Ventricular Tachyarrhythmia DrAmirhosseinAzhari Electrophysiologist
VENTRICULAR TACHYARRHYTHMIAS • VENTRICULAR TACHYCARDIA • VENTRICULAR FIBRILLATION
Underlying Arrhythmia of Sudden Death Primary VF 8% Torsades de Pointes 13% VT 62% Bradycardia 17% Adapted from Bayés de Luna A. Am Heart J. 1989;117:151-159.
DEFINITION • Occurrence of a series of three or more consecutive abnormaly shaped premature ventricular complexes, • WHOSE DURATION EXCEEDS 120 ms, • With the ST-T vector pointing opposite the major QRS deflection
Symptoms occurring during VT depend on • The ventricular rate, • Duration of tachycardia, • Presence and extent of the underlying heart disease and peripheral vascular disease.
VT can occur in several forms: • Short, asymptomatic, Nonsustainedepisodes; • Sustained, • Hemodynamicallystable events, generally occurring at slower rates or in otherwise normal hearts; • Unstable runs, often degenerating into VF
VENTRICULAR TACHYCARDIA VT NONSUSTAINED SUSTAINED
NONSUSTAINED VT Three or more consecutive ventricular premature depolarizations, up to a maximum duration of 30seconds before spontaeous termination
Importance of NSVT • Most tachyarrhythmias come to our attention because of the symptoms they produce • In contrast,most instances of NSVTdo not cause symptoms • Rather it derives its importance from the prognostic significance it carries in some patient populations
SUSTAINED VT MONOMORPHIC UNIFORM POLYMORPHIC MULTIFORM ,PLEOMORPHIC
SUSTAINED VT IN PATIENTS WITH ORGANIC HEART DISEASE IN PATIENTS WITH NORMAL HEARTS
VT in normal hearts • 1-Idiopathic VT • 2-long Q-T syndrome • 3-Brugada syndrome • 4-Catecholaminergic polymorphic VT • 5-Short Q-T syndrome
IDIOPATHIC VT PROPRANOLOL -SENSITIVE VT AUTOMATICITY ADENOSINE -SENSITIVE VT TRIGGEREDACTIVITY VERAPAMIL -SENSITIVE VT INTRAFASCICULAR REENTRY
ADENOSINE-SENSITIVE VT CLINICAL CHARACTERISTICS • THE MOST COMMON FORM OF IDIOPATHIC VT(75-90%) • ORIGINATES FROM RIGHT VENTRICULAR OUTFLOW TRACT
RVOT VT USUALLY EXHIBITS ONE OF TWO PHENOTYPES • NONSUSTAINED REPETITIVE MONOMORPHIC VT(RMVT) • PAROXYSMAL EXERCISE INDUCED SUSTAINED VT
THERE IS A CONSIDERABLE OVERLAP BETWEEN THESE TWO PHENOTYPES OF ADENOSINE-SENSITIVE RVOT VT
Long QT • Acquired • Congenital
The acquired form has a long-QT interval caused by various drugs, such as • Quinidine, procainamide, sotalol, amiodarone, disopyramide, phenothiazines, tricyclic antidepressants, erythromycin, pentamidine, antimalarials, cisapride, and probucols
Electrolyte abnormalities, such as • Hypokalemia and hypomagnesemia; • The effects of a liquid protein diet and starvation; • Central nervous system lesions; significant bradyarrhythmias.
CLINICAL MANIFESTATIONS • The principal symptoms are syncope and SCD,from TDP • Most often,TDP is self-terminating and cause a syncopal episode from which the patient quickly recovers • Cardiac arrest occurs if the TDP is more persistent,and SCD results if the rhythm does not return to normal spontaneously
QT Duration • A widely accepted method for correcting QT interval for rate is Bazett’s formula • Lead II is generally the best single lead for measuring QT interval. • Traditionally, QTc >440 msec were considered prolonged; however, values up to 460 msec may still be normal among females • Affected gene carriers can have a QTc of 410 msec or less and no normal person has a QTc of 470 or more (men) or 480 or more (women)
ECG MANIFESTATIONS • A QTC of 0.47 sec in men and 0.48 sec in women is 100% sensitive for LQTS • A QTC less than 0.40 sec in menand 0.42 sec in women is 100% specific for excluding LQTS
Treatment • Intravenous magnesium is the initial treatment of choice for torsades de pointes from an acquired cause, followed by temporary ventricular or atrial pacing. • In all patients with torsades de pointes, administration of class IA, possibly some class IC, and class III antiarrhythmic agents ( amiodarone, dofetilide, sotalol) can increase the abnormal QT interval and worsen the arrhythmia.
For patients who have idiopathic long-QT syndrome but • Not syncope, • Complex ventricular arrhythmias, • Afamily history of sudden cardiac death, • QTc no longer than 500 milliseconds • No therapy or treatment with a beta blocker is generally recommended
In patients with : • Syncope caused by ventricular arrhythmias or aborted sudden death, • An ICD is warranted
Brugada Syndrome • Brugada syndrome is a distinct form of idiopathic VF in which patients have right bundle branch block and ST-segment elevation in the anterior precordial leads, without evidence of structural heart disease • Mutations in genes responsible for the sodium channel (SCN5A) and calcium channel have been identified in many families with Brugada syndrome
Currently, no pharmacologic treatment reliably prevents VF in these patients. ICDs are the only effective treatment to prevent sudden death
Ischemic Cardiomyopathy • Patients with previous myocardial infarction are at risk for development of VT. In the setting of a remote myocardial infarction, the mechanism of VT is reentry, involving the infarct scar and in particular the border zone or other areas of the scar with deranged conduction. As a result, the VT in this setting is typically monomorphic
1 sec VT
In general, ICDs are indicated to prevent sudden cardiac death from VT in this group of patients, especially in those with depressed LV function
VT IN DCM • BUNDLE BRANCH REENTRY MAY BE SEEN IN THIS POPULATION AND CAN BE TREATED BY ABLATING THE RBB
VT IN HCM RISK FACTORS FOR SCD IN HCM • CARDIAC ARREST(VF) • SUSTAINED VT • SYNCOPE PARTICULARLY IF RECURRENT AND EXERTIONAL • FAMILIAL SUDDEN HCM- RELATED DEATH IN FIRST DEGREE RELATIVES • NSVT ON HOLTER FREQUENT,REPETITIVE AND PROLONGED • ABNORMAL BP RESPONSE IN EXERCISE >20 mm HG • EXTREME LV HYPERTROPHY >30 mm
Acute Management of Sustained Ventricular Tachycardia • VT that does not cause hemodynamic decompensation can be treated medically to achieve acute termination by the intravenous administration of amiodarone, lidocaine, or procainamide, followed by an infusion of the successful drug
In general, amiodarone • loading dose of 15 mg/min is given during a 10-minute period. • This dose is followed by an infusion of 1 mg/min for 6 hours and then • a maintenance dose of 0.5 mg/min for the remaining 18 hours and for the next several days, as necessary
If the arrhythmia does not respond to medical therapy • Hypotension,Shock • Angina, • Congestive heart failure • Symptoms of cerebral hypoperfusion should be treated promptly with DC cardioversion.
Very low energies can terminate VT, beginning with a synchronized shock of 10 to 50 J.
The goal of long-term therapy is to prevent sudden cardiac death and recurrence of symptomatic VT. • Asymptomatic nonsustained ventricular arrhythmias in low-risk populations (preserved LV function) often need not be treated. • In patients with symptomatic nonsustained tachycardia, beta blockers are frequently effective in preventing recurrences.
In patients refractory to beta blockers, class IC agents, sotalol, or amiodarone can be effective. • However, class IC agents should be avoided in patients with structural heart disease, especially those with coronary artery disease because of the increased mortality associated with these drugs caused by proarrhythmia.
Sotalolshould be used cautiously because of its potential for prolonging the QT interval and producing torsades de pointes. • Patients with nonsustained VT after myocardial infarction and poor LV function are at significant risk for sudden death