Premature ventricular contraction (PVC), also known as ventricular premature beat (VPB) or extrasystole, is a form of irregular heartbeat in which the ventricle contracts prematurely. This may be perceived as a "skipped beat" or as palpitations. The depolarization of cardiac myocytes begins in the ventricle instead of the usual place, the sinoatrial node. PVCs can be a useful natural probe, since they induce Heart rate turbulence whose characteristics can be measured, and used to evaluate cardiac function.
In children, PVCs occur less frequently than in adults, although healthy children are known to have episodes of PVC. In fact, on routine monitoring of children aged 10-13 years with a Holter monitor, about 20% of healthy boys had occurrences of PVC. In otherwise healthy newborns, PVCs will often resolve on their own by the 12th week of life, and almost never require treatment.
In people who work swing shifts and nights, studies have shown as high as 40% have PVCs. Most people over 40 years of age have PVCs whether they realize it or not.
Heart conditions or a previous history of heart attack, ischemia, myocarditis, dilated or hypertrophic cardiomyopathy, myocardial contusion, atrial fibrillation and mitral valve prolapse may cause PVC. Patients with hypomagnesemia, hypokalemia, and hypercalcemia may also present with PVC.
PVCs in young children are thought to be associated with developmental factors of the autonomic nervous system. In older children, sympathomimetic drugs, such as cold or asthma medication may cause PVCs, along with mild cases of viral myocarditis.
In the case of ventricular premature beats, a focus in the ventricle depolarizes before the SA node has time to recover and initiate another wave of depolarization. Because the focus is usually outside of the intraventricular conduction system, the ventricles will not contract synchronously, and the wave of depolarization will spread in an abnormal manner. Partly because ventricular diastole is interrupted, causing incomplete filling, and partly because the wave of depolarization is abnormal and may not generate a sufficiently organized contraction, the premature beat is generally weaker than a normally conducted beat. This may be perceived as a "skipped beat", as the arterial impulse will be weaker than normal. This results in a decreased stroke volume and an increased end-systolic volume. It is thought that the normal P wave originating from the SA node occurs during the PVC, causing the atria to remain refractory to any stimuli. This results in a complete compensatory pause as the interval between the last normal QRS and the next normal QRS is generally equal to twice the average R-R interval. In some cases, the abnormal wave of depolarization will also travel through the conduction system in a retrograde fashion, and depolarize the atria and SA node as well, and allowing repolarization to occur sooner. This results in an incomplete compensatory pause and the interval between the last normal QRS and the next normal QRS will be less than twice the average R-R interval. In some cases, the PVC does not affect the atria at all, and the next P wave and normal QRS occurs as if the PVC was not present, and there is no compensatory pause. These types of PVC are called interpolated PVCs.
Because diastole is prolonged due to the delay while the SA node repolarizes, the end-diastolic volume is higher than normal as well. In a healthy heart, in concordance with the Frank-Starling curve, this will create a higher than normal stroke volume on the next normal beat. This transient increase in stroke volume may be perceived as a palpitation.
On history, the patient may describe "skipped beats", pauses, or palpitations.
On physical exam, PVCs will manifest as an S1 occurring earlier than expected. The following S1 will occur much later than expected. On the actual PVC, the arterial impulse may be weaker than normal, while on the following normal QRS, the arterial impulse may be stronger than normal.
PVCs must be differentiated from premature atrial contractions (PACs). If the pause is present but the beat is not obviously premature, then alternative diagnoses must be considered.
PVCs are definitively diagnosed by an ECG or a TMT but some patients will need to wear a Holter monitor or a cardiac event monitor to record PVCs that occur outside the doctor's office or hospital. PVCs are often benign but may be a sign of a heart condition. On the ECG, PVCs are diagnosed by: 1. prematurity (occurring before the next expected normal QRS) 2. an abnormal appearing, wide QRS complex 3. the presence (usually) of a compensatory pause. PVCs may be unifocal (coming from the same area of the ventricles) or multifocal (coming from different areas of the ventricle). Unifocal PVCs are more characteristic of a benign condition, and manifest as abnormal, wide QRS complexes with identical morphologies. These are described as monomorphic PVCs. Multifocal PVCs manifest with varying morphologies and varying dominant axises, and are described as polymorphic PVCs. Multifocal PVCs are more concerning of a possible pathology.
PVCs may occur at regular intervals. If a PVC occurs after every normal QRS, this is termed ventricular bigeminy. If it occurs after every two normal QRS complexes, this is termed ventricular trigeminy. If it occurs after every three normal QRS complexes, this is termed ventricular quadrigeminy. On physical exam, this will manifest as an irregular rhythm, usually described as regularly irregular (in contrast to the irregularly irregular rhythm of atrial fibrillation.) While these rhythms may be benign as well, they may also herald dysfunction in the conduction system.
If more than one ventricular beat occurs in sequence, this is a sign of a more ominous condition. Two ventricular beats in sequence are termed a couplet. Three or more ventricular beats in sequence occurring at a rapid rate (above 100 bpm, but usually greater than 150 bpm) is termed ventricular tachycardia. At slower rates, it is called idioventricular rhythm.
Anxiety and physiologic stress (for example, hypovolemia caused by dehydration or hemorrhage) will activate the sympathetic nervous system, causing a surge of catecholamines (epinephrine and norepinephrine) Both of these neuroendocrine hormones will bind to β1 receptors on cardiac myocytes, activating Gs proteins and resulting in a signal transduction cascade that generates cyclic AMP(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.
Phosphodiesterase inhibitors such as caffeine, theobromine (found in chocolate), theophylline, and milrinone 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 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 ions affect the flow of calcium ions, affect the function of the Na+/K+ ATPase, and is necessary for maintaining potassium levels. Hypomagnesemia therefore also makes spontaneous depolarization more likely.
Existing damage to the myocardium can also provoke PVCs. The 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.
Isolated PVCs with benign characteristics require no treatment.
In the setting of existing cardiac disease, however, PVCs must be watched carefully, as they may result in a run of ventricular tachycardia, or even ventricular fibrillation. It is recommended that serum potassium should be in the high-normal range (K+>4 meq/dl) as hypokalemia favors the development of arrhythmia. In patients with existing coronary artery disease or ischemic cardiomyopathy, they should be on a beta-blocker. If the ejection fraction is less than 30%, placement of an automatic implantable cardioverter-defibrillator is indicated.
One hundred and seven middle aged and senile cases of coronary heart disease with ventricular premature beat treated by Qing Xin An Shen Fang.(Abstracts: The Journal of Traditional Chinese Medicine Abstracts December 2001)
Jun 01, 2002; Treatment of premature ventricular beat in 164 cases of coronary heart disease, using the formula Qing Xin An Shen Fang was...