Arrhythmias and EKGs

1. Arrhythmias and EKGs Part 3

2. Outline Triggered Activity and Torsade de Pointes Sinus Node Block Differentiating VT from SVT with aberrancy

3. Mechanisms of Arrhythmogenesis

4. Triggered Activity A third general mechanism for generating tachyarrhythmias (in addition to enhanced/abnormal automaticity and reentry). When triggered activity occurs, a normal action potential is followed by oscillations of the membrane potential, known as afterdepolarizations. This triggers additional depolarization which have the potential to lead to extra atrial or ventricular contractions, and/or tachyarrhythmias.

5. Triggered Activity(early afterdepolarizations)

6. Triggered Activity(late afterdepolarizations)

7. Torsade de Pointes

8. Torsade de Pointes Torsade de pointes means �twisting of the points� It is most commonly seen in the setting of a prolonged QT interval (either congenital or acquired), and is caused by early afterdepolarizations. This rhythm is usually short lived, and resolves spontaneously within seconds, but can progress to ventricular fibrillation if prolonged.

9. Sinoatrial (SA) Nodal Block Less common than AV nodal block, and more difficult to detect Is classified similarly to AV block into 1st, 2nd, and 3rd degree, although only 2nd degree SA block is detectable on EKG.

10. 1st Degree SA Block Since the discharge of the sinus node cannot be measured externally, this will appear to be normal sinus rhythm on EKG. Can only be diagnosed via EP study.

11. Type 1 2nd Degree SA Block

12. Type 2 2nd Degree SA Block

13. 3rd Degree SA Block Indistinguishable from complete sinus arrest on EKG. Can only be diagnosed via EP study.

14. Distinguishing VT from SVT with aberrancy SVT can occasionally present as an unknown wide-complex tachycardia if if occurs in the presence of: Preexisting bundle branch block Rate related bundle branch block An accessory pathway Treatment with class IA or IC antiarrhythmics

15. Distinguishing VT from SVT with aberrancy VT accounts for ~80% of all cases of regular wide-complex tachycardias, and ~95% of all cases of regular wide-complex tachycardias which occur in patients with a history of MI. One of the most common lethal errors made in arrhythmia diagnosis is to mistake VT for SVT and treat with verapamil, diltiazem, and adenosine, all of which can precipitate ventricular fibrillation in patients in VT, even if initially stable.

16. Distinguishing VT from SVT with aberrancy Therefore, all wide-complex tachycardias should be assumed to be VT until proven otherwise.

17. EKG features moderately suggestive of VT: QRS duration > 160ms An extreme QRS axis (-90 to -180 degrees) Precordial QRS concordance Variations in the QRS and ST-T morphologies Slight irregularity at the onset of the arrhythmia

18. EKG features highly suggestive of VT: Fusion beats Capture beats (aka Dressler beats) Dissociated P waves

19. Physical findings highly suggestive of VT: Signs of AV dissociation, including: Canon A waves in the jugular venous pulsations Varying BP measurement from beat to beat Varying intensity of S1