Catecholaminergic polymorphic ventricular tachycardia is a rare devastating lethal inherited disorder or sporadic cardiac ion channelopathy characterized by unexplained syncopal episodes, and/or sudden cardiac death (SCD), aborted SCD (ASCD), or sudden cardiac arrest (SCA) observed in children, adolescents, and young adults without structural heart disease, consequence of adrenergically mediated arrhythmias: exercise-induced, by acute emotional stress, atrial pacing, or β-stimulant infusion, even when the electrocardiogram is normal. The entity is difficult to diagnose in the emergency department, given the range of presentations; thus, a familiarity with and high index of suspicion for this pathology are crucial. Furthermore, recognition of the characteristic findings and knowledge of the management of symptomatic patients are necessary, given the risk of arrhythmia recurrence and SCA. In this review, we will discuss the concept, epidemiology, genetic background, genetic subtypes, clinical presentation, electrocardiographic features, diagnosis criteria, differential diagnosis, and management.

P-wave dispersion (PWD, Pd or Pdis) is a noninvasive electrocardiographic (ECG) marker for atrial remodeling and predictor for atrial fibrillation (AF). PWD is defined as the difference between the widest and the narrowest P-wave duration recorded from the 12 ECG leads. Increased P-wave duration and PWD reflect prolongation of intraatrial and interatrial conduction time with lack of a well-coordinated conduction system within the atrial muscles, with inhomogeneous, asynchronic, pro-inflammatory and anti-inflammatory effect mediated by interleukin-6 (IL-6) in patients with the CG + GG genotype IL-6 -634C/G polymorphism [1] and discontinuous propagation of sinus impulses mainly between the left and right atria, interstitial/extracellular fibroblast activation and collagen deposition with fibrosis (via TGF-β) in atrial tissue, insufficient blood supply, significant not isotropic myoelectric activity, and thin wall thickness and consequent expansion tendency all well-known electrophysiological characteristics in patients with atrial arrhythmias and especially paroxysmal atrial fibrillation (PAF) [2].

In the 12-lead electrocardiogram (ECG), the time from the onset of the QRS complex (Q or R wave) to the apex or peak of R or to R' (when present), using indirect or semidirect surface unipolar precordial leads, bipolar limb leads or unipolar limb leads, is called ventricular activation time (VAT), R wave peak time (RWPT), R-peak time or intrinsicoid deflection (ID). The R-peak time in a specific ECG lead is the interval from the earliest onset of the QRS complex, preferably determined from multiple simultaneously recorded leads, to the peak (maximum) of the R wave or R' if present. Irrespective of the relative height of the R and R' waves, the R-peak time is measured to the second peak. The parameter corresponds to the time of the electrical activation occurring from the endocardium to the epicardium as reflected by the recording electrode located at a variable distance on the body surface, depending on the lead type: a unipolar precordial lead, a bipolar or unipolar limb lead. In normal conditions, the R-peak time for the thinner-walled right ventricle is measured from lead V1 or V2 and its upper limit of normal is 35 ms. The R-peak time for the left ventricle (LV) is measured from leads V5 to V6 and 45 ms is considered the upper limit of normal. In this manuscript, we review the clinical applications of this parameter.

Brugada phenocopies (BrP) have emerged as new clinical entities that are etiologically distinct from true Brugada syndrome (BrS). BrP are characterized by an ECG pattern that is phenotypically identical to true BrS (type 1 or type 2); however, BrP are caused by various other factors such as mechanical mediastinal compression, myocardial ischemia, pericarditis, myocarditis, pulmonary embolism, and metabolic disturbances. We report a case of an electrocardiographic BrP in a patient with pectus excavatum deformity in the absence of true BrS using currently defined BrP diagnostic criteria. A systematic review of ECG manifestations associated with pectus excavatum is also discussed.

Electrocardiographic artifacts are defined as electrocardiographic alterations, not related to cardiac electrical activity. As a result of artifacts, the components of the electrocardiogram (ECG) such as the baseline and waves can be distorted. Motion artifacts are due to shaking with rhythmic movement. Examples of motion artifacts include tremors with no evident cause, Parkinson's disease, cerebellar or intention tremor, anxiety, hyperthyroidism, multiple sclerosis, and drugs such as amphetamines, xanthines, lithium, benzodiazepines, or shivering (due to hypothermia, fever (rigor due to shaking), cardiopulmonary resuscitation by chest compression (oscillations of great amplitude) and patients who move their limbs during the test, causing sudden irregularities in the ECG baseline that may resemble premature contractions or interfere with ECG wave shapes, or other supraventricular and ventricular arrhythmias. When the skeletal muscles experience shaking, the ECG is "bombarded" by apparently random electrical activity.