Seizure and Tachycardia

This was written by one of our fantastic Emergency Medicine 3rd year residents, Emily Ferrari:

A young man presented with AMS and seizure like activity. EMS called by PD from a scene, where the patient had been seen ingesting powder and pills, then began acting more erratically. He was seizing on arrival to the ED, but this ceased after 5mg Versed given by medics. 

Once on the monitor, he had an odd appearing QRS complex, consistent with wide complex sinus tachycardia. We called for ECG, and while exposing the patient during our secondary survey - he notably had a large amount of white powder in a baggy but also free form around his genitalia...

His first ED ECG as below :

What do you think?

Sinus rhythm.  Now borderline tachycardic.  A very wide QRS (178ms), large R-wave in aVR, and Brugada morphology in V1-V2.  

This is typical Sodium channel blockade morphology.  One might appropriately be worried about hyperkalemai, but this ECG is so pathognomonic of Na channel blockade that one should immediately administer the antidote, which is Na-bicarbonate.

What specific drugs/medications do this?  

1. Tricyclic antidepressants.

2. Type 1 antidysrhythmics, especially flecainide.

3. Cocaine

With the reported ingestion of the white powder, and seizure, there was strong suspicion of cocaine toxicity in this patient (in other settings, we would need to be cognizant of possible TCA overdose). 

An IV was placed, and bloods were drawn, including a venous blood gas.

He was immediately given 2 "amps" of sodium bicarbonate (100 mL of 8.4% NaHCO3 = 100 mEq of Na and 100 mEq of HCO3), with the resulting ECG: 

The QRS is now 160 ms

The Brugada pattern persists

His initial venous blood gas returned with pH 6.96, pCO2 64, pO2 84, bicarb 14.

We continued with serial administration of 2 doses of bicarbonate, with the following ECGs showing narrowing of his QRS to 130 ms:

Another VBG returned with 7.21/47/67/18

And with more bicarbonate, the QRS normalized:

QRS is now 110 ms, upper limit of normal

The patient required intubation for airway protection and concern for concomitant respiratory acidosis and persistent stupor. A bicarbonate drip was ordered, but subsequently not used as his QRS remained normal. Later, his urine drug screen was positive for both cocaine and fentanyl, and he was discharged from the ICU three days later. 

Reminders about pathognomonic ECG patterns in Sodium Channel Blockade:

1. R-wave in aVR that is > 3mm or an R:S > 0.7 is highly suspicious for sodium channel blockade. 
2. In  TCA overdoses, QRS duration > 100ms is 100% sensitive for detecting patients that are high risk for seizure, though this is specifically noted in. 

Notably this patient also had a drug-induced Brugada pattern in V1 and V2. Dr. Smith has noted this phenomenon in a previous blog post. 

Follow up ECGs:

A few more Cases:

Cardiac arrest, severe acidosis, and a bizarre ECG

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***

Brugada pattern induced by tricyclic antidepressant

Pre-syncope and a bizarre wide complex

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MY Comment, by KEN GRAUER, MD (5/6/2025):

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Today's case by Dr. Smith is another "must know" for emergency providers — in that the history of seizures and the initial ECG (that I've reproduced in Figure-1) means that we need to immediately consider any toxicity producing Sodium-Channel Blockade (ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agent listed in the excellent reviews by Dr. Ed Burns from Life-In-The-Fast-Lane or by Josh Farkas in the Internet Book of Critical Care).

• As shown above by Dr. Smith — serial treatment with Sodium Bicarbonate typically produces rapid clinical improvement.

As a visual reminder — ECG #1 shows the characteristic signs of Sodium-Channel Blockade:

• Sinus Tachycardia.
• QRS prolongation to ≥0.10 second (It is especially the terminal portion of the QRS that is prolonged with sodium channel blockade). QRS morphology may look bizarre.
• QT prolongation (the result of slowed ventricular depolarization).
• Terminal RAD (Right Axis Deviation) — as is characteristically manifest by a terminal S wave in lead I (that may be wide) — and/or — a significant terminal R wave component to the QRS complex in lead aVR (that is uaully ≥3 mm in amplitude). These effects are thought to be due to slow conduction through the myocardium, leading to delayed depolarization of the RV (therefore the last vector of ventricular depolarization is directed to the right).
• Brugada Phenocopy.

NOTE: The ECG of a patient with sodium channel blockade may resemble that of hyperkalemia (bizarre, widened QRS, right axis, Brugada-1 ECG pattern). 

• Both of these entities may be present at the same time — such that both empiric IV Calcium and IV Bicarbonate may be tried until definitive diagnosis is made.

Figure-1: I've labeled the initial ECG in today's case. (To improve visualization — the original ECGs have been digitized using PMcardio).