- Definition
- Etiology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Clinical Case Studies
- Study Questions
This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation (VF), asystole, and sudden death.
Electrocardiogram shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse.
Heart disease
Previous heart attack, a congenital heart defect, hypertrophic or dilated cardiomyopathy, or myocarditis. Sometimes ventricular tachycardia occurs after heart surgery. Inherited heart rhythm problems, such as long QT syndrome or Brugada syndrome, are rare causes of ventricular tachycardia.
Medications
Some medicines-including antiarrhythmic medicines, which are used to treat other types of abnormal heart rhythms-can cause ventricular tachycardia.
Nonprescription decongestants, herbal remedies (especially those that contain ma huang or ephedra), diet pills, and "pep" pills often contain stimulants that can trigger episodes of ventricular tachycardia.
Illegal drugs (such as stimulants, like cocaine) also may cause ventricular tachycardia.
Electrolytes ImbalancesLess common causes include blood imbalances, such as low potassium levels and other electrolyte imbalances.
Ventricular tachycardia (VT) or ventricular fibrillation (VF) is responsible for most of the sudden cardiac deaths in the United States, [1] at an estimated rate of approximately 300,000 deaths per year. [2, 3]
dETERMINING sTABILITY
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Hypotension
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Altered level of consciousness
Signs or symptoms of instability include:
Dyspnea
Unstable versus Stable
Patients suffering from pulseless VT or unstable VT require immediate cardioversion and CPR.
Stable
For patients who are hemodynamically stable, antiarrythmic agents such as:
amiodarone, lidocaine, procainamide, or sotolol should be used.
Intravenous dosage1
For the first 24 hours is the following infusion regimen: initial IV rapid infusion of 150 mg over the first 10 minutes. Then begin a slow IV infusion of 1 mg/min for the next 6 hours (total dose infused = 360 mg). Then, the infusion rate is lowered to 0.5 mg/min for the next 18 hours (total dose infused = 540 mg). After the first 24 hours, a maintenance IV infusion of 0.5 mg/minute (720 mg/day) is recommended. Adjust infusion rate to achieve effective arrhythmia suppression. Intravenous amiodarone is not intended for maintenance therapy and should not be administered for longer than 3 weeks. NOTE: The dose of amiodarone may be individualized, however, during controlled clinical trials doses more than 2100 mg were associated with an increased risk of hypotension.
Conversion from intravenous to oral therapy
If the duration of IV infusion was less than 1 week, the initial oral dose is 800 to 1600 mg/day PO. If the duration of IV infusion was 1 to 3 weeks, the initial oral dose is 600 to 800 mg/day PO. If the duration of IV infusion was longer than 3 weeks, the initial oral dose is 400 mg/day PO.
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(What are the doses?)
Catheter ablation is more effective than escalation of antiarrythmic therapy at reducing the occurrence of recurrent VT in patients with ischemic cardiomyopathy, when the initial VT occurred on amiodarone therapy.1
Anticoagulation with warfarin has significant risks, so should be reserved for patients with high CHADS2 scores.
implantable device.
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A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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In the setting of significant structural heart disease, sustained VT (defined as an episode longer than 30 seconds) predicts a poor prognosis.
This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation. With ventricular fibrillation, the heartbeats are so fast and irregular that the heart stops pumping blood.
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A 75-year-old male with a past medical history significant for hypertension, diabetes, and coronary artery disease presents to the emergency department with a 1-hour history of sudden shortness of breath and generalized weakness.
On examination, he is noted to have a blood pressure of 90/58. He is clammy and diaphoretic. His lungs are clear to auscultation. His heart examination reveals tachycardia.
His EKG is shown
