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
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