Introduction

The heart has specialized cells called conduction cells which generate an electrical impulse that alters the resting membrane of the myocardial tissue. This leads to myocardial contraction and the ejection of blood. As well as the conduction system, the myocardium also possesses other electrical properties that facilitate cardiac function. The myocardium has automaticity and excitability; this allows an electrical impulse to be self-generated and able to be depolarized if a stimulus is present. If an impulse reaches a sufficient threshold, the myocardium will depolarize and conduct this electrical impulse throughout the myocardium, which leads to myocardial contraction. Finally, in the all-or-none principle, which is specific to cardiac muscle, if an electrical impulse is sufficient, complete depolarization and full contraction of the myocardium occurs.

In the presence of a cardiac disease or disorder, and through the natural process of aging, there is an increased incidence of dysfunction of the conduction system. This dysfunction may be benign and not disrupt general heart function or it can have life-threatening consequences. The type of conduction dysfunction, its rate and occurrence or frequency determines the clinical significance of the arrhythmia. The bottom line for the clinician is how the arrhythmia affects myocardial perfusion and what happens to cardiac output. For example, in the presence of ischemic heart disease, a fast conducting rhythm, such as supraventricular tachycardia (SVT), rapid ventricular rate or atrial fibrillation, will decrease the diastolic filling time, which leads to a decline in myocardium perfusion and further ischemia, resulting in a vicious cycle. The same tachycardiac arrhythmias can lead to a decrease in cardiac output because of the decrease in filling time. In the presence of myocardial or pump dysfunction, the ventricles rely on volume to improve the contractile force, which is known as the Frank–Starling law. However, with the decrease in the filling time caused by a fast conduction rate, there is a decrease in the volume entering the ventricles leading to a loss of myocardial stretch. The end result is a decrease in contractility. Bradycardiac rhythms allow sufficient time for ventricular filling but the rate may be too slow to maintain the cardiac output needed to meet the metabolic demands of the body. The loss of cardiac output is associated with the following common clinical signs and symptoms: light-headedness, dizziness, visual disturbances, altered mentation, syncope and increased risk of falls. The frequency with which arrhythmia occurs can also disrupt perfusion and cardiac output, particularly in cardiac dysfunction.

Cardiac arrhythmias may be temporary or permanent, depending on the etiology. Transient arrhythmias may be caused by significant alterations in electrolytes. This may result from gastrointestinal distress because of nausea, vomiting and diarrhea, or from the use of medications, such as diuretics and potassium supplements. Transient arrhythmias may also be caused by myocardial hypersensitivity resulting from heart catheterization, open heart procedures, myocardial infarct or trauma. More permanent arrhythmias may be caused by ischemic disease that directly impairs the cells of the conduction system. This may lead to various conduction arrhythmias, such as heart blocks, atrial or ventricular bradycardia or tachycardia. Heart failure (HF) is commonly associated with atrial fibrillation and abnormal ventricular electrical conduction or ectopy. Aging may also lead to a significant loss of conduction cells, which may lead to such conduction dysfunction as sick sinus syndrome. Arrhythmias can be managed via technology, including pacemakers and defibrillators. They are discussed below.

Pacemakers