ECG Topic - Brugada Be Kidding Me

Last updated 6/6/25

Introduction

Brugada syndrome is a deadly channelopathy marked by characteristic ECG findings in V1–V3 plus clinical criteria. It’s a cause of sudden cardiac death in young, otherwise healthy patients and recognizing this pattern can be life-saving.

Pathophysiology

About 20–30% of Brugada cases are due to mutations in the SCN5A gene, which encodes the cardiac sodium channel (Nav1.5). These mutations impair the inward Na⁺ current (INa) during depolarization.

• Mutation in SCN5A → ↓ inward Na⁺ current during phase 0
• Leads to phase 2 reentry and polymorphic VT/VF

The majority (~70–80%) of Brugada patients do not have identifiable SCN5A mutations, and other ionic currents and genes have been implicated. These mutations shift the balance of ionic currents in epicardial RV outflow tract (RVOT) cells, promoting phase 2 reentry → VT/VF.

ECG Criteria for Brugada Syndrome

Type I Brugada pattern

Along with clinical criteria, type I Brugada is potentially diagnostic.

• Coved ST elevation >2 mm in ≥1 of V1–V3
• Followed by a negative T wave
• Usually no reciprocal ST depression
• QRS duration usually <120 ms (not a true RBBB)

Type II and III Brugada Pattern

• Type 2 Brugada ECG pattern is not diagnostic, but may serve as a screening marker to identify patients who could benefit from further testing if clinical suspicion is high.
• Type 3 is no longer a recognized diagnostic category in the classification or management of Brugada syndrome.

Type	ST Morphology	T Wave	ST Elevation
II	Saddleback (rSr′)	Upright	> 2mm
III	Coved or saddleback	Variable	<2 mm

ECG Technique Pearl

Repeating the ECG by moving V1 and V2 leads from the 4th intercostal space to the 2nd or 3rd ICS significantly increases the sensitivity for detecting Type 1 Brugada pattern, especially in patients with intermittent or concealed disease. This approach is recommended by major cardiology societies and can unmask Brugada in up to 40% of cases with initially normal ECGs. It's standard practice when Brugada is suspected but not evident on standard leads—particularly in cases of syncope or positive family history.

Clinical Criteria

• Documented VF or polymorphic VT
• Family history of sudden cardiac death <45 y/o
• Type I ECG in family members
• Syncope
• Nocturnal agonal respirations
• VT/VF inducible with programmed electrical stimulation

Triggers That Unmask or Exacerbate Brugada Syndrome

Brugada Syndrome is a dynamic electrophysiologic disorder — the ECG pattern may be absent at baseline and only unmasked under specific physiologic or pharmacologic conditions. Recognizing and managing these triggers is important.

Clinical Pearl

Even in asymptomatic patients, fever should be treated aggressively in Brugada pattern. Expert guidelines from the ACC, AHA, and HRS recommend early antipyretic therapy to reduce arrhythmic risk. Fever decreases sodium channel availability and is a documented trigger for ventricular fibrillation, particularly in children and patients with SCN5A mutations. This recommendation is based off observational studies and case series (no prospective studies).

Brugada vs Mimics

Brugada Cases

ECG 1

Clinical Context: syncope

ECG 2

Clinical Context: syncope

ECG 3

Clinical Context: 21 year old with type I DM presents with SOB after running out of insulin for a week. FS > 500.

ECG 4

Clinical Context: 30 year old presenting with 106F and delirium. (Source 🔗)

ECG 5

Clinical Context: 70-something with fever of 38.0, and was diagnosed with influenza (Source 🔗)

ECG 6

Clinical Context: An elderly woman presents with altered mental status; she was found by her family lying on her bed in her apartment on a hot summer day found to have a 107.9F rectal temp. (Source 🔗)

ECG 7

Clinical Contect: “An elderly man had a post-operative ECG following left lower lobectomy for lung cancer. A pre-operative ECG was normal. He had no chest discomfort or other cardiac symptoms. He was on a continuous epidural infusion of bupivacaine. Echocardiogram showed normal ventricular wall motion and serial CK-MB enzyme tests were normal.” (Source 🔗)

Management

Key Points

• Brugada Syndrome is dynamic — ECG findings may be intermittent and require repeat testing, especially during fever or pharmacologic challenge.
• Type I Brugada pattern (coved ST elevation + T wave inversion in V1–V3) is diagnostic only when paired with clinical criteria (e.g., syncope, VF, family history).
• Moving V1 and V2 to the 2nd or 3rd intercostal space increases diagnostic yield and is recommended in all patients with suspected Brugada but nondiagnostic ECGs.
• Fever is potentially an arrhythmic trigger — aggressively treat febrile Brugada patients even if asymptomatic, particularly in pediatric and SCN5A-positive individuals.
• Common mimics include STEMI, early repolarization, WPW, hyperkalemia, incomplete RBBB, and ARVC.
• ICD placement remains the definitive therapy for symptomatic Brugada or patients with documented ventricular arrhythmias; asymptomatic patients require individualized EP risk stratification.