Arrhythmia is loss of cardiac rhythm, especially irregularity of heartbeat.
Common supraventricular tachycardia requiring drug treatment are atrial fibrillation (AF), atrial flutter, and paroxysmal supraventricular tachycardia (PSVT). Other arrhythmias that usually do not require drug therapy are not discussed here (e.g., premature atrial complexes, sinus arrhythmia, and sinus tachycardia).
Atrial Fibrillation and Atrial Flutter
AF has extremely rapid (400–600 atrial beats/min) and disorganized atrial activation. There is loss of atrial contraction (atrial kick), and supraventricular impulses penetrate the atrioventricular (AV) conduction system to variable degrees, resulting in irregular ventricular activation and irregularly irregular pulse (120–180 beats/min).
Atrial flutter has rapid (270–330 atrial beats/min) but regular atrial activation. Ventricular response usually has a regular pattern and a pulse of 300 beats/min. This arrhythmia occurs less frequently than AF but has similar precipitating factors, consequences, and drug therapy.
The predominant mechanism of AF and atrial flutter is reentry, which is usually associated with organic heart disease that causes atrial distention (e.g., ischemia or infarction, hypertensive heart disease, and valvular disorders). Additional associated disorders include acute pulmonary embolus and chronic lung disease, resulting in pulmonary hypertension and states of high adrenergic tone such as thyrotoxicosis, alcohol withdrawal, sepsis, and excessive physical exertion.Paroxysmal Supraventricular Tachycardia Caused by Reentry
PSVT arising by reentrant mechanisms includes arrhythmias caused by AV nodal reentry, AV reentry incorporating an anomalous AV pathway, sinoatrial (SA) nodal reentry, and intraatrial reentry.
Premature Ventricular Complexes
Premature ventricular complexes (PVCs) can occur in patients with or without heart disease.
Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It is a wide QRS tachycardia that may result acutely from severe electrolyte abnormalities (hypokalemia or hypomagnesemia), hypoxia, drug toxicity (e.g., digoxin), or (most commonly) during an acute myocardial infarction (MI) or ischemia complicated by heart failure (HF). The chronic recurrent form is almost always associated with organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm).
Sustained VT is that which requires intervention to restore a stable rhythm or persists a relatively long time (usually above 30 s). Nonsustained VT self-terminates after a brief duration (usually below 30 s). Incessant VT refers to VT occurring more frequently than sinus rhythm, so that VT becomes the dominant rhythm. Monomorphic VT has a consistent QRS configuration, whereas polymorphic VT has varying QRS complexes. Torsade de pointes (TdP) is a polymorphic VT in which the QRS complexes appear to undulate around a central axis.
Proarrhythmia refers to the development of a significant new arrhythmia, such as VT, ventricular fibrillation (VF), or TdP, or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. 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 class Ia and class III IKr blockers.
VF is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Sudden cardiac death occurs most commonly in patients with coronary artery disease and those with LV dysfunction. VF associated with acute MI may be classified as either (1) primary (an uncomplicated MI not associated with HF) or (2) secondary or complicated (an MI complicated by HF).
Sinus bradyarrhythmias (heart rate below 60 beats/min) are common, especially in young, athletically active individuals, and are usually asymptomatic and do not require intervention. 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 tachycardia such as AF. Alternating bradyarrhythmias and tachyarrhythmia are referred to as the tachy–brady syndrome.
AV block or conduction delay may occur in any area of the AV conduction system. AV block may be found in patients without underlying heart disease (e.g., trained athletes) or during sleep when vagal tone is high. It may be transient when the underlying etiology is reversible (e.g., myocarditis, myocardial ischemia, after cardiovascular surgery, or during drug therapy). β-Blockers, digoxin, or nondihydropyridine calcium antagonists may cause AV block, primarily in the AV nodal area. Class I antiarrhythmic may exacerbate conduction delays below the level of the AV node. AV block may be irreversible if the cause is acute MI, rare degenerative diseases, primary myocardial disease, or congenital heart disease.
Supraventricular tachycardia may cause clinical manifestations ranging from no symptoms to minor palpitations or irregular pulse to severe and even life-threatening symptoms. Patients may experience dizziness or acute syncopal episodes, symptoms of HF, angina chest pain, or, more often, a choking or pressure sensation during the tachycardia episode.
AF or atrial flutter may be manifested by the entire range of symptoms associated with other supraventricular tachycardia, but syncope is uncommon. Arterial embolization from atrial stasis and poorly adherent mural thrombi may result in embolic stroke.
PVCs often cause no symptoms or only mild palpitations. The presentation of VT may vary from totally asymptomatic to pulseless hemodynamic collapse. Consequences of proarrhythmia range from no symptoms to worsening of symptoms to sudden death. VF results in hemodynamic collapse, syncope, and cardiac arrest.
Patients with bradyarrhythmias experience symptoms associated with hypotension, such as dizziness, syncope, fatigue, and confusion. If LV dysfunction exists, patients may experience worsening HF symptoms.
• Electrocardiogram (ECG) is the cornerstone of diagnosis for cardiac rhythm disturbances.
• Cardiac auscultation can reveal the irregularly irregular pulse characteristic of AF.
• 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.
• Based on ECG findings, AV block is usually categorized as first-, second-, or third-degree AV block.
The desired outcome depends on the underlying arrhythmia. For example, the goals of treating AF or atrial flutter are restoring sinus rhythm, preventing thromboembolic complications, and preventing further recurrences. Use of antiarrhythmic drugs has declined because major trials showed increased mortality with use in several situations, the realization of pro-arrhythmia as a significant side effect, and the advancing technology of nondrug therapies, such as ablation and the implantable cardioverter-defibrillator (ICD).Reference