What are ventricular ectopic beats (VPC)? Cardiology Basics

What are ventricular ectopic beats (VPC)? Cardiology Basics

Ventricular ectopic beats are premature heart beats originating from the ventricles. Normal heart beats originate from the sinus node, situated in the upper part of right atrium. Sinus node is the natural pacemaker of the heart which gives out regular impulses to induce sequential contractions of atria and ventricles.

Ventricular ectopic beats (VEB) are also known by other names like ventricular premature beat (VPB), ventricular premature complex (VPC) and premature ventricular complex (PVC). Ventricular ectopic is the commonest form of cardiac arrhythmia.

In a ventricular ectopic beat, the sequence of activation is different from that in a normal sinus beat. Normal sinus beat activates the atria first and then the ventricles, after a short delay. The delay is produced by the atrioventricular (AV) node, situated in the lower part of right atrium near the AV junction.

The delay between the activation of the atria and ventricles ensure that the atrial emptying is over before the ventricles start contracting. This ensures that the ventricles get a booster filling effect when the atria contract, known as atrial help to ventricular filling. Rest of the filling of the ventricles occur passively when they relax after a contraction. In ventricular ectopic beats, this sequence is lost.

Ventricles contract first in ventricular ectopic beat. The impulse may be conducted back to the atria which contract after the ventricles. So, the ventricles do not get help in filling from the atria. Moreover, as the contraction of the ventricles occur earlier than normally, they do not get enough time to fill. Poorly filled ventricle is not able to eject much blood so that the volume of the pulse is low or even absent.

When the atria contract soon after the ventricles, the blood from the atria cannot enter the ventricles as the atrioventricular valves are closed during ventricular systole. This results in back flow of blood into the superior and inferior vena cava. This manifests as a cannon wave in the jugular venous pulse. Cannon waves can occur along with every ventricular ectopic if there is regular retrograde conduction.

Even if there is no retrograde conduction, some ventricular ectopics may occur during atrial systole from a sinus impulse and cause cannon waves. Ventricular ectopics are the commonest cause of cannon waves as they are much more frequent than complete heart block, the classical cause of cannon waves.

If the number of ventricular ectopics is more than 10% of the total heart beats, it can cause left ventricular dysfunction in the long run due to ventricular dyssynchrony. In ventricular ectopic, dyssynchrony between contractions of various regions of the left ventricle occurs due to the abnormal sequence of activation. But if the frequency of ventricular ectopics is low, it hardly affects the function of the heart.

Ventricular ectopics are often seen with no evidence of structural heart disease. They can occur in those with myocardial scars after a myocardial infarction and in those with electrical and structural disorders of the heart, when it is more sinister. Ventricular ectopy is quite common in the early hours after acute myocardial infarction and may lead on to ventricular fibrillation and cardiac arrest sometimes. Ventricular fibrillation in acute myocardial infarction without heart failure is known as primary ventricular fibrillation and needs prompt electrical cardioversion with a defibrillator.

Though isolated ventricular ectopic beats are of no great significance, sometimes they can be the forerunner of more serious heart rhythm disorders. Ventricular ectopy in general indicates an irritable ventricle. This can sometimes lead to continuous firing of the abnormal focus, leading to ventricular tachycardia. It is a potentially serious condition requiring antiarrhythmics and electrical cardioversion if needed. Multiple morphologies of ventricular ectopics are considered to be more dangerous than monomorphic VPC. Highly premature VPCs are more likely to precipitate ventricular tachyarrhythmias by the R on T phenomenon.

Ventricular ectopics can occur without significant other heart disease and it is the usual pattern. Abnormalities in the serum electrolytes like hypokalemia or hypomagnesemia can increase the irritability of the ventricles and lead to ectopic beats. A structurally abnormal heart is more prone for VPC. Left ventricular dysfunction due to any cause like myocardial infarction, cardiomyopathy and valvular heart disease can increase the chance of VPC. Risk of progression to ventricular tachycardia or ventricular fibrillation is higher if there is structural heart disease.

Ventricular ectopics are often appreciated as missed beats while feeling the pulse. This is because the poorly filled ventricles produce a weak pulse. The beat after that is stronger as it gets more time to fill after a short pause which is usual after a VPC. This forceful contraction is often felt by the individual and causes palpitation.

Some individuals get higher frequency of VPC on taking caffeinated drinks. Hence it is better to avoid them. ECG is a simple test which can document a PVC. They stand out as broad premature complexes in the ECG, followed by a pause and can be easily recognized by even a minimally trained person. The total number of PVC in a day can be documented by an ambulatory Holter monitor. Holter monitor is a continuous ECG recorder attached to the belt and connected to the chest with lead wires.

If there is an associated structural heart disease or heart failure, it needs immediate attention and can reduce the number of PVCs. Abnormalities of serum potassium and magnesium levels have to be corrected. Occasionally there may be some medications taken by the person which has induced the VPCs. Stopping them can also reduce the number of ventricular ectopics.

Antiarrhythmic medications to suppress ventricular ectopics are not generally preferred if the PVCs are isolated and not associated with structural heart disease or heart failure. This is because of potential long term adverse effects of some of these medications. They may be given if essential, as decided by the physician, with monitoring for adverse effects.

Very rarely, large number of VPCs can produce heart failure and need extra treatment. In selected cases, an electrophysiology study (EP study) is done to find out the exact location of the abnormal focus. This is done by introducing electrodes into the heart under local anaesthesia and recording the electrical signals from various parts of the heart. If a significant abnormality is found, it can be treated by radiofrequency catheter ablation. In catheter ablation, the tiny region producing the abnormality is ablated by radiofrequency energy delivered at the exact spot by a thicker ablation catheter.