Background: Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than

120 beats per minute and wide !" comple#es$ VT may be monomorphic (typically regular rhythm originating from a single focus with identical !" comple#es) or polymorphic (may be irregular rhythm, with varying !" comple#es)$ %onsustained VT is defined as a run of tachycardia of less than &0 seconds duration' a longer duration is considered sustained VT$ %o absolute ()* criteria e#ist for establishing the presence of VT$ +owever, several factors suggest VT, including the following,

!ate greater than 100 beats per minute (usually 1-0.200) /ide !" comple#es (0120 ms) 1resence of atrioventricular (2V) dissociation 3usion beats

Ventricular tachycardia may develop without hemodynamic deterioration, yet it often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation (V3)$ This tachydysrhythmia must be addressed swiftly to avoid morbidity or mortality$ Pathophysiology: VT usually is a conse4uence of structural heart disease, with brea5down of normal conduction patterns, increased automaticity (which tends to favor ectopic foci), and activation of re.entrant pathways in the ventricular conduction system$ (lectrolyte disturbances and sympathomimetics may increase the li5elihood of VT in the susceptible heart$ 2V dissociation usually is present$ !etrograde ventriculoatrial conduction may occur, which can generate an ()* comple# similar to paro#ysmal supraventricular tachycardia (1"VT) with aberrant conduction$ 2 distinctive variant of VT is torsade de pointes, with its unusual shifting.a#is !" comple#es that appear (on ()*) as if the heart is rotating upon an a#is$ 6t typically occurs from drugs or conditions that prolong the T interval (eg, type 12 antiarrhythmics and hypomagnesemia)$ 2rrhythmia may occur with or without either myocardial ischemia or infarction$ 2 second variant of VT is accelerated idioventricular rhythm$ "ometimes termed slow ventricular tachycardia, this arrhythmia presents with a rate of 70.100 beats per minute$ 6t typically occurs with underlying heart disease (ischemic or structural), is transient, and only rarely is associated with hemodynamic compromise or collapse$ Treatment usually is not re4uired unless hemodynamic impairment develops$ Frequency:

In the US: VT is one of the most fre4uently observed dysrhythmias$

Internationally: VT and coronary disease are common throughout most of the developed world$ 6n developing countries, VT and other heart diseases are relatively less common$

Mortality/Morbidity: VT can produce congestive heart failure and hemodynamic compromise, yet the principal morbidity comes from its tendency to degenerate spontaneously into V3$ This degeneration also is the usual source of mortality in VT$ Sex: 8ost patients presenting with VT are men$ +owever, as coronary artery disease ()29) becomes more common in women, incidence of VT in women will increase$ Age:

VT is very unusual among pediatric patients$ Tachydysrhythmias in this population usually are 1"VT$ VT incidence rates pea5 in the middle decades of life, following the incidence of structural heart disease$

istory: 8ost patients present to the (9 with symptoms of either ischemic heart disease or hemodynamic compromise resulting from poor perfusion$ "ymptoms may include the following,

)hest pain 1alpitations 2n#iety 9iaphoresis

Physical: 3indings generally reflect the degree of hemodynamic instability$

"ymptoms of congestive heart failure ()+3)

o o o

9yspnea and hypo#emia !ales from pulmonary edema :ugular venous distention

+ypotension 8ental status changes

o o

2n#iety 2gitation

o o

;ethargy 3ran5 coma

!auses: 2s noted above, VT generally is a symptom of )29 or structural heart disease$

VT can be triggered by electrolyte deficiencies (eg, hypo5alemia, hypocalcemia, hypomagnesia)$ <se of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine) may stimulate VT in vulnerable hearts$

Stable "ono"orphic #entricular tachycardia

Algorith" $or"al %F: 8ay proceed directly to synchronised cardio#ersion or use one of the following drugs, . procaina"ide, or a"iodarone& or lidocaine, or sotalol =0 synchronised cardio#ersion is mandatory if elected drug therapy is not successful (100: =0 200: =0 &00: =0 &70:, or e4uivalent biphasic' 0$- . 1:>5g . pediatric) %F lo'/! F: 8ay proceed directly to synchronised cardio#ersion or use one of the following drugs, a"iodarone or lidocaine () synchronised cardio#ersion is mandatory if elected drug therapy is not successful Adult doses and precautions

procaina"ide dose = 20mg>min 6V infusion up to a ma#imum dose of 1?mg>5g, discontinue procainamide if patient becomes hypotensive, or if !" comple# prolongs 0 -0@, or if the ma#imum recommended dose of 1?mg>5g is given =0 1 . A mg>min 6V infusion if chemical conversion is successful lidocaine dose = 0$-.0$?-mg>5g 6V, and the same dose can be repeated 4 B . 10 mins to a ma#imum dose of &mg>5g =0 1 . A mg>min 6V infusion if chemical conversion is successful a"iodarone dose = 1-0mg 6V over 10 minutes at 1-mg>min, continue 6V infusion at a rate of 1mg>min if chemical conversion is successful' ma#imum daily dose of 2g>day sotalol dose = 1.1$-mg>5g 6V at 10mg>min Pediatric doses and precautions procaina"ide dose = 1-mg>5g over &0 . 70 minutes 6V

lidocaine dose = 1mg>5g 6V bolus a"iodarone dose = -mg>5g over 20 . 70 minutes 6V *arnings use cardioversion as primary therapy if there is any uncertainty about clinical stability prior to, or during drug therapy avoid using multiple anti.arrhythmic drugs in se4uence because of potential pro.arrhythmic effects

Stable poly"orphic #entricular tachycardia + $or"al ,- inter#al

Algorith" %F nor"al: 8ay proceed directly to synchronised cardio#ersion or use one of the following drugs,. a"iodarone or beta blocker or lidocaine or procaina"ide or sotalol =0 synchronised cardio#ersion is mandatory if elected drug therapy is unsuccessful %F lo'/! F: 8ay proceed directly to synchronised cardio#ersion or use one of the following drugs,. a"iodarone or lidocaine =0 synchronised cardio#ersion is mandatory if elected drug therapy is unsuccessful Adult doses and precautions

a"iodarone dose = 1-0mg over 10 minutes 6V at 1-mg>min =0 1 mg>min 6V infusion rate if chemical conversion is successful lidocaine dose = 0$?-mg>5g 6V push =0 0$-.0$?-mg>5g 6V prn 4 B .10 minutes to a ma#imum total dose of &mg>5g =0 1 . Amg>min 6V infusion rate if chemical conversion is successful procaina"ide dose = 20mg>min 6V infusion to a ma#imum dose of 1?mg>5g =0 1 . A mg>min 6V infusion rate if chemical conversion is successful sotalol dose = 1.1$-mg>5g 6V at 10mg>min Pediatric doses and precautions a"iodarone dose = -mg>5g over 20 . 70 minutes 6V>6C lidocaine dose = 1mg>5g 6V>6C bolus procaina"ide dose = 1-mg>5g over &0 . 70 minutes 6V>6C *arnings use cardioversion as primary therapy if there is any uncertainty about clinical stability prior to, or during drug therapy avoid using multiple anti.arrhythmic drugs in se4uence because of potential pro.arrhythmic effects

Stable poly"orphic #entricular tachycardia + prolonged ,- inter#al

Algorith" $or"al %F: 8ay proceed directly to synchronised cardio#ersion& or correct electrolyte abnor"alities D drug>pacing therapy . any one of "agnesiu", o#erdri#e pacing, lidocaine, phenytoin or isoproterenol =0 synchronised cardio#ersion is mandatory if elective drug therapy is unsuccessful .o' %F/! F: 8ay proceed directly to synchronised cardio#ersion& or a"iodarone or lidocaine =0 synchronised cardio#ersion is mandatory if elective drug therapy is unsuccessful Adult doses and precautions

"agnesiu" dose = 1 . 2g 6V (diluted in -0 . 100cc of saline) over - . 20 minutes =0 0$- . 1g>hour 6V infusion rate if chemical conversion is successful lidocaine dose = 0$?-mg>5g by rapid 6V bolus, repeated prn 4 B . 10 minutes to a ma#imum total dose of &mg>5g =0 1. Amg>min 6V infusion rate if chemical conversion is successful phenytoin dose = -0mg>min 6V to a ma#imum dose of 1?mg>5g' slow>discontinue 6V infusion if hypotension ensues or !" comple# prolongs 0 -0@ isoproterenol in/usion can be used as a temporising measure until overdrive pacing can be instituted . start at 2.10mcg>min (6V solution prepared by diluting 1mg in -00ml of -@9>/) a"iodarone dose . 1-0mg 6V over 10 minutes at 1-mg>min =0 1mg>min 6V infusion rate if chemical conversion is successful Pediatric doses and precautions "agnesiu" dose = 20. -0mg>5g 6V>6C over - . 20 minutes 6V to ma#imum dose of 2g lidocaine dose = 1m5>5g 6V>6C bolus a"iodarone dose = -mg>5g over 20 . 70 minutes 6V>6C *arnings use synchronised cardioversion as primary therapy if there is any uncertainty about clinical stability prior to, or during administration of drug therapy avoid using multiple anti.arrhythmic drugs in se4uence because of potential pro.arrhythmic effects avoid using procainamide (or similar drugs) in a patient with a prolonged T interval or torsade des pointes