Premature ventricular contraction
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|Premature ventricular contraction|
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A premature ventricular contraction marked by the arrow.
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 ventricular extrasystole (VES), is a relatively common event where the heartbeat is initiated by Purkinje fibres in the 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. Although a PVC can be a sign of decreased oxygenation to the myocardium (cardiac muscle) often PVCs are benign and may even be found in otherwise healthy hearts. 
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 lungs and to the rest of the body. In a PVC, the ventricles contract first and before the atria have optimally filled the ventricles with blood, which means that circulation is inefficient. However, single beat PVC arrhythmias do not usually pose a danger and can be asymptomatic in healthy individuals.
Premature ventricular contractions can occur in a healthy person of any age, but are more prevalent in the elderly and in men. They frequently occur spontaneously with no known cause. Heart rate turbulence (HRT) is a phenomenon representing the return to equilibrium of the heart rate after a PVC. HRT parameters correlate significantly with mortality after myocardial infarction (heart attack). Some possible causes of PVCs include:
- Adrenaline excess;
- Calcium excess;
- Cardiomyopathy, hypertrophic or dilated;
- Certain medicines such as digoxin, which increases heart contraction
- Chemical (electrolyte) problems in the blood;
- Contact with Carina (trachea/bronchi) when performing medical suctioning stimulates vagus nerve
- Drugs such as:
- Heart attack;
- Hypercapnia (CO2 poisoning);
- Lack of sleep/exhaustion;
- Magnesium and potassium deficiency;
- Mitral valve prolapse;
- Myocardial contusion;
- Sarcoidosis;
- Theobromine;
- Thyroid problems;
- Tricyclic antidepressants;
Signs and symptoms
Although there are many signs and symptoms associated with PVCs, PVCs may have no symptom at all. An isolated PVC is hard to catch without the use of a Holter monitor. PVCs may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a potentially fatal cardiac arrhythmia.
Some other possible signs and symptoms of PVCs:
- Abnormal EKG
- Irregular heart beat
- Shortness of breath
- Feeling your heart beat (palpitations)
- Feeling of occasional, forceful beats
- Increased awareness of your heart beat
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.
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. For example, some cases of premature ventricular contraction have a mitral-valve prolapse which can be determined through the physical examination. The next step in diagnosis is a 12 lead ECG which can be performed in the doctors’ office over a short period of time however this is often non-conclusive in diagnosis because it is not very sensitive and there is only a small chance of 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 24 hours, or event monitoring which records noncontinuously for 30 days or indefinitely. This increases the likelihood of a premature ventricular contraction occurring during the recording period and is therefore more useful in diagnosis.
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 from 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. PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions.
There are four different named patterns of regularly occurring PVCs. Depending whether there are 1, 2, or 3 normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. Unifocal PVCs are triggered from a single site in the ventricle, causing the peaks on the ECG to look the same. Multifocal PVCs arise when more than one site in the ventricles initiate depolarization, causing each peak on the ECG to have a different shape. If 3 or more PVCs occur in a row it may be called Ventricular tachycardia.
One study has suggested that in the absence of structural heart disease, even frequent (> 60/h or 1/min) and complex premature ventricular contractions are associated with a benign prognosis. On the other hand, the Framingham Heart Study reported that PVCs were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death. These results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.
Isolated PVCs with benign characteristics require no treatment. In healthy individuals, PVCs can often be resolved 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 use of substances such as caffeine, and certain drugs.)
- Pharmacological agents
- Electrolytes replacement
- Magnesium supplements (e.g. magnesium citrate, orotate, Maalox, etc.)
- Potassium supplements (e.g. chloride potassium with citrate ion)
- Radiofrequency catheter ablation treatment
- Lifestyle modification
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. In patients with no known coronary artery disease (CAD), the presence of frequent premature ventricular contractions (PVCs) is linked to acute myocardial infarction and sudden death. The Framingham Heart Study defines frequent as >30 PVCs per hour. The American College of Cardiology and the American Heart Association recommend evaluation for CAD in patients who have frequent PVCs and cardiac risk factors, such as hypertension and smoking (SOR C). Evaluation for CAD may include stress testing, echocardiography, and ambulatory rhythm monitoring.
Normally impulses pass through both ventricles almost simultaneously 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 neutralisation 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 signalling, 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 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).
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 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.
- 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 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 are 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.
- What is a PVC[dead link]
- Stanfield, C.; Germann, W. (2008), Principles of Human Physiology (3rd ed.), Pearson International Edition, p. 378, ISBN 0-321-45506-1
- Premature ventricular contraction at eMedicine
- Francis J, Watanabe MA, Schmidt G. (January 2005), "Heart rate turbulence: a new predictor for risk of sudden cardiac death.", Ann Noninvasive Electrocardiol. 10: 102–9, PMID 15649245
- http://www.uptodate.com/patients/content/topic.do?topicKey=hrt_dis/11733, Up-to-date
- MedlinePlus Encyclopedia Ectopic heartbeat
- Emilsson K (June 2008), "Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report", J Med Case Reports 2: 192, doi:10.1186/1752-1947-2-192, PMC 2427047, PMID 18522736
- "Premature ventricular contractions (PVCs) Causes". Diseases and Conditions. Mayo Clinic.
- Guyton MD, Arthur C.; Hall, John E. (2006). Textbook of medical physiology (11th ed.). p. 151. ISBN 0-7216-0240-1.
- "Premature Ventricular Contractions". HealthCentral.
- Zimetbaum P, Josephson ME (1998). "Evaluation of patients with palpitations". N. Engl. J. Med. 338 (19): 1369–73. doi:10.1056/NEJM199805073381907. PMID 9571258.
- Meurs KM, Spier AW, Wright NA, Hamlin RL (January 2001). "Comparison of in-hospital versus 24-hour ambulatory electrocardiography for detection of ventricular premature complexes in mature Boxers". J. Am. Vet. Med. Assoc. 218 (2): 222–4. doi:10.2460/javma.2001.218.222. PMID 11195827.
- Levy 2007, pp. 49–50
- Haist, Steven A.; Gomella, Leonard G. (2004), "19 Basic ECG Reading: Ventricular Arrhythmias", Clinician's pocket reference (10th ed.), New York: McGraw-Hill, p. 390, ISBN 0-07-140255-1
- Ng GA (2006). "Treating patients with ventricular ectopic beats". Heart 92 (11): 1707. doi:10.1136/hrt.2005.067843. PMID 17041126.
- Belhassen B (2005). "Radiofrequency ablation of "benign" right ventricular outflow tract extrasystoles: a therapy that has found its disease?". J. Am. Coll. Cardiol. 45 (8): 1266–8. doi:10.1016/j.jacc.2005.01.028. PMID 15837260.
- Shiraishi H, Ishibashi K, Urao N, Tsukamoto M, Hyogo M, Keira N, Hirasaki S, Shirayama T, Nakagawa M (2002). "A case of cardiomyopathy induced by premature ventricular complexes". Circ. J. 66 (11): 1065–7. doi:10.1253/circj.66.1065. PMID 12419942.
- Medscape: Medscape Access, Emedicine.medscape.com, retrieved 2014-02-15
- Nelson 2008, p. 424
- Levy 2007, p. 62
- Levy 2007, p. 24
- Nelson 2008, p. 430
- Levy, M.N.; Pappano, A.J. (2007). Cardiovascular physiology (9th ed.). Mosby Elsevier. ISBN 0-323-03446-2.
- Nelson, D.L.; Cox, M.M. (2008). Lehninger Principles of Biochemistry (5th ed.). WH Freeman. ISBN 0-7167-7108-X.