CONTENTS

• Sodium channel blocker
• Brugada
  • Brugada Type I
    • Five mimics of Brugada I
  • Brugada Type II
  • Brugada syndrome vs. Brugada pattern

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sodium channel blocker (e.g. tricyclic)

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key features of sodium channel intoxication

• 🔑 Terminal right-axis deviation:
  • Terminal S-wave in Lead I.
  • Terminal tall R-wave in aVR (R>3 mm or R/S ratio >0.7).
  • RSR' in V1 can occur.
• 🔑 QT & QRS prolongation.
• 🔑 Brugada pattern can occur.

differential diagnosis

• Hyperkalemia 📖
  • Both may cause:
    • Brugada-like pseudoinfarction pattern. 📖
    • Marked QRS prolongation & QT prolongation.
    • Tall R-wave in aVR.
    • Peaked T-waves.
  • Sorting this out:
    • Preserved P-waves might suggest sodium channel blockade. (Hyperkalemia often causes flattening and disappearance of the P-waves).
    • Tall R-wave in aVR (R' >3 or R'>S) is more closely associated with sodium channel blockade (although it can happen in hyperkalemia).
    • ⚠️ It may be challenging to sort out based on ECG (clinical approach may include checking point-of-care potassium, reviewing medication list, or trialing hypertonic bicarbonate and/or calcium).
• Brugada syndrome. 📖
• RBBB: (Sorting out RBBB vs. Na-blocker is discussed here: 📖)
• RVH 📖 Both can cause an SI-SII-SIII pattern.
• Ventricular tachycardia: Tachycardia with wide QRS may mimic VT.

rhythm

• Sinus tachycardia:
  • This is commonly seen due to other effects of the intoxication, for example, anticholinergic effects (TCAs, diphenhydramine) or sympathomimetic effects (e.g., cocaine).
  • Tachycardia with prolonged QRS may mimic ventricular tachycardia.
• Sinus bradycardia:
  • May occur with some antiarrhythmics or beta-blockers.
  • May also reflect severe intoxication, due to a direct effect of sodium-channel inhibition.  This is usually a sign of severe sodium channel toxicity. (Berberian 2021)
• Ventricular tachycardia & VF may occur.

intervals

• PR prolongation & various AV blocks can occur
• QRS prolongation is a key feature. If the patient has a normal baseline QRS interval, the QRS measurement quantifies how severe the intoxication is:
  • QRS >100 ms suggests an elevated risk of seizures. (4022081)
    • ⚠️ QRS >100 ms that is new (or presumably new) is an indication for the administration of sodium bicarbonate.
    • >120 ms associated with a 33% risk of seizure
  • QRS >160 ms suggests an elevated risk (~50%) of ventricular tachycardia. (4022081)
  • RBBB is commonly seen (right bundle more susceptible), or this can mimic RBBB.
  • Sine wave patterns may eventually occur.
• QT prolongation may occur due to slow ventricular depolarization. However, torsade de pointes doesn't commonly occur (perhaps because patients are commonly tachycardic).

terminal right-axis deviation (RAD) with tall R-aVR

• One key to diagnosing sodium channel blockade is recognition of terminal rightward axis deviation. Electrophysiologically, this is caused by slow conduction through the myocardium, leading to delayed depolarization of the right ventricle (such that the last bit of the QRS complex points in a rightward direction). This creates the following pattern:
  • (1) Deep, terminal S-wave in Lead I (which may be broad or slurred).
  • (2) aVR to have a tall terminal R-wave (R>3 mm or R/S ratio >0.7).  This is associated with seizure and malignant arrhythmia. (7618783)
• The differential diagnosis of this pattern focuses on three entities: sodium channel blockade, hyperkalemia, or Brugada syndrome.
  • Hyperkalemia can generally be excluded rapidly based on other features of the ECG, or laboratory studies.
  • Brugada syndrome is discussed further below (but as a rule of thumb, a true Brugada Syndrome patient is extremely rare – so Brugada syndrome is a bit of a diagnosis of exclusion).

morphology

• Brugada pattern may occur in ~15% of patients.
• Incomplete RBBB can occur (RSR' in V1).
• Sine wave patterns may occur in extreme cases (due to prolongation of the QRS complex).

ECG is the test of choice for sodium channel blocker toxicity

• ECG is the most direct reflection of cardiac sodium channel blockade.
• ECG is the only test capable of suggesting sodium channel blockade in a patient with an unreliable or unobtainable history.
• If ECG abnormalities are suspected to be due to sodium channel blocker toxicity, two ampules (100 mEq total) of hypertonic bicarbonate should be given with a repeat ECG subsequently. Improvement in ECG findings following bicarbonate administration supports the presence of sodium channel blockade.
• In a patient who overdosed on a medication known to block sodium channels (e.g., TCA), the ECG should be repeated frequently to allow for early detection of sodium channel toxicity.

additional information on sodium channel blockers

• The chapter on sodium blocker poisoning: 📖
• List of medications that inhibit sodium channels: 📖

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Brugada type I

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key aspects of Type I Brugada

• 🔑 V1 and/or V2 with the following configuration:
  • STE ≧2 mm followed by a downward-sloping ST segment that is coved or straight.
  • ST segment dives downwards into a negative, symmetric T-wave (TWI).
  • After 40 ms, the decrease in amplitude is <0.4 mV (much less than in RBBB or athletes).
• 🔑 ST shifts can mimic anteroseptal MI:
  • STE in aVL.
  • STD in lateral precordial leads.
  • STD in the inferior leads.
  • (Discussion of sorting out Brugada vs. anteroseptal MI below.)
• 🔑 QT is generally normal (aside from the right precordial leads).
  • QT prolongation should suggest:
    • Brugada 2/2 to sodium channel blockade.
    • Hyperkalemia mimic of Brugada.
    • Brugada + 2nd process causing QT prolongation. 📖
• Other findings:
  • Early repolarization patterns may be observed in inferior leads.
  • May see fractionated QRS. (22920782)

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differential diagnosis: closest mimics of Brugada I 

[#1/5] Causes of RSR' in V1

• Consider this differential list for patients where RSR' in V1 is a predominant abnormality.
• Especially if R' is sharp, consider non-Brugada etiologies.
• Discussed further here: 📖

[#2/5] RBBB vs. Brugada I 

• Features favoring RBBB:
  • Broad S-wave in leads I and V6.
  • QRS is wide (>120 ms) throughout the ECG.
• Features favoring Brugada-I: The right precordial leads mimic an RBBB pattern, but the remainder of the ECG leads don't look like RBBB (e.g., V6 lacks a broad S-wave).

[#3/5] hyperkalemia vs. Brugada I 📖

• Key features suggesting hyperkalemia in this context:
• [1] Peaked T-waves.
• [2] QRS and QT prolongation to a greater extent than expected with Brugada I (e.g., unequivocal QRS and QT prolongation in limb leads).
• [3] P-waves flatten, PR increases, and eventually, P-waves disappear.

[#4/5] anteroseptal MI vs. Brugada I

• ⚠️ Sometimes, anteroseptal MI and Brugada-I can be nearly indistinguishable. If history, examination, and/or POCUS suggest an anteroseptal MI, then you should probably assume an acute MI until proven otherwise.
• Features that would might suggest anteroseptal MI:
  • STE extends out more laterally (e.g., beyond V3).
  • Frankly ischemia morphologies (e.g., terminal QRS distortion).
  • Loss of R-wave voltage in the right precordial leads.
  • Q-waves extending beyond V1.

[#5/5] Sodium channel blocker poisoning

• Sodium channel blocker poisoning may cause a Type I Brugada pattern. This may be accompanied by additional findings of sodium channel blocker intoxication. ⚡️

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Brugada type II

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key findings of Brugada II

• 🔑 V2 lead (V1 is variable):
  • Saddleback STE is usually ≧1-2 mm, followed by a taller, positive T-wave.
  • Terminal R' is rounded, wide, and relatively low voltage (unlike benign variant patterns).
  • Relatively broad beta-angle (>60 degrees). This causes the duration of the base triangle of r' at 5 mm from the high take-off to be >3.5 mm.  Other causes of a broad beta-angle include ARVC and hyperkalemia. (22920782)
• 🔑 QT is generally normal (may be prolonged in right precordial leads).
• Other potential findings:
  • Early repolarization patterns may be observed in inferior leads.
  • May see fractionated QRS.

differential diagnosis of Brugada-II 

• Anterior MI.
• Benign early repolarization.
• RBBB.
• Incomplete RBBB:
  • Terminal R' in incomplete RBBB is peaked, whereas in Brugada-II, the terminal R' wave is rounded, wide, and usually relatively low voltage.
  • In incomplete RBBB, the QRS duration in V1 equals V6.  Alternatively, in Brugada-II, the QRS is longer in V1 than V6.
• High lead placement (especially in young athletes). (Berberian 2021)
• (Further differential diagnosis: Approach to rSr' in V1 📖)

clinical significance of Brugada-II ECG?

• An ECG alone with Brugada type II is considered non-diagnostic (especially without clinical symptoms). This ECG is less strongly diagnostic of Brugada syndrome than a Brugada type I ECG.

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Brugada syndrome vs. Brugada pattern

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Brugada phenocopy = Brugada-pattern ECG pattern elicited by one of the following:

• Sodium channel-blocking medications (Patients with normal sodium channels may manifest with a Brugada pattern following an overdose of sodium channel-blocking medications; this pattern is seen in ~15% of patients with tricyclic intoxication.):
  • Tricyclics
  • IA antiarrhythmics
  • Cocaine
  • Tricyclics
  • Methadone
  • Antihistamines
  • Psychotropics
  • Tramadol
  • Complete list here: 📖
• Electrolyte abnormalities:
  • Hyperkalemia
  • Hypokalemia
• Fever, hypothermia
• Vagal stimulation.

Brugada syndrome

• Criteria:
  • (1) Brugada pattern on ECG, plus
  • (2) One of the following:
    • Survivor of cardiac arrest.
    • Polymorphic VT.
    • History of nonvagal syncope.
    • Familial antecedents of sudden death in patients <45 YO without coronary artery disease.
    • Type I pattern in relatives.
• Patients are often diagnosed in their 40s-50s.
• Patients are at risk for polymorphic VT. Treatment may include the placement of an ICD.

medical management of VT storm in a patient with Brugada syndrome

• Quinidine is the medical treatment of choice for Brugada syndrome (if available). Quinidine blocks the transient outward potassium current (I_to).
• Isoproterenol infusion may be helpful acutely for electrical storm (or, if unavailable, presumably another inotropic infusion could be substituted, such as epinephrine). (17556186) 

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questions & discussion

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