1. Unstable patients or those in cardiac arrest should be treated with synchronized cardioversion. Ventricular tachycardia can be converted with energies as low as
1 J, and over 90 percent can be converted with less than 10 J. Rarely is more than 100 J needed. Current advanced cardiac life support (ACLS) guidelines recommend that pulseless ventricular tachycardia be defibrillated (unsynchronized cardioversion) with 200 J.
2. Clinically stable patients should be treated with intravenous antiarrhythmics.
a. Lidocaine 75 mg (1.0 to 1.5 mg/kg) IV over 60 to 90 s, followed by a constant infusion at 1 to 4 mg/min (10 to 40 pg/kg per minute). A repeat bolus dose of 50 mg lidocaine may be required during the first 20 min to avoid a subtherapeutic dip in serum level due to the early distribution phase.
b. Bretylium 500 mg (5 to 10 mg/kg) IV over 10 min, followed by a constant infusion at 1 to 2 mg/min.
c. Procainamide at a rate of less than 50 mg/min IV until the dysrhythmia converts, the total dose reaches 15 to 17 mg/kg in normals (12 mg/kg in patients with congestive heart failure), or early signs of toxicity develop with hypotension or QRS prolongation. The loading dose should be followed by a maintenance infusion of 2.8 mg/kg per hour in normal subjects (1.4 mg/kg per hour in patients with renal insufficiency).
d. A variety of other antiarrhythmics have been studied for the treatment of ventricular tachycardia. Most class I and III agents are effective for the acute termination of ventricular tachycardia when given intravenously. Recommendations concerning their routine use will have to await further studies.
VENTRICULAR FIBRILLATION Ventricular fibrillation is the totally disorganized depolarization and contraction of small areas of ventricular myocardium—there is no effective ventricular pumping activity. The ECG of ventricular fibrillation shows a fine to coarse zigzag pattern without discernible P waves or QRS complexes ( Fig.
A pulse or blood pressure never accompanies ventricular fibrillation. In patients who are awake and responsive, the ECG pattern of ventricular fibrillation is caused by a loose lead artifact or electrical interference.
Clinical Significance Ventricular fibrillation is most commonly seen in patients with severe ischemic heart disease, with or without an acute MI. Primary ventricular fibrillation occurs suddenly, without preceding hemodynamic deterioration, while secondary ventricular fibrillation occurs after a prolonged period of left ventricular failure and/or circulatory shock. Ventricular fibrillation may also occur from digoxin toxicity, quinidine toxicity, hypothermia, blunt chest trauma, severe electrolyte abnormality, or myocardial irritation caused by an intracardiac catheter or pacemaker electrode.
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