24

Ventricular Tachyarrhythmias
Roger D. White, M.D.

It is often not appreciated that ventricular tachy-
cardia (VT) can be accompanied by hemodynamic
stability. Therapeutic urgency is therefore based on
the patient’s hemodynamic response and not simply
on the tachycardia’s ventricular origin.
In monomorphic ventricular tachycardia (MVT),
the QRS complexes are wide and of uniform mor-
phology. Intermittent P waves unrelated to the QRS
complexes (AV dissociation) and fusion/capture com-
plexes are strong indicators of ventricular origin
(Fig. 24–1). Other helpful evidence is a QRS width
greater than 140 msec and QRS concordance across
the precordium on a 12-lead ECG. Although these
ECG findings should be searched for, they may not
be evident. Clinical clues provide strong evidence
that the tachycardia is ventricular in origin. A his-
tory of previous myocardial infarction or coronary
artery disease with angina is strongly indicative of
a ventricular origin of the tachycardia. Any wide–
QRS complex tachycardia should be considered ven-
tricular in origin until shown to be otherwise, and
therapy should be directed with this consideration
in mind.
In hemodynamically stable patients, cardiover-
sion is the intervention of choice. Drug therapy can
also be used in these patients. Lidocaine, procain-
amide, and amiodarone are all therapeutic options.
Polymorphic ventricular tachycardia (PVT) is
characterized by irregular, wide QRS complexes
that vary in amplitude and twist about the isoelec-
tric baseline (Fig. 24–2). PVT can occur in various
settings; therapy is as described for MVT.
Torsades de pointes is a form of PVT. In addition
to the QRS morphologic features, there is lengthen-
ing of the QT interval (prolonged repolarization)
before and after the episodes of tachycardia. Correc-
tion of the underlying cause is essential for ultimate
control of the arrhythmia. Magnesium should be
considered the first drug of choice in the treatment
of torsades de pointes, given as magnesium sulfate
1 to 2 g over 1 to 2 minutes. If this is not effective,
then overdrive pacing can be used. Traditional anti-
arrhythmic therapy is not likely to be successful in
controlling torsades de pointes. Class IA antiar-
rhythmic drugs, such as procainamide, disopyr-
amide, and quinidine, can be the cause of torsades

Figure 24–1. Wide-complex tachycardia at a rate of 210 beats/min. A fusion/capture QRS complex is present (second complex from
the right), preceded by a P wave. Such complexes are evidence of AV dissociation and strongly support a diagnosis of VT.

Figure 24–2. Onset of PVT in a patient with acute myocardial infarction. The characteristic twisting of the QRS complexes around
the baseline is evident. PVT is identified as torsades de pointes when the QT interval is prolonged from congenital or acquired causes.

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56 ▫ Anesthesiology Review
Figure 24–3. VT in the presence of hyperkalemia. The QRS complexes show a sine wave pattern.
de pointes as well as other prolonged repolariza-
tion.
VT accompanying acute hyperkalemia is often
characterized by a sine wave QRS pattern (Fig.
24–3). Clinical suspicion or documentation of hyper-
kalemia can lead to prompt therapy with sodium
bicarbonate, calcium chloride, and glucose and insu-
lin. Such therapy can include IV sodium bicarbon-
ate 1 to 2 mEq/kg, calcium chloride 1 g, and glucose
1 g/kg with regular insulin 0.3 U/g glucose, the
latter given over 1 hour.
In the absence of evidence to support a diagnosis
of VT, the assumption is that the tachycardia is
ventricular in origin. Cardioversion is always a
therapeutic option, especially in unstable patients.
Suggested References
Akhtar M. Clinical spectrum of ventricular tachycardia. Circula-
tion 1990;82:1561–1573.
American Heart Association in collaboration with International
Liaison Committee on Resuscitation. Guidelines 2000 for Car-
diopulmonary Resuscitation and Emergency Cardiovascular
Care. Circulation 2000; 102 (suppl I):1.
Miller JM. The many manifestations of ventricular tachycardia.
J Cardiovasc Electrophysiol 1992;3:88–107.
Napolitano C, Priori SG, Schwartz PJ. Torsade de pointes: Mech-
anisms and management. Drugs 1994;47:51–65.
White RD. Acute therapy in patients with cardiac arrhythmias.
In Murray MJ, Coursin DB, Pearl RG, Prough DS, eds. Critical
Care Medicine: Perioperative Management. Philadelphia: Lip-
pincott-Raven, 1997:327–340.
White RD. Pharmacologic management of arrhythmias during
advanced cardiac life support. Anesthesiol Clin North Am
1995;13:849–868.