Cardiac arrhythmia for cardiologist

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”

3. Arrhythmia
Definition
It may be abnormality in
impulse formation or
 it’s conduction
 Arrhythmia –means
abnormal electrical
activity of the heart.
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 JunctionalTachy
-Triggered activity.
- Re-entry (or circus movements)

5. Re-entry (or circus movement)
Mechanism of Arrjyth.
 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 .

6. Normal Sinus Rhythm- slow
pathway block

7. MMechanism of Arrhythmia
Re-enterant
Tachycardia

8. Mechanism of SVT
AV Nodal ReentryTachy.
(AVNRT) AVRT

9. CLASSIFICATION
of Arrhythmia
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

10. Ectopic- Atrial,Junctional(AV-nodal),Ventricular.
Narrow complex tachy= 0.12 sec
S.T
A.T
Junctional Tachy
Atrial Flutter.
A. F
Wide complex tachycardia
VT
VF
Supraventricular tachy with BBB.
Bradycardia
 Sinus Brady
 Sinus Pause
 CHB
 2nd. DegreeAVB.
 SSS
Block
 SA block
 AV block- 1st.2nd.3rd. Degre
 RBBB
 LBBB
 Hemiblock

11. Vaughan William’m 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**

12. Classification of
Antiarrhythmics.
Class I and III
Acts on i) ATRIAL ,
ii)VENTRICULAR
iii)ACCESSORY
PATHWAY.
OnAV nodal
dependant
arrhythmia
Class II, IV,V

13. (APC) – Itisearlierthannextsinusbeat (sopremature),
MorphologyofPisdifferentfromsinusP.
MorphologyoftheQRScomplexisnormalasthat fromsinus.

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

15. 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.

16. Premature ventricular contractions
(PVCs)

17. Sinus Node Dysfunction
SND
S.T
S.B
S. Arrhythmia
Sinus Pause- SA block & S. arrest.

18. Sinus Tachycardia.
(SND)
 Causes –
physiological(anxiety/exercise/pregnancy)
Pathological ( Anaemia, Fever, hyperthyroidism, HF, Drugs)
 Treatment-
Rx of underlying causes.
BB- Propranolol, Metoprolol, Atenolol, Carvidilol, Esmolol,Sotalol, Nabivolol
CCB,Verapamil, Dilteazem
Ivabradin
?Amiodaron, ? Digoxin

19. Sinus Tachycardia-cont..
N.B. Don’t confuse S.Tachy (HR <150/m) with SVT(HR>150/m).

20. S.Tachy to NSR.
D/D- SVT.

21. Sinus Bradycardia
 Causes-
Physiological- athletes.
Pathological
 Drugs,
 IHD.
 SSS,
 Vasovagal syncope
 raised ICP,
 Hypothyroidis,
 hypothermia,
 Obstr. Jaundice.

22. 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 % .
*

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

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

25. Atrial Arrhythmias
Atrial Ectopic/APC/PAC ( Premature Atrial omplex, not contraction).
A.Tachycardia :- Paroxysmal A.T(PAT),
MAT( Multifocal AtrialTachycardia),
IncessantAT
A. Flutter.
A.Fibrillation.

26. SVT
Supraventricular
Tachyarryhthmia
ECG Features Remarks
S.Tachycardia Rapid Rate.
Normal P,
normal QRS.
Gradual onset,
Slow recovery. Find out &
Rx underlying cause.
AtrialTachycardia Rapid rate.
P is different from sinus
P, as atrial depolarization
is abnormal.
Normal QRS, as
ventricular depolarization
is normal.
Usually occurs in patients
with structural heart
disease or COPD , Lung
Infection.
Accelerated Junctional
Tachycardia
ECG is similar to
SVT/AVNRT
Rare in adult.

27. SVT- cont..
Supra-
ventricular
Tachycardia
ECG Remarks
AVNRT Rapid Rate ( 150-250).
No P wave.
Normal QRS.
Common inYoung
people.
Episodic, rapid onset,
rapid recovery,
Usually recurrent.
AVRT Do Do
Atrial Flutter Saw tooth apearance of P waves,
usually 2:1 AV conduction.
Atrial Rate usually arround 300/mint.
QRS is normal
S/S and Rx likeA.F with
RVR
Atrial Fibrillation Irregularly irregular Rhythm.
Normal P is absent, Fibrillatory P
( abnormal, small, bizarre and variable
size-shape),
QRS is usually normal.
Cardiadiac or
extracardiac causes.

28. SinusTachycardia
Junnctional Rhythm

29. 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.

30. SVT cont..
AVNRT AVRT – in WPW synd.
 4 times more common
than AVRT.
 Mostly in younger people
with structurally normal
heart.
 Metabolic factors, anxiety,
coffee, tea may ppt. the
condition ( not the cause)
 Macro re-entrance
tachycardia.WPW synd.
 Resting ECG may show
Delta wave/ pre-excitation.
 Nearly impossible to
differentiate fromAVNRT-
ECG.

31. 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.

32. 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.

33. 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

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

35. 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).

36. 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.

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

38. Mechanism
A.F A.Flutter

39. Management of A.F
 Control ofVentricular Rate ,
class-II or IV
 Revert to Sinus Rhythm by DC,
Class-I,III.
 Maintenance of SR -Class I,III
 Anticoagulation.
Hemodynamically
Stable &
normal
Heart
To Revert &
maintenance
to S.R-
Class- Ic..III.IA
To controll
ventricular Rate-
Class-II, IV,
Unstable or pre-existing
heart disease.
(AF Duration <48 hrs).
DC
Cardioversion.
100-200 J .

40. 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 HeartValve
H/O CVD ,TIA or
systemic embolism.
More than 1
intermediate risk factors
For any one risk factor-
Warfarin with target INR
as above.

41. Ventricular Arrhythmias
PVC
Idioventricular Rhythm, accelleratedV.
Rhythm
VT
VF

42. V.T
Salvos of 3-5 consecutive PVCs
NonsustainedVT – consecutive 6 PVCs upto
< 30 sec.
Sustained- succession of PVCs >30 sec at
@>=100/mint.
MonomorphicVs. polymorphic
( Pleomorphic)VT. AndTorsade de pointes.
Differentiation betweenVT and SVT with
aberrant conduction.

43. VT- ventricular tachycardia. D/D SVT with aberrant conduction.

44. Torsade de pointes
Torsades de pointes -
 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.
 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.
 Treatment includes; correction of any electrolyte disturbances, stopping of
causative drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol (mg2+)
over 10-15 min for acquired long QT, IV isoprenaline in acquired cases and B
blockers in congenital types
 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
pacemaker therapy. Patients who remain symptomatic despite conventional
therapy and those with a strong family history of sudden death usually need ICD
therapy.

46. VF – totally disorganized and bizarre electrical activity.
There is pattern similar to “ torsade de pointes “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 .

47. Conduction Defect/ Block
SA block- already discussed
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.

48. 1st degree AV block – PR interval is >0.20 sec (1 small square)

50. 2nd degree AB block . Progressive prolongation of PR- interval followed by a drop
beat ( nonconducted P ) . Wenkebach’s type ( Mobitz’s type-1 ).
2nd degree AV block. 2:1 AV block.Whether it is Mobitz type 1 or 2 , can’t be
differentiate.

51. Third Degree A-V block
PP regular
RR regular
PR( AV dissociation)

52. 2nd Degree Mobitz type 2 AV block. PR intervale is constant. 3rd & 5th P waves failed
to be conducted to ventricle.
CHB or 3rd degree AV block. Atrial rate is nearly 100/min.Ventricular rate is about
33/mint. Complete atrio-ventricular dissociation . QRS are narrow , so possible escape
rhythm arises from bundle of His.

53. LBBB – QRS is wide , M or RsR pattern inV5-6. Secondary ST-T changes in lateral leads.
There may be LAD.
RBBB-QRS are wide, RSR’ pattern inV1-2 , deep S in lateral leads, secondary ST-T
changes inV1-3.

54. Normal Axis
 Lead I, aVL- Mean deflection = +ve So Lt. thump is above baseline
 II,III,aVF mean deflectio is +veSo Rt.Thump is aboe basline

55. LAHB-LAD; LPHB-RAD
LAD in LVH,normal variation, RAD in ASD secondum-RVH.
Never normal.
Lt. Thump down
Rt. Thump down
Rt. Thump up

56. ThankYou