Sudden Cardiac Death - Brugada Syndrome | ECG Cases | EM Cases
Highlights
- ../../../Knowledge/Medicine/Brugada syndrome was described in 1992 in 8 previously healthy patients aged 2 to 53, who presented with syncope without prodrome, and then developed polymorphic ventricular tachycardia—which either self terminated or led to sudden cardiac death.
- The family history, febrile provocation and ECG findings have been linked to an inherited, temperature-sensitive, right ventricular sodium channelopathy. Sometimes the ECG pattern can be concealed and other times provoked—by fever, medications, or vagal stimulation—and provocative testing with sodium channel blockers can be used to confirm the diagnosis.
- V1-2 coved ST elevation and symmetric T wave inversion = Brugada pattern type 1 V1-2 saddle back ST elevation and upright T wave P wave fully inverted in V1 or biphasic in V1 = high lead placement Normal P wave with narrow base of triangle = normal variant Normal P wave with wide base of triangle = Brugada type 1 pattern
- Step 2. treat reversible causes of Brugada phenocopy If there is Brugada pattern on ECG, the next step to put it in clinical context: are there any reversible causes of Brugada phenocopy? These are clinical conditions that can mimic Brugada pattern but are reversible. These causes include metabolic conditions that alter condution (severe hyper/hypokalemia, hyponatremia, hypocalcemia, hypothyroid, or hypothermia), mechanical compression of the right ventricle (mediastinal mass, tension pneumothorax), V1-3 ischemia (anterior or RV infarct, pulmonary embolism), and myo/pericarditis. Brugada phenocopies can be suspected when there is a) Brugada pattern on ECG, but b) a secondary cause is found, and c) the pattern resolves with treatment, and d) the patient has a low pre-test of Brugada syndrome (i.e no history of syncope, seizure or nocturnal agonal breathing, and no family history of sudden cardiac death). This can be further confirmed by referral to electrophysiologist for provocative or genetic testing, both of which are negative in Brugada phenocopies.[4]
- ECG interpretation of Brugada pattern: type 1 (coved) is pathognomonic, but type 2 (saddle-back) requires checking lead placement (negative P in V1 or biphasic P in V2 are too high) and measuring the base of the triangle (>4mm measured 5mm from the apex of r’) Treat reversible causes of Brugada phenocopy (eg hyperkalemia, RV/anterior ischemia) Diagnosis, management and risk stratification of Brugada syndrome: treat fever and stop inciting meds/drugs; type 1 patients who are symptomatic (arrest, nonvagal syncope, seizure, agonal breathing) require ICD, and asymptomatic patients can be referred for provocative testing
Sudden Cardiac Death - Brugada Syndrome | ECG Cases | EM Cases
Highlights
- Brugada syndrome was described in 1992 in 8 previously healthy patients aged 2 to 53, who presented with syncope without prodrome, and then developed polymorphic ventricular tachycardia—which either self terminated or led to sudden cardiac death.
- The family history, febrile provocation and ECG findings have been linked to an inherited, temperature-sensitive, right ventricular sodium channelopathy. Sometimes the ECG pattern can be concealed and other times provoked—by fever, medications, or vagal stimulation—and provocative testing with sodium channel blockers can be used to confirm the diagnosis.
- V1-2 coved ST elevation and symmetric T wave inversion = Brugada pattern type 1 V1-2 saddle back ST elevation and upright T wave P wave fully inverted in V1 or biphasic in V1 = high lead placement Normal P wave with narrow base of triangle = normal variant Normal P wave with wide base of triangle = Brugada type 1 pattern
- Step 2. treat reversible causes of Brugada phenocopy If there is Brugada pattern on ECG, the next step to put it in clinical context: are there any reversible causes of Brugada phenocopy? These are clinical conditions that can mimic Brugada pattern but are reversible. These causes include metabolic conditions that alter condution (severe hyper/hypokalemia, hyponatremia, hypocalcemia, hypothyroid, or hypothermia), mechanical compression of the right ventricle (mediastinal mass, tension pneumothorax), V1-3 ischemia (anterior or RV infarct, pulmonary embolism), and myo/pericarditis. Brugada phenocopies can be suspected when there is a) Brugada pattern on ECG, but b) a secondary cause is found, and c) the pattern resolves with treatment, and d) the patient has a low pre-test of Brugada syndrome (i.e no history of syncope, seizure or nocturnal agonal breathing, and no family history of sudden cardiac death). This can be further confirmed by referral to electrophysiologist for provocative or genetic testing, both of which are negative in Brugada phenocopies.[4]
- ECG interpretation of Brugada pattern: type 1 (coved) is pathognomonic, but type 2 (saddle-back) requires checking lead placement (negative P in V1 or biphasic P in V2 are too high) and measuring the base of the triangle (>4mm measured 5mm from the apex of r’) Treat reversible causes of Brugada phenocopy (eg hyperkalemia, RV/anterior ischemia) Diagnosis, management and risk stratification of Brugada syndrome: treat fever and stop inciting meds/drugs; type 1 patients who are symptomatic (arrest, nonvagal syncope, seizure, agonal breathing) require ICD, and asymptomatic patients can be referred for provocative testing