Despite considerable progress in management over the recent years, coronary artery disease (CAD) remains the leading cause of death in the industrialized world. It is estimated that CAD is responsible for causing 152,000 deaths per year in the United Kingdom. 400,000 deaths per year in the United State of America, and one in eight deaths worldwide. Many of these deaths are attributed to the development of cardiac arrhythmias, especially ventricular fibrillation during periods of myocardial ischemia or infarction. Myocardial ischemia is characterized by ionic and biochemical alterations, creating an unstable electrical substrate capable of initiating and sustaining arrhythmias, and infarction creates areas of electrical inactivity (1-3) and blocks conduction, which also promotes arrhythmogenesis.
Arrhythmias are dysfunctions which cause abnormalities (4-6) in impulse formation (automaticity), conduction (conductivity), or both in the myocardium. Most disturbance of cardiac rhythm arises when a small group of cardiac cells competes with or replaces the normal pacemaker. Any circumscribed region that acts in such a way is called an ectopic focus, meaning that it is not located in the usual pacemaker region, the sinoatrial node. The result can be abnormal ectopic beats and rhythms. The three basic mechanisms or causes responsible for ectopic beats (6-9) and rhythms (arrhythmias) are enhanced automaticity, reentry, and triggered activity.
The sinoatrial node shows the fastest rate of phase 4 depolarization and therefore, exhibits a higher rate of discharge than that occurring in other pacemaker cells exhibiting automaticity. The SA node normally sets the pace of contraction for the myocardium, and latent pacemakers (5-7,9,10) are depolarized by impulses coming from the SA node. So, if cardiac sites other than the SA node show enhanced automaticity, they may generate competing stimuli, and arrhythmias may arise.
Common causes of enhanced automaticity are an increase in chatecholamines, digitalis toxicity, hypoxia, potassium imbalance (5,10), and myocardial ischemia or infarction.
A common mechanism by which abnormal conduction causes arrhythmias is called reentry excitation, which occurs if a unidirectional block is caused by myocardial injury or prolonged refractory period. With normal conduction, the electrical impulse moves freely down the conduction system until it reaches recently excited tissue that is refractory to stimulation. This causes the impulse to be extinguished. The SA node then recovers and fires spontaneously, and the conduction process starts all over again. Reentry excitation means that an impulse continues to reenter an area of the heart rather than coming to an end. For this to occur, the impulse must encounter an obstacle in the normal conducting pathway. The obstacle is usually an area which allows conduction (5,7,9,10) in only one direction and causes a circular movement of the impulse. Re-entry is the most common cause of arrhythmias (5) and this can occur in any level of the cardiac conduction system.
Triggered activity is an abnormal conduction of latent pacemaker and myocardial cells in which the cells may depolarize more than once following stimulation by a single electrical impulse. The level of membrane action potential spontaneously and rhythmically increases after depolarization until it reaches threshold potential, causing the cells to depolarize.
This phenomenon, called after depolarization, can occur immediately following repolarization early, in phase 3 (early after depolarization), or late in phase 4 (delayed after depolarization).
Triggered activity can result in atrial or ventricular ectopic beats occurring singly, in groups of two (paired or coupled beats), or in bursts (7,10) of three or more beats (paroxysms of beats or tachycardia).
Common cause of triggered activity (10) include an increase of catecholamines, digitalis toxicity, hypoxia, and myocardial ischemia.
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