Ventricular tachycardia is characterized as a wide complex (QRS duration greater than 120 milliseconds) tachyarrhythmia at a heart rate greater than 100 beats per minute. It is classified by duration as non-sustained or sustained. Non-sustained ventricular tachycardia is defined as more than 3 beats of ventricular origin at a rate greater than 100 beats per minute that lasts less than 30 seconds in duration. When the rhythm lasts longer than 30 seconds or hemodynamic instability occurs in less than 30 seconds, it is considered sustained ventricular tachycardia.
Further classification is made into monomorphic and polymorphic on the basis of QRS morphology. Monomorphic ventricular tachycardia demonstrates a stable QRS morphology from beat to beat while polymorphic ventricular tachycardia has changing or multiform QRS variance from beat to beat. Torsades de pointes is a polymorphic ventricular tachycardia that occurs in the setting of a long QT interval and appears as waxing and waxing QRS amplitude on ECG.
The final form of ventricular tachycardia is bidirectional ventricular tachycardia which has a beat-to-beat alternation in the QRS frontal plane axis. It is associated with digitalis toxicity or catecholaminergic polymorphic VT.
The most common cause of VT is ischemic heart disease.
Ventricular tachycardia accounts for approximately 8% of cases of wide complex tachycardia. The most common cause of ventricular tachycardia is underlying ischemic heart disease. Other causes include adult and congenital structural heart disease, acquired and inherited channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity. Infiltrative cardiomyopathy can result from: systemic lupus erythematosus, sarcoidosis, amyloidosis, rheumatoid arthritis, and hemochromatosis.
A common trigger is hypokalemia followed by hypomagnesemia. Some cases may also be triggered by hyperkalemia, especially in patients with structural heart disease. sleep apnea and atrial fibrillation can also trigger V.
QT prolongation either acquired or inherited, is fast becoming recognized as a trigger for VT. In both cases, the repolarization phase is prolonged leading to torsade de pointes.
In young people, the cause of VT includes:
Catecholaminergic polymorphic VT is known to be triggered by exercise, stress and intense emotional states.
The Brugada syndrome is characterized by RBBB and ST-segment elevation in the early precordial leads (V1-V3) can also cause VT and is often associated with sudden death.
Ventricular tachycardia and ventricular fibrillation cause most cases of sudden cardiac death with an estimated rate of 300,000 deaths each year in the United States. This accounts for approximately half of the deaths related to cardiac causes. Risk factors for ventricular tachycardia are hypertension, previous myocardial infarction, chronic obstructive pulmonary disease (COPD), and ST-segment changes at presentation. Patients presenting with acute myocardial infarction have ventricular fibrillation or ventricular tachycardia at a rate of 5% to 10%. Ventricular tachycardia 48 hours after hospital presentation is associated with an increased risk of death compared to ventricular tachycardia occurring within the first 48 hours of hospital presentation.
VT is rare in children but can occur in the presence of structural heart disease. Overall, VT is more common in men than in women.
The mechanism for ventricular tachyarrhythmias includes enhancement of normal automaticity or abnormal automaticity, activity triggered by early or late afterdepolarizations, and reentry. In acute myocardial infarction, the transient ischemia results in an increased concentration of extracellular potassium, which causes partial depolarization of the resting membrane potential. This creates injury currents between the infarcted tissue and healthy myocardium that may trigger spontaneous activity.
A good history and physical can help you differentiate ventricular tachycardia from supraventricular tachycardia. Patients presenting with ventricular tachycardia are more likely to be older with a history of heart disease. A past medical history of heart failure, recent angina, and prior myocardial infarction all have a greater than 9% positive predictive value for ventricular tachycardia.
The physical examination findings of cannon A waves and variable intensity of the S1 heart sound suggest AV dissociation, a criterion favoring the diagnosis of ventricular tachycardia.
Patients may present with hypotension, altered mental status, diaphoresis, and pallor.
The first step in the evaluation of presumed ventricular tachycardia is a 12-lead electrocardiogram (ECG). Patients with ventricular tachycardia symptoms associated with exertion, ischemic heart disease, or catecholaminergic polymorphic ventricular tachycardia should undergo further testing with a treadmill stress test. Patients having syncope, presyncope or palpitations with no arrhythmia detected on a single 12-lead ECG should undergo further evaluation with ambulatory ECG monitoring. In patients with ventricular tachycardia and possible structural heart disease, .an echocardiogram is recommended. Patients who undergo an episode of unexplained sudden cardiac arrest secondary to a ventricular tachyarrhythmia, CT, or coronary angiography can be used to confirm the presence or absence of ischemic heart disease.
If there is a family history of prolonged QT interval, hypertrophic cardiomyopathy or right ventricular dysplasia, then siblings should be offered genetic testing.
Appropriate laboratory workup is necessary. Levels of potassium, magnesium, calcium, and phosphate should be measured serially. Levels of digoxin and a toxicology screen should be obtained. Cardiac enzymes should be obtained to rule of an MI.
Echocardiography is useful in patients at risk for sudden death. The technique can assess ejection fraction, myocardial infiltrative disease, and presence of any wall motion abnormality.
A myocardial biopsy is only done in patients with infiltrative cardiomyopathies. If no cause is found, electrophysiologic studies may be required to determine the presence of reentry circuits.
Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying cardiac comorbidities require no additional therapy. Patients that are symptomatic and without cardiac comorbidities should be started on a beta-blocker due to favorable efficacy and safety profile. If these patients continue to have episodes of non-sustained VT despite beta-blocker therapy, or cannot tolerate beta-blocker therapy, a calcium channel with atrioventricular nodal action such as verapamil or diltiazem can be used. The previously mentioned nondihydropyridine calcium channel blockers are contraindicated in the setting of structural heart disease or heart failure with reduced ejection fraction.
Patients with sustained monomorphic ventricular tachycardia (SMVT) that are unstable should be managed following advanced cardiac life support (ACLS) guidelines. Hemodynamically stable patients should be pharmacologically cardioverted using an anti-arrhythmic medication. Intravenous amiodarone or procainamide can be used for this purpose. Procainamide will terminate between 50% and 80% of ventricular tachycardias, and it will slow the conduction of those that it does not terminate. Amiodarone will convert about 30% of patients to sinus rhythm but is very effective in reducing the reversion rate of refractory SMVT.
The first-line therapy for chronic treatment of patients with ischemic heart disease and VT is a beta-blocker therapy which is associated with a reduced risk of sudden cardiac death. In patients with ischemic heart disease who have recurrent VT despite beta-blocker therapy, amiodarone or sotalol can be initiated however neither therapy has been associated with a decrease in mortality. Amiodarone plus a beta-blocker has been associated with a greater decrease in the number of ICD shocks compared to sotalol monotherapy.
Patients with ischemic heart disease that survive sudden cardiac arrest due to ventricular tachycardia, or experience hemodynamically unstable or stable sustained ventricular tachycardia, should have an implantable cardiac defibrillator (ICD) placed if their estimated meaningful survival is greater than 1 year. Patients with syncope who have ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who do not meet criteria for an ICD can undergo an electrophysiological study to assess the risk of sustained ventricular tachycardia; however, performing the study solely for risk stratification is not indicated.
Catheter ablation has a class 1 recommendation for patients with a history of myocardial infarction who continue to suffer from symptomatic sustained VT, or have failed or are intolerant of amiodarone or other antiarrhythmic medications.
If a patient with VT is hemodynamically unstable, immediate cardioversion is necessary. This is accomplished by a 100-200J biphasic shock. All reversible factors must be corrected. VT in patients with an MI should be treated with lidocaine. If the patient has torsade de pointes then magnesium sulfate is preferred.
If possible, ventricular tachycardia should be differentiated from supraventricular tachycardia with aberrant conduction as the treatment strategies are different. Factors favoring the diagnosis of ventricular tachycardia include: QRS width greater than 0.14 seconds with right bundle branch block pattern or greater than 0.16 seconds with left bundle branch block pattern, AV dissociation, RS interval longer than 100 milliseconds in a precordial lead (Brugada's sign), QRS with negative concordance in the precordial leads, and ventricular fusion beats.
The prognosis of VT depends on the cause and cardiac status. Patients who develop VT can suffer from hemodynamic failure and the mortality can exceed 30% if no treatment is provided. In the setting of percutaneous coronary intervention, VT occurring prior to revascularization is associated with very high mortality. The prognosis does not correlate with ejection fraction. Patients with hypertrophic cardiomyopathy, long QT syndrome and right ventricular dysplasia often have normal heart function but yet are a high risk for sudden death.
Patients who have monomorphic VT with normal heart anatomy are at low risk for sudden death and can be managed by medications or ablation
In the presence of LV dysfunction, the antiarrhythmic drugs have been disappointing. The drug of choice is amiodarone and can be combined with beta-blockers.
Early recognition, bystander CPR, and public access defibrillation have all helped to increase the rate of survival for patients who have an out-of-hospital cardiac arrest however survival remains low at under 10%. (Level I) After arrival at the hospital, post-arrest care order sets that pay significant attention to temperature control and cardio-cerebral resuscitation, have further improved survival. (Level 2)
In-hospital cardiac arrest shares the similarity with out-of-hospital cardiac arrest in that early cardiopulmonary resuscitation (CPR), and defibrillation are important factors in survival. (Level I) Every minute that treatment is delayed reduces survival by approximately 10%. This makes the resuscitation team an important part in improving outcomes of in-hospital cardiac arrest. However, there is significant variation amongst different hospitals in efficacy. Resuscitation teams universally consist of physicians, nurses, anesthesia, and respiratory therapists coordinating their efforts. Hospitals that were high performing included more support staff (pharmacy, clerical, security, spiritual staff).
Patients with ischemic heart disease should be seen by a dietitian because they may benefit from low cholesterol and low sodium diet. Strenuous exercise should be avoided as it may precipitate VT in some patients. All patients should be encouraged to discontinue smoking. The pharmacist should educate the patient on medication compliance and the need to follow up with the cardiologist. They should also assist the clinical team in managing drug-drug interactions and making appropriate drug treatment selection.
Top-performing hospitals were also more likely to have a dedicated resuscitation team that had no clinical responsibilities that interfered with their participation in the team. Effective communication among team members was also identified as a positive factor in improving outcomes.
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