Ventricular tachycardia pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Ventricular tachycardia}} | {{Ventricular tachycardia}} | ||
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | ||
==Overview== | ==Overview== | ||
The underlying mechanism of VT is due to [[automaticity]] arising in either the [[myocardium]] or in the distal conduction system. | The underlying mechanism of [[VT]] is due to [[automaticity]] arising in either the [[myocardium]] or in the distal [[conduction system]]. The most common underlying substrate for [[ventricular tachycardia]] is [[ischemic heart disease]]. [[ Myocardial]] scarring from any process increases the likelihood of electrical [[reentrant]] circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. [[Ventricular]] scar formation from a prior [[Myocardial infarction|myocardial infarction (MI)]] is the most common cause of sustained [[monomorphic VT]]. The morphology of [[ventricular tachycardia]] often depends on its cause. [[VT]] in a [[structurally normal heart]] typically results from mechanisms such as triggered activity and enhanced [[automaticity]]. If [[VT]] is hemodynamically tolerated, the incessant [[tachyarrhythmia]] may cause a [[dilated cardiomyopathy]]. This may develop over a period of weeks to years and may resolve with successful suppression of the [[VT]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Pathophysiology of ventricular tachycardia can be better studied depending upon the subclass:<ref name="pmid28855272">{{cite journal |vauthors=Martin CA, Lambiase PD |title=Pathophysiology, diagnosis and treatment of tachycardiomyopathy |journal=Heart |volume=103 |issue=19 |pages=1543–1552 |date=October 2017 |pmid=28855272 |pmc=5629945 |doi=10.1136/heartjnl-2016-310391 |url=}}</ref><ref name="pmid9058854">{{cite journal |vauthors=Simons GR, Klein GJ, Natale A |title=Ventricular tachycardia: pathophysiology and radiofrequency catheter ablation |journal=Pacing Clin Electrophysiol |volume=20 |issue=2 Pt 2 |pages=534–51 |date=February 1997 |pmid=9058854 |doi=10.1111/j.1540-8159.1997.tb06209.x |url=}}</ref><ref name="pmid15137521">{{cite journal |vauthors=Brunckhorst C, Delacretaz E |title=[Ventricular tachycardia--etiology, mechanisms and therapy] |language=German |journal=Ther Umsch |volume=61 |issue=4 |pages=257–64 |date=April 2004 |pmid=15137521 |doi=10.1024/0040-5930.61.4.257 |url=}}</ref><ref name="pmid19589116">{{cite journal |vauthors=Srivathsan K, Ng DW, Mookadam F |title=Ventricular tachycardia and ventricular fibrillation |journal=Expert Rev Cardiovasc Ther |volume=7 |issue=7 |pages=801–9 |date=July 2009 |pmid=19589116 |doi=10.1586/erc.09.69 |url=}}</ref> | |||
==== Cellular level ==== | |||
* [[Electrical reentry]] or abnormal [[automaticity]] is the main reason behind [[ventricular tachycardia]]. | |||
** [[Myocardial]] scarring from any process increases the likelihood of [[electrical reentrant circuits]]. | |||
** These circuits generally include a zone where normal electrical propagation is slowed by the [[scar]]. | |||
**[[ Ventricular scar]] formation from a prior [[Myocardial infarction|myocardial infarction (MI)]] is the most common cause of sustained monomorphic VT. | |||
* [[VT]] in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced [[automaticity]]. | |||
*[[Torsade de pointes]] seen in the [[Long QT syndrome|long QT syndromes]] is likely a combination of triggered activity and [[ventricular reentry]]. | |||
* During [[VT]], [[cardiac output]] is reduced as a consequence of decreased [[ventricular] filling from the rapid heart rate and the lack of properly timed or coordinated [[atrial]] contraction. | |||
* [[Ischemia]] and [[mitral insufficiency]] may also contribute to decreased [[ventricular]] stroke output and hemodynamic intolerance. | |||
* Hemodynamic collapse is more likely when underlying [[left ventricular]] dysfunction is present or when [[heart rates ]] are very rapid. | |||
* Diminished [[cardiac output]] may result in diminished [[myocardial perfusion]], worsening [[inotropic]] response, and degeneration to [[Ventricular fibrillation|ventricular fibrillation (VF)]], resulting in [[sudden death]]. | |||
* In [[patients]] with [[monomorphic VT]], [[mortality]] risk correlates with the degree of [[structural heart disease]]. Underlying [[structural heart diseases]] such as [[ischemic cardiomyopathy]], [[dilated cardiomyopathy]], [[hypertrophic cardiomyopathy]], [[Chagas disease]], and [[Right ventricular failure|right ventricular dysplasia]] have all been associated with degeneration of [[monomorphic ]] or [[polymorphic VT]] to [[VF]]. | |||
* Even without such degeneration, [[VT]] can also produce [[congestive heart failure]] and hemodynamic compromise, with subsequent [[morbidity ]] and [[mortality]]. | |||
* If [[VT]] is hemodynamically tolerated, the incessant [[tachyarrhythmia]] may cause a [[dilated cardiomyopathy]]. This may develop over a period of weeks to years and may resolve with successful suppression of the [[VT]]. | |||
===Monomorphic Ventricular Tachycardia=== | ===Monomorphic Ventricular Tachycardia=== | ||
=== | * There are two reasons the morphology of the [[QRS]] does not vary in [[monomorphic ventricular tachycardia]]: | ||
* | **A single site that generates [[cardiac arrhythmia#origin of impulse|automaticity]] of a single point in either the left or right [[ventricle]]. | ||
*[[ | **A [[cardiac arrhythmia#origin of impulse|reentry]] circuit within the [[ventricle]]. | ||
* | |||
===[[Polymorphic Ventricular Tachycardia]]=== | |||
* [[Polymorphic ventricular tachycardia]], on the other hand, is most commonly caused by abnormalities of [[myocardium|ventricular muscle]] repolarization. | |||
* The predisposition to this problem usually manifests on the [[ECG]] as a prolongation of the [[QT interval]]. | |||
* [[QT prolongation]] may be congenital or acquired. | |||
* Congenital problems include [[long QT syndrome]] and [[catecholaminergic polymorphic ventricular tachycardia]]. | |||
* Acquired problems are usually related to [[drug toxicity]] or [[electrolyte abnormalities]], but can occur as a result of [[myocardial ischemia]]. | |||
* Class III [[anti-arrhythmic]] drugs such as [[sotalol]] and [[amiodarone]] prolong the [[QT interval]] and may in some circumstances be pro-arrhythmic. | |||
* Other relatively common drugs including some [[antibiotics]] and [[antihistamines]] may also be a danger, particularly in combination with one another. | |||
* Problems with [[blood]] levels of [[potassium]], [[magnesium]] and [[calcium]] may also contribute. High dose [[magnesium]] is often used as an [[antidote]] in [[cardiac arrest]] protocols. | |||
=== | ===[[Bundle Branch Re-entrant Ventricular Tachycardia]]=== | ||
* [[Bundle branch reentry]] [[ventricular tachycardia]] usually occurs either in patients with [[structural heart disease]] or in patients with conduction disturbances with a structurally normal heart. | |||
[[ | * [[Bundle branch reentry]] is a macro-reentrant [[tachycardia]] that incorporates the [[His-Purkinje system]], the bundle branches, and trans-septal [[myocardial]] conduction in the circuit. | ||
- | * Typical [[bundle branch reentry]] [[tachycardia]] uses the [[Purkinje fibers|right bundle]] as the anterograde limb and the [[Purkinje fibers|left bundle]] as the retrograde limb. | ||
* Atypical [[bundle branch reentry]] uses the [[left bundle]] (anterior fascicle, posterior fascicle, or both) as the antegrade limb and the [[right bundle]] as the retrograde limb. | |||
* The [[tachycardia]] appears as a typical [[left bundle branch block]] or [[right bundle branch block]]. | |||
===[[Accelerated idioventricular rhythm]]=== | |||
* [[Accelerated idioventricular rhythm]] commonly seen in the setting of [[reperfusion]] following [[myocardial]] [[ischemia]] or [[infarction]]. However, [[spontaneous coronary artery dissection]] should be considered when the [[atherosclotic disease]] is unlikely. <ref>{{cite journal|doi=10.1001/jamaintern-med.2020.8999}}</ref> | |||
*The [[Known]] [[mechanism]] is [[automaticity]] and can be seen in [[patients]] with [[digoxin]] [[toxicity]] and rarely seen in [[structurally normal heart]]. | |||
* Self-limited [[condition]], resolved spontaneously | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Best pages]] | |||
[[Category:Up-To-Date cardiology]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Disease]] | [[Category:Disease]] | ||
Latest revision as of 05:41, 28 July 2021
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Differentiating Ventricular Tachycardia from other Disorders |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. Myocardial scarring from any process increases the likelihood of electrical reentrant circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT. The morphology of ventricular tachycardia often depends on its cause. VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity. If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.
Pathophysiology
Pathophysiology of ventricular tachycardia can be better studied depending upon the subclass:[1][2][3][4]
Cellular level
- Electrical reentry or abnormal automaticity is the main reason behind ventricular tachycardia.
- Myocardial scarring from any process increases the likelihood of electrical reentrant circuits.
- These circuits generally include a zone where normal electrical propagation is slowed by the scar.
- Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT.
- VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity.
- Torsade de pointes seen in the long QT syndromes is likely a combination of triggered activity and ventricular reentry.
- During VT, cardiac output is reduced as a consequence of decreased [[ventricular] filling from the rapid heart rate and the lack of properly timed or coordinated atrial contraction.
- Ischemia and mitral insufficiency may also contribute to decreased ventricular stroke output and hemodynamic intolerance.
- Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or when heart rates are very rapid.
- Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to ventricular fibrillation (VF), resulting in sudden death.
- In patients with monomorphic VT, mortality risk correlates with the degree of structural heart disease. Underlying structural heart diseases such as ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, and right ventricular dysplasia have all been associated with degeneration of monomorphic or polymorphic VT to VF.
- Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.
- If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.
Monomorphic Ventricular Tachycardia
- There are two reasons the morphology of the QRS does not vary in monomorphic ventricular tachycardia:
- A single site that generates automaticity of a single point in either the left or right ventricle.
- A reentry circuit within the ventricle.
Polymorphic Ventricular Tachycardia
- Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization.
- The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval.
- QT prolongation may be congenital or acquired.
- Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.
- Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia.
- Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic.
- Other relatively common drugs including some antibiotics and antihistamines may also be a danger, particularly in combination with one another.
- Problems with blood levels of potassium, magnesium and calcium may also contribute. High dose magnesium is often used as an antidote in cardiac arrest protocols.
Bundle Branch Re-entrant Ventricular Tachycardia
- Bundle branch reentry ventricular tachycardia usually occurs either in patients with structural heart disease or in patients with conduction disturbances with a structurally normal heart.
- Bundle branch reentry is a macro-reentrant tachycardia that incorporates the His-Purkinje system, the bundle branches, and trans-septal myocardial conduction in the circuit.
- Typical bundle branch reentry tachycardia uses the right bundle as the anterograde limb and the left bundle as the retrograde limb.
- Atypical bundle branch reentry uses the left bundle (anterior fascicle, posterior fascicle, or both) as the antegrade limb and the right bundle as the retrograde limb.
- The tachycardia appears as a typical left bundle branch block or right bundle branch block.
Accelerated idioventricular rhythm
- Accelerated idioventricular rhythm commonly seen in the setting of reperfusion following myocardial ischemia or infarction. However, spontaneous coronary artery dissection should be considered when the atherosclotic disease is unlikely. [5]
- The Known mechanism is automaticity and can be seen in patients with digoxin toxicity and rarely seen in structurally normal heart.
- Self-limited condition, resolved spontaneously
References
- ↑ Martin CA, Lambiase PD (October 2017). "Pathophysiology, diagnosis and treatment of tachycardiomyopathy". Heart. 103 (19): 1543–1552. doi:10.1136/heartjnl-2016-310391. PMC 5629945. PMID 28855272.
- ↑ Simons GR, Klein GJ, Natale A (February 1997). "Ventricular tachycardia: pathophysiology and radiofrequency catheter ablation". Pacing Clin Electrophysiol. 20 (2 Pt 2): 534–51. doi:10.1111/j.1540-8159.1997.tb06209.x. PMID 9058854.
- ↑ Brunckhorst C, Delacretaz E (April 2004). "[Ventricular tachycardia--etiology, mechanisms and therapy]". Ther Umsch (in German). 61 (4): 257–64. doi:10.1024/0040-5930.61.4.257. PMID 15137521.
- ↑ Srivathsan K, Ng DW, Mookadam F (July 2009). "Ventricular tachycardia and ventricular fibrillation". Expert Rev Cardiovasc Ther. 7 (7): 801–9. doi:10.1586/erc.09.69. PMID 19589116.
- ↑ . doi:10.1001/jamaintern-med.2020.8999. Missing or empty
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