Ventricular Premature Complexes Differential Diagnoses

Updated: Nov 27, 2016
  • Author: Jatin Dave, MD, MPH; Chief Editor: Jeffrey N Rottman, MD  more...
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DDx

Diagnostic ConsiderationsAberrant premature atrial contractionsFusion beatPremature junctional contractionsIdioventricular escape rhythmsVentricular tachycardiaParasystoleFixed versus variable coupling intervalInterpolated VPCVPCs as a proarrhythmic effect

Differentiating VPCs from other arrhythmias can be challenging, because several arrhythmias may mimic VPCs, as discussed below.

The diagnosis of VPCs is primarily electrocardiogaphic. Rarely, when catheters are present in the heart (as for EP studies, or with implanted cardiac devices capable of telemetry), VPCs can be definitively diagnosed by establishing the earliest temporal origin or an extrasystole in the ventricles. Often, however, this is not true and VPCs must be imperfectly diagnosed on the basis of surface electrocardiographic data. In this case, an important consideration is distinguished VPCs from other supraventricular extrasystoles that result in a broader QRS complex, typically from aberration. Thus, data from multiple leads must be evaluated: Depending on the origin of the VPC and the specific surface ECG lead observed, occasionally, a VPC may appear narrower than the sinus complex, but it still is generally broader when all leads are considered together.

The presence of ectopic P waves, usually absence of full compensatory pause (R-R interval containing the premature contraction is < 2 times the R-R interval of basic rhythm), and a relatively narrow QRS complex morphology help differentiate atrial premature complexes from VPCs. The compensatory pause results when the sinus node is not reset by VPCs. This typically occurs when the ectopic impulse colides with the sinus impulse remote to the sinus node (either at the AV node or in the ventricles), or when it otherwise fails to propogate to the atrium and enter and reset the sinus node.

On occasion, the ectopic impulse conducts retrogradely to the sinus node; resets the sinus node; and a shorter, noncompensatory pause occurs. If the sinus impulse is able to conduct despite the VPC, then the VPC is termed interpolated and no compensatory pause occurs. However, the presence or absence of a compensatory pause is not a diagnostic finding for a VPC, as a beat of ventricular origin may retrograde traverse the AV node and enter and reset the sinus node; conversely, beats of non-ventricular origin may not always enter and reset the sinus node, and sinus node function is not always predictable. 

Simultaneous activation of the ventricle by 2 sources can lead to a beat with characteristics between the conducted sinus beat and the ectopic beat.

The origin of this arrhythmia is automaticity or reentry in AV junctional tissues. The P waves usually are inverted because of retrograde atrial depolarization. If the ectopic beat originates in high nodal tissue, the QRS complex can be narrow.

A very slow pacemaker in the ventricle takes over when sinoatrial node and AV junctional pacemakers fail to function. The rate usually is less than 45 beats per minute, which helps to differentiate it from other arrhythmias.

When 3 or more consecutive ventricular contractions occur, they are called VT. VT that persists for 30 seconds or causes hemodynamic collapse is called sustained VT.

Parasystole occurs when a protected focus discharges independently of the dominant pacemaker. The characteristics of parasystole include wide QRS complexes with a varying coupling interval between the ectopic (parasystolic) and the dominant (usually sinus) complex, fusion beats, and variable coupling interval.

Fixed coupling refers to a fixed interval between the sinus QRS complex and the VPC; this indicates reentry or a triggered focus as the possible cause. Variable coupling could be due to parasystole or multifocal ectopy.

When the sinus rate is slow, a short-coupled VPC can occur between sinus beats. If concealed retrograde conduction occurs, the subsequent PR interval can be prolonged.

VPCs can be exacerbated by catheters in the heart or pacemaker leads. They can occur in response to an antiarrhythmic drug. If they are worsened with an antiarrhythmic drug and the QT is prolonged from the drug, a risk of torsades de pointes exists.