Pathophysiology of Cardiac Arrhythmias: Arrhythmogenesis and Types of Arrhythmias

Abstract

As a pumping organ with an intrinsic electrical system, the heart is unique. For most individuals, it remains efficient for decades. However, as a pump, it can fail. Often the failure is due to inherent or acquired problems with the electrical system. Failure of maintenance of normal sinus rhythm often results in adverse or no heart rhythm, a term referred to as “arrhythmias.” These can result in the heart rate being too fast (“tachy-”) or too slow (“brady-”) and alter blood flow resulting in patient morbidities and mortalities. Arrhythmias can occur anywhere in the heart and may not always be caused by any adverse lifestyle events such as coronary disease. Certain inherited congenital heart defects can cause abnormalities within the developing electrical system that can appear even before birth. Alternatively, the simple process of normal aging can adversely affect the heart’s ability to maintain normal rhythms. Once initiated, arrhythmias can be sustained by the normal anatomical variations of cardiac structures. There are three common arrhythmia etiologies: “automaticity” “reentry,” and “triggered.” Automaticity results from alterations of the basic cellular ion exchange mechanism which is depicted as a distinct electrical pattern, the action potential. Once an electrical impulse is initiated, it typically propagates cell to cell in a relatively uninterrupted fashion. However, if an obstruction (valves, veins) or postinfarction scar tissue occurs, the impulse can circle around the obstruction, creating a reentrant pathway. In rare instances, drugs or disease states can alter cell action potentials, triggering abnormal impulse initiation. This chapter will address all of these issues.