tachyarrhythmias

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Khushbu on Jul 16, 2012 Says :

good presentation on heart beat disorders.

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TACHYARRHYTHMIAS Meeniga Srinivasulu

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Tachyarrhythmia-Non sustained and sustained forms of tachycardia originating from myocardial foci or reentrant circuits Tachycardia is a rhythm that produces a ventricular rate >100 bpm Premature complexes are considered under this category, because they may cause arrhythmia related symptoms and/or serve as triggering events for more sustained forms of tachycardia

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Investigations 12 lead ECG Holter monitor Loop recorder Monitoring for whom? Tachycardia induced cardiomyopathy Asymptomatic VPCs, Non sustained VTs- risk of SCD Asymptomatic AF ECG + exercise test Echo

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Primary disorders of Rhythm Abnormal Impulse formation Abnormal Impulse propagation

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Abnormal Impulse Formation Increased automaticity Increase in slope of phase 4 depolarization or a reduced threshold for AP depolarization(other than SA node) Trigger activity is related to cellular afterdepolarisation that occur at the end of AP, If it occurs during phase3 they called as early afterdepolarisation If it occurs during phase 4 they are called late afterdepolarisation

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Ex: APCs, VPCs, Some ATs Early-VPCs causing TDP Late- atrial, junctional and fascicular tachyarrhythmias caused by digoxin toxicity and catecholamine sensitive VT

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Classification Sinus rhythms Sinus arrhythmia Sinus bradycardia Sinus tachycardia 2.Ectopic atrial rhythms Atrial extrasystoles PAT AF AFl 3.AV nodal rhythms AV nodal extrasystoles Extrasystolic PAVNT Idionodal tachycardia 4.Ventricular rhythms Ventricular extrasystoles Extrasystolic VT Idioventricular tachycardia VFl VF Ventricular parasystole

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Abnormal Impulse Propagation Inhomogeneties in myocardial conduction and/or recovery properties leads to re-entry These may be exaggerated by Extra pathways (e.g. WPW) Genetically determined ion channel abnormalities(e.g. LQTs) or Due to fibrosis Re-entry appears to be the basis for most abnormal sustained SVTs & VTs

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Re-entry which is caused by extra pathways, leads to stable, uniform tachycardia (monomorphic) Some times it may be due to functional and dynamic changes in electrophysiological properties leading to unstable and polymorphic appearance E.g. VF in MI and polymorphic VT in LQTs, Brugada syndrome or catecholaminergic VT

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Classification SA Block AV Block WPW Syndrome Reciprocal rhythm

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Secondary Rhythm disorders Escape rhythms Atrial escape AV Nodal escape Ventricular escape AV dissociation Phasic aberrant ventricular conduction

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Basic Approach Atrial deflection Normal P wave Ectopic or P’ deflection Flutter-F-wave Chaotic fibrillation-f-wave 2.Atrial rate 3.Regularity of rhythm 4.Relationship of atrial deflections with QRS complexes 5.QRS configuration

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Sinus Arrhythmia Faster rate towards end of inspiration, slower rate towards end of expiration Due to reflex stimulation of vagus nerve from receptors in the lung Physiological phenomenon

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Sinus Tachycardia SA node discharges >100/min Normal P-QRS-T pattern Physiological response to stress, underlying condition or drugs

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APC MC arrhythmia identified during extended ECG monitoring Premature discharge of an ectopic atrial focus Bizarre P wave- pointed, notched, biphasic or inverted ECG features depends upon timing and conduction through atria, AV node and ventricles 3 or more APCs termed paroxysmal atrial tachycardia

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Timing- premature, compensatory pause, theoretically incomplete Atrial conduction AV conduction Intraventricular conuduction Abnormal bizarre P wave blocked conducted PR Interval short normal prolonged normal aberrant

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JUNCTIONAL PREMATURE COMPLEXES Uncommon, originates from AV node and His bundle region and may produce retrograde atrial activation with the P wave distorting the QRS complex Pseudo Q or S wave in leads II, III, and aVF PR prolongation

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Atrial Fibrillation Most common sustained arrhythmia Excitation and recovery of the atria are disorganized and chaotic Ventricular response to the rapid atrial activation is also irregular Atrial rate 400-600/min Ventricular rate 120-160/min(low or high)

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ECG Irregular and chaotic atrial deflections with ragged baseline with numerous rounded or spiked waves In chronic cases, the deflections may be of low amplitude and baseline may be almost straight with minimal undulations

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Atrial Flutter Due to rapid and regular atrial excitation Due to 1.ciruit rotates in a clockwise/counter clockwise in RA around tricuspid annulus 2.ectopic atrial focus Associated with block 1:1, 2:1, 4:1, 6:1 or 8:1 Odd ratios are less common than even ratios

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ECG Presence of regular, undulating, closely spaced but relatively wide atrial deflections or flutter-F waves Resulting in saw tooth appearance Best seen in L II and V1 Some times saw tooth appearance shows some irregularity or distortion, like AF referred as impure flutter or flutter fibrillation

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MULTI FOCAL ATRIAL TACHYCARDIA In patients with significant pulmonary disease Characterized by at least three distinct P wave morphologies and often three different PR intervals Atrial and Ventricular rates between 100-150 bpm D.Dx 1. AF- absence of isoelectric line 2.APCs- presence of intervening sinus rhythms

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AVNRT AV nodal reentrant tachycardia is the most common paroxysmal regular SVT Presence of two pathways Fast pathway in the more superior part of the node has a longer refractory period, Whereas the pathway lower in the AV region conducts more slowly but has a shorter refractory period

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ECG An APC followed by long PR interval(slow pathway) Narrow QRS complex tachycardia ranging form 120-250bpm P wave frequently is buried inside the QRS complex and either will not be visible or will distort the initial or terminal part of QRS complex Negative deflections in L II III aVF (atrial activation in AV node)

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AV junctional tachycardia Due to enhanced normal automaticity, abnormal automaticity or triggered activity May not be associated with retrograde conduction May occur as a manifest of increased adrenergic tone or drug effect (digoxin) or post surgical or post ablation

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ECG Dissociated sinus activity or intermittent capture beats with long PR interval Accelerated junctional rhythm- rate between 50-100bpm

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WPW Syndrome Wolff-Parkinson-White syndrome is due to expression of an anomalous AV conduction pathway which is congenital in origin The anomalous bypass, also known as bundle of Kent-thin filamentous structure, situated anywhere along the atrioventricular ring

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Whenever a SVT manifests with narrow QRS complex with 1:1 conduction at a rate >200/min, WPW should be considered AF may be conducted anterogradely to the ventricles through one of three forms Anomalous pathway(MC) Normal AV nodal pathway Both

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D.Dx RVH PWMI IWMI BBB VT

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LOWN-GANONG-LEVINE SYNDROME Due to bypass(James) which arises in atria and bypasses the main region of bundle of His So it doesn’t end in, or activate the myocardium directly Normal P wave Short PR interval Delta wave

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VPCs Due to premature discharge of an ectopic ventricular focus Bigeminy-every sinus beat is followed by VPC Trigeminy-two sinus beats are followed by VPC Couplets/pairs-two VPCs consecutively Three or more consecutive VPCs termed VT when the HR >100bpm If it is terminates spontaneously and are more than three beats in duration, it is called nonsustained VT

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AIVR Due to abnormal automaticity Three or more complexes at a rate of 40-120bpm Overlap between AIVR and slow VT Idiopathic, acute MI, cocaine, myocarditis, digoxin and post-op cardiac surgery Hemodynamic compromise can occur due to loss of AV synchrony

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VT Rapid discharge of an ectopic ventricular pacemaking focus Three or more consecutive VPCs recorded in rapid succession The QRS complex may be uniform (monomorphic) or may vary from beat to beat (polymorphic) Polymorphic VT in LQT interval exhibits- torsade des pointes

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Monomorphic VT Uniform QRS Suggests stable tachycardia with out structural heart disease Reproducible and reentrant phenomenon Polymorphic VT Variable QRS Due to MI, myocarditis or dynamic changes in the QT interval Not initiated with pacing or programmed stimulation

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Non-Sustained VT, which lasts for <30 sec VT which lasts for >30 sec sustained Hemodynamically unstable VT VT VT terminated by ICD

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ECG AV dissociation(capture beats, fusion beats) QRS duration >140 ms for RBBB type V1 morphology, V1 >160 ms for LBBB type v1 morphology Frontal plane axis -900 to 1800 delayed activation during initial phase of QRS complex- LBBB- R wave in V1, V2>40ms -RBBB- onset of R wave to nadir S wave >100ms

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Bizarre QRS pattern that does not mimic typical RBBB/LBBB QRS complex Concordance of QRS complex in all precordial leads RS or dominant S in V6 for RBBB VT Q wave in V6 with LBBB QRS pattern 4. Monophasic R or biphasic qR or R/S in V1 with RBBB pattern

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VT syndromes Idiopahtic outflow tract VT Idiopathic LV septal/fascicular VT VT associated with LV DCM Bundle branch reentrant VT VT a/w HCM VT a/w infiltrative CM or NM disorders ARVCM/D VT in post op TOF Fascicular tachycardia caused by Digoxin

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ARVD

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Digoxin

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Genetic diseases-polymorphic VT Long QT syndrome- congenital forms due to channelopathies Defects that enhance sodium or calcium currents or inhibit potassium currents in the plateau phase of AP Types- LQT 1-8 Jervell LN1&2, Brugada, catecholaminergic VT

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Romano Ward syndrome

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Brugada syndrome

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Brugada syndrome

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Catecholaminergic VT

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D.Dx SVT with Aberrant ventricular conduction due to L/R BBB Ventricular Flutter

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Ventricular fibrillation Due to chaotic, uncoordinated ventricular depolarisation Regular waveforms such as P, QRS, ST and T cannot be identifeid

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Ventricular flutter Very rapid & regular ectopic ventricular discharge Grossly abnormal intraventricular conduction Bizarre sine like waveform

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VFl

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THANK YOU

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