ventricular tachycardia - budi baktijasa, md, fiha.pdf

CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

VENTRICULARTACHYCARDIA

Budi Baktijasa DharmadjatiOryza Sativa


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


CLASSIFICATION OFVENTRICULAR TACHYCARDIA


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


TORSADES DE POINTES


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


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


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


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


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


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


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


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



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



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



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


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;


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)



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.



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


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


Positive concordance of VT


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


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


Morphology Criteria of VT


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


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


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)


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


Thank you


CASE

ventricular tachycardia - budi baktijasa, md, fiha.pdf

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