Premature ventricular contraction pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* | * 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 in one direction, so there is no neutralisation effect and this results in the high voltage QRS wave in the electrocardiograph. | ||
* | * There are two main physiological explanations for premature ventricular contractions: | ||
**1. [[Cardiac dysrhythmia#Re-entry|Re-entrant signalling]] | |||
**2. 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. | |||
===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 or [[hypovolemia]]. This activation can cause a release of [[catecholamines]] such as [[epinephrine]] (adrenaline) which can bind to [[beta-1 adrenergic receptor]] (β<sub>1</sub> receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called [[Gs (protein)|G<sub>s</sub> protein]].<ref name="nelson">{{harvnb|Nelson|2008|p=424}}</ref> This type of protein stimulates the production of cAMP,<ref>{{harvnb|Levy|2007|p=62}}</ref> ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.<ref>{{harvnb|Levy|2007|p=24}}</ref><br /> This has the effect of increasing the strength of contraction (inotropy) and 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<ref>{{harvnb|Nelson|2008|p=430}}</ref> by inhibiting the enzyme that catalyzes the breakdown of cAMP,<ref name="nelson"/> 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. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 17:24, 27 August 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]
Overview
Premature ventricular contraction 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.
Pathophysiology
- 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 in one direction, so there is no neutralisation effect and this results in the high voltage QRS wave in the electrocardiograph.
- There are two main physiological explanations for premature ventricular contractions:
- 1. Re-entrant signalling
- 2. 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.
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 or hypovolemia. 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.[1] This type of protein stimulates the production of cAMP,[2] ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.[3]
This has the effect of increasing the strength of contraction (inotropy) and 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[4] by inhibiting the enzyme that catalyzes the breakdown of cAMP,[1] 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.
References
- ↑ 1.0 1.1 Nelson 2008, p. 424
- ↑ Levy 2007, p. 62
- ↑ Levy 2007, p. 24
- ↑ Nelson 2008, p. 430