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TACHYARRYTHMIAS
Dr RAVI KANTH
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DEFINITION
ANATOMY OF CONDUCTION
ELECTROPHYSIOLOGY
DIAGNOSTIC APPROACH
TREATMENT MODALITIES
DESCRIPTION ABOUT INDIVIDUAL ARRYTHMIAS 2
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DEFINITION Any disturbance of the heart's rhythm,
regular or irregular, resulting by convention in a rate over 100 beats/min .
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CONDUCTION SYSTEM OF THE HEART AND ELECTROCARDIOGRAPHY
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Conduction System of the Heart• SA node: sinoatrial node. The pacemaker.
– Specialized cardiac muscle cells.– Generate spontaneous action potentials (autorhythmic tissue). – Action potentials pass to atrial muscle cells and to the AV node
• AV node: atrioventricular node.– Action potentials conducted more slowly here than in any other
part of system. – Ensures ventricles receive signal to contract after atria have
contracted• AV bundle: passes through hole in cardiac skeleton to reach
interventricular septum• Right and left bundle branches: extend beneath
endocardium to apices of right and left ventricles• Purkinje fibers:
– Large diameter cardiac muscle cells with few myofibrils. – Many gap junctions. – Conduct action potential to ventricular muscle cells (myocardium)
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Conducting System of Heart
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IMPULSE CONDUCTION THROUGH THE HEART
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ACTION POTENTIAL Duration – 200- 400 msec Regulated by activity of time & voltage
dependent ionic currents Ionic currents maintained by
Ionic channels –passively conduct ions along electrochemical gradient
Pumps, transporters – transport ions against gradients
Exchangers- electrgenically exchange species AP are regionally distinct
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Electrical Properties of Myocardial Fibers
1. Rising phase of action potential • Due to opening of fast Na+ channels
2. Plateau phase • Closure of sodium channels• Opening of calcium channels• Slight increase in K+ permeability• Prevents summation and thus tetanus of
cardiac muscle3. Repolarization phase
• Calcium channels closed• Increased K+ permeability
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Heart Physiology: Intrinsic Conduction System
• Autorhythmic cells:– Initiate action potentials – Have unstable resting potentials
called pacemaker potentials– Use calcium influx (rather than
sodium) for rising phase of the action potential
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DEPOLARIZATION OF SA NODE SA node - no stable resting membrane potential Pacemaker potential
gradual depolarization from -60 mV, slow influx of Na+
Action potential occurs at threshold of -40 mV depolarizing phase to 0 mV
fast Ca2+ channels open, (Ca2+ in) repolarizing phase
K+ channels open, (K+ out) at -60 mV K+ channels close, pacemaker potential starts over
Each depolarization creates one heartbeat SA node at rest fires at 0.8 sec, about 75 bpm
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Pacemaker and Action Potentials of the Heart
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DEPOLARIZATION AND IMPULSE CONDUCTION Depolarization in
SA node precedes depolarization in atria, AV node, ventricles
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ELECTROCARDIOGRAM
P wave Depolarization of atria Followed by
contraction QRS complex
3 waves (Q, R, & S) Depolarization of
ventricles Followed by
contraction T wave
Repolarization of ventricles
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ELECTROCARDIOGRAM
P-Q intervalTime atria
depolarize & remain depolarized
Q-T intervalTime ventricles
depolarize & remain depolarized
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ELECTROCARDIOGRAM Intervals show timing of cardiac cycle
P-P = one cardiac cycle P-Q = time for atrial depolarization Q-T = time for ventricular depolarization T-P = time for relaxation
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MECHANISMS OF ARRYTHMOGENESIS Some tacyarythmias start by one mechanism
& gets perpetuated by another mechanism Some caused by one mechanism can
precipitate another episode caused by different mechanism
Mechanisms are Disorders of impulse formation Disorders of impulse conduction both
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DISORDERS OF IMPULSE FORMATION Characterised by
Inappropriate discharge rate of normal pacemaker
Inappropriate discharge of ectopic pacemaker
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Abnormal automaticity Arise from cells that have reduced maximum
diastolic potentials Don’t need prior stimulationTriggered activity Initiated by after depolarisations Induced by one or more preceding action
potentials
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After depolarisations are of two types Early after depolarisation- occurs during
phase 2 & phase 3 Delayed after depolarisation- occurs
during phase 4 All depolariations doesn’t reach threshold
potential but if they reach they trigger another after depolarisation & thus perpetuate
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DAD’S Result from activation of calcium sensitive
inward current due to increase in intra cellular ca concentrations
Acquired or inherited abnormalities in Sarcoplasmic reticulum properties CA release channels SR calcium binding proteins
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EAD’S AP prolongation may increase ca influx
through l-type ca channels during cardiac cycle , causing excessive ca accumulation in SR & spontaneous SR ca release
Increased intracellular ca cause depolarisation by activation of ca dependent cl currents ,NA +/CA + exchanger provoking EAD,S
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Re-entry Two types
Anatomical re-entry Functional reentryANATOMICAL REENTRYCharacters
-2 or more pathways with different electropohysiological properties-impulse blocked in one pathway-impulse conducts slowly in alternate pathway &returns in pathway initially blocked in reversed direction to re exite tissue proximal to site of block
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For re entry to occur anatomical length of circuit should be greater than reentrant wave length
Conditions that depress conduction velocity & refractory period promote development of re entry[λ = c.v x rp]
Sustained reentry occurs due to excitable gap between activating head & recovery tail.
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Fuctional reentry Occur in fibres that exhibit functionally
different EP properties caused by local differences in transmembrane AP
functional heterogenities can be fixed or change dynamically
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Mechanisms of termination are When conduction & recovery characters of
circuit change When activating head of wave collides with
tail
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DETERMINANTS OF AMPLITUDES OF AFTER DEPOLARISATIONSintervention Effect on
amplitude of EAD’S
Effect on amplitude of DAD’S
Long cycles ↑ ↓Long AP duration ↑ ↑Reduced membrane potential
↑ ↓
Na channel blockers No effect ↓Ca channel blockers ↓ ↓catecholamines ↑ ↑
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APPROACH TO TACHYARRYTHMIAS
HISTORY• Mode of
onset• Mode of
termination• Drug
history• Dietary
history• H/o
systemic illness
• Family history
PHYSICAL EXAMINATION
• Symptoms• Signs
NON INVASIVE INVESTIGATIONS• 12 lead ECG• Holter
monitor• Patient
activated event monitor
• Implanted loop ECG monitor
• HUT• Exercise ECG• 2D ECHO
INVASIVE INVESTIGATIONS
• Electrophysiological studies
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HISTORY
MODE OF ONSET Occuring in the setting of exercise and stress – caused by
catecholamine sensitive automatic or triggered activity At rest – may be caused by vagal initiation (AF) Lightheadedness, syncope in setting of tightly fitting collar,
turning head- suggests carotid hypersensitivity
• MODE OF TERMINATION• If terminated by vagal manevoure – suggests AV node as integral part of
tachyarrythmias
May help determine diagnosis or further guide to diagnostic tests
• DRUG HISTORY• nasal decongestants• Beta blockers• Drugs prolonging QT interval. 36
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DIETARY HISTORY Alcoholic intake Food containing Ephedrine
H/O SYSTEMIC ILLNESS COPD Thyrotoxicosis Pericarditis Congestive heart failure
FAMILY HISTORY HOCM Long QT syndromes Myotonic dystrophies
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PHYSICAL EXAMINATIONMORE HELPFUL IF DONE DURING SYMPTOMATIC PERIOD HR
>100 Regularly irregular Irregularly irregular
JVP Increased JVP Cannon waves
Heart sounds Variable heart sounds murmurs
BP -- Variable Physical manoeveurs– Can have diagnostic and therapeutic
value. Valsalva/Carotid sinus massage - terminate or slow tachyarrythmias that depend on AV node. 38
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12 LEAD ECG
Primary tool in arrhythmia analysis 3 steps in diagnosing tachyarrythmia.
Step 1 – determine if QRS complex is narrow or wide. Step 2 – determine if QRS complex is regular or irregular. Step 3 -- look for p waves and relation to QRS complex.
Major branch point in DD is QRS duration. QRS < .12 – always almost SVT QRS >.12 – often VT
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24 hr Holter monitoring - for patients with daily symptoms
Patient activated event monitor – for patients with intermittent symptoms
Implanted loop ECG monitor – for patients with infrequent severe symptoms
Exercise ECG - to determine myocardial ischemia -For analysis of morphology of QT
interval. HUT – used in patients with recurrent syncope
Syncope with injuries in absence of heart disease
2D ECHO – for cardiac chamber size and function.To rule out valvular diseases.
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ELECTROPHYSIOLOGICAL STUDIES For diagnostic purposes For therapeutic purposes
COMPONENTS OF TEST Measuement of conduction under resting , stress
conditions and maneuvers
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SITE OF ORIGIN
Atrial SA node Atrial muscle
Junctional AV node His bundle Kent bundle
Bundle branches Purkinje fibres Ventricular muscle
SUPRAVENTRICULAR VENTRICULAR
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Atrial Fibrillation Paroxysmal
supraventriculartachycardias(PSVT)-AV nodal reentry tachycardia (AVNRT)
-AV junctional tachycardia-AV reentry tachycardia (AVRT)-WPW-AV reentry over concealed bypass tract–Atrial Tachycardia
VPC’S VT Ventricular flutter Ventricular
fibrillation Brugada syndrome
Supraventricular arryhthmias Ventricular arryhthmias
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WIDE QRS TACHY CARDIA
Ventricular tachycardia
SVT with BBB Antidromic AV re –
entry tachycardia
Torsades de – pointes
LBBB with AF or Atrial flutter with variable block
WPW with AF or AFL with variable block
WITH REGULAR RHYTHM
WITH IRREGULAR RHYTHM
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DIFFERENTIAL DIAGNOSIS OF WIDE QRS TACHYCARDIA
Initiation with premature P wave
Changes in P-P interval precedes R – R interval changes
Slowing or termination by vagal maneuvers
Initiation with premature QRS complex
Changes in R – R interval precedes P – P interval
AV – dissociation Fusion ,capture beats QRS duration-
RBBB type V1 morphology - >140 msLBBB type V1 - > 160 ms
Delayed activation –LBBB - R- wave > 40 msRBBB- onset of R- wave to nadir of S – wave > 100 ms
Concordance of QRS complexes in all precordial leads
SVT VT
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ANTIARRYHTHMIC DRUGS
Class IA. This includes drugs that reduce V.max (rate of rise of
action potential upstroke [phase 0]) and prolong action potential duration
Eg-quinidine, procainamide, disopyramide.Class IB. This class of drugs does not reduce V.max and shortens
action potential duration—Eg-mexiletine, phenytoin, and lidocaine.
Class IC. This class of drugs can reduce V.max, primarily slow
conduction, and prolong refractoriness minimallEg-flecainide, propafenone, and moricizine.
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Class II. These drugs block beta-adrenergic receptors.
Eg- propranolol, timolol, and metoprolol.Class III. This class of drugs predominantly blocks
potassium channels (such as IKr) and prolongs repolarization. Eg-sotalol, amiodarone, and bretylium.
Class IV. This class of drugs predominantly blocks the
slow calcium channel (ICa.L)—Eg-verapamil, diltiazem, nifedipine,
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SINUS TACHYCARDIA PHYSIOLOGICAL
fever anxiety anemia sepsis hyperthyroidism congetive heart failure hypoxemia
INAPPROPRIATE viral – post viral dysautonomia
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TREATMENT
Treat underlying cause
Beta blockers
Increase hydration Beta blockers Catheter
ablation/pacing
PHYSIOLOGICAL INAPPROPRIATE
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APC’S – Incidence increases with age ECG – Premature & abnormal P wave Short PR interval Precedes normal QRS complex Compensatory pause is incompleteTREATMENT – No treatment needed If severely symptomatic – Β-blocker, Catheter ablation .
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FOCAL ATRIAL TACHYCARDIAS
Can not be initaiated by programmed atrial stimulation
First P wave same as othr P waves
Response to adenosine –AV block seen
-- slow or terminate
Initiated by programmed stimulation
First P wave different from others
Response to adenosine
-AV block seen -cant slow or
terminate
Automatic AT Focal reenterant AT
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ECG – P wave distinct from sinus P wave PR interval shorter than RP intervalTREATMENT
Rate control Rhytm control Anticoagulation if LA diameter > 5cm Catheter ablative theraphy DC version
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MULTIFOCAL ATRIAL TACHYCARDIA – Mostly seen in patients of pulmonary disease ECG – Atrial & ventricular rate – 100 – 150 bts / min > 3 distinct P wave morphology > 3 distinct PR intervalTREATMENT – Treat underlying pulmonary disease CCB’s , amiodarone
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ATRIAL FIBRILLATION Most common sustained arrhythmia Disorganised , rapid and irregular atrial activation and
ventricular responses Atrial rate – 400- 600 bpm Ventricular rate – 120-150 bpm
CLASSIFICATION Recurrent Paroxysmal Persistent Permanent
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CAUSES RHD Ischaemic heart disease Hypertension Constrictive pericarditis Hyperthyroidism Acute alcoholism Vascular,abdominal and thoracic surgery Anemia Acute vagotonic episode Lone atrial fibrillation ( no structural heart disease)
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ECG Atrial deflections are irregular and chaotic – ragged baseline Ventricular rate is irregular In longstanding cases, baseline almost straight with minimal
undulation .
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TREATMENT
Control ventricular rate Betablockers Ca channel blockers Digoxin
Anticoagulation When AF >12hrs and
risk factors for stroke present.
Maintain INR – 2 to 3 Warfarin
DC cardioversion – 200 J Pharmacological
To terminate - Amiodarone , Procainamide iv To maintain restored sinus rhytm – beta
blockers ,class Ic drugs. Emergency
If AF >24 - 48hrs TEE done to r/o atrial thrombus Heparin given with warfarin until INR > 1.8 Anticoagulate for 1 month after restoration of
sinus rythm Elective
Anticoagulate for atleast 3 weeks before cardioversion.
RATE CONTROL TERMINATION OF AFACUTE
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CHRONIC
Beta blockers Ca channel blockers Digoxin His bundle / AV junction
ablation with implantation of activity sensor pacemaker
Anti coagulation Surgical ablation of left
atrial appendage
Catheter ablation – of atrial muscle sleeves entering pulmonary veins
Surgical ablation – COX – MAZE procedure
RATE CONTROL TERMINATION OF AF
SURVIVAL OUTCOME Restoration of sinus rhytm not superior to rate control with anticogulation as evidenced by AFFIRM and RACE trials 65
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ATRIAL FLUTTERatrial rate = 250-350 cycles/min Ventricle rate is closer to 150, 100 or 75
beats/min 2:1, 3:1 and 4:1F waves“sawtooth” shape
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ATRIAL FLUTTER
Reentrant type arrhythmia
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ATRIAL FLUTTER Treatment
DC – version 50 – 100 j Anticoagulation If asymptomatic –
- rate control -rhythm control - catheter ablation
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AV NOAL RE ENTERANT TACHYCARDIA – Most common Mostly in women Repetitive activation down slow pathway &
up fast pathway results in tachycardiaECG – Rate – 120 – 150 P waves negative Narrow QRS complexes P wave not visible or distorts QRS complex
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TREATMENT – ACUTE Vagal maneuvers Adenosine – 6 – 12 mg iv B – blockers ,CCB’s DC - version -100- 200 j
PREVENTION B-blockers , CCB’s Catheter ablation – slow pathway
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AV JUNCTIONAL RHYTHM Rate – 40 – 50 Accelerated AVJR – 50 – 100TREATMENT
Stop digoxin B – blockers Catheter ablation
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WPW SYNDROMEECG
Short PR interval.
Short or long RP interval.
Delta waves Narrow QRS
complex.
SITES OF BYPASS TRACTS
Left lateral Right lateral Posteroseptal Anteroseptal
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A comment on PSVT in patient with WPW:
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MAIN SITES OF BYPASS
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COMPLICATIONS Reciprocating tachycardia
Orthodromic – AV reentry – conduction to ventricle via AV node and reentry via AP.Antidromic - conduction to ventricle via AP and reentry via His purkinje system – mimics VT
Atrial fibrillation50% predisposed
-fast ventricular rate results in hemodynamic compromise. 83
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TREATMENTACUTE
Orthodromic tachycardiaVagal stimulationAdenosineCCB sBetablockers
AFDC cardioversionProcainamideIbutelideDigoxin avoided
CHRONIC
Beta blockers CCB s Class Ia or Ic drugsCATHETER
ABLATION Indications --
recurrent symptomatic SVTs HR >200
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AIVR
>3 or more consecutive VPCs VR >40 and <120 Benign rhytm CAUSES
Idiopathic Acute MI Acute myocarditis Digoxin intoxication Postoperative cardiac surgery Cocaine intoxication
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TREATMENT If hemodynamic compromise occurs
atropine Atrial pacing
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PREMATURE VENTRICULAR COMLEXES Broad QRS > 120ms T wave is large ,opposite in direction to QRS No preceding p waves Compensatory or noncompensatory pause Fixed or variable coupling interval.
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TYPES BIGEMINY TRIGEMINY QUADRIGEMINY COUPLET TRIPLET MONOMORPHIC POLYMORPHIC
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Incidence >60% of healthy males during 24hr Holter
>80% post MI Benign ectopics disappear on exercise Pts –normal life span.
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CLINICAL SIGNIFICANCE LOWNs grading system of VPCs Determines prognostic significance after MI As grade advances, there is increased risk of
SCD
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GRADES VPCs0 none1 <30/hr2 >30/hr3 multiform
4A 2 consecutive4B >3 consecutive5 R on T phenomenon
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MANAGEMENTIn Normal heart Asym- No treatment Sym - betablockersStructural heart disease betablockers Class IA, III drugs
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VENTRICULAR TACHYCARDIA
VT consists of at least three or more consecutive VPCs at a rate of 100bpm.
Types- -Nonsustained <30s -sustained > 30s
Rhythm- Regular / slightly irregular Rate 70 to 250 / min
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ECG DIAGNOSIS QRS duration RBBB > 140 ms LBBB > 160 ms Wellens et al QRS >140ms good indicator of VT QRS 120- 140 ms only 50% have VT
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VT with RBBB (Wellens & Gulamhusein)
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FUSION & CAPTURE BEATS 33 % cases of VT Diagnosis of VT is certain Seen in VT of lower rates(< 160) Capture beat- sinus beat Fusion beat- hybrid beat due to both atrial &
ventricular activation.
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VT IN PATIENTS WITH CORONARY ARTERY DISEASE
Non-sustained VT (NSVT) -67% Sustained VT 3.5% VF – 4.1% VT + VF – 2.7 %Mortality VT - 18.6% VT + VF – 44% 1 yr mortality 7% Without VT is 3 %
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CLINICAL PRESENTATION Symptoms are variable Depend upon rate of VT & degree of LV
dysfunction Syncope / presyncope / dizziness Palpitations Sudden death
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TREATMENT OF VT
HEMODYNAMIC COMPROMISE --
DC – version asynchronously 200j , repeat with ↑energy if no response
IV lidocaine, amiodarone
DC –version synchronously with R wave
IV lidocaine , procainamide , amiodarone
Polymorphic VT Monomorphic VT
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NO HEMODYNAMIC COMPROMISE
Correction of k+ & mg
Removal of offending drug
B – blocker iv Treat acute ischemia Pacing Catheter ablation Quinidine,procainam
ide for BRUGADA syndrome
Lidocaine , procainamide , amiodarone
Catheter ablation
Polymorphic VT Monomorphic VT
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•B-BLOCKERSFocal out flow tract VT
•VERAPAMILSeptal VT
•ICD’S VT with structural
heart disease 114
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SPECIFIC TYPES OF VTARRHYTHMOGENIC RT
VENTRICULAR DYSPLASIA(0.4%)
LBBB contour with right axis deviation during VT
ICRBBB ,T waves inverted over the right precordial leads
Type of Cardiomyopathy, possibly familial, with hypokinetic thin walled RV
Abnormality in Chr 1 & Chr 10 -apoptosis
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Imp cause of VT in children & young adults with normal hearts
Rt heart failure or asymptomatic rt ventricular enlargement can be present with normal pulmonary vasculature
Males predominate Pathology- Fatty & fibrofatty infiltration
OR myocardial atrophy
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Preferentially affects rt ventricular inflow & outflow tracts & the apex
ECG- T wave inversion in V1 to V3, Terminal notch in QRS called “epsilon” wave can be present due to slowed intra ventricular conduction
ICDs are preferable to pharmacological Radio frequency catheter ablation is often
not successful
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LEFT SEPTAL VT Arises in the left posterior septum, often
preceded by a fascicular potential. It is sometimes called Fascicular
tachycardia Cause – Re-entry Mgm – Verapamil or Diltiazem Oral verapamil is less effective than iv
verapamil
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LEFT SEPTAL VT(FASCICULAR VT) Seen in normal heart. 70% males ,15-40 yrs Resting ECG normal
VT – RBBB pattern with left superior axis QRS < 140 ms
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Left septal ventricular tachycardia. This tachycardia is characterized by a right bundle branch block contour. the axis is rightward.
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C/F – palpitations, syncope Not associated with sudden death
Treatment- Verapamil . RF ablation 85-100% Prognosis – good
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CATECHOLAMINERGIC POLYMORPHIC VT
Uncommon form of inherited VT Occurs in children & adolescents
without any overt structural heart disease
Adenosine sensitive Pts present with syncope or aborted
sudden death with highly reproducible stress induced VT that is often bidirectional
QT interval – Normal Family history present in 30%
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During exercise typical responses, initial sinus tachycardia & ventricular extrasystoles followed by monomorphic or bidirectional VT, which eventually leads to polymorphic VT as exercise continues
Mgm – Beta blockers & ICDs Lt cervicothoraic sympathetic
ganglionectomy
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BRUGADA SYNDROME
30-40% of idiopathic VF AD, M:F 8:1 2-4th decade Distinct form of idiopathic VT,V fib RBBB & ST segment elevation in anterior
precordial leads No evidence of structural heart disease Mutation in gene responsible for sodium
channel
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Acceleration of Na channel recovery or nonfunctional channels
Common in apparently healthy south east Asians – 40-60%
Precise mechanism is not known Can be reproduced by sodium channel
blockers ICDs are the only effective treatment to
prevent sudden deaths
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LONG QT SYNDROMES Normal QT males - 440 ms females – 470ms Congenital Jervell Lange-Neilsen syndrome- AR with
deafness Ramano-Ward syndrome - AD with normal
hearing Defect in Na, K channels.
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LQTS ECG PATTERNS
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AcquiredDrugs Antiarrhythmic Phenothiazines Antihistaminics Antimalarials,pentamidine Tricyclic antidepressants Ketoconazoles Erythromycin cisapride Hypokalemia Hypomagnesemia
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C/F Syncope, dizziness,sudden deathTreatment Underlying condition Betablockers ICD
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CARDIOMYOPATHIESDILATED CARDIOMYOPATHY
Focus basal septum Mutiple macrorentry ICDs -life threatening ventricular
arrhythmias Comparing amiodarone v/s ICD,
improved survival was found with ICD In case bundle branch re-entry is the
basis, ablate the RBB
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HYPERTROPHIC CARDIOMYOPATHY
Risk of sudden death is increased by presence of syncope, family h/o, sudden death in 1st degree relative, septal thickness >3cms or presence of non sustained VT in 24 hr recordings
Infrequent episodes of non sustained VT have low mortality
Amiodarone – Useful symptomatic non sustained VT but not in improving survival
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MITRAL VALVE PROLAPSE
VT in MVP has good prognosis although sudden death can occur
Treated with betablockers.
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CHD Can occur in pts some years after repair Sustained VT can be caused by re entry at
the site of surgery Mgm- resection or catheter ablation of the
area
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VENTRICULAR FLUTTER Severe derangement of heart beat Macro-reentrant Sine wave appearance, with large
regular oscillations (150-300 Bpm) Distinct QRS ,ST T are absent Difficult to distinguish between rapid
VT & V.flutter
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VENTRICULAR FIBRILLATION Grossly irregular ,undulation of varying
amplitudes, contours with rates >300 /min Starts with VT Distinct QRS ,ST T are absent Multiple wavelets of reentry 75% of sudden death after MI have VF.
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MANAGEMENT
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TORSADES DE POINTES
VT characterized by QRS complexes of changing amplitude
that appear to twist around the isoelectric line & occur at rates of 200 to 250 /min
Prolonged ventricular repolarization with QT intervals generally exceeding 500 msec
U wave can also become prominent& merge with T wave
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Torsades de Pointes can terminate with progressive prolongation in cycle length with distinctly formed QRS complexes & culminate into basal rhythm, ventricular standstill, or VFib
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Common causes Potassium depletion Congenital LQTS Antiarrhythmic drugs IA,IC,III c/f Palpitations, syncope, death Women are at a greater risk
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Management IV magnesium Temporary ventricular or atrial pacing+
ICD Lidocaine, mexiletine or phenytoin can
be tried K channel activating drugs pinacidil,
cromakalim Cause of long QT should be treated
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REFERENCES BRAUNWALD ‘S HEART DISEASE 8 th ed HARRISONS INTERNAL MEDICINE 17 th ed HURST ‘S HEART DISEASES SHAMMROTH ECG MARRIOTS ECG MEDICINE UPDATE
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