. anti-arrhythmic drugs normal cardiac rhythm: SA node produces electrical impulse-allow for cardiac contraction ↳ impulse spreads thru atria - enters AV node → slow conduction allows atria to propel blood into ventricles → impulse propagates thru His Purkinje system to all parts of ventricles * activation of entire ventricular myocardium so. 1sec arrhythmia: electrical activity denating from T, result of abnormality in impulse initiation and/or propagation * tx of mild/asymptomatic arrhythmias → avoid me cham 'm s: - Ischemia -excessive catecholamine exposure -hypoxia -autonomic influences - acidosis, alkalosis - drug toxicities - electrolyte disturbance DEMPLEX R. {Amp:! T WAVE P wave IIYnimni.es . Aggie atrial depolarization ventricular ventricular repolarization ⑥ g, g contraction bundle of his cardiac AP: change" "in"'voltage across myocardial cells ↳ movement of ions: Nat, Kt, C Azt NORMAL SAT AV NODE ACTION POTENTIAL 2 * SLOW * cart blockers * RATE CONTROL - Verapimil -Dittiazem O drugs that suppress Cast influx can slow/Stop AV conduction. 3 cast depolarization * B- blockers - PROPANOLOL -METOPROLOL 4 I 4 drugs that work here suppress phase 4 depolarization SA node automacity NORMAL ATRIAL, VENTRICULAR, & HIS-PURKINJE MYOCYTE AP * FAST drugs here rate of phase on * RHYTHM CONTROL low impulse conduction thru His,jzm, I 2 erjinke + myocardium -drugs here delay repolarization c it " -prolongs EPP I NP duration Cart - prolongs ERP + AP duration * sodium agents contraction la. Quinidine, Procainamide ↳ moderate O z * potassium agents lb. Lidocaine, Phenytoin -Amiodarone Nat - Sota lol I c. Fletainide, Propatenone ↳ Strong depolarization 4 rekptolarization 4 < > -96mV 200ms rate control: Il + IV SLOW; AV node t SA node rhythm. control: 1+111 FAST; atria, ventricles or His-Purkinje DISTURBANCES IN IMPULSE FORMATION early after-depolarizations (EADS) -triggered by factors that prolong AP duration in ventricle → QT prolongation ↳ torsade de pontes (rack), tachycardia others - OF prolongation: caused by blockage of rapidly activating delayed Kt channels • intrinsic (congenital long) vs extrinsic (drugs) • slow Hr + Hypokalemia exacerbate → life-threatening delayed after depolarizations (DADS) - occurs when there is excess accumulation of intracellular cart, esp@FAST HR ↳ Ventricular tachycardia > Ventricular Lac/car l -triggers: digitalis toxicity, excess catecholamines, myocardial ischemia ⇒ r u run Ap multiple triggered APs normal AP DAD single triggered DISTURBANCES IN IMPULSE CONDUCTION -Mfc affects Av node → various degrees of❤block ↳ Slowing vs. complete complete PM block: latent Purkinje pacemaker cells dictate ventricular rate * Av node under tonic influence of parasymp. NS to conduction ↳ * atropine can relieve reentry: one impulse re-enters, excites area of B 71 time ↳ can be small or involve large portions * Wolff-parkinson white syndrome: reentry circuit of atrial tissue, Av node, ventricular tissue, accessory AV conduction ↳ few extra beats ro. sustained tachycardia • "daughter impulses" can be generated-VT or A-FIB Clinical Presentation: - entranced gytomaticity: acceleration of AP th m abl normal cardiac tissue - triggered' tactitity: abnormal AP trig by preceding AP (EAD/DAD) ↳ AF, VT - reentry: impulse fails to die out after normal activation ↳ AVN RT, W PW ex/ obstacle prevents impulse conduction → unidirectional block (impulse cannot propagate thru obstruction) ↳ impulse travels diff path → returns to obstacle from diff direction but tissue no longer blocking → so travels in retrograde direction Anti-Arrythmic Classes now, O: blocks HCN 4 → It (funny channel) * Ivrabradine at channel f: sodium channel blockade-7 AP duration tab lockers 2: sympatholytic → reduce B-adrenergic activity gypped, 3: prolongation of AP duration → block rapid component of delayed rectifier Kt current (ikr) cart 4: blockade of Cat current → slows conduction in regions where AP upstroke Cartdepent (SA + AV nodes charggerers I 2 absolute refractory period (ARP) . ↳ time where another stimulus will not lead to another AP O 3 relative refractory period (RRP) ↳ interval following ARP → 2nd stimulus inhibited but not impossible 4 4 effective refractory pen od (ERP) < ARP > L I n I l 1 ) ↳ time In which cell does not produce new AP 10, 1,2, 3) > { ERP > m, saggy, CLASS T decreased slope of phase - f slope of phase 0 depolarization y depolarization prolonged repolarization @nYde CLASS TA Q ERP CLASS 11 PR interval AP duration prolonged . if.. CLASS TB GLASS 111 ERP ERP AP duration ( [ " " " " CLASSIC CLASS N NORMAL ERP PR interval normal AP duration , I ERP - rate control: Il + IV SLOW; AV node + SA node rhythm. control: I +111 FAST; atria, ventricles or His-Purkinje CLASS IA AGENTS CLASS IB AGENTS -block activated/inactivated Nat channels * rapid kinetics -glow phase 0 depolarization m ventricular -shorten phase z repolarization, AP duration muscle fiber by binding to open/inactive Nat channels → PREVENT Nat influx * can