1、The BasicsSA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamilAtrium, Bundle of His, and ventricle cells are fast conducting and activated by sodium, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as q
2、uinidine, lidocaine and propafenone.4 Mechanisms of Arrhythmia reentry (most common) automaticity parasystole triggered activityFast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryReentry RequiresElectrical ImpulseCardiac Conduction Tissue1. 2 distinct pathways that come together at be
3、ginning and end to form a loop. 2. A unidirectional block in one of those pathways. 3. Slow conduction in the unblocked pathway. Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryPremature Beat ImpulseCardiac Conduction Tissue1. An arrhythmia is triggered by a premature beat 2. The f
4、ast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathwayRepolarizing Tissue (long refractory period)Reentry Mechanism3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, whi
5、ch has now recovered and therefore travels retrogradely (backwards) up the fast pathway Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueReentry Mechanism4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the
6、wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuitFast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueReentry MechanismAtrial Reentry atrial tachycardia atrial fibrillation atrial flutterAtrio-Ventri
7、cular Reentry WPW SVTVentricular Re-entry ventricular tachycardiaAV Nodal ReentrySVTReentry CircuitsSA NodeReentry Requires1. 2 distinct pathways that come together at beginning and end to form a loop. 2. A unidirectional block in one of those pathways. 3. Slow conduction in the unblocked pathway. L
8、arge reentry circuits, like a-flutter, involve the atrium. Reentry in WPW involves atrium, AV node, ventricle and accessory pathways.Automaticity Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker. Factors that enhance automati
9、city include: SANS, PANS, CO2, O2, H+, stretch, hypokalemia and hypocalcaemia. Examples: Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung disease OR ventricular ectopy after MIParasystole is a benign type of automaticity problem that affects only a small region of a
10、trial or ventricular cells. 3% of PVCsTriggered activity is like a domino effect where the arrhythmia is due to the preceding beat. Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias. Early after-depolarizations arise d
11、uring the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)Event Monitors Holter monitoring: Document symptomatic and asymptomatic arrhythmias over 24-48 hours. Can also evaluate treatment effectiveness in a-fib, pacemaker
12、effectiveness and identify silent MIs. Trans-telephonic event recording: patient either wears monitor for several days or attaches it during symptomatic events and an ECG is recorded and transmitted for evaluation via telephone. Only 20% are positive, but still helpful.Exercise testing Symptoms only
13、 appear or worsen with exercise. Also used to evaluate medication effectiveness (esp. flecanide & propafenone) You can assess SA node function with exercise testing.Mobitz 1 (Wenkebach) is blockage at the AV node, so catecholamines from exercise actually help! Mobitz 2 is blockage at bundle of His,
14、so it worsens as catecholamines from exercise increase AV node conduction, thus prognosis is worse.*PVCs occur in 10% without and 60% of patients with CAD. *PVCs DO NOT predict severity of CAD (neither for nor against)! Signal Averaged ECG Used only in people post MI to evaluate risk for v-fib or v-
15、tach. Damage around the infarct is variable, so this measures late potentials (low-signal, delayed action potentials) as they pass through damaged areas. Positive predictive value is 25%-50% but negative predictive value is 90%-95%, thus if test is negative, patient is at low risk. Electrophysiologi
16、c Testing Catheters are placed in RA, AV node, Bundle of HIS, right ventricle, and coronary sinus (to monitor LA and LV). Used to evaluate cardiogenic syncope of unknown origin, symptomatic SVT, symptomatic WPW, and sustained v-tach. *Ablative therapy is beneficial in AV node reentry, WPW, atrial ta
17、chycardia, a-flutter, and some v-tach. Complication is 1%Sick Sinus Syndrome Conduction problem with no junctional escape during sinus pause Diagnose with ECG or Holter. If inconclusive, need electrophysiologic testing. If asymptomatic, leave alone. If symptomatic, needs pacemaker.First Degree AV Bl
18、ock Delay at the AV node results in prolonged PR interval PR interval0.2 sec. Leave it aloneSecond Degree AV Block Type 1 (Wenckebach) Increasing delay at AV node until a p wave is not conducted. Often comes post inferior MI with AV node ischemia Gradual prolongation of the PR interval before a skip
19、ped QRS. QRS are normal! No pacing as long as no bradycardia. Second Degree AV Block Type 2 Diseased bundle of HIS with BBB. Sudden loss of a QRS wave because p wave was not transmitted beyond AV node. QRS are abnormal! May be precursor to complete heart block and needs pacing.Third Degree AV Block
20、Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles. Must treat with pacemaker.LBBBLeft Bundle Branch Block Left ventricle gets a delayed impulse QRS is widened (at least 3 boxes) V5 and V6 have RR (rabbit ears) Be careful not to miss any hiding q
21、 waves! Pacemaker if syncope occursRight Bundle Branch BlockRight Bundle Branch Block Right ventricle gets a delayed impulse QRS is widened (at least 3 boxes) V1 and V2 have rSR Pacemaker if syncope occurs.Bifascicular Block RBBB plus LABB OR RBBB plus LPBB QRS is widened (at least 3 boxes) V5 and V
22、6 have RR (rabbit ears) V1 and V2 have rSR Pacemaker if syncope occursTachyarrhythmias Supraventricular tachycardia Atrial fibrillation Atrial flutter Ventricular tachycardia MonomorphicPolymorphic (Torsades de pointe) Ventricular fibrillationSupraventricular TachycardiaSVT Reentrant arrhythmia at A
23、V node that is spontaneous in onset May have neck fullness, hypotension and/or polyuria due to ANP Narrow QRS with tachycardia First line is vagal maneuvers Second line is adenosine or verapamil For chronic SVT, class 1A or 1C or amiodarone or sotalol work well Ablation will cure it too, but we usua
24、lly do this only in young patientsMultifocal Atrial TachycardiaMAT Automatic atrial rhythm from various different foci Seen in hypoxia, COPD, atrial stretch and local metabolic imbalance. Three or more types of p waves and a rate 100 Digoxin worsens it, so treat with oxygen and slow channel blocker
25、like verapamil or diltiazem. Wolf Parkinson WhiteWPW Ventricles receive partial signal normally and partially through accessory pathway Symptomatic tachycardia, short PR interval (0.12) Electrophysiologic testing helps to identify the reentry pathway and location of the accessory pathwayWPW Because
26、WPW has both normal conduction through the AV node and accessory pathway conduction that bypasses the AV node, a-fib can happen via the accessory pathway Inhibition of the AV node will end up in worsening the a-fib because none of the signals are slowed down by the AV node before hitting the ventric
27、le. * Do not use any meds that will slow AV node conduction, ie digoxin, beta-blockers, adenosine or calcium channel blockers. * The best choice is procainamide as it slows the accessory pathway. *If patient becomes hypotensive, cardiovert immediately!Atrial FlutterAtrial Flutter Atrial activity of
28、240-320 with sawtooth pattern. Usually a 2:1 conduction pattern; if it is 3:1 or higher, there is AV node damage Treatment is to slow AV node conduction with amiodarone, propafenone or sotalol DC cardiovert if 48 hours or unstable You can also ablate the reentry pathway within the atrium between the
29、 tricuspid and the IVC. Atrial FibrillationA-Fib Can be due to HTN, cardiomyopathy, valvular heart desease, sick sinus, WPW, thyrotoxicosis or ETOH Therapy is either rate control via slowing AV node conduction with stroke prophylaxis or rhythm controlRate control Beta-blockersContinuation after CABG
30、 may prevent a-fibGood for hyperthyroid or post-MI patients with a-fibCarvedilol decreases mortality in patients with CHFEsmolol is good for acute management Digoxin actually increases vagal tone, thus indirectly slowing AV node conduction. But it is used essentially only in patients with LV dysfunc
31、tion because its inotropic. Rate control Calcium Channel BlockersNondihydropyridines (verapamil or dilitiazem) block AV node conduction but also have negative inotropy, so dont use in CHF. Dihydropyridines (nifedipine, amlodipine, felodipine) have no effect on AV node conduction Adenosine is too sho
32、rt acting to be of any use in a-fib Last choice is AV node ablation and permanent pacingRhythm control Rhythm control does not decrease thromboembolic risk and may be proarrhythmicClass 1A (quinidine, procainamide, disopyramide) slows conduction through HIS can cause torsades de pointes during conve
33、rsion. They also enhance AV node conduction, so they should be used only after rate is controlledClass 1B (lidocaine, meilitine, tocainide) are useless for a-fibClass 1C (propafenone, and flecainide) slow conduction through HIS are good first choice. Amiodarone is good if patient is post-MI or has s
34、ystolic dysfunction.Cardioversion for A-Fib Cardiovert if symptomatic Patients with a-fib for more than 2 days should be receive 3 weeks of anticoagulation before electrical cardioversion. Give coumadin for 4 weeks after cardioversionAnticoagulation Rules for A-Fib Everybody who has rheumatic heart
35、disease should be anticoagulated If 75 yo give coumadin but keep INR 2-2.5 due to increased risk of bleedVentricular Tachycardia Impulse is initiated from the ventricle itself Wide QRS, Rate is 140-250 If unstable DC cardiovert If not, IV Amiodarone and/or DCCV Consider procainamide Nonsustained ven
36、tricular tachycardia needs no treatmentVentricular TachycardiaTorsades de Pointes “Twisting of the points” is usually caused by medication (quinidine, disopyramide, sotalol, TCA), hypokalemia or bradycardia especially after MI Has prolonged QT interval Acute: Remove offending medication. Shorten the
37、 QT interval with magnesium, lidocaine, isoproterenol, or temporary overdrive pacing Chronic: may need pacemaker/ICD, amiodarone, beta-blockers Ventricular Fibrillation Most common in acute MI, also drug overdose, anesthesia, hypothermia & electric shock can precipitate Absence of ventricular comple
38、xes Usually terminal event Use Amiodarone if refractory to DCCV.Classification of Anti-arrhythmicsC l assA ct i onExam pl esSi de Eff ect s1AFast sodi um chan nel bl ocker var i esdepol ari zat i on and act i on pot ent i aldurat i onQ ui ni di ne,procai nam i de,di s op yram i deC l ass: nausea, vo
39、m i t i ngQ ui ni di ne: hem ol yt i canem i a, t hrom bo cyt openi a,t i nni t usPr ocainam i de: l upus1BLi do cai ne,M ex i l et i neLi do cai ne: di zzi ness,conf usi on, sei zures, com aM ex i l et i ne: t rem or, at axi a,rash1CFl ecai ni de,Pr op afen oneFl ecai ni de: pro- arrhyt hm i a,naus
40、ea, di zzyness2beta- b l ockers Where did you say you worked?Locati on of A cti vi t yA nt i - arrh yt hm i cA V N odeA den osine, Cal ci um channel bl ockers, B-bl ockers, D i goxi nA V N ode, A ccessory Pat hway, Bundl e ofH I S, ventr i cl ePropafenone, A m i oda rone, Sotol olA t ri al , Vent ri
41、 cul ar, A ccessory Pat hwa y,Bundl e of H I SQ ui ni di ne, Procai nam i de, Li docai ne,D i sopyram i de, F l ecani de, I buti l i de,Bretyl i um , D ofeti l i deWhen in doubtAmiodaroneSVTVTAtrial Fib or flutterAmiodaroneIVAmiodarone.Modes of action. Mainly class III action on the outgoing K+ chan
42、nels. Class Ib action on the Na+ channels. Non competitive alpha antagonism (class III)Magnesium indications. 1. Torsades de point from any reason. 2. Arrhythmias in a patient with known hypomagnesaemia. 3. Consider its use in acute ischaemia to prevent early ventricular arrhythmias. 4. Digoxin indu
43、ced arrhythmias.Who gets a pacemaker?Syncope, presyncope or exercise intolerance that can be attributed to bradycardia Symptomatic 2nd or 3rd degree AV block Congenital 3rd degree AV block with wide QRS Advanced AV block after cardiac surgery Recurrent type 2 2nd degree AV block after MI 3rd degree AV block with wide QRS or BBB.
