1. WELCOME

2. arrhythmias
Basil

3. arrhythmias

4. Properties of cardiac cells
Automaticity
• Ability to initiate an impulse spontaneously and
continuously.
Excitability.
• Ability to be electrically stimulated.
Conductivity
• Ability to transmit an impulse along a membrane in
an orderly manner.
Contractility
• Ability to respond mechanically to an impulse.

5. Pacemakers of the Heart
• SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
• AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker with
an intrinsic rate of 20 - 45 bpm.

6. Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

7. The “PQRST”
• P wave - Atrial
depolarization
• T wave - Ventricular
repolarization
• QRS - Ventricular
depolarization

8. The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)

9. The ECG Paper
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box - 0.5 mV

11. ECG Composed of Waves And Complexes
P- WAVE QT- INTERVAL
QRS- COMPLEX PR- INTERVAL
T- WAVE ST- SEGMENT

12. Criteria's of a normal heart rhythm
1. Presence of one upright and consistent-
appearing P wave before each QRS
complex.
2. P-R interval between 0.12-0.20 seconds
3. A consistent appearing QRS complex of
less than 0.12 seconds.
4. Consistent R-R interval
5. A heart rate between 60-100 beats/minute
6. The ST segment should be isoelectrical

13. Arrhythmias
• It is a disturbance in the
rhythmic patterns of the heart.
Results from abnormal
impulse initiation, abnormal
conduction or both mechanism
together.

14. Four Steps to Identify Arrhythmias
1- Begin by labeling the P wave, QRS
complex, T wave, PR interval, and QT
interval.
2- Calculate the atrial and ventricular heart
rates.
3- Determine if the rhythm is regular or
irregular.
4- Evaluate the waveform of the ECG in
detail for additional clues:

16. Mechanisms Of Arrhythmias
Arrhythmias result from
1-Abnormal impulse initiation and
2-Abnormal impulse conduction.

17. Mechanisms Of Arrhythmias
The major mechanisms of arrhythmias are
ABNORMAL IMPULSE INITIATION
Enhanced normal automaticity
Abnormal automaticity
Triggered activity due to afterdepolarization
ABNORMAL IMPULSE CONDUCTION
Conduction blocks
Reentry
1
2

18. Enhanced normal automaticity
• Automaticity is defined as the ability of a cell
to independently initiate an action potential.

19. Classification Of Arrhythmias
• Disorders of Impulse
Generation
• Disorders of Impulse
Conduction

21. II. Disorder of impulse conduction
• S.A. Block
• First degree AV Block
• Second Degree A.V.Block
» Mobitz type I
» Mobitz type II
• Third Degree or Complete A.V Block

22. Common causes
• Underline cardiac disease
• Sympathetic stimulation
• Vagal stimulation
• Electrolyte imbalance
• Hypoxia

23. Mechanism responsible for phase 4
depolarization
1. Decreased outward permeability to
potassium
2. Increased inward permeability to sodium
3. Reduced sodium pump activity
4. Increased inward permeability to calcium

24. Rhythms Originating in SA Node
SINUS BRADYCARDIA
• It is characterized by atrial and ventricular rates
of less than 60 beats/minutes.
• It occur gradually or suddenly for a brief period.
• It is usually a benign dysrhythmias and is
common among general population
• It is commonly seen in athletes and also be
associated with sleep

25. Sinus Bradycardia
CAUSES Stimulation
Carotid Sinus Massage
Increased vagal tone
 vomiting
 suctioning
 severe pain
 extreme emotions
Decreased sympathetic tone
Intra Occular Pressure
Valsalva maneuver

26. Disease Process
MI
Uremia
Raised ICP
Anorexia Nervosa
Hypothermia
Hypothyroidism

27. • Right and left Vagus nerve fibers of the
parasympathetic nerve system plays an
important role in the rate of impulse formation,
the speed of conduction and the strength of
cardiac contraction.
• Stimulation of the Vagus nerve causes a
decrease rate of firing of the SA node, slowed
impulse conduction of the AV node, and
decreased force of cardiac muscle contraction.

28. • Stimulation of the sympathetic nerve
system that supply the heart has essentially
the opposite effect on the heart.

29. Valsalva maneuver
• The Valsalva maneuver or Valsalva
manoeuvre is performed by moderately forceful
attempted exhalation against a closed airway,
usually done by closing one's mouth and
pinching one's nose shut.

32. • Variations of the maneuver can be used either in
medical examination as a test of cardiac function
and autonomic nervous control of the heart, or to
"clear" the ears and sinuses (that is, to equalize
pressure between them) when ambient pressure
changes, as in diving, hyperbaric oxygen therapy,
or aviation.
• The technique is named after Antonio Maria
Valsalva

33. The normal physiological response
consists of 4 phases
• Initial pressure rise: On application of
expiratory force, pressure rises inside the chest
forcing blood out of the pulmonary circulation
into the left atrium. This causes a mild rise in
stroke volume.

34. • Reduced venous return and compensation:
Return of systemic blood to the heart is impeded
by the pressure inside the chest. The output of the
heart is reduced and stroke volume falls. This
occurs from 5 to about 14 seconds in the
illustration. The fall in stroke volume reflexively
causes blood vessels to constrict with some rise in
pressure (15 to 20 seconds).

35. • This compensation can be quite marked
with pressure returning to near or even
above normal, but the cardiac output and
blood flow to the body remains low. During
this time the pulse rate increases.

36. • Pressure release: The pressure on the chest is
released, allowing the pulmonary vessels and
the aorta to re-expand causing a further initial
slight fall in stroke volume (20 to 23 seconds)
due to decreased left ventricular return and
increased aortic volume, respectively. Venous
blood can once more enter the chest and the
heart, cardiac output begins to increase.

37. • Return of cardiac output: Blood return to
the heart is enhanced by the effect of entry
of blood which had been dammed back,
causing a rapid increase in cardiac output
(24 seconds on). The stroke volume usually
rises above normal before returning to a
normal level. With return of blood pressure,
the pulse rate returns towards normal.

40. Drugs
Digitalis
Morphine sulfate
Sedatives
Beta-Blockers
Ca-Channel Blockers
Amiodarone

42. 30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia

43. Sinus Bradycardia
• Deviation from NSR
- Rate < 60 bpm

44. Sinus Bradycardia
• Etiology: SA node is depolarizing slower
than normal, impulse is conducted normally
(i.e. normal PR and QRS interval).

45. Management
Inj Atropine Sulphate is administered if
presented with hypotension, restless, chest
pain, other signs of hemodynamic changes
Decrease the Vagal stimulation
Avoid drugs which causes Bradycardia
Transcutaneous pacing
Dopamine
Epinephrine
Isoproterenol

46. Sinus Tachycardia
• It is characterized by an atrial and ventricular
rate of 100 beats/minute or more.
• Generally the upper limit of sinus tachycardia
is 160 beats/ minute.

47. Sinus Tachycardia
Causes
• Increased Sympathetic Stimulation
 Exercise
 Emotions/ excitement
 Fever
 Fear
 Acute pain
Any condition that require a higher
basal metabolism

48. Causes……..
• Hyper metabolic States
• Blood Loss
• Consumption of alcohol, caffeine and tobacco.
• Drugs like
Atropine
Dopamine
Dobutamine
Nor epinephrine
amphetamines

49. • It can be a short term compensatory response
to heart failure, anemia, hypovolemia, and
hypotension.
• Hyperthyroidism
Causes……..

51. Sinus Tachycardia

52. 130 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia

53. Sinus Tachycardia
• Deviation from NSR
- Rate > 100 bpm

54. Sinus Tachycardia
• Etiology: SA node is depolarizing faster
than normal, impulse is conducted
normally.
• Remember: sinus tachycardia is a response
to physical or psychological stress, not a
primary arrhythmia.

55. Management
• Treatment is directed at the cause
• Digitalis
• Beta-blockers
• Diltiazem
• Carotid Sinus Massage

56. Sinus Arrest/Sinus Pause
• Sinus node automaticity is depressed
• Impulses are not formed when expected
• No P wave or no QRS complex is generated
• Patient may feel palpitation from the
increased stroke volume that accompanies
the next beet after the pause.

57. Etiology
• Vagal Stimulation
• Hypoxia
• Myocardial ischemia
• Injury to SA node
• Carotid sinus sensitivity
• MI
• Drugs:- Digitalis, Beta-Blocker and Ca-
Channel Blockers

58. ECG Characteristics
• Rate- Normal unless sinus node fails to
form impulse
• Rhythm-Irregular
• P_waves- present when SA Node Initiates
• PR interval –normal if P waves present
• QRS –present, absent when arrest

60. Management
• Treatment is directed to the Cause
• Discontinue/withheld offending drugs
• Minimize Vagal Stimulation
• Inj Atropine sulphate
• Insertion of a permanent pacemaker

61. Sick Sinus Syndrome
• The term sick sinus syndrome is used to
describe the rhythm in which there is
marked sinus bradycardia, sinus pause or
periods of sinus arrest alternating with
paroxysms of rapid atrial arrhythmias.
• The term brady- tachy syndrome is
commonly used to describe the same
arrhythmias.

62. Causes
• Inflammatory cardiac disease.
• Cardiomyopathy
• Sclerodegenerative process involving both
the SA and AV node
• Drugs
beta-blockers
calcium-channel blockers
digitalis, amiodarone, and adenosine.

63. Etiologies of Sick Sinus Syndrome
More Common
Sinus node fibrosis
Atherosclerosis of the
SA artery
Congenital heart
disease
Excessive vagal tone
Drugs
Less Common
Familial SSS (due to
mutations in SCN5A)
Infiltrative diseases
Pericarditis
Lyme disease
Hypothyroidism
Rheumatic fever

64. ECG characteristics
• Rate :varies from bradycardiac to tachycardiac
rates depending on sinus node function and
presence of atrial tachy dysrhythmias
• Rhythm: irregular
• P waves : normal during sinus rhythm
• PR interval : may be normal depend upon the
state of AV conduction
• QRS complex: usually normal

65. Sinus bradycardia (rate of ~43 bpm) with
a sinus pause

66. Abrupt termination of atrial flutter with variable AV block,
followed by sinus arrest with a junctional escape beat.

67. Clinical manifestations
• Patients are usually elderly and present with
lightheadedness and/or syncope,
• but it can also manifest as
• angina,
• dyspnea,
• and palpitations.

68. Treatment
• Ing.Atropine sulphate for brady arrhythmias
• Atntiarrhyhmics like quinidine or
procainamide
• Permanent pacemaker insertion

69. Rhythms originating in atria

70. Atrial Tachycardia
It is rapid atrial rhythm at a rate of 120 to 250
b/min. It is due to rapid firing of an ectopic
foci present in the atria
Atrial tachycardia frequently occurs in
paroxysms.

71. Possible mechanisms of atrial Tachy
arrhythmias.
• Two groups of fundamentally different
mechanisms are responsible for producing
Tachy arrhythmias
• 1- those mechanisms based on some form of
abnormal impulse formation
• 2- based on a disorder of impulse conduction,
leading to circulating excitation or reentry.

72. Pathophysiology
• The spontaneous depolarization in the fibers
in the center of the sinus node is normally
the fastest, and therefore this depolarization
brings these fibers to a discharge before
others. Thus under normal conditions,
automaticity of the dominant pacemaker in
the center of the sinus node suppress the
subsidiary pacemakers in the atria.

73. • Abnormal impulse formation may be
defined as the generation of impulses by
fibers other than the dominant pacemaker
fibers in the centre of the sinus node
regardless of whether the abnormal
impulse is generated spontaneously or
induced by foregoing normal or abnormal
activities.

74. • Normal impulse formation is the occurrence
of a spontaneous depolarization before the
onset of an action potential, the so- called
diastolic depolarization.
• If depolarization occurs either during
repolarization or under special conditions
directly after repolarization the term
abnormal impulse formation may be used.

75. • There are some muscle fibers in the right
atrium close to the crista terminalis that have a
some characteristics of purkinje fibers (ie.
Relatively low resting potential and develops
spontaneous depolarization under certain
conditions)

76. Etiology
• RHD
• COPD
• Mitral valve Disease
• Acute MI
• Digitalis Toxicity
• Caffeine
• Tobacco
• Alcohol

77. ECG Characteristics
• Rate- 140-250/min,
• Rhythm- regular unless there is block
• P-wave- differ in configuration
• PR interval- may be shorter and difficult to
measure
• QRS- Usually normal

79. Signs and Symptoms
• Palpitation
• Light headedness
• Angina
• Syncope

80. Management
• Sedation to terminate the rate
• Carotid sinus massage
• Cardioversion if severe symptoms occurs
• Beta-blockers
• Radiofrequency catheter ablation of the
ectopic focus

81. Atrial Flutter
A rapid well-organized contraction of the atrium
at a rate of 200-350 contractions per minute
which is fired by ectopic foci present in the
atria.
Atrial flutter can be classified in to two types
type-1 which is the commonest one has an
atrial rate of 240-340 beats/ minute

83. Causes
• Mitral valve disease
• Pulmonary embolism
• Thoracic surgery
• Myocardial hypoxia
• Electrolyte disturbances
• Hypercalcaemia

84. ECG Characteristics
• Rate- Atrial 250 to 350b/min
Ventricular 150 to 200b/min
• Rhythm- Atrial Rhythm is regular
Ventricular may be irregular
• P waves- saw tooth appearance
• QRS- usually normal
• PR Interval not measurable

85. ATRIAL FLUTTER

86. 2:1 Atrial flutter

87. Signs and Symptoms
• Palpitation
• Chest pain
• Dizziness
• Blurred vision

88. Management
• Carotid Sinus Massage
• Digitalis
• Ca Channel Blockers
• Beta Blockers
• Synchronized Cardioversion if 1:1

89. ATRIAL FIBRILLATION
• Atrial fibrillation is an extremely
rapid and disorganized pattern of
depolarization in the atria where the
rate is 400 to 600b/min.

90. Atrial fibrillation
Showing multiple ectopics
Firing erratically

91. Causes
• Coronary Artery Diseases
• Atrial enlargement
• Valve diseases
• Sick sinus syndrome
• Pericarditis
• Lung disease
• Congenital heart defects
• Thyrotoxicosis

92. ECG Characteristics
• Rate- atrial- 400 to 600b/min
ventricular- 110 to160b/min
• Rhythm- irregular
• P wave- not present. Atrial
activity is chaotic.
• PR Interval- not measurable
• QRS- Usually normal

93. ATRIAL FIBRILLATION

94. Management
• Cardioversion if
Hemodynamically unstable
• Inj Dilitiazem
Verapmil
Beta-blockers
• Anticoagulation if fibrillation is
chronic

95. Complication
• Mural Thrombi
• Pulmonary Emboli
• CHF

96. VENTRICULAR
ARRHYTHMIAS
• PREMATURE VENTRICULAR
CONTRACTION
• VENTRICULAR TACHYCARDIA
• VENTRICULAR FIBRILLATION

97. Premature Ventricular Contraction
• Premature contraction that is
generated by the ectopic foci
present in the ventricles. Which
fires independently.

98. Premature ventricular contraction

99. Etiology
• Ischemia or MI
• Hypoxia
• Hypokalemia
• Digitalis toxicity
• Acidosis
• Hyper metabolic states

100. P V C s
• UNIFOCAL
• MULTIFOCAL
• BIGEMINY
• TRIGEMINY
• COUPLETS
• TRIPLETS

101. • After each normal QRS complex there is one
Ectopic appear

102. • After two QRS complex which
are from normal sinus rhythm
then the ectopic foci fires called
Trigeminy

104. • When 2 ectopic appears
sequentially in a row or pairs
called Couplets

105. • When 3 ectopic occurs
sequentially in one row is
called Triplets

106. ECG Characteristics
• Rate- 60-100b/min
• Rhythm- Irregular
• P-waves usually present in sinus
rhythm not related to PVC
• QRS- wide and bizarre, greater
than 0.12sec

107. Management
• Treatment is directed to the cause
• If PVCs are associated with heart
disease can be treated
• Inj lidocaine bolus followed by
titrated drip

108. Ventricular Tachycardia
• It is repetitive firing of the
ventricular ectopic foci at a rate
more than 100 to 200b/min, which
may cause the heart to beat
inefficiently.

109. Etiology
• Ischemia
• Acute MI
• Hypoxia
• Hypokalemia
• Digitalis toxicity
• Acidosis
• Hypermetabolic states

110. ECG Characteristics
• Rate- ventricular rate 100 to
200b/min
• Rhythm- usually regular
• P-waves present if S.A.Node fires
may be buried in QRS or T
• PR Interval- not measurable
• QRS- wide, bizarre and greater
than 0.12sec

111. V-TACH

113. Management
• Cardioversion
• Defibrillation can be done when the
patient is pulseless
• Inj Lidocaine bolus and drip as
maintenance dose
• Antiarrhythmic like inj Amidarone
or inj MgSo4
• Resuscitative measures to kept
ready

114. Ventricular Fibrillation
• An erratic, disorganized firing of
impulses from the ventricles.

115. Etiology
• Myocardial Infarction
• V-Tach
• Drug toxicity
• Electrocution
• Drowning

116. ECG Characteristics
• Rate- rapid, uncoordinated, ineffective
• Rhythm- Chaotic, irregular
• P waves- not seen
• PR interval- none
• QRS – no formed QRS complex

118. Management
• Defibrillation
• CPR must be performed
• Anti-arrhythmic like
inj Lidocaine
inj Procainmide
inj MgSo4 most commonly
used
• Beta-Blockers

119. Disorders of impulse Conduction
• S.A. Block
• First degree AV Block
• Second Degree A.V.Block
» Mobitz type I
» Mobitz type II
• Third Degree or Complete A.V Block
• Bundle Branch Block
» RBBB
» LBBB

120. First Degree A.V.Block
• It is defined as prolonged AV
conduction time of supraventricular
impulses into the ventricles.

121. Etiology
• Congestive Heart Disease
• Rheumatic Heart Disease
• Vagal Stimulation
• Digitalis
• Beta-Blockers
• Ca-channel Blockers

122. ECG Characteristics
• Rate- 60 to 100b/min
• Rhythm- Regular
• P waves- normal, precede every QRS
• PR Interval- Greater than 0.20 sec
• QRS complex- usually normal

124. Management
• Usually does not require treatment
• It should be observed for progression

125. Second Degree A.V.Block
• It occurs when one atrial impulse
at a time fails to be conducted to
the ventricles.
It is classified into two
• Mobitz type I
• Mobitz type II

126. Type I Second degree A.V.Block
• It is a progressive increase in
conduction times of consecutive atrial
impulses into the ventricles until one
impulse fail to conduct or is ‘dropped’

127. Etiology
• Aortic Valve Disease
• Congestive Heart Failure
• Inferior Wall MI
• ASD
• Drugs
• Mitral Valve Prolapse

128. ECG Characteristics
• Rate- usually normal
• Rhythm- irregular unless 2:1
conduction present
• P waves- normal. Some p waves are
not conducted to the ventricle, but
only one at time fails.
• PR Interval- gradually lengthens in
consecutive beats.
• QRS- normal unless BBB

129. IInd Degree type I

130. Management
• Treatment depends on the
conduction ratio, ventricular rate
• If the ventricular rate slow give
inj Atropine Sulphate
• Removal of precipitating factor
• Temporary pacing can be done.

131. Type II Second degree A.V.Block
• It is sudden failure of conduction of
an atrial impulse to the ventricles
without progressive increase in
conduction time.

132. ECG Characteristics
• Rate- normal
• Rhythm- irregular
• P waves- usually regular and
precede QRS.
Periodically a P
wave is not followed by a
QRS
• PR interval- constant unless there
is block
• QRS- usually normal

134. IInd Degree type II

135. Management
• Pacemaker therapy because it is
often permanent and progress to
complete block

136. Third Degree A.V. Block(Complete Block)
• It is complete failure of conduction
of all atrial impulses to the
ventricles.

137. Etiology
• Congestive Heart Disease
• MI
• Lenegre’s disease
• Cardiac Surgery
• Congenital Heart Disease
• Digitalis Toxicity

138. ECG Characteristics
• Rate- atrial normal, Ventricular
rate is less that 45/min
• Rhythm- Regular
• P waves- independent
• PR Interval- no consistent PR
interval
• QRS- Normal If ventricles
controlled by Junctional
pacemaker, may be wide

140. Management
• Onset is sudden or associated with
MI pacing can be done without delay
• CPR should performed if the cardiac
out put severly diminished

147. Ventricular Asystole
• It refers to the absence of any
ventricular rhythm; there is no QRS
complex, no pulse and no cardiac
output.

149. Management
• Cardio Pulmonary Resuscitation
• Endotracheal Intubation immediately
• Obtain IV Access
• Confirm Asystole in more than one lead
• Consider immediate Transcutaneous
Pacing
• Epinephrine 1 mg IV push q3-5 minutes
– Consider Vasopressin as alternative
• Atropine 1 mg IV q3-5 minutes

150. The P wave is caused by atrial
depolarization. The P wave duration is
normally less than 0.12 sec. The P wave is
usually smooth and positive.
The QRS complex represents ventricular
depolarization. The normal QRS interval
range is from 0.04 sec - 0.12 sec, measured
from the first deflection to the end of the
QRS complex
The T wave due to ventricular
repolarization The wave is normally
rounded and positive.

151. • The PR interval is the beginning of the P wave to
beginning of QRS complex. It is normally 0.12 -
0.20 seconds. (onset of atrial depolarization to onset of
ventricular depolarization)
• The QT interval begins at the onset of the QRS
complex and to the end of the T wave.
• The ST Segment represents the period of
ventricular muscle contraction before
repolarization.

152. • The ECG below illustrates primary ST-T wave abnormalities (leads
I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave
abnormalities such as these may be related to ischemia, infarction,
electrolyte abnormalities, medications, CNS disease, etc.

153. • In the above ECG the ST-T waves are "normal" for
LBBB; i.e., they are secondary to the change in the
ventricular depolarization sequence.

155. Wolff-Parkinson-White Preexcitation
• Early ventricular activation in region of the accessory AV pathway
• Short PR interval (<0.12s)
• Initial slurring of QRS complex (delta wave) representing early ventricular
activation through normal ventricular muscle in region of the accessory
pathway
• Prolonged QRS duration (usually >0.10s)
• Secondary ST-T changes due to the altered ventricular activation sequence

159. The ectopic atrial rate is 150 bpm. Some of the ectopic P waves are easily seen and indicated by the
arrows. Other P waves are burried in the T waves and not so easily identified. Atrial tachycardia with AV
block is often a sign of digitalis intoxication. 3:2 and 2:1 AV block is seen in this example.

160. Premature Atrial Contractions
When an irritable focus in the atria
fires before the next sinus impulse
is due

161. Premature atrial contractions

163. Thank You