Manejo Clinico de Arritmias Ventriculares

1. Manejo Clinico de Arritmias Ventriculares Oscar L Paredes G; M.D., Ph.D.

2. Arrtimias ventriculares • Bajo la denominacion de arritmias ventriculares se incluyen a despolarizaciones originadas en un foco ventricular, precoces, repetitivas, disociadas de las aurículas.

3. Fisiologia • Celulas musculares cardiacas son excitables • En reposo su voltaje intracelular es negativo -90mV (SA node is -40mV) • En reposo el - K+ se encuentra dentro y el Na+ fuera de las celulas (Na+/K+ pump) • El potencial de accion ocurre cuando el Na+ entra a la celula originando una corriente de despolarizacion • La estimulacion de una sola celula causa que la actividad electrica se disperse por el miocardio.

4. Phase 0 rapid depolarisation (inflow of Na+) Phase 1 partial repolarisation (inward Na+ current deactivated, outflow of K+) Phase 2 plateau (slow inward calcium current) Phase 3 repolarisation (calcium current inactivates, K+ outflow) Phase 4 pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) ‘autorhythmicity’ Refractory period (phases 1-3) Phase 1 Phase 2 0 mV Phase 0 Phase 3 -80mV Phase 4 Fases del potencial de accion

5. Arritmias - Mecanismos • Reentrant • Reentry circuit (fast and slow pathway) is confined to the ventricles and/or bundle branches • Automatic • Automatic focus occurs within the ventricles “focos ectopicos” • Triggered activity • Early afterdepolarizations (phase 3) • Delayed afterdepolarizations (phase 4)

6. Re-entrantes • Reentrant ventricular arrhythmias • Extrasistoles ventriculares • Idiopathic left ventricular tachycardia • Bundle branch reentry • Ventricular tachycardia and fibrillation when associated with chronic heart disease: • Previous myocardial infarction • Cardiomyopathy

7. Automaticas • Automatic ventricular arrhythmias • 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

8. Abnormal Acceleration of Phase 4 Automaticity Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.

9. Gatilladas • Triggered activity ventricular arrhythmias • Pause-dependent triggered activity • Early after depolarization (phase 3) • Polymorphic ventricular tachycardia • Catechol-dependent triggered activity • Late afterdepolarizations (phase 4) • Idiopathic right ventricular tachycardia • Digoxina • Long QT congenito

10. Triggered Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.

11. Antiarritmicos * Farmacos que modifican las propiedades electrofisiológicas del tejido cardiaco. 􀁉 Clasificación: En base al efecto electrofisiológico predominante in vitro.

12. Antiarritmicos Vaughan - Williams • Repolarización • IA Alarga • I Bloqueadores canales de Na → IB Acorta • IC Sin cambios • II Bloqueadores β adrenérgicos. • III Prolongan repolarización. • IV Bloqueadores canales de Ca. • - Otros - no clasificados.

13. Class I: block sodium channels Ia (quinidine, procainamide, disopyramide -*ajmalina) AP Ib (lidocaine) AP Ic (flecainide -propafenona) AP Class II: ß-adrenoceptor antagonists (atenolol, bisoprolol) Class III: prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol) Class IV: Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil) Vaughan - Williams classification of anti-arrhythmic drugs Phase 1 IV Phase 2 0 mV III I Phase 0 Phase 3 -80mV Phase 4 II

14. Antiarritmicos (Proarritmia) Antiarrhythmic DrugProarrhythmia Class I - Flecainide, Propafenone Sustained VT, slow atrial flutter rate causing 1:1 conduction to the ventricle Class II - Beta blocker Severe sinus bradycardia Class III - Sotalol, Dofetilide Torsades de pointes Class IV - Verapamil, Diltiazem Severe sinus bradycardia

15. Amiodarona • Toxicidad • Fibrosis pulmonar • Hipo-hipertiroidismo • Hepatotoxicidad • Aplasia de medula osea • Insuficiencia renal • Fotosencibilidad • Depositos corneanos • Efectos colaterales • Mialgias • Trasntornos de la marcha • Insomnio • Prolongacion del TP • Aumenta biodisponibilidad de la digoxina

16. Amiodarona: Estudios • Chest RX • Hemograma • Funcional hepatico • Funcional renal • Hormonas tiroideas • Evaluacion oftalmologica • Test de funcionalidad pulmonar

17. Dronedarone SR33589 • Inhibe los Ikr , Iks, B1 ,ICa (L-type), Ito • • No es iodinado • • No thyroid or pulmonary toxicity • • Similar electrophysiology to amiodarone • • Half-life = 24 h, dose BID • • Food increases levels 2-3 x • • Undergoes 1st pass metabolism, ~ 15% • Available • Circulation 1999;100:2276

18. Dronedarone SR33589 Dronedarone-Clinical Trials •DAFNE-Dronedarone Atrial Fibrillation study aFter Electrical cardioversion– Persistent AF, RRR 55% of reversion to AF •EURIDIS-EUropean trial in atrial fibrillation or flutter patients Receiving Dronedarone for the maintenance of Sinus rhythm •ADONIS-American-Australian-African Trial with Dronedarone in Atrial Fibrillation/Flutter Patients for the Maintenance of Sinus Rhythm

19. Arritmias ventriculares • CLASIFICACION • Extrasistoles ventriculares • Ritmo idioventricular • Lento • Acelerado • Ventricular tachycardia • Momorfas • Polimorfas: Torsades De Pointes • Flutter Ventricular • Fibrilacion Ventricular

20. Extrasistole Ventricular • Ectopic beat originate in the ventricles and earlier than expected • Herald the development of lethal ventriular arrhythmia (VT, VF) • Uniform: single ectopic ventricular pacemaker site • Multiform: having different QRS complex size, shape or direction

21. Extrasistole Ventricular • Cause: enhanced automaticity in the ventricular conduction or muscle tissue • Electrolyte imbalance (K↑or↓, Mg ↓, Ca ↓) • Metabolic acidosis • Hypoxia • Drug intoxication (coccaine, amphetamines, tricyclic antidepressants) • Enlargement or hypertrophy of ventricular chamber • Increased sympathetic stimulation • Myocarditis • Caffeine or alcohol ingestion • Tobacco use • Irritation of ventricles by pacemaker or pulmonary artery catheter • Sympathomimetic drug(epi, isoproterenol)

22. Ausencia de onda p. Aspecto distinto a los demas QRS, bizarro Complejo ancho, duracion>0.12 sec. Onda T opuesta Sigue una pausa compensadora EKG

23. R-on-T phenomenon：una extrasistole cae justo encima del down slope de la onda T precedente.

24. Clasificacion de las EV (Lown modificado) • GRADO IA menos de un latido anticipado por hora • GRADO IB mas de 1 latido por h. pero menos de 30 • GRADO II mas de 30 latidos anticipados por hora • GRADO III Extrasístoles polimorfas • GRADO IV A Extrasístole apareadas y bigeminadas • GRADO IV B Taquicardia ventricular • GRADO V Fenómeno R sobre T

25. Signos / Sintomas • A weaker pulse after the premature beat and a longer pause between pulse waves. • Auscultation: early heart sound with each PVC. • Maybe asymptomatic or palpitation or other S/S due to decrease of cardiac output.

26. Manejo de las EV • Cuando tratar: • Son frecuentes: mas de 10 por minuto • Prematuras con fenomeno R/T • Formas repetitivas: duplas, tripletas. • Cuando son poli focales o polimorfas. • Cuando se presentan en salvas • Tratamiento: • Depende de la etiología, características y clínica del paciente. • Cardiac origin: drug to suppress ventricular irritability( procainamide, amiodarone and lidocaine) • Other PVC: underlying heart disease or medical condition

27. Ritmo Idioventricular • Ritmo ventricular de “escape” secundario a falla o bloqueo en la senal supraventricular / nodo-AV. • Inherent firing rate of ectopic pacemaker: 30-40 beat/minuteprevent ventricular standstill or asystole • <3 QRS complex from the escape pacemaker  called “ventricular escape beats or complex” • Ritmo idioventricular acelerado: HR<100 beat/min but > 30-40 beat/min related to enhanced automaticity of ventricular tissue. • Dx Diferencial • AIVR: 100 > AIVR > 30-40 beat/min • Idioventricular rhythm: 30-40 beat/min

28. Cause and significance • Idioventricular rhythm may accompany 3rd-degree heart block • Cause: • Myocardial ischemia • Myocardial infarction(MI) • Digoxin toxicity, beta-adrenergic blockers, calcium antagonist, tricyclic antidepressant • Pacemaker failure • Metabolic imbalances • Transient ventricular escape rhythm: ↑parasympathetic effect on higher pacemaker site • Continuous idioventricular rhythm: serious situation • Slow rate and loss of atrial kick ↓cardiac output death

29. Ritmo: 20-40 bpm Complejo QRS : duracion de mas de 0.12 sec, configuracion “QRS ancho” Ausencia de onda P Onda T: opuesta a la ultima parte del QRS QT intervalo prolongado Often occurs with 3rd-degree AV block EKG

30. AIVR: 100 > AIVR > 30-40 beat/minIdioventricular rhythm: 30-40 beat/min

31. Signos y Sintomas • Inestabilidad hemodinamica • Continuous idioventricular rhythm: due to ↓cardiac output dizziness, light-headedness, syncope or loss of consiousness

32. Tratamiento • Objetivo: incrementar HR, para mejorar el cardiac output. Restablecer el ritmo de base. • Not to suppress the idioventricular rhythm never use lidocaine or other antiarrhythmia to suppress the escape beat • Atropine: increase HR • If hypotension or clinical instability pacemaker • Transcutaneous pacemaker in an emergency • ECG monitor until restore hemodymamic stability • Bed rest

33. Ventricular tachycardia • Se define como la sucesión de tres o mas latidos cardiacos con una frecuencia superior a 100 latidos por minuto, originados por debajo del Haz de His, por tanto con un complejo QRS ancho ( mayor de 12 mseg.). (Brugada et all. Circ.1997)

34. Ventricular tachycardia • Causas: • Myocardial ischemia • Coronary artery disease • Valvular heart disease • Heart failure • Cardiomyopathy • Electrolyte imbalance(↓K) • Drug intoxication: procainamide, quinidine or cocaine • ↓ventricular refilling time and drop of cardiac output cardiovascular collapse

35. Clasificacion de las TV • Duracion TV no sostenida (menos de 30 segundos) TV sostenida ( mas de 30 segundos) • Patron ECG TV monomorfica TV polimorfica QT largo (torsade de pointes) QT normal

36. Rhythm: ventricular rate: 100~250 beat/min Absent P wave or obscured or retrograde QRS: duration > 0.12 sec, bizarre and increased amplitude Opposite T wave if visible Variation: Ventricular flutter Torsades de pointes(polymorphic VT) ECG

37. ECG criterios • Disociación AV durante la taquicardia. • Ausencia de RS en precordiales horizontales. • Duración del RS mayor a 100 mseg. • Eje eléctrico a la izquierda en TV con imagen de BRD. (valor predictivo 87%). Eje eléctrico a la derecha en TV con imagen de BRI ( valor predictivo 94% ) • Presencia de capturas y/o latidos de fusión (Andries et all. SEC 1995)

38. Taquicardia con QRS ancho Ausencia de RS en precordiales si no TV Intervalo RS > a 100ms si no TV Disoc. A-V no si TV Criterios morfológicos V1 V6 no si TV Taq. Supravent. Aberrante. (Brugada et all. Circ. 1997)

39. Medida del Intervalo RS(Brugada et all Circ. 1997)

40. Taquicardia con QRS ancho Disociacion AV esta presente? si no TV R inicial en derivación AVR? si no TV Criterios morfológicos de BBB no si TV Vi / Vt<1 no si TV Aberrancia (Vereckei et all. EHJ.2007)

41. Velocidad activacion inicial (Vi) Vi<Vt = TV (Vereckei et all. EHJ.2007) Velocidad activacion terminal (Vt) (Brugada et all Circ. 1997)

42. ECG Recognition Kay NG. Am J Med 1996; 100: 344-356.

43. ECG Recognition

44. Torsades De Pointes • French term meaning "twisting of the points • torsade de pointes occurs in the setting of delayed ventricular repolarization, evidenced by prolongation of the QT intervals or the presence of prominent U waves. • Drugs– • Quinidine and related antiarrhythmic agents (disopyramide and procainamide), • Sotalol, amiodarone (less commonly), • Psychotropic agents (phenothiazines and tricyclic antidepressants) • Terfenadine, and others • Electrolyte imbalances, including hypokalemia, hypomagnesemia, and less commonly, hypocalcemia, which prolong repolarization • Miscellaneous factors such as severe bradyarrhythmias, liquid protein diets, and hereditary long-QT syndromes

45. Torsades De Pointes • This ventricular tachycardia is often caused by drugs conventionally recommended for the treatment of arrhythmias. • Tx: • Removing or correcting causative factors such as drug toxicity, electrolyte imbalance, or underlying bradycardia. • In emergency settings a temporary pacemaker may be inserted to accomplish "overdrive" suppression of the arrhythmia by increasing the underlying heart rate and thereby decreasing ventricular repolarization time. • Intravenous magnesium sulfate has proved highly useful for suppressing this arrhythmia. • Drug therapy with isoproterenol or bretylium has been used in selected cases. • Sustained episodes of torsade de pointes attempted cardioversion

46. Rapid ventricular rate: 250~350 beat/min • Character: QRS complex change back and forth, with amplitude of each successive complex gradually increasing and decreasing • DDx: ventricular flutter: rapid, regular, repetitive beating of ventricle single ventricular focus firing at a rapid rate of 250~350 beat/min smooth and “sine-wave”appearance

49. What is QTc? • The QT interval varies with the heart rate • Longer when the heart is beating slower and shorter when the heart beats faster • The QT interval is "corrected" through the use of a mathematical formula to what it would be if the heart rate was 60 beats per minute (bpm). • Many correction formulas have been proposed and tested; however, the formulas most commonly in use are the Bazett, the Fridericia, and the Hodges correction formulas. • Bazett(QTc=QT/RR1/2). • Fridericia QTc=QT/RR0.33 • Hodges QT (QTc) = QT + 1.75 (rate - 60)] • The Bazett Formula is usually programmed into the machine that measures your ECG and the QTc value is part of the information printed on the ECG. • For men the QTc < 420 msec and for women the QTc < 440 msec. • QTc values higher than normal are associated with increased risk of serious heart rhythm abnormalities (Torsades de Pointes).

50. Tratamiento de las TVs • Evaluation of consciousness, respiration and circulation • If pulseless immediate defibrillation • Unstable : ventricular rate > 150 beat/min with S/S: hypotension, chest pain or alternated consciousness immediate synchronized cardioversion • Stable with wide-complex VT and no signs of heart failure • Monomorphic: • Polymorphic: • Chronic, recurrent episodes of VT unresponsive to drug therapy implantation cardioversion-defibrillator (ICD)