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Ventricular arrhythmias
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
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Ventricular arrhythmias
- 1. VENTRICULAR ARRHYTHMIAS Moderator : LtCol Brahamjit Singh Presenter : Lt Phuntsho Choden
- 2. Arrhythmias that originatein the ventricular myocardium or His Purkinje system include: •Premature ventricular beats •Ventricular tachycardia •Ventricular fibrillation
- 3. • Emerge fromfocus of myocardium and purkinje fibres • Conduction away from the ventricular focus through the ventricular myocardium is slower than activation of the ventricles over the Purkinje system. • QRS wide, typically >0.12 s
- 4. Premature Ventricular Contraction •Premature ventricular ectopic beats arising in the diastolic period of preceding sinus beat • Unifocal • Multifocal • Ventricular Couplets • Caused by electrical irritability • Ischemia • Electrolyte imbalances • Drug intoxication
- 6. Multiform premature ventricularcomplexes (PVCs) The normally conducted QRS complexes exhibit a left bundle branch block contour (arrowhead) and are followed by PVCs with three different morphologies.
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- 8. • Three ormore PVC's in a row (run of V-tach) • They come close to or on top of a preceding T-wave (R on T) • They are frequent (> 30% of complexes) • They are increasing in frequency • PVC's come from different foci ("multifocal" or "multiformed") May preclude the occurrence of : • Ventricular Tachycardia • Ventricular Fibrillation PVCs : CLINICAL SIGNIFICANCE sinus beats Unconverted V-tach r V-fibV-tach “R on T phenomenon” time
- 9. Fusion beat - notep-wave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal. Fusion and capture beats during ventricular tachycardia.
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- 11. Ventricular Tachycardia (VT) •Three or more consecutive ventricular ectopic beats at a rate > 100 beats/min • Originates in the ventricles • Nonsustained < 30secs • Sustained > 30secs • Most patients have significant heart disease • Coronary artery disease • A previous myocardial infarction • Cardiomyopathy
- 12. V1 Ventricular Tachycardia (VT) • Ratesrange from 100-250 beats/min • Non-sustained or sustained • P waves often dissociated (as seen here)
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- 14. Mechanisms of VT •Reentrant • Reentry circuit (fast and slow pathway) is confined to the ventricles and/or bundle branches • Automatic • Automatic focus occurs within the ventricles • Triggered activity • Early after depolarizations (phase 3) • Delayed after depolarizations (phase 4)
- 15. Reentrant • Reentrant ventriculararrhythmias • Premature ventricular complexes • Idiopathic left ventricular tachycardia • Bundle branch reentry • Ventricular tachycardia and fibrillation when associated with chronic heart disease: • Previous myocardial infarction • Cardiomyopathy
- 16. Automatic • Automatic ventriculararrhythmias • Premature ventricular complexes • Ischemic ventricular tachycardia • Ventricular tachycardia and fibrillation when associated with acute medical conditions: • Acute myocardial infarction or ischemia • Electrolyte and acid-base disturbances, hypoxemia • Increased sympathetic tone • Drugs
- 17. Automaticity Abnormal Acceleration ofPhase 4 Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.
- 18. Triggered • Triggered activityventricular arrhythmias • Pause-dependent triggered activity • Early afterdepolarization (phase 3) • Hypokalemia, TdP • Polymorphic ventricular tachycardia • Catechol-dependent triggered activity • Late afterdepolarizations (phase 4) • Local catecholamines, hypercalcemia • Digitalis intoxication • Idiopathic right ventricular tachycardia
- 19. IDIOVENTRICULAR TACHYCARDIA • Enhancedinherent idioventricular rhythm • Manifests when the rate equals sinus rate • Characterised by: • Bizarre QRS complexes or Fusion beats • Rapid idioventricular rate (70-80beats/min) • AV dissociation and capture beats • Absence of pacemaker protection – abolished by faster sinus rhythm
- 20. Ectopic ventricular activation Normal ventricular activation Fusion beat AcceleratedIdioventricular Rhythm (> Ventricular Escape Rate, but < 100 bpm) Sinus acceleration
- 22. • Hemodynamically welltolerated • Beta blockers and CCBs for prevention • Catheter ablation • No risk of sudden cardiac deaths
- 23. ECG Clues Supportingthe Diagnosis of Ventricular Tachycardia • AV dissociation (capture beats, fusion beats) • Concordance of QRS complex in all precordial leads • Frontal plane: LAD with QRS > 140 ms • Precordial leads: RS pattern ; Onset of R to Nadir of S >100ms • RBBB pattern with - V6 : QS or dominant S - V1 : R > R’ - V1 : Monophasic R or biphasic qR or R/S with initial deflection different from sinus initiated QRS • LBBB pattern with - Right axis : Negative deflection in V1 > V6 - V6 : qR or QS - V1 : R > 40 ms
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- 27. TORSADES DE POINTES •‘Twisting of the points’ • Etiology: • Congenital long QT • Drugs – Quinidine, Phenothiazines • Hypokalemia/ hypomagnesemia • Bradyarrhythmias -3rd degree blocks
- 28. ECG Recognition • QRSmorphology continuously changes • Complexes alternates from positive to negative
- 29. Mechanism • Events leadingto TdP are: • Hypokalemia • Prolongation of the action potential duration • Early afterdepolarizations • Critically slow conduction that contributes to reentry
- 30. Brugada Syndrome • RBBB+ persistent ST elevation in Right precordial leads • Sudden cardiac death • 3 patterns • Type 1 - J point elevation with ST segment elevation ≥0.2mV followed by Negative T wave • Type 2 – saddle back configuration of ST elevation >0.2mV – downsloping ST elevation – positive or biphasic T wave not touching baseline • Type 3 – ST elevation <0.1mV with either of the morphologies
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- 34. Morphology Criteria forVT qRqRAbsent Q
- 35. ACUTE MANAGEMENT OF SUSTAINEDVT Hemodynamic decompensation NO YES Termination by medical treatment AMIODARONE PROCAINAMIDE SOTALOL LIDOCAINE No Response DC Cardioversion AMIODARONE 15 mg/min over 10 min f/b 1 mg/min for 6 hours f/b 0.5 mg/min for 18 hours.
- 36. LONG TERM THERAPY PREVENTIONOF RECURRENCE/SUDDEN DEATH • Asymptomatic Nonsustained Preserved LV function • Symptomatic Nonsustained Preserved LV function • Symptomatic Nonsustained LV dysfunction (EF < 0.35) Need not be treated Beta blockers Class IC agents Sotalol Amiodarone ICD
- 37. LONG TERM THERAPY SECONDARYPREVENTION Survivors of cardiac arrest/ Sustained VT with hemodynamic compromise PLUS Poor LV function ICD IS THE TREATMENT OF CHOICE Empirical Amiodarone/ Beta blocker is the next best therapy
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Editor's Notes
- #2 Welcome to VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW. This module contains a discussion of the various characteristics and classifications of ventricular tachycardia (VT). ECG recognition and treatment of the various tachycardias will be explored. Focus is given to the use of RF ablation as a treatment for certain VTs.
- #5 PVC’s can lead to ventricular tachycardia or fibrillation in individuals with ischemic or damaged hearts. PVCs can occur in many combinations (e.g., bigeminal, trigeminal, couplets) or from many ectopic foci, (e.g., multifocal PVCs).
- #7 FIGURE 35–30 Multiform premature ventricular complexes (PVCs). The normally conducted QRS complexes exhibit a left bundle branch block contour (arrowhead) and are followed by PVCs with three different morphologies.
- #11 This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.
- #12 Idiopathic left ventricular tachycardia has been seen in younger patients with normal hearts.
- #14 Sudden death affects approximately 250,000 or more Americans annually according to the AHA. Most causes of sudden death can be attributed to VT or ventricular fibrillation (VF). As the name implies, ventricular tachycardia, originates in the ventricles. Rates can range from 110 – 250 bpm. Ventricular tachyarrhythmias are often, life threatening and require immediate intervention. Occasionally, slower VTs may be relatively well tolerated. While most ventricular arrhythmias occur in patients with a history of heart disease, they have also been seen in patients with healthy hearts.
- #21 Ventricular tachycardia can be attributed to one of three mechanisms.
- #22 Reentry is a common cause of ventricular tachyarrhythmias. It is the mechanism that is responsible for the arrhythmias listed on this slide. Left idiopathic ventricular tachycardia is rare.
- #23 Automaticity enables the cell to spontaneously produce an electrical impulse without an external stimulus. It is the mechanism for arrhythmias listed on this slide. Of note, hypoxemia is deficient oxygenation of the blood.
- #24 This graphic illustrates the cause of automaticity: abnormal acceleration of phase 4 of the action potential in a cardiac cell. This reduces the time of repolarization, and allows the cell to depolarize again. Automaticity enables some cardiac cells (ectopic cells) to act as backup pacemakers when the SA node malfunctions. Ectopic sites may generate impulses in addition to the impulses generated by the SA node, or the ectopic sites may generate impulses out of sync with the normal heart rhythm. Enhanced automaticity occurs when the SA node or ectopic sites generate electrical impulses too quickly, which may affect heart rhythm or rate. Ectopic sites may be located in the atria, AV node, or in the ventricles and can produce tachycardias reflective of the site of origination.
- #25 Characteristically, triggered activity resembles both automaticity and reentry. Triggered activity can be divided into two different categories: pause-dependent and catechol-dependent. Pause-dependent triggered activity is caused by early afterdepolarizations in phase 3 of the action potential. These VTs are usually polymorphic. Catechol-dependent triggered activity is caused by late afterdepolarizations in phase 4 of the action potential. They may be seen in patients with digitoxicity, cardiac ischemia, or congenitally prolonged QT intervals. Increased sympathetic tone also plays a part in these arrhythmias. Idiopathic right ventricular tachycardia is attributed to this mechanism.
- #30 LBBB with V1 : R &gt; 40 ms indicates (Delayed activation during initial phase of the QRS complex)
- #35 Torsades de pointes (twists of points) is a unique VT in which the QRS complexes change from positive to negative and appear to twist around the isoelectric line.
- #36 The early afterdepolarizations initiate the tachycardia; reentry sustains it.