History
The important element in obtaining a history from patients with ventricular ectopy is 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. Note the following:
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Patients are usually asymptomatic
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Cannon A waves or the increased force of contraction resulting from postextrasystolic potentiation of contractility can cause palpitations and neck and/or chest discomfort
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The patient may report feeling that his or her heart "stops" after a PVC
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Patients with frequent PVCs or bigeminy may report syncope. a symptom that is due to either inadequate stroke volume or decreased cardiac output caused by the condition effectively halving the heart rate
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Long runs of PVCs can result in hypotension
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Exercise can increase or decrease the PVC rate
Physical Examination
Important findings on the physical examination are those that provide clues to the underlying cause of the ventricular ectopy, including the following:
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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
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Pulse - The ectopic beat may produce a diminished or absent pulse, depending on the force of the ventricular contraction
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Pulse oximetry - Hypoxia may precipitate PVCs
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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
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Cardiopulmonary findings - Findings in conjunction with longstanding hypertension (elevated BP and an S 4 ) or congestive heart failure (S 3 and rales) are important clues to the cause and clinical significance of PVCs
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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
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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.
