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. calcium excess:  One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the muscle cells of the hearts ventricles leading to increased flow of calcium ions into the cell. This may happen for the following reasons:Activation of the sympathetic nervous system, due to anxiety and/or physiological stress, for example hypovolemia caused by dehydration or bleeding. This activation can cause a release of catecholamines such as epinephrine (adrenaline) which can bind to beta-1 adrenergic receptor (β1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein. This type of protein stimulates the production of cAMP, ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol. This has the effect of (1) increasing the strength of contraction (inotropy) and (2) depolarizing the myocyte more rapidly (chronotropy). The ventricular myocytes are therefore 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.
Therapists may use a combination of physical and psychological measures, such as cognitive-behavioral-therapy and applied tension (AT), in order to aid in extinguishing the individuals fear response.Early studies of methods to combat vasovagal fainting found that certain leg exercises and that individuals making themselves angry over imagined scenarios could increase blood pressure, thus elevating cerebral blood flow and preventing fainting upon exposure to a phobic trigger. A later study tested applied muscle tension as a way of preventing fainting when an individual with a fear of injuries was exposed to triggering visual stimuli. Lars-Göran Öst expanded upon this research, having BII-phobic individuals engage in applied muscle tension while shown blood stimuli. Those who were trained in the technique showed notable symptom improvement over the course of five one-hour treatment sessions.An AT treatment program most often involves an individual being instructed to clench their arm, leg, and chest muscles in 10 to 15 second intervals as they are systematically exposed to triggers of increasing likeness to real blood or needles. This program is designed to increase heart rate and blood pressure, counteracting vasovagal response.The method of applied tension remains popular — it is the most common BII phobia treatment suggestion, and has been found to be highly effective in a majority of BII-phobics. However, exposure-only cognitive-behavioral therapy (CBT) can also be effective, as can the method of applied relaxation (AR).CBT is a technique which promotes fear extinguishment by way of gradual, repeated exposure to feared stimuli.