Heart disease (8) Arrhythmias: Part 1
An arrhythmia is any abnormality in heart rate (HR) or rhythm. Some arrhythmias are benign, but others can cause sudden death. It is estimated that 5.3 per cent of people are managing an arrhythmia at any given time. Many arrhythmias remain undiagnosed.
Contraction of heart muscle is controlled by an electrical system. Specialised cells (pacemaker cells) in the myocardium trigger electrical activity, which travels across the atria into the ventricles, stimulating contraction and hence controlling the rate and rhythm of the heart. An arrhythmia is caused by a disturbance in the electrical conduction system. Panel 1 (p369) provides background information on cardiac contraction.
Arrhythmias can be described in terms of where they occur or their effect on heart rhythm. For example, the term “supraventricular arrhythmia” encompasses disturbances of rhythm arising above the AV node (atrial arrhythmias) and those arising at the AV junction or within the AV node itself and the term “ventricular arrhythmia” refers to disturbances in rhythm arising within the ventricles. Changes in HR may be referred to as “bradycardia” (slow rate) or “tachycardia” (fast rate).
Common symptoms of arrhythmia include dizziness or lightheadedness, palpitations, chest pain and fatigue. Some arrhythmias can result in loss of consciousness secondary to hypotension or compromise blood supply to the major organs because blood no longer circulates effectively. A small number of patients may be at risk of cardiac arrest. The best way to diagnose an arrhythmia is to use an electrocardiogram (ECG). The P wave indicates atrial depolarisation, the QRS complex indicates ventricular depolarisation and the T wave ventricular repolarisation (see Figure 1).
Management of arrhythmias
In many cases arrhythmias occur as a result of heart disease (eg, cardiomyopathies) and management may focus on addressing the underlying cause. Strategies to manage arrhythmias include drug therapy, electrical cardioversion (see Panel 2, p370) and the insertion of pacemaker or defibrillator devices. Anti-arrhythmic drugs work by modifying the electrical activity of the heart. The advent of successful procedures, such as radiofrequency (RF) ablation (see Panel 2), has decreased the role of drugs in managing arrhythmias. However use of RF ablation in the United Kingdom is limited because there are few specialists who can perform the procedure and there is a risk of several complications (eg, stroke). Cost is also an issue.
A wide variety of anti-arrhythmic drugs exists and they are commonly classified according to the Vaughan Williams system, which divides anti-arrhythmic drugs into groups according to their actions. Class I antiarrhythmics (eg, quinidine, disopyramide, flecainide) block the sodium channels. This group can be further subdivided (IA, IB, IC) according to their effect on repolarisation. Class II anti-arrhythmics (eg, propranolol, sotalol) primarily consist of the beta-blockers. These agents reduce the arrhythmogenic effects of circulating catecholamines, delay depolarisation and also close calcium channels by an indirect mechanism. Class III agents (eg, amiodarone, bretilium) block potassium channels and hence prolong the action potential, delaying repolarisation, while class IV (eg, verapamil, diltiazem) block calcium channels at the AV node, delaying conduction to the ventricles. A number of additional agents are not classified within the Vaughan Williams system (eg, adenosine, digoxin). Alternatively, anti-arrhythmics can be described as those used primarily for the management of supraventricular arrhythmias and those targeting ventricular arrhythmias (although there is some overlap between the two groups).
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Citation: The Pharmaceutical Journal URI: 10985910
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