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Ventricular arrhythmias
This document provides an outline for a module on ventricular tachyarrhythmias. It begins with module objectives of differentiating types of ventricular tachycardias using ECGs. The outline then describes ventricular tachyarrhythmias, discusses characteristics like mechanisms and sustained vs nonsustained types. It classifies ventricular tachyarrhythmias as monomorphic or polymorphic, and provides subcategories within each with descriptions and ECG recognition details. Specific arrhythmias discussed include idiopathic VT, bundle branch reentry, ventricular flutter, fibrillation, and Torsades de Pointes.
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Ventricular arrhythmias
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- 2. Module Objectives – VentricularTachyarrhythmias After completion of this module, the participant should be able to: • Differentiate types of ventricular tachycardias using ECG
- 3. Module Outline – VentricularTachyarrhythmias I. Description II. Characteristics A. Mechanisms B. Sustained vs. nonsustained C. Premature ventricular contractions
- 4. Module Outline – VentricularTachyarrhythmias III. Classification A. Monomorphic 1. Idiopathic a. b. ECG recognition c. 2. Description Treatment – ablation Bundle branch a. Description b. ECG recognition c. Treatment –ablation
- 5. Module Outline – VentricularTachyarrhythmias III. Classifications - continued 1. Ventricular flutter a. 4. Ventricular fibrillation a. B. ECG recognition ECG recognition Polymorphic 1. Torsades de pointes a. b. Description ECG recognition
- 6. Ventricular Tachycardia (VT) •Originates in the ventricles • Can be life threatening • Most patients have significant heart disease – Coronary artery disease – A previous myocardial infarction – Cardiomyopathy
- 7. 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 afterdepolarizations (phase 3) – Delayed afterdepolarizations (phase 4)
- 8. 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
- 9. 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
- 10. Automaticity Abnormal Acceleration ofPhase 4 Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.
- 11. Triggered Fogoros: Electrophysiologic Testing.3rd ed. Blackwell Scientific 1999; 158.
- 12. Sustained vs. Nonsustained •Sustained VT – Episodes last at least 30 seconds – Commonly seen in adults with prior: • Myocardial infarction • Chronic coronary artery disease • Dilated cardiomyopathy • Non-sustained VT – Episodes last at least 6 beats but < 30 seconds
- 13. Premature Ventricular Contraction • PVC – Ectopicbeat in the ventricle that can occur singly or in clusters – Caused by electrical irritability • Factors influencing electrical irritability – Ischemia – Electrolyte imbalances – Drug intoxication
- 14. Classification • Ventricular Tachycardia – Monomorphic • • Bundlebranch reentry tachycardia • Ventricular flutter • – Idiopathic VT Ventricular fibrillation Polymorphic • Torsades de pointes (TdP)
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- 16. Monomorphic VT • Heartrate: 100 bpm or greater • Rhythm: Regular • Mechanism – Reentry – Abnormal automaticity – Triggered activity • Recognition – Broad QRS – Stable and uniform beat-to-beat appearance
- 17. ECG Recognition ECG usedwith permission of Dr. Brian Olshansky.
- 18. Distinguishing wide complexSVT from ventricular tachycardia In VENTRICULAR TACHYCARDIA • H/O coronary disease or infarction • QRS width >0.14 sec • AV dissociation showing capture or fusion beats • Extreme right axis deviation • Q wave in V6
- 19. The Brugada Criteria TableI. Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm Step 1. Is there absence of an RS complex in all precordial leads V1 – V6? If yes, then the rhythm is VT. • Sens 0.21 Spec 1.0 Step 2. Is the interval from the onset of the R wave to the nadir of the S wave greater than 100 msec in any precordial leads? If yes, then the rhythm is VT. • Sens 0.66 Spec 0.98 Step 3. Is there AV dissociation? If yes, then the rhythm is VT. • Sens 0.82 Spec 0.98 Step 4. Are morphology criteria for VT present? See Table II. If yes, then the rhythm is VT. • Sens 0.99 Spec 0.97
- 20. Morphology Criteria forVT Table II. Morphology Criteria for VT Right bundle type requires waveform from both V1 and V6. V1 V6 Monophasic R wave QR or QS RS or QR R/S <1 Left bundle type requires any of the below morphologies. V1or V2 V6 R wave > 30 msec QR or QS Notched downstroke S wave. Greater than 60msec nadir S wave. Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649-59.
- 21. Idiopathic Right Ventricular Tachycardia •Right ventricular idiopathic VT – Focus originates within the right ventricular outflow tract – Ventricular function is usually normal – Usually LBBB, inferior axis • Treatment options: – Pharmacologic therapy (beta blockers, verapamil) – RF ablation
- 22. ECG Recognition Kay NG.Am J Med 1996; 100: 344-356.
- 23. Case History: IdiopathicVT 39 y.o. female with no prior cardiac history • First episode – 9 hours of palpitations – In ER, found to be in wide-complex tachycardia of LBBB, inferior axis, at 205 bpm – Converted with IV lidocaine; placed on tenormin • Second episode – While on tenormin, patient had onset of palpitations at airport – In ER, converted with IV lidocaine • Patient underwent EP study
- 24. Case History: IdiopathicVT • At EP study, tachycardia focus was mapped and localized to right ventricular outflow tract • The focus was successfully ablated using radiofrequency energy, with no subsequent inducible or clinical VT
- 25. Idiopathic Left Ventricular Tachycardia •RBBB – Involves the Purkinje network • Treatment options: – RF ablation – Pharmacologic therapy (verapamil, beta blockers)
- 26. ECG Recognition ECG usedwith permission of Kay NG.
- 27. Bundle Branch Reentry •Reentry circuit is confined to the left and right bundle branches • Usually LBBB, during sinus rhythm • Presents with: – Syncope – Palpitations – Sudden cardiac death • Treatment: RF ablation of right bundle
- 28. VT Due toBundle Branch Reentry
- 29. Ventricular Flutter • Heartrate: 300 bpm • Rhythm: Regular and uniform • Mechanism: Reentry • Recognition: – No isoelectric interval – No visible T wave – Degenerates to ventricular fibrillation • Treatment: Cardioversion
- 30. Ventricular Fibrillation • Heartrate: Chaotic, random and asynchronous • Rhythm: Irregular • Mechanism: Multiple wavelets of reentry • Recognition: – No discrete QRS complexes • Treatment: – Defibrillation
- 31. ECG Recognition • Pwaves and QRS complexes not present • Heart rhythm highly irregular • Heart rate not defined
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- 33. Polymorphic VT • Heartrate: Variable • Rhythm: Irregular • Mechanism: – Reentry – Triggered activity • Recognition: – Wide QRS with phasic variation – Torsades de pointes
- 34. ECG Recognition EGM usedwith permission of Texas Cardiac Arrhythmia, P.A.
- 35. Torsades de Pointes(TdP) • Heart rate: 200 - 250 bpm • Rhythm: Irregular • Recognition: – Long QT interval – Wide QRS – Continuously changing QRS morphology
- 36. Mechanism • Events leadingto TdP are: – Hypokalemia – Prolongation of the action potential duration – Early afterdepolarizations – Critically slow conduction that contributes to reentry
- 37. ECG Recognition • QRSmorphology continuously changes • Complexes alternates from positive to negative
- 38. A 67 yearold male with history of previous infarct and reduced LV function presents with palpitations and dizziness. His blood pressure is 80/40. The appropriate next step is ? • A. Synchronized cardioversion for VT • B. I.V. Procainamide for Atrial Fibrillation with WPW syndrome • C. Synchronized cardioversion for unstable SVT with aberrancy. • D. I.V. Amiodarone for SVT with aberrancy in a patient with reduced LV function.
- 40. Answer A. • Thispatient has ventricular tachycardia. An RS interval of greater than 100 msec is clearly visible. In addition, by history this patient is overwhelmingly likely to present with VT with a wide complex rhythm. Also this patient is not stable with relative hypotension requiring immediate cardioversion as opposed to pharmacologic therapy.
- 41. A 46 yearold female is admitted with dizziness. She is an alcoholic, on methadone, with schizophrenia. She began feeling dizzy after starting a fluoroquinalone for a UTI. Which of the following should be your next step? • A. Administer I.V . Procainamide • B. Consult E.P. for placement of a defibrillator • C. Discontinue antibiotic, treat with I.V. magnesium, discontinue antipsychotic, and consider temporary pacing • D. Administer I.V. amiodarone because it is unlikely Torsades de Pointes. cause
- 43. Answer C. • Thispatient has Torsades de Pointes with classic polymorphic VT and prolonged QT demonstrated in the bottom strip. Antipsychotics, hypomagnesemia, quinolones all may predispose to this arrhythmia. Procainamide or amiodarone would worsen this rhythm. ICD is not indicated .
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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.
- #3 Participant objectives, for this module, are as listed.
- #4 This module will start by discussing the characteristics of VT.
- #5 VTs are generally classified as being either monomorphic or polymorphic. Detailed discussions of monomorphic VTs, (idiopathic, bundle branch, ventricular flutter,and ventricular fibrillation) will include a description of the rhythm, ECG characteristics, and treatment options.
- #6 The presentation will conclude with a discussion of Torsades de pointes.
- #7 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.
- #8 Ventricular tachycardia can be attributed to one of three mechanisms.
- #9 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.
- #10 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.
- #11 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.
- #12 Figure A illustrates the early afterdepolarizations in phase 3 of the action potential, responsible for pause-dependent triggered activity. Figure B illustrates late afterdepolarizations seen in late phase 3 or phase 4 of the action potential, responsible for catechol-dependent triggered activity.
- #13 Another characteristic, used to describe VT, is whether it is sustained or non-sustained.
- #14 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).
- #15 Ventricular tachycardia can be classified as being either monomorphic or polymorphic. The following slides present a discussion for each rhythm listed, along with EGC identification and treatment options. Ventricular flutter is rarely seen, and may be seen just prior to the onset of ventricular fibrillation. Torsades de pointes is associated with a long QT interval.
- #17 Monomorphic VT is regular, with uniform beat-to-beat morphology. It can be sustained, nonsustained, idiopathic or caused by bundle branch reentry.
- #18 ECG characteristics that help define VTs are: The QRS complexes are rapid, wide, and distorted. The T waves are large with deflections opposite the QRS complexes. The ventricular rhythm is usually regular. P waves are usually not visible. The PR interval is not measurable. A-V dissociation may be present. V-A conduction may or may not be present. It may be difficult to distinguish VT from SVT with aberrancy from a surface ECG. Many texts offer tips for distinguishing these rhythms. The presence of capture and fusion beats generally occur in VT.
- #22 This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.
- #23 This slide is a recording of RVOT VT.
- #24 The following slides discuss the case of a 39 year old white female, who presented with idiopathic VT.
- #26 Idiopathic left ventricular tachycardia has been seen in younger patients with normal hearts.
- #27 This ECG is left ventricular tachycardia.
- #28 Bundle branch reentry tachycardia is another VT that is treatable with RF ablation. With this type of tachycardia, the HV interval is increased. Ablation of the right bundle does cure this form of reentry. However, given the underlying LBBB, ablation of the RBBB results in either very impaired His/Purkinje function or in complete heart block. A pacer is usually required.
- #29 The most helpful criteria to consider when diagnosing VT due to bundle branch reentry is the comparison of this LBBB morphology to the LBBB seen in sinus. The morphology does not have to be exactly the same (if there is some conduction down the left bundle) but it should be really similar.
- #30 Rarely seen, ventricular flutter may occur just prior to the onset of ventricular fibrillation. It degenerates into ventricular fibrillation in a matter of seconds.
- #31 Ventricular fibrillation (VF) will convert to fine VF and then no electrical activity will be seen. Patients resuscitated from VF are deemed sudden cardiac death survivors.
- #32 The following ECG findings help electrophysiologists to diagnose VF: P waves and QRS complexes are not present. Heart rhythm is highly irregular. The heart rate is not defined (without QRS complexes).
- #34 A second classification of VT is polymorphic VT.
- #36 TdP is a rapid and distinct VT with a twisting configuration of the QRS morphology, associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT.
- #37 The early afterdepolarizations initiate the tachycardia; reentry sustains it.
- #38 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.