What is vpc in ecg?

A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.[1]

The electrical events of the heart detected by the electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. However, very frequent PVCs can be symptomatic of an underlying heart condition (such as arrhythmogenic right ventricular cardiomyopathy). Furthermore, very frequent (over 20% of all heartbeats) PVCs are considered a risk factor for arrhythmia-induced cardiomyopathy, in which the heart muscle becomes less effective and symptoms of heart failure may develop.[2] Ultrasound of the heart is therefore recommended in people with frequent PVCs.

If PVCs are frequent or troublesome, medication (beta blockers or certain calcium channel blockers) may be used. Very frequent PVCs in people with dilated cardiomyopathy may be treated with radiofrequency ablation.[2][1]

Although there are many possible symptoms associated with PVCs, PVCs may also have no symptoms at all. PVCs may be perceived as a skipped heart beat, a strong beat, palpitations, or lightheadedness. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise.[2] Symptoms may be more pronounced at times of stress. Women may be more aware of PVCs at the time of the menstrual period.[2]

Premature ventricular contractions may be associated with underlying heart disease, and certain characteristics are therefore elicited routinely: the presence of signs of heart disease or a known history of heart disease (e.g. previous myocardial infarction), as well as heart disease or sudden cardiac death in close relatives. PVCs and palpitation associated with syncope (transient loss of consciousness) or provoked by exertion are also concerning.[2] Physical examination is focused on identifying evidence of underlying heart disease.[2]

Premature ventricular contractions occur in healthy persons of any age, but are more prevalent in the elderly and in men.[3] In a very significant proportion of people they occur spontaneously with no known cause.[citation needed]

Some possible underlying causes of PVCs include:

Normally, impulses pass through both ventricles almost at the same time and the depolarization waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels through only one bundle fiber, so there is no neutralization effect; this results in the high voltage QRS wave in the electrocardiograph.

There are three main physiological explanations for premature ventricular contractions: enhanced ectopic nodal automaticity, re-entry signaling, and toxic/reperfusion triggered.

Ectopic enhanced nodal automaticity suggests foci of sub-pulmonic valvular pacemaker cells that have a subthreshold potential for firing. The basic rhythm of the heart raises these cells to threshold, which precipitates an ectopic beat. This process is the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly low blood potassium, known as hypokalemia.

Reentry occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, one bundle tract's area of slow conduction activates the other tract's bundle fibers post block after the rest of the ventricle has recovered. This resulting in an extra beat. Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia.

Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).

This ectopy of the ventricles when associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract (RVOT) under the pulmonic valve. The mechanism behind this is thought to be enhanced automaticity versus triggered activity.[3]

There are a number of different molecular explanations for PVCs.

PVCs may be found incidentally on cardiac tests such as a 12-lead electrocardiogram (ECG/EKG) performed for another reason. In those with symptoms suggestive of premature ventricular complexes, the ECG/EKG is the first investigation that may identify PVCs as well as other cardiac rhythm issues that may cause similar symptoms. If symptoms are infrequent, other forms of continuous heart beat recording may be used, such as a 24 or 48-hour Holter monitor or even 14- to 30-day recorders if the symptoms are very occasional.[2] The advantage of these monitors is that they allow a quantification of the amount of abnormal beats ("burden") and ensure that there are no heart arrhythmias present that might require attention, such as ventricular tachycardia.[2] If symptoms are associated with exercise, a supervised cardiac stress test may be required to reproduce the abnormality. Specifically, if this shows exercise-induced ventricular tachycardia this would require specific treatment.[2] If PVCs are suppressed by exercise, this is an encouraging finding.[citation needed]

On electrocardiography (ECG or Holter) premature ventricular contractions have a specific appearance of the QRS complexes and T waves, which are different from normal readings. By definition, a PVC occurs earlier than the regular normally conducted beat. Subsequently, the time between the PVC and the next normal beat is longer as the result of a compensatory pause.[19] PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions, in addition to a difference in QRS appearance.[20]

In some people, PVCs occur in a predictable pattern. Two PVCs in a row are called doublets and three PVCs in a rows are triplets. Depending whether there are one, two, or three normal (sinus) beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. If 3 or more consecutive PVCs occur in a row it may be called ventricular tachycardia.[20] The precise shape of the QRS can give an indication as to where precisely in the heart muscle the abnormal electrical activity arises. If someone has PVCs that all have the same appearance, they are considered "monofocal", if PVC’s have different appearance, they are considerevole “multifocal”.[2]

Isolated PVCs with benign characteristics and no underlying heart disease require no treatment, especially if there are limited symptoms.[2]

The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and certain drugs, like tobacco).[21] If frequent, it’s possible to use:

PVCs are harmless, but frequent PVCs may increase the risk of developing cardiomyopathy, which can greatly impair heart function. On a more serious and severe scale, very frequent PVCs can accompany underlying heart disease.[25]

People who do not have heart disease (with ejection fractions greater than 40%) have the same long-term prognoses as the minorance of people without PVCs on the 24 hours. Emerging data also suggest that very frequent ventricular ectopy may be associated with cardiomyopathy through a mechanism thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy. For patients with underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.[3]

In meta-analysis of 11 studies, people with frequent PVCs (≥ once during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death twice as great as that of participants with occasional PVCs. Although most researchers attempted to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.[26]

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease (i.e. in the presence of normal heart function) there were no serious cardiac events through 5.6 years on average, but there was correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. In this study absence of heart of disease was established by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.[27]

Another study has suggested that in the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis.[22] It was study of 70 people followed by 6.5 years on average. Healthy status was verified by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.[28]

On the other hand, the Framingham Heart Study reported that frequent PVCs in healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death.[22] In men with coronary heart disease and in women with or without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk.[29] The at-risk people might have subclinical coronary disease.[30] These Framingham results have been criticized for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.[22]

In the ARIC study of 14,783 people followed for 15 to 17 years those with detected PVC during 2 minute ECG, and without hypertension or diabetes on the beginning, had risk of stroke increased by 109%.[31] Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVCs.[31] It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes.[31] Those in ARIC study with any PVC had risk of heart failure increased by 63%[32] and were > twice as likely to die from coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.[33]

In the Niigata study of 63,386 people with a 10-year follow-up period, subjects with PVC during a 10-second recording had triple the risk of atrial fibrillation of those without PVCs, independently of these risk factors: age; male sex; high simple body mass index (a possible signifier of obesity); hypertension (systolic and diastolic blood pressure within certain abnormal limits); and diabetes.[34]

Reducing very frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.[22][24]

Recent studies have shown that those subjects with extremely frequent PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy regresses.[24][35]

Single PVCs are common in healthy persons. When 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs.[36] Rates vary by age with extremely rare for those under the age of 11 and extremely common in those older than 75 years.[37] These differences may be due to rates of high blood pressure and atherosclerosis, which are more easy to find in older persons.[38] In 101 people free of heart disease during 24 hours Holter monitoring, 39 had at least 1 PVC, and 4 at least 100. Heart disease was excluded after physical examination, chest x-ray, ECG, echocardiography, maximal exercise stress test, right- and left-heart catheterization and coronary angiography.[39] In 122,043 United States Air Force flyers and cadet applicants during approximately 48 seconds of ECG 0.78% (952 males) had PVC within all age groups, but with increased incidence with increasing age.[40] Ventricular ectopy is more prevalent in men than in women of the same age data from large, population-based studies indicate that the prevalence is less for young white women without heart disease and greater for older African American individuals with hypertension.[3]

Ventricular premature complexes (VPCs), or premature ventricular complexes/contractions (PVCs), are ectopic beats that arise from within the ventricles. They are common and can occur in a wide variety of clinical scenarios and a diverse population.

Premature ventricular complexes are also referred to as premature ventricular beats, premature ventricular contractions or just ventricular beats/contractions/complexes. These terms will be used interchangeably in this discussion.

A premature ventricular complex is recognized on the ECG as an abnormal and wide QRS complex occurring earlier than expected in the cardiac cycle. It is caused by an impulse discharged from an ectopic focus which may be located anywhere in the ventricles. The ectopic impulse depolarizes the ventricles; because the impulse is discharged in the ventricles it will spread partly or entirely outside of the conduction system and thus produce a wide QRS complex (QRS duration ≥0.12 s). Refer to Figure 1 for an example.

The premature ventricular impulse replaces a sinus beat and induces a delay to the next sinus beat (the RR interval is increased after a premature ventricular complex). This yields more time to fill the ventricles with blood (increased ventricular filling). The person with premature beats might perceive this as palpitations, because of the stronger ventricular contractions caused by the increased filling.

Ventricular premature complexes are not preceded by P-waves, because the ectopic impulse originates in the ventricles and do not affect the atria (there are exceptions to this rule, discussed below).

Although premature ventricular contractions are mostly harmless, they may trigger sustained ventricular tachyarrhythmias. This will also be discussed later.

The impulse discharchged from en ectopic focus in the ventricles will spread abnormally (because the impulse did not enter the ventricles through the bundle of His). Abnormal depolarization will consequently lead to abnormal repolarization. This explains the secondary ST-T changes seen on premature ventricular complexes; the ST-T vector will be directed oppositely to the QRS vector. As seen in Figure 1 the premature ventricular complex displays a positive QRS complex followed by a negative ST-T segment. Thus, the ST-T segment is directed oppositely to the QRS (this is called discordant ST-T segment).

A premature ventricular contraction is followed by a complete compensatory pause which means that the next sinus beat will occur on schedule. The interval between the sinus beats occurring before and after the premature beat will be two sinus cycles (2 RR intervals). This is explained by the fact that the premature ventricular impulse does not discharge and reset the sinoatrial node, which will therefore continue on schedule. Refer to Figure 2.

When every other beat on the ECG is a premature ventricular complex (PVC), the rhythm is referred to as PVC in bigeminy (Figure 3). If every third beat is a PVC, it is referred to as PVC in trigeminy. Similarly there can be quadrigeminy and so on.

Two consecutive premature ventricular contractions are referred to as a pair or couplet. If 3 to 30 premature ventricular contractions occur consecutively, it is referred to as non-sustained ventricular tachycardia (if the rate is >100 beats/min) or ventricular rhythm (if the rate is <100 beats/min). If more than 30 consecutive beats are premature ventricular contractions it is referred to as sustained ventricular tachycardia if the rate is >100 beats/min.

Premature ventricular complexes discharged by the same ectopic focus will typically have similar morphology (appearance) and constant timing. Such premature ventricular complexes are referred to as monomorphic (or unifocal). This is exemplified in Figure 3.

Polymorphic premature ventricular complexes display constant timing but varying morphology. These beats typically originate in the same ectopic focus but the spread of the impulse (from that ectopic focus) varies from one beat to another (Figure 4).

Multifocal premature ventricular complexes have varying morphology and varying timing. These beats are discharged by several ectopic foci in the ventricles (Figure 5).

It is also possible to determine where the ectopic focus is located by assessing the morphology of the premature beat in lead V1. If the morphology in lead V1 is similar to a right bundle branch block (i.e predominantly positive), the ectopic focus is located in the left ventricles. If the morphology in lead V1 is similar to a left bundle branch block (i.e predominantly negative), the ectopic focus is located in the right ventricles.

If a normal atrial impulse is conducted to the ventricles approximately simultaneously as a premature ventricular impulse is discharged, the ventricles might be depolarized by both these impulses. This typically occurs if the premature ventricular impulse is discharged late, around the time of the normal sinus impulse. The morphology resulting QRS complex will resemble a combination (a fusion) of the normal beat and the PVC. Refer to Figure 6.

Although the complete compensatory pause is very typical of the premature ventricular complex (PVC), there are instances where it does not occur.

Premature ventricular contractions are common among both healthy individuals and there is robust evidence that do not affect long term cardiovascular prognosis among those individuals. Premature ventricular complexes are even more common among individuals with heart disease. Premature ventricular complexes can be debilitating, even for healthy individuals.

It is acceptable to have one or two dozens of premature ventricular contractions every day. Almost 30% of all healthy individuals display premature ventricular contractions during exercise stress testing. Male sex, stress, nervousness, tobacco, coffee, hypokalemia, infection, alcohol, sleep deprivation and certain drugs are associated with increased occurrence of premature ventricular beats. Moreover, the frequency of premature beats increase with age.

Healthy individuals might display premature ventricular complexes on ECG during screening. It may be symptomatic or asymptomatic. Palpitations and the feeling that the heart "skips a beat" are common symptoms. Chest or throat discomfort is less common.

A few premature ventricular contractions on a daily basis in otherwise healthy individuals is considered benign and has no effect on cardiovascular prognosis. However, if ventricular premature beats make up a significant proportion of all heart beats during the day, the situation is more problematic. If >15% of all beats are premature ventricular beats there is actually a risk of PVC-induced cardiomyopathy and left ventricular dysfunction. In such cases it is wise to refer to patient for invasive examination; it is often possible to eliminate the ectopic focus (foci) by means of ablation therapy. This can also reverse established cardiomyopathy.

Premature ventricular beats are common among those with heart disease. The frequency of premature beats is increased in a wide range of conditions, such as ischemic (coronary) heart disease. These individuals are generally more affected by the premature beats, as they already have compromised cardiac function. Because premature ventricular beats have ineffective ventricular contraction, it can reduce cardiac output and thus cause deterioration of ischemic heart disease and heart failure.

R-on-T phenomenon has been discussed here.

Underlying heart disease must be ruled out among persons without previously known heart disease. The procedure must be individualized and guided by ECG, anamnesis and findings from physical examination. Rather few otherwise healthy individuals necessitate treatment. Among those with heart disease, the proclivity to treat should be higher. Before treatment is instigated, it is important to analyse potassium and magnesium levels because hypokalemia and hypomagnesemia may cause PVCs and these causes are reversible.

Treatment is instigated if (1) symptoms are significant, (2) of PVCs make up a significant portion of all beats during the day (examined with Holter-ECG), or (3) if the PVCs have a negative hemodynamic effect. First choice of drug is beta-blockers (bisoprolol 5–10 mg once daily or sustained-release metoprolol 50–100 mg once daily). However, beta-blockers are often insufficient and symptoms may persist. Class I antiarrhythmic drugs can be tried, as can amiodarone. One should have invasive treatment with ablation in mind.

Normal Sinus Rhythm

Premature atrial contractions

Aberrant ventricular conduction (aberration, aberrancy)

A premature ventricular complex (PVC) is a premature beat arising from an ectopic focus within the ventricles. AKA: ventricular ectopics, ventricular extrasystoles, ventricular premature beats, ventricular premature depolarisations.

Appropriate discordance describes a pattern of repolarisation abnormality (typically seen with left bundle branch block, paced rhythms, VT) in which the ST segment and T wave are directed opposite to the main vector of the QRS complex. Because there is abnormal depolarisation, there is subsequent abnormal repolarisation which is discordant:

With a full compensatory pause, the next normal beat arrives after an interval that is equal to double the preceding R-R interval

Retrograde capture describes the process whereby the ectopic impulse is conducted retrogradely through the AV node, producing atrial depolarisation. This is visible on the ECG as an inverted P wave (“retrograde P wave“), usually occurring after the QRS complex.

PVCs are said to be “frequent” if there are more than 5 PVCs per minute on the routine ECG, or more than 10-30 per hour during ambulatory monitoring.

PVCs may be either:

The origin of each PVC can be discerned from the QRS morphology:

PVCs often occur in repeating patterns:

Frequent PVCs are usually benign, except in the context of an prolonged QTc, when they may predispose to malignant ventricular arrhythmias such as Torsades de Pointes by causing “R on T” phenomenon

Frequent or symptomatic PVCs may be due to:

When is a PVC not a PVC?

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