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.
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.
In left bundle branch block (LBBB), the ventricles are activated in a sequential manner with alterations in left ventricular mechanics, perfusion, and workload resulting in cardiac remodeling. Underlying molecular, cellular, and interstitial changes manifest clinically as changes in size, mass, geometry, and function of the heart. Cardiac remodeling is associated with progressive ventricular dysfunction, arrhythmias, and impaired prognosis. Clinical and diagnostic notions about LBBB have evolved from a simple electrocardiographic alteration to a critically important finding affecting diagnostic and clinical management of many patients. Advances in cardiac magnetic resonance imaging have significantly improved the assessment of patients with LBBB and provided additional insights into pathophysiological mechanisms of left ventricular remodeling. In this review, we will discuss the epidemiology, etiologies, and electrovectorcardiographic features of LBBB and propose a classification of the conduction disturbance.
The epsilon wave of the electrocardiogram (ECG) together with fragmented QRS (fQRS), the terminal conduction delay, incomplete right bundle branch block (IRBBB) and complete/advanced RBBB (CRBBB) of peripheral origin are part of a spectrum of ventricular depolarization abnormalities of arrhythmogenic cardiomyopathy ( AC). Although the epsilon wave is considered a major diagnostic criterion for AC since 2010 (AC Task Force Criteria), its diagnostic value is limited because it is a sign of the later stage of the disease. It would be more appropriate to say that the epsilon wave is a “hallmark” of AC, but is of low diagnostic sensitivity. Although the epsilon wave has high specificity for AC, it can be present in other pathological conditions. In this update we will cover the nomenclature, association with disease states and electrocardiographic aspects of the epsilon wave.
The patient is a 65-year-old white male with history of type 2 diabetes mellitus, hypertension, chronic smoking, and prior stroke with residual left hemiparesis and aphasia. His medication included losartan, furosemide, simvastatin, and metformin.He was admitted to the emergency room in cardiac arrest and was quickly resuscitated with cardiopulmonary resuscitation and external electric cardioversion maneuvers. Immediately after return of spontaneous circulation, a 12-lead ECG was performed (Figure 1).Based on the ECG, what is the most likely etiology of his cardiac arrest? Please turn the page to read the diagnosis.
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