Serial ECGs are mandatory in SCA survivors for the diagnosis of acute myocardial ischemia/infarction, conduction abnormalities, and depolarization and repolarization abnormalities. Additional right- -sided, lateral and posterior leads may be helpful if acute myocardial ischemia/infarction is suspected from adjacent standard leads or elevated markers of myocardial damage. Continuous ECG telemetry (> 72 h) can identify recurrent myocardial ischemia and sustained or non-sustained arrhythmias, and should be routine during hospitalization.
Bradyarrhythmias account for about 1 in 5 of all SCA based on recordings from ambulatory ECGs. Myocarditis, infiltrative cardiomyopathies and neuromuscular disorders may be associated with significant conduction abnormalities. Paroxysmal atrio-ventricular block as a result of disease in the His-Purkinje system is characterized by an abrupt change from 1:1 conduction to complete heart block, which can lead to prolonged ventricular asystole or torsades de pointes. A preceding history of syncope is common and normal 1:1 conduction on resting ECG does not exclude this condition. Diagnosis requires clinical vigilance, continuous ECG telemetry and serial ECGs. A prolonged PR interval (> 210 ms) may also identify patients with Brugada syndrome with SCN5A mutation.
Areas of myocardial necrosis, scar or ischemia result in inhomogenous ventricular depolarization and present a substrate for reentrant ventricular arrhythmias. This may manifest as additional notching (R’ or S’) or fragmentation of the QRS complexes on surface ECG. Quantitatively defined fragmentation of the QRS complexes based on specific scoring algorithms is associated with increased mortality and arrhythmic events in patients with implantable defibrillators. Areas of slow conduction due to myocardial scarring can also be detected as late potentials at the terminal portion of the QRS on signal-averaged ECG (SAECG). The latter is a useful tool to assess for a potential latent myopathic process such as arrhythmogenic right ventricular cardiomyopathy (ARVC), sarcoidosis, or myocarditis. A filtered QRS duration longer than 114 ms is the most sensitive parameter on SAECG at predicting the risk of sudden cardiac death. Other parameters that are considered abnormal are low-amplitude signal duration ≥ 38 ms and a root mean square voltage of the terminal 40 ms of the QRS complex less than 20 µV at 40-Hz filter settings. These parameters in the SAECG have recently been included as minor criteria in the 2010 Task Force Criteria for the diagnosis of ARVC.
Sudden cardiac death related to abnormalities of ventricular repolarization (eg: long QT, Brugada and early repolarization syndromes) is well recognized. The T wave morphology and QT interval should be measured and adjusted for heart rate. Linear regression functions have been recommended for the adjustment of the QT interval for heart rate, but the Bazett formula (measured QT divided by the square root of the RR interval) remains widely used. The method of QT adjustment for heart rate should be specified. Transient repolarization changes and QT prolongation related to acute myocardial infarction, anoxic brain injury and induced hypothermia is common. Conversely, repolarization changes may be absent on the resting ECGs in patients with congenital repolarization abnormalities. In this regard, serial ECGs and provocation testing are helpful (see below).