Brugada pattern and other sudden-death ECGs

What it is

Brugada syndrome is an inherited channelopathy, most often from loss-of-function variants in the cardiac sodium channel gene SCN5A, that causes polymorphic ventricular tachycardia and ventricular fibrillation in a structurally normal heart. It is more common in men, often presents in the third or fourth decade, and arrhythmias tend to occur at rest, during sleep or with fever. The ECG sign sits in the right precordial leads. The type 1 (coved) pattern is ST elevation of at least 2 mm (0.2 mV) at the J point in at least one of V1–V2, with a convex, down-sloping ST segment running into a negative T wave; it is the only pattern that is diagnostic, whether spontaneous or brought out by a sodium channel blocker challenge. The type 2 (saddleback) pattern has a high take-off with a trough and a positive or flat T wave; it is suggestive only. The pattern is dynamic: it comes and goes, and fever, some drugs and a vagal state unmask it. Recording V1–V2 one or two intercostal spaces higher (second or third space) raises the yield. Brugada is one of a short list of resting ECGs that can warn of sudden cardiac death in the young, and in an ECG station after syncope you should look for each of them: Brugada type 1, a long or very short QT, pre-excitation (WPW), left ventricular hypertrophy with deep narrow Q waves (hypertrophic cardiomyopathy), epsilon waves and right precordial T inversion (arrhythmogenic right ventricular cardiomyopathy), and high-grade AV block.

How to recognise it

• Type 1: ST elevation ≥2 mm (0.2 mV) at the J point in ≥1 right precordial lead (V1–V2, in the fourth, third or second intercostal space), coved, followed by an inverted T wave.
• Type 2: J-point elevation with a saddleback ST segment that dips and rises again, ending in a positive or flat T wave in V2.
• QRS is often slightly wide in V1–V2 with an rSR'-like look, but there is no broad slurred S wave in I and V6 as in true right bundle branch block.
• PR may be mildly prolonged (conduction slowing from the sodium channel defect); the QT is usually normal.
• The pattern fluctuates from day to day: one normal ECG does not exclude the diagnosis.
• Other sudden-death ECGs: QTc clearly prolonged or very short, a short PR with a delta wave, very high voltage with deep narrow Q waves or deep T inversion, epsilon waves after the QRS in V1–V3.

Why it happens

• Reduced inward sodium current in the right ventricular outflow tract epicardium leaves an unopposed outward potassium current (Ito) early in phase 1, creating a voltage gradient across the wall.
• That gradient shows as J-point and ST elevation in the leads that face the right ventricular outflow tract (V1–V2), and its heterogeneity allows phase 2 re-entry and polymorphic VT or VF.
• Fever, sodium channel blockers and high vagal tone further reduce the sodium current or increase Ito, which is why they unmask the pattern.

Step by step

1. Look at V1–V2 first in any ECG after syncope or a family sudden death — the Brugada sign lives only in the right precordial leads.
2. Measure J-point elevation in mm and describe the ST shape (coved or saddleback) and T wave — only coved with a negative T is type 1.
3. Check I and V6 for a broad S wave — its presence points to right bundle branch block rather than Brugada.
4. Ask about fever, drugs and electrolytes — temperature and sodium channel blockers can create the pattern for hours.
5. If suspicion stays, request high V1–V2 leads (second and third intercostal spaces) — the outflow tract may sit higher.
6. Then screen the rest of the tracing for QTc, delta waves, hypertrophy, epsilon waves and AV block — other inherited causes of sudden death.

Resting ECGs that can warn of sudden death

Differential and pitfalls

• Brugada phenocopies: hyperkalaemia, hypercalcaemia, fever, right ventricular ischaemia or infarction, pulmonary embolism, pericarditis, pectus excavatum and lead V1–V2 placed too high in a normal person.
• Incomplete right bundle branch block, athlete's early repolarisation and ARVC can resemble type 2; compare the T wave and look for a broad S in I and V6.
• Acute anterior STEMI may look coved in V1–V2 but extends to V3–V4 with reciprocal change and a clinical story of chest pain.
• Many drugs can unmask Brugada (class I antiarrhythmics, some psychotropic drugs, some anaesthetics); check before prescribing to a known patient.
• Pitfall: dismissing a coved pattern seen only during fever; record a follow-up ECG when afebrile and still refer.
• Pitfall: a normal resting ECG in a young person with exertional syncope does not exclude catecholaminergic polymorphic VT or a long QT that varies.

Next step

• Type 1 pattern with syncope, seizure-like episodes at night or a family history of sudden death: admit to a monitored bed and call cardiology now.
• Any patient with polymorphic VT or VF and a Brugada pattern follows the arrest algorithm; specialists decide on an implantable cardioverter-defibrillator.
• Asymptomatic or type 2 pattern: refer to electrophysiology for risk assessment and, if indicated, a supervised sodium channel blocker challenge.
• Treat fever early, correct potassium and calcium, and give the patient a list of drugs to avoid.
• Advise screening ECGs for first-degree relatives and genetic counselling.

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Elsewhere in DurgiPedia

• ECG basics: waves, intervals and leads
• How arrhythmias arise
• The ventricular action potential

Connections

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Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: Brugada Syndrome (StatPearls (NCBI Bookshelf), 2025).

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