Medical Care
The optimal indications for therapy for premature ventricular contractions (PVCs) have not yet been elucidated. [4] Involvement of a cardiologist may be indicated if the patient's condition is refractory to standard therapy.
Prehospital care
Perform telemetry, and secure intravenous (IV) access. Administer oxygen, if any hypoxia exists. Complex ectopy in the setting of myocardial ischemia or causing hemodynamic instability should be suppressed. Use lidocaine for patients with myocardial ischemia.
Emergency department care
The decision to treat PVCs in the emergency or outpatient settings depends on the clinical scenario. In the absence of cardiac disease, isolated, asymptomatic ventricular ectopy, regardless of configuration or frequency, requires no treatment. With cardiac disease, certain toxic effects, and electrolyte imbalances, treatment may be required. Establish telemetry and IV access, initiate oxygen, and obtain a 12-lead electrocardiogram (ECG). Note the following:
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Hypoxia - Treat the underlying cause; secure the ABCs and provide oxygen.
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Drug toxicity - Specific therapy is indicated for certain toxic effects—for example, digoxin (Fab antibodies), tricyclics (bicarbonate), and aminophylline (gastrointestinal decontamination and possibly hemodialysis)
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Correct electrolyte imbalances, particularly those of magnesium, calcium, and potassium
Acute ischemia or infarction
Early diagnosis and treatment of acute infarction/ischemia are the cornerstones of therapy. Note the following:
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Routine use of lidocaine and other type I antiarrhythmic agents in the setting of acute MI is no longer recommended, because of their toxic effects
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Acute ischemia or infarction includes patients with ectopy in the period immediately after receipt of thrombolytic agents, during which complex ectopy frequently is seen
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First-line therapy for ectopy without hemodynamic significance in patients who have sustained a myocardial infarction (MI) is beta-blockade
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Only in the setting of symptomatic, complex ectopy is lidocaine likely to benefit a patient having an MI
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Lidocaine is especially useful when symptomatic ectopy is associated with a prolonged QT interval, in that it does not lengthen the QT interval as other antiarrhythmic agents do
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Amiodarone [12] is also a useful agent for suppressing ectopy or ventricular tachycardia (if hemodynamically significant); additional beneficial effects include coronary vasodilation and increased cardiac output via a reduction in systemic vascular resistance
Catheter Ablation
Catheter ablative therapy has a role in the management of patients with PVCs. [13, 14] This is in the setting of PVCs from the right or left ventricular outflow tract that occur in structurally normal hearts. Ablation is indicated for frequent, symptomatic PVCs that occur despite medical therapy. Success is variable, depending on frequency and inducibility at the time of electrophysiologic study (EPS).
Guidelines on the use of catheter ablation in ventricular arrhythmia are available from the European Heart Rhythm Association (EHRA) and the Heart Rhythm Society (HRS) in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). [15]
Fichtner et al evaluated the outcome and success of PVC ablation in 408 patients in the German Ablation Registry from March 2007 to May 2011. [16] The acute ablation success rate was 82%; all patients were discharged alive after a median of 3 days; and no patient suffered an acute MI, stroke, or major bleeding. After 12 months of follow-up, 99% of patients were still alive, and 76% showed significantly improved symptoms.
Im et al investigated ECG criteria for predicting successful ablation of PVCs from the right coronary cusp (RCC). They found that the presence of a dominant positive lead I, an R-wave duration index (RWDI) higher than 43.6%, and an S-wave amplitude lower than 0.95mV in aVL predicted RCC PVCs in patients with a sensitivity of 83% and a specificity of 94%. [17]
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ECG shows frequent, unifocal PVCs with a fixed coupling interval between the ectopic beat and the previous beat. These PVCs result in a fully compensatory pause; the interval between the 2 sinus beats surrounding the PVC are exactly twice the normal R-R interval. This finding indicates that the sinus node continues to pace at its normal rhythm despite the PVC, which fails to reset the sinus node.
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On this ECG, the PVCs occur near the peak of the T wave of the preceding beat. These beats predispose the patient to ventricular tachycardia or fibrillation. This R-on-T pattern is often seen in patients with acute myocardial infarction or long Q-T intervals. In the latter case, the triggered arrhythmia would be torsade.
