Premature Ventricular Contractions (PVC)

Look for structural disease - New or frequent PVCs earn a 12-lead ECG and, where structural disease is suspected, a transthoracic echocardiogram for left ventricular dysfunction; isolated PVCs in a normal heart need reassurance, not treatment.

Correctable triggers first - Serum potassium, magnesium, calcium, and TSH, plus oxygenation and a look at the med list for digoxin and stimulants. Hypokalemia, hypomagnesemia, hypoxia, and excess catecholamines are the fixable drivers, and repletion often quiets the ectopy on its own.

Rule out ischemia - PVCs appearing acutely are treated as ischemia until a 12-lead ECG and troponin say otherwise; electrolyte imbalance and drug toxicity get ruled out at the same time.

Quantify the burden - A 24- to 48-hour Holter or event monitor is what puts a number on it. Burden above 10% of beats (or roughly 10,000 per day) is what drives PVC-induced cardiomyopathy and earns an EP referral before an elective case.

Adrenergic tone matters - Benign PVCs are usually the product of excessive adrenergic stimulation, so deepen anesthesia and treat pain before reaching for a drug. Catecholamine-sensitive and exercise-induced ectopy responds well to beta-blockade.

Beta-blockers are first line - If the ectopy is symptomatic or frequent enough to treat, beta-blockade first; non-dihydropyridine calcium channel blockers are the alternative when beta-blockers are contraindicated.

Do not reflex to lidocaine - Routine antiarrhythmics for PVCs in acute MI are not recommended. Class Ic agents (flecainide, propafenone) are proarrhythmic and contraindicated with pre-existing coronary disease.

R-on-T is the emergency - A PVC landing on the T wave can degenerate into ventricular fibrillation; that gets immediate defibrillation.

Watch the perfusion, not the rate - Frequent or sustained runs can drop the blood pressure and cause presyncope; the arterial trace or plethysmograph shows the non-perfusing beats that the ECG rate does not.

Know where VT starts - More than three consecutive PVCs is nonsustained VT; past 30 seconds it is sustained VT. Escalate accordingly.

Post-ablation patients - Catheter ablation usually reverses PVC-induced cardiomyopathy, but some LV systolic dysfunction occasionally persists - check the post-ablation echo rather than assuming a normal ventricle.

Premature ventricular contractions (PVCs) are ectopic beats that arise below the AV node, from Purkinje tissue or ventricular myocardium, so the ventricles depolarize outside the specialized conduction system and the QRS widens past 120 ms. Three mechanisms drive them: enhanced automaticity from a spontaneously firing ectopic focus, re-entry through scarred or ischemic tissue, and triggered activity from after-depolarizations. Hypokalemia, hypomagnesemia, excess calcium, excess catecholamines, hypoxia, myocardial ischemia, and digoxin toxicity all lower the threshold.

Most PVCs are followed by a full compensatory pause because the sinus node timing is never reset. Isolated PVCs in a structurally normal heart carry the same prognosis as the general population, but a high burden - more than 10,000 ectopic beats or over 10% of all beats on 24-hour monitoring - can produce a largely reversible cardiomyopathy, and in patients with existing heart disease PVCs mark higher mortality.