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.
Phosphodiesterase inhibitors such as caffeine directly affect the G-coupled signal transduction cascade by inhibiting the enzyme that catalyzes the breakdown of cAMP, again leading to the increased concentration of calcium ions in the cytosol.potassium deficiency: Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells, and hypokalemia makes it more likely that cells will depolarize spontaneously. Hypercalcemia has a similar effect, although clinically it is of less concern. magnesium deficiency: 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. Low blood magnesium therefore also makes spontaneous depolarization more likely. myocardium damage:  Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes. Diagnosis
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.