Ventricular tachycardia overview: Difference between revisions
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[[Ventricular tachycardia]] is a [[tachycardia]] that originates in one of the [[left ventricle|ventricles]] of the [[heart]]. This is a potentially life-threatening [[arrhythmia]] because it may lead to [[ventricular fibrillation]] and [[sudden cardiac death|sudden death]]. In 1906 Gallavardin discovered the reasons behind the [[cardiac]] [[instability]] which leads to ventricular tachycardia, and put forth the idea that VT could convert into [[ventricular fibrillation]]. Thomas Lewis gave the first [[electrocardiographic]] description of ventricular tachycardia in 1909. It was first suggested in 1921 that [[coronary]] occlusion could be the main cause of ventricular tachycardia. Many advancements have been made in the [[diagnosis]] and management protocols of [[ventricular tachycardia]] since that time.[[Ventricular tachycardia]] refers to a [[rhythm]] with a [[heart rate]] in excess of 100 (and in some definitions 120) [[beats per minute]] that arises distal to the [[bundle of His]]. [[Ventricular tachycardia]] can be classified based on morphology and duration of [[tachyarrhythmia]]. The [[morphology]] of the [[QRS complexes]] on the [[ECG]] maybe ([[monomorphic ventricular tachycardia]]or [[polymorphic ventricular tachycardia]]). In sustained [[VT]] duration of [[VT]] lasts > 30 sec or [[VT]]< 30 sec that needs to termination due to compromised [[hemodynamic]]. Nonsustained, or unsustained [[VT]] is more than 3 consecutive [[premature ventricular complexes]] with spontaneously termination. [[Bidirectional VT]] is a type of [[VT]] with beat to beat changing [[QRS]] frontal plane [[axis]] indicating of [[digoxin toxicity]] or [[catecholaminergic polymorphic VT]].[[Torsades de pointed]] is a type of [[polymorphic VT]] in the setting of [[long QT]] interval which is characterized by [[twisting of the points]], waxing and waning [[QRS]] amplitude, Long-short sequence with long-coupling interval to the first [[VT]] beat, maybe initiated after [[bradycardia]] such as [[high grade AV block]].[[Ventricular flutter]] | [[Ventricular tachycardia]] is a [[tachycardia]] that originates in one of the [[left ventricle|ventricles]] of the [[heart]]. This is a potentially life-threatening [[arrhythmia]] because it may lead to [[ventricular fibrillation]] and [[sudden cardiac death|sudden death]]. In 1906 Gallavardin discovered the reasons behind the [[cardiac]] [[instability]] which leads to ventricular tachycardia, and put forth the idea that VT could convert into [[ventricular fibrillation]]. Thomas Lewis gave the first [[electrocardiographic]] description of ventricular tachycardia in 1909. It was first suggested in 1921 that [[coronary]] occlusion could be the main cause of ventricular tachycardia. Many advancements have been made in the [[diagnosis]] and management protocols of [[ventricular tachycardia]] since that time.[[Ventricular tachycardia]] refers to a [[rhythm]] with a [[heart rate]] in excess of 100 (and in some definitions 120) [[beats per minute]] that arises distal to the [[bundle of His]]. [[Ventricular tachycardia]] can be classified based on morphology and duration of [[tachyarrhythmia]]. The [[morphology]] of the [[QRS complexes]] on the [[ECG]] maybe ([[monomorphic ventricular tachycardia]]or [[polymorphic ventricular tachycardia]]). In sustained [[VT]] duration of [[VT]] lasts > 30 sec or [[VT]]< 30 sec that needs to termination due to compromised [[hemodynamic]]. Nonsustained, or unsustained [[VT]] is more than 3 consecutive [[premature ventricular complexes]] with spontaneously termination. [[Bidirectional VT]] is a type of [[VT]] with beat to beat changing [[QRS]] frontal plane [[axis]] indicating of [[digoxin toxicity]] or [[catecholaminergic polymorphic VT]].[[Torsades de pointed]] is a type of [[polymorphic VT]] in the setting of [[long QT]] interval which is characterized by [[twisting of the points]], waxing and waning [[QRS]] amplitude, Long-short sequence with long-coupling interval to the first [[VT]] beat, maybe initiated after [[bradycardia]] such as [[high grade AV block]].[[Ventricular flutter]] | ||
is explained as a regular [[ventricular arrhythmia]] with rate about 300 [[beat per minute]] (bpm), or cycle length 200 ms, [[sinusoidal]] [[monophorphic]] [[QRS]] complexes, [[Without]] any isoelecterical interval between successive [[QRS]] complexes. [[Ventricular fibrillation]] is a [[rapid]], grossly irregular [[electrical]] activity with variation in morphologic waveforms by [[ventricular]] rate >300bpm, [[cycle length]] <200 ms. [[VT]]/ [[VF]] storm is an electerical storm or [[cardiac]] instability due to ≥ 3 episodes of sustained [[VT]], [[VF]] or shock delivery from [[ICD]] within 24 hours. 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]].[[Ischemic heart disease]] is a common cause of [[ventricular tachycardia]]. Other causes of [[ventricular tachycardia]] include [[congenital heart disease]], [[valvular heart disease]], dilated [[non-ischemic cardiomyopathy]], [[sarcoidosis]], [[infiltrative cardiomyopathy]], [[inflammatory cardiomyopathy]], and inherited [[channelopathies]]. In addition, illicit drug use with [[sympathetic activity]] such as [[cocaine]] and [[methamphetamine]], and drugs with [[QT interval prolongation]] effect and also [[electrolyte disturbances]] such as [[hypokalemia]], [[hypomagnesemia]], and [[hypocalcemia]] may cause [[ventricular tachycardia]].When [[wide QRS]] tachycardia is present on the [[electrocardiogram] [[ECG]], it is necessary to rapidly differentiate whether it is caused by [[ventricular tachycardia]] ([[VT]]) or a [[supraventricular tachycardia]] ([[SVT]]) with aberrant conduction. While the [[ECG]] provides the most reliable data to distinguish [[VT]] from [[SVT]] with aberrant conduction, the [[clinical]] history and the age of the [[patient]] may also provide additional discriminatory information regarding the cause of the wide [[QRS]] [[tachycardia]]. While older [[patients]] with a prior history of [[myocardial infarction]] are more likely to have [[VT]], young hemodynamically stable [[patients]] presenting with [[paroxysmal tachycardia]] are more likely to have [[SVT]] with aberrant conduction. Nevertheless, the primary tool to differentiate [[VT]] from [[SVT]] with aberrant conduction is the [[ECG]]. There are several findings that are more common in [[ventricular tachycardia]], and there are also more sophisticated [[electrophysiologic]] algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish [[VT]] from [[SVT]] with aberrant conduction. The diagnosis of [[VT]] is more likely if: There is a history of [[myocardial infarction]] or [[structural heart disease]], the [[electrical axis]] is -90 to -180 degrees (a “northwest” or “superior” axis), the [[QRS]] is > 140 msec, there is [[AV dissociation]], there are positive or negative [[QRS]] complexes in all the precordial leads, and the morphology of the [[QRS]] complexes resembles that of a previous [[premature ventricular contraction]] ([[PVC]]).Common risk factors associated with [[VT]]/ [[VF]] include prior history of [[hypertension]], Prior [[MI]], [[ST-segment]] changes at presentation, [[chronic obstructive pulmonary disease]]. Risk factors of occurrence of [[VF]] before [[ primary PCI]] in [[STEMI]] [[patients]] include [[alcohol]] consumption, preinfarction [[angina]], [[ anterior infarct ]] location, complete [[coronary ]] occlusion at the time of [[coronary angiography]]. Risk factors associated with [[VT]]/ [[VF]] after [[primary PCI]] include lower [[ blood pressure]], higher [[heart rate]], poor [[coronary flow ]] at the end of the [[procedure]], incomplete [[resolution]] of [[ST elevation]]. Risk factors associated with [[monomorphic VT]] early after [[CABG]] include [[prior]] [[MI]], [[ventricular scar]], [[LV]] dysfunction, placement of a [[bypass graft]] across a [[noncollateralized]] occluded [[coronary]] vessel to a chronic [[infarct]] zone.[[Ventricular arrhythmia]] may include the range from triple premature [[ventricular contraction ]]s ([[PVC]]s) to [[ ventricular fibrillation]]. Clinical presentation varies from asymptomatic to [[cardiac arrest]]. | is explained as a regular [[ventricular arrhythmia]] with rate about 300 [[beat per minute]] (bpm), or cycle length 200 ms, [[sinusoidal]] [[monophorphic]] [[QRS]] complexes, [[Without]] any isoelecterical interval between successive [[QRS]] complexes. [[Ventricular fibrillation]] is a [[rapid]], grossly irregular [[electrical]] activity with variation in morphologic waveforms by [[ventricular]] rate >300bpm, [[cycle length]] <200 ms. [[VT]]/ [[VF]] storm is an electerical storm or [[cardiac]] instability due to ≥ 3 episodes of sustained [[VT]], [[VF]] or shock delivery from [[ICD]] within 24 hours. 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]].[[Ischemic heart disease]] is a common cause of [[ventricular tachycardia]]. Other causes of [[ventricular tachycardia]] include [[congenital heart disease]], [[valvular heart disease]], dilated [[non-ischemic cardiomyopathy]], [[sarcoidosis]], [[infiltrative cardiomyopathy]], [[inflammatory cardiomyopathy]], and inherited [[channelopathies]]. In addition, illicit drug use with [[sympathetic activity]] such as [[cocaine]] and [[methamphetamine]], and drugs with [[QT interval prolongation]] effect and also [[electrolyte disturbances]] such as [[hypokalemia]], [[hypomagnesemia]], and [[hypocalcemia]] may cause [[ventricular tachycardia]].When [[wide QRS]] tachycardia is present on the [[electrocardiogram] [[ECG]], it is necessary to rapidly differentiate whether it is caused by [[ventricular tachycardia]] ([[VT]]) or a [[supraventricular tachycardia]] ([[SVT]]) with aberrant conduction. While the [[ECG]] provides the most reliable data to distinguish [[VT]] from [[SVT]] with aberrant conduction, the [[clinical]] history and the age of the [[patient]] may also provide additional discriminatory information regarding the cause of the wide [[QRS]] [[tachycardia]]. While older [[patients]] with a prior history of [[myocardial infarction]] are more likely to have [[VT]], young hemodynamically stable [[patients]] presenting with [[paroxysmal tachycardia]] are more likely to have [[SVT]] with aberrant conduction. Nevertheless, the primary tool to differentiate [[VT]] from [[SVT]] with aberrant conduction is the [[ECG]]. There are several findings that are more common in [[ventricular tachycardia]], and there are also more sophisticated [[electrophysiologic]] algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish [[VT]] from [[SVT]] with aberrant conduction. The diagnosis of [[VT]] is more likely if: There is a history of [[myocardial infarction]] or [[structural heart disease]], the [[electrical axis]] is -90 to -180 degrees (a “northwest” or “superior” axis), the [[QRS]] is > 140 msec, there is [[AV dissociation]], there are positive or negative [[QRS]] complexes in all the precordial leads, and the morphology of the [[QRS]] complexes resembles that of a previous [[premature ventricular contraction]] ([[PVC]]).Common risk factors associated with [[VT]]/ [[VF]] include prior history of [[hypertension]], Prior [[MI]], [[ST-segment]] changes at presentation, [[chronic obstructive pulmonary disease]]. Risk factors of occurrence of [[VF]] before [[ primary PCI]] in [[STEMI]] [[patients]] include [[alcohol]] consumption, preinfarction [[angina]], [[ anterior infarct ]] location, complete [[coronary ]] occlusion at the time of [[coronary angiography]]. Risk factors associated with [[VT]]/ [[VF]] after [[primary PCI]] include lower [[ blood pressure]], higher [[heart rate]], poor [[coronary flow ]] at the end of the [[procedure]], incomplete [[resolution]] of [[ST elevation]]. Risk factors associated with [[monomorphic VT]] early after [[CABG]] include [[prior]] [[MI]], [[ventricular scar]], [[LV]] dysfunction, placement of a [[bypass graft]] across a [[noncollateralized]] occluded [[coronary]] vessel to a chronic [[infarct]] zone.[[Ventricular arrhythmia]] may include the range from triple premature [[ventricular contraction ]]s ([[PVC]]s) to [[ ventricular fibrillation]]. Clinical presentation varies from asymptomatic to [[cardiac arrest]]. | ||
[[Ventricular tachycardia]] can cause life-threatening or fatal [[hemodynamic compromise]] or it can degenerate into a life-threatening rhythm called [[ventricular fibrillation]]. Common complications of [[ventricular tachycardia]] include [[sudden cardiac death]], [[cardiomyopathy]], [[ventricular fibrillation]], and infection related to [[ICD]]. The prognosis of [[ventricular tachycardia]] in patients largely depends upon the presence and severity of underlying [[cardiac]] disease. [[Mortality]] of [[ventricular tachycardia]] is higher in [[patients]] with [[coronary artery disease]] and presence of [[LV]] dysfunction. Prognosis is generally good in [[patients]] with [[right ventricular dysplasia]], [[idiopathic ventricular tachycardia]] or [[ventricular fibrillation]] treated medically. Contrary to previous studies, [[VT]] or [[VF]] at any time after [[STEMI]] was associated with higher [[mortality]] rate within 90 days. Late [[VT]] or [[VF]] (after 48 hours of hospital admission) after [[STEMI]] was associated with a higher risk of [[death]] than early [[VT]] or [[VF]] (within 48 hours of hospital admission). | [[Ventricular tachycardia]] can cause life-threatening or fatal [[hemodynamic compromise]] or it can degenerate into a life-threatening rhythm called [[ventricular fibrillation]]. Common complications of [[ventricular tachycardia]] include [[sudden cardiac death]], [[cardiomyopathy]], [[ventricular fibrillation]], and infection related to [[ICD]]. The prognosis of [[ventricular tachycardia]] in patients largely depends upon the presence and severity of underlying [[cardiac]] disease. [[Mortality]] of [[ventricular tachycardia]] is higher in [[patients]] with [[coronary artery disease]] and presence of [[LV]] dysfunction. Prognosis is generally good in [[patients]] with [[right ventricular dysplasia]], [[idiopathic ventricular tachycardia]] or [[ventricular fibrillation]] treated medically. Contrary to previous studies, [[VT]] or [[VF]] at any time after [[STEMI]] was associated with higher [[mortality]] rate within 90 days. Late [[VT]] or [[VF]] (after 48 hours of hospital admission) after [[STEMI]] was associated with a higher risk of [[death]] than early [[VT]] or [[VF]] (within 48 hours of hospital admission).[[ECG]] is the first diagnostic test that should be obtained in hemodynamically stable [[Ventricular tachycardia]]. For detection of [[tachyarrhythmia]] [[symptoms]] related exercise such as [[cathecolaminergic polymorphic VT]], [[Exercise stress test]] is recommended. Findings on resting [[ECG]] associated with diagnosis of [[VT]] include evidence of [[structural hear disease]] such as prior [[MI]] or [[chamber enlargement]], evidence of [[inherited arrhythmia disorders]] such as [[long QT syndrome]], [[Brugada syndrome]], [[arrhythmogenic right ventricular cardiomyopathy]]. [[QRS]] duration and [[conduction abnormality]] may have prognostic value in [[structural heart disease]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Revision as of 06:13, 27 May 2021
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Ventricular tachycardia Microchapters |
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Differentiating Ventricular Tachycardia from other Disorders |
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Diagnosis |
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Treatment |
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Case Studies |
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Ventricular tachycardia overview On the Web |
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Risk calculators and risk factors for Ventricular tachycardia overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Avirup Guha, M.B.B.S.[3]
Overview
Ventricular tachycardia is a tachycardia that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and sudden death. In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could be the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time.Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified based on morphology and duration of tachyarrhythmia. The morphology of the QRS complexes on the ECG maybe (monomorphic ventricular tachycardiaor polymorphic ventricular tachycardia). In sustained VT duration of VT lasts > 30 sec or VT< 30 sec that needs to termination due to compromised hemodynamic. Nonsustained, or unsustained VT is more than 3 consecutive premature ventricular complexes with spontaneously termination. Bidirectional VT is a type of VT with beat to beat changing QRS frontal plane axis indicating of digoxin toxicity or catecholaminergic polymorphic VT.Torsades de pointed is a type of polymorphic VT in the setting of long QT interval which is characterized by twisting of the points, waxing and waning QRS amplitude, Long-short sequence with long-coupling interval to the first VT beat, maybe initiated after bradycardia such as high grade AV block.Ventricular flutter is explained as a regular ventricular arrhythmia with rate about 300 beat per minute (bpm), or cycle length 200 ms, sinusoidal monophorphic QRS complexes, Without any isoelecterical interval between successive QRS complexes. Ventricular fibrillation is a rapid, grossly irregular electrical activity with variation in morphologic waveforms by ventricular rate >300bpm, cycle length <200 ms. VT/ VF storm is an electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours. 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.Ischemic heart disease is a common cause of ventricular tachycardia. Other causes of ventricular tachycardia include congenital heart disease, valvular heart disease, dilated non-ischemic cardiomyopathy, sarcoidosis, infiltrative cardiomyopathy, inflammatory cardiomyopathy, and inherited channelopathies. In addition, illicit drug use with sympathetic activity such as cocaine and methamphetamine, and drugs with QT interval prolongation effect and also electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia may cause ventricular tachycardia.When wide QRS tachycardia is present on the [[electrocardiogram] ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide QRS tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if: There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).Common risk factors associated with VT/ VF include prior history of hypertension, Prior MI, ST-segment changes at presentation, chronic obstructive pulmonary disease. Risk factors of occurrence of VF before primary PCI in STEMI patients include alcohol consumption, preinfarction angina, anterior infarct location, complete coronary occlusion at the time of coronary angiography. Risk factors associated with VT/ VF after primary PCI include lower blood pressure, higher heart rate, poor coronary flow at the end of the procedure, incomplete resolution of ST elevation. Risk factors associated with monomorphic VT early after CABG include prior MI, ventricular scar, LV dysfunction, placement of a bypass graft across a noncollateralized occluded coronary vessel to a chronic infarct zone.Ventricular arrhythmia may include the range from triple premature ventricular contraction s (PVCs) to ventricular fibrillation. Clinical presentation varies from asymptomatic to cardiac arrest. Ventricular tachycardia can cause life-threatening or fatal hemodynamic compromise or it can degenerate into a life-threatening rhythm called ventricular fibrillation. Common complications of ventricular tachycardia include sudden cardiac death, cardiomyopathy, ventricular fibrillation, and infection related to ICD. The prognosis of ventricular tachycardia in patients largely depends upon the presence and severity of underlying cardiac disease. Mortality of ventricular tachycardia is higher in patients with coronary artery disease and presence of LV dysfunction. Prognosis is generally good in patients with right ventricular dysplasia, idiopathic ventricular tachycardia or ventricular fibrillation treated medically. Contrary to previous studies, VT or VF at any time after STEMI was associated with higher mortality rate within 90 days. Late VT or VF (after 48 hours of hospital admission) after STEMI was associated with a higher risk of death than early VT or VF (within 48 hours of hospital admission).ECG is the first diagnostic test that should be obtained in hemodynamically stable Ventricular tachycardia. For detection of tachyarrhythmia symptoms related exercise such as cathecolaminergic polymorphic VT, Exercise stress test is recommended. Findings on resting ECG associated with diagnosis of VT include evidence of structural hear disease such as prior MI or chamber enlargement, evidence of inherited arrhythmia disorders such as long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy. QRS duration and conduction abnormality may have prognostic value in structural heart disease.
Historical Perspective
In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time.
Classification
Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified based on morphology and duration of tachyarrhythmia. The morphology of the QRS complexes on the ECG maybe (monomorphic ventricular tachycardiaor polymorphic ventricular tachycardia). In sustained VT duration of VT lasts > 30 sec or VT< 30 sec that needs to termination due to compromised hemodynamic. Nonsustained, or unsustained VT is more than 3 consecutive premature ventricular complexes with spontaneously termination. Bidirectional VT is a type of VT with beat to beat changing QRS frontal plane axis indicating of digoxin toxicity or catecholaminergic polymorphic VT.Torsades de pointed is a type of polymorphic VT in the setting of long QT interval which is characterized by twisting of the points, waxing and waning QRS amplitude, Long-short sequence with long-coupling interval to the first VT beat, maybe initiated after bradycardia such as high grade AV block.Ventricular flutter is explained as a regular ventricular arrhythmia with rate about 300 beat per minute (bpm), or cycle length 200 ms, sinusoidal monophorphic QRS complexes, Without any isoelecterical interval between successive QRS complexes. Ventricular fibrillation is a rapid, grossly irregular electrical activity with variation in morphologic waveforms by ventricular rate >300bpm, cycle length <200 ms. VT/ VF storm is an electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours.
Pathophysiology
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.
Causes
Ischemic heart disease is a common cause of ventricular tachycardia. Other causes of ventricular tachycardia include congenital heart disease, valvular heart disease, dilated non-ischemic cardiomyopathy, sarcoidosis, infiltrative cardiomyopathy, inflammatory cardiomyopathy, and inherited channelopathies. In addition, illicit drug use with sympathetic activity such as cocaine and methamphetamine, and drugs with QT interval prolongation effect and also electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia may cause ventricular tachycardia.
Differentiating Ventricular Tachycardia from other Disorders
When wide QRS tachycardia is present on the [[electrocardiogram] ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide QRS tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if: There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).
Epidemiology and Demographics
Ischemic heart disease is the most common cause of ventricular tachycardia in the US, followed by cardiomyopathy. VT is causes approximately of half of the 300,000 sudden deaths which occur out of hospital annually in the US. Brugada syndrome is thought to be the cause of half of the sudden cardiac deaths which occurs in young individuals without structural heart disease.
Risk Factors
Common risk factors associated with VT/ VF include prior history of hypertension, Prior MI, ST-segment changes at presentation, chronic obstructive pulmonary disease. Risk factors of occurrence of VF before primary PCI in STEMI patients include alcohol consumption, preinfarction angina, anterior infarct location, complete coronary occlusion at the time of coronary angiography. Risk factors associated with VT/ VF after primary PCI include lower blood pressure, higher heart rate, poor coronary flow at the end of the procedure, incomplete resolution of ST elevation. Risk factors associated with monomorphic VT early after CABG include prior MI, ventricular scar, LV dysfunction, placement of a bypass graft across a noncollateralized occluded coronary vessel to a chronic infarct zone.
Screening
In a young patient with lone atrial fibrillation, short QT syndrome should be excluded. In a patient with a family history of sudden cardiac death a physical examination should be performed.
Natural History, Complications and Prognosis
Ventricular arrhythmia may include the range from triple premature ventricular contraction s (PVCs) to ventricular fibrillation. Clinical presentation varies from asymptomatic to cardiac arrest. Ventricular tachycardia can cause life-threatening or fatal hemodynamic compromise or it can degenerate into a life-threatening rhythm called ventricular fibrillation. Common complications of ventricular tachycardia include sudden cardiac death, cardiomyopathy, ventricular fibrillation, and infection related to ICD. The prognosis of ventricular tachycardia in patients largely depends upon the presence and severity of underlying cardiac disease. Mortality of ventricular tachycardia is higher in patients with coronary artery disease and presence of LV dysfunction. Prognosis is generally good in patients with right ventricular dysplasia, idiopathic ventricular tachycardia or ventricular fibrillation treated medically. Contrary to previous studies, VT or VF at any time after STEMI was associated with higher mortality rate within 90 days. Late VT or VF (after 48 hours of hospital admission) after STEMI was associated with a higher risk of death than early VT or VF (within 48 hours of hospital admission).
Diagnosis
History and Symptoms
The symptoms of ventricular tachycardia will depend on the ventricular rate, the duration of tachycardia, and the presence of underlying disease. In general, the symptoms include shortness of breath, weakness, palpitations, fatigue, and syncope.
Physical Examination
Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Jugular pulsation may be noted in the neck exam.
Laboratory Findings
Serial cardiac enzymes, serum electrolytes as well as calcium, magnesium and phosphate levels, should be obtained. A toxicology screen should also be obtained to assess for illicit drugs as the cause of the VT, as well as levels of medications that may have caused the VT.
Electrocardiogram
The diagnosis of ventricular tachycardia almost completely depends on EKG findings. The details are illustrated below. It is important to differentiate it from other wide complex tachycardias. The rate is > 100 beats per minute and is usually 150-200 beats per minute. The QRS complex is wide (>140 milliseconds). AV dissociation is always present, but is evident in only 20% of cases of VT.
Chest X Ray
Chest X ray is done only when ventricular tachycardia leads to congestive heart failure or if a secondary pathological disease is suspected as the cause of ventricular tachycardia.
Echocardiography
Echocardiography can be performed in the patient with ventricular tachycardia to rule out structural abnormalities such as a right ventricular cardiomyopathy and silent ischemia on stress testing. Coronary arteriography is often performed in the patient with ventricular tachycardia to rule out obstructive coronary artery disease.
Treatment
Electrical Cardioversion
Therapy may be directed at either terminating an episode of the arrhythmia or for suppressing a future episode from occurring. The treatment is tailored to the specific patient, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. It is usually possible to terminate a VT episode with a direct current shock across the heart. This is ideally synchronized to the patient's heartbeat. As it is quite uncomfortable, shocks should be delivered only to an unconscious or sedated patient.
Surgery
Surgery is not a mainstay or a preferred method of treatment for ventricular tachycardia. There are some specific scenarios however in which revascularization may be considered, and may help in preventing VT.