Premature ventricular contraction

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Premature ventricular contraction
Classification and external resources
Premature ventricular contraction in an ECG (arrows)
ICD-10	I49.3
ICD-9	427.69
DiseasesDB	32412
eMedicine	emerg/773
MeSH	D018879

A Premature Ventricular Contraction (PVC), also known as a premature ventricular complex, ventricular premature contraction (or complex or complexes) (VPC), ventricular premature beat (VPB), or extrasystole, is a relatively common event where the heartbeat is initiated by the heart ventricles rather than by the sinoatrial node, the normal heartbeat initiator. The electrical events of the heart detected by the electrocardiogram allow a PVC to be easily distinguished from a normal heart beat.

A PVC may be perceived as a "skipped beat" or felt as palpitations in the chest. In a normal heartbeat, the ventricles contract after the atria have helped to fill them by contracting; in this way the ventricles can pump a maximized amount of blood both to the body and to the lungs. In a PVC, the ventricles contract first, which means that circulation is inefficient. However, single beat PVC arrhythmias do not usually pose a danger and can be asymptomatic in healthy individuals^[1].

	PVC recording An audio clip recording of a PVC symptom, made with a cardiac event monitor.
Problems listening to this file? See media help.

	PVC recording A full 2 minute cardiac event monitor recording with many PVC symptoms around mid-recording.
Problems listening to this file? See media help.

Causes/triggers

Premature ventricular contraction can occur in a healthy person of any age, but becomes more frequent in the elderly, and is more commonly found in men^[2]. PVC frequently occurs spontaneously with no cause.

List of possible causes:

• Ischemia^[3];
• Certain medicines such as digoxin, which increases heart contraction^[2];
• Myocarditis^[2];
• Cardiomyopathy, hypertrophic or dilated^[2];
• Myocardial contusion^[2];
• Hypoxia^[2];
• Hypercapnia (CO2 poisoning)^[2];
• Mitral valve prolapse^[2];
• Smoking^[3];
• Alcohol^[3];
• Drugs such as cocaine^[2];
• Caffeine^[2];
• Tricyclic antidepressants^[2];
• Decreased levels of magnesium and potassium in blood^[2];
• Increased levels of calcium in blood^[2];
• Thyroid problems^[4];
• Chemical (electrolyte) problems in the blood^[5];
• Heart attack^[6];
• Increased levels of adrenaline^[6];
• Lack of sleep/exhaustion^[7];
• Stress^[7];

Symptoms

Premature ventricular contraction is often caused by an underlying disease, which will be exhibiting symptoms of its own, but most PVCs are never felt and thus have no symptoms. However, some people experience heart palpitations (the sensation of a skipped beat)^[6]; and/or

• Chest pain^[6];
• Faint feeling^[6];
• Fatigue^[6];
• Hyperventilation (after exercise)^[6].

Frequent episodes of continuous PVCs becomes a form of ventricular tachycardia (VT), which is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction (Fig1).

Diagnosis

PVCs are usually diagnosed after the patient has described “skipped beats”, pauses or palpitations. Typically the palpitations felt by PVC patients are very irregular and less sustained than patients with other types of arrhythmia. They are likely to have “flip flopping” sensations where it feels like the heart is flipping over or pounding due to there being a pause after the premature contraction and then a powerful contraction after the pause. There is a possibility that they might feel a ‘fluttering’ in their chest or a pounding in their neck but these two types of palpitations aren’t very common in PVC patients^[8].

A physical examination should be conducted after a full history has been taken. This is useful in determining any possible heart defects that might be causing the palpitations. Most cases of premature ventricular contraction have a mitral-valve prolapse which can be determined through the physical examination^[8]. The next step in diagnosis is a 12 lead ECG which can be performed in the doctors’ surgery over a short period of time however this is often non-conclusive in diagnosis because it is not very sensitive and there is a small chance a premature ventricular contraction occurring in the short period of time. Holter monitoring is a far better method for diagnosis as it is continuous recording of the heart’s rhythm over a period of 24hours. This increases the likelihood of a premature ventricular contraction occurring during the recording period and is therefore more useful in diagnosis^[9].

When looking at an electrocardiograph premature ventricular contractions are easily spotted and therefore a definitive diagnosis can be made. The QRS and T waves look very different to normal readings. The spacing between the PVC and the preceding QRS wave is a lot shorter than usual and the time between the PVC and the proceeding QRS is a lot longer. However, the time between the preceding and proceeding QRS waves stays the same as normal due to the compensatory pause^[10]. PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions^[11].

There are four different patterns of premature ventricular contractions. Bigeminy is where one PVC occurs after every normal beat, in an alternating pattern. Trigeminy is where one PVC occurs after every two normal beats. Quadrigeminy is where one PVC occurs after every 3 normal beats of the heart. A unifocal premature ventricular contraction is where the depolarisation is triggered from the one site in the ventricle meaning that the peaks on the ECG look the same. Multifocal premature ventricular contractions arise when more than one site in the ventricles cause depolarisation meaning each peak on the ECG will have a different shape. If 3 or more PVCs occur in a row it is indicative of ventricular tachycardia^[11].

Treatment

Isolated PVCs with beginning characteristics require no treatment. In healthy individuals, PVCs can often be resolved with by restoring the balance of magnesium, calcium and potassium within the body. The most effective treatment is the elimination of triggers (particularly the cessation of the abuse of substances such as caffeine, and illegal drugs.)

• Pharmacological agents
  • Beta blockers^[6]
  • Calcium channel blockers^[6]
• Electrolytes replacement
  • Magnesium supplements (e.g. magnesium citrate, orate, Maalox, etc.)
  • Potassium supplements
• Radiofrequency catheter ablation treatment^[6]
• Lifestyle modification
  • Frequently stressed individuals should consider therapy, or joining a support group.
  • Heart attacks can increase the likelihood of having PVCs^[6], so exercise and a healthy diet will decrease PVCs by reducing the risk of heart attacks.

In the setting of existing cardiac disease, however, PVCs must be watched carefully, as they may cause a form of ventricular tachycardia (rapid heartbeat).

Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses^[12][13].

Pathophysiology

Normally impulses pass through both ventricles almost simultaneously, the depolarisation waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels in one direction therefore there is no neutralisation effect which results in the high voltage QRS wave in the electrocardiograph.

There are two main physiological explanations for premature ventricular contractions: re-entrant signalling and “enhanced automaticity in some ectopic focus”. The enhanced automaticity means that the ectopic centre fires more regularly than usual and is protected from depolarisation that results in premature contractions^[10].

Molecular Basis

There are a number of different molecular explanations for PVCs. One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the ventricular cardiac myocytes 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 hemorrhage. 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 calledG_s proteins^[14] . This type of protein stimulates the production of cAMP^[15], ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol^[16].
  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 directly affect the G-coupled signal transduction cascade^[17] by inhibiting the enzyme that catalyzes the breakdown of cAMP^[14], 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, and they 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 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.

See also

• Bigeminy
• Heart rate turbulence
• Premature atrial contraction

References