 cause of ventricular tachycardia, it is important to be able to differentiate these entities. The older the patient and the more significant the heart disease, the more likely is ventricular tachycardia. The Brugada group has also developed an algorithm to differentiate antidromic AVRT from ventricular tachycardia. The algorithm follows:
Brugada’s algorithm for differentiating ventricular tachycardia and antidromic AVRT
- If the QRS complex is net negative in V4–V6, ventricular tachycardia is more likely.
- If the QRS complex is net positive in V4–V6 and any of the leads V2–V6 display a qR complex, ventricular tachycardia is very likely.
- If there is AV dissociation, ventricular tachycardia is very likely.
- If there are no signs of ventricular tachycardia, antidromic AVRT should be strongly considered.
Management of ventricular tachycardia
Treatment in the emergency setting
Unconscious patients: start cardiopulmonary resuscitation.
Hemodynamically unstable patients (hypotension, angina, heart failure, shock, pre-syncope/syncope): the patient should be treated immediately with electrical cardioversion (during anesthesia). Ventricular tachycardia can be terminated already at 20–50 J biphasic shock. Beta-blockers are administered intravenously, unless the patient has bradycardia induced ventricular tachycardia. In that scenario, amiodarone is to be preferred after cardioversion (amiodarone 50 mg/ml, 6 ml with 14 ml glucose 50 mg/ml, i.v during 2 min). Hypokalemia and hypomagnesaemia should be corrected rapidly. Causes underlying the ventricular tachycardia must be targeted; heart failure, ischemia, hypotension, hypokalemia etc can all be treated rapidly. Thumpversion (hitting the patient’s chest with a fist) is no longer recommended although it might terminate the tachcyardia in some cases.
Hemodynamically stable patients may be treated pharmacologically (amiodarone, lidocaine, sotalol, procainamide). Only one of these drugs are administered and a loading dose is followed by infusion. Amiodarone is the primary choice with a loading dose of 150 mg i.v bolus given during 10 minutes. An infusion at 1 mg/min during 6 hours, followed by 0.5 mg/min during 18 hours is also started. The loading dose may be repeated with 15 minute intervals. Maximum dose amiodarone is 2.2 g/day. If amiodarone fails, one should consider electrical cardioversion before considering pharmacological alternatives. Lidocaine is given as iv bolus of 0.75 mg/kg which can be repeated after 5–10 minutes. Infusion lidocaine 1–4 mg/min (maximum dose 3 mg/kg/h) is started simultaneously.
Digoxin induced ventricular tachycardia may be treated as a hemodynamically stable patients above. Note that there are antibodies against digoxin.
Transcutaneous or transvenous pacing: Pacing at higher frequency than the ventricular tachycardia may terminate it (but there is a risk of degeneration into ventricular fibrillation).
Intermittent ventricular tachycardia with frequent capture beats should be treated pharmacologically.
Polymorphic ventricular tachycardia should be considered unstable and treated immediately with electrical cardioversion. Beta-blockers may be administered if the ECG does not show long QT interval. If the ECG does show long QT interval, the condition is classified as torsade de pointes; refer to this article for treatment recommendations. Amiodarone may also be administered if there is no evidence of long QT interval.
Bradycardia induced ventricular tachycardia (sinus bradycardia, AV-block etc): Bradycardia may induce premature ventricular complexes and ventricular arrhythmias. These are treated with atropine, isoproterenol (isoprenaline) or transvenous pacing.
Long-term treatment of ventricular tachycardia
Patients with preserved left ventricular function and asymptomatic non-sustained ventricular tachycardias may be adequately treated with beta-blockers. Sotalol (may cause QT prolongation) and amiodarone may also be considered. Verapamil is contraindicated. If the individual has suffered a myocardial infarction, an ICD should be considered.
Patients 