Program Information

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.