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. 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. 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.
Signs and symptoms 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. Symptoms may be more pronounced 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, 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. Physical examination is focused on identifying evidence of underlying heart disease.
Causes
Premature ventricular contractions occur in healthy persons of any age, but are more prevalent in the elderly and in men. In a very significant proportion of people they occur spontaneously with no known cause. Some possible underlying causes of PVCs include:
Non-cardiac causes Adrenaline excess Anemia Catecholamine excess Certain medicines such as tricyclic antidepressants, digoxin, sympathomimetics, aminophylline Chemical (electrolyte) abnormalities in the blood (for example hypokalemia (low blood potassium), which can occur in those taking diuretics ("water pills") and hypomagnesaemia (magnesium deficiency)). Contact with the carina (trachea/bronchi) when performing medical suctioning stimulates vagus nerve Drugs/substances such as: Amphetamines Alcohol Caffeine Cocaine Nicotine Theobromine Hypercapnia (CO2 poisoning) Hypertension (high blood pressure) Hyperthyroidism High blood calcium Hypoxia and/or hypercapnia Lack of sleep/exhaustion Sarcoidosis Smoking Stress Anxiety
Cardiac causes Any structural heart disease which alters electrical conduction pathways due to tissue alterations Cardiomyopathy, hypertrophic or dilated Myocardial infarction Myocarditis Myocardial contusion Mitral valve prolapse
Pathophysiology
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.
Molecular basis There are a number of different molecular explanations for PVCs.
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