ECG

1. TACHYARRYTHMIAS
Presentation by :- Dr. Ajay T Raj
2nd Year Resident
Dept. of Internal Medicine

2. INTRODUCTION
 The only normal rhythm of the heart is a normal sinus rhythm.
 An impulse is generated in the sinoatrial (SA) node, which is
conducted through and slowed down while passing through
the atrioventricular node (AV).
 It is then conducted through the bundle of His, to the left and right
bundle branches, and eventually into the Purkinje fibers

3. CARDIAC CONDUCTION SYSTEM
Sinoatrial
(SA) node
Atrioventricular
(AV) node
Right bundle
branch
Bundle
of His
Left bundle
branch
Left anterior
fascicle
Left posterior
fascicle

4. THE NOMENCLATURE
Waves are the positive/negative deflections.
Segment is a straight line connecting 2 waves.
Interval consist of at least one wave plus the connecting line.
P wave - Atrial depolarization
PR interval - Start of atrial depolarization to start of
ventricular depolarization
QRS complex - Ventricular depolarization
ST segment - Pause in ventricular electrical activity before
repolarization
T wave - Ventricular repolarization
QT interval - Total time taken by ventricular depolarization
and repolarization
U wave - Uncertain, possibly:
interventricular septal repolarization
slow ventricular repolarization

5. SINUS RHYTHM
Sinus rhythm is the normal cardiac rhythm, in which the SA node acts
as the natural pacemaker, discharging at a rate of 60–100/min. The
characteristic features of sinus rhythm are:
• Heart rate is 60–100/min.
• P wave morphology is normal (e.g. upright in lead II and inverted
in lead aVR).
• Every P wave is followed by a QRS complex.

6. TACHYARRYTHMIAS
Arrhythmia is an abnormal rhythm of the heart
Tachyarrhythmia is defined as an abnormal rhythm with a
heart rate of 100 beats per minute or more.

7. CLASSIFICATION BASED ON ORIGIN OF ARRYTHMIA
 Supraventricular Tachycardia (SVT): Arrhythmia originating from above the AV
node (from atrial origin or AV junction origin).
• Atrial fibrillation (AFib)
• Atrial flutter
• Atrial tachycardia
• Atrial premature complex (PAC)
• Atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tachycardia (AVRT)
• AV junctional extrasystoles
 Ventricular Tachycardia (VT): The origin of the arrhythmia is below the AV
node.
• Ventricular fibrillation (V-fib)
• Ventricular premature beats (PVC)
• Ventricular tachycardia (sustained or non-sustained)

9. MECHANISMS OF TACHYARRYTHMIA GENERATION
1. Enhanced Automaticity- Can be normal (sinus tachycardia), or abnormal
(focal AT and MAT, junctional tachycardia, ventricular tachycardia-ischemic
VT)
2. Triggered Activity- Early after depolarization and late after depolarization
(catecholamine sensitive arrythmias – Sympathetic VT)
3. Re-Entry – premature atrial/ ventricular complex
1. Micro – re entry circuit – AV NRT, Brugada Syndrome, AF
2. Macro – re entry circuit – AV RT, Atrial Flutter. Scar VT
NOTE:- ONE ARRYTHMIA CAN HAVE MORE THAN ONE MECHANISM

10. SINUS TACHYCARDIA
Sinus tachycardia is sinus rhythm with a
• Heart rate is greater than 100/min.
• P wave morphology is normal and every P
wave is followed by a QRS complex.
• Physiological causes can be anxiety, pain,
fear, fever or exercise.
• Other causes :
1. Drugs (e.g. adrenaline, atropine,
salbutamol inhalers and nebulizers),
caffeine and alcohol
2. ischemic heart disease and acute
myocardial infarction
3. heart failure
4. pulmonary embolism
5. fluid loss
6. anemia
7. hyperthyroidism

11. ATRIAL TACHYCARDIA
 Structurally abnormal heart
 In this, impulses are generated by an ectopic focus somewhere
within the atrial myocardium other than the sinus node
 Because of either increased automaticity (m/c), triggered activity or
a re-entry circuit.
 It can be focal (arising from one small focus in the atria) or
multifocal (arising from three or more foci), and can be paroxysmal
or sustained.
 Atrial rate is usually 100–250/min
 Isoelectric baseline between 2 P waves
 Abnormally shaped P waves
 Warm up and cool down Phenomenon – rate will slowly increase
and decrease

12. Multifocal atrial tachycardia
inverted P waves (in lead II) indicating an atrial rhythm arising from near the AV node.

13. ATRIAL FLUTTER
 m/c post op arrythmia
 It is characterized by a macro re-entry circuit, typically within the
right atrium. Usually occur in relation to an area of scar tissue (prior
cardiac surgery).
 In atrial flutter the atrial rate is usually 250–350/min and often
almost exactly 300/min (it takes about 0.2 s for the impulse to
complete a circuit in the right atrium). The AV node cannot
normally keep up with such a high atrial rate and AV block occurs.
 Atrial rate around 300/min
 ‘Sawtooth’ waves
 AV block (commonly 2:1, but can be 3:1, 4:1 or variable)

15. Treatment of Atrial Flutter
1. DC Cardioversion with 50J initially and 100J (if required) is
the treatment of choice
2. Ibutilide is also effective
3. Catheter ablation – site- Cavo-tricuspid isthmus

16. ATRIAL FIBRILLATION
 AF is rapid, chaotic depolarization occurring throughout the atria as a
consequence of multiple ‘wavelets’ of activation.
 Risk factors – increasing age, hypertension, any cardiac disease and lung
disease, CKD, OSAS, Psoriasis, Alcoholism, Thyrotoxicosis, hypo K, hypo Mg
 Characteristic ECG features are: Absence of distinct P waves, Irregularly
irregular ventricular rhythm
 ECG baseline consists of low-amplitude oscillations (fibrillation or ‘f’ waves)
 Around 400–600 impulses reach the AV node every minute, but not all are
transmitted to the ventricles. Therefore, ventricular rate can be fast, normal or
even slow.

18. Types of AF
1. Permanent AF – a/w structural heart disease, usually there is LA
dilatation more than 4cm, here we go for rate control
2. Paroxysmal AF – any self terminating AF /cardioverted AF within 7
days
3. Persistent AF - >7 days
4. Long standing persistent AF - >1year
MS and Prosthetic Mitral valve associated AF is called VALVULAR
AF
AF is associated with stasis of blood – hence there is risk for
Embolic CVA

19. Management of AF
1. Hemodynamically Unstable – Synchronized Cardioversion –
200 J
2. Hemodynamically Stable – if LA dilated >4cm – go for rate
control, if LA not dilated then rhythm control
if AF <48hrs- no risk for embolism – rhythm control
DOC is Vernakalent, Others Ibutilide, Amiodarone
if AF >48 hrs – high risk for embolism – do a TEE/ Cardiac CT
3. If in TEE there is a clot  3 weeks of anticoagulation f/b
rhythm control f/b 4 weeks of anticoagulation  then
calculate CHADS2 VaSC score- if high then go for long term anti
coagulation (Daibigatran)

22. HAS-BLED Score for Major Bleeding
Risk
Estimates risk of major bleeding for patients on anticoagulation to assess
risk-benefit in atrial fibrillation care

23. AV RE-ENTRY TACHYCARDIA
 Seen in Wolff-Parkinson-White (WPW) - An accessory pathway exists
between atria and ventricles, known as Bundle of Kent.
 Short PR interval (<0.12 s)
 Rare
 Delta wave (a slurred early upstroke of the QRS complex  ventricular pre-
excitation)
 Two Types –
1. Orthodromic AVRT- impulses travel atria  AV node  bundle of Kent
(Narrow QRS)
2. Antidromic AVRT – impulses travel via atria  Bundle of Kent  AV node
(Wide QRS tachycardia)
Accessory
pathway
Delta
wave

25.  Two types of AVRT –
 1 – Typical
 2 – Atypical – here there is a very slow retrograde pathway, p wave lies just
before QRS complex (D/D atrial tachycardia)
MANAGEMENT OF AVRT
 Hemodynamically UNSTABLE – dc SHOCK 50J
 Hemodynamically Stable –
1. Vagal Maneuvers – carotid sinus massage, occulo sinus massage, Valsalva
maneuver
2. Adenosine , BB, CCB

26. AV NODAL RE-ENTRY TACHYCARDIA
 narrow complex tachycardia, with regular R-R interval
 P wave absent
 Ventricular rate usually 180–250/min
 Can occur in a structurally normal heart
 m/c in females
 a/w good prognosis

27. Slow
pathway
Fast
pathway
Slow
pathway
Refractory
fast pathway
Slow
pathway
Fast
pathway
Atrial ectopic
beat
In AV node there are 2 pathways
1- Fast Pathway – Long refractory period
2- Slow Pathway – short refractory period
Normally only one impulse activates the ventricles, in AVNRT there is a premature
supraventricular impulse – this impulse is timed in such a way that the short
pathway has recovered from refractory period and fast pathway is in refractory
period.
Impulse activates the atria retrograde, in 2/3 patients p wave formed at the same
time of qrs complex – atria and ventricles activated at the same time

28.  AVNRT is of 2 types-
1. Typical AVNRT – 95% - slow-fast – triggered by premature
supraventricular complex -(m/c atrial)
 In 2/3 of patients atria and ventricles are activated at the same time
hence no p wave
 In 1/3 of patients atria and ventricles are not activated at the same time
hence p wave can be seen – PSEUDO s WAVE (II) / PSEUDO r’ WAVE (V1)
2. Atypical AVNRT – 5% - fast-slow – triggered by Premature ventricular
complex this is a D/D for atrial tachycardia

30. MANAGEMENT OF AVNRT
 Hemodynamically UNSTABLE – dc SHOCK
 Hemodynamically Stable –
1. Vagal Maneuvers – carotid sinus massage, occulo sinus massage,
Valsalva maneuver
2. Adenosine , BB, CCB
3. Long term prevention – BB/CCB, or ablation of pathways

31. AVNRT VS AVRT
 In AVRT atria and ventricles are 2 different circuits – synchronous
activation will not happen, but in AVNRT synchronous activation
can happen
 P wave will be outside QRS complex in AVRT
 R-P interval (>80 ms in AVRT but <80ms in AV-NRT)

32. BROAD QRS TACHYARRYTHMIAS
 Impulses generated from ventricles –
 Rate 15- 40  idioventricular rhythm
 Rate 40 – 100  Accelerated Idioventricular rhythm
 Rate >100  Ventricular Tachycardia

33. VENTRICULAR PREMATURE COMPLEX (VPC)
 Also called as Extrasystole
 Premature discharge arising from ventricles, occurs earlier than next
sinus beat
 No P wave seen before VPC
 Wide QRS with ST- T changes
 Coupling Interval – distance between a VPC and preceding QRS
complex will be constant (VPC with different coupling intervals is called
Parasystole)
 Compensatory Pause – Distance btw 2 sinus impulse across VPC is
same as the distance btw 2 sinus impulses across a normal beat or one
sinus P-wave is not able to reach the ventricles because they are
still refractory from the VPC

38.  When VPCs arise after every sinus beat – Ventricular Bigeminy
 When VPCs arise after every 2 sinus beats – Ventricular Trigeminy
 2 VPC occurring in a row – Pair/ Couplet
 3 or more VPC occurring in a row - VT

39.  Clinically – VPCs are usually asymptomatic but can be associated
with palpitations
 Treatment – Use of antiarrhythmics in isolated VPCs are not
recommended
 But VPCs – if occuring frequently, multifocal, bigeminy, >40yrs,
parasystole  more chance of VT

40. VENTRICULAR TACHYCARDIA
 VT is a broad-complex tachycardia, defined as three or more successive
ventricular beats at a heart rate above 100 beats/min and with a broad QRS
complex >0.16sec.
 VT arises most commonly due to a re-entry circuit around an area of myocardial
scarring, increased automaticity of a specific ventricular focus and abnormal
triggering.

41. VT can be described as:
Non-sustained (self-terminating in <30sec)
Sustained (lasting >30sec, or requiring urgent termination
within 30sec due to hemodynamic compromise)
Monomorphic (arises from a single ventricular focus, and
has a uniform QRS morphology)
Polymorphic (with a changing focus and varying QRS
morphology).

42. Fusion beats appear when
the ventricles are activated
by an atrial impulse and a
ventricular impulse
arriving simultaneously.
 Capture beats occurs when
an atrial impulse manages to
‘capture’ the ventricles for a
beat, causing a normal QRS
complex, which may be
preceded by a normal P
wave. There is one normal
QRS complex

44. BRUGADA CRITERIA FOR VT VS SVT WITH BBB
1. ABSENCE OF RS COMPLEX IN V1 TO V6
2. RS COMPLEX DURATION >100MS
3. AV DISSCOCIATION

45. POLYMORPHIC VENTRICULAR TACHYCARDIA
Varying QRS morphology. Polymorphic VT falls into two distinct categories based
upon the duration of the QT interval (measured during sinus rhythm):
• Polymorphic VT in the setting of a normal QT interval.
• Polymorphic VT in the setting of a prolonged QT interval (hypocalcemia, acute
myocarditis, long QT syndrome). It is commonly called torsades de pointes
(‘twisting of the points’).

46.  Polymorphic VT carries a risk of precipitating VF and so urgent
assessment is warranted.
 CONGENITAL POLYMORPHIC VT – LQTs- MANAGED BY BETA
BLOCKERS
 ACQUIRED POLYMORPHIC VT – CAUSED BY LOW K, LOW CA, LOW
MG, HYPOTHERMIA
Polymorphic VT is always unstable and requires
immediate defib- 200J and 2 g iv MGSO4 over 10min is
given

47. TREATMENT
 PULSELESS VT – ASYNCHRONISED CARDIOVERSION 200J
 HEMODYNAMICALLY UNSTABLE  SYNCHRONISED DC
CARDIOVERSION WITH 200 J
 HEMODYNAMICALLY STABLE 
 AMIODARONE – LV DYSFUNCTION – 150MG IV BOLUS OVER 10MIN
F/B 1MG/MIN X 6HRS F/B 0.5MG/MIN X 18HOURS
 PROCAINAMIDE – STRUCTURALLY NORMAL HEART
 LIGNOCAINE – POST MI

48. VENTRICULAR FIBRILLATION
• A chaotic rhythm without clearly discernible P waves, QRS complexes
or T waves.
• Classified as ‘coarse’ or ‘fine’ depending upon the amplitude of the
chaotic activity on the ECG.
• Untreated VF is a rapidly fatal arrhythmia and therefore requires
immediate diagnosis and treatment.

49. • Ventricular fibrillation can occur in :
Myocardial ischemia/infarction
Cardiomyopathy
Myocarditis
Electrolyte disturbances
Pro-arrhythmic drugs
Long QT syndrome
Cardiac trauma
Electrical shock
Treatment : According to ACLS Guidelines – shockable rhythm – 200J

50. CLASSIFICATION OF ANTIARRHYTHMIC DRUGS
(VAUGHAN WILLIAM CLASSIFICATION)

51. Classification based on Mechanism of Action
Na Channel Blocker : decrease slope of phase 0, further classified
based on action on K Channel-
Ia – blocks K channels eg Quinidine, Procainamide
Ib – opens K channels eg Lignocaine, Phenytoin
Ic – no effect on K channels eg Encainide, Flecainide, Propafenone
Beta Blockers eg Metoprolol, Esmolol
DOC for catecholamine induced arrythmia
K Channel Blocker eg Ibutilide, Amiodarone, Bretyllium
Ca Channel Blockers eg Verapamil, Diltiazem, Amlodipine,
Nifedipine
Others eg Adenosine, MgSO4, Atropine, Digoxin

52. TACHYCARDIOMYOPATHY
 caused by persistent SVT/VT
 it can be defines as atrial/ ventricular dysfunction secondary to
rapid/ asynchronous irregular myocardial contraction --- partially or
completely reversed after treatment of cause
 Heart rate normalization by rate or rhythm control is the main
therapy,

54. VT STORM
Ventricular tachycardia (VT) electrical storm (ES) is a severe
clinical condition characterized by clustering episodes of
ventricular arrhythmia in a short amount of time.
Occurrence of at least 3 distinct episodes of sustained VT or
ventricular fibrillation (VF) within the last 24-h or the
occurrence of incessant VT for at least 12-h

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