hustle. I’m sure someone from pharmacy, probably Scott, will be right behind you with the code bag. Hurry up, I’ll run with you. I know the only two spots you know how to get to in this hospital are the ED and the cafeteria”
“I feel so seen,” you think to yourself as you hustle upstairs and see chaos coming from room 1529. You quickly introduce yourself as the ED doc and take control of the code. The charge nurse catches you up.
“Doc, I’m Heather, the charge nurse from this floor. This patient was admitted for nausea, vomiting, and diarrhea. He had some electrolyte abnormalities in the ED, something about a really low potassium. There was a delay in getting some of his medications from central pharmacy and we haven’t started repleting his lytes yet. This was his ECG from the ED, take a quick look:”
Rate: about 60
Rhythm: normal sinus rhythm
Axis: Normal
Intervals: Normal PR, narrow QRS, Prolonged QTc! (probably around 550-600, which is way too long).
Morphology: If you look closely at V2, you can see u waves, likely due to his hypokalemia.
Final Read: Sinus rhythm with a very prolonged QTc, around 550-600 msec. There are also u waves present, suggestive of electrolyte abnormalites.
“Yeah, Heather, this ECG looks like the patient had some severe electroltye derrangements. What happened next?”
“Rigth, right. Then, all of a sudden, he started saying that he was going to pass out. He vomited twice and, per protocol, we gave him zofran. We were able to get this telemetry strip as he went unresponsive. He lost his pulse quickly and we’ve been doing ACLS ever since. Take a look at that ECG quick; next pulse check is in 90 seconds.”
Well. Another time where we get two ECGs for the price of one. Let’s take a look:
Rate: initially low 50s, then 280s or so.
Rhythm: initially sinus, then definitely not sinus.
Axis: Initially normal, then probably extreme left axis.
Intervals: Prolonged QTc, but not as terrible as the first ECG.
Morphology: Initially pretty good, then more consistent with a polymorphic ventricular tachycardia. There are PVCs present in the first portion of the ECG.
Final read: This tele strip shows the patient going into polymorphic VT. You can see the prolonged QTc before he jumps into it about halfway through the strip. Given his prolonged QTc before the polymorphic VT and his prolonged QTc on his first ECG, this is consistent with Torsades de Pointes.
Side note: My favorite part of this ECG is that you can see the “R on T Phenomenon” happen in real time. Take a look at this zoomed in portion:
The blue arrow is pointing out the “R on T Phenomenon.” This refers to something that can happen when a PVC occurs on top of the current beat’s T wave. So, think of it as the R wave of the PVC complex occurring at the same time as the T wave is finishing up. You have a heart that is trying to depolarize and repolarize at the same time. If you’re thinking to yourself, “This can’t be good,” you are correct. This can precipitate Torsades De Pointes, as seen above.
But what can cause Torsades? And how do we treat it? Scott? A little help from Pharmacy would be nice…
“Oh, hey Lloyd! Don’t mind me, I’ll just run up 6 flights of stairs with the code bag. Thanks so much for offering to help carry literally any of it. Anyway, as long as you don’t care that I’m panting and probably need oxygen, here’s a quick primer on how to fix Torsades.
Hypokalemia and hypomagnesemia are the predominant electrolyte abnormalities associated with Torsades. In patients with Torsades target repleted serum potassium and magnesium levels of 4.0 and 2.0, respectively. Magnesium decreases IKr and L-type Ca2+ activity leading to suppression of early afterdepolarizations (think of early afterdepolarizations as “pre-PVCs”) and automaticity. Just think, more Mag, less PVCs! Through this mechanism, magnesium supplementation is theoretically expected to cause rhythm termination though current data only supports its utility in preventing recurrence.
Magnesium’s suppression of early afterdepolarizations explains its efficacy in Torsades even for patients with normal serum magnesium concentrations (serum magnesium levels are poorly reflective of intracellular concentrations anyway). As the risk of magnesium toxicity is low with standard treatment doses, therapy should not be delayed for labs. In an unstable patient, 2 g of magnesium can be given IV push, or IVPB over 10 minutes in a more stable patient. It is important to note that while the AHA 2025 guidelines for adult advanced life support the use of magnesium in polymorphic ventricular tachycardia associated with a long QT interval, there is no proven benefit to magnesium administration in patients with normal QT interval.
If both magnesium and potassium are low, magnesium should be repleted first to help improve potassium retention. Maintaining adequate potassium levels is especially important when concerned for drug-induced torsades. Potassium can be repleted intravenously at 10 mEq/hr when administered peripherally or at 20 mEq/hr if the patient has a central line.
But what if you’re 100% sure the cardiac arrest is caused by hypokalemia? Can you run the potassium any quicker? Well in 2000, the AHA guidelines recommended a rapid potassium bolus for patients in arrest due to hypokalemia. They recommended 2 mEq/min for 10 mEq, which could be repeated, if necessary. Was this based on science? Unsure, since there were no references cited for this recommendation. In 2010 and 2020,those recs have disappeared and were replaced with a Class 3 (will cause harm) recommendation against bolusing potassium. However, the European Resuscitation Council Guidelines of 2021 recommend 20 mEq KCl over 2-3 min and then an additional 10 mEq over 2 min, again, only if you know the patient is arresting due to hypokalemia. Routine administration of potassium in an undifferentiated arrest is NOT recommended. In conclusion, the science is a little unclear.
Aside from unsynchronized cardioversion and electrolyte repletion, are there any medications that can be given for Torsades? Typically, no. Antiarrhythmic medications should be avoided in Torsades patients due to the risk of QT prolongation and pro-arrhythmic effects. β-blocker-induced bradycardia may also induce Torsades, so β-blockers should be avoided in the acute treatment phase as well. In rare cases, isoproterenol, a β-adrenergic agonist may be used (with expert consultation) as an alternative to temporary pacing for patients with pause-precipitated Torsades.”
“Scott, for someone so out of breath, that sure was a lot of science. That felt like at least 5 or 6 paragraphs… So, let me get this straight. To Dos are ACLS, shock him to get him out of unstable torsades, then blast him with magnesium and be gentle with potassium (maybe)? And don’t give anti-arrhythmics, since they’ll cause hemodynamic collapse and that’s just poor form?”
“Exactly. Remember, Torsades is usually short lived, so you’ll hopefully get him back and have some time to fix his electrolytes. But it can also degrade into ventricular fibrillation, so better get moving. Here’s 2 grams of Magnesium, you can just give it push since he’s coding, which counts as an unstable patient.”
“Thanks Scott… I probably could have guessed he was unstable.”
“I never like to leave anything to chance with you. Now stop asking me questions and run this code while I catch my breath.”
Case wrap up:
You work on the patient for 45 minutes. He get defibrillated multiple times, you push mag and even try running in potassium during the code. Unfortunately, despite your best efforts the patient never achieves ROSC.
Recap:
- A prolonged QTc can predispose patients to Torsades De Pointes via the R on T phenomenon.
- The R on T phenomenon occurs when the heart is trying to both repolarize and depolarize at the same time.
- “This is bad” – Scott
- The R on T phenomenon occurs when the heart is trying to both repolarize and depolarize at the same time.
- Low Potassium and Low Magnesium are often associated with TdP.
- If both K and Mg are low, prioritize magnesium replacement first, as you need magnesium to replete potassium.
- There aren’t many other medications you can give if your patient is coding from TdP due to electrolyte abnormalities.
- Most anti-arrhythmics are contraindicated as they will increase the QTc even more.
