Ventricular Tachycardia (VT) A. General Characteristics 1.

Defined as rapid and repetitive firing of 3 or more PVCs in a row, at a rate of between 100 and 200 bpm 2. AV dissociation is present, i.e., sinus P waves continue with their cycle, unaffected by the tachycardia 3. Originates below the bundle of His 4. VT or VFib cause 75% of episodes of cardiac arrest 5. Causes a. CAD with prior and I is most common cause b. Active ischemia, hypotension c. Cardiomyopathies d. Congenital defects e. Prolonged QT syndrome f. Drug toxicity 6. Sustained versus nonsustained VT a. Sustained VT (persists in absence of intervention) Lasts longer than 30 seconds and is almost always symptomatic Often associated with marked hemodynamic compromise (i.e. hypertension) and/or development of myocardial ischemia A life-threatening arrhythmia Can progress to ventricular fibrillation if untreated b. Nonsustained VT Brief, self-limited runs of VT Usually asymptomatic When CAD and LV dysfunction are present, it is an independent risk factor for sudden-death. Therefore, patients with nonsustained VT should be thoroughly evaluated for underlying heart disease and LV dysfunction. 7. Prognosis depends on the presence of heart disease and on whether VT is sustained or nonsustained. VT after an MI usually has a poor prognosis, especially if it is sustained. In patients with no underlying heart disease, the prognosis is good. 8. In sum, the presence of ventricular irritability (frequent PVCs, VT) is especially worrisome in patients with underlying heart disease and left ventricular dysfunction. These patients are at a high risk for sudden death B. Clinical features 1. Palpitations, dyspnea, lightheadedness, angina, impaired consciousness (syncope or near syncope) 2. May present with sudden cardiac death 3. Signs of cardiogenic shock maybe present 4. May be asymptomatic if rate is slow

5. Physical findings include cannon a waves in the neck (secondary to AV disassociation, which results in atrial contraction during ventricular contraction) and an S1 that varies in intensity C. Diagnosis 1. ECG: wide and bizarre QRS complexes a. Always suspect VT in a patient with a wide (>0.12 sec) QRS tachycardia b. Torsades de pointes: is a rapid polymorphic VT. It is a dangerous arrhythmia that often can lead to VFib. It is associated with many factors that prolong QT interval (e.g. congenital QT syndromes, tricyclic antidepressants, anticholinergics, electrolyte abnormalities, ischemia) IV magnesium provides cardiac stabilization. Address the underlying cause 2. QRS complexes maybe monomorphic or polymorphic a. In monomorphic VT, all QRS complexes are identical It is important to distinguish monomorphic VT from SVT with abarrant conduction Wide complex tachycardia in adults with a history of structural heart disease is much more likely to be due to VT than SVT with aberrancy b. In polymorphic VT, the QRS complexes are different 3. Unlike PSVT, VT does not respond to vagal maneuvers or adenosine D. Treatment 1. Identify and treat reversible causes 2. Sustained VT a. Hemodynamicallly stable patients with mild symptoms systolic BP >90 pharmacologic therapy New ACLS guidelines recommend IV amiodarone, IV procainamide, or IV sotalol over IV lidocaine or IV bretylium Hemodynamically unstable patients or patients with severe symptoms Immediate synchronous DC cardioversion Follow with IV amiodarone to maintain sinus rhythm b. Ideally, all patients with sustained VT should undergo placement of an ICD, unless EF is normal (then consider amiodarone) 3. Nonsustained VT a. If no underlying heart disease and asymptomatic, do not treat. These patients are not at increased risk for sudden death. b. If the patient has underlying heart disease, a recent MI, evidence of LV dysfunction, or is symptomatic, order an electrophysiologic test: if it shows inducible, sustained VT, ICD placement is appropriate c. Pharmacologic therapy is second line treatment. However, amiodarone has the best results of all of the antiarrhythmic

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