Drugs that further prolong repolarization—quinidine, disopyramide, procainamide, phenothiazines, and tricyclic antidepressants—exacerbate this dysrhythmia. Conventional treatment with lidocaine often is ineffective. To date, treatment for TdP consisted of accelerating the heart rate (thereby shortening ventricular repolarization) with isoproterenol (2 to 8 pg/min) while making arrangements for a ventricular pacemaker to overdrive the heart at rates of 90 to 120. Temporary pacing is the most effective and safest method to treat TdP and prevent its recurrence in the emergency setting. Recent reports have revealed that magnesium sulfate 1 to 2 g IV over 60 to 90 s followed by an infusion of 1 to 2 g/h is effective in abolishing these runs of TdP, although recurrences are seen despite continued infusion. A wide variety of other agents and antiarrhythmics have reported anecdotal success, but overall efficacy has been inconsistent.
Clinical Significance Ventricular tachycardia is very rare in patients without underlying heart disease. The most common causes of ventricular tachycardia are ischemic heart disease and acute MI. Less common causes include hypertrophic cardiomyopathy, mitral valve prolapse, and toxicity from many drugs (digoxin, quinidine, procainamide, and sympathomimetics). Hypoxia, alkalosis, and electrolyte abnormalities exacerbate the tendency toward ventricular ectopy and tachycardia.
It is a common misconception that patients with ventricular tachycardia appear clinically unstable; this is the basis for the mistaken assumption that patients who appear stable with a wide complex tachycardia have SVT with aberrancy rather than ventricular tachycardia. This is definitely wrong. Ventricular tachycardia cannot be differentiated from SVT with aberrancy on the basis of clinical symptoms, blood pressure, or heart rate. Patients who are unstable should be cardioverted; this is effective for both dysrhythmias. In patients who are stable, a 12-lead ECG should be obtained first and examined for evidence favoring one dysrhythmia over another; but even then, it is often difficult to decide. Therefore, in general, it is best to treat all wide complex tachycardias as ventricular tachycardia with lidocaine or procainamide. These drugs are obviously effective in ventricular tachycardia and often surprisingly effective in SVT with aberrancy, and they carry little risk of harming the patient. Conversely, verapamil is harmful in most patients with ventricular tachycardia, accelerating the heart rate and the decreasing blood pressure without converting the rhythm. Adenosine appears to do little harm in patients with ventricular tachycardia and has potential merit for the treatment for wide QRS complex tachycardias. However, until further experience is gained with this agent, it cannot be recommended for routine use in this setting.
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