Ventricular tachycardia pathophysiology: Difference between revisions
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==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]]. The morphology of ventricular tachycardia often depends on its cause. | ||
The morphology of | |||
==Monomorphic Ventricular Tachycardia== | |||
In [[monomorphic ventricular tachycardia]], the reason all the beats look the same is because the impulse is being generated from either increased [[cardiac arrhythmia#origin of impulse|automaticity]] of a single point in either the left or right ventricle, or due to a [[cardiac arrhythmia#origin of impulse|reentry]] circuit within the ventricle. The most common cause of [[monomorphic ventricular tachycardia]] is damaged or dead (scar) tissue from a previous [[myocardial infarction]] (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit ''around'' the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of [[atrial flutter]] and the re-entrant forms of [[supraventricular tachycardia]]. Other rarer congenital causes of [[monomorphic ventricular tachycardia|monomorphic VT]] include right ventricular dysplasia, and right and left ventricular outflow tract VT. | In [[monomorphic ventricular tachycardia]], the reason all the beats look the same is because the impulse is being generated from either increased [[cardiac arrhythmia#origin of impulse|automaticity]] of a single point in either the left or right ventricle, or due to a [[cardiac arrhythmia#origin of impulse|reentry]] circuit within the ventricle. The most common cause of [[monomorphic ventricular tachycardia]] is damaged or dead (scar) tissue from a previous [[myocardial infarction]] (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit ''around'' the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of [[atrial flutter]] and the re-entrant forms of [[supraventricular tachycardia]]. Other rarer congenital causes of [[monomorphic ventricular tachycardia|monomorphic VT]] include right ventricular dysplasia, and right and left ventricular outflow tract VT. | ||
==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 EKG 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 ischaemia. 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. | 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 EKG 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 ischaemia. 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. | ||
Revision as of 17:10, 22 September 2012
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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. The morphology of ventricular tachycardia often depends on its cause.
Monomorphic Ventricular Tachycardia
In monomorphic ventricular tachycardia, the reason all the beats look the same is because the impulse is being generated from either increased automaticity of a single point in either the left or right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is damaged or dead (scar) tissue from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.
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 EKG 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 ischaemia. 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.
