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Understanding Arrhythmias: Mechanisms, Types, and Treatments

This presentation by Dr. Karima Sajadi and Dr. Sarah Stahmer from Cooper University Hospital covers the fundamental mechanisms of arrhythmias, including enhanced automaticity, triggered activity, and reentry. It reviews types of tachyarrhythmias such as sinus tachycardia, atrial fibrillation, and ventricular tachycardia, alongside their treatments. Additionally, the presentation explores bradyarrhythmias and emphasizes the importance of ECG recognition for accurate diagnosis. Learn how various factors can contribute to arrhythmias and their therapeutic approaches.

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Understanding Arrhythmias: Mechanisms, Types, and Treatments

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  1. Program Information

  2. Arrhythmias - Part 1 Karima Sajadi, MD Sarah A. Stahmer MD Cooper University Hospital

  3. Objectives Understand the basic mechanisms that give rise to arrhythmias Review the basic types of tachy-arrhythmias and their treatment Review the presentation of wide complex tachycardias and their treatment Review the basic types of brady-arrhythmias and their treatment Slide 3

  4. Mechanisms Enhanced automaticity – spontaneous depolarization of the myocytes that are normally not arrhythmogenic Triggered activity – depolarizations that are triggered by the preceding beat and occur during or after repolarization Reentry – existence of slow and fast conducting pathways that allow antero- and retrograde conduction Slide 4

  5. Tachydysrhythmias Regular Irregular Narrowcomplex Wide complex Narrow complex Wide complex Sinus Tachycardia Atrial Tachycardia Atrial Flutter AVNRT/AVRT Ventricular tachycardia Pacer-mediated tachycardia SVT with pre-existing BBB SVT with rate-dependent BBB MAT Atrial Fibrillation Atrial Flutter with variable block Torsade des Pointes Ventricular fibrillation Tachydysrhythmias Slide 5

  6. Regular Narrow-Complex Tachyarrhythmias Sinus tachycardia Atrial tachycardia 3. Atrial flutter 4. Paroxysmal supraventricular tachycardia A. AVNRT (AV nodal reentry tachycardia) B. AVRT or ORT (Orthodromic reciprocating tachycardia) Slide 6

  7. Sinus Tachycardia Physiologic response rather than a pathologic rhythm Maximal rate = 220 bpm – age (years) Slide 7

  8. Sinus Tachycardia Causes: Fever, anxiety, hypovolemia, thyrotoxicosis Peripheral vasodilatation Exogenous catecholamines (cocaine, amphetamine, dopamine) Anticholinergics (TCAs, Benadryl) LV dysfunction (CHF, myocardial ischemia) RV dysfunction (PE, RV infarct) Slide 8

  9. Sinus Tachycardia ECG Recognition: Discrete P waves before every QRS, constant PR interval Rate should vary in response to respirations, vagal stimulation, pain, stress An isolated sinus tachycardia is a potentially life threatening rhythm until the underlying cause is identified and treated! Slide 9

  10. Sinus Tachycardia Slide 10

  11. Atrial Tachycardia A single ectopic atrial pacemaker Causes: Enhanced automaticity Reentry – patients with a history of cardiac surgery Triggered activity – think digoxin toxicity ECG recognition: Atrial rate 150-250 bpm – slower than atrial flutter, with which it can be confused Ectopic P wave morphology distinct from baseline sinus node P wave Slide 11

  12. Atrial Tachycardia Slide 12

  13. Atrial Flutter Mechanism: regular microreentry circuit that rotates counterclockwise around right atrium Inherently unstable and converts to NSR or atrial fibrillation Causes: ischemic heart disease, congestive CM, PE, myocarditis, hyperthyroidism, etc Slide 13

  14. Atrial Flutter ECG recognition: atrial rate 250-230, ventricular rate 75-150 bpm if variable ventricular response then it is irregular sawtooth wave pattern in inferior leads. Treatment: depends on time of onset (> or < than 48 hrs) preserved or impaired heart function presence of WPW syndrome Slide 14

  15. Atrial Flutter: 1:1 Slide 15

  16. Atrial Flutter 2:1 Slide 16

  17. AVNRT Mechanism: reentry at AV node or perinodal tissue. triggered by premature atrial conduction (PAC) PAC conduction is blocked down the fast pathway (with a long refractory period) conducted anterograde through the slow pathway (with a short refractory period) reenters via recovered fast pathway Slide 17

  18. AVNRT ECG recognition: Narrow complex regular tachycardia at 140-280 bpm P wave not seen due to simultaneous atria/ventricular activation Causes: Atrial stretch (ACS, CHF) irritability (exogenous catecholamines) inflammation (pericarditis) Treatment: Vagal maneuvers, adenosine beta-blockers, diltiazem, digoxin Slide 18

  19. AVNRT Slide 19

  20. Atypical AVNRT Slide 20

  21. AVRT or ORT Less common than AVNRT, difficult to distinguish from AVNRT on EKG Mechanism: macroreentry through normal conducting system and an accessory AV pathway impulse conducts anterograde down the AVN reenters via an accessory pathway, resulting in narrow-complex tachycardia P wave visible due to delayed activation of the atria ECG recognition: P wave follows QRS Slide 21

  22. ORT Causes: same as AVNRT Treatment: AV-nodal blocking agents are usually effective due to antegrade activation of the ventricles via the AVN Ablation treatment has a 95% success rate Slide 22

  23. AVRT or ORT Slide 23

  24. ORT Slide 24

  25. ORT after Adenosine Slide 25

  26. Irregular Narrow-Complex Tachyarrhythmias 1.Multifocal Atrial Tachycardia (MAT) 2.Atrial fibrillation 3.Atrial flutter with variable block Slide 26

  27. MAT Mechanism: absent single dominant pacemaker multiple atrial foci fire independently ECG recognition: at least 3 different P wave morphologies variable P-R, P-P, R-R intervals isoelectric baseline present to distinguish from atrial fibrillation Slide 27

  28. MAT Causes: COPD, hypoxia Pulmonary Hypertension CHF Theophylline toxicity Electrolyte abnormalities (low K/Mg) Treatment: treat underlying cause Magnesium, Verapamil may be beneficial Slide 28

  29. MAT Slide 29

  30. Atrial Fibrillation Slide 30

  31. Atrial Fibrillation Mechanism: due to multiple reentrant wavelets between left and right atria ECG recognition: irregularly irregular rhythm disorganized atrial activity no clear P waves between QRS complexes Slide 31

  32. Atrial Fibrillation Causes: Ischemic heart disease, HTN pericarditis “holiday heart” thyrotoxicosis, etc Treatment: Rate control Cardioversion (chemical or electrical) Anticoagulation Slide 32

  33. Atrial Flutter with Variable Block Mechanism: Atrial rate up to 300 bpm not all depolarizations conduct through the AV node especially in patients on medications that block AV node ECG recognition: irregular narrow QRS complexes the ratio of atrial flutter waves to QRS complexes varies (2:1, 3:1, etc) Slide 33

  34. Atrial Flutter with Variable Block Slide 34

  35. Conclusion • This concludes part 1 of the arrhythmia presentation. • Continue to Arrhythmias Part 2 for the next installment of this lecture. • Cases studies and references for this section are found at the end of Arrhythmias Part 3.

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