A premature beat arising from an ectopic focus within the ventricles.

AKA: ventricular ectopics, ventricular extrasystoles, ventricular premature beats, ventricular premature depolarisations.

• Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation.
• The rate of depolarisation decreases from top to bottom: fastest at the sinoatrial node; slowest within the ventricles.
• Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above, but depolarisation occurs early enough — prior to the arrival of the next sinus impulse — a premature contraction may result.
• Classified by origin — atrial (PACs), junctional (PJCs) or ventricular (PVCs).

• Focus within the ventricles bypasses the His-Purkinje system and depolarises the ventricles directly, disrupting the normal sequence of cardiac activation, leading to asynchronous activation of the two ventricles. The consequent interventricular conduction delay produces QRS complexes with prolonged duration and abnormal morphology.

PVCs have the following features:

• Broad QRS complex (≥ 120 ms) with abnormal morphology.
• Premature — i.e. occurs earlier than would be expected for the next sinus impulse.
• Discordant ST segment and T wave changes.
• Usually followed by a full compensatory pause.
• Retrograde capture of the atria may or may not occur.

Appropriate discordance describes a pattern of repolarisation abnormality (typically seen with LBBB, paced rhythms, VT) in which the ST segment and T wave are directed opposite to the main vector of the QRS complex:

• ST depression and T wave inversion in leads with a dominant R wave.
• ST elevation with upright T waves in leads with a dominant S wave.

• Unifocal — Arising from a single ectopic focus; each PVC is identical.
• Multifocal — Arising from two or more ectopic foci; multiple QRS morphologies.

The origin of each PVC can be discerned from the QRS morphology:

• PVCs arising from the right ventricle have a left bundle branch block morphology (dominant S wave in V1).
• PVCs arising from the left ventricle have a right bundle branch block morphology (dominant R wave in V1).

• Bigeminy — every other beat is a PVC.
• Trigeminy — every third beat is a PVC.
• Quadrigeminy — every fourth beat is a PVC.
• Couplet — two consecutive PVCs.
• NSVT — three-thirty consecutive PVCs (see below).

PVCs are a normal electrophysiological phenomenon not usually requiring investigation or treatment. Frequent PVCs may cause palpitations and a sense of the heart “skipping a beat”. In patients with underlying predispositions (e.g. ischaemic heart disease, WPW), a PVC may trigger the onset of a re-entrant tachydysrhythmia — e.g. VT, AVNRT, AVRT.

Frequent PVCs are usually benign, except in the context of prolonged QTc, when predispose to malignant ventricular arrhythmias eg. Torsades de Pointes due to “R on T” phenomenon

• Anxiety
• Sympathomimetics, Beta-agonists, digoxin, TCA's, aminophylline
• Excess caffeine, cocaine, alcohol, tobacco, amphetamines
• Hypokalaemia, Hypomagnesaemia, hypercalcaemia
• Myocardial ischemia, myocarditis, cardiomyopathy
• Hyperthyroidism, pheochromocytoma
• Hypercapnia, hypoxia

In the absence of structural disease, prognosis is debatable with some studies suggesting frequent PVCs are associated with increased risk of sudden cardiac death and others suggesting higher mortality during exercise.

• Treat correctable causes - correct electrolyte abnormalities, reduce stimulants, review usual medications.
• In the absence of symptoms and structural disease, no treatment is necessary.
• Low dose ẞ blocker for symptomatic management.

Control of underlying cardiovascular disease is mainstay of treatment.

• management of hypertension
• ẞ blockers
• Amiodarone
• implantable defib may be useful

References include:
https://litfl.com/premature-ventricular-complex-pvc-ecg-library/