1. Arrhythmias and EKGs Amirhossein Azhari 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. Enhanced Normal Automaticity
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 Is characterized by:
SA node discharge rate of 100 to 180 x m.
Normal P waves and QRS complexes
Most often arises from increased sympathetic stimulation of the SA node.
Physiologic response to exercise.
Pathologic conditions including fever, 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 premature depolarization

12. PACs: Bigeminal Pattern

13. (Physiologic Delay in the His Purkinje System)
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
RBBB
LBBB
Normal
conduction

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
beats per min

17. Atrial Fibrillation EKG Characteristics: Absent P waves
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 ResponseII
Irregularity may be subtle

20. AF is the most common sustained arrhythmia
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 transthoracic cardioversion 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. (“Typical,”Counterclockwise)
Atrial Flutter
(“Typical,”Counterclockwise)
Reentrant
mechanism

31. Atrial flutter (SVT) 50 Joules, Ibutilide/Amiodarone
Re-entrant loop just above AVN in right atrium
Atrial rate 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 II “sawtooth” flutter waves
at 300 min-1
(best seen in
II, III and AVF) II
4:1
2:1 V1
Note variable
ventricular
response

33. Atrial Flutter V. rate 2:1 140-160 Conduction beats/min (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 = fast AV
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. AV Nodal Reentrant Tachycardia
Sustainment of
AV Nodal Reentrant Tachycardia
Rate
beats per min
P waves
generated
retrogradely
(AV node
 atria) and
fall within or
at tail of QRS

40. Sustained AV Nodal Reentrant TachycardiaP 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. Ventricular Preexcitation (Wolff-Parkinson-White Syndrome)
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 ECG Characteristics of WPW: 1. Short PR interval
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. Ventricular Preexcitation
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

51. Orthodromic AV Reentrant Tachycardia
Anterogade
conduction
via normal
pathway
Retrograde
conduction
via ac
pathway (AP) AP

52. AV Reentrant Tachycardia
Initiation of Orthodromic
AV Reentrant Tachycardia
PAC
Atria AP
AVN
Ventricles
PAC = premature atrial
complex (beat)

53. Sustainment of Orthodromic AV Reciprocating Tachycardia
Atria
Rate
beats per min AP
AVN
Ventricles
Retrograde P’s fall
in the ST segment
with fixed, short RP

54. Orthodromic AV Reentrant Tachycardia
NSR with
V Preex
Note
retrograde
P waves
in the
ST segment
SVT:
V Preex
gone

55. AVRT (30% of SVT) Wolff-Parkinson-White (WPW) pattern: “death pattern”
The initial delta wave
PR < 120ms
The QRS > 100ms

56. AVRT: orthodromic (95%) and antidromic tachycardia
Normal PR
(short RP SVT)

57. A fib. in a patient with WPW
1.) can degenerate into V fib (death)
2.) No beta-blocker, calcium channel blocker, digoxin.
3.) drug blocks AP: procainamide, amiodarone, ibutilide, Ic drug

58. AVRT Therapy
1.) No beta-blocker, calcium channel blocker, digoxin in WPW.
2.) drug blocks AP: procainmide, amiodarone, ibutilide, Ic
But do not reduce SCD risk.
3.) Asymptomatic WPW, EP study if in high risk profession
4.) AVRT in WPW patients needs ESP and likely RFA.

59. AT 10% (now more)
Normal PR
Can have AVN block
Long RP (most)

60. Adenosine for SVT Terminate all AVNRT or AVRT Terminate 30 AT only
ECG at the same time please!

61. AT Therapy
1.) More likely to be treated with medications traditionally.
(success rate: 20-50%).
2.) Now more and more ATs are treated with RFA,
(success rate: 70-95%).

62. PSVT Initial eval: Is the patient stable?
Determine quickly if sinus rhythm
If not sinus and unstable, cardioversion
Unstable sinus tachycardia---treat cause
Sxs of instability would include: chest pain, decreased consciousness, short of breath, shock, hypotension—unstable sxs require shock

63. SVT
If stable, determine whether regular rhythm (sinus or PSVT) vs irregular (afib/flutter, MAT)? p waves (MAT vs. AF)?
If regular, determine whether p waves are present, if can’t see---At first CSM or other vagal maneuvers then administer adenosine (6mg, can give 2 doses)

64. SVT
CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRT
Can also use CCB or beta blockers to terminate, if available
Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stress

65. Adenosine

66. Adenosine interacts with A1 receptors present on the extracellular surface of cardiac cells, activating K+ channels (IK.Ach, IK.Ade) in a fashion similar to that produced by acetylcholine.
Transient prolongation of the A-H interval results, often with transient first-, second-, or third-degree AV node block.

67. Pharmacokinetics
washout, enzymatically by degradation to inosine, by phosphorylation to adenosine monophosphate.
The vascular endothelium and the formed blood elements contain these elimination systems, which result in very rapid clearance of adenosine from the circulation. Elimination half-life is 1 to 6 seconds.

68. Dosage and Administration
To terminate tachycardia, a bolus of adenosine is rapidly injected intravenously at doses of 6 to 12 mg, followed by a flush.
Pediatric dosing should be 0.1 to 0.3 mg/kg.
When it is given into a central vein and in patients after heart transplantation or those receiving dipyridamole, the initial dose should be reduced to 3 mg.

69. Transient sinus slowing or AV node block results, lasting less than 5 seconds. Doses of more than 18 mg are unlikely to revert a tachycardia and should not be used.

70. Indications
Adenosine has become the drug of first choice to terminate an SVT acutely, such as AV node or AV reentry .
It is useful in pediatric patients and to judge the effectiveness of ablation of accessory pathways.
It results in only transient AV block during atrial flutter or fibrillation and is thus useful only for diagnosis, not therapy.
Adenosine terminates a group of VTs most often located in the right ventricular outflow tract.

71. Calcium Channel Antagonists

72. Verapamil
Verapamil, a synthetic papaverine derivative, is the prototype of a class of drugs that block the slow calcium channel and reduce ICa.L in cardiac muscle

73. In humans, verapamil prolongs conduction time through the AV node (the A-H interval) without affecting the P wave or QRS duration or H-V interval and lengthens AV nodal anterograde and retrograde refractory periods.
More commonly, the sinus rate does not change significantly because verapamil causes peripheral vasodilation, transient hypotension, and reflex sympathetic stimulation.

74. After intravenous administration, AV nodal conduction delay occurs within 1 to 2 minutes and A-H interval prolongation is still detectable after 6 hours.
The elimination half-life of verapamil is 3 to 7 hours, with up to 70% of the drug excreted by the kidneys.

75. For acute termination of SVT or rapid achievement of ventricular rate control during atrial fibrillation, the most commonly used intravenous dose of verapamil is 10 mg infused during 1 to 2 minutes while cardiac rhythm and blood pressure are monitored.
A second injection of an equal dose may be given 30 minutes later.

76. Adverse Effects
Verapamil must be used cautiously in patients with significant hemodynamic impairment or in those receiving beta blockers, as noted earlier. Hypotension, bradycardia, AV block, and asystole are more likely to occur when the drug is given to patients who are already receiving beta-blocking agents
Hemodynamic collapse has been noted in infants, and verapamil should be used cautiously in patients younger than 1 year.

77. Contraindications 1) advanced heart failure
2) second- or third-degree AV block without a pacemaker in place
3) atrial fibrillation and anterograde conduction over an accessory pathway
4) hypotensive states
5) significant sinus node dysfunction
6) Iv B-blocker

78. Diagnosis ?

79. Diagnosis ?

80. What is this arrhythmia?
Antidromic AVRT

83. Classification Scheme for Arrhythmias
Abnormalities in Conduction
Abnormalities in Automaticity
Bradyarrhythmias
Conduction Block
SA node – SA block
Atria - NA
AV node – AV block
Ventricles – NA
Decreased Automaticity
SA node – Sinus bradycardia
Atria – NA
AV node – NA
Ventricles - NA
Tachyarrhythmias
Reentry
SA node – SA nodal reentry
Atria – Intraatrial reentrant
tachycardia, a-flutter, a-fib
AV node – AVNRT
Ventricles – Ventricular tachycardia (common)
Accessory pathways – AVRT
Increased/Abnormal
Automaticity
SA node – Sinus tachycardia
Atria – Ectopic atrial
tachycardia
AV – Junctional tachycardia
Ventricles – Ventricular tachycardia (rare)
Additional important arrhythmias: Multifocal atrial tachycardia, torsade de pointes

84. The end