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Review 순환기 내과 R3 서정호 Specific type of VT Torsades de pointes Polymorphic tachycardia with normal QT interval with ischemic heart disease Polymorphic VT Associated with QT prolongation (often >0.60sec) Initiated by “R-on-T” VPC Should not be consisidered Torsades Class I or III agents Abolition of ischemia, revascularization Polymorphic VT initiated by short coupled VPC during exercise or catecholamine state Accelerated Idioventricular Rhythm Torsade de Pointes Twisting of the points Polymorphic VT 기저선 위아래로 교대로 나타나는 다양한 폭을 가진 파형 보통 비지속적 대부분 QTc 간격 연장이 선행 Antiarrhythmics Macrolide TCA Hypokalemia, hypomagnesemia, Ischemic heart disease, congenital long QTS Torsade de Pointes Early afterdepolarization M/c cause: congenital, severe bradycardia, potassium depeletion,Medication (class IA,IC,III) IV magnesium Temporary pacing Isoproterenol Lidocaine, mexiletine, phenytoin Potassium channel opener Torsades de Pointes-Treatment Removing precipitating factor Correcting metabolic abnormalities Removing drugs that induce QT prolongation Electrolyte abnormality(hypokalemia, hypomagnesemia) Antiarrhythmic Drug(quinidine) Phenothiazine , TCA, Liquid protein diet, Intracranial event, bradyarrhythmia Torsades de Pointes-Treatment Removing precipitating factor Correcting metabolic abnormalities Removing drugs that induce QT prolongation Drug induced torsades de pointes Atrial or ventricular overdrive pacing and Mg Congenital long QT syndrome B-blocker Phenytoin(shorten QT interval) Cervicothoracic sympathectomy ICD with dual chambered pacing capability and B blocker Contents Normal QT interval Long QT syndrome Definition Causes Management Drug induced long QT syndrome 심장의 전도계 ECG Measurements ECG measures electrical activity of heart P wave: atrial depolarization Q-R-S wave: ventricular depolarization T wave: ventricular repolarization http://www.cbi.dongnocchi.it/glossary/TWave.html • • • • • • • P : 2.5mm * 0.12초 PR 간격 : 0.12 ~ 0.20초 QRS군 : 30mm * 0.06 ~ 0.10초 Q파 : R파의 25% 미만 * 0.04초 미만 ST 분절 : -0.5 ~ +2mm T파 : 5 ~ 10mm이하 QT간격 : RR간격의 50%이하 남<0.42초, 여<0.43초 Normal QT interval QT interval: 심실 근육의 전기적 활성도와 회복 시간 간의 간격 심박수에 역비례 Bazett’s formula Hodges and coworkers: QTc= QT + 0.00175(심실 박동수 –60) 상한 범위는 0.46 sec 여성에서 약간 길고 나이가 들수록 증가 여러 유도 간 차이- 가장 긴 QT interval QT prolongation Age and Sex Prolonged QTc (sec) Reference Range (sec) Children (< 15 y) > .46 < .44 Adult Males > .45 < .43 Adult Females > .46 < .45 http://www.emedicine.com/med/topic1983.htm LQT Syndrome (LQTS) LQT syndrome is a genetic disease One of several causes of cardiac arrhythmias ECG Characteristics: Prolongation of the Q-T interval Deformation of T wave/presence of U wave Action Potentials: Normal vs. LQT1 http://www.cvrti.utah.edu/~macleod/bioen/be6460/notes/Channels-LQTS.pdf LQT Syndrome: Types LQTS Type Chromosomal Locus Mutated Gene Ion Current Affected LQT1 11p15.5 KVLQT1 IKs LQT2 7q35-36 HERG IKr LQT3 3p21-24 SCN5A INa LQT4 4q25-27 ? ? LQT5 21q22.1-22.2 KCNE1 (heterozygotes) IKs LQT6 21q22.1-22.2 MiRP1 IKr http://www.emedicine.com/med/topic1983.htm Disease Statistics Affects 1 in about 3000-5000 individuals Potassium channel mutations (KvLQT1 and HERG) estimated to cause 87% of all LQT syndromes LQT3 (SCN5A): approximately 8% LQT5 (KCNE1/minK), LQT6 (MiRP1): 5% Genetic Basis Type 1 arises as a result of a genetic mutation Chromosome 11 KvLQT1 gene Encodes potassium channel α subunit Mutation leads to loss of function of K+ channel Delayed potassium rectifying current (IKs) Inherited Dominantly Recessively Chromosome 11 11p15.5 http://ghr.nlm.nih.gov/chromosome=11 Cardiac myocyte repolarization IK responsible for repolarization of cell during action potential IKs helps keep action potential duration at normal levels Problems with channel longer APD (lengthened because of abnormal repolarization) Romano-Ward and JLN Associated with KvLQT1 gene Related to LQT1 Romano-Ward: autosomal dominant Characterized by gradual hearing loss Jervell-Lange-Nielsen (JLN): autosomal recessive Characterized by congenital deafness Cardiac related symptoms Abnormal heartbeat Tachyarrhythmias – fast heart rate (>100 bpm) Torsades de Pointes Syncope (Fainting) Cardiac arrest (heart failure) Sudden death Caution! Arrhythmia can be induced by: Stress/ Exercise Accelerated heart rate Superposition of action potentials Treatment β-blockers (suppresses sympathetic nervous system) ICD/Pacemakers (control heart rhythm) Gene therapy ? Cellular Structure • Phospholipid bilayer • Impermeable • Spanning proteins • Channels, receptors and pumps Ion Pumps Na+/K+ ATPase, 3 Na+ out 2 K+ in Ion Channels Macromolecular protein tunnels Highly selective to particular ion Respond to various modifiers (voltage, time, other ion concentrations) Conformational changes Act as switches to energy created by pumps Resting Membrane Potential Intracellular K+, 140 mM/L, extracelluar 4 mM/L Intracelluar Na+, 1015mM/L, extracelluar 140 mM/L At rest K+ channel is open, others closed Receptors Na+ channels Phase 0 in fast response (ventricular atrial and Purkinje) tissue Voltage and time dependent Class I agents Ca2+ Channels T type (transient, tiny), pacemaker L type (long-lasting) dominant depolarizing current (phase 0) of SA and AV node, plateau (phase 2) of ventricle, atrium L type, target of Ca2+ channel blockers K+ Channels IKl – voltage dependent, generates RMP IK – responsible for repolarization, 2 components, IKr (rapid), IKs (slow) Cardiac Action Potential Antiarrhythmics Vaughn-Williams Classification Class I – Na+ channel blockers IA – Procainamide, Disopyramide, Quinidine IB – Lidocaine, Mexiletine, Tocainide IC – Flecainide, Propafenone Class II – Beta-blockers Class III – K+ channel blockers Sotalol, Ibutilide, Amiodarone, Dofetilide Class IV – Ca2+ channel blockers Class I Na+ channel Blockers Slow conduction (IC>IA>IB) Useful for reentrant rhythms in Na+ dependent tissue Depress automaticity IC’s prolong refractoriness without affecting APD IA’s block several K+ channels, inc APD Class I Na+ Channel Blockers Proarrhythmia risk slow conduction prolong QT IC’s increase mortality in ischemic CM Contraindicated Class I Na+ Channel Blockers IA/IC, atrial fib/flutter or atrial tach with normal LV/no ischemia IB no significant effect on atrial tissue Lidocaine indicated for VF/VT Class II Beta-Blockers Reversibly bind to beta-receptors Decrease pacemaker current, increase threshold (dec automaticity) Indirect inhibition of L type Ca2+ channels (slow conduction in AVN) Class II Beta-Blockers Hyperadrenergic states reduce SCD risk post MI, CHF automatic rhythms (atrial tach) Reentrant rhythms using AVN AVRT, AVNRT Slow ventricular rate in atrial fibrillation No ventricular proarrhythmia Bradycardia/heart block can limit use Class III K+ Channel Blockers Sotalol, Ibutilide, Dofetilde inhibit IKr Amiodarone inhibits IKr and IKs Markedly prolong APD Sotalol betablocker Amio class I, II, IV Class III K+ Channel Blockers IKr blockers display reverse use dependence Torsade risk up to 8%! Variant of LQTS Amio no significant risk of ventricular proarrhythmia Possibly mediated by IKs block Class III K+ Channel Blockers IKr blockers, wide variety of reentrant arrhythmias (afib, atrial flutter) Avoided in presence of LVH and poor LV function Sotalol reduces ICD shocks Amio broadest range of indications Limited by bradycardia/AVN block and extracardiac effects Ca2+ Class IV Channel Blockers Inhibit L type Ca2+ channels Slow phase 4 (reduce automaticity) in SA and AV nodes Slow conduction/prolong refractoriness in AV node Useful for PSVT, slow ventricular rate in atrial fibrillation, rare form of VT Limited by bradycardia/AVN block Mortality neutral, no ventricular proarrhythmia Adenosine Endogenous nucleoside Adenosine (A1) receptor agonist Activates outward IKAdo K+ current causing hyperpolarization Inhibits pacemaker current Results in profound slowing of sinus rate, AV nodal block Agent of choice for PSVT Digoxin Inhibits Na+/K+ pump Increases intracellular Ca2+ Increases Vagal tone Atrial fibrillation in presence of CHF PSVT in pregnancy Mortality neutral Antiarrhythmics