Arrhythmias : Definition, Pathophysiology, Diagnosis, and Treatment
Arrhythmia is defined as loss of cardiac rhythm, especially irregularity of heartbeat. This chapter covers the group of conditions caused by an abnormality in the rate, regularity, or sequence of cardiac activation.
Pathopyshiology of Arrhytmia :
Common supraventricular tachycardias requiring drug treatment are atrial fibrillation or atrial flutter, paroxysmal supraventricular tachycardia, and automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy (e.g., premature atrial complexes, wandering atrial pacemaker, sinus arrhythmia, sinus tachycardia).
Atrial Fibrillation and Atrial Flutter
Atrial fibrillation is characterized as an extremely rapid (400 to 600 atrial beats/min) and disorganized atrial activation. There is a loss of atrial contraction (atrial kick), and supraventricular impulses penetrate the atrioventricular (AV) conduction system in variable degrees, resulting in irregular ventricular activation and irregularly irregular pulse (120 to 180 beats/min).
Atrial flutter is characterized by rapid (270 to 330 atrial beats/min) but regular atrial activation. The ventricular response usually has a regular pattern and a pulse of 300 beats/min. This arrhythmia occurs less frequently than atrial fibrillation but has similar precipitating factors, consequences, and drug therapy.
Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI); other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm).
Torsades de Pointes
TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type Ia and type III IKr blockers. Quinidine-induced TdP or quinidine syncope occurs in 4% to 8% of patients treated with this agent.
Asymptomatic sinus bradyarrhythmias (heart rate less than 60 beats/min) are common especially in young, athletically active individuals. However, some patients have sinus node dysfunction (sick sinus syndrome) because of underlying organic heart disease and the normal aging process, which attenuates SA nodal function. Sinus node dysfunction is usually representative of diffuse conduction disease, which may be accompanied by AV block and by paroxysmal tachycardias such as atrial fibrillation. Alternating bradyarrhythmias and tachyarrhythmias are referred to as the tachy-brady syndrome.
Clinical Presentation of Arrhthymias :
Supraventricular tachycardias may cause a variety of clinical manifestations ranging from no symptoms to minor palpitations and/or irregular pulse to severe and even life-threatening symptoms. Patients may experience dizziness or acute syncopal episodes; symptoms of heart failure; anginal chest pain; or, more often, a choking or pressure sensation during the tachycardia episode.
Atrial fibrillation or flutter may be manifested by the entire range of symptoms associated with other supraventricular tachycardias, but syncope is not a common presenting symptom. An additional complication of atrial fibrillation is arterial embolization resulting from atrial stasis and poorly adherent mural thrombi, which accounts for the most devastating complication: embolic stroke. Patients with atrial fibrillation and concurrent mitral stenosis or severe systolic heart failure are at particularly high risk for cerebral embolism.
Patients with bradyarrhythmias experience symptoms associated with hypotension such as dizziness, syncope, fatigue, and confusion. If LV dysfunction exists, symptoms of congestive heart failure may be exacerbated.
Diagnosis of Arrhytmias :
The surface electrocardiogram (ECG) is the cornerstone of diagnosis for cardiac rhythm disturbances.
Less sophisticated methods are often the initial tools for detecting qualitative and quantitative alterations of heartbeat. For example, direct auscultation can reveal the irregularly irregular pulse that is characteristic of atrial fibrillation.
Proarrhythmia can be difficult to diagnose because of the variable nature of underlying arrhythmias.
TdP is characterized by long QT intervals or prominent U waves on the surface ECG.
Specific maneuvers may be required to delineate the etiology of syncope associated with bradyarrhythmias. Diagnosis of carotid sinus hypersensitivity can be confirmed by performing carotid sinus massage with ECG and blood pressure monitoring. Vasovagal syncope can be diagnosed using the upright body-tilt test.
Treatment of Arrhytmias :
The use of antiarrhythmic drugs in the United States is declining because of major trials that showed increased mortality with their use in several clinical situations, the realization of proarrhythmia as a significant side effect, and the advancing technology of nondrug therapies such as ablation and the internal cardioverter-defibrillator.
Drugs may have antiarrhythmic activity by directly altering conduction in several ways. Drugs may depress the automatic properties of abnormal pacemaker cells by decreasing the slope of phase 4 depolarization and/or by elevating threshold potential. Drugs may alter the conduction characteristics of the pathways of a reentrant loop.