Ventricular tachycardia
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| Ventricular tachycardia Classification and external resources | |
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|---|---|
| Lead II: rhythm, ventricular tachycardia | |
| ICD-10 | I47.2 |
| ICD-9 | 427.1 |
| DiseasesDB | 13819 |
| eMedicine | emerg/634 med/2367 ped/2546 |
| MeSH | D017180 |
| Cardiology Network |
 Discuss Ventricular tachycardia further in the WikiDoc Cardiology Network |
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Overview
Ventricular tachycardia (V-tach or VT) is a tachycardia, or fast heart rhythm 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.
Classification
1. Classification Based Upon Morphology of Complexes
Ventricular tachycardia can be classified based on its morphology: Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (EKG).
Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This most commonly appears as a cyclical progressive change in cardiac axis referred to by its French eponym Torsade de pointes (literally twisting of the points).
2. Classification Based Upon Duration of Episode
Another way to classify ventricular tachycardias is the duration of the episodes: Technically, three or more beats in a row on an EKG that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia. If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia. If the rhythm lasts more than 30 seconds it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds).
Sustained Ventricular Tachycardia
- Ventricular tachycardia originates from a ventricular focus
- Lasts more than 30 seconds
- Broad QRS complexes: rate of >90 beats/minute
Paroxysmal Ventricular Tachycardia
- Rapid succession of three or more ectopic beats.
- Sustained if it lasts longer than 30 seconds.
Incessant Ventricular Tachycardia
- The ventricular tachycardia is recurrent and the episodes are interrupted by only a few sinus beats.
3. Classification Based Upon Symptoms
A third way to classify ventricular tachycardia is on the basis of its symptoms: Pulseless VT is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest. In this circumstance it is best treated the same way as ventricular fibrillation (VF) and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some VT is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless VT or to VF.
Pathophysiology
The morphology of the tachycardia depends on its cause.
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, 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.
Diagnosis
The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12 lead EKG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include ashman beats and antedromic atrioventricular re-entry tachcyardias.
Various diagnostic criteria have been developed to determine if a wide complex tachycardia is ventricular tachycardia or a more benign rhythm.[1][1] In addition to these diagnostic criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia.[1]
The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil are used to attempt to terminate a presumed supraventricular tachycardia.[1] It is therefore wisest to assume that all wide complex tachycardia is VT until proven otherwise.
EKG Findings
- Abnormal and wide QRS complexes with secondary ST segment and T wave changes.
- Usual QRS duration is > 0.12 seconds, may be shorter if the ectopic focus is located in the ventricular septum.
- The secondary ST segment and T wave changes are in a direction that is opposite the major deflection of the QRS.
- A ventricular rate between 140 and 200 BPM.
- When the rate is >200 and has a sine wave appearance, it is called ventricular flutter.
- When the rate is <110 BPM it is called non-paroxysmal VT.
- A regular or slightly irregular (up to 0.03 seconds) rhythm.
- Abrupt onset and termination.
- AV dissociation.
- Atrial rate slower than ventricular rate.
- No relationship between atrial activity and ventricular activity.
- There can be VA conduction.
- The RP interval is >0.11 seconds.
- Occurs in about 50% of cases.
- Uncommon when the ventricular rate is rapid (only 1/7 when the rate was>200).
- Capture beats.
- Occurs when a supraventricular impulse is conducted and captures the ventricle.
- They are rare.
- Fusion beats.
Examples of Ventricular Tachycardia:
 12 lead EKG: Ventricular tachycardia. |
 12 lead EKG: Ventricular tachycardia. Image courtesy of Dr Jose Ganseman |
 12 lead EKG: Ventricular tachycardia. Image courtesy of Dr Jose Ganseman |
 12 lead EKG: Ventricular tachycardia. Image courtesy of Dr Jose Ganseman |
 12 lead EKG: Ventricular tachycardia. Image courtesy of Dr Jose Ganseman |
 12 lead EKG: Ventricular tachycardia. Image courtesy of Dr Jose Ganseman |
 Ventricular tachycardia of 140 bpm with a left bundle branch block pattern and left heart axis. |
 Ventricular tachycardia of 250 bpm with a right bundle branch block pattern and right heart axis. |
 Ventricular tachycardia of 150 bpm with a right bundle branch block pattern and right heart axis. Note the 5th and 6th complex from the right side. These are fusion complexes. |
 Ventricular flutter on a 12 lead ECG |
Differential Diagnosis of Underlying Causes of Ventricular Tachycardia
- Caffeine
- Cardiomyopathy
- Cocaine
- Congenital Heart Disease
- Congestive heart failure
- Electrolyte imbalance
- Hypertrophic cardiomyopathy
- Hypocalcemia
- Hypokalemia
- Hypomagnesia
- Iatrogenic due to pulmonary artery catheter, right heart catheterization, or electrophysiologic sutdy
- Methamphetamine
- STEMI
- Ventricular aneurysm
Treatment
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.
Electrical Cardioversion / Defibrillation
It is usually possible to terminate a VT episode with a direct current shock across the heart. This is ideally synchronised to the patient's heartbeat. As it is quite uncomfortable, shocks should be delivered only to an unconscious or sedated patient. A patient with pulseless VT will be unconscious and treated as an emergency on a cardiac arrest protocol. Elective cardioversion is usually performed in controlled circumstances with anaesthetic and airway support.
The shock may be delivered to the outside of the chest using an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted.
An ICD may also be set to attempt to overdrive pace the ventricle. Pacing the ventricle at a rate faster than the underlying tachycardia can sometimes be effective in terminating the rhythm. If this fails after a short trial, the ICD will usually stop pacing, charge up and deliver a defibrillation grade shock.
Antiarrhythmic drug therapy
Drugs such as amiodarone, epinephrine and vasopressin may be used in addition to [defibrillation] to terminate VT while the underlying cause of the VT can be determined. Possible causes or contributing factors to VT can be remembered as the six H's and five T's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo- or Hyperglycemia, Hypothermia; and Toxins, Tamponade (cardiac), Tension pneumothorax, Thrombosis, Trauma.
Long term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used.
For some of the rare congenital syndromes of VT, other drugs, and sometimes even catheter ablation therapy may be useful.
The implantation of an ICD is more effective than drug therapy for prevention of sudden cardiac death due to VT and VF, but may be constrained by cost issues, and well as patient co-morbidities and patient preference.
Bundle Branch Reentry Ventricular Tachycardia
Characteristics
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 transseptal 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 respectively.
Diagnosis
- Each ventricular activation is preceeded by His bundle activation (see Figure)
- Changes in the HH Interval precede changes in the VV interval
- Tachycardia induction is associated with critical delay in the HPS Initiation or a V-H increment (“V-H jump”) (see Figure)
- A longer H-V interval during tachycardia as compared with sinus rhythm. This is paradoxical because one would expect it to be analogous to the situation with fascicular tachycardia, the wavefront in Bundle Branch Reentry Ventricular Tachycardia usually proceeds retrogradely through the left bundle branch system. It then divides with a portion continuing retrogradely to the site of the His bundle recording, and another portion turning anterogradely along the right bundle branch to the ventricle. Since this impulse enters the distal His bundle, and then proceeds retrogradely to the His bundle recording site and simultaneously anterogradely down the right bundle branch, one might expect the ventricle to be depolarized with an HV interval shorter than during sinus rhythm. This does not occur and the longer HV interval typically seen in BBRT is probably due to a combination of some effects of relative refractoriness of the right bundle and a predominant role of anisotropic conduction.
- Tachycardia is terminated by block in the HPS
- Tachycardia is abolished by ablation of the RBBB
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Helpful Maneuvers
- Single PVC advances His
- Entrainment from Left bundle. The interval from the stimulus to QRS approximates that from the LBB potential to onset of QRS. PPI and TCL are the same.
References
External Links
- ECGpedia: Course for interpretation of ECG
- The whole ECG - A basic ECG primer
- 12-lead ECG library
- Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
- ECG information from Children's Hospital Heart Center, Seattle
- National Heart, Lung, and Blood Institute, Diseases and Conditions Index
- A history of electrocardiography
- EKG Interpretations in infants and children
Additional Readings
- Journal of Interventional Cardiac Electrophysiology 1997;1:73–77
- Journal of Interventional Cardiac Electrophysiology 5, 173-176, 2001