7.2 Ventricular tachycardia

Ventricular Tachycardia (VT)

Ventricular tachycardia is defined as three or more consecutive PVCs at a rate of approximately 100-250 beats per minute. The rhythm originates from an ectopic ventricular focus — or a re-entry circuit within ventricular tissue — that fires rapidly and repetitively, seizing control of the heart from the SA node. Because activation again bypasses the normal His-Purkinje system, every complex is wide (≥0.12 s) and bizarre, and the complexes typically march out in a rapid, usually regular succession. VT is a direct extension of the PVC concept: link three or more together and you have VT.

Recognition criteria

• Rate: approximately 100-250 bpm (most commonly 150-200).
• Rhythm: usually regular, though it may be slightly irregular.
• QRS: wide (≥0.12 s) and bizarre, resembling a rapid string of PVCs marching across the strip.
• P waves: usually absent or dissociated — when visible, the atria march independently of the ventricles (AV dissociation).
• T waves: often difficult to identify and usually deflect opposite the QRS.
• Onset: often begins abruptly with a PVC, sometimes an R-on-T beat.

The presence of AV dissociation, fusion beats, and capture beats favors VT over other wide-complex tachycardias such as supraventricular tachycardia (SVT) conducted with aberrancy. A capture beat is an occasional normal, narrow QRS that appears amid the wide complexes when a sinus impulse briefly "captures" the ventricles through the normal pathway; a fusion beat is a hybrid formed when a sinus impulse and the ventricular focus depolarize the ventricle at the same moment. Both prove the atria and ventricles are beating independently, which cements the diagnosis of VT rather than SVT with aberrancy. As a practical rule, a regular wide-complex tachycardia should be assumed to be VT until proven otherwise, especially in a patient with known heart disease.

Common causes

VT most often arises from a re-entry circuit around scar tissue — classically the scar left by a prior myocardial infarction — which is the usual substrate for monomorphic VT. Other triggers include active ischemia, cardiomyopathy, heart failure, electrolyte imbalance (potassium and magnesium disturbances), and QT-prolonging drugs, the last of which favor the polymorphic torsades pattern. Recognizing that a stable structural scar produces uniform, single-shape complexes helps connect morphology to mechanism.

Monomorphic versus polymorphic

VT is subclassified by the shape of its QRS complexes:

• Monomorphic VT — all QRS complexes share the same shape and amplitude, indicating a single stable focus or re-entry circuit. The complexes are uniform beat to beat.
• Polymorphic VT — the QRS complexes vary in shape and amplitude from beat to beat, reflecting an unstable, shifting activation pattern. Polymorphic VT is generally more unstable and more likely to degenerate into ventricular fibrillation.

Torsades de pointes

Torsades de pointes ("twisting of the points") is a distinctive form of polymorphic VT in which the QRS complexes appear to twist around the isoelectric baseline, spindling up and down so the amplitude waxes and wanes. Its defining association is a prolonged QT interval in the underlying rhythm — whether from congenital long-QT syndrome, electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), or QT-prolonging drugs. Recognizing the twisting pattern and linking it to a long QT is a high-yield CRAT association; the treatment context (intravenous magnesium) is worth knowing even though the technician does not administer it.

Sustained versus non-sustained

Duration further classifies VT:

A brief triplet or a short burst that self-terminates is NSVT; a run that persists is sustained VT and demands immediate clinical attention.

Pulseless VT: an emergency

The most important clinical concept is that VT can be perfusing or pulseless. When the ventricular rate is very rapid, the ventricles may not fill adequately between beats, so cardiac output collapses and the patient loses a pulse. Pulseless VT is a cardiac-arrest rhythm — treated identically to ventricular fibrillation, with immediate defibrillation and CPR. This is why VT is never dismissed on the monitor: a technician who sees sustained wide-complex tachycardia must alert the team at once, because the tracing on the screen cannot, by itself, tell you whether the patient has a pulse. Even perfusing (stable) VT is dangerous, because it can deteriorate into pulseless VT or ventricular fibrillation without warning.

Clinically, VT with a pulse may be stable (the patient is awake and perfusing) or unstable (hypotension, chest pain, altered mental status, or other signs of shock). Unstable VT with a pulse is treated with synchronized cardioversion, whereas pulseless VT is defibrillated; both scenarios are handled by the clinical team, but the technician's rapid recognition and escalation set the entire response in motion.

The takeaway for exam purposes: three or more wide, bizarre complexes in a row at 100-250 bpm is VT. Classify it by morphology (monomorphic versus polymorphic, with torsades as long-QT polymorphic VT) and by duration (non-sustained versus sustained), and always treat sustained or pulseless VT as a life-threatening emergency requiring immediate escalation.