Dr, A. Banerjee. D.M(Cardiology)

1. Cardiac Arrhythmia
Dr. A. Bandyopadhyay
D.M.(Cardiology)

2. Cardiac Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
Impulses originate regularly at a
frequency of 60-100 beat/ min

3. Non-nodal Cell Action Potentials
Non-nodal action potentials, sometimes referred to as "fast response" action potentials,
are characteristic of atrial and ventricular myocytes.
Phase 0: Rapid depolarization
- increased Na+
conductance
- decreased K+
conductance
Phase 1: Initial repolarization
- decreased Na+
conductance
- increased K+
conductance
Phase 2: Plateau phase
- increased Ca++
conductance
Phase 3: Repolarization
- increased K+
conductance
- decreased Ca++
conductance
Phase 4: Resting potential
- increased K+
conductance
- decreased Na+
conductance
- decreased Ca++
conductance

4. Nodal Cell Action Potentials
Nodal action potentials, sometimes referred to as "slow response" action potentials, are characteristic of
action potentials found in the SA node and AV node.
These action potentials display automaticity, or pacemaker activity, and therefore undergo
spontaneous depolarization.
Their depolarization phase is slower and they have a shorter action potential duration than
non-nodal, fast response action potentials.
Furthermore, they have no phase 1 or phase 2.
Phase 0: Depolarization
- increased Ca++
conductance
- decreased K+
conductance
Phase 3: Repolarization
- increased K+
conductance
- decreased Ca++
conductance
Phase 4: Spontaneous depolarization
- "Funny" currents (If)
- increased Ca++
conductance
- decreased K+
conductance

5. Refractory period
Defined as the time from phase 0 until the next possible depolarization of a myocyte, i.e. once
enough fast Na+
channels have recovered (as TMP decreases below −50 mV).
Absolute refractory period (ARP): the cell is completely unexcitable to a new stimulus.
Effective refractory period (ERP): ARP + short segment of phase 3 during which a
stimulus may cause the cell to depolarize minimally but will not result in a propagated action
potential.
Relative refractory period (RRP): a greater than normal stimulus will depolarize the
cell and cause an action potential.
Supranormal period: a hyperexcitable period during which a weaker than normal stimulus
will depolarize the cells and cause an action potential.

7. Mechanisms of Cardiac Arrhythmias
Cardiac arrhythmias arise by 2 potential mechanisms:
A.Disorders of impulse formation.
•Disturbed normal automaticity: e.g. Inappropriate sinus tachycardia.
•Abnormal automaticity: e.g. Atrial tachycardia, VT.
•Triggered activity(early and delayed after depolarization):
early afterdepolarization(EAD): phases 2, 3; Ca2+
inward flow, increased by drugs, K+
↓
delayed afterdepolarization(DAD): phase 4; Ca2+
inward flow leads to transient Na+
flow
induced by digitalis intoxication, plasma Ca2+
↑, K+
↓

8. B. Disorders of impulse conduction.
•Simple conduction block:
slow and small depolarization in phase 0, reduced MDP level in phase 4. e.g. different types of
heart block due to ischemia, inflammation, metabolic disorders.
•Reentry:
Presence of two functional pathways for conduction(anatomically identical or distinct).
Unidirectional block in one pathway(allows impulse conduction antegradely through 2nd
pathway and to re-enter the 1st
pathway).
Slow conduction through 2nd
pathway.

10. Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
R.M.P
(Plateau Phase)
Class I:
Na+
channel blockers.
- Pacemaker potential
-
-
-
Class III:
K +
channel blockers
-
Class IV:
Ca++
channel blockers
Class II:
Beta blockers
Classification of Anti-Arrhythmic Drugs

11. Classification of Vaughan Williams Antiarrhythmic Drugs
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
Flecainide
II. Beta-Adrenergic Blockers Propranolol, esmolol
III. K+
Channel Blockers
)prolong repolarization(
Amiodarone, Sotalol,
Ibutilide
IV. Calcium Channel Blockade Verapamil, Diltiazem

12. Classification of Arrhythmias

13. ARRHYTHMIAS
Bradyarrhythmias (HR < 60/m) Tachyarrhythmias (HR> 100/m)
SND
AVND
IVCD
Asystole
Narrow QRS(<120ms) Wide QRS(≥120ms)

14. Tachyarrhythmias

15. Physiological:
Sinus Tachycardia
Sinus Arrhythmia
Pathological:
 Valvular heart disease.
 Electrolyte disturbances.
 Structural heart disease.
 Ischemic heart disease.
 Hypertensive heart diseases.
 Congenital heart disease.
 Cardiomyopathies.
 Myocarditis and Pericarditis.
 Right Ventricular dysplasia.
 Drug related.
 Pulmonary diseases.
 Ideopathic.
Etiology

17. SVTs from a sinoatrial source:
Inappropriate Sinus Tachycardia (IST)
Sinoatrial Nodal Re- entrant Tachycardia (SNRT)
SVTs from an atrial source:
Ectopic (Focal) Atrial Tachycardia (EAT)
Multifocal Atrial Tachycardia (MAT)
Atrial fibrillation with a rapid ventricular response
Atrial flutter with a rapid ventricular response
SVTs from an atrioventricular source (junctional tachycardia):
AV nodal re- entrant Tachycardia(AVNRT)
Atrioventricular re- entrant Tachycardia (AVRT- including WPW syndrome)
Accelerated junctional Tachycardia

18. Sinus Arrhythmia
• All criteria of normal rhythm except heart and pulse rates increase with inspiration
and decrease with expiration
• Normal finding in brachycephalic breeds and in chronic respiratory disease
• Increased number of cardiac cycles during inspiration;
decreased number during expiration
• This is usually a benign condition

19. Causes of SVT
Tachycardia ECG features Comment
AV nodal re-entry tachycardia (AVNRT) No visible P wave, or inverted P
wave immediately before or after
QRS complex
Commonest cause of palpitations in
patients with normal hearts
AV reciprocating tachycardia (AVRT) P wave visible between QRS and T
wave complexes
Due to an accessory pathway.
Atrial fibrillation Irregularly irregular RR intervals
and absence of organized atrial
activity
Commonest tachycardia in patients over
65 years
Atrial flutter Visible flutter waves at 300/min
(saw-tooth appearance) usually with
2 : 1 AV conduction
Suspect in any patient with regular SVT
at 150/min
Atrial tachycardia Organized atrial activity with P wave
morphology different from sinus
rhythm
Usually occurs in patients with structural
heart disease
Multifocal atrial tachycardia Multiple P wave morphologies (≥3)
and irregular RR intervals
Rare arrhythmia;
most commonly associated with
significant chronic lung disease

20. SVT – Acute Treatment
COR Recommendations
I
Carotid massage is recommended for patients with regular SVT.
I
Intravenous adenosine is recommended for patients with regular SVT.
I
Synchronized cardioversion is recommended for patients with hemodynamically
unstable SVT.
I
Synchronized cardioversion is recommended for patients with hemodynamically
stable SVT when pharmacological therapy is ineffective or contraindicated.
IIa
Intravenous diltiazem or verapamil can be effective for acute treatment in patients
with hemodynamically stable SVT.
IIa
Intravenous beta blockers are reasonable for acute treatment in patients with
hemodynamically stable SVT.

23. SVT – Ongoing Treatment
COR Recommendations
I
Oral beta blockers, diltiazem, or verapamil is useful for ongoing management in
patients with symptomatic SVT without pre-excitation.
IIa
Flecainide or propafenone is reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have symptomatic
SVT who are not candidates for catheter ablation.
IIb
Sotalol may be reasonable for ongoing management in patients with
symptomatic SVT who are not candidates for catheter ablation.
IIb
Dofetilide and oral amiodarone may be reasonable for ongoing management in
patients with symptomatic SVT who are not candidates for catheter ablation and
in whom beta blockers, diltiazem, flecainide, propafenone, or verapamil are
ineffective or contraindicated.
IIb
Oral digoxin may be reasonable for ongoing management in patients with
symptomatic SVT without pre-excitation who are not candidates for catheter
ablation.

25. Inappropriate Sinus Tachycardia
persistent increase in resting heart rate unrelated to the level of physical, emotional,
pathological or pharmacologic stress due to enhanced automaticity of the sinus node.
Diagnosis-
presence of a persistent sinus tachycardia during the day with excessive rate increase in
response to activity and nocturnal normalization of rate as confirmed by a 24-hour Holter
recording.
tachycardia (and symptoms) is non paroxysmal.
P-wave morphology and endocardial activation identical to sinus rhythm.

26. IST – Ongoing Treatment
COR Recommendations
I
Evaluation for and treatment of reversible causes are recommended in
patients with suspected IST.
IIa
Ivabradine is reasonable for ongoing management in patients with
symptomatic IST.
IIb
Beta blockers may be considered for ongoing management in patients with
symptomatic IST.
IIb
The combination of beta blockers and ivabradine may be considered for
ongoing management in patients with IST.

27. Focal Atrial Tachycardia
Rapid (usually <250 beats/ min), regular rhythms that originate in the atrial musculature.
Mechanisms include abnormal automaticity and triggered activity.
Foci are most frequently found in the pulmonary veins in the LA and the crista terminalis in
the right atrium.
Myocardial infarction, non ischemic heart disease, obstructive lung disease,
serum electrolyte disorders and drug toxicity.

28. Multifocal Atrial Tachycardia(MAT)
• rapid, irregular rhythm with at least 3 different morphologies of P waves on the ECG
• distinct isoelectric period between P waves.
• The P-P, PR, and R-R intervals are variable.
• associated with pulmonary disease, pulmonary hypertension, coronary disease, and
valvular heart disease , hypomagnesemia and theophylline therapy.
• first-line treatment is management of the underlying condition

29. Focal Atrial Tachycardia and MAT – Acute Treatment
COR Recommendations
I
Intravenous beta blockers, diltiazem, or verapamil is useful for acute
treatment in hemodynamically stable patients with focal AT.
I
Synchronized cardioversion is recommended for acute treatment in patients
with hemodynamically unstable focal AT.
IIa
Adenosine can be useful in the acute setting to either restore sinus rhythm or
diagnose the tachycardia mechanism in patients with suspected focal AT.
IIa
Intravenous metoprolol or verapamil can be useful for acute treatment in
patients with MAT.
IIb
Intravenous amiodarone or Ibutilide may be reasonable in the acute setting to
either restore sinus rhythm or slow the ventricular rate in hemodynamically
stable patients with focal AT.

31. Focal Atrial Tachycardia and MAT – Ongoing Treatment
COR Recommendations
I
Catheter ablation is recommended in patients with symptomatic focal AT as an
alternative to pharmacological therapy.
IIa
Oral beta blockers, diltiazem, or verapamil are reasonable for ongoing
management in patients with symptomatic focal AT.
IIa
Flecainide or propafenone can be effective for ongoing management in patients
without structural heart disease or ischemic heart disease who have focal AT.
IIb
Oral sotalol or amiodarone may be reasonable for ongoing management in
patients with focal AT.
IIa
Oral verapamil or diltiazem is reasonable for ongoing management in patients
with recurrent symptomatic MAT.
IIa
Metoprolol is reasonable for ongoing management in patients with recurrent
symptomatic MAT.

33. AV NODAL RE-ENTRANT TACHYCARDIA
• Presence of a narrow complex tachycardia with regular R-R intervals and no visible p waves.
• P waves are retrograde and are inverted in leads II, III, aVF.
• P waves are buried in the QRS complexes –simultaneous activation of atria and ventricles –
most common presentation of AVNRT –66%.
• If not synchronous –pseudo s wave in inferior leads, pseudo r’ wave in lead V1---30% cases .

34. AV NODAL REENTRANT TACHYCARDIA

40. Atrioventricular Nodal Reentrant Tachycardia – Acute Treatment
COR Recommendations
I
Vagal maneuvers are recommended for acute treatment in patients with AVNRT.
I
Adenosine is recommended for acute treatment in patients with AVNRT.
I
Synchronized cardioversion for hemodynamically unstable patients with AVNRT .
I
Synchronized cardioversion is recommended for acute treatment in
hemodynamically stable patients with AVNRT when pharmacological therapy does
not terminate the tachycardia or is contraindicated.
IIa
Intravenous beta blockers, diltiazem, or verapamil are reasonable for acute
treatment in hemodynamically stable patients with AVNRT.
IIb
Oral beta blockers, diltiazem, or verapamil may be reasonable for acute treatment
in hemodynamically stable patients with AVNRT.
IIb
Intravenous amiodarone may be considered for acute treatment in
hemodynamically stable patients with AVNRT.

42. ANRT – Ongoing Treatment
COR Recommendations
I
Oral verapamil, diltiazem or beta blockers is recommended for ongoing
management who are not candidates for catheter ablation.
I
Catheter ablation is recommended in patients with AVNRT.
IIa
Flecainide or propafenone is reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have AVNRT who
are not candidates for catheter ablation and in whom beta blockers, diltiazem, or
verapamil are ineffective or contraindicated.
IIb
Oral digoxin or amiodarone may be reasonable for ongoing treatment of AVNRT
in patients who are not candidates for, or prefer not to undergo, catheter
ablation.

44. AV RE-ENTRANT TACHYCARDIA
Typical – RP interval < PR interval
RP interval > 70 milli sec
Atypical –RP interval > PR interval
Concealed bypass tract – only retrograde conduction
Manifest bypass tract– both anterograde and retrograde.
Electrical alternans –the amplitude of QRS complexes varies by 5 mm alternatively.
Rate related BBB occurring and the rate of tachycardia is decreasing.

45. AV REENTRANT TACHYCARDIA

49. WPW syndrome
An abnormal band of atrial tissue connects the atria and ventricles and can electrically
bypass the normal pathways of conduction;
a re-entry circuit can develop causing paroxysms of tachycardia.
WPW may be two types: Orthodromic and Antidromic
Antidromic is wide complex tachycardia.
ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
WPW may be described as type A or B:
• Type A has a positive delta wave in all precordial leads with R/S > 1 in V1
• Type B has a negative delta wave in leads V1 and V2
Can precipitate into AF and VF on use of AV nodal blockers

54. Orthodromic AVRT

55. Atrioventricular Reentrant Tachycardia – Acute Treatment
COR Recommendations
I
Vagal maneuvers are recommended for acute treatment in patients with
orthodromic AVRT.
I
Adenosine is beneficial for acute treatment in patients with orthodromic AVRT.
I
Synchronized cardioversion should be performed for acute treatment in
hemodynamically unstable patients.
I
Synchronized cardioversion is recommended for acute treatment in
hemodynamically stable patients with AVRT when pharmacological therapy is
ineffective or contraindicated.
I
Ibutilide or intravenous procainamide is beneficial for acute treatment in
patients with pre-excited AF who are hemodynamically stable.

56. I
Synchronized cardioversion should be performed for acute treatment in
hemodynamically unstable patients with pre-excited AF.
I
Ibutilide or intravenous procainamide is beneficial for acute treatment in
patients with pre-excited AF who are hemodynamically stable.
IIa
Intravenous diltiazem, verapamil or beta blockers can be effective for acute
treatment in patients with orthodromic AVRT who do not have pre-excitation
on their resting ECG during sinus rhythm.
III: Harm
Intravenous digoxin, intravenous amiodarone, intravenous or oral beta
blockers, diltiazem, and verapamil are potentially harmful for acute treatment
in patients with pre-excited AF.
Contd…..

58. Atrioventricular Reentrant Tachycardia – Ongoing Treatment
COR Recommendations
I
Catheter ablation of the accessory pathway is recommended in patients with
AVRT and/or pre-excited AF.
I
Oral beta blockers, diltiazem, or verapamil are indicated for ongoing
management of AVRT in patients without pre-excitation in ECG.
IIa
Oral flecainide or propafenone is reasonable for ongoing management in
patients without structural heart disease or ischemic heart disease who are not
candidates for catheter ablation.
IIb
Oral amiodarone may be considered for ongoing management in patients with
AVRT and/or pre-excited AF who are not candidates for catheter ablation and
in whom beta blockers, diltiazem, flecainide, propafenone, and verapamil are
ineffective or contraindicated.
III: Harm
Oral digoxin is potentially harmful for ongoing management in patients with
AVRT or AF and pre-excitation in the ECG.

60. Atrial Flutter
Usually a single, irritable foci in the atria (right) due to macro re-entry circuit.
AV node protects the ventricles by blocking some of the atrial impulses.
P waves take on a ͞saw-tooth appearance and are called flutter waves.
Atrial rhythm and ventricular response are usually regular
Atrial rate 250-350 beats/min.
Ventricular rate varies depending on the number of impulses the AV node is blocking.
No P waves or PR interval
QRS normal width or with aberrancy

63. Atrial Flutter – Acute Treatment
COR Recommendations
I
Oral dofetilide or intravenous ibutilide is useful for acute pharmacological
cardioversion in patients with atrial flutter.
I
Intravenous or oral beta blockers, diltiazem, or verapamil are useful for acute rate
control in patients with atrial flutter who are hemodynamically stable.
I
Elective synchronized cardioversion is indicated in stable patients with well-
tolerated atrial flutter when a rhythm-control strategy is pursued.
I
Synchronized cardioversion is recommended for acute treatment of patients with
atrial flutter who are hemodynamically unstable.

66. Atrial Flutter – Ongoing Management
COR Recommendations
I
Catheter ablation of the is useful in patients with atrial flutter that is either
symptomatic or refractory to pharmacological rate control.
I
Beta blockers, diltiazem, or verapamil are useful to control the ventricular rate
in patients with hemodynamically tolerated atrial flutter.
I
Catheter ablation is useful in patients with recurrent symptomatic
non cavo-tricuspid dependent flutter.
I
Ongoing management with antithrombotic therapy is recommended in patients
with atrial flutter to align with recommended antithrombotic therapy for
patients with AF.
IIa
The following drugs can be useful to maintain sinus rhythm:
a. Amiodarone
b. Dofetilide
c. Sotalol

68. Junctional Tachycardia
Origin from the AV node or His bundle heart rates of 110 to 250 bpm and a narrow complex or
typical BBB conduction pattern
Atrioventricular dissociation is often present
Arrhythmia is thought to be either abnormal automaticity or triggered activity.
Uncommon in adults
Non paroxysmal Junctional Tachycardia
Benign arrhythmia
Narrow complex tachycardia with rates of 70 to 120 bpm. Cannot be terminated by pacing
maneuvers.
Cause-
•digitalis toxicity,
•hypokalemia,
•myocardial ischemia.
•inflammatory myocarditis.

70. Junctional Tachycardia – Acute and Ongoing Treatment
COR Recommendations
IIa
Intravenous beta blockers are reasonable for acute treatment in patients with
symptomatic junctional tachycardia.
IIa
Intravenous diltiazem, procainamide, or verapamil is reasonable for acute
treatment in patients with junctional tachycardia.
IIa
Oral beta blockers, diltiazem or verapamil are reasonable for ongoing
management in patients with junctional tachycardia.
IIb
Catheter ablation may be reasonable in patients with junctional tachycardia
when medical therapy is not effective or contraindicated.

72. SVT with Pregnancy – Acute Treatment
COR Recommendations
I
Vagal maneuvers are recommended for acute treatment in pregnant patients
with SVT.
I
Adenosine is recommended for acute treatment in pregnant patients with SVT.
I
Synchronized cardioversion is recommended for acute treatment in pregnant
patients with hemodynamically unstable SVT when pharmacological therapy is
ineffective or contraindicated.
IIa
Intravenous metoprolol or verapamil is reasonable for acute treatment in
pregnant patients with SVT when adenosine is ineffective or contraindicated.
IIb
Intravenous procainamide may be reasonable for acute treatment in pregnant
patients with SVT.
IIb
Intravenous amiodarone may be considered for acute treatment in pregnant
patients with potentially life-threatening SVT when other therapies are
ineffective or contraindicated.

73. SVT with Pregnancy – Acute Treatment
COR Recommendations
IIa
The following drugs, alone or in combination, can be effective for ongoing
management in pregnant patients with highly symptomatic SVT:
a. Digoxin
b. Flecainide
c. Metoprolol
d. Propafenone
e. Propranolol
f. Sotalol
g. Verapamil
IIb
Catheter ablation may be reasonable in pregnant patients with highly
symptomatic, recurrent, drug-refractory SVT.
IIb
Oral amiodarone may be considered for ongoing management in pregnant
patients when treatment of highly symptomatic, recurrent SVT is required and
other therapies are ineffective or contraindicated.

74. Atrial Fibrillation
The most common sustained cardiac arrhythmia.
AF is an arrhythmia characterized by chaotic impulses propagating in different directions and
causing disorganized atrial depolarization without effective atrial contraction
In patients with poor ventricular function or valve disease, it may precipitate or aggravate
cardiac failure.
Irregularly irregular rhythm. No P waves. Absence of an isoelectric baseline.
Variable ventricular rate. QRS complexes usually < 120 ms unless pre- existing bundle branch
block, accessory pathway, or rate related aberrant conduction.
Fibrillatory waves may be present.
Ashman’s Phenomenon – presences of aberrantly conducted beats, usually of RBBB
morphology, due a long refractory period as determined by the preceding R-R interval.
Commonly AF is associated with a ventricular rate ~ 110 – 160.
AF is often described as having ‘rapid ventricular response’ if the ventricular rate is > 100/m.
‘Slow’ AF is a term often used to describe AF with a ventricular rate < 60/m.

76. Common causes of AF
Coronary artery disease (including acute MI)
Valvular heart disease, especially rheumatic mitral valve disease
Hypertension
Sinoatrial disease
Hyperthyroidism
Alcohol
Cardiomyopathy
Congenital heart disease
Acute chest infection
Pulmonary embolism
Pericardial disease
Idiopathic (lone atrial fibrillation): are 60 years of age or younger.

77. Pathogenesis
Recent theories suggest that it is due to multiple re-entrant wavelets conducted between the
Right & Left atria.
Initiators: It is now known that foci of rapid ectopic activity, often located in muscular sleeves
that extend from the left atrium into the proximal parts of pulmonary veins, play a pivotal role
in the initiation of AF.
Triggers: Sympathetic ganglia situated in the vicinity of PVs are acting as triggering factors
for AF.
Substrate: Both experimental and human mapping studies have demonstrated that persistent
AF is generally characterised by the presence of multiple wavelets of excitation that propagate
around the atrial myocardium.
Perpetuation of AF is facilitated by the existence or development of an abnormal atrial tissue
substrate capable of maintaining the arrhythmia
Electrophysiological remodelling: AF in itself can cause progressive changes in atrial
electrophysiology such as substantial refractory period shortening, which further facilitate
perpetuation of the arrhythmia.

83. DO NOTs in AF management:
Do not use antiplatelet therapy for stroke prevention in AF.
Do not permanently discontinue oral anticoagulation in AF patients at increased
risk of stroke unless such a decision is taken by a multidisciplinary team.
Do not use rhythm control therapy in asymptomatic AF patients, nor in
patients with permanent AF.
Do not perform cardioversion or catheter ablation without anticoagulation, unless
an atrial thrombus has been ruled out by trans -oesophageal echocardiogram.

91. Rhythm control

94. Heparin-Induced Thrombocytopenia
A decrease in the platelet count of more than 50% from the highest platelet count value after the
start of heparin
An onset 5 to 10 days after the start of heparin
Hypercoagulability
Presence of heparin-dependent, platelet-activating IgG antibodies(PF4 antibody)
A strongly positive test for Antibody against PF-4 would strongly support the diagnosis of HIT
Type 1 HIT is a mild, transient decrease in platelet count that occurs during the first few days of
heparin exposure due to platelet agglutination.
This form is benign, and the platelet count will return to normal while heparin is
continued.
Type 2 HIT, an antibody-mediated thrombocytopenia that is associated with a high risk of
developing thrombosis.
An onset 5 to 10 days after the start of heparin.

95. Initiation of long term rhythm control

114. Regular wide complex tachycardia includes:
1.Ventricular tachycardia (VT)
2 Supraventricular tachycardia (SVT) with aberrancy
3 Preexcited tachycardia.
Irregular wide complex tachycardia includes:
• Atrial fibrillation with pre-excitation.
• Atrial fibrillation with BBB.
• Atrial flutter with BBB.
• Multifocal Atrial Tachycardia with BBB.
Differential Diagnosis: ECG Diagnosis – points to be seen:
AV dissociation.
Width of the QRS complex.
QRS axis in the frontal plane.
Morphology of the QRS complex.
ECG during sinus rhythm.
Vagal manoeuvres

115. Ventricular Tachycardia
Most common cause of wide complex tachycardia.(80%)
Major cause of morbidity and mortality in patients with structural heart disease.
Major cause of sudden cardiac death –60 % cases on Holter monitoring.
Relatively organized tachy-arrhythmias with discrete QRS complexes.
Diagnosis still a challenge ….on presentation.
Reentry is the most common mechanism.
Recurrence is more common in less than one year of onset.
ICD implantation is the absolute indication as primary prevention in presence of
LVEF <35%.

116. Definition
The occurrence of three or more VPCs with a rate of > 100 bpm in succession is called as VT.
Non sustained is termination of VT by self less than 30 sec.
Sustained VT is presence of VT for > 30 sec. or hemodynamically unstable.
Slow VT –HR >100 < 120 bpm.
Pulseless VT – VT with hemodynamic collapse that requires DC cardioversion.
Refractory VT –that does not revert to sinus rhythm on medication use or use of three shocks.
VT storm --- > Two VT episodes in 24hrs, requiring the DC shocks/ICD shocks .
Rate is 100—300 bpm

117. Etiology Reversible causes of VT
Acute MI
After chronic infarction
Ischaemic heart disease
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Post CABG
Post TOF surgery
Electrolyte abnormalities
Idiopathic
Specific etiology-- genetic
Hypoxia
Hyperthyroidism
catecholamines
Hypokalemia
Metabolic acidosis
Hypomagenesemia
Hypocalcemia
Drugs
Alcohol
Starvation

118. Monomorphic VT and Polymorphic VT
MONO MORPHIC VT POLYMORPHIC VT
1. Stable tachycardia Unstable, dynamic
2. Reproducible, recurrent phenomenon Less reproducible
3. Initiated by pacing, programmed
ventricular stimulation
Not reliably initiated
4. Normal hearts/structural heart
disease
Acute ischemia, myocarditis, drugs
5. Reentry circuit Pause dependent VT, Triggering
6. Hemodynamically stable Hemodynamically unstable
7. MVT—PVT—VF/VFL PVT—VF/VFL
8. Catheter ablation, pacing, AAD BBs, pacing…/ablation?

119. Monomorphic VT with RBBB morphology.

120. Clinical features Diagnosis
Asymptomatic
May have palpitations –
transient, sustained.
Chest pain – angina
Syncope
Presyncope
Dizziness
Cannon a waves
Absent pulse
Hypotension
Variable s 1
AV dissociation (capture, fusion beats)
QRS duration>140 ms for RBBB type morphology in V1:
QRS duration>160 ms for LBBB type morphology in V1.
Frontal plane axis ---90 to 180
Delayed activation during initial phase of QRS complex:
LBBB pattern –R wave in V1, V2 >40 ms
RBBB pattern –onset of R wave to nadir of S wave > 100 ms
Bizzare QRS pattern that does not mimic typical RBBB or
LBBB type QRS complex
concordance of QRS complex in all precordial leads.
RS or dominant S in V6 with RBBB morphology
Q wave in V6 with LBBB morphology
Monophasic R or biphasic qR or rS in V1 with RBBB
morphology

122. SUPRAVENTRICULAR TACHYCARDIA VENTRICULAR TACHYCARDIA
Aberrant QRS pattern that matches exactly that of the
wide complex rhythm.
not in morphology of LBBB, RBBB,
wide complexes present
Presence of p wave before QRS complex P waves and QRS complexes are
dissosciated.
Preexcited QRS pattern on Sinus Rhythm
ECG indicates atrial arrhythmia—AFL, focal AT,
antidromic macro re-entrant tachycardia.
Bizzare QRS complex
Responds to vagal Maneuver, Valsalva, adenosine Not so
Verapamil effective Worsens the LV dysfunction
SUPRAVENTRICULAR and VENTRICULAR TACHYCARDIA

124. Positive concordance in VT:
Negative concordance of VT:

125. Brugada sign, Rabbit ear sign

130. Initiation of VT BY VPCs

131. Torsades de pointes due to

132. Idiopathic Monomorphic VT

133. Acute Management of VT
In patients in cardiac arrest, CPR should be performed according to published Basic and
Advanced Cardiac Life Support algorithms.
In patients with hemodynamically unstable VT that persist or recur after a maximal energy
shock, intravenous amiodarone should be administered to attempt to achieve a stable rhythm
after further defibrillation.
Patients presenting with VT with hemodynamic instability should undergo direct current
cardioversion.
In patients with polymorphic VT or VF with ST elevation MI, angiography with emergent
revascularization is recommended.
Patients with a wide-QRS tachycardia should be presumed to have VT if the diagnosis is unclear.

134. In patients with hemodynamically stable VT, administration of intravenous procainamide can
be useful to attempt to terminate VT .
In patients with a witnessed cardiac arrest due to VF or polymorphic VT that is unresponsive to
CPR, defibrillation, and vasopressor therapy, intravenous lidocaine can be beneficial.
In patients with polymorphic VT due to myocardial ischemia, intravenous beta blockers can be
useful.
In patients with a recent MI who have VT/VF that repeatedly recurs despite direct current
cardioversion and antiarrhythmic medications (VT/VF storm), an intravenous beta blocker can
be useful.
In patients in cardiac arrest, administration of epinephrine (1 mg every 3 to 5 minutes) during
CPR may be reasonable.

137. Sustained
Monomorphic VT
Direct current
cardioversion &
ACLS
UnstableStable
Hemodynamic
stablility
12-lead ECG,
history & physical
Cardioversion
(Class I)
IV amiodarone or
sotalol
(Class IIb)
Therapy guided
by underlying
heart disease
IV procainamide
(Class IIa)
VT
termination
Catheter ablation
(Class I)
Consider disease
specific VTs
Structural
heart disease
Therapy to prevent
recurrence preferred
VT
termination
Verapamil sensitive VT* : verapamil
or
Outflow tract VT: beta blocker
for acute termination of VT
(Class IIa)
Cardioversion
(Class I)
Yes
Sedation/anesthesia,
reassess antiarrhythmic
therapeutic options,
repeat cardioversion
No
VT
termination
No
Yes No
No
Catheter ablation
(Class I)
Verapamil or
beta blocker
(Class IIa)
Typical ECG
morphology for
idiopathic VA
Cardioversion
(Class I)
Effective No
Yes
Yes
Yes

140. Primary and Secondary Prevention of VT
In patients with LVEF of 35% or less that is due to ischemic heart disease who are at least 40
days’ post-MI and at least 90 days post revascularization, and with NYHA class II or III HF
despite GDMT, an ICD is recommended if meaningful survival of greater than 1 year is expected.
In patients with LVEF of 30% or less that is due to ischemic heart disease who are at least 40
days’ post-MI and at least 90 days post revascularization, and with NYHA class I HF despite
GDMT, an ICD is recommended if meaningful survival of greater than 1 year is expected.
In patients with ischemic heart disease who either survive SCA due to VT/VF or experience
hemodynamically unstable VT or stable VT not due to reversible causes, an ICD is recommended
if meaningful survival greater than 1 year is expected.
In patients with ischemic heart disease and unexplained syncope who have inducible sustained
monomorphic VT on electrophysiological study, an ICD is recommended if meaningful survival
of greater than 1 year is expected.

142. Secondary prevention in
pts with IHD
Revascularize
& reassess
SCD risk
(Class I)
No
LVEF≤35%
Yes
EP study
(Class IIa)
No
Extended
monitoring
ICD
(Class I)
GDMT
(Class I)
Ischemia
warranting
revascularization
Yes
ICD candidate║
No
ICD
(Class I)
Yes
Inducible
VT
NoYes
SCA survivor*
or sustained
spontaneous
monomorphic VT*
Cardiac syncope†
ICD
(Class I)

143. Some special form of Ventricular Tachycardia
Idiopathic Outflow Tract VT or Adenosine sensitive VT:
No structural heart disease. RV 80%, LV 20%. More in women.
Not associated with SCD. Symptoms on exercise, stress, caffeine ingestion.
Hemodynamically stable and nonsustained IV BBs useful in termination
BBs and CCBs are for chronic therapy
Catheter ablation in resistant cases.
Calcium dependent triggered activity.
Large monophasic R waves in inferior leads.
LBBB pattern in V1 –RVOT
RBBB pattern in V1 ---LVOT

144. Fascicular VT or verapamil sensitive VT:
Second most common.
Macro re-entry involving calcium dependent slow response fibres.
Narrow RBBB+ LAD ---posterior fascicles
Narrow RBBB+RAD – anterior fascicles
Unique nature –suppression by verapamil
Catheter ablation therapy effective.
Bundle branch re-entrant VT:
Macro reentry circuit
Antegrade direction down the right branch
Retrograde up the left posterior or anterior fascicles/LBB
Mimic RV pacing with LBBB pattern, leftward superior axis.
Readily amenable to catheter ablation therapy.
Coupled with ICD due to risk of SCD.

145. Arrhythmogenic RV dysplasia:
Genetically determined dysplastic process or after a suspected viral myocarditis.
Sporadic nonfamilial nondysplastic is more common.
ECG:
Epsilon wave (most specific finding, seen in 30% of patients)
T wave inversions in V1-3 (85% of patients)
Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
Localized QRS widening of 110ms in V1-3
Paroxysmal episodes of ventricular tachycardia with a LBBB morphology
Treatment:
ICD treatment of choice.
Catheter ablation
Beta blockers with other antiarrhythmic drugs.

147. REPOLARIZATION SYNDROMES:
1. ST-segment elevation
a.Early repolarization pattern(elevated J point)
b.Brugada syndrome
2. QT-interval abnormalities
a.Short QT syndromes
b.Long QT syndromes
Early repolarization pattern:
Type 1: The ERP only in the lateral leads= benign outcome=young, healthy men.
Type 2: ERP = inferior or inferolateral leads and is associated with moderate risk of
Arrhythmic SCD, especially in individuals with syncope and personal or F/H of SCD.
Type 3: ERP = globally =inferior+ lateral+ right precordial leads /highest risk of malignant
ventricular arrhythmias, VT/VF storms, and sudden death.

149. BRUGADA SYNDROME:
RBBB, ST-segment elevation and T inversion.
sudden cardiac death in up to 20%.
Type 1 pattern: is characterized by J-point or coved
ST-segment elevation 2 mm followed by a negative
T wave in V1.
Type 2 pattern: is characterized by J-point or saddle-shaped
ST segment elevation 2 mm followed by positive or biphasic
T wave in V1.
Type 3 pattern: is characterized by coved or saddle-shaped
ST-segment elevation 1 mm.

150. Occurs in the setting of digoxin use, the signature VT of digoxin toxicity—triggered activity
—calcium overload, inhibition of Na, K pump
Originates from LBB anterior and posterior fascicles –alternating change in axis

151. Ventricular fibrillation (VF)
A condition in which many electrical signals are sent from the ventricles at a very fast and
erratic rate.
As a result, the ventricles are unable to fill with blood and pump.
This rhythm is life-threatening because there is no pulse and complete loss of consciousness.
The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes
A person in VF requires prompt defibrillation to restore the normal rhythm and function of
the heart.
It may cause sudden cardiac death.
Basic and advanced cardiac life support is
needed
Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of
these survivors of ventricular Fibrillation

152. Ventricular Fibrillation

153. Bradyarrhythmias

154. The Pacemakers

155. Sinus Bradycardia:
Physiological variant due to strong vagal tone or athletic training.
Rate as low as 50 at rest and 40 during sleep.
Common causes of sinus bradycardia include:
Extrinsic causes: Hypothermia, hypothyroidism, cholestatic jaundice and raised ICP.
Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs.
Intrinsic causes: Acute ischaemia and infarction of the sinus node (as a complication of acute
myocardial infarction).
Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick
sinus syndrome).

156. Sick-Sinus Syndrome
Syndrome encompassing a number of sinus nodal abnormalities.
The abnormalities can be:
Persistent spontaneous sinus bradycardia not caused by drugs.
Sinus arrest(pause) or exit block
Combinations of SA and AV node conduction disturbances
Bradycardia-tachycardia syndrome
More than one of these conditions can be recorded in the same patient on different
occasions.
Clinical features:
May be completely Asymptomatic
Sinus bradycardia may present with symptoms such as hypotension, Syncope, presyncope,
fatigue and weakness
Patients with SSS may develop signs and symptoms of heart failure
Patients with SSS are also at risk of developing thromboembolism

158. Sinus pause or arrest
In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing function. If failure is
brief and recovery is prompt, the result is only a missed beat (sinus pause). If recovery is
delayed and no other focus assumes pacing function, cardiac arrest follows.

159. SA node Exit Block
Intermittent failure of conduction from the SA node.
First degree SA block: Prolonged SA conduction time(non-detectable on EKG;
no missing P waves)
Type I second degree SA block: Progressive prolongation of SA node conduction with
intermittent failure of the impulses originating in the Sinus node to conduct to the surrounding
atrial tissue
Type II second degree block there is no change in SA node conduction before the pause.
Third degree SA block results in absence of P waves on the ECG.

160. Wandering atrial pacemaker
As the heart rate slows, the P waves become inverted and then gradually revert toward normal
when the heart rate speeds up again.
The PR interval shortens to 0.14 second with the inverted P wave and is 0.16 second with the
upright P wave.
This phasic variation in cycle length with varying P wave contour
suggests a shift in pacemaker site and is characteristic of a wandering atrial pacemaker

161. Tachy-Brady Syndrome

162. Diagnostic Testing
SA nodal dysfunction is most commonly a clinical or electrocardiographic diagnosis.
The diagnostic modalities used are:
Resting ECG
Holter monitors
Implantable ECG monitors
Exercise testing
Autonomic Nervous system testing
Electrophysiologic testing:
•SNRT(Sinus Node Recovery Time) This is defined as the longest pause after cessation of
overdrive pacing of the right atrium near the SA node( normal: <1500 ms or corrected for
sinus cycle length, <550 ms)
•SACT( Sino-Atrial Conduction Time) This is defined as one half the difference between the
intrinsic sinus cycle length and a non-compensatory pause after a premature atrial stimulus(
normal<125 ms)

163. Treatment
Exclusion of the Extrinsic causes of SA node dysfunction.
Pacemaker Implantation: This is the primary therapeutic intervention in patients with
symptomatic SA nodal dysfunction.
Pharmacotherapy:
IV Isoproterenol
IV Atropine
Theophylline
Orciprenaline

167. Hypersensitive Carotid Sinus Syndrome
A. Right carotid sinus massage (RCSM, arrow ) results in sinus arrest and a ventricular
escape beat (probably fascicular) 5.4 seconds later.
Sinus discharge then resumes.
B. Carotid sinus massage (CSM, arrow; monitor lead) results in slight sinus slowing but,
more important, advanced AV block.

168. AV blocks in CAD
CAD may produce transient or persistent AV block.
In acute MI AV block develops transiently in 10-25% patients.
Most commonly the AV block is first or second degree block.
Second degree and higher grade AV blocks occur more often in inferior than anterior acute MI.
Acute anterior MI is associated with block in the distal AV nodal complex, His bundle or bundle
branches and results in wide complex, unstable escape rhythms and a worse prognosis with high
mortality rates.

169. First degree heart block
P wave precedes QRS complex but P-R intervals prolong (>5 small squares)
and remain constant from beat to beat

170. Second degree heart block
1. Mobitz Type I or Wenckenbach phenomenon:
Runs in cycle, first P-R interval is often normal.
With successive beat, P-R interval lengthens until there will be a P
wave with no following QRS complex.
The block is at AV node,
often transient, maybe asymptomatic.

171. Second degree heart block
2. Mobitz Type 2:
P-R interval is constant, duration is normal.
Periodically, no conduction between atria and ventricles- producing a wave with no
associated QRS complex. (blocked p wave).
The block is most often below AV node, at bundle of His Bundle or Bundle Branch.
May progress to third degree heart block.

172. Third degree heart block (Complete heart block)
No relationship between P waves and QRS complexes
An accessory pacemaker in the lower chambers will typically activate the
ventricles- escape rhythm.
Atrial rate= 60-100bpm.
Ventricular rate based on site of escape pacemaker.
Atrial and ventricular rhythm both are regular.

176. IVCD
RBBB WITH LAFB
RBBB WITH LPFB
TRIFASICULAR BLOCK

177. Class I
Intermittent third-degree AV block.
Type II second-degree AV block.
Class IIa
Alternating bundle branch block.
HV interval ≥100 msec in asymptomatic patient.
EPS of pacing-induced infra-His block that is not physiological.
Class IIb
Neuromuscular diseases with any degree of fascicular block.
Guidelines for Permanent Pacing in Chronic Bi and Tri-fascicular

182. THANK
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