Premature ventricular contraction (PVCs)




A premature ventricular contraction (PVC) is a relatively common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. 



PVCs may cause no symptoms.



In general, PVCs are harmless, but frequent PVCs may increase the risk of developing arrhythmias or cardiomyopathy, which can greatly and permanently impair heart function.


Single PVCs are common in healthy persons. 41% of healthy volunteers below the age of 45 years have been found to have PVCs on 24-hour Holter ECG recording.


Frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms .


PVCs may be perceived as a skipped beat or felt as palpitations in the chest. 


Single beat PVCs do not usually pose a danger.


The  electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. 


Frequent PVCs can be symptomatic of an underlying heart condition.


With very frequent, over 20% of all heartbeats, PVCs are considered a risk factor for arrhythmia-induced cardiomyopathy when heart muscle becomes less effective and symptoms of heart failure may develop.


Echocardiography of the heart is commanded  study in people with PVCs.


Frequent or troublesome PVCs can be managed with beta blockers, certain calcium channel blockers,and 

dilated cardiomyopathy may be treated with radiofrequency ablation.


While PVCs may be asymptomatic, they may be felt as a skipped heart beat, a strong beat, palpitations, lightheadedness, and may cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise.


Symptoms are enhanced at times of stress. 


Women may be more aware of PVCs at the time of the menstrual period


Premature ventricular contractions may be associated with underlying heart disease.


In evaluating PVCs, history of the presence of signs of heart disease or a known history of heart disease, as well as heart disease or sudden cardiac death in close relatives is important.


PVCs and palpitation associated with syncope or provoked by exertion are also concerning.


Premature ventricular contractions can occur in a healthy person of any age.


PVCs are more prevalent in the elderly and in men.


PVCs occur in a very significant proportion of people spontaneously with no known cause. 


Underlying causes of PVCs include:


Adrenaline excess


High blood calcium


Cardiomyopathy, hypertrophic or dilated


Medicines such as digoxin, which increases heart contraction or tricyclic antidepressants


Electrolyte abnormalities in the blood: hypokalemia, hypomagnesaemia.


Irritation of the carina/ trachea/bronchi when performing medical suctioning stimulates vagus nerve










Myocardial infarction








Lack of sleep/exhaustion


Mitral valve prolapse


Myocardial contusion










Cardiac 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. 

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.

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

Ectopic enhanced nodal automaticity indicates a foci of sub-pulmonic valvular pacemaker cells that have a subthreshold potential for firing: the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly hypokalemia.


The  reentry mechanism occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. 


The  reentry mechanism 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 in the reentry mechanism, 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: resulting in an extra beat. 


Reentry can produce single ectopic beats, or paroxysmal tachycardia.


Triggered premature ventricular beats are considered to be due to after-depolarizations that are triggered by the preceding action potential. 


Triggered premature ventricular beats are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).


Molecular explanations for PVCs: 


Calcium excess: due to an increased amount of cyclic AMP(cAMP) in the muscle cells of the heart’s ventricles leading to increased flow of calcium ions into the cell. 


Calcium excess: occurs with the activation of the sympathetic nervous system, due to anxiety and/or physiological stress.


Sympathetic activation causes a release of catecholamines such as epinephrine which can bind to beta-1 adrenergic receptors on cardiac myocytes, activating guanosine nucleotide-binding protein (Gs protein) which stimulates the production of cAMP.


cAMP ultimately increased the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.


cAMP activation via the sympathetic nervous system increases the strength of contraction and depolarizers the myocyte more rapidly.


The ventricular myocytes become more irritable than usual, and may depolarize spontaneously before the SA node depolarizes. 


Other sympathomimetic molecules such as amphetamines and cocaine will also cause this effect.


Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells.



Hypokalemia makes it more likely that cells will depolarize spontaneously. 


Hypercalcemia has a similar effect to depolarize, although clinically it is of less concern.


Magnesium ions affect the flow of calcium ions, and they affect the function of the Na+/K+ ATPase, and are necessary for maintaining potassium levels: hypomagesemia makes spontaneous depolarization more likely.


Existing myocardial injury can also provoke PVCs. 


Myyocardial scarring in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. 


Myocardial inflammation in myocarditis and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for  myocardial irritability.


PVCs may be found incidentally on a 12-lead electrocardiogram (ECG/EKG) that is performed for another reason. 



Continuous heart beat recordings are used if symptoms are infrequent, such as a 24- or 48-hour Holter monitor or even 14- to 30-day recorders if the symptoms are very occasional.


Continuous heart beat recordings allow a quantification of the amount of abnormal beats and ensure are no additional heart arrhythmias are present.


PVCs suppressed by exercise, is a favorable finding.


On electrocardiography premature ventricular contractions have a specific appearance of the QRS complexes and T waves, which are different from normal readings. 


PVCs occurs earlier than the regular normally conducted beat. 


The  time between the PVC and the next normal beat is longer as the result of a compensatory pause.


PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions.


Premature atrial contractions and PVCs have different appearances on EKG.



PVCs occur in a predictable pattern:  Depending whether there are one, two, or three normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. 


When 3 or more PVCs occur in a row it may be called ventricular tachycardia.



Monofocal PVCs that all have the same appearance, is a more benign phenomenon. 



PVCs of multiple different appearances, they are multifocal, and this is a possible sign of a greater risk of complications.


Isolated PVCs with benign characteristics and no underlying heart disease require no treatment.


The most effective treatment is the elimination of triggers:  caffeine and certain drugs, like tobacco.


Antiarrhythmics agents alter the electrophysiologic mechanisms responsible for PVCs. 


Encainide and flecainide, suppress PVCs, in patients experiencing myocardial infarction, but they also increase the risk of death. 


Other useful agents measures:


Beta blockers


Calcium channel blockers


Electrolytes replacement


Magnesium supplements 


Potassium supplements 


Radiofrequency catheter ablation treatment.


Radiofrequency catheter ablation treatment is advised for people with ventricular dysfunction and frequent arrhythmias or very frequent PVC (>20% in 24 h) and normal ventricular function.



Implantable cardioverter-defibrillator


Lifestyle modification in stressed individuals.


In general, PVCs are harmless, but frequent PVCs may increase the risk of developing arrhythmias or cardiomyopathy, which can greatly and permanently impair heart function. 


Asymptomatic patients with PVCs who do not have heart disease have long-term prognoses very similar to the general population.


Asymptomatic patients with PVCs and ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. 


Very frequent ventricular ectopy may be associated with cardiomyopathy.


In patients with underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.


Meta-analyses show that people with frequent PVC:  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 without frequent PVC. 

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease: there were no serious cardiac events through 5.6 years on average.


There is an correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. 

In the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis.

The Framingham Heart Study reported that PVCs in apparently healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death.

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%.

Those in ARIC study with any PVC had risk of heart failure increased by 63% and were twice as likely to die from coronary heart disease (CHD). 

The Niigata study of 63,386 people with a 10-year follow-up period of individuals with PVC during a 10-second recording had triple the risk of atrial fibrillation of those without PVC.

Reducing frequent PVC by 20% or more, by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.

Extremely frequent PVCs of several thousand a day, can be associated with a dilated cardiomyopathy. 

Rates of PVCs vary by age with under 1% for those under the age of 11 and 69% in those older than 75 years.

Ventricular ectopy is more prevalent in men than in women of the same age.

Ventricular ectopy prevalence ranges from less than 3% for young white women without heart disease to almost 20% for older African American individuals with hypertension.






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