ventricular tachycardia - budi baktijasa, md, fiha.pdf
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CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
VENTRICULARTACHYCARDIA
Budi Baktijasa DharmadjatiOryza Sativa
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
DEFINITION
Characterized by three or more consecutive, abnormallyshaped PVCs with rate > 100 bpm (usually 150-200 bpm)with wide QRS complexes (QRS > 0.12 s)
The focus originated from ventricle (left or right) or as aresult of reentry process in some part of the bundlebranch (bundle branch reentry VT)
broad complex tachycardia originating in the ventricles
Olgin J, Zipes DP. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
CLASSIFICATION OFVENTRICULAR TACHYCARDIA
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
QRS COMPLEXESMORPHOLOGY
Monomorphic VT
Most common
Uniform complexes
Polymorphic VT
Beat to beat changes ofQRS complexesappears twist around thebaseline
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Olgin J, Zipes DP, 2012;Katrisis DG, Zareba W, Camm AJ, 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
TORSADES DE POINTES
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
ETIOLOGY
Idiopathic Right ventricular outflow tract (RVOT) VT Left ventricular outflow tract (LVOT) VT Idiopathic left ventricular tachycardia (ILVT) Cathecolaminergic Polymorphic VT (CPVT)
VT in cardiomyopathy (non-ischemic) Bundle Branch Reentrant VT Arrhythmogenic Right Ventricular Cardiomyopathy
(ARVC)
Ischemic VT
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
CLINICAL MANIFESTATION
Stable VT Hemodynamically stable
Usually don’t requirespecific intervention
Unstable VT Hemodynamically
compromised
Hypotension, chest pain,heart failure, decreaseLOC
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
DURATION
Sustained VT
Duration > 30 seconds
Leads to hemodynamiccompromise
Requires furtherintervention to terminatethe episode
Non-sustained VT
Duration < 30 seconds
Self terminating
Usually withouthemodynamic instability
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Katrisis DG, Zareba W, Camm AJ. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
EPIDEMIOLOGY
Most common cause of VT is coronary artery disease
VT/VF is the most frequent complication caused by ACS thatleads to sudden cardiac death
CAD will cause scar tissue which, when accompanied by anincreased activity of reentrant circuit will trigger VT
Panchon M, Almendral J. 2011; Goldberger JJ, Basu A, Boineau R. 2011;Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015; Zipes DP, Camm AJ, Borggrefe M. 2006
Non structural heart disease px associated with morebenign form of VT
Prystowsky EN, Padanilam BJ, Joshi S. 2012; Katrisis DG, Zareba W, Camm AJ. 2012;Koplan BA, Stevenson WG. 2009
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Predisposing factors includes: Tissue ischemia Hypoxemia Autonomic system (sympathetic activity that would
increased HR) Metabolic abnormality (lactic acidosis) Haemodynamic disturbance (decreased coronary
perfusion) Drugs (digitalis) Electrolyte imbalance (hypokalemia due to forced
diuresis) Acute reperfusion due to trombolytic agents
Olgin J, Zipes DP. 2012; Prystowsky EN, Padanilam BJ, Joshi S. 2012;Katrisis DG, Zareba W, Camm AJ. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
PATHOPHYSIOLOGY
• Most common mechanismof VT: reentry
• Caused by scarredmyocardium orcardiomyopathy
• Scarred myocardium orischemic tissue interspersedbetween normal viablemyocardium may providedsubstrate for reentrymechanism
• Triggered activity is morecommon in the nonischemic or normal heart
Olgin J, Zipes DP. 2012; Gaztanaga L, Marchlinski FE, Betensky BP. 2012;Chen P, Antzelevitch E. 2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
REENTRY
Scar tissue isolated viablebundles of conductingmyocardium with slowconduction from the normalconducting myocard in theremainder of ventricle
When a stimulus reaching thearea surrounded by scar, it willtravel with such delay that thewavefront arrives at distalterminus of the bundle toencounter fully repolarizedmyocardium allowingreentrant circuit
Gaztanaga L, Marchlinski FE, Betensky BP. 2012;Chen P, Antzelevitch E.2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
TRIGGERED ACTIVITY Impulse initiation caused
afterdepolarizations (membranepotential oscillations that occurduring or immediately following apreceding AP)
Afterdepolarizations occur onlyin the presence of a previous AP(the trigger), and when theyreach the threshold potential, anew AP is generated
This may be the source of a newtriggered response, leading toself-sustaining VT.
Myocardial damage oscillations transmembranepotential ‘after depolarization” treshold potential VT
Gaztanaga L, Marchlinski FE, Betensky BP. 2012;Chen P, Antzelevitch E.2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
EAD Arise during the plateau
phase or the repolarizationphase of the last beat andmay be the cause oftorsades de pointes
DAD Arise during the resting
phase of the last beat andmaybe the cause ofdigitalis-inducedarrhythmia
Gaztanaga L, Marchlinski FE, Betensky BP. 2012;Chen P, Antzelevitch E.2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Occurs as a response to a preceeding impulse(the trigger)
Automatic rhythms can arrive de novo in theabsence of prior electrical activity
Triggered activity is not a self genertaing rhythm
Gaztanaga L, Marchlinski FE, Betensky BP. 2012;Chen P, Antzelevitch E.2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
CLINICAL EXAMINATION
VT frequently precede significant haemodynamiccollapse
Asymptomatic individuals with or withoutelectrocardiographic abnormalities
Persons with symptoms potentially attributable toVT Palpitations Dyspnea Chest pain Syncope and presyncope
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Risk factors for developing VT : MI, SHD, or familyhistory of SCD
Every px aged < 40 yo with family history of SCDshould be evaluated for genetic arrhythmiassyndrome (LQTS, Brugada syndrome, RVarrhythmogenic dysplasia, hypertrophiccardiomyopathy)
Goldberger JJ, Basu A, Boineau R. 2011; Priori SG, Blomstorm-Lundqvist C,Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006Prystowsky EN, Padanilam BJ, Joshi S.2012; Katrisis DG, Zareba W, Camm AJ. 2012;
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
From physical examination : Tachycardia (related to hypotension and
tachypnea) Lack of tissue perfussion leads to decreased LOC,
diaphoresis and shock Variated 1st heart sound (AV dissociation) Murmur or S3 gallop (related to underlaying heart
disease)
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
WORK UP
Detect underlying heart disease (including inheritedand acquired cardiomyopathy)
Resting 12 lead electrocardiography evaluate thepresence of myocardial scar (Q-waves or fractionatedQRS complexes), the QT interval, ventricularhypertrophy
Echocardiography RV and LV structure and function,valvular abnormalities, and pulmonary artery systolicpressure Recommended for px symptomatic PVCs, a high
frequency of PVCs (.10% burden), or when the presenceof SHD is suspected.
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP. 2012
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
ECG DIAGNOSTIC CRITERIA
1. Three or more consecutivePVCs
2. Heart rate 100-250 bpm3. AV dissociation Independent P wave, not
related with QRScomplexes, with differentrate
Fusion beat, when impulsesoriginated from SA Nodeconducted to ventricle by andmerging with impulses originatedfrom ventricle
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Captured beat, impulsesoriginated from atriumdepolarize ventricle throughnormal conduction pathway early and narrow QRS complexes
4. Extreme axis deviation(northwest axis) : positive QRScomplexes in aVR, negative inlead I and aVF
5. Positive or negativeconcordance
6. Brugada’s sign, the distancefrom the onset of the QRScomplexes to the nadir of the S-wave is > 100 ms
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Positive concordance of VT
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
7. Josephson’s sign, notchingnear the nadir of the S-wave.
8. RSR’ complexes with higherleft rabbit ear
Priori SG, Blomstorm-Lundqvist C, Amzzanti A. 2015;Zipes DP, Camm AJ, Borggrefe M. 2006; Olgin J, Zipes DP, 2012;Prystowsky EN, Padanilam BJ, Joshi S. 2012; Alzand BS, Crijins HJ.. 2011
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
VT vs SVT with abberancy
Absence of on R2 complex inall precordial leads
R to S interval > 100ms inone precordial lead?
AV dissociation ?
Morphology criteria for VTpresent in both in precordialleads V1-2 and V6 ?
SVT
VT
VT
VT
VT
No
No
No
No
Yes
Yes
Yes
Yes
Brugada Algorithm
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Morphology Criteria of VT
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
LONG TERM MANAGEMENTBeta blocker
• Counters thearrhythmogenic effectsof excesscathecolaminestimulations countering the theproarrhythmic effectsof increased cAMP andCa-dependenttriggered arrhytmias
• If channel effects;indirect Ca channelsblocker
• All px with VT,precluded byhypotension,bradycardia, and otherclinical factor
Amiodarone• Class III• Repolarizing K+
currents, markedlyprolongs repolarizationtimes
• First choice in VT withhemodynamicinstability in the settingof CHD
• Prevents monomorphicVT reccurency
• Manages refractory VTin CHD or withdecreased ventricularfunctions
Procainamide• Class 1A• Sodium blockers,
prolongs repolarizationtimes
• Inotropic -• Stable sustained VT
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
LONG TERM MANAGEMENT
ICD(implantable cardiac device)
VT in cardiomyopathy andischemic VT
Decreased LVEF (< 35%) lower mortality rate thanOMT
Selection criteria Primary : no history of
cardiac arrest or sustainedVT
Secondary : survivedcardiac arrest, lifethreatening VT or syncopeepisode related to VT
CATHETER ABLATION Refractory monomorphic VT
unresponsive to medicine
Mostly used for idiopathic VT
Failed procedure structuralproblem
Mortality during procedureuncontrollable life threateningVT
Complication : tamponadealongside perforation andcoronary occlusion inpericardial or aortic root
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
PROGNOSIS
VT associated with cardiac arrest in many cases
LV function projected by EF and functional capacity (NYHAclass, maximum oxygen uptake, duration of activity) is amajor determinant of mortality and SCD risk
Cardiac arrest or SCD more frequent in px with same historyof VT
Stable recurrent VT have lower risk of SCD
Idiopathic VT have better prognosis than ischemic VT and/orVT in cardiomyopathy (non ischemic), which have higher riskof cardiac arrest (syncope and decreased LV functionrelated to worse prognosis)
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
SUMMARY
VT diagnosed by three or more consecutive PVC, with regular andwide QRS complexes.
The electrical mechanism are reentry (in ischemic heart diseaseand cardiomyopathy) and triggered activity in (non-ischemic heartdisease or with normal heart)
The presence of structural heart disease affects pathophysiology,treatment and worsen the prognosis of VT episodes
After acute management based on ACLS guideline, it isrecommended to prevent reccurency of VT episodes with OMT ordevice therapy
ICD is the choice for VT in cardiomyopathy and ischemic VT
Catheter ablation is the better choice for refractory monomorphicVT unresponsive to OMT or VT episode in SHD
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Thank you
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
CASE
CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015