Arrhythmias 101 Fundamentals and what you should know for the big, bad BOARDS!

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Transcript of Arrhythmias 101 Fundamentals and what you should know for the big, bad BOARDS!

  • Slide 1
  • Slide 2
  • Arrhythmias 101 Fundamentals and what you should know for the big, bad BOARDS!
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  • The Basics SA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamil Atrium, 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 quinidine, lidocaine and propafenone.
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  • 4 Mechanisms of Arrhythmia reentry (most common) automaticity parasystole triggered activity
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  • Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Reentry Requires Electrical Impulse Cardiac Conduction Tissue 1. 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.
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  • Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Premature Beat Impulse 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
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  • 3. The wave of excitation 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
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  • 4. On arriving 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 Tissue Reentry Mechanism
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  • Atrial Reentry atrial tachycardia atrial fibrillation atrial flutter Atrio-Ventricular Reentry WPW SVT Ventricular Re-entry ventricular tachycardia AV Nodal Reentry SVT Reentry Circuits SA Node
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  • Reentry Requires 1. 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. Large reentry circuits, like a-flutter, involve the atrium. Reentry in WPW involves atrium, AV node, ventricle and accessory pathways.
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  • 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 automaticity include: SANS, PANS, CO 2, O 2, H +, stretch, hypokalemia and hypocalcaemia. Examples: Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung disease OR ventricular ectopy after MI
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  • Parasystole is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells. 3% of PVCs
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  • 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 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)
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  • DiagnosisDiagnosis What tools to use and when to use it
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  • Event Monitors Holter 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 events and an ECG is recorded and transmitted for evaluation via telephone. Only 20% are positive, but still helpful.
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  • 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 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, 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)!
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  • 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. Positive predictive value is 25%-50% but negative predictive value is 90%-95%, thus if test is negative, patient is at low risk.
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  • 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 syncope 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%
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  • BradyarrhythmiasBradyarrhythmias The slow pokes (HR
  • First Degree AV Block Delay at the AV node results in prolonged PR interval PR interval>0.2 sec. Leave it alone
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  • Second 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 skipped QRS. QRS are normal! No pacing as long as no bradycardia.
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  • 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.
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  • Third Degree AV Block Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles. Must treat with pacemaker.
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  • LBBB
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  • Left Bundle Branch Block Left ventricle gets a delayed impulse QRS is widened (at least 3 boxes) V 5 and V 6 have RR (rabbit ears) Be careful not to miss any hiding q waves! Pacemaker if syncope occurs
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  • Right Bundle Branch Block
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  • Right ventricle gets a delayed impulse QRS is widened (at least 3 boxes) V 1 and V 2 have rSR Pacemaker if syncope occurs.
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  • Bifascicular Block RBBB plus LABB OR RBBB plus LPBB QRS is widened (at least 3 boxes) V 5 and V 6 have RR (rabbit ears) V 1 and V 2 have rSR Pacemaker if syncope occurs
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  • TachyarrhythmiasTachyarrhythmias The speed demons(HR >100)
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  • Tachyarrhythmias Supraventricular tachycardia Atrial fibrillation Atrial flutter Ventricular tachycardia Monomorphic Polymorphic (Torsades de pointe) Ventricular fibrillation
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  • Supraventricular Tachycardia
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  • SVT Reentrant arrhythmia at AV 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 usually do this only in young patients
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  • Multifocal Atrial Tachycardia
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  • 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.
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  • Wolf Parkinson White
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  • WPW 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 pathway
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  • WPW Because 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 ventricle. * 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!
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  • Atrial Flutter
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  • Atrial activity of 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 w