Arrhythmias

Introduction

Arrhythmia is loss of cardiac rhythm, especially irregularity of heartbeat.

Pathophysiology: Supraventricular arrhythmias

Common supraventricular tachycardias 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 (eg, premature atrial complexes, sinus arrhythmia, 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

• 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 intraarterial reentry.

VENTRICULAR ARRHYTHMIAS: Premature Ventricular Complexes

Premature ventricular complexes (PVCs) can occur in patients with or without heart disease.

Ventricular Tachycardia

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).

Ventricular Proarrhythmia

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.

Ventricular Fibrillation

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).

CLINICAL PRESENTATION

• Supraventricular tachycardias 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, anginal 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 tachycardias, 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.

DIAGNOSIS

• 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.

TREATMENT

Goals of Treatment: 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 proarrhythmia as a significant side effect, and the advancing technology of nondrug therapies, such as ablation and the implantable cardioverter-defibrillator (ICD).

Typical Maintenance Doses of Oral Antiarrhythmic Drugs

Disopyramide 100–150 mg every 6 h 200–300 mg every 12 h

Quinidine 200–300 mg sulfate salts every 6 h 324–648 mg gluconate salts every 8–12 h

Maxiletine 200–300 mg every 8 h

Amiodarone 400 mg 2 or 3 times daily until 10 g total, then 200–400 mg daily

Dofetilide 500 mcg every 12 h

Sotalol 80–160 mg every 12 h

Intravenous Antiarrhythmic Dosing

Amiodarone in Pulseless VT/VF, Dose is 300 mg IV/IO push (can give additional 150 mg IV/ IO push if persistent VT/VF), followed by infusion of 1 mg/min for 6 h, then 0.5 mg/min

In stable VT (with a pulse), Dose is 150 mg IV over 10 min, followed by infusion of 1 mg/min for 6 h, then 0.5 mg/min

In AF (termination) 5 mg/kg IV over 30 min, followed by infusion of 1 mg/min for 6 h, then 0.5 mg/min

Diltiazem PSVT; AF (rate control) 0.25 mg/kg IV over 2 min (may repeat with 0.35 mg/kg IV over 2 min), followed by infusion of 5 to 15 mg/h

Ibutilide AF (termination) 1 mg IV over 10 min (may repeat if needed)

Procainamide AF (termination); stable VT (with a pulse) 15–18 mg/kg IV over 60 min, followed by infusion of 1–4 mg/min

Verapamil PSVT; AF (rate control) 2.5–5 mg IV over 2 min (may repeat up to maximum cumulative dose of 20 mg); can follow with infusion of 2.5–10 mg/h

Sotalola AF/AFl (SR maintenance) Ventricular arrhythmias 75–150 mg IV once or twice daily (infused over 5 hr