This document discusses cardiac arrhythmias including their definitions, mechanisms, classifications, and management. Some key points: - Arrhythmias refer to abnormal electrical activity of the heart and can involve abnormal impulse formation, conduction, rate, or rhythm. Common mechanisms include accelerated automaticity, triggered activity, and reentry. - Arrhythmias are classified anatomically based on site of origin or electrocardiographically based on features seen on ECG such as rate, rhythm, and conduction abnormalities. - Common arrhythmias include sinus tachycardia, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and heart block. - Management depends

1. Cardiac Arrhythmia
Dr. Ashok Dutta
FCPS.MD.FACC

2. AXIOM
• All Rhythm Interpretation must be correlated with sign,
symptoms and patients condition….
“Treat the patient,
NOT the monitor”.
Because sometimes artifact may mimic arrhythmia-
Straight line ECG/Asystole- loss of chest lead contact/connection,
vibration – may mimic VT/VF.
Speed of recording ECG- Bradycardia, tachycardia.

3. Arrhythmia
Definition
• Arrhythmia –means
abnormal electrical
activity of the heart.
It may be abnormality in
impulse formation or
 it’s conduction
Abnormality in
Rate ( HR=60-100/min),
Rhythm (normal sinus, may be
atrial ,nodal/junctional, ventricular)
Conduction
(SA,AVN,BBB,IVCD)

4. Mechanisms of Cardiac Arrhythmias
Mechanisms of bradicardia:
Sinus bradycardia is a result of abnormally slow
automaticity while bradycardia due to AV block is
caused by abnormal conduction within the AV node or
His bundle, the distal AV conduction system.
Mechanisms generating tachycardia include:
- Accelerated automaticity- S.T. & Accellerated Junctional Tachy
- Triggered activity- ACS setting
- Re-entry (or circus movements)- most common
mechanism- SVT, A. fluttar, scar VT, SANRT.

5. The original concept of Coumel on the left (a), and its generally well-
known final form (b), as the triangle of Coumel, explaining
how the interaction of substrate, triggers and the autonomic
nervous system are important in arrhythmogenesis.

6. Re-entry (or circus movement)
Mechanism of Arrhythmia
• The mechanism of re-entry occurs when a 'ring' of cardiac
tissue having 2 different pathway surrounds an in-excitable
core e.g. in a region of scarred myocardium.
• Alfa/fast pathway is rapid conducting & slow recovery and
• Beta pathway/slow pathway is slow conducting and rapid
recovery .

7. Mechanism of Arrhythmia- Re-entry
SVT, A. flutter, VT.
APC-
Conducted through slow
path because fast path is
refractory
When APC
at appropriate time & site-
Re-enterant
Tachycardia

8. CLASSIFICATION-anatomical.
S.Tachy.
S. Brady.
S.Arry
**S.Pause
(s.arrest & SA
block)
APC
A.Tachy.
A.F
A.flutter
J.Ect
SVT.
**AVB
PVC.
VT.
VF
*IVCD
*RBBB
*LBBB

9. Elecrocardiographic-Classificarion of Arrhythmia
Ectopics-
Atrial, Junctional(AV-nodal), Ventricular.
Narrow complex tachy= 0.12 sec
S.T
A.T- Focal AT, MAT.
Junctional Tachy.
AVNRT/AVRT.
Atrial Flutter.
A. F
Bradycardia
Sinus Brady
Sinus Pause
CHB
2nd. Degree AVB.
SSS
Wide complex tachycardia
VT- Regular ( except-TdP)
VF- irregular.
Supraventricular tachy with
BBB/IVCD- Regular/irregular.
Heart Block
SA block
AV block- 1st.2nd.3rd. Degre
RBBB
LBBB
Hemiblock

10.  Tachyarrhythmia-ECG Dx.
Atrial rate in supraventricular tachyarrhythmia
(400-300-200-150 bpm)-
AF atrial rate 400+/-100 (300-500) bpm,
A. flutter it’s 300+/- 100 (200-400),
SVT(AVNRT/AVRT) atrial rate 200 +/- 50(150-250) bpm,
Sinus tachycardia – 150+/-50 (100-200) bpm.
All SV tachy – NCT if not aberrantly conducted.
All V Tachy- are WCT- except Fascicular VT, VT close to HB.
Irregular tachy- AF, A flutter with variable AVB, MAT, VF, TdP.

11. SV Tachycardia-
effect of Adenosine/vagal maneuver.

12. General approach to Tachyarrhythmia
• Group-1. DC-shock
• Patients with Cardiac arrest.
• Group-2. DC shock ( Except- Chr.AF)
• Patients with signs of severe hemodynamic
compromise (hemodynamically unstable).
• Group-3. Medical Mx
• Patient without hemodynamic compromise
(stable patients).

13. Vaughan William’s Classification of antiarrhythmic Drugs
based on Drug Action
CLASS ACTION DRUGS
I. Sodium Channel Blockers
1A.
Moderate phase 0 depression and slowed
conduction (2+); prolong repolarization
Quinidine,
Procainamide,
Disopyramide
1B.
Minimal phase 0 depression and slow
conduction (0-1+); shorten repolarization **Lidocaine
1C.
Marked phase 0 depression and slow
conduction (4+); little effect on
repolarization
** propafenone,
Flecainide
II. Beta-Adrenergic Blockers Propranolol, esmolol**
III. K+ Channel Blockers
(prolong repolarization)
Amiodarone**,
Sotalol**, Ibutilide
IV. Calcium Channel Blockade Verapamil**, Diltiazem
V Increase parasympathetic activity Digoxin**, Adenosin**

14. Classification of Antiarrhythmics.
Acts on i) ATRIAL ,
ii) VENTRICULAR
iii) ACCESSORY
PATHWAY.
Class I and III
AV nodal dependant arrhythmia
Class II, IV, V
(BB,CCB,Digoxin & Adenosine.
All anti-arrhythmic drugs are pro-arrhythmic except BB.
All are negative chronotropic.
All are negative ionotropic except digoxin.
class I, IV > class-III

15. Sinus Node Dysfunction
SND
S.T
S.B
S. Arrhythmia
Sinus Pause- SA block & S. arrest.
S.Tachy.
S. Brady.
S.Arry
**S.Pause
(s.arrest & SA
block)

16. Sinus Tachycardia.
(SND)
 Causes –
physiological(anxiety/exercise/pregnancy)
Pathological ( Anaemia, Fever, hyperthyroidism, HF, Drugs)
Treatment-
Rx of underlying causes.
BB- Propranolol, sotalol ( antiarrhythmia>anti-Htn).
Atenolol, Carvidilol, nabivilol ( anti-Htn> anti-arrhyth)
Metoprolol,Bisoprolol (both).
CCB-Verapamil, Dilteazem
Ivabradin- SA node specific.
?Amiodaron, ? Digoxin

17. Sinus Tachycardia-cont..
N.B. Don’t confuse S.Tachy (HR <150/m) with SVT(HR>150/m) or AF.
How ECG monitor can help?

18. How ECG monitor can help?
ST, SVT,AF-FVR
Rate-rhythm. Increase the gain and speed

19. SV- tachy Differentiation
SV- Tachycardia
ECG Remarks
AVNRT  Rapid Rate (150-250).
 No P wave.
 Normal QRS.
Common in Young people.
Episodic, rapid onset, rapid
recovery.Usually recurrent.
AVRT Do Do
Atrial Flutter  Saw tooth appearance of P waves,
 usually 2:1 AV conduction.
 Atrial Rate usually around 300/mint.200-400 bpm
 QRS is normal
S/S and Rx like A.F with Fast VR
Atrial
Fibrillation
 Irregularly irregular Rhythm.
 Normal P is absent, Fibrillatory P
(abnormal, small, bizarre and variable size-shape),
 QRS is usually normal.
Cardiac or extra cardiac
causes.

20. Sinus Bradycardia
Causes-
Physiological- athletes.
Pathological
• Drugs,
• IHD.
• SSS,
• Vasovagal syncope
• Raised ICP,
• Hypothyroidis,
• hypothermia,
• Obstr. Jaundice.

21. S. Arrhythmia
Sinus arrhythmia of young man and children.
 Respiratory or non-respiratory variation of HR .
 In inspiration rate is higher .
Variation of HR > 10 % .
It indicates good autonomic n. system & good SA node.
*

22. Sinus arrhythmia of young man . Respiratory or nonrespiratory variation of HR .
In inspiration rate is higher . Variation of HR > 10 % .

23. Sinus Pause
Cause: SSS.
S.A BLOCK
• PP/RR interval is exactly the
double of normal PP/RR.
S. ARREST
• Not double.

24. Atrial Arrhythmias
Atrial Ectopic/APC/PAC ( Premature Atrial complex, not contraction).
A. Tachycardia :- Paroxysmal A.T(PAT),
MAT( Multifocal Atrial Tachycardia),
Incessant A T
A. Flutter.
A.Fibrillation.
APC
A.Tachy.
A.F
A.flutter

25. (APC)
It is earlier than next sinus beat ( so premature),
Morphology of P is different from sinus P.
Morphology of the QRS complex is normal as that from sinus.

26. APC in Bigeminy form
APC – after every normal Sinus Complex. Atrial Bigeminy.

27. PVC/VPC – occurs earlier than expected , no P wave, QRS is wide, T
wave is in opposite to mean QRS . In bigeminy form (each of the PVC is
paired with one normal complex).
PVC in trigeminy form.

28. Premature ventricular contractions (PVCs)

29. Ectopics

30. Ectopics

31. A.T.D/D SVT.
N.B. Don’t confuse with AF with FVR. Look at the monitor.
In AF HR will be variable, in SVT HR – fixed/regular.

32. Atrial Fibrillation.
Disorganised atrial activity and irregular AV
conduction.
International consensus on nomenclature and
classification of AF:
 Initial ( First detected) event.
Paroxysmal that terminates spontaneously within 48 hrs. it may recurs.
 Persistent – not self limiting, and lasting >7 days or after cardio version.
 Permanent( established)- may or may not be terminated or
relapse after cardio version.
(This classification is for guideline of therapy).

33. Atrial Fibrillation ( A.F) with fast ventricular rate.
P waves are absent.
Low amplitude fibrillatory waves .
RR intervals at first glance looks regular but, on closure inspection they are
irregular .
 ST-T changes are nonspecific due tachycardia.

34. Causes of A.F
• RHD
• Hypertensive Heart disease.
• IHD
• Thyrotoxicosis.
• CMP
• Lone A.F
• ASD
• P. Embolism.
• Alcohol
• Metabolic

35. Management of A.F
Control of Ventricular Rate , class-II /IV.
(BB,CCB,digoxin).
Revert to Sinus Rhythm by DC, Class-I,III
( amiodarone, propafenone).
Maintenance of SR -Class I,III
Anticoagulation.
DC shock.

36. Anticoagulation for AF
Risk Level Risk Factors Therapeutic Guideline
Low Risk Age<65 yrs
No additional risk factor
Aspirin 325 mg/day
Intermediate Risk Age 65-75 yrs
DM
CAD
For 1 Risk Factor-
Aspirin 325 mg/day.
For 2 Risk factors-
Warfarin with target INR
2.5 ( range=2.0-3.0)
High Risk Age >75 yrs.
H/O HTN
LVD
MVD
Prosthetic Heart Valve
H/O CVD ,TIA or systemic
embolism.
More than 1
intermediate risk factors
For any one risk factor-
Warfarin with target INR as
above.

37. SVT
-AVNRT,AVRT

38. SVT- it may be AV nodal reentry tachycardia- AVNRT ( 80% ) or AV (
atrioventricular) reentry tachycardia- AVRT ( 20 %) . AVRT is less
common and it occurs due to accessory pathway ( WPW syndrome ) .
WPW syndrome . Q in inferior leads is not due to OMI.

39. Sign-symptoms of SVT
• Palpitation.
• Dizziness, Blurring vision.
• Vertigo.
• Chest Pain ( due to reduced coronary flow).
• Sweating. Cold –clammy extremities.
• Pre-syncope ( due to reduced cerebral circulation)
• Syncope ( due to reduced cerebral circulation)
• Rapid onset , may suddenly disappears without Rx
or by vomiting.

40. SVT -Mx
Hemodynamically
Stable
Vagal menuvers-
Carotid Msg.
Cold water immersion,
Self induced vomiting,
Valsalva
IV adenosine, 0.25 mg/kg
Verapamil,
Dilteazem
BB
Unstable
DC Cardioversion.
50-100 J .
Synchronized

41. SVT –Mx Cont…
Preventation of Recurrence:
Class-II – BB- Propranolol, Metoprolol, Sotalol.
Class-IV- CCB( Verapamil, Dilteazem).
Pill in Pocket- Propafenone ( Rythmosin 150 mg)
EPS & RFA: i) Recurrent attack.
ii) Attack with unstable hemodynamics.
iii) High risk professions- Public transport
driver.

42. Ventricular Arrhythmias
PVC
Idioventricular Rhythm, accellerated V. Rhythm
VT
VF
PVC.
VT.
VF
*IVCD

43. V.T
Salvos of 3-5 consecutive PVCs
Nonsustained VT – consecutive 6 PVCs upto < 30 sec.
Sustained- succession of PVCs >30 sec at
@>=100/mint.
Monomorphic Vs. polymorphic ( Pleomorphic) VT.
And Torsade de pointes.
Differentiation between VT and SVT with aberrant
conduction.

44. Causes of VT
• Primary VT- ARVD (RVOT -VT), fascicular VT.
• Secondary VT- 80-90 % of cases of VT.
• Primary and secondary VT in AMI ?

45. Middle aged man , WCT for hrs. together.
IV amiodarone, adenosine – with no effect.

46. AV dissociation- VT/CHB.

47. After DC cardioversion-
Difference between Cardioversion and Defrillation?.

48. HR- irregular, wide complex, discordance.
Dx- AF with LBBB.

49. Dx- AF- WPW/VT.

50. Fascicular VT-Narrow complex VT& verapamil sensitive.
• Is it SVT-RBB or VT ?
• Points in favor of each .

51. Other features of VT
• Extreme axis deviation (“northwest axis”) — QRS is
positive in aVR and negative in I + aVF.
• Brugada’s sign – The distance from the onset of the QRS
complex to the nadir of the S-wave is > 100ms
• Josephson’s sign – Notching near the nadir of the S-wave
• RSR’ complexes with a taller left rabbit ear. This is the most
specific finding in favour of VT. This is in contrast to RBBB,
where the right rabbit ear is taller.

52. Additional factors associated with VT or SVT
• The likelihood of VT is increased with:
• Age > 35 (positive predictive value of 85%)
• Structural heart disease
• Ischaemic heart disease
• Previous MI
• Congestive heart failure
• Cardiomyopathy,
• H/O syncope.
• Family history of sudden cardiac death (suggesting conditions
such as HOCM, congenital long QT syndrome, Brugada
syndrome or arrhythmogenic right ventricular dysplasia(ARVD)
that are associated with episodes of VT)

53. 3. AV dissociation
•The ECG is scrutinised for hidden P waves; these are often superimposed on the
QRS complexes and may be difficult to see.
•If P waves are present at a different rate to the QRS complexes –> AV
dissociation is present and VT is diagnosed.
•If no evidence of AV dissociation can be seen –> go to step 4.
AV dissociation: P waves can be spotted in between QRS complexes (circled)
and superimposed upon the T wave causing a peaked appearance (arrow)

54. Capture Beat

55. Fusion beats –
the first of the narrower complexes is a fusion beat (the
next two are capture beats)

56. Concordance & discordance

57. QRS- very wide. Axis- NWAD,
Concordance –negative.

58. Brugada’s sign (red callipers) and Josephson’s sign (blue arrow)

59. Torsade de pointes( Torsad de pont).
• This is a type of short duration tachycardia that reverts to sinus rhythm
spontaneously.
• It may be due to:
- Congenital
- Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia.
- Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics.
Quinolone, cispride, antihistamine, clarithromycine.
Toxins- Herbal, Toxic fish.
• It may present with syncopal attacks and occasionally ventricular fibrillation.
• QRS complexes are irregular and rapid that twist around the baseline. In
between the spells of tachycardia the ECG show prolonged QT interval.

60. Long QT- QT >1/2 of RR interval.

61. VF – totally disorganized and bizarre electrical activity.
There is pattern similar to “ torsade de pointes “- torsad de point
VT .
This man collapsed during recording. He was defibrillated, treated
for MI & survive. Don’t try to take 12 lead ECG . It will delay
treatment only .

62. Polymorphic VT

64. Treatment of TDP
• Correction of any electrolyte disturbances,
• stopping of causative drug,
• Magnesium sulphate 8 mmol (mg2+) over 10-15 min for
acquired long QT,
• IV isoprenaline in acquired cases and B blockers in
congenital types .
• atrial or ventricular pacing @ >70 bpm.
• Long-term management of acquired long QT syndrome
involves avoidance of all drugs known to prolong the QT
interval.
• Congenital long QT syndrome is generally treated by beta-
blockade, left cardiac sympathetic denervation and ICD.

65. Arrhythmia in AMI
• PVC.
• Idioventricular Rhythm- rate <100 bpm. Slow VT. Not related to in
hospital or 1 yr. mortality.
• Non-sustained VT- >3 consequitive PVCs but persist <30 sec.
• 67% cases in AMI- specially in large infarc.
• Sustained VT- 3.5%.
• VF-4%. Both VT and VF in same patient- 2.7%.
• Sustained VT- n hospital mortality 18%.
• VT+VF group-44%.
• 1 yr mortality is also high.
• A.F- Rx ?
• Primary VT- in absence LVF
• Secondary VT- in LVF, electrolyte imbalance.

66. AV node & BB disorders-
Conduction Defect/ Block
AV Block- 1st. Degree
2nd. Degree – Mobitz type- I , type-II.
3rd. Degree/ complete AVB/CHB.
LBBB.
RBBB
Fascicular block- LAF ( LAD).LPF(RAD).
IVCD.

67. 1st degree AVB

68. 2nd. Degree AVB

69. 2:1 AVB.

70. 2nd. Degree AVB.

71. 3rd. Degree AVB.
RR is regular, PP –regular. No relation between R and P.

72. J. Rhythm.- Escape Rhythm.

73. CHB, Irregular Escape

74. Thank You