DESCRIPTION 
- Ventricular tachycardia (VT) is wide QRS tachycardia originating in the ventricles due to reentry, triggered activity, or automaticity.
- Synonym(s): The following have been used interchangeably but are not synonymous: Cardiac arrest (refers to collapse due to ventricular tachycardia or fibrillation); VT followed by ventricular fibrillation is the usual cause of sudden death.
Pregnancy Considerations
Pregnancy may precipitate ventricular arrhythmias in long QT syndrome.
EPIDEMIOLOGY
- Coronary artery disease is the most common cause and is not specifically a genetic disease, although there is a genetic component.
- Prevalence is variable and depends on presence or absence of structural heart disease.
- All ages can be affected, but VT is more common in older individuals because coronary artery disease is more common.
- Cardiomyopathies, both hypertrophic and dilated, are associated with nonsustained and sustained VT.
- Some clear genetic syndromes, such as long QT syndrome, Brugada syndrome, and arrhythmogenic RV dysplasia, are associated with VT.
RISK FACTORS
- Same as in coronary artery disease (cigarette use, hyperlipidemia, and HTN)
- EKG abnormalities (though nonspecific), often determined by ambulatory monitoring, including:
- Premature ventricular contractions and nonsustained ventricular tachycardia, LV hypertrophy, nonspecific ST-T wave changes, intraventricular conduction delays, increased QT dispersion, T-wave alternans, and decreased heart rate variability
- Low LV ejection fraction
- Increased age
- Inducible VT in high-risk patient (after MI, low LV ejection fraction)
ETIOLOGY
- Myocardial scar from any cause
- Drug toxicity [digoxin (bidirectional VT) or QT-prolonging drugs (torsade de pointes VT)]
- Electrolyte abnormalities (hypokalemia)
- Ischemia
- Bundle–branch reentry
- Congenital heart disease, especially postoperatively where there has been a ventriculotomy (as in tetralogy of Fallot)
- In structurally normal hearts two VT syndromes can occur:
- RV outflow tract VT
- Idiopathic left septal VT
COMMONLY ASSOCIATED CONDITIONS
See Risk Factors and Etiology.
Outline
Signs and symptoms:
- Signs and symptoms depend on rate and duration of VT, and extent of underlying heart disease, if any:
- None
- Syncope
- Cardiac arrest
- Dyspnea
- Palpitations
- Chest discomfort/angina
DIAGNOSTIC TESTS & INTERPRETATION
- EKG is the cornerstone of the diagnosis. When a 12-lead EKG is available, the criteria listed below can be used not only to diagnose VT (to distinguish it from supraventricular tachycardia), but also to help guide therapy when ablation is considered.
- General: Atrioventricular (AV) dissociation and fusion (capture) beats prove VT, extremely wide QRS (>160 ms), QRS axis –90–180 degrees favor VT over supraventricular tachycardia with aberrancy.
- Morphology may be uniform (monomorphic) or variable (polymorphic)
- If left bundle beats all favor VT over supraventricular tachycardia branch block morphology, VT suggested if:
- In V1 or V2, R wave is >30 ms
- In V1 or V2, there is a notch on the downstroke of the QRS
- In V1 or V2, the interval from the onset of the QRS to the nadir of the S or Q wave is
60 msec - In V6 there is a Q wave
- If right bundle–branch block morphology, VT suggested if:
- In V1, QRS is monophasic or if QRS biphasic R is greater in amplitude than R’
- In V6, R to S ratio is <1 by either amplitude or area under the QRS complex
- Also useful to document if prior or new MI present
- Electrophysiologic study
Lab
None, except to assess electrolytes and drug levels where appropriate
Imaging
- Echo (to evaluate cardiomyopathy, localized wall-motion abnormalities such as in coronary artery disease, arrhythmogenic RV dysplasia)
- Coronary and LV angiography
- Cardiac MRI (especially useful in diagnosing arrhythmogenic RV dysplasia or infiltrative diseases)
- Exercise test with perfusion imaging to assess ischemia
Pathological Findings
Pathology depends on substrate, including coronary artery disease, any cause of myocardial fibrosis (cardiomyopathy, trauma), fibroadipose infiltration of the myocardium (arrhythmogenic RV dysplasia), inflammatory disease (myocarditis, sarcoidosis), or none (RV outflow tract tachycardia, idiopathic left VT, Brugada syndrome).
DIFFERENTIAL DIAGNOSIS
- Supraventricular tachycardia with aberrancy
- Preexcited tachycardia [antidromic reentrant tachycardia, or preexcitation as an innocent bystander such as during atrial flutter with atrioventricular (AV) conduction over a Mahaim accessory pathway]
Outline
ADDITIONAL TREATMENT
General Measures
- Treat underlying heart disease, especially ischemia and LV dysfunction.
- Treat reversible causes (withdraw toxic drugs, correct electrolyte disturbances).
- Be sure to synchronize if performing electrical cardioversion.
SURGERY
- In selected patients, curative therapy is possible with ablation or surgery.
- Catheter ablation is especially useful and efficacious for RV outflow tract and idiopathic left VT in patients without heart disease.
- VT in the setting of coronary artery disease may be amenable to catheter ablation, but ablation is often combined with drug therapy or implantable cardioverter-defibrillator (ICD) therapy.
- Endocardial resection was used to treat VTs arising from MI scars, and is still used in highly selected patients (presence of surgical coronary artery disease and an anterior aneurysm).
- The Antiarrhythmics Vs. Implantable Defibrillators (AVID) Trial, showed superior survival in patients with hemodynamically unstable VTs when treated with ICDs compared with antiarrhythmic drugs.
- Finally, surgery is used to correct and/or treat reversible/contributing causes of VF, such as coronary artery disease and aortic stenosis.
IN-PATIENT CONSIDERATIONS
Admission Criteria
- Admission criteria are variable and depend on hemodynamics during VT and the underlying substrate.
- VT from the RV outflow tract and idiopathic LV tachycardias occur in patients with otherwise normal hearts. Hemodynamics are usually preserved, and death due to these VTs is extremely uncommon. These patients can be managed in part on an outpatient basis.
- Admission is warranted for RF ablation of these VTs or the initiation of drug therapy.
- Conversely, VT in patients with coronary artery disease warrants admission because VT can degenerate to cardiac arrest (ventricular fibrillation).
Outline
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
- If drug therapy is chosen, follow to assess compliance, drug levels, effect on EKG, and changes in myocardial substrate.
- Device follow-up for ICD
- Drugs can alter the rate of ventricular tachycardias and affect the ease of defibrillation (defibrillation threshold) such that when antiarrhythmic drugs are begun in patients with ICDs, these potential effects need to be considered and an electrophysiologic study may be necessary.
DIET
Choose diet appropriate for underlying heart disease (low-cholesterol if coronary artery disease, low-sodium if CHF, calorie-restricted if diabetic).
PATIENT EDUCATION
- Counseling depends in part on the VT substrate.
- For those with genetic syndromes, genetic screening of family members should be discussed.
- Patients with torsade de pointes VT need to be educated about which drugs to avoid (www.qtdrugs.org), and for those with congenital long QT syndrome avoidance of precipitating causes of VT (startle reflexes).
- Activity:
- If VT is exercise-related, exercise should be restricted.
PROGNOSIS
Outcome depends on underlying heart disease and comorbid conditions. For patients with VT and a structurally normal heart, prognosis is excellent (RV outflow tract and idiopathic LV tachycardias).
Outline
CODES
ICD9
427.1 Paroxysmal ventricular tachycardia
SNOMED
- 25569003 ventricular tachycardia (disorder)
- 251156000 wide QRS ventricular tachycardia (disorder)