Arrhythmias 101.ppt

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1、Arrhythmias 101,Fundamentals and what you should know for the big, bad BOARDS!,The Basics,SA 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 sodi

2、um, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as quinidine, lidocaine and propafenone.,4 Mechanisms of Arrhythmia,reentry (most common)automaticityparasystole triggered activity,Fast Conduction Path Slow Recovery,Slow Conduction Path Fast Recovery,Reentry Requires,Elect

3、rical Impulse,Cardiac Conduction Tissue,2 distinct pathways that come together at beginning and end to form a loop. A unidirectional block in one of those pathways. Slow conduction in the unblocked pathway.,Fast Conduction Path Slow Recovery,Slow Conduction Path Fast Recovery,Premature Beat Impulse,

4、Cardiac Conduction Tissue,1. An arrhythmia is triggered by a premature beat 2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway,Repolarizing Tissue (long refractory period),Reentry Mechanism,3. The wave of excitatio

5、n from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway,Fast Conduction Path Slow Recovery,Slow Conduction Path Fast Recovery,Cardiac Conduction Tissue,Reentry Mechanism,4. On arriv

6、ing at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuit,Fast Conduction Path Slow Recovery,Slow Conduction Path Fast Recovery,Cardiac Conduction Tissu

7、e,Reentry Mechanism,Atrial Reentryatrial tachycardiaatrial fibrillationatrial flutter,Atrio-Ventricular ReentryWPWSVT,Ventricular Re-entryventricular tachycardia,AV Nodal Reentry SVT,Reentry Circuits,SA Node,Reentry Requires,2 distinct pathways that come together at beginning and end to form a loop.

8、 A unidirectional block in one of those pathways. Slow conduction in the unblocked pathway. Large 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 faste

9、r than SA node cells, and take control as the cardiac pacemaker. Factors that enhance automaticity 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 afte

10、r MI,Parasystole,is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells. 3% of PVCs,Triggered 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

11、 beat and may be the cause of digitalis-induced arrhythmias. Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced),Diagnosis,What tools to use and when to use it,Event Monitors,Holte

12、r monitoring: Document symptomatic and asymptomatic arrhythmias over 24-48 hours. Can also evaluate treatment effectiveness in a-fib, pacemaker effectiveness and identify silent MIs. Trans-telephonic event recording: patient either wears monitor for several days or attaches it during symptomatic eve

13、nts and an ECG is recorded and transmitted for evaluation via telephone. Only 20% are positive, but still helpful.,Exercise testing,Symptoms only appear or worsen with exercise. Also used to evaluate medication effectiveness (esp. flecanide & propafenone) You can assess SA node function with exercis

14、e testing. Mobitz 1 (Wenkebach) is blockage at the AV node, so catecholamines from exercise actually help! Mobitz 2 is blockage at bundle of His, 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 CA

15、D. *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-tach. Damage around the infarct is variable, so this measures late potentials (low-signal, delayed action potentials) as they pass through damaged areas.

16、 Positive predictive value is 25%-50% but negative predictive value is 90%-95%, thus if test is negative, patient is at low risk.,Electrophysiologic 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 sy

17、ncope of unknown origin, symptomatic SVT, symptomatic WPW, and sustained v-tach. *Ablative therapy is beneficial in AV node reentry, WPW, atrial tachycardia, a-flutter, and some v-tach. Complication is 1%,Bradyarrhythmias,The slow pokes (HR60),Sick Sinus Syndrome,Conduction problem with no junctiona

18、l 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 Block,Delay at the AV node results in prolonged PR intervalPR interval0.2 sec.Leave it alone,Second Degree AV Bloc

19、k Type 1 (Wenckebach),Increasing delay at AV node until a p wave is not conducted. Often comes post inferior MI with AV node ischemiaGradual prolongation of the PR interval before a skipped QRS. QRS are normal! No pacing as long as no bradycardia.,Second Degree AV Block Type 2,Diseased bundle of HIS

20、 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,Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles. Must tre

21、at with pacemaker.,LBBB,Left 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 waves! Pacemaker if syncope occurs,Right Bundle Branch Block,Right Bundle Branch Block,Right ventricle gets a d

22、elayed 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 V6 have RR (rabbit ears) V1 and V2 have rSR Pacemaker if syncope occurs,Tachyarrhythmias,The speed demons(HR 1

23、00),Tachyarrhythmias,Supraventricular tachycardia Atrial fibrillation Atrial flutter Ventricular tachycardia Monomorphic Polymorphic (Torsades de pointe) Ventricular fibrillation,Supraventricular Tachycardia,SVT,Reentrant arrhythmia at AV node that is spontaneous in onset May have neck fullness, hyp

24、otension 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 usually do this only in young patients,Multifocal Atrial Tachycardi

25、a,MAT,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 like verapamil or diltiazem.,Wolf Parkinson White,WPW,Ventric

26、les 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 pathway,WPW,Because WPW has both normal conduction through the AV node and acce

27、ssory 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 ventricle. * Do not use any meds that will slow AV node conduction

28、, 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 Flutter,Atrial Flutter,Atrial activity of 240-320 with sawtooth pattern. Usually a 2:1 conduction p

29、attern; 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 tricuspid and the IVC.,Atrial Fibrillation,A-Fib,Can be

30、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 control,Rate control,Beta-blockers Continuation after CABG may prevent a-fib Good for hyperthyroid or post-MI pa

31、tients with a-fib Carvedilol decreases mortality in patients with CHF Esmolol 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 dysfunction because its inotropic.,Rate control,Calcium Ch

32、annel Blockers Nondihydropyridines (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 short acting to be of any use in a-fib Last choice is

33、 AV node ablation and permanent pacing,Rhythm control,Rhythm control does not decrease thromboembolic risk and may be proarrhythmic Class 1A (quinidine, procainamide, disopyramide) slows conduction through HIS can cause torsades de pointes during conversion. They also enhance AV node conduction, so

34、they should be used only after rate is controlled Class 1B (lidocaine, meilitine, tocainide) are useless for a-fib Class 1C (propafenone, and flecainide) slow conduction through HIS are good first choice. Amiodarone is good if patient is post-MI or has systolic dysfunction.,Cardioversion for A-Fib,C

35、ardiovert 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 cardioversion,Anticoagulation Rules for A-Fib,Everybody who has rheumatic heart disease should be anticoagulated If 75 yo gi

36、ve coumadin but keep INR 2-2.5 due to increased risk of bleed,Ventricular 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 ventricular tachycardia needs no treatment,Ven

37、tricular Tachycardia,Torsades 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 QT interval with magnesium, lidocaine, i

38、soproterenol, 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 complexesUsually terminal event Use Amiodarone

39、if refractory to DCCV.,Treatment,Here comes the fun part!,Classification of Anti-arrhythmics,Where did you say you worked?,When in doubtAmiodarone,Amiodarone. Modes of action.,Mainly class III action on the outgoing K+ channels. Class Ib action on the Na+ channels. Non competitive alpha antagonism (

40、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 induced arrhythmias.,Who gets a pacemaker?, Syncope, presyncope or exercise intolerance that can be attributed to bradycardiaSymptomatic 2nd or 3rd degree AV blockCongenital 3rd degree AV block with wide QRSAdvanced AV block after cardiac surgery Recurrent type 2 2nd degree AV block after MI 3rd degree AV block with wide QRS or BBB.,QUESTIONS,