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VT and EP Studies Lauren Butler

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  • VT and EP Studies

    Lauren Butler

  • Value of EP testing

    • Monomorphic VT

    • Less value – non-sustained or polymorphic

    • EP testing = induction, characterisation and termination

    • Programmed stimulation used – VT usually re-entry mechanism

  • Wide complex tachycardia(>120ms) –differential diagnosis

    • SVT with abberancy

    • SVT with pre-exitation

    • VT

  • Characteristics VT

    • Cycle length• Haemodynamic effects• QRS morphology – RBBB, LBBB pattern

    – RBBB = arising from LV or septum– LBBB = arising from RV

    • Axis – superior, inferior– Superior = arising from apex– Inferior = arising from base, usually outflow

    tracts

  • Programmed ventricular stimulation

    • To evaluate inducibility of those patients thought to be at risk

    • To characterize the VT and assist in choice of therapy

    • For the purpose of mapping and ablation• To evaluate efficacy of treatment

  • Mechanisms of VT

    • Re-entry (e.g. scar) macro-rentry caused by areas of slow conduction– Pace induced, terminated, entrained

    • Automaticity (e.g. RVOT)– Isoprenaline, epinephrine, atropine, exercise

    • Triggered– Multiple extrastimuli, short-long burst pacing,

    drugs as above

  • Automaticity• Usually abnormal automatic focus• Difficult to induce – EP lab• Usually accounts 10 % all arrhythmias• May not have sudden onset & termination

    – Gradual warm up and warm down• Often associated with ischeamia, hypoxia,

    hypokaleamia, hypomagnesemia

    Action

    Potential

  • Re-entry

    • Features– 2 pathways connected distal & proximal

    provide circuit– 1 pathway/limb has longer refractory period

    than the other– The longer refractory limb has a quicker

    conduction time

  • Mechanism of re-enty

    • Initiated with an appropriately timed extra• Enters circuit to find long refractory limb (B) is

    refractory and passes down slow conducting pathway (A)

    A B

  • Triggered• Has some features of Automaticity and re-entry• Leakage of positive ions into cell – leading to a bump

    in late phase 3 / phase 4 on the action potential called afterdepolarisation

    • Afterdepolarisation if strong enough generates another action potential

    • Can be difficult to diagnose in EP lab but can be induced with pacing (feature of re-entry)

    • ∴to distinguish between re-entry and automatic – Triggered displays warm up/down– May respond to Ca channel blockers– Most likely re-entry in the presence of structural

    heart disease

  • Entrainment

    • A stimulus entered into a re-entrant circuit (faster than the tachycardia rate) will either terminate the tachycardia as it collides with the advancing wavefront and extinguishes it or ‘entrains’ it and advances the tachycardia (resets it at a higher rate)

    • Demonstration of entrainment is proof of a tachycardia with an exitable gap between the tail of one wavefront and the head of another

  • Types of VT

    • VT –associated with structural heart disease– Infarct related– Dilated cardiomyopathy– Hypertrophic myopathy– Arrhythmogenic RV dysplasia– Bundle branch re-entry

    • Idiopathic VT– Right ventricular outflow tract VT (RVOT)– Idiopathic LV VT (fascicularVT)– LVOT VT

  • Specificity of VT induced by programmed stimulation

    • The ease with which VT is induced = substrate (scar) and stage of aggressiveness of protocol achieved

    • Yield increases with increasing aggressiveness but specificity lessens

    • Second stimulation site and infusion isoprenaline increases yield but reduces specificity

  • • Routine risk assessment – protocol 3 extras, 2 cycle lengths, 2 sites

    • To induce a known VT for mapping and ablation – more aggressive

    • Remember – mechanism idiopathic VT is usually ‘automaticity’ and programmed stimulation normally is used for ‘re-entrant’ VT ie. scar

  • Scar related VT• Ingredients for re-entry are present

    – Scar provides a central obstacle around which the circuit revolves

    – Area surrounding scar containing areas of viable myocardium provides areas of slow conduction

    • Any morphology and axis, usually QRS width >140ms

    • LV origin is more common than RV origin• Abnormal axis is more common than

    normal axis

  • Other types structural heart disease

    • Myopathies, RV dysplasia– Myocardial disarray provides the substrate for slow

    conduction

    Mechanism is the same as for scar related

    i.e re-entry, usually induced by extra-stimulus

  • Bundle Branch re-entry

    • Macro-reentrant circuit within IV septum around the 2 bundle branches

    • Often Associated with LV dilatation, partial or complete LBBB and long PR interval

    • Remember slow conduction within some part of the circuit is necessary for re-entry

  • Bundle branch re-entry

    His is penetrated with each circuit therefore each (v) activation is preceeded by a His potential

    Ablation RBB – cures VT but creates Heart block and requires pacing

  • Idiopathic VTRVOT

    • LBBB pattern, inferior axis• Increased frequency exercise, stress, iso, epi• Terminated adenosine and some patients respond

    to beta blockade• Usually benign• Difficult to induce in EP lab• Mechanism – usually automatic• Activation mapping – more accurate than pace

    mapping

  • RVOT VT

  • Idiopathic VTLV VT (fascicular)

    • Sensitive to verapamil• RBBB + LAD• Normal LV function, moderator band in LV often

    seen • Mechanism thought to be triggered, ? Due to re-

    entry with a slowly conducting diastolic segment along septum

    • Often see a sharp fascicular potential on site of exit at septum on mapping electrogram

  • Brugada syndrome

    • Polymorphic VT• Torsade de points• Long QT resting ECG• Normal QT< 0.43 SECS• RBBB and ST elevation V1 and V2• EP LAB

    – Flecainide,– ECG recording every minute– Prepare for VT/VF

  • Brugada – resting ECG

  • Ablation VT

    • Pace mapping – 12 lead ECG during pacing approximates 12 lead ECG during spontaneous VT

    • All 12 leads are needed• Ensure pacing rate is same as VT rate as

    rate can change morphology slightly

  • • Activation mapping – mapping electrode looks for earliest activation relative to a fixed reference point

    • Fixed reference – onset of ventricular complex on surface ECG (often difficult as sharp inflections are not always seen

    • Negative QS seen in the unipolarelectrogram

    VT and EP StudiesValue of EP testingWide complex tachycardia(>120ms) – differential diagnosisCharacteristics VTProgrammed ventricular stimulationMechanisms of VTAutomaticityRe-entryMechanism of re-entyTriggeredEntrainmentTypes of VTSpecificity of VT induced by programmed stimulationScar related VTOther types structural heart diseaseBundle Branch re-entryBundle branch re-entry Idiopathic VT�RVOTRVOT VTIdiopathic VT�LV VT (fascicular)Brugada syndromeBrugada – resting ECGAblation VT