Arrhythmias and EKGs

1. Arrhythmias and EKGs AmirhosseinAzhari M.D Fellowship of electrophysiology Chamran heart center

2. Mechanisms of Arrhythmogenesis

3. Tachycardia Abnormally rapid heart rhythm May result from: • Abnormal impulse formation • Automaticity • Triggered activity • Abnormal impulse conduction • Reentry

4. Tachycardia Enhanced Normal Automaticity Basal condition Increased slope of phase 4 depolarization

5. Symptoms the following:Include • Your pulse rate becomes 150 – 200 beats per minute. • Palpitations (Feeling your heart beat) • Dizziness, or Feeling Light Headed • You may become breathless • If you have angina, then an angina pain may be • triggered by an episode of SVT • You may have no symptoms, • You may only be aware that your • heart is beating fast.

7. Sinus Tachycardia

8. Sinus Tachycardia • Ischaracterizedby: • SA nodedischargerate of 100 to 180 x m. • Normal P waves and QRS complexes • Mostoftenarisesfrom increased sympatheticstimulation of the SA node. • Physiologic response toexercise. • Pathologicconditionsincludingfever, hyperthyroidism and hypoxemia.

9. Physiologic Sinus Tachycardia: Treatment • Treatment of sinus tachycardia is directed at the underlying condition causing the tachycardia response. • Uncommonly, beta blockers are used to minimize the tachycardia response if it is determined to be potentially harmful, as may occur in a patient with ischemic heart disease and rate-related anginal symptoms.

10. Premature Atrial Complex (PAC) V5 Non-Compensatory Pause P P P P’ P Timing of Expected P

11. Premature Atrial Complex (PAC): Alternative Terminology • Premature atrial contraction • Atrial extrasystole • Atrial premature beat • Atrial ectopic beat • Atrial prematuredepolarization

12. PACs: Bigeminal Pattern P P’ P P’ P P’

13. PAC with “Aberrant Conduction” (Physiologic Delay in the His Purkinje System) V1 P P P’ P RRbbBBB

14. PACs with Aberrant Conduction (Physiologic RBBB and LBBB) V1 Normal conduction LBBB RBBB

15. Treatment • PACs uncommonly require intervention. For extremely symptomatic patients who do not respond to explanation and reassurance, an attempt can be made to suppress the PACs with pharmacologic agents. • Beta blockers are typical first-line therapy. • The repetitive focus can even be targeted for catheter ablation.

16. Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min

17. Atrial Fibrillation www.uptodate.com EKG Characteristics: Absent P waves Presence of fine “fibrillatory” waves which vary in amplitude and morphology Irregularly irregular ventricular response

18. Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response II

19. Atrial Fibrillation with Rapid Ventricular Response II Irregularity may be subtle

20. AF is the most common sustained arrhythmia. It is marked by disorganized, rapid, and irregular atrial activation. The ventricular response to the rapid atrial activation is also irregular. • In the untreated patient, the ventricular rate also tends to be rapid and is entirely dependent on the conduction properties of the AV junction. Although typically the rate will vary between 120 and 160 beats/min.

21. The mechanism • multiple wavelets of (micro)reentry. • The drivers appears to originate predominantly from the atrialized musculature that enters the pulmonary veins . • Sustained forms of microreentry as drivers have also been documented around the orifice of pulmonary veins; nonpulmonary vein drivers have also been demonstrated.

22. incidence • The incidence of AF increases with age such that >5% of the adult population over 70 will experience the arrhythmia. • Occasionally AF appears to have a well-defined etiology, such as acute hyperthyroidism, an acute vagotonic episode, or acute alcohol intoxication.

23. Clinical symptoms clinical importance related to: • (1) the loss of atrial contractility, • (2) the inappropriate fast ventricular response • (3) the loss of atrial appendage contractility and emptying leading to the risk of clot formation and subsequent thromboembolic events

24. Acute Management of Atrial Fibrillation • In emergency department because of AF generally have a rapid ventricular rate, and control of the ventricular rate is most rapidly achieved with intravenous diltiazem or esmolol. • If the patient is hemodynamically unstable, immediate transthoraciccardioversion may be appropriate.

25. If the AF has been present for more than 48 hours or if the duration is unclear and the patient is not already anticoagulated, cardioversion ideally should be preceded by transesophageal echocardiography to rule out a left atrial thrombus. • However, a delay in cardioversion may not be appropriate in the setting of severe cardiovascular decompensation

26. If the patient is hemodynamically stable, the decision to restore sinus rhythm by cardioversion is based on several factors, including symptoms, prior AF episodes, age, left atrial size, and current antiarrhythmic drug therapy. .

27. For example, in an elderly patient whose symptoms resolve once the ventricular rate is controlled and who already has had early recurrences of AF despite rhythm-control drug therapy, further attempts at cardioversion usually are not appropriate. • On the other hand, cardioversion usually is appropriate for patients with symptomatic AF who present with a first episode of AF or who have had long intervals of sinus rhythm between prior episodes.

28. anticoagulation • Regardless of whether cardioversion is performed pharmacologically or electrically, therapeutic anticoagulation is necessary for 3 weeks or more before cardioversion to prevent thromboembolic complications if the AF has been ongoing for more than 48 hours. If the time of onset of AF is unclear, for the sake of safety, the AF duration should be assumed to be more than 48 hours

30. Atrial Flutter (“Typical,”Counterclockwise) Reentrant mechanism

31. Atrial flutter (SVT) • Re-entrant loop just above AVN in right atrium • Atrial rate 240-360 without medications • 2:1 block, vent rate 150 most common • Regular, fixed; or regularly irregular • Narrow if no aberrancy • Flutter waves, sawtooth pattern--Always visible in lead II • Adenosine can help to diagnose, not treat • Conversion vs. Ventricular slowing • 50 Joules, Ibutilide/Amiodarone

32. Atrial Flutter Classic inverted “sawtooth” flutter waves at 300 min-1 (best seen in II, III and AVF) II 2:1 4:1 V1 Note variable ventricular response

33. Atrial Flutter V. rate 140-160 beats/min 2:1 Conduction (common) 2:1 & 3:2 Conduction 1:1 Conduction (rare but dangerous)

34. Multifocal Atrial Tachycardia EKG Characteristics: Discrete P waves with at least 3 different morphologies. Atrial rate > 100 bpm. The PP, PR, and RR intervals all vary.

36. Paroxysmal Supraventricular Tachycardia • Refers to supraventricular tachycardia other than afib, aflutter and MAT • Occurs in 35 per 100,000 person-years • Usually due to reentry—AVNRT or AVRT

37. AV Nodal Reentrant Tachycardia Circuit F = fastAV nodal pathway S = slow AV nodal pathway (His Bundle) During sinus rhythm, impulses conduct preferentially via the fast pathway

38. Initiation of AV Nodal Reentrant Tachycardia PAC PAC PAC = premature atrial complex (beat)

39. Sustainment of AV Nodal Reentrant Tachycardia Rate 150-250 beats per min P waves generated retrogradely (AV node  atria) and fall within or at tail of QRS

40. Sustained AV Nodal Reentrant Tachycardia V1 P P P P Note fixed, short RP interval mimicking r’ deflection of QRS

41. AVNRT (60% of SVT) Typical AVNRT: (90% AVNRT) 1. A and V Simultaneously 2.Pseudo “r” in V1/AVR

42. AVNRT Therapy Acute therapy: Please record ECG at the same time. 1.) Vagal maneuver 2.) Adenosine 3.) Verapamil Chronic therapy: 1.) RFA (cure >95%, complication rate of <1%, Mortality < 1/10,000, heart block 0.5%) 2.) Medications beta-blocker, calcium channel blocker Flecainide, propafenone

43. Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Sinus beat Hybrid QRS shape “Delta” Wave PR < .12 s AP QRS  .12 s Fusion activation of the ventricles

44. Preexcitation Preexcitation is a condition characterized by an accessory pathway of conduction, which allows the heart to depolarize in an atypical sequence. The most common form of preexcitation is called Wolfe-Parkinson-White (WPW) syndrome, in which a direct atrioventricular connection allows the ventricles to begin depolarization while the standard action potential is still traveling through the AV node. ECG Characteristics of WPW: 1. Short PR interval 2. QRS prolongation 3. Delta wave

45. Varying Degrees of Ventricular Preexcitation

46. Intermittent Accessory Pathway Conduction V Preex V Preex Normal Conduction Note “all-or-none” nature of AP conduction

47. AV Reentrant Tachycardia (AVRT) In patients with WPW, a reentrant rhythm can be generated where the AV node serves as one arm of the reentrant circuit, and the accessory pathway as the other.

48. Types of AVRT • Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of depolarization travels down the AV node and retrograde up the accessory pathway. • Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of depolarization travels down the accessory pathway and retrograde up the AV node.

49. Mechanism of orthodromic AVRT

50. Mechanism of antidromic AVRT