Premature ventricular contraction


Premature ventricular contraction
Premature ventricular contraction
Classification and external resources

A premature ventricular contraction marked by the arrow.
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 lungs and to the rest of the body. 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]

Contents

Causes

Premature ventricular contraction in an ECG (arrows)

Premature ventricular contractions can occur in a healthy person of any age, but are more prevalent in the elderly and in men.[2] They frequently occur spontaneously with no known cause.

Some possible causes include:

Symptoms

A PVC 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.[6] Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a dangerous rapid heartbeat.

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’ 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.[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 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. A unifocal PVC is where the depolarisation is triggered from the one 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 depolarisation 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.[11]

Treatment

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
    • Antiarrhythmics:[2] these agents alter the electrophysiologic mechanisms responsible for PVCs
    • Beta blockers[6]
    • Calcium channel blockers[6]
  • Electrolytes replacement
    • Magnesium supplements (e.g. magnesium citrate, orotate, 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]

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][clarification needed]

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 receptor1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein.[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 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.

See also

References

  1. ^ Stanfield, C.; Germann, W. (2008), Principles of Human Physiology (3rd ed.), Pearson International Edition, p. 378, ISBN 0321455061 
  2. ^ a b c d e f g h i j k l m n Premature ventricular contraction at eMedicine
  3. ^ a b c 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, http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2427047 
  4. ^ Health encyclopedia – diseases and conditions. The heathcentral network. Accessed Feb 8th 2009.
  5. ^ MedlinePlus Encyclopedia Ectopic heartbeat
  6. ^ a b c d e f g [Leonard I Ganz, MD, http://www.uptodate.com/patients/content/topic.do?topicKey=hrt_dis/11733, Up-to-date patient information, Updated Sep 11th 2007, reviewed Oct 2008, Accessed Feb 9th 2009.]
  7. ^ a b Guyton MD, Arthur C.; Hall, John E. (2006), Textbook of medical physiology (11th ed.), p. 151, ISBN 0721602401 
  8. ^ a b Zimetbaum P, Josephson ME (May 1998), "Evaluation of patients with palpitations", N. Engl. J. Med. 338 (19): 1369–73, doi:10.1056/NEJM199805073381907, PMID 9571258, http://content.nejm.org/cgi/content/full/338/19/1369 
  9. ^ 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 
  10. ^ a b Levy 2007, pp. 49–50
  11. ^ a b 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, http://books.google.com/books?id=KaegPx6LK2sC&pg=PA390&dq=unifocal+premature+ventricular+contraction&client 
  12. ^ Belhassen B (April 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, http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(05)00234-2 
  13. ^ Shiraishi, Hirokazu; Ishibashi, Kazuya; Urao, Norifumi; Tsukamoto, Masaki; Hyogo, Masayuki; Keira, Natsuya; Hirasaki, Satoshi; Shirayama, Takeshi et al. (2002), "A case of cardiomyopathy induced by premature ventricular complexes", Circulation 66 (11): 1065–7, doi:10.1253/circj.66.1065 
  14. ^ a b Nelson 2008, p. 424
  15. ^ Levy 2007, p. 62
  16. ^ Levy 2007, p. 24
  17. ^ Nelson 2008, p. 430

Further reading

  • Levy, M.N.; Pappano, A.J. (2007), Cardiovascular physiology (9th ed.), Mosby Elsevier, ISBN 0323034462 
  • Nelson, D.L.; Cox, M.M. (2008), Lehninger Principles of Biochemistry (5th ed.), WH Freeman, ISBN 071677108X 

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