Ventricular premature complexes(VPCs) result from the spontaneous depolarization of the ventricular myocardium. The result a QRS complex that wide 120 has a bizarre morphology, and occurs earlier than expected.
The repolarization phase is also abnormal and results in ST segment and T wave changes opposite the major deflection of the QRS complex. The AV node, depolarize the atria, and result in a retro- de P wave on the surface ECG. Usually, this wave of depolarization does not reach the sinoatrial node before its spontaneous discharge and, thus, the sinus rate is unaffected.

Most VPCs are, therefore, followed by a fully compensatory pause; that is, the RR interval surrounding the VPC is twice the normal RR interval(Fig 10-8B). Occasionally, a VPC may occur without affecting the underlying sinus or ventricular rate(an interpolated VPC). VPCs may occur as single contractions, in pairs(a ventricular couplet), or in runs of three or more consecutive beats(i.e., VT). They may occur as other complex(ventricular bigeminy), every third complex(ventricular trigeminy), and so on. They may be of uniform morphology or vary in appear(polymorphic). VPCs commonly have a fixed relationship preceding ORS complex.

When this relationship to the relationship varies, it suggests that there is a ventricular focus sinus node, a so-called parasystolic focus. VPCs occur with increased frequency in the presence of underlying heart disease(coronary artery disease, cardiomyopathy, mitral valve prolapse) ,advancing age, metabolic abnormalities ( hyperkalemia, hypokalemia , hypoxia), infection, acute myocardial ischemia, and emotional stress, and with the excessive use of caffeine, tobacco, or alcohol. They are frequently asymptomatic, although they may produce palpitations and rarely hypotension.

In the absence of underlying cardiac disease, VPCs are probably of no prognostic importance.