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Arrhythmia and conduction disorders http://www.uzhnu.edu.ua/uk/infocentre/2006 ІІ Taras V. Chendey, MD, PhD, Ass. Prof. Chair of hospital therapy Cardiac arrhythmias (dysrhythmias) Disorders of frequency (rate), regularity and/or sequence of heart excitation and contraction. Arrhythmias may occur at any age, they may affect either healthy subjects or patients with heart disease or other disease. Arrhythmias vary from benign to fatal; they are amongst major causes of sudden death. Arrhythmology’s basics: action potential Refractory period Arrhythmology’s basics: automaticity S. bradycardia (<50') SА-node: 50-100' AV-junction: 40-50' NSR S. tachycardia (>100') Junctional rhythm Accelerated J. rhythm (50-100') J. tachycardia (>100') Bundle branches: 15-20' ІІ Idioventricular rhythm Accelerated I. rhythm (50-100') Ventricular tachycardia (>100') Mechanisms of arrhythmias Disorders of automaticity Re-entry Triggered activity Conduction block Re-entry concept Triggered activity Vaughan-Williams antiarrhythmic drug classification Class І: Na-channels blockers: -Class Іа: quinidine, procainamide -Class Іb: mexiletine -Class Іс: propafenone, etacizine, flecainide Class Ia Class Ib Class ІІ: beta-blockers Class ІІІ: Potassium channels blockers – amiodarone, sotalol, dronedarone Class IV: non-DHP Са-channel blockers (verapamil) Class Ic Class III Class IV (action potential of AV-node Other AAD: glycosides, ATP, potassium and magnesium salts, sympatomimetics, atropine Classification of arrhythmias I. II. III. IV. V. Disorders of impulse formation Disorders of impulse conduction Combined disorders of impulse formation and conduction Diseases, syndromes and phenomena Arrhythmias in normal or altered function of different types of artificial pacemakers. Etiology of arrhythmias Disorders of cardiovascular system Internal and neurological disease Electrolyte disorders (K, Ca, Mg) Certain drugs Genetic causes (LQTS, SQTS, Brugada syndrome etc.) Extrasystoles Extrasystole (ectopy, premature beat) – premature depolarization of the heart Site of origin: Other characteristics: •Supraventricular: •Single (isolated), pair (two in a row), group (3-triplet or 4) •atrial •junctional (u/, m/, l/p) •Ventricular (from LV, RV) •Allorhythmic (bi-, tri-, quadrigemini) •early (R on T)/ late •interpolated Atrial premature beats 0,92 сек 0,52 сек 1,0 сек Premature occurrence of QRS complex with preceding deformed/wide P wave of non-sinus origin, often superimposed on preceding T-wave. Extrasystolic PQ may be prolonged due to incomplete recovery of AV-junction after prior sinus cycle. Exrtrasystolic QRS width may normal (<120 msec), it may be wide and deformed, resembling a bundle branch block due to incomplete recovery of bundle branch (aberrant conduction). Distance between R wave of sinus complex before APB and R wave of sinus complex after APB less than double normal RR interval – “incomplete post-extrasystolic pause”. Junctional premature beats JPB w/prior atrial excitation А JPB w/simult. ex. of atria and ventr. V JPB w/prior ventricular excitation Ventricular premature beats Premature appearance of wide (≥120 msec), deformed ventricular complex with ST segment and T wave shifted discordantly relative to QRS. No P-wave before VPB. “Complete” post-extrasystolic pause. No complete pause in interpolated VPBs, which occur in sinus bradycardia. Ventricular trigeminy Ventricular pairs and groups V1,2 V5,6 In right ventricular premature beat QRS complex resembles left BBB (positive complexes in left chest leads). In left ventricular premature beat QRS complex resembles right BBB (positive complexes in right chest leads). Right bundle branch block – Deep and wide S-waves in limb and left chest (V5,6) leads. – Wide and deformed QRS complex (rSR') in right chest leads (V1,2). – Reciprocal ST-T changes (i.e. ST depression and T-wave inversion) in right chest leads. – Prolonged activation time in right chest leads. – Clinical significance: mostly benign finding associated with normal heart function. Almost always present in dilatation/ hypertrophy or failure of right heart chambers. – In classical type of RBBB heart electrical axis shifted rightwards or normal in Wilson type electrical axis deviated leftwards. Left bundle branch block Wide (>120 msec) and deformed QRS in limb and left chest leads. Deep and wide S-waves in right chest leads (“cut sward” sign). ST-T moves discordantly (in the opposite direction) from the QRS complex – ST elevated in right chest leas and depressed in left chest leads. Prolonged activation time in left chest leads. Clinical significance: always associated with heart dysfunction. Left anterior fascicular block Extreme left axis deviation, when α<60°which is characterized by SII>RII, RaVR≥QaVR, deep SIII deep, tall RaVL>RI. Clinical significance: always associated with heart dysfunction. Posterior fascicular block AV-blocks – impairment of impulse conduction from atria onto ventricles via AVjunction First-grade AV-block: all implulses are being conducted onto ventricles with some and same delay. ECG: prolonged PQ(R) interval (> 0.2 sec). HR unaffected, and there is a P-wave before each QRS complex. PQ=0,4" Second-degree AV-block – more pronounced impairment of AV-conduction in which NOT ALL impulses are being conducted to ventricles. 2nd degree AV-block type Mobitz-I (Wenckebach block) : progressive prolongation of PQ(R) in consecutive cycles with non-conducted subsequent P and no QRS. (Wenckebach periods). This block caused by the alteration at the level of AV-node (nodal block). 2nd grade AV-block type Mobitz-II Constant (normal or prolonged) PQ(R) interval with irregular sequence of conducted and nonconducted P-waves (no Wenckebach periods) High-grade AV-block (Mobitz-ІІІ) Normal PQ(R) interval with regular sequence of conducted and nonconducted P-waves (mostly 2:1 or 3:1) 3rd grade AV-block (complete): no conduction from atria to ventricles AV-dissociation – rhythm of P-waves independent from the Proximal (nodal) complete block: escape pacemaker located in rhythm of QRS complexes His bundle and produces 30-40 narrow (<120 msec) QRS complexes per minute (junctional escape rhythm). Distal (infranodal): escape pacemaker located in the left or right bundle branch and produces 20-30 wide QRS complexes per minute (idioventricular escape rhythm). Treatment of complete AV-block Implantation of artificial pacemaker Tachyarrhythmias arrhythmias with HR>100' QRS width Narrow QRS (<120 мс) Regularity Wide QRS (>120 мс) Regular Irregular Narrow-complex tachycardia Sinus tachycardia Paroxysmal supraventricular tachycardia HR 188/min Atrial fibrillation Wide-complex tachycardia: ventricular tachycardia Atrial fibrillation Supraventricular tachycardia with irregular ventricular response Most common chronic arrhythmia AFib linked to increased risk of heart failure, embolism (mostly embolic stroke) and death Common causes/favoring conditions in AFib: IHD (all forms) Мyоcarditis Cardiomyopathies Valvular heart disease (esp. mitral stenosis) Thyrotoxicosis Sick sinus syndrome Atrial fibrillation: classification and terminology Paroxysmal – normal sinus rhythm restores spontaneously without intervention; usually lasts up to 48 hours. Persistent – restoration of NSR requires pharmacological or electrical intervention (cardioversion); lasts up to several days or weeks. Permanent – restoration of NSR is not possible or not feasible. Primary and recurrent atrial fibrillation Isolated atrial fibrillation Tachy- and normosystolic atrial fibrillation Mechanisms of Atrial Fibrillation Left atrial microreentry near pulmonary veins ostia Daughter wavelets of re-entry Irregular ventricular response due to physiologic AVblock 2 1 4 ECG-signs of AFib: 1) absence of P-waves 2) irregular ventricular rhythm 3) f-waves 4) electrical alternation 3 Atrial flutter F F F F Regular tachyarrhythmia with HR 150/min F-waves at rhe rate of 300/min Conduction F/QRS = 2:1 Treated atrial flutter Regular rhythm with HR 75 bpm F-waves at the rate of 300/min Conduction F/QRS = 4:1 Patient with AF Restoration and attainment of NSR (“rhythm control”) Class Іс drugs Class ІІІ drugs Electrical cardioversion Ablation Attainment of normal HR (“rate control”) Class ІІ drugs Class ІV drugs Digoxin AV-node destruction + pacemaker Thromboembolism prevention Aspirin Vit. K antagonists Novel anticoagulants Left atrial appendage isolation Stroke risk assessment in atrial fibrillation – CHA2-DS2-VaSc score C H A2 D S2 Va Sc Cardiac failure – 1 point Hypertension – 1 point Age > 65 – 1 point, >75 yrs – 2 points Diabetes – 1 point S2 Stroke or TIA – 2 points Vascular disease – MI/PAD – 1 point Sex category – female sex – 1 point Total score: 0-9 0-1 point – low risk (1,9-2,8% per year) → aspirin 150 mg/d ≥2 points – high risk (>4% per year) → VKAs (warfarin) or novel anticoagulants Rationale for the therapeutic range of INR Thrombosis Bleeds Target range INR