CLINICIAN PVC & VT GUIDE · SECTION 1 OF 3

Understanding PVCs & VT

Recognize ventricular ectopy, VT patterns, and the importance of underlying heart disease.

Rhythms from the lower chambers

A premature ventricular contraction (PVC) is an early beat arising in a ventricle. Ventricular tachycardia (VT) is a fast sequence of ventricular beats. These rhythms range from occasional ectopy to life-threatening arrhythmias.

Patients may describe skipped beats, thumps, racing, dizziness, or fainting. Risk depends on the rhythm and the underlying heart: coronary disease, scar, cardiomyopathy, inflammation, and inherited electrical disorders all matter.^[1]^[2]

Labeled cutaway heart showing the SA node, AV node, bundle of His, right and left bundle branches, Purkinje fibers, and left atrial appendage. — Follow one normal heartbeat
**SA node → Atria → AV node → Ventricles**
**The SA node starts the signal.** The heart’s natural pacemaker in the right upper chamber begins each normal sinus beat.
**The signal spreads through both atria.** The upper chambers contract, moving blood into the ventricles.
**The AV node briefly delays the signal.** This pause gives the ventricles time to finish filling.
**The signal activates the ventricles.** It travels through the bundle of His, right and left bundle branches, and Purkinje fibers. The lower chambers contract, pumping blood to the lungs and body.
**The atria contract first; the ventricles follow.** This organized sequence produces a coordinated heartbeat.
NHLBI: How the heart beats MedlinePlus: Cardiac conduction system
Normal activation begins in the sinus node and travels to the ventricles.

Premature electrical activation originating in a ventricle — A PVC begins in a lower chamber before the next expected sinus beat.

Learn the vocabulary

Bigeminy / trigeminy

Every second / third beat is a PVC.

Couplet

Two consecutive ventricular beats.

Nonsustained VT (NSVT)

At least 3 consecutive ventricular beats at >100/min, ending spontaneously in <30 seconds.

Sustained VT

VT lasting >30 seconds, or requiring earlier termination because of hemodynamic compromise.

Monomorphic / polymorphic

Similar / changing QRS morphology during VT.

^[3]

Recognize the EKG pattern

Four schematic EKG strips showing an isolated PVC, ventricular bigeminy, a four-beat run of NSVT, and monomorphic VT — Teaching examples with white backgrounds. The last strip illustrates VT morphology, not a full sustained episode. Confirm findings on the actual tracing; a monitor label alone is insufficient.

PVCs usually have a wide QRS without a preceding conducted sinus P wave. During VT, AV dissociation, capture beats, or fusion beats can support the diagnosis, but their absence does not exclude it.

Why PVC burden matters

Burden = PVCs ÷ total beats. Frequent PVCs may weaken ventricular function. An unexplained reduced EF with a burden around ≥10% warrants assessment for PVC-induced cardiomyopathy; this is not a universal cutoff or an automatic ablation indication. PVCs may also be a consequence of existing disease.^[4]

Polymorphic VT and torsades

Torsades de pointes is polymorphic VT associated with a prolonged QT interval between episodes. Other polymorphic VT can occur with a normal QT, including during acute ischemia. Both require urgent assessment.^[5]

Clinical references

Educational review draft · EKGs are schematic examples · References reviewed October 11, 2026.