This document provides an overview of arrhythmias, including their mechanisms, types, diagnosis, and treatment. It discusses the basics of the cardiac action potential and ion channels involved. Common arrhythmias described include sinus tachycardia, premature beats, supraventricular tachycardias like AVNRT and atrial flutter, ventricular arrhythmias, and atrial fibrillation. Diagnostic tools like ECG findings and symptoms are outlined. Treatment options covered consist of medications, cardioversion, ablation procedures, and surgery.

1. Arrythmias
Basics, AF, AVRT, AVNRT
Dr Sravan kumar G
Assistant Professor
MRIMS

2. Action Potential

3. Chemical compositions of extracellular and intracellular fluids
-900

4. Resting Membrane Potential
• SA node -60
• Ventricular myocyte -90 (outward K
movement contributes to RMP)

6. Phase 0 – Slow channels I Ca L
Phase 4 diastolic depolarisations – funny (Na)
& T Ca
Phase 0 – fast channels Nav 1.5 (SCN5A)
Phase 1 – Ito
Phase 2 - L type Ca
Phase 3 – K channel (LQTS 1 & 2)

7. • Nernst equation
EMF (electromotive force ) in (millivolts)
= ±61 log inside/outside
• K = +61 log 140/4 = - 61 x 1.54 = - 94
• Na = +61 log 10/142 = - 61 x – 1.15 = + 70
• Ca = + 129

9. Triangle of Koch - AVnode

11. Arrhythmias
Dr Sravan kumar G
Assistant Professor
MRIMS

12. Mechanisms of Arrhythmogenesis
• Disorders of Impulse Formation
– Automaticity
• Normal automaticity(phase 4 diastolic depolarisation) - Sinus tachycardia or
bradycardia
• Abnormal automaticity - ventricular rhythms after myocardial infarction
– Triggered activity
• EADs - low Sr K, Acquired LQTS and associated ventricular arrhythmias
• DADs – Ca Overload of myocyte
• Disorders of Impulse Conduction
Block
– Bidirectional or unidirectional without reentry
• Sinoatrial Block, AV block, bundle branch block
– Unidirectional block with reentry
• Reciprocating tachycardia in Wolff-Parkinson-White syndrome,
• AV nodal reentry tachycardia, ventricular tachycardia caused by bundle branch
reentry

14. Delayed Afterdepolarizations
Increase in intracellular Ca
Activate Na/Ca exchange
Na influx - depolarisation

15. Early Afterdepolarizations
• Long-QT Syndrome
• Increased influx L type Ca channels – more
calcium release – Na Ca exchange - EAD

17. Para systole
secondary pacemaker in the heart, which works in parallel with the SA node.
Parasystolic pacemakers are protected from depolarization by the SA node by
some kind of entrance block.

18. Impulse conduction
• Reentry
• Atrial flutter

19. AVNRT

22. • Palpitations – Post extrasystolic beats (PVCs,
PACs)
• Syncope – rapid onset, brief duration, no post
ictal confusion

23. • Sudden Cardiac Death
– Ventricular Tachycardia
– Ventricular Fibrillation
– Asystole
– Rarely CHB

24. • Regular Cannon A waves
– AVRT, AVNRT
• AV dissociation -intermittent cannon A waves
– VT
• Carotid Sinus Massage
– AVRT, AVNRT

25. RESTING ECG

26. Resting ECG
WPW SYNDROME

27. Resting ECG
EPSILON WAVES

28. Resting ECG
Brugada Syndrome - gene SCN5A

29. Resting ECG
Long QT Syndrome

30. Resting ECG
SHORT QT SYNDROME

31. • Head-UP Tilt Table Testing – neurocardiogenic
Syncope

32. RP Interval

34. LQT SYNDROME
• QTc > 480 ms
• QTc < 340 ms
SQT SYNDROME

36. BETA BLOCKERS MEXILETINE, FLECAINIDE, RANOLAZINE

37. Triadin Knockout Syndrome
• Cardiac triadin is responsible for stabilization of the T
tubule junctional sarcoplasmic reticulum (jSR)
association by linking calsequestrin 2 (Casq2), ryanodine
receptor 2 (RyR2), and junctophilin-2 (JPH2)
proteins together in proximity to the L-type calcium
channel (LTCC), thus facilitating a proper negative
feedback loop for Ca2+ handling.
• Ablation of cardiac triadin results in cardiac dyad structural
remodeling and Ca2+ overload as a result of slower Ca2+-
dependent inactivation of the LTCC. Slower LTCC
inactivation could lengthen the cardiac action potential and
manifest as QT prolongation on the ECG

38. Andersen-Tawil Syndrome (KCNJ2)
• periodic paralysis,
• dysmorphic features (low set ears)
• ventricular arrhythmias
• ECG
– pronounced QTU prolongation,
prominent U waves
– ventricular ectopy, including polymorphic ventricular
tachycardia (VT),
– bigeminy, and bidirectional VT

39. Timothy Syndrome(CACNA1C-
encoded LTCC)
• fetal bradycardia
• extreme prolongation of the QT interval
(QTc >500 msec)
• macroscopic T wave alternans
• 2 : 1 AV block at birth.

40. SQT SYNDROME
• Atrial fibrillation
• syncope

41. Drug-Induced Torsade de Pointes
• IKr/Kv11.1 channel blockers (HERG channel
blockers).
• QT-prolonging drugs create an “LQT2-like”
phenotype

42. Catecholaminergic Polymorphic
Ventricular Tachycardia
• exercise-induced syncope and a QTc less than
460 milliseconds
• exercise-induced premature ventricular
complexes in bigeminy & bidirectional VT.
• RYR2-encoded cardiac ryanodine
receptor/calcium release channel mutation
• calcium overload, delayed depolarizations

43. Brugada Syndrome
• Coved-type ST-segment elevation (≥2 mm)
followed by a negative T wave in the right
precordial leads V1 through V3
• SCN5A

44. SVT

45. Sinus Tachycardia
Accelerated phase 4 depolarisation
Hyperthyroidism
Anemia
Infection
inflammation
hypovolemia
Beta blockers
T Metoprolol 25mg BD/ T Met XL 25 mg OD
Calcium Channel Blockers
Diltiazem 30 mg TID/ T DILZEM-CD 90 mg OD
Blocker of Pacemaker current(If) – Ivabradine
T IVABRAD 5 mg BD

46. Premature Atrial Complexes

47. ATRIAL TACHYCARDIAS

48. ATRIAL FLUTTER
• macroreentrant atrial rhythm
• circulate in a counterclockwise direction
around the tricuspid annulus in the frontal
plane (counterclockwise flutter)
•

49. o Rate 250 to 350 beats/min
o Regular, sawtooth flutter waves
o Continual electrical activity (lack of an isoelectric interval between
flutter waves), often best visualized in leads II, III, aVF, or V1
o flutter waves for the most common form, counterclockwise typical
atrial flutter, are inverted (negative) in these leads
o ratio of flutter waves to conducted ventricular complexes is most often
an even number (e.g., 2 : 1, 4 :1)

50. • Rhythm control
– Cardioversion - synchronous direct current (DC) -
approximately 50 J
– Inj Ibutilide 1 mg iv over 10 min
• Rate control
• CCBs
– Inj Verapamil 2.5 mg slow i.v
– Inj Diltiazem (0.25 mg/kg) 15 mg slow i.v
• Betablockers (Esmolol)
• Digoxin
• Amiodarone

51. Focal atrial tachycardia
• atrial rates of 150 to 200 beats/min
• P wave contour different from that of the
sinus P wave
• CCBs/betablockers

53. Multifocal atrial tachycardia(Chaotic Atrial Tachycardia)
• atrial rates between 100 and 130 beats/min
• marked variation in P wave morphology
• at least three P wave contours are noted
• COPD & CHF
• CCBs

55. AVNRT
• 150 to 250 beats/min
• P wave occurs just before or just after the end of the QRS complex
• causes a subtle alteration that results in a pseudo-S or pseudo-r′

57. Typical AVNRT (SLOW FAST
FORM)
Atypical AVNRT(FAST SLOW
FORM)

58. • palpitations, heart failure, syncope, or shock
• Vagal maneuvers
– carotid sinus massage
– Valsalva and Müller maneuvers
– exposure of the face to ice water
• Inj Adenosine 6 mg I.V administered rapidly
• Inj Verapamil
• Inj Diltiazem
• DC Cardioversion 50 J

59. AFFECTED TISSUE DRUGS
Accessory pathway Class IA
AV node Class II
Class IV
Adenosine
Digitalis
Both Class IC
Class III (amiodarone)

60. Accessory Atrioventricular Pathways
WPW Syndrome
preexcitation
Concealed
No preexcitation
Pathway conducts only
anterogradely

61. Reentry Over a Concealed
(Retrograde-Only) Accessory Pathway
• Resting ECG: manifestations of WPW
syndrome are absent, and the accessory
pathway is “concealed.”
• Tachycardia ECG: QRS complex is normal,
retrograde P wave occurs after completion of
QRS complex, in the ST segment, or early in
the T wave
• Left ventricle & left atrium

62. Preexcitation Syndrome
1) PR interval less than 120 milliseconds during
sinus rhythm
2) QRS complex duration exceeding 120
milliseconds with a slurred, slowly rising onset
of the QRS in some leads (delta wave)
and usually a normal terminal QRS portion
3) Secondary ST-T wave changes that are generally
directed in an opposite direction to the major
delta and QRS vectors.

64. • The major difference between the two is the
capacity for anterograde conduction
over the accessory pathway during atrial
flutter or AF

65. orthodromic AV reciprocating
tachycardia

67. Right Anteroseptal AP

68. Left lateral AP

69. Right free wall AP

70. PJRT (Permanent form of junctional
reciprocating tachycardia)

71. Atrial fibrillation - AP

72. SHORT RP, LONG PR
INTERVAL
LONG RP, SHORT PR
INTERVAL
AV nodal reentry Atrial tachycardia
AV reentry Sinus node reentry
Atypical AV nodal reentry
AVRT with a slowly
conducting accessory
pathway (e.g., PJRT)

73. ATRIAL FIBRILLATION

74. • paroxysmal AF - AF that terminates spontaneously within 7
days
– vagotonic AF – evening during relaxation or sleep
– Adrenergic AF – strenous exertion
• persistent AF - AF present continuously for more than 7
days
• longstanding persistent -AF that persists for longer than 1
year is termed
• Permanent - longstanding AF refractory to cardioversion is
termed
• Lone atrial fibrillation - AF that occurs in patients younger
than 60 years who do not have hypertension or any
evidence of structural heart disease

76. • Sites of origin
• Pulmonary veins – paroxysmal AF

77. AF vs Atrial flutter

78. causes
• hypertensive heart disease
• ischemic heart disease
• Mitral valve disease
• hypertrophic cardiomyopathy
• dilated cardiomyopathy
• Obstructive sleep apnea and obesity
• Holiday heart – alcohol
• Hyperthyroidism

79. symptoms
• Palpitations
• Polyuria -release of atrial natriuretic peptidee
• Syncope
• Stroke
• Variable intensity of S1
• Irregularly irregular pulse
• Pulse deficit

80. Prevention of Thromboembolic
Complications
CHA2DS2 VASc Score – 0 - No Anticoagulation
CHA2DS2 VASc Score – 1 – may consider
CHA2DS2 VASc Score – 2 – Anticoagulation with Warfarin/NOACs

82. • Acitrom /Warfarin 2 or 3 mg OD at 6.00 pm
monitor INR alternate day, increase dose by 1
mg till INR 2 to 3

83. Novel Oral Anticoagulants(NOACs)
T Dabigatran 150 mg BD – Idarucizumab 5 gm i.v bolus
T Rivaroxaban 20 mg OD
T Apixaban 5 mg BD Andexanet Alfa
T Endoxaban 60 mg OD
Ciraparantag – for all the above 4
Prothrombin Concentrates
Less Intracranial bleed than warfarin
High GI bleed compared with warfarin
Withold 1 to 2 days before surgery

84. Excision or Closure of the Left Atrial
Appendage
• 90% of left atrial thrombi form in the left atrial
appendage (LAA)

85. WATCHMAN DEVICE

86. LARIAT SUTURE

87. Rate control
• Target Ventricular Rate – 60 to 80 /mt
• BetaBlockers – Inj Metoprolol (BETALOC) 5 mg
in 10 ml NS I.V over 2 min repeat doses every
5 to 10 min till 3 doses to bring Heart Rate to
less than 100 to 120/mt
• CCBs – Inj Ditiazem 15 mg slow I.V over 2 min
repeat 10 mg slow i.v every 5 to 10 min till 3
doses

88. • T MET XL 50 mg OD
• T DILZEM SR 90mg OD

89. ACUTE RHYTHM CONTROL – if AF less than 48 hours
if > 48 hours – 3 weeks of Anticoagulation before rhytm control
Anticoagulation continued for next 4 weeks after rhythm control
PHARMACOLOGICAL
• Inj Ibutilide 1 mg I.V over 10
min
• Inj Amiodarone (cordarone)
150 mg I.V over 10 min fb
900 mg in 50 ml NS @ 3.4
ml/hr(1 mg/min) for 6 hrs fb
1.7 ml/hr (0.5 mg/min) for
next 18 hrs
CARDIOVERSION
• 200 J synchronised shock

90. Pharmacological rhytm control
• Lone AF & no Structural heart disease – IC –
Flecainide, Propafenone, Sotalol, Dronedarone
• Structural heart disease or CHF - Amiodarone

91. Catheter Ablation of Atrial Fibrillation
• Radiofrequency Catheter Ablation
• Cryoballoon Ablation
– almost all ablation strategies include electrical
isolation of the PVs
• Ablation of the Atrioventricular Node
– complete AV nodal block and substitutes a regular,
paced rhythm for an irregular and rapid native rhythm

92. surgery
• “cut-and-sew” maze procedure

93. • Post operative AF –
after CABG – 40%
• WPW Syndrome AF
• Digitalis & CCBs are contraindicated