Ventricular premature complexes (VPCs)

Just like APCs, VPCs are “ectopic” to the normal pacemaker system of the heart, appearing prior to when they are expected. They can come in singles, couplets, triplets, or “runs” (series of three or more in a row, a phenomenon sometimes termed “ventricular tachycardia”).

When a premature QRS complex originates from a ventricular focus such as the left ventricular, right ventricular, or interventricular septal myocardium, it does not take advantage of the fast-conducting cardiomyocytes belonging to the His bundles and Purkinje fibers, but rather bypasses them via other, normal cardiomyocytes (that do not specialize in fast conduction but rather in effective contraction and relaxation), on a slower, cell-to-cell basis. This is why its electrocardiographic morphology is most often different from that of normal QRS complexes originating from the sino-atrial (SA) node, or from any other supra-ventricular focus (in other words, different from the “gold standard” of that individual patient), that do travel into the ventricular myocardium via these specialized fast conducting pathways.

Other than their premature timing (which renders the electrical diastole, or TQ interval preceding them, much shorter than expected for that patient based on other intervals), their unusual morphology helps to identify them even by the less experienced eye, and this is why their identification is often less challenging than that of APCs. Because of their relatively slow conduction across ventricular myocytes, they are often, albeit not always wider than normal, but are still necessarily morphologically different in other ways from supraventricular QRS complexes in that same patient. One should not confuse their often longer-than-normal duration with their prematurity, as the former has to do with their relatively low rate of conduction while the latter has to do only with the unusually early timing of their onset.

Typically there is no P-wave preceding VPCs but occasionally an incidental P-wave does precede them, without having been their trigger or even a contributor (in other words, there is no causal relationship between it and the VPC). For this reason, the absence of a P-wave before a QRS cannot be used as a pathognomonic diagnostic feature of a VPC.

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However, when the underlying sinus rhythm and the repetitive ventricular rhythm are similar in heart rate and, therefore, appear to “compete” with each other, an occasional preceding P-wave in front of a VPC-like complex is more common. This phenomenon may reflect an “idioventricular rhythm” (also known as an “accelerated ventricular rhythm”, see in the ECG viewer above) where both the SA-node AND a ventricular ectopic focus happen to contribute to a merged (“fused”) complex. Such fused complexes sometimes have morphological features that belong to one or to both of their two simultaneous sources.

This is more often recorded in severe extra-cardiac disease with diffuse tissue damage (but no direct cardiac damage) such as gastric dilatation and volvulus, road car accidents with pelvic fractures, snake envenomation, necrotizing pancreatitis, heat stroke, etc. In such patients, the idioventricular/accelerated ventricular rhythm is seldom fast enough to endanger the patient or hemodynamically compromise it. However, the underlying, extra-cardiac condition might pose life-threatening risks. Therefore, *it* should be addressed accordingly and promptly. When two different foci, the sinoatrial node and a ventricular focus “compete” like that, their resultant “fusion beats” are more likely to be identified during gradual transition phases between them (i.e., during the onset and/or offset of the accelerated ventricular rhythm).

When the VPC originates from the right ventricular myocardium (as sometimes occurs, for example, with arrhythmogenic right ventricular cardiomyopathy, or with congenital pulmonic stenosis), the QRS dominant wave is positive (an R-wave) in Lead-I, such as in the following case:

HR = 186 bpm, QRS = 80 ms, R = 2.125 mV, QT = 205 ms, 90>MEA>0 (normal)  | view the full report

In contrast, when it originates from the left ventricular myocardium (as sometimes occurs, for example, with congenital subaortic stenosis, dilated cardiomyopathy, or severe, chronic, mitral valve regurgitation), the dominant QRS wave is typically negative (and late in the QRS complex, i.e., an S-wave) in this very same lead as in the case below. When in doubt, carefully look at the same-suspected VPC as seen in several (simultaneously inscribed) leads, rather than just at a single lead.

HR = 130 bpm, P = 50 ms, 0.15 mV, PR = 120 ms, QRS = 70 ms, R = 1.4 mV

Often, because the depolarization process is abnormal, the following repolarization process is abnormal as well, resulting in a wide and tall/deep T-wave starting just as soon as the QRS complex ends, with a slurred or sometimes absent ST-segment between the two. In addition, the T-wave is commonly “discordant” rather than “concordant” to the QRS complex, namely opposite in polarity to the dominant wave within the QRS complex.

In human beings with ischemic myocardial disease, a VPC that occurs prematurely enough to be inscribed even before the end of the previous T-wave is thought to pose a risk of severe (“malignant”) ventricular arrhythmia. This is termed an “R-on-T phenomenon” (the “R” representing the entire premature QRS, even if its dominant wave happens to actually be an S). Fortunately, veterinary patients do not often develop ischemic myocardial disease and therefore, even if they do present with an R-on-T phenomenon, the risk of malignant arrhythmia is usually not as high, unless they do have an underlying myocardial disease such as cardiomyopathy or myocardial complications of other severe conditions such as severe (and typically congenital) subaortic or pulmonic stenosis.