Development of Arrhythmias
Mechanisms by which arrhythmias can develop (Jaeger 2010):
Enhanced or suppressed automaticity. Automaticity is the ability of the heart muscle cells to generate an electrical impulse. All cells in the heart have this capacity, but only certain cells, such as those in SA node, are responsible for generating heartbeats. The SA node is the heart’s natural pacemaker and it determines when an impulse should be fired. Any impulses fired from elsewhere in the heart before or concurrently with SA node firing can lead to premature heartbeats or sustained abnormal heartbeats. This can cause sinus node dysfunction (SND), a term used to describe various types of heart rhythm disorders. Enhanced automaticity, on the other hand, can lead to tachycardia (>100 beats per minute) and several types of atrial and ventricular arrhythmia. Various factors, including electrolyte imbalances, medications, and age can alter automaticity in specific areas of the heart, thereby leading to arrhythmias.
Triggered activity. Triggered activity, the abnormal propagation of electrical activity in individual heart cells, can lead to sustained abnormal heart rhythms (Wit 2007). Arrhythmias due to triggered activity are rare; when they occur, they are often due to problems in the ion channels in the heart muscle cells. They can also occur as a side effect of certain anti-arrhythmic drugs such as digitalis.
Re-entry. Re-entry is a common mechanism for the initiation of tachyarrhythmia (a rapid irregular heartbeat) (Merriam-Webster 2012). This happens when the electrical impulse travels backwards from the ventricles to the atria, initiating another heartbeat while the first heartbeat is still descending into the ventricles.