Premature ventricular contraction (PVC) is caused by an ectopic cardiac pacemaker located in the ventricle. PVCs are characterized by premature and bizarrely shaped QRS complexes usually wider than 120 msec on with the width of the ECG. These complexes are not preceded by a P wave, and the T wave is usually large, and its direction is opposite the major deflection of the QRS.
The clinical significance of PVCs depends on their frequency, complexity, and hemodynamic response.
For additional information, see Medscape’s Cardiology Specialty page.
PVCs reflect activation of the ventricles from a site below the atrioventricular node (AVN). Suggested mechanisms for PVCs are reentry, triggered activity, and enhanced automaticity.
Reentry occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, the area of slow conduction activates the blocked part of the system after the rest of the ventricle has recovered, resulting in an extra beat. Reentry can produce single ectopic beats ,or it can trigger paroxysmal tachycardia.
Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).
Enhanced automaticity suggests an ectopic focus of pacemaker cells in the ventricle that has a subthreshold potential for firing. The basic rhythm of the heart raises these cells to threshold, which precipitates an ectopic beat. This process is the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly hyperkalemia.
Ventricular ectopy associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract beneath the pulmonic valve. The mechanism is thought to be enhanced automaticity versus triggered activity. These arrhythmias are often induced by exercise, isoproterenol (in the EP lab), the recovery phase of exercise, or hormonal changes in female patients (pregnancy, menses, menopause). The characteristic ECG pattern for these arrhythmias is a large, tall R wave in the inferior leads with a left bundle-branch block pattern in V 1 . If the source is the left ventricular outflow tract, there is a right bundle-branch block pattern in V 1 . Beta-blocker therapy is first-line therapy if symptomatic.
Factors that increase the risk of PVCs include male sex, advanced age, African American race, hypertension and underlying ischemic heart disease, a bundle-branch block on 12-lead ECG, hypomagnesemia, and hypokalemia.
PVCs are one of the most common arrhythmias and can occur in patients with or without heart disease. The prevalence of PVCs varies greatly, with estimates of less than 3% to more than 60% in asymptomatic individuals.
Data from large, population-based studies indicate that the prevalence ranges from less than 3% for young white women without heart disease to almost 20% for older African American individuals with hypertension.
The clinical significance of PVCs depends on the clinical context in which they occur.
PVCs in young, healthy patients without underlying structural heart disease are usually not associated with any increased rate of mortality.
PVCs in older patients, in particular those with underlying heart disease, are associated with an increased risk of adverse cardiac events, particularly sustained ventricular dysrhythmias and sudden death.
In patients who have had a MI, the risk of malignant ventricular arrhythmias and sudden death is related to the complexity and frequency of the PVCs. Patients with PVCs in Lown classes 3-5 are at greatest risk (see Lown grading criteria below).
African American race is associated with an increased frequency of PVCs on routine monitoring. In a large population-based study of PVC prevalence, African American race alone increased the risk of PVCs by 30% compared with the risk in white individuals.
Ventricular ectopy is more prevalent in men than in women of the same age. Male sex alone increases the risk of identifying PVCs on routine screening, with an odds ratio for male sex of 1.39 compared with women.
PVC frequency increases with age, reflecting the increased prevalence of hypertension and cardiac disease in aging populations.
The important elements in obtaining a history from patients with ventricular ectopy are a history of cardiac disease or structural heart disease. Current medications that may be proarrhythmic or that may increase the risk of abnormal potassium or magnesium levels and use of drugs or medications that are sympathomimetic (eg, ephedrine-containing products, cocaine), may also provide important clues to the source of the premature ventricular contractions (PVCs).
Symptoms pertinent to the management of the PVCs are those that suggest underlying ischemic cardiac disease, such as chest pain or its anginal equivalent, or those suggesting hemodynamic compromise, such as lightheadedness or syncope.
Patients are usually asymptomatic.
Cannon A waves or the increased force of contraction due to postextrasystolic potentiation of contractility can cause palpitations and neck and/or chest discomfort.
The patient may report feeling that his or her heart “stops” after a PVC.
Patients with frequent PVCs or bigeminy may report syncope. This symptom is due to either inadequate stroke volume or decreased cardiac output caused by the condition effectively halving the heart rate.
Long runs of PVCs can result in hypotension.
Exercise can increase or decrease the PVC rate.
Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy.
Blood pressure: Frequent PVCs may result in hemodynamic compromise. Frank hypotension is rare, but relative hypotension is not uncommon, particularly in patients with underlying cardiac disease.
Pulse: The ectopic beat may produce a diminished or absent pulse depending on the force of the ventricular contraction.
Pulse oximetry: Hypoxia may precipitate PVCs.
Cardiac findings: Cannon A waves may be observed in the jugular venous pulse if the timing of the PVC causes an atrial contraction against a closed tricuspid valve.
Cardiopulmonary findings: Findings in conjunction with longstanding hypertension (elevated BP and an S 4 ) or CHF (S 3 and rales) are important clues to the cause and clinical significance of PVCs.
Neurologic findings: Agitation and findings of sympathetic activation (eg, dilated pupils, warm and dry skin, tremor, tachycardia, hypertension) suggest that catecholamines may be the cause of the ectopy.
Acute MI or ischemia
Cardiomyopathy, dilated or hypertrophic
Mitral valve prolapse
Hypoxia and/or hypercapnia
Medications (eg, digoxin, sympathomimetics, tricyclic antidepressants, aminophylline, caffeine)
Illicit substances (eg, cocaine, amphetamines, alcohol, tobacco)
Hypomagnesemia, hypokalemia, hypercalcemia