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VENTRICULAR TACHYCARDIA
Overview of approach to ventricular tachycardia
EKG Features of VT
•
If patient is hemodynamically stable, take a deep breath and get a 12-lead EKG!
Leads of choice to analyze: V1-2 and 6 for bundle branch morphology; I and F for axis EKG findings suggestive of VT: 1) AV dissociation/VA block with Wenckebach: “cherchez le p” and try to march them out using the 2) Fusion/capture beats 3) Concordance V1-6: can also be seen in WPW however 4) V1: slurred downstroke; RBBB morphology Rsr’, monophasic or biphasic 5) V6: LBBB morphology monophasic 6) NW axis: negative I, aVF 7) QRS > 0.14
Approach to differential diagnosis of VT
Step 1: Look at EKG morphology
Monomorphic or polymorphic?
If monomorphic, try to identify location of VT focus:
•
If VT has an LBBB pattern (i.e. positive in I, V6, negative in V1), it is likely coming from the RIGHT ventricle (particularly if patient is young and/or ostensible has no structural heart disease) If VT has an RBBB pattern (i.e. isoelectric in I, positive in V1), it is likely coming from the LEFT ventricle If VT has a superior axis (i.e. positive in I, negative in F), it is likely coming from the region of the ventricular apex or diaphragmatic region If VT has an inferior axis (i.e. negative in I, positive in F), it is likely coming from the region of the outflow tract To help remember the above, just think OPPOSITE bundle, OPPOSITE axis EKG morphology
from anatomic source
Step 2: Is the heart structurally normal?
Monomorphic VT with
Structurally abnormal heart:
•
CAD: Ischemia induced v. Scar induced
Cardiomyopathy (dilated CM, hypertrophic CM, valvular CM)
Infiltrative disease (amyloidosis, sarcoidosis)
Valvular disease: mitral valve prolapse association
Bundle branch reentry: associated with DCM, valve surgery and myotonic dystrophy
Arrhythmogenic right ventricular dysplasia (ARVD)
•
Seen primarily in young patients; marked replacement of right ventricular myocardium by fibrofatty tissue with development of RV cardiomyopathy ECG during VT: LBBB morphology with inferior (pulmonary infundibular source) or superior axis (apical source) ECG during NSR: T wave inversions beyond V1 (50%), incomplete RBBB (18%), epsilon waves (postexcitation activation of right ventricular fibers) are seen in 30% cases- defined as potential in V1-3 (can look like pseudo R’) that is >25 msec beyond end of QRS in V6 (or QRS > 110 ms V1-V3) DX: MRI, right ventriculography (infundibular aneurysm, hypertrophic trabeculae, TVP)
TX: ICD, antiarrhythmics, RFA (usually adjunctive), surgical isolation, cardiac transplant
Structurally normal heart:
•
RV outflow tract tachycardia (adenosine-sensitive VT)
•
Two types: repetitive monomorphic VT (RMVT) and exercise-induced VT LBBB morphology with inferior axis (usual y originates from RVOT) Cornel Cardiology Curriculum 2003-2004 32 Mechanism: adenosine sensitivity with catecholamine-mediated triggered activity and DADs (cAMP stimulation of oscil atory calcium channel release, giving rise to DAD (due to ITi) TX: RFA (definitive), beta blockers, CCB, class I agents
NOTE: variants include LVOT source (10%) with either RBBB pattern in V1 or LBBB with
early precordial transition in V2 (aortic sinus cusp source; Ouyang et al., JACC 2002)
Idiopathic LV tachycardia (verapamil-sensitive fascicular VT)
•
Usual y RBBB morphology with relatively narrow QRS and superior axis Mechanism: reentry; left posterior fascicular origin (inferoposterior origin with short retrograde VH interval), EP study will reveal location of retrograde Purkinje potentials (also known as mid or late diastolic potentials) that reflect depolarization of the slow conduction portion of reentrant circuit TX: RFA (definitive), CCB
Automatic (propanolol sensitive) VT* (see Familial polymorphic VT syndrome below)
•
Younger patients, precipitated by exercise Inflammatory LV microaneuryms: RBBB morphology, seen in cases of myocarditis with general y
good prognosis

Polymorphic VT with:
Normal QT
•
MYOCARDIAL ISCHEMIA (MOST COMMON CAUSE)
Brugada syndrome:
•
Association of VT/VF with characteristic ECG pattern: RBBB morphology with ST elevation in V1-3 (unrelated to ischemia, electrolyte abnormalities or structural heart disease) Mechanism: some forms linked to SCN5A gene mutation (also in LQT3 form of long QT); impaired Na channel function leads to unopposed Ito current during phase 1 of the action potential leading to early repolarization (this occurs primarily in the epicardium leading to a transmural voltage gradient that is manifest by J point elevation)  dispersion of repolarization  phase 2 reentry  extrasystole  circus movement reentry – VT/VF TX: ICDs primarily given high mortality rate
Familial polymorphic VT syndrome (also known as catecholaminergic VT) – now thought to be a
major subset of automatic (propranolol sensitive) VT
•
Classical y presents with stress-induced bidirectional VT; look for strong FH of SCD Autosomal dominant with association with RyR2 mutation (ryanodine receptor/calcium release channel); RyR sits on sarcoplasmic reticulum (SR) membrane and is activated by Ca influx through L-type calcium channels; RyR in turn activates calcium-induced calcium release channels of the SR
Long QT
•
Acquired long QT:
•
Class IA, class IC, and class III antiarrhythmic agents; Haldol, erythromycin, Seldane/Cisapride (pul ed off market), Reglan, TCAs Mutations in HERG and MiRP1 genes have been associated with drug-induced torsades Congenital long QT
•
LQT1-6 (linked to variety of sodium channel and potassium channel mutations- KVLQT1, minK, HERG, MiRP1, SCN5A) See Torsades de Pointes section for details
33 Cornel Cardiology Curriculum 2003-2004
Acute treatment of ventricular tachycardia
Unstable VT/VF arrest
•
See ACLS protocol and Resuscitation (in this curriculum) section for details
DC cardioversion (UN-synchronized): monophasic shocks 200J – 300J – 360J (biphasic shocks
require less energy and have been shown to result in higher rates of successful defibrillation with 1st
shock)
Epinephrine 1 mg or Vasopressin 40U IV
Amiodarone 300 mg bolus (can repeat 150 mg) IV; can then infuse at 1 mg/min initially
Its use has been supported by the ARREST trial (amiodarone v. placebo in out-of-hospital
VF/pulseless VT arrests) and the ALIVE trial (amiodarone v. lidocaine in VF/pulseless VT arrests)
Lidocaine 1.5 mg/kg bolus (can repeat 0.5-0.75 mg/kg) IV; can then infuse at 2-4 mg/h
•
Although lidocaine is general y safe, its effectiveness in terminating VT/VF has been cal ed into question by various studies comparing it to placebo and other antiarrhythmics Procainamide 30 mg/min (17 mg/kg max) load IV  stop if hypotension, QRS prolonged > 50%, or
QT prolongation  can then infuse at 1-6 mg/min initially (check NAPA/procainamide levels after
24hs if renal failure or if infusion rate>= 2 mg/min)
•
While procainamide has been shown to be effective in terminating stable VT, its use is general y NOT recommended during arrests given the long time required for its infusion and its hypotensive effects Magnesium 1-2 mg IV push should be given if torsade de pointes or hypomagnesemic states are
suspected
REMEMBER TO CONTINUE TO ADMINISTER DEFIBRILLATION SHOCKS WITH EACH
MEDICATION ADMINISTRATION OR AFTER 1 MINUTE OF CPR WHILE STILL IN VT/VF

Stable VT
•
DC cardioversion (synchronized)
Pharmacological therapy
If low EF, consider:
Amiodarone 150 mg/min bolus IV over 10 min then 1 mg/min x 6hs then 0.5 mg/min x 18hs
initial y
Lidocaine 1 mg/kg load IV then 1-4 mg/min maintenance
Procainamide 100 mg IV q10 min or infuse at 20 mg/min to total 17 mg/kg (renal elim)
Amiodarone
Lidocaine
Other pharmacological agents can be considered which should be tailored to specific etiologies of the arrhythmia (e.g. verapamil in idiopathic left ventricular tachycardia)
Pearls
•
Immediate post-MI ectopy (within 48ds) such as PVCs or asymptomatic NSVT does NOT need to be treated Post MI AIVR (rate 50-120) is NOT treated because 1) it is usually transient, benign and a sign of reperfusion and 2) are at times an escape rhythm due to intrinsic pacemaker failure Cornel Cardiology Curriculum 2003-2004 34
Chronic treatment of sustained VT: ICD Therapy

Key questions to answer when considering ICD therapy
1) Did VT/VF occur in the setting of ACUTE ischemia? (answer with cardiac enzymes, cardiac
catheterization)
2) Does the patient have significant coronary disease? (answer with stress testing, cath)
3) Does the patient have a structurally normal heart? (answer with echo +/- cardiac MRI)
4) Does the patient have a family history of sudden cardiac death?

Primary prevention of SCD
If low EF (i.e. < 30-40%) AND ischemic cardiomyopathy
•
If patient has NSVT, perform EP study; if inducible, place ICD  this has been supported by the
MADIT-I (EF 35% cutoff) and MUSTT (EF 40% cut off) trials
However, MADIT-II data (EF 30% cut off) currently supports ICD placement regardless of presence
of ectopy
If low EF AND nonischemic cardiomyopathy
•
There is poor data at this point to guide the use of ICD therapy Patients with NICM, low EF and history of syncope are at high risk of SCD and ICDs are often indicated It is unclear what to do with patients with NICM, low EF and NSVT • EP studies are of limited utility in these situations (it would al ow detection of bundle branch reentry which is an ablatable rhythm) GESICA and subgroup analysis of CHF STAT trials would support the use of amiodarone
although this is controversial
Several ongoing studies including DEFINITE and SCD-HeFT trial should answer some of these
questions
If normal EF and apparently structurally normal heart
•
Consider ICD and/or pharmacological therapy if etiology of SCD is understood Examples:
•
Brugada syndrome: consider ICD therapy given high risk of SCD
Secondary prevention of SCD
•
The use of ICDs have been supported by the AVID study (to a greater extent than the CIDS and
CASH studies) in patients with one of the fol owing:
•
History of resuscitation from VF/pulseless VT arrest Sustained VT with EF < 40% resulting in hemodynamic compromise (i.e. near syncope, CHF and angina In the above cases, would need to rule out acute myocardial infarction as cause of VF/VT episode before considering ICD implantation as coronary revascularization would be treatment of choice in such cases
REFERENCES
ACLS guidelines. Circulation 2000 102 [Suppl I]: I-86 - I-171.
ALIVE Dorian et al., Amiodarone as compared with lidocaine for shock-resistant ventricular defibril ation.
NEJM 2002; 346: 884-90.
Altemose et al. Idiopathic ventricular tachycardia. Annu Rev Med 1999; 50: 159-77.
ARREST Kudenchuk et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to
ventricular fibril ation. NEJM 1999;341:871-878.
AVID A comparison of antiarrhythmic drug therapy with implantable defibril ators in patients resuscitated
from near fatal ventricular arrhythmias. NEJM 1997; 337: 1576-83.
35 Cornel Cardiology Curriculum 2003-2004 Chimenti et al. Inflammatory left ventricular microaneurysms as a cause of apparently idiopathic
ventricular tachyarrhythmias. Circulation 2001; 104: 168-73.
Fontaine et al. Arrhythmogenic right ventricular dysplasia. Annu Rev Med 1999; 50: 17-35.
GESICA Doval et al. Randomised trial of low-dose amiodarone in severe congestive heart failure.
Klein et al. New primary prevention trials of sudden cardiac death in patients with left ventricular
dysfunction: SCD-HEFT and MADIT-II. Am J Cardiol 199; 83: 19D-97D.
MADIT Moss et al. Improved survival with an implanted defibrillator in patients with coronary disease at
high risk for ventricular arrhythmia. NEJM 1996; 335: 1933-40.
MUSTT Buxton et al. A randomized study of the prevention of sudden death in patients with coronary
artery disease. NEJM 1999; 341: 1882-90.
Viskin, S. Long QT syndromes and torsade de pointes. Lancet 1999; 354: 1625-33.
Zipes and Wellens. Sudden Cardiac Death. Circulation 1998; 98: 2334-2351.
Cornel Cardiology Curriculum 2003-2004 36

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