ECG

Short Rapid Review

For Non-Cardiologists

Edition 2.1
(PocketBook)
Review Medicine with us at :
www.twitter.com/MedRx22

Dr. CHIRAG NAVADIA

2013

1
 **ABOUT BOOK **

Hello Dear Friends ,

I am Dr. Chirag Navadia & Its my pleasure to present this

ECG book as a compact version of other detailed ECG books.
This book is meant to be for all the Doctors , Nurses and
Students around the world. If you are curious to learn ECG
Basics, then this is the book for you which is prepared after
reviewing many other books out there. These are some 50+
must know basic ECG with Interpretations, Clinical
Presentation, Etiologies & Managements.

As this is a Review Book , It does not contain All Treatments

in Detail. Emphasize has been made to include all clinically
relevant important points. Please See the index for more
details about the topics in this book.

I hope you will enjoy this book and will not regret your
purchase.

Best Wishes For Your Brilliant Future.

Sincerely

Dr. Chirag Navadia

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Book is dedicated to my Parents , Friends, All College
professors and Tutors of Kaplan Medical , USMLE First
Aid , Dr Edward Goljan , Dr Hussain Sattar , Dr Najeeb.
Thanks for giving me most valuable knowledge of my
life

Copyrights 2013 Chirag Navadia

Certain ECG images were freely available on Internet &

belongs to their Owner . No part of this book may be
reproduced in any form , by Photostat , microfilm ,
xerography or any other mean , or incorporated into any
information retrieval system , electronic or mechanical ,
without the written permission of Chirag Navadia.

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 TABLE OF CONTENTS

CHAPTER 1 : ECG BASICS8

1.1 SHORT INTRODUCTION ......................................................................... 8

1.2 CONDUCTION PATHWAY.................................................................... 11

1.3 BLOOD SUPPLY TO HEART ................................................................ 12

1.4 ACTION POTENTIALS ........................................................................... 14

1.5 PHASES OF CARDIAC CYCLE ............................................................. 17

GENERAL PHYSIOLOGICAL TERMS ....................................................... 20

1.6 ECG RECORDING ..................................................................................... 22

1.8 BEST METHOD TO DETERMINE HEART RATE ........................ 29

1.9 TYPES OF ECG ........................................................................................... 30

1.10 STANDARD CHEST LEAD PLACEMENT OF ELECTRODES 33

1.11 CORONARY TERRITORY ON 12 LEAD ECG .............................. 35

1.12 ANALYSING THE RHYTHM .............................................................. 36

CHAPTER 2 : SINUS RHYTHMS38

Normal ECG ....................................................................................................... 38

Normal 12-Lead ECG ..................................................................................... 39

SINUS ARRYTHMIAS ..................................................................................... 40

SINUS BRADYCARDIA................................................................................... 41

SINUS TACHYCARDIA ................................................................................... 43

SINUS PAUSE..................................................................................................... 45

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CHAPTER 3 : ATRIO-VENTRICULAR ARRYTHMIAS 47

ATRIAL TACHYCARDIA ............................................................................... 47

MULTIFOCAL ATRIAL TACHYCARDIA ................................................. 49

ATRIAL FLUTTER ........................................................................................... 50

ATRIAL FIBRILLATION ................................................................................ 52

PREMATURE ATRIAL CONTRACTION .................................................. 54

SUPRAVENTRICULAR TACHYCARDIA ................................................. 56

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA .................. 57

WANDERING ATRIAL PACEMAKER ...................................................... 60

CHAPTER 4 : VENTRICULAR ARRYTHMIAS..61

IDIOVENTRICULAR RHYTHM ................................................................... 61

ACCELETATED IDIOVENTRICULAR RHYTHM ................................ 62

VENTRICULAR TACHYCARDIA (MONOMORPHIC) ........................ 63

VENTRICULAR TACHYCARDIA (POLYMORPHIC) .......................... 65

VENTRICULAR FIBRILLATION................................................................. 66

TORSADE DE POINTES ................................................................................ 68

PULSELESS ELECTRICAL ACTIVITY ...................................................... 69

ASYSTOLE ........................................................................................................... 71

CHAPTER 4 : HEART BLOCKS..72

ATRIOVENTRICULAR BLOCKS (FIRST DEGREE BLOCK) ............ 72

2ND DEGREE AV BLOCK : MOBITZ TYPE I ........................................... 74

2ND DEGREE AV BLOCK : MOBITZ TYPE II.......................................... 75

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 3RD DEGREE AV BLOCK ................................................................................ 77

SINOATRIAL BLOCK (SA BLOCK) ........................................................... 78

RIGHT & lEFT BUNDLE BRANCH BLOCKS ......................................... 79

CHAPTER 5 : MYOCARDIAL INFARCTION82

ECG CHANGE FROM DAY 1 TO YEAR LATER .................................... 86

ST SEGMENT CHANGES FROM ISCHEMIA TO MI ........................... 87

ST SEGMENT ELEVATION & DEPRESSION ........................................ 88

INFERIOR WALL MI ....................................................................................... 91

ANTERIOR WALL MI ..................................................................................... 92

LATERAL WALL MI ........................................................................................ 93

CHAPTER 6 : JUNCTIONAL ARRYTHMIAS.94

JUNCTIONAL RHYTHM ................................................................................ 94

ACCELERATED JUNCTIONAL RHYTHM ............................................... 95

JUNCTIONAL ESCAPE BEATS .................................................................... 96

WOLF-PARKINSON WHITE SYNDROME ............................................. 97

PREMATURE JUCTIONAL CONTRACTIONS ....................................... 98

SINGLE CHAMBER PACEMAKER RHYTHM - VENTRICULAR .... 99

SINGLE CHAMBER PACEMAKER RHYTHM - ATRIAL ................ 100

DUAL CHAMBER PACEMAKER RHYTHM ATRIAL &

VENTRICULAR .............................................................................................. 100

CHAPTER 7 : PREMATURE VENTRICULAR CONTRACTIONS101

PVC : UNIFORM VS MULTIFORM ......................................................... 102

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 PVC : VENTRICULAR BIGEMINY VS TRIGEMINY ......................... 103

PVC : VENTRICULAR QUADRIGEMINY VS COUPLETS ............... 104

CHAPTER 8 : MISCELLANEOUS..106

HYPERKALEMIA VS HYPOKALEMIA .................................................. 106

HYPERCALCEMIA VS HYPOCALCEMIA ............................................. 109

CHAPTER 9 : P & Q WAVE RELATIONSHIPS112

P MITRALE/P SINISTROCARDIALE (MITRAL STENOSIS) ....... 113

P PULMONALE (COR PULMONALE) ................................................... 114

RIGHT ATRIAL ENLARGEMENT ........................................................... 114

LEFT ATRIAL ENLARGEMENT. ............................................................. 115

MECHANISM OF Q WAVE ........................................................................ 116

ACUTE PERICARDITIS ............................................................................... 117

CARDIAC PHARMACOLOGY.118

ANTI-ARRYTHMIC DRUGS ...................................................................... 118

ANTIHYPERTENSIVE DRUGS................................................................. 125

ANTIHYPERLIPIDEMIC DRUGS ............................................................ 128

NON PHARMACOLOGICAL TREATMENTS ...................................... 130

References ....................................................................................................... 132

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 CHAPTER 1 : ECG BASI CS

1.1 SHORT INTRODUCTION

Electrocardiogram (ECG)
The electrocardiogram is commonly used to detect
abnormal heart rhythms and to investigate the cause of
chest pains.

What is an electrocardiogram?
An electrocardiogram (ECG) records the electrical
activity of the heart. The heart produces tiny electrical
impulses which spread through the heart muscle to
make the heart contract. These impulses can be detected
by the ECG machine. You may have an ECG to help find
the cause of symptoms such as palpitations or chest pain.
Sometimes it is done as part of routine tests - for
example, before you have an operation.
The ECG test is painless and harmless. (The ECG machine
records electrical impulses coming from your body - it
does not put any electricity into your body.)

How is it done?
Small metal electrodes are stuck on to your arms, legs
and chest. Wires from the electrodes are connected to
the ECG machine. The machine detects and amplifies the
electrical impulses that occur at each heartbeat and
records them on to a paper or computer. A few
heartbeats are recorded from different sets of electrodes.
The test takes about five minutes to do.
Usually, more than two electrodes are used, and they can
be combined into a number of pairs (For example: left
arm (LA), right arm (RA) and left leg (LL) electrodes
form the three pairs LA+RA, LA+LL, and RA+LL). The
output from each pair is known as a lead. Each lead

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looks at the heart from a different angle. Different types
of ECGs can be referred to by the number of leads that
are recorded, for example 3-lead, 5-lead or 12-lead ECGs
(sometimes simply "a 12-lead").
A 12-lead ECG is one in which 12 different electrical
signals are recorded at approximately the same time and
will often be used as a one-off recording of an ECG,
traditionally printed out as a paper copy. Three- and 5-
lead ECGs tend to be monitored continuously and viewed
only on the screen of an appropriate monitoring device,
for example during an operation or while being
transported in an ambulance. There may or may not be
any permanent record of a 3- or 5-lead ECG, depending
on the equipment used.

What does an electrocardiogram show?

The electrodes on the different parts of the body detect
electrical impulses coming from different directions
within the heart. There are normal patterns for each
electrode. Various heart disorders produce abnormal
patterns. The heart disorders that can be detected
include :
-Abnormal heart rhythms. If the heart rate is very
fast, very slow, or irregular. There are various
types of irregular heart rhythm with
characteristic ECG patterns.
-A heart attack (myocardial infarction), Whether it
was recent or some time ago. A heart attack
causes damage to heart muscle, and heals with
scar tissue. These can be detected by abnormal
ECG patterns.
-An enlarged heart. Basically, this causes bigger
impulses than normal.
All Other ECG are discussed in detail from Chapter 2
onwards.

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Limitations of the electrocardiogram
An ECG is a simple and valuable test. Sometimes it can
definitely diagnose a heart problem. However, a normal
ECG does not rule out serious heart disease. For example,
you may have an irregular heart rhythm that 'comes and
goes', and the recording can be normal between
episodes. Also, not all heart attacks can be detected by
ECG. Angina, a common heart disorder, cannot usually be
detected by a routine ECG.

Specialised ECG recordings sometimes help to

overcome some limitations. For example:

Exercise ECG This is where the tracing is done when you

exercise (on a treadmill or exercise bike). This helps to
assess the severity of the narrowing of the coronary
arteries which causes angina.

Ambulatory ECG. This is where you wear a small

monitor which constantly records your heart rhythm.
This test records the electrical activity of your heart
when you are walking about (ambulatory) and doing
your normal activities. It aims to detect abnormal heart
rhythms that may 'come and go'. The electrical activity is
usually recorded for 24-48 hours.

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 1.2 CONDUCTION PATHWAY

Image courtesy : Holes human anatomy and physiology , 7 th edition by

Shier

An electrical stimulus is generated by the sinus node.

Sinus Node is also called the Sinoatrial node or SA node,

It Consist of a small mass of specialized tissue located in
the right atrium (right upper chamber) of the heart.

The sinus node generates a regular electrical stimulus,

which for adults, is usually 60 to 100 times per minute
under normal conditions. This electrical stimulus travels
down through the conduction pathways and causes the
heart's lower chambers to contract and pump out blood.
The right and left atria (the two upper chambers of the
heart) are stimulated first and contract for a short period
of time before the right and left ventricles (the two lower
chambers of the heart).

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The electrical impulse travels from the sinus node to the
atrioventricular node (also called AV node), where
impulses are slowed down for a very short period & then
allowed to continue down the conduction pathway via an
electrical channel called as bundle of His into the
ventricles. The bundle of His divides into right and left
pathways to provide electrical stimulation to the right
and left ventricles. Each contraction of the ventricles
represents one heartbeat

1.3 BLOOD SUPPLY TO HEART

Image Courtesy : Principles of anatomy and physiology , 11e John Wiley &
Sons

The Heart is supplied by the Coronary arteries which

arises Behind the Aortic Valves. 1) Left Coronary Artery
& 2) Right coronary artery.
The left coronary artery is Further Devided into Left
circumflex artery and Left Anterior descending artery

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aka Anterior Interventricular Branch.
The Right Coronary Artery is Further Divided into
Marginal Arteries, Nodal Arteries & Posterior
Interventricular Branch.
Various Anastomoses & Collaterals are formed between
branches of Left & Right Coronary Artery. No Symptoms
of Ischemic Heart Disease are noticeable until more than
70% of Coronary Artery Lumen is occluded.
Risk of Infarction Increases when more than 90% of
Arterial Lumen is occluded.
SA & AV Node are Supplied by Nodal branches of Right
Coronary Artery in 90% Population called as Right
Dominant Heart.
SA & AV Node Are Supplied by Branches of Left Coronary
Artery in 10% Population called as Left Dominant Heart.

Blood Vessel Area Supplied

Right Coronary Artery To the Right atrium, Right
ventricle and part of the left
ventricle
Posterior Interventricular
Artery Posterior Third of
Interventricular Septum

Left Coronary Artery

Left anterior descending To the Anterior wall of the

artery left ventricle, Anterior 2/3rd
Interventricular septum,
Bundle of His, Right bundle
branch, and Left anterior
fasciculus of the left bundle
branch

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Left Circumflex artery To the lateral walls of the
left ventricle, left atrium,
and left posterior fasciculus
of the left bundle branch

Cardiac veins Collect blood from the

capillaries of the
myocardium
Coronary sinus Returns blood to the right
atrium.

1.4 ACTION POTENTIALS

Action potentials are generated by special types of

voltage-gated ion channels embedded in a cell's plasma
membrane. They are responsible for the generation of
electrical impulses in the Heart.

ACTION POTENTIAL IN FAST RESPONSE FIBRES

Fast Response Fibres : Cardiac Muscle , His-Purkinje System

Phase 0 : Phase of Depolarization : Depends on

number of Sodium Channels (Na+ coming into the cell)
which in turn depends on Resting membrane potential of
cell. Contraction occur during this phase (Atrial

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depolarisation P wave , Ventricular depolarization
first half of QRS complex). Class I antiarrythmics
(Procainamide, Quinidine, Disopyrimide) Blocks Phase 0
in fast response fibres.

Phase I : Na+ channels are inactivated. Overshoot

develops because of Potassium (K+) going out of cell &
inward Chlorine current.

Phase II : Plateau Phase : Balanced by slow Calcium

current going into the cell and Slow K+ going out of cell.

Phase III : Repolarisation Phase : Delayed K+ rectifier

current rapidly increases and calcium channels get
inactivated. Atrial repolarization is not seen on ECG, It is
believed to be hidden behind QRS complex , T wave
indicates Ventricular repolarization. Class III
antiarrythmics (Amiodarone , sotalol )slow down this
phase.

Phase IV : Return of membrane to resting potential .

Maintained by Na+/K+ ATPase pump which send Sodium
out of cell in exchange of Potassium. Phase IV is flat in
Fast fibres.

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 ACTION POTENTIAL IN SLOW RESPONSE FIBRES

Slow Response Fibres : SA Node & AV Node

Phase 0 : Dependent on Calcium Channels (Not on

Sodium Channels . With each depolarization SA node
sends signal to contract the heart . Class IV
antiarrythmics (Verapamil , Diltiazem) can slow or block
this phase .

Phase I & II is not present in SA & AV node

Phase III : Repolarisation phase , due to Potassium going

out of cell.

Phase IV : Rising Slope (Not flat as in fast fibres) ,

referred to as Pacemaker current . its due to inward Na+
& Ca++ current and outward K+ current (not well
understood yet). Class II (B blockers) & Class IV (Ca+
channel blockers) act on this phase and decreases heart
rate.

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 1.5 PHASES OF CARDIAC CYCLE

Image Courtesy : Hypocaffeinic.pbworks.com

5 Phases of Cardiac cycle are as follow :

Isovolumetric ventricular contraction : Volume in the

ventricles does not change during this phase .

In response to ventricular depolarization, tension in the

ventricles increases. This increase in pressure within the
ventricles leads to closure of the mitral and tricuspid

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valves which give rise to the S1 heart sound. The
pulmonic and aortic valves stay closed during the entire
phase. Ventricular Contraction is reflected by QRS
complex on the ECG .

The pressure during this phase gradually increases &

when the pressure exceeds aortic and pulmonary
arterial pressure (ie at 80 mmHg), the aortic and
pulmonic valves open and the ventricles eject blood. This
phase is called as Ejection Phase.
Opening of Aortic & Pulmonary valves does not cause
any heart sound.
After an ejection phase the pressure inside ventricles
start falling due to relaxation of ventricles. When
ventricular pressure falls below the pressure in aorta
and pulmonary artery, the Aortic and Pulmonic valves
closes. This phase is called as isovolumetric relaxation.

The closure of Pulmonary & Aortic valves give rise to S2

sound. All valves are closed during this phase. Atrial
diastole occurs during this time and the blood fills the
atria. On the ECG it will be reflected by T Wave .

Just on the side note remember that the pulmonic valve

closes before the aortic valves which give rise to Split in
2nd heart sound which can be heard during inspiration
on auscultation. Anything which delays Pulmonary valve
closure will increase Splitting. All Cardiac Sounds are
discussed in more detail in our last section of Murmers .

The phase of Rapid Ventricular filling : As the blood

continue to fill Atrium, The Atrial pressure exceeds
ventricular pressure, which causes the mitral and
tricuspid valves to open, it will lead the Blood to flows
passively from the atria into the ventricles.

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About 70% of ventricular filling takes place during this
phase. Sometimes S3 heart sound Is heard during this
phase due to the rapid filling of ventricles example
(Normal in Youngs). Pathologically associated with
Dilated cardiomyopathy and some other pathologies
which will be discussed in Pathology section.

After Rapid filling , Atrial systole will occur : Known as

the atrial kick, atrial systole (coinciding with late
ventricular diastole) It supplies the ventricles with the
remaining 30% of the blood for each heartbeat & the
new cycle keeps going .

Heart is Innervated mainly by Parasympathetic

(Vagus) Fibres & Sympathetic Fibres.

Sympathetic Stimulation Increases Heart Rate. The

Pain which arises during Angina travels through
Sympathetic Fibres to Spinal Cord segment T1-T5.
Parasympathetic Stimulation Decreases Heart Rate.
Sensory Fibres that Carry Afferent Limb of Cardiac Reflex
Travel with Vagus Nerve.

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 GENERAL PHYSIOLOGICAL TERMS

Preload is the load on Ventricular Muscles at the end of

Diastole. It is determined mainly by Left Ventricular End
Diastolic Volume & Left Ventricular End Diastolic
Pressure ie by Venous Return.

Increase in Preload results in increase in Contractility

which in turn increases Stroke Volume & thus increase in
Ejection Fraction

A Rise in Pulmonary Capillary Wedge Pressure is

evidence of increased Preload on the Left Ventricle. In
Some Cases like Mitral Stenosis or Mitral Valve Prolapse
it is not a good index of Left Ventricular Preload..

Stroke Volume is the amount of blood that heart pump

out with each beat . It is affected by Contractility,
Afterload & Preload.
Stroke Volume is Calculated as : SV = EDV (End Diastolic
Volume) ESV (End Systolic Volume)
EDV Volume that is in the Left Ventricle after Diastole.
ESV Volume That Remains in the Left Ventricle After
Systole

Ejection fraction is the fraction of blood which heart

pumps out during 1 contraction which is usually 60% in
healthy normal adult
Ejection Fraction = SV/End diastolic volume = EDV-
ESV/EDV.
Normal SV is 70 ml and EDV is 120 ml in 70kg man . So if
you calculate , it will come out to be 60% .

Cardiac output = Heart Rate * Stroke Volume .

So if the heart rate is 72 per minute , and stroke volume

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is 70 ml , then Cardiac output in 1 minute = 5000ml or 5
Litres per minutes . Chronic increase in preload is
Responsible for Dilated Cardiomyopathy
Ficks Principle says that : CO = Rate of O2 Consumption /
Arterial O2 Content Venous O2 Content

Mean Arterial Pressure is defined as Average arterial

pressure during since cardiac cycle. It is calculated as :
(i) MAP = Cardiac Output * Total Peripheral Resistance.
(ii) MAP = 2/3rd Diastolic Pressure + 1/3rd Systolic
Pressure.
Ex : If Mr. John has Blood Pressure of 120/80 mmHg ,
His MAP will be 2/3rd (80) + 1/3rd (120) = 92 mmHg

Pulse Pressure is merely the Difference between

Systolic Pressure and Diastolic Pressure, It is Calculated
as PP = Systolic Pressure Diastolic Pressure. In Above
Case, Mr. John will have Pulse Pressure of 40mmHg.

Afterload : The pressure AGAINST which heart will

work determined by Peripheral Arterial resistance
Chronic increase in Afterload (eg Hypertension) will lead
to Left ventricular hypertrophy
From physiological formula : Blood flow = Pressure /
Resistance (Q=P/R) .
So if the resistance will increase, the blood flow will
decrease and the heart will have to pump more amount
of blood against more resistance. Chronically it will lead
to ventricular muscle hypertrophy.

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 1.6 ECG RECORDING

The horizontal axis of the ECG strip represents time.

Each small block equals 0.04 second, and five small
blocks form a large block, which equals 0.20 second.

This time increment is determined by multiplying 0.04

second (for one small block) by 5, the number of small
blocks that compose a large block.
Five large blocks equal 1 second (5 0.2). When
measuring or calculating a patients heart rate, a 6-
second strip consisting of 30 large blocks is usually used.

The ECG strips vertical axis measures amplitude in

millimeters (mm) or electrical voltage in millivolts (mV)
Each small block represents 1 mm or 0.1 mV; each large
block, 5 mm or 0.5 mV.

To determine the amplitude of a wave, segment, or

interval, count the number of small blocks from the
baseline to the highest or lowest point of the wave,
segment, or interval.

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 1.7 INTERVALS AND SEGMENTS

RR It is the interval between a R wave 0.6s to

interval and the next R wave, Normal resting 1.2sec
heart rate is between 60 and 100
bpm.

During Normal Atrial depolarization, < 0.08s

the main electrical vector is directed
from the SA node towards the AV Height <
node and spreads from the right 2.5mm
P wave
atrium to the left atrium . This turns
into the P wave on the ECG.

For abnormal P waves see Right

Atrial Hypertrophy, Left Atrial
Hypertrophy, Atrial Premature
Beat, Hyperkalaemia

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 The PR interval is measured from 0.12 to
the beginning of the P wave to the 0.20s(3-
beginning of the QRS complex. The 5 Small
PR interval reflects the time the squares
electrical impulse takes to travel )
PR from the sinus node through the AV
interval node and entering the ventricles.
The PR interval is therefore a good
estimate of AV node function.

For Short PR segment consider

Wolf-Parkinson-White syndrome or
Lown-Ganong-Levine syndrome
(other causes - Duchenne muscular
dystrophy, type II glycogen storage
disease (Pompe's), Hypertrophic
Obstructive CardioMyopathy).

For long PR interval see first degree

heart block and 'trifasicular' block

The PR segment connects the P wave 0.05 to

and the QRS complex. 0.12s

The impulse vector is from the AV

PR node to the bundle of His to the
segment bundle branches and then to the
Purkinje fibers. This electrical
activity does not produce a
contraction directly and is merely
traveling down towards the
ventricles, and this shows up flat on

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 the ECG. The PR interval is more
clinically relevant.

The QRS complex reflects the rapid 0.08 to

depolarization of the right and left 0.12s (2-
ventricles. The ventricles have a 3 small
large muscle mass compared to the squares)
QRS
atria, so the QRS complex usually has
complex
a much larger amplitude than the P-
wave.

For Abnormally wide QRS consider

right or left bundle branch block,
ventricular rhythm, hyperkalaemia,
etc.

The point at which the QRS complex N/A

finishes and the ST segment begins.
J-point It is used to measure the degree of
ST elevation or depression.

The ST segment connects the QRS 0.08 to

complex and the T wave. The ST 0.12s
segment represents the period when
the ventricles are depolarized. It is
ST
isoelectric. No elevation or
segment
depression is normally seen.

Causes of elevation include

Acute MI (e.g. anterior,
inferior), left bundle branch
block, normal variants (e.g.
athletic heart, Edeiken

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 pattern, high-take off),
acute pericarditis
Causes of depression
include myocardial
ischemia, digoxin effect,
ventricular hypertrophy,
acute posterior MI,
pulmonary embolus, left
bundle branch block

The T wave represents the 0.16s

repolarization of the ventricles. The
interval from the beginning of the
QRS complex to the apex of the T
wave is referred to as the absolute
refractory period. The last half of the
T wave is referred to as the relative
T wave refractory period (or vulnerable
period).

Causes of tall T waves include

hyperkalaemia, hyperacute
myocardial infarction and left
bundle branch block

Causes of small, flattened or

inverted T waves are numerous and
include ischaemia, age, race,
hyperventilation, anxiety, drinking
iced water, LVH, drugs (e.g.
digoxin), pericarditis, PE,
intraventricular conduction delay
(e.g. RBBB)and electrolyte
disturbance.

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ST The ST interval is measured from the 0.32s
interval J point to the end of the T wave.

The QT interval is measured from Up to

the beginning of the QRS complex to 0.42s in
the end of the T wave. A prolonged heart
QT interval is a risk factor for rate of
QT
ventricular tachyarrhythmias and 60 bpm
interval
sudden death.Many drugs will
increase QT interval like :
amiodarone , antipshycotics ,
antidepressant , which increases the
risk to develop Torsade-de-pointes .

Other Causes of long QT interval

Myocardial infarction
Myocarditis
Diffuse Myocardial Disease
Hypocalcaemia
Hypothyrodism
Subarachnoid haemorrhage,
intracerebral haemorrhage

Hereditary :

-Romano Ward syndrome

(autosomal dominant)
-Jervill + Lange Nielson
syndrome (autosomal
recessive) associated with
sensorineural deafness

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 The U wave is hypothesized to be
caused by the repolarization of the
U wave interventricular septum. It normally
has a low amplitude, and even more
often is completely absent.

It always follows the T wave, and

also follows the same direction in
amplitude. If it is too prominent,
suspect hypokalemia, hypercalcemia
or hyperthyroidism.

The J wave, elevated J-point or

Osborn wave appears as a late delta
J wave wave following the QRS or as a small
secondary R wave.

It is considered pathognomonic of
hypothermia or hypocalcemia.

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1.8 BEST METHOD TO DETERMINE HEART RATE

Remember 60 sec/min divided by 0.20 sec/large box =

300 large boxes/min

Number of Boxes (between Heat Rate

two R waves)

1 300

2 150

3 100

4 75

5 60

6 50

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 1.9 TYPES OF ECG

1 : 12-lead ECG records electrical activity from 12 views

of the heart.
2 : Single-lead or dual-lead monitoring provides
continuous cardiac monitoring.

12-lead ECG
Six limb leads provide information about the
hearts frontal (vertical) plane.
Bipolar (leads I, II, and III) require a negative
and positive electrode for monitoring.
Unipolar (leads aVR, aVL, and aVF) record
information from one lead and require only one
electrode.
The six precordial leads (leads V1 through V6)
provide information about the hearts horizontal
plane.

Leads I, II, and III

Leads I, II, and III typically produce positive
deflection on ECG tracings.
Lead I helps monitor atrial arrhythmias and
hemiblocks.
Lead II commonly aids in routine monitoring and
detecting of sinus node and atrial arrhythmias.
Normally , R wave is tallest in Lead ll .
Lead III helps detect changes associated with
inferior wall myocardial infarction.

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 30
Normal Normal Normal
to 90

May indicate left Left axis deviation

30 anterior is considered
Left axis
to fascicular block normal in
deviation
90 or Q waves from pregnant women
inferior MI. & in emphysema

May indicate left

posterior
Right deviation is
fascicular block,
+90 considered normal
Right axis Q waves from
to in children and is
deviation high lateral MI, or
+180 a standard effect
a right
of dextrocardia.
ventricular strain
pattern

Is rare, and
Extreme +180
considered an
right axis to
'electrical no-
deviation 90
man's land'

Causes of axis deviation :

Left : Reflected by a QRS complex positive in lead I

(usually QRS complex peak in Lead l > Lead 2) and
negative in leads aVF and II.

Inferior wall myocardial infarction(MI)

Wolf-Parkinson-White syndrome (right sided accessory
pathway)

31 | P a g e
 Mechanical shifts (ascites,pregnancy, tumors)
Left bundle-branch block
Left ventricular hypertrophy
Aging , Artificial Cardiac pacing , Emphysema ,
Hyperkalaemia , tricuspid atresia, ostium primum ASD,
Injection of contrast into left coronary artery
Note: left ventricular hypertrophy is not a cause left axis
deviation

Right : Reflected by a QRS complex in lead I negative

and aVF positive.
Normal finding in children and tall thin adults
Right ventricular hypertrophy
Chronic lung disease even without pulmonary
hypertension
Anterolateral myocardial infarction
Left posterior hemiblock
Pulmonary embolus
Wolff-Parkinson-White syndrome - left sided
accessory pathway
Atrial & Ventricular septal defect

Augmented Leads
Leads aVR, aVL, and aVF are called augmented
leads
Lead aVR provides no specific view of the heart.
Lead aVL shows electrical activity coming from
the hearts lateral wall.
Lead aVF shows electrical activity coming from
the hearts inferior wall

32 | P a g e
 1.10 STANDARD CHEST LEAD PLACEMENT
OF ELECTRODES

LEAD POSITIVE ELECTRODE VIEW

PLACEMENT & PROPERTIES OF
HEART
V1 4th Intercostal space to right of Septum
sternum. Biphasic, Distinguishes
between right and left ventricular
ectopic beats. Monitors ventricular
arrhythmias, ST-segment changes
and bundle-branch blocks

V2 4th intercostal space to left of Septum

sternum

Biphasic , Monitors ST-segment

33 | P a g e
 elevation

V3 Directly between V2 and V4 Anterior

Biphasic , Monitors ST-segment

elevation

V4 5th Intercostal space at left Anterior

midclavicular line.

Produces a biphasic waveform

,Monitors ST-segment and T-wave
changes.

V5 Level with V4 at left anterior Lateral

axillary line.

Produces a positive deflection on

the ECG , Monitors ST-segment or
T-wave changes (when used with
lead V4).

V6 Level with V5 at left midaxillary Lateral

line.

Produces a positive deflection on

the ECG , Detects bundle-branch
blocks.

34 | P a g e
 1.11 CORONARY TERRITORY ON 12 LEAD ECG

LCx = Left circumflex artery , LAD = Left anterior

Descending artery , RCA = Right coronary artery. Injury
to following vessels will be reflected in this lead

ECG
Area Coronary artery
changes
Anteroseptal V1-V4 Left anterior descending
Inferior II, III, Avf Right coronary
Anterolatera Left anterior descending
V4-6, I, Avl
. or left circumflex
I, aVL +/-
Lateral Left circumflex
V5-6

Usually left circumflex,

Tall R waves
Posterior also right coronary. . .
V1-2 .
.

35 | P a g e
 1.12 ANALYSING THE RHYTHM

COMPONENTS CHARACTERISTIC

Rate & The bpm(Beats Per Minute) is

Rhythm commonly the ventricular rate.

If the atrial and ventricular rates differ

as in a 3rd degree AV block, Measure
both rates.

Each P wave is followed by a QRS

P waves normal for the subject

P wave rate 60 - 100 bpm with <10%

variation Rate <60 = sinus bradycardia

Rate >100 = sinus tachycardia

Variation >10% = sinus arrhythmia

Regularity Measure R-R interval and P-P intervals.

Regular : Consistent intervals

Regularly Irregular : Repeating pattern

Irregular : No rhythm

P waves If present : determine whether they are

Same in size , shape , position ? Does
each QRS have a P wave ?

Normal : Upright (Positive) and

36 | P a g e
 uniform

Inverted : Negative

Notched : P

None : Rhythm is junctional or

ventricular

PR interval Constant : Interval are same

Variable : Interval Differs

Normal : 0.12-0.20 sec and constant

QRS interval Normal : 0.06 0.10 sec

Wide : >0.10 sec

None : Absent

QT interval Beginning of R wave to the end of T

wave

Varies with heart rate.

Normal : less than half the R-R interval

Dropped beats Occur in AV blocks

Occur in Sinus arrest

37 | P a g e
 CHAPTER 2 : SINUS RH YTHMS

NORMAL ECG

Rate : Normal (60-100bpm). 4 boxes = 60 bpm in this

ECG
Rhythm : Regular
P wave : Normal (upright and uniform)
PR interval : Normal (0.12 sec to 0.20 sec )= - 1 box
QRS : Normal (0.06-0.10 sec)

Please Go through Normals discussed in Chapter 1 .Easy

pneumonic to remember this Intervals is Rule of
0.08+/- 0.04 sec.

See , P wave is about 0.08 Sec , PR Segment 0.08 Sec .

On combining them you will get PR Interval which is 0.16
Seconds ( +/- 0.04 sec = 0.12-0.20 sec )

Now QRS complex is 0.08 , ST segment is 0.08 Sec , while

T wave is 0.08*2 = 0.16 Sec . Combining all of them you
get QT interval , 0.32 Sec + 0.08 sec = 0.40 seconds ,
which must be less then 0.42sec normally . this is little
confusing but I hope , you will deal with it .

38 | P a g e
 NORMAL 12-LEAD ECG

Normal ECG does not rule out underlying Valvular

pathologies .Many times Valvuvar problems like Mitral
Prolapse will have normal ECG findings. You can
diagnose valvular pathologies by Auscultation and
Confirm by Echocardiography .

Mitral valve prolapse is usually identified by cardiac

auscultation (Systolic Click) in asymptomatic patients or
incidentally through echocardiography for other reason .

The most common complain is palpitation secondary to

supraventricular arrhythmias or premature ventricular
beats (discussed later in this book). ECGs however are
frequently normal. Other manifestation include chest
pain , that is not associated with Myocardial Ischemia ,
Exertional dyspnea , Syncope and Low blood pressure

39 | P a g e
 SINUS ARRYTHMIAS

The SA node discharge irregularly , so , R-R interval is

irregular.

Rate : Usually normal

Rhythm : Irregular In this ECG , 1st R-R interval 0.80
sec , in 2nd R-R interval is 1.0 seconds , 3rd R-R interval
is 0.7 sec .
P wave : Normal
PR interval : Normal
QRS : Normal
During Inspiration R-R interval decrease and during
expiration it increases.

During inspiration, there will be an increase in the flow

of blood back to the heart & Decrease in Stroke Volume
that reduces vagal tone. Normally , Vagal tone makes the
heart to beat slowly , and when the vagal tone decreases ,
Sympathetic tone will predominate , which in turn
increases the heart rate & ECG complexes fall closer
together,that shortens the R-R interval.

During expiration, venous return decreases and Stroke

Volume increases , which in turn increases vagal tone
that slows the heart rate, and lengthens the R-R interval.
Sinus arrhythmia can occur naturally in athletes and

40 | P a g e
children, but it rarely occurs in infants. Conditions which
are not related to respiration may also produce sinus
arrhythmia like : inferior wall myocardial infarction (MI)
, Advanced age, use of Digoxin or morphine and
conditions involving increased intracranial pressure.

Treatment : Usually No treatment is necessary if the

patient is asymptomatic.

SINUS BRADYCARDIA

Sinus Bradycardia is due to slow firing of the SA node , it

is defined as heart beat less than 60 bpm ..

Rate : Slow (less than 60 bpm) - 50 bpm in this ECG .

Rhythm : Regular
P wave : Normal
PR interval : Normal
QRS : Normal
Sinus bradycardia is normal in athletes and during sleep.
In acute MI , it may be beneficial or the slow rate may
compromise cardiac output

Patients present to you is usually asymptomatic and

unaware of this condition . However, symptomatic
patient will present to you as Syncope , Dizziness ,
Lightheadedness , Chest pain , Shortness of breath ,

41 | P a g e
Exercise intolerance all this symptoms are due to
decrease in blood supply to their respective organs .

Sinus bradycardia usually occurs as the normal response

to a reduced demand for blood flow. In this case, vagal
stimulation increases and sympathetic stimulation
decreases , as a result, automaticity (the tendency of cells
to initiate their own impulses) in the SA node diminishes.

Sinus bradycardia commonly occurs after an inferior

wall MI that involves the right coronary artery, which
supplies blood to the SA node.

The clinical significance of sinus bradycardia depends on

how low the rate is and whether the patient is
symptomatic. For example, most adults can tolerate a
sinus bradycardia of 45 to 59 beats/minute but are less
tolerant of a rate below 45 beats/minute.

Causes of sinus bradycardia :

Hyperkalaemia (cell will not depolarize due to

change in K+ gradient)

Increased intracranial pressure (stimulates vagal

outflow)

Hypothyroidism (decrease in SNS mediators )

Increased vagal stimulation or decreased

sympathetic stimulation, such as sleep, deep
relaxation, Valsalvas maneuver, carotid sinus
massage
Sinoatrial node disease (decrease in impulse
generation), Myocarditis

42 | P a g e
 Drugs like beta-adrenergic blockers (BBs) ,
calcium channel blockers (CCBs) , digoxin
,quinidine and other Due to decrease in AV
nodal conduction . Details are discussed in
Pharma. Section.

Treatment : Usually asymptomatics are not treated and

are monitored regularly . use atropine if severe and
symptomatic.

SINUS TACHYCARDIA

Results from increased in SA node discharge

Rate : Fast (greater than 100bpm). 150 bpm in this ECG

Rhythm : Regular
P wave : Normal
PR interval : Normal
QRS : Normal
Sinus tachycardia is a normal response to exercise ,
anxiety , fever , hypoxemia , hypovolemia , strong
emotions like Fear , Shock, Anemia . failure to do so , is a
pathology.

Usually , Patient will be asymptomatic , but the

symptomatic may present with palpitations, dyspnea,

43 | P a g e
dizziness, light-headedness, fatigue, or chest pressure.

Other Causes of sinus tachycardia

heart failure
cardiogenic shock, pericarditis
Pulmonary embolism, sepsis, and
hyperthyroidism
Drugs as atropine, dopamine, dobutamine,
epinephrine, caffeine, nicotine

Tachycardia can lower cardiac output by reducing

ventricular filling time and the amount of blood
pumped by the ventricles during each contraction.
Normally, ventricular volume reaches 120 to 130 ml
during diastole. In tachycardia, decreased
ventricular volume leads to hypotension and
decreased peripheral perfusion.
As cardiac output plummets, arterial pressure and
peripheral perfusion decrease.

Tachycardia worsens myocardial ischemia by

increasing the hearts demand for oxygen and
reducing the duration of diastolethe period of
greatest coronary flow.

Treatment : Usually none , correct underlying cause .

use B-Blocker if symptomatic

44 | P a g e
 SINUS PAUSE

The SA node fails to discharge and then resumes.

Electrical activity resumes either when the SA node
resets itself or when a lower latent pacemaker (AV
node or bundle of His) begins to discharge

Rate : Normal to Slow (depends upon , the duration of

sinus pause)
Rhythm : Irregular (during the time of pause ,
afterward it may be its actual Rate ). Here beat is
normal after Pause , indicating that the patient is
having a normal rhythm .
P wave : Normal Except , no P wave will be formed
during the time of pause
PR interval : Normal
QRS : Normal

If the Pause duration was same as Normal R-R Duration

ie 0.80sec , then this would be called as Sinus Escape. In
Sinus Escape 1 beat is Dropped.

If the Pause remains for longer period of time , it may

result into Syncope and Dizziness.

Hypoperfusion of brain can lead to ischemic injury of

brain.

45 | P a g e
Pauses of 2 to 3 seconds normally occur in healthy adults
during sleep and occasionally in patients with increased
vagal tone or hypersensitive carotid sinus disease.

Causes of sinus arrest :

Fibrosis and idiopathic degeneration of SA node

Increased vagal tone

Digoxin , quinidine, procainamide and salicylates

Excessive doses of beta- blockers and many

other causes.

Sinus Arrest are usually asymptomatic but ,the

Symptomatic patient will classically present to you as
Recurrent dizziness, syncope & unexplained falls.

Asymptomatics usually dont require treatment .

In any pathology in which asymptomatic patients dont

require treatment , you must educate your patient about
his condition and lifestyle modifications.

In symptomatic, not a single Pharmacological agent has

been proven to provide long-term effectiveness, so
Permanent pacemaker implantation is generally
considered an effective treatment.

46 | P a g e
 CHAPTER 3 : ATRIO -VENTRICULAR
ARRYTHMIAS

ATRIAL TACHYCARDIA

Atrial tachycardia is a rhythm disturbance that arises in

the atria. A rapid atrial rate overrides the SA node and
become the dominant pacemaker. Some st wave and t
wave abnormalities may be present

Rate : 150-250 bpm (In this ECG Appro. 200 bpm)

Rhythm : Regular
P wave : Normal but differs in shape from sinus P waves
PR interval : May be short (.12sec) in rapid rates
QRS : Normal (0.06-0.10 sec) but can be aberrant at
times

The rapid rate shortens diastole resulting in a loss of

atrial kick reduced cardiac output reduced
coronary perfusion ischemic myocardial changes
multiorgan failure due to underperfusion most affected
is Brain.
Patients presents to you with : Rapid regular pulse ,
Dyspnea, dizziness, light-headedness, fatigue, or chest
pressure. In tachycardic episodes - Sudden onset of
palpitations & the Warm-up phenomenon

47 | P a g e
(Tachycardia gradually speeds up soon after onset)
Cardiac conditions that can cause atrial tachycardia
include :

MI , Cardiomyopathy , Congenital anomalies

Wolff-Parkinson-White syndrome , Valvular
heart disease
Cor pulmonale (Right Ventricular failure due to
pathology in lungs or pulmonary vessels).
Hyperthyroidism , Systemic hypertension ,
Digoxin toxicity

Treatment aims to control the rate with the helps of BBs

& CCBs.

For the patients who are not managed by drugs :

Cardioversion , Radiofrequency catheter ablation,
Surgical ablation

48 | P a g e
 MULTIFOCAL ATRIAL TACHYCARDIA

It is a type of wandering atrial pacemaker (discussed later)

which is associated with ventricular rate > 100 bpm. In
MAT , Number of different clusters of cells outside of the SA
node take over control of the heart rate.To distinguish it
from Atrial fibrillation , see the presence of recognizable P
wave

Rate : Fast (>100 bpm)

Rhythm : Irregular
P wave : Atleast 3 different forms , which are
determined by the focus in the atria
PR interval : Variable , depends on the focus
QRS : Normal

MAT is commonly seen in patients with Chronic

Obstructive pulmonary disease but may also occur in
acute myocardial infarction , Metabolic disorders &
endocrinopathies.
Patients will presents to you with the primary pathology
symptoms + Symptoms of atrial tachycardia .
Treat the underlying cause of MAT . Pharmacological
management by Calcium channel blockers (first line of
treatment) , Magnesium sulfate , Beta blockers.

Rarely it can be Refractory of pharm. Rx , so at that time

AV junctional radiofrequency ablation and permanent
pacemaker Implantation should be considered.

49 | P a g e
 ATRIAL FLUTTER

It is characterized by atrial rates of 250-400 beats/min

with some degree of AV Block . AV node conduct
impulses to the ventricles at 2:1 , 3:1 .$:1 or greater ratio.
Rarely it can also be 1:1. Degree of AV block may be
consistence or variable

Rate : Atrial 250-350 bpm , Ventricular : Slow or fast

Rhythm :Usually regular but may be variable
P wave : Waves have saw tooth appearance
PR interval :Variable
QRS : usually normal , but may appear widened if flutter
waves are buried in QRS

Originating in a single atrial focus, this rhythm results

from circus reentry and possibly increased automaticity.

On an ECG, the P waves lose their distinction due to the

rapid atrial rate. The waves blend together in a saw-
toothed appearance and are called flutter waves, or f
waves.
Atrial flutter may be caused by conditions that enlarge
atrial tissue and elevate atrial pressure. Found in
patients with severe mitral valve disease,
hyperthyroidism, pericardial disease, & primary
myocardial disease.

50 | P a g e
Clinical note : Patient usually use to be asymptomatic ,
signs and symptom depends on ventricular response
rate. Patient will typically have decreased cardiac output
, Palpitations , Fatigue or poor exercise tolerance , Mild
dyspnea , Presyncope.

The pulse may be regular or slightly irregular ,

Hypotension is possible, but normal blood pressure is
more commonly observed. Tachycardia may or may not
be present, it depends on the degree of AV block
associated with the atrial flutter activity.

Atrial flutter and sinus tachycardia

Whenever you see sinus tachycardia with a rate of 150
beats/minute, take another look. That rate is a common
one for atrial flutter with 2:1 conduction. Look closely for
flutter waves, which may be difficult to see if theyre
hidden in the QRS complex. You may need to check
another lead to clearly see them.

Treatment aim to Control the ventricular rate (BBs ,

CCBs) to prevent Clot formation by anticoagulants . Also
done.

Restoration of sinus rhythm (cardioversion or RFA

)Ablations will minimize the usage of anticoagulant
drugs and its toxicity .

51 | P a g e
 ATRIAL FIBRILLATION

Characterized by an irregular and often rapid heartbeat.

Rapid , erratic electrical discharge comes from multiple
ectopic foci in the atrium. No organized atrial contraction
are detectable.

Rate : Atrial : 350 bpm or greater , ventricular rate :

Slow or Fast
Rhythm : Irregular
P wave : No recognizable P wave , Chaotic atrial activity
PR interval : None (because there is no recognizable P
wave)
QRS : Normal (because ventricles were not affected)

A-fib is usually a chronic arrhythmia associated with

underlying heart disease. They are never considered
normal.

Signs and symptoms depend on ventricular response

rate. 90% of AF episodes may not cause symptoms, Many
patients experience a wide variety of symptoms,
including palpitations, dyspnea, fatigue, dizziness,
angina, and decompensated heart failure.

52 | P a g e
The irregular conduction of impulses through the AV
node produces a characteristic irregularly irregular
ventricular response. If you see R waves that look
irregularly irregular, suspect atrial fibrillation.

Atrial fibrillation can occur : Following cardiac surgery,

By long-standing hypotension, Pulmonary embolism,
Hyperthyroidism , Acute MI, Pericarditis, Hypoxia and
other, Catecholamine release during exercise may also
trigger the arrhythmia.

A patient with atrial fibrillation is at increased risk for

developing atrial thrombus and systemic arterial
embolism. Because the atria dont contract, blood may
pool on the atrial wall, and thrombi can form , which can
dislodge and embolized any small vessel leading to
infarction of the particular structure that vessel supplies.

Treatment : Anticoagulation (Prevent embolism).

Control rate by : B-blockers , Calcium channel blockers ,
or digoxin.

Acute onset (<24 hours)- cardiovert with

amiodarone , procainamide or electrical
cardioversion.

chronic : first anticoagulate and then cardiovert.

If above Rx fails and A-fib reoccurs : Leave

patient on rate control medications (B-Blocker ,,
CCBs) and warfarin

53 | P a g e
 PREMATURE ATRIAL CONTRACTION

PACs occur when another region of the atria depolarizes

before the sinoatrial node and thus triggers a premature
heartbeat .On ECG a single whole complex occur earlier
than the next expected sinus complex. Sinus rhythm
usually resumes after PAC

Rate : Depends on the rate of underlying rhythm

Rhythm : Irregular whenever PAC occur , at other time ,
it will be normal
P wave : Present , in PAC might have different size
PR interval : Varies in PAC , otherwise normal
QRS : Normal

Frequent PAC may preceed paroxysmal supraventricular

tachycardia , A-fib or A-flutter.

In PAC , The SA node fires an impulse, but then an

irritable focus jumps in, firing its own impulse before the
SA node can fire again.

Patients are mostly asymptomatic and PAC are not

considered abnormal findings .

PAC used to be diagnose incidentally during routine

check ups. Rarely , Patient might feel palpitations.

PACs may be conducted through the atrioventricular

54 | P a g e
(AV) node and the rest of the heart, depending on their
prematurity and the status of the AV and intraventricular
conduction system.

Nonconducted or blocked PACs dont trigger a QRS

complex.

Nicotine in Cigarette smoking is responsible for PAC.

Also , triggered
by alcohol , anxiety, fatigue, fever, and infectious
diseases.

PACs may also be associated with coronary or valvular

heart disease, acute respiratory failure, hypoxia,
pulmonary disease, digoxin toxicity, and certain
electrolyte imbalances.

Treatment : No treatment is Required , Reassure the

patients about this findings . Beta blockers will help in
symptomatics .

55 | P a g e
 SUPRAVENTRICULAR TACHYCARDIA

Rapid heart rhythm originating at or above the

atrioventricular node. If it occurs episodically , then it is
called as Paroxysmal SVTs . P waves are not seen due to
the fast rate

Rate : 150-250 bpm (Around 200bpm on this ECG)

Rhythm : Regular
P wave : Frequently buried in preceeding T wave and
difficult to see
PR interval : Usually not possible to measure
QRS : Normal but may be widened if conducted through
ventricles

SVT may be related to caffeine intake , nicotin , anxiety ,

stress and many other reasons in healthy individual.

56 | P a g e
 PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA

PVTs are rapid rhythm that starts and stop suddenly.

Rate : 150-250 bpm

Rhythm : Regular
P waves : Frequently buried in preceeding T waves and
difficult to see.
PR interval : not possible to measure
QRS : Normal , but may be wide if abnormally
conducted through ventricles

For acute interpretation of ECG , beginning or end of

PSVT must be seen.

Symptoms can arise suddenly and may resolve without

treatment , Episodes can last from a few minutes to one
or two days, sometimes persisting until treated. The
rapid heart rate reduces the opportunity for the "pump"
to fill between beats decreasing cardiac output and
consequently blood pressure.

Patient will present to you with the following symptoms

(typical with a rate of 150270 bpm) Pounding heart ,

57 | P a g e
Shortness of breath, Chest pain , Rapid breathing ,
Anxiety , Dizziness , Loss of consciousness (in only the
most serious cases) .

PSVTs is sometimes called as Paroxysmal Atrial

Tachycardia (PAT) . AV nodal re-entry is most common
cause of this arrhythmias which occurs in around 75% of
old patients with underlying other heart pathology .In
this condition , the AV node is pathologically devided
into two functional pathways. The electrical impulse
usually proceeds anterograde down the slow pathway
and retrograde up the fast pathway.

The P waves are recorded simultaneously with the QRS

complexes (which occur in rapid sequences) and are
therefore obscured on ECG.

Reentry PSVTs can be reverted to normal sinus rhythm

by interrupting the re-entry pathway , for example : the
performance of vagal maneuvers often improves the
condition by increasing AV nodal refractoriness

Atrial re-entry causes about 10% of all PSVTs. The re-

entry pathway is in atria.

The P wave if recorded before QRS complex, usually

associated with organic heart disease.

Automatic atrial conduction results in 5% of all PVSTs.

These are not paroxysmal, last days to years and
resistant to treatment. P wave will have abnormal
configuration

Treatment : Valsalva Manuevers or Carotid Massage

58 | P a g e
usually alleviate the symptoms & are first choice to do
when patient presents with SVTs. Pharmacological
management depends mainly on the Types of SVTs .

Aim is to prevent rapid impulse conduction to Ventricles

(Because Ventricular Tachycardia can be Fatal ). Prevent
using drugs like Beta blockers , CCBs if the cause of SVTs
is atrial fibrillation .

Otherwise - Procainamide , Digoxin should be

administered in stable patient.

If the patient is unstable, direct current cardioversion

should be performed.

Digoxin can be use in SVTs because Digoxin will block

AV node and decrease AV conductivity + increase
contractility of heart , so it will also , increases cardiac
output which is very important to provide enough blood
supply to organs to prevent hypoperfusion injury.

59 | P a g e
 WANDERING ATRIAL PACEMAKER

Pacemaker site transfer between the SA node and AV

node. It transfer from SA node to other latent pacemaker
sites in the atria and the AV junction and then moves
back to SA node

Rate : Normal
Rhythm : Irregular
P wave : At least three different forms , determined by
the focus in the atria
PR interval : Variable , depend upon the origin of site
QRS : Normal

Wandering Atrial Pacemaker and MAT are in the DDx.

Both share P wave changes in shape and size but the rate
in MAT is fast and in WAP is normal.
Wandering pacemaker may be caused by:
Varying vagal tone
Digoxin toxicity
Organic heart disease such as rheumatic carditis.
WAP may be normal in young patients , very old patients
and is common in athletes who have slow heart rates ,
arrhythmia is usually transient , Usually No symptoms
present and so difficult to identify.

Treatment
No treatment if asymptomatic
Correction of the underlying cause

60 | P a g e
 CHAPTER 4 : VENTRICU LAR ARRYTHMIAS

IDIOVENTRICULAR RHYTHM

If the ventricle does not receive triggering signals , the

ventricular myocardium itself becomes the pacemaker
(escape rhythm). This is called Idioventricular Rhythm.
Ventricular signals are transmitted cell-to-cell between
cardiomyocytes and not by the conduction system,
creating wide sometimes bizarre QRS complexes(> 0.12
sec)
.

Rate : 20-40 bpm

Rhythm : Regular
P waves : None
PR interval : None
QRS : Wide (>0.10 sec) . Bizzare type appearance

Idioventricular rhythms occur when all of the hearts

other pacemakers fail to function or when
supraventricular impulses cant reach the ventricles
because of a block in the conduction system.
Ventricular arrhythmias originate in the ventricles below
the bundle of His and fires at the rate of 20-40 bpm .

Idioventricular rhytm may also be called as agonal

rhythm. If the rate is >40 bpm, it is called accelerated
idioventricular rhythm. The rate of 20-40 is the

61 | P a g e
"intrinsic automaticity" of the ventricular myocardium.

Bizzare appearance : The T wave and the QRS complex

deflect in opposite directions because of the difference in
the action potential during ventricular depolarization
and repolarization. P wave is absent because
depolarization of atria does not occur.
The arrhythmias may accompany third-degree heart
block or be caused by anything which damages AV node
like infarction or blocks it like digoxin.

ACCELETATED IDIOVENTRICULAR RHYTHM

Same as Idioventricular rhytm , only difference is , heart

rate. Here its 40-100 bpm , while in IVR its been 20-40
bpm

Rate : 40-100 bpm

Rhythm : Regular
P waves :None
PR interval :None
QRS : Wide (>10 sec) , Bizzare appearance

Idioventricular rhythms appear when supraventricular

pacing sites are depressed or absent. If the heart rate

62 | P a g e
become slow , diminished cardiac output is expected.

History is helpful for identifying the underlying etiology

for AIVR. Most patients with AIVR presents with chest
pain or shortness of breath (symptoms related to
myocardial ischemia with history of myocardial
reperfusion with drugs or coronary artery
interventions.) ,Plus Peripheral edema, cyanosis,
clubbing, (With the history of cardiomyopathy,
myocarditis, and congenital heart diseases )

Treatment : Idioventricular rhythm should never be

treated with lidocaine or other antiarrhythmics that
would suppress that safety mechanism.

If the symptoms develops , immediate treatment

required to increase his heart rate, improve cardiac
output and establish a normal rhythm. Treat the
Underlying Cause .

In life-threatening situations in which time is critical, a

transcutaneous pacemaker may be used to regulate
heart rate.

VENTRICULAR TACHYCARDIA (MONOMORPHIC)

Ventricular tachycardia refers to any rhythm faster than

100 beats per minute, with 3 or more irregular beats in a
row, arising distal to the bundle of His. In Monomorphic
type , The shape, size and amplitude of QRS complex will
be same

63 | P a g e
Rate : 100-250 bpm
Rhythm : Regular
P waves : None or not associated with the QRS
PR interval : None
QRS : Wide (>0.10sec) , Bizzare appearance
It is important for a physician to confirm the presence or
absence of pulses because monomorphic VT may be
perfusing or non perfusing. Sustained SVTs requiring
immediate treatment to prevent death, monomorphic VT
will probably deteriote into VF or unstable VT if
sustained and not treated.

Ventricular tachycardia usually results from increased

myocardial irritability, which may be triggered by
enhanced automaticity or reentry within the Purkinje
system or by PVCs.

Conditions that can cause ventricular tachycardia

include:
Myocardial ischemia & Infarction
Coronary artery disease
Valvular heart disease
Heart failure, Cardiomyopathy
Hypokalemia
Drugs like digoxin , procainamide, quinidine or
cocaine

64 | P a g e
 VENTRICULAR TACHYCARDIA (POLYMORPHIC)

The difference between monomorphic and polymorphic

is the presence of different type of complexes in
polymorphic.

Rate : 100-250 bpm

Rhythm : Regular
P waves : None or not associated with the QRS
PR interval : None
QRS : Wide (>0.10sec) , Bizzare appearance

Electrolyte abnormality is a possible etiology behind this.

Patient in VT will present with Palpitation,

lightheadedness, and syncope (from diminished cerebral
perfusion). Chest pain (due to ischemia or to the rhythm
itself. Anxiety usually present. Some patients describe a
sensation of neck fullness, which may be related to
increased central venous pressure and cannon a waves.

Cannon A waves are related to right atrial contraction

against a closed tricuspid valve (Jugular Venous Pressure
Graph is Discussed later on) . Dyspnea (due to increased
pulmonary venous pressures when left atrial contraction

65 | P a g e
against a closed mitral valve). Ventricular Tachycardia
can convert into Ventricular Fibrillation if not treated . V.
fib is a medical emergency .

It is important to confirm the presence or absence of

pulses because polymorphic VT may be perfusing or non
perfusing.

Treatment of VT: They are Treated aggressively by Anti

arrythmimc drugs . Coronary revascularization is
indicated to reduce the risk of SCD in patients with VF
when there is presence of direct evidence of acute
myocardial ischemia . Amiodarone or lidocaine are
usually used.

VENTRICULAR FIBRILLATION

Is when ventricles fire rapidly and asynchronously at rate

more than 300.Most common cause of death in cardiac ER.
Massive hypoperfusion will occur throughout the body

Rate : 300-600
Rhythm : Extremely Irregular
P wave : Absent
PR interval : N/A
QRS : Fibrillatory baseline

66 | P a g e
Ventricular fibrillation is defined when Ventricles beat
>250bpm.

V-fib, is a pattern of electrical activity in the ventricles in

which electrical impulses arise from many different foci.
It produces no effective muscular contraction and no
cardiac output. Untreated ventricular fibrillation causes
most cases of sudden cardiac death in people outside of a
hospital.

The ventricular rate, P wave, PR interval, QRS complex, T

wave, and QT interval cannot be determined.
Patient will present with Prodrome of symptoms of chest
pain, fatigue, palpitations, and other nonspecific
complaints (50% patients visit in 4 week before death) ,
A history of Left Ventricular impairment (LV ejection
fraction < 30-35%) is the single greatest risk factor for
sudden death from VF.

Otherwise , symptoms depend upon the underlying

cause of V-Fib : Coronary artery Disease , Hypertrohpic
or dilated cardiomyopathy , valvular pathology ,
Myocarditis , Congenital Heart Disease (All this
pathology are discussed in Pathology Section)

Treatment : if pulseless , treat with immediate

defibrillation followed by epinephrine , vasopressin ,
amiodarone or lidocaine.

If pulse is present treat with amiodarone and

synchronized cardioversion.

67 | P a g e
 TORSADE DE POINTES

Characterized by a gradual change in the amplitude and

twisting of the QRS complexes around the isoelectric line

Rate : 200-250 bpm

Rhythm : Irregular
P waves : None
PR interval : None
QRS : Wide (>0.10sec) , Bizzare appearance

The main causes of Torsades are Drugs that prolong QT

interval and electrolyte abnormalities such as
Hypomagnessemia.

This rhythm is unusual variant of polymorphic VT with

the normal or long QT intervals. It may deteriotes to
Ventricular fibrillation or asystole. Patient usually
present with recurrent episodes of palpitations,
dizziness, and syncope; however, sudden cardiac death
can occur with the first episode. Nausea, cold sweats,
shortness of breath, and chest pain also may occur but
are nonspecific and can be produced by any form of
tachyarrhythmia.

HALLMARK : QRS complexes that rotate about the

68 | P a g e
baseline, deflecting downward and upward for several
beats.

Treatment : Magnesium (Decreases the influx of calcium,

thus lowering the amplitude of Action Potentials ).

Beta-1 Agonist Drugs (to increase Heart rate and

decrease Prolonged QT interval).

If torsades convert into V-Fib Direct Current

Cardioversion is required .

PULSELESS ELECTRICAL ACTIVITY

When you try to measure pulse ,you will not detect them
, but , when you will perform ECG , identifiable electrical
rhythms are produced.

Rate , Rhythm , P waves .PR interval ,QRS - All reflects

the underlying rhythm.

Rhythm may be sinus , atrial , juinctional , or ventricular

in origin. PEA is also called as electromechanical
dissociation .

69 | P a g e
In pulseless electrical activity, the heart muscle loses its
ability to contract even though electrical activity is
preserved. As a result, the patient goes into cardiac
arrest.
On an electrocardiogram, youll see evidence of
organized electrical activity, but you wont be able to
palpate a pulse or measure the blood pressure.

This condition requires rapid identification and

treatment.
Causes include :
Hypovolemia , Hypoxia,
Acidosis, Tension pneumothorax,
Cardiac tamponade, massive pulmonary
embolism
Hypothermia, hyperkalemia,
Overdose of drugs such as tricyclic
antidepressants , calcium channel blockers ,
digoxin

Treatment : Cardiopulmonary resuscitation is the

immediate treatment, along with epinephrine. Atropine
may be given to patients with bradycardia. Subsequent
treatment focuses on identifying and correcting the
underlying cause.

70 | P a g e
 ASYSTOLE

Electical activity in the ventricles is completely absent

A straight line

Rate, Rhythm, P waves, PR interval, QRS : None

Always confirm asystole by checking the ECG in two

different leads . Also search to identify underlying
ventricular fibrillation.

This most commonly occur from a prolonged period of

cardiac arrest without effective resuscitation. Seek to
identify the underlying cause as in PEA.

The patient is in cardiopulmonary arrest. Without rapid

initiation of CPR (Cardio-pulmonary Resuscitation) and
appropriate treatment, the situation quickly becomes
irreversible

Anything that causes inadequate blood flow to the heart

may lead to asystole

The immediate treatment for asystole is CPR

71 | P a g e
 CHAPTER 4 : HEART B L OCKS

ATRIOVENTRICULAR BLOCKS (FIRST DEGREE

BLOCK)

It is the prolongation of the PR interval on an

electrocardiogram (ECG) to more than 200 msec.

Rate : Depends on the underlying rhythm

Rhythm : Regular
P waves : Normal
PR interval : Prolonged (>0.20sec)
QRS : Normal

Usually AV block is benign , but if associated with an

acute MI. it may lead to futher AV defects.. Whenever
there is increase in PR interval , think about AV node
problem

First-degree AV block occurs when impulses from the

atria are consistently delayed during conduction through
the AV node. Conduction eventually occurs , it just takes
longer than normal. just the underlying cause will be
treated, not the conduction disturbance itself.

72 | P a g e
Patient is usually asymptomatic at REST . Markedly
prolonged PR interval may reduce exercise tolerance in
some patients with left ventricular systolic dysfunction.

Syncope may result from transient high-degree AV block,

especially in those with infranodal block and wide QRS
complex. Other symptoms might be present depending
upon the causes of AV Block.

Causes of AV block :

Temporary block : Myocardial infarction (MI), usually

inferior wall MI , Digoxin toxicity ,Calcium Channel and
Beta blockers , Cardiac surgery

Permanent block : Changes associated with aging ,

Congenital abnormalities , MI, usually anteroseptal MI ,
Cardiomyopathy , Cardiac surgery

Treatment :

Asymptomatics : No treatment ,

Symptomatics : If PR interval > 300 msec, Placement of a

dual-chamber pacemaker, medications (eg, atropine,
isoproterenol) can be used in anticipation of insertion of
a cardiac pacemaker.

Warning : Avoid B-blockers and CCBs (both slowers the

conduction)

73 | P a g e
 2 N D DEGREE AV BLOCK : MOBITZ TYPE I

P-R interval becomes progressively longer and then one P

wave will be block , resulting in no QRS production. Note
that P wave is formed .and later on normal cycle
continues.

Rate : Depends on the rate of underlying rhythm

Rhythm: Irregular
P waves : Normal
PR interval : Progressively become long until one P
wave is blocked and a QRS is dropped
QRS : Normal (Absent during block)

Ischemia involving right coronary artery is one potential

cause. Because RCA supplies AV node in 80% of Patients.

Hallmark : increasing PR interval with successive beat

and sudden drop and cycle repeats

Usually asymptomatic, a patient with type I second-

degree AV block may show signs and symptoms of
decreased cardiac output, such as light-headedness or
hypotension.
Symptoms may be especially pronounced if the
ventricular rate is slow.

74 | P a g e
Treatment :
For asymptomatics No Rx
For symptomatics : Atropine may improve AV
node conduction
For long term relief : Temporary Pacemaker.

2 N D DEGREE AV BLOCK : MOBITZ TYPE II

Conduction ratio (P waves to QRS complexes) is

commonly 2:1 , 3:1, or 4:1
QRR complexes are usually wide because this block
usually involves bot right and left bundle branch block

Rate : Atrial rate (60-100bpm) , Faster than the

ventricular rate (because they are blocked)
Rhythm : Atrial regular, and ventricular : Irregular
P Waves : Normal , more P waves than QRS complexes
PR interval : Normal or prolonged but constant
QRS : Usually wide

Resulting Bradycardia can compromise cadiac output

and lead to complete AV block. This rhythm often

75 | P a g e
occurs with cardiac ischemia or an MI.

Occasional impulses from the SA node fail to conduct to

the ventricles so a drop beat will be seen

In 2:1 second-degree atrioventricular (AV) block, every

other QRS complex is dropped, so there are always two P
waves for every QRS complex.

In 3:1 three P waves for every QRS complex. The

resulting ventricular rhythm is regular.

Patient is usually asymptomatic , but , as the number of

dropped beats increases, patients may experience
palpitations, fatigue, dyspnea, chest pain, or light-
headedness.

On physical examination, you may note hypotension, and

the pulse may be slow and regular or irregular.

Patient must be kept under frequent observation . if

symptoms develop
Aim in treatment use to be

Increase cardiac output by increasing heart rate

to prevent underperfusion of organs. Atropine,
dopamine, or epinephrine may be given for
symptomatic bradycardia

Pacemaker

Discontinue digoxin, if its the cause of the

arrhythmia

76 | P a g e
 3 R D DEGREE AV BLOCK

Electrical block is at or below the AV node , and so ,

conduction between the atria and ventricle is absent. 3rd
degree heart block is also called as complete heart block

Rate : Atrial (60-100bpm) , Ventricular : 40-60 bpm if

escape focus is junctional , <40 bpm if escape focus is
ventricular
Rhythm : Usually regular , but atria and ventricles
contracts independently
P Waves : Normal , may be superimposed on QRS
complexes or T waves
PR interval : Varies greatly
QRS : Normal , if ventricles are activated by junctional
escape focus , wide if escape focus is ventricular

It is most commonly a congenital condition. This block

may also be caused by :
Coronary artery disease an anterior or inferior
wall MI, degenerative changes in the heart
Drugs like Digoxin toxicity, calcium channel
blockers, beta-adrenergic blockers, or surgical
injury

Patients are symptomatics, symptoms include severe

fatigue, dyspnea, chest pain, lightheadedness, changes in
mental status, and loss of consciousness.
You may note hypotension, pallor, diaphoresis,

77 | P a g e
bradycardia, and a variation in the intensity of the pulse.
Therapy aims to improve the ventricular rate.

Treatment : Atropine , Dopamine , Epinephrine,

temporary pacing. For permanent block requires
permanent pacemaker.

SINOATRIAL BLOCK (SA BLOCK)

There is drop of beat , but , after beat drop , cycle

continues with normal rate and rhythm.

Rate : Normal to slow , depends upon the duration and

frequency of SA block
Rhythm : Irregular whenever SA blocks occur , Regular
after that
P waves : Absent during drop beat, but once cycle
continues it will be normal
PR interval : Depends upon the duration of drop beat ,
afterward , it will be normal
QRS : Depends upon the duration of drop beat ,
afterward , it will be normal

Cardiac output can decrease during drop beat . usually

asymptomatic , but if last longer , syncope or dizziness

78 | P a g e
can occur. SA Blocks must not be confuse with A)
Mobitz type l AV Block (discussed next) where there is
prolongation of PR intervation with every successive
beat and then beat is dropped. B) P waves are present ,
ventricular beat is dropped. Here , PR interval remains
same after all beats and problem is with SA node.

Patients are usually asymptomatics , while In some

people they can cause fainting, altered mental status,
chest pain, hypoperfusion, and signs of shock.

Treatment : Not required for asymptomatics , but in

emergent situation use Atropine or Transuctaneous
Pacing .

RIGHT & LEFT BUNDLE BRANCH BLOCKS

Notches in the QRS complex are classics of BBB

Rate : Depends upon the rate of underlying rhythm

Rhythm : Regular
P Waves : Normal
PR interval : Normal
QRS : Usually wide (>0.10 sec) with a notched
appearance

79 | P a g e
Commonly , BBB occur in Coronary artery Disease

Potential complication of an Myocardial Infarction is a

bundle-branch block

Right bundle-branch block

RBBB occurs with such conditions as anterior wall MI,
CAD, cardiomyopathy, cor pulmonale, and pulmonary
embolism

Left bundle-branch block

Left bundle-branch block (LBBB) never occurs normally.
This block is usually caused by hypertensive heart
disease, aortic stenosis, degenerative changes of the
conduction system, or Coronary artery disease.

Left anterior fascicular block is a cardiac condition

distinguished from left bundle branch block. It is caused
by only the anterior half of the left bundle branch being

80 | P a g e
defective. It is manifest on the ECG by left axis
deviation.

It is the most common type of intraventricular

conduction defect seen in acute anterior
myocardial infarction, and the left anterior
descending artery is usually the culprit vessel.
It can be seen with acute inferior wall
myocardial infarction.
It also associated with hypertensive heart
disease, aortic valvular disease,
cardiomyopathies, and degenerative fibrotic
disease of the cardiac skeleton.

Left posterior fascicular block (LPFB) is a condition

where the left posterior fascicle, i.e. the backside part of
the left cardiac bundle, does not conduct the electrical
impulses from the atrioventricular node. The electricity
then has to go through the other fascicle, and thus is a
frontal right axis deviation seen on the ECG.

BBB are usually normal , even some people are born with
this , but , in Some people it describes the underlying
defect (Causes mentioned above).

Treatment is not required for asymptomatics , Treat

according to the underlying cause . In severe Cases
Pacemaker might be required.

81 | P a g e
 CHAPTER 5 : MYOCARD IAL INFARCTION

Acute myocardial infarction : Pain is the most common

presenting symptom in patients with AMI. The pain is
typically felt substernally or in the epigastrium. Its often
described as Crushing or Stabbing or Burning pain .
Pain may also irradiate to left arm and/or jaw (because
the sympathetic fibres from T1-T2 will supply both heart
and left arm, jaw) , sudden onset of shortness of breath ,
fatigue or adrenergic symptoms .

Pain is not controlled by Nitroglycerin.

Serum Cardiac markers will be released into the blood

due to Cell lysis/death . Markers will not be present in
blood if myocardiocyte does not die (example : in Angina
Pectoralis)

Troponin I (Specific marker)- Rises by first 4

hours and remain elevated for 7-10 days.(usually
drawn every 8 hours three times till MI is ruled
out)
Creatine Kinase-MB peaks about 20 hours after
AMI.
LDH (Lactate dehydrogenase) is marker of
reinfarction within 7 days.

On ECG , Total occlusion of artery will result in ST

elevation (depression means ischemia , elevation means
injury) .

In Subtotal occlusion or transient occlusion , there will

be adequate collateral circulation , then ST segment
elevation does not occur. Most patients who present with
ST segment elevation , eventually develop Q wave on

82 | P a g e
ECG (which will indicate as a marker of previous MI)

Causes of MI :
Angina, reinfarction, infarct extension
Ischemic
Heart failure, cardiogenic shock, mitral
Mechanical valve dysfunction, aneurysms, cardiac
Rupture
Atrial or ventricular arrhythmias, sinus or
Arrhythmic atrioventricular node dysfunction

Central nervous system or peripheral

Embolic embolization

Inflammatory Pericarditis

Differentials for MI : Gastroesophageal reflux disease &

Peptic ulcer disease (pain related to certain food ,
relieved by antacids) , Stable angina (Pain on exertion ,
ST segment depression) , Unstable angina (pain at rest,
ST segment depression ) , Esophageal problems ,
Pericarditis (Diffuse ST-segment elevation) , Pleuritis,
Prinzmental angina (pain at rest, ST ELEVATION)

Post MI Complications :
Cardiac arrest : This most commonly occurs due to
patients developing ventricular fibrillation and is the
most common cause of death following a MI. Patients are
managed with defibrillation.

Cardiogenic shock : If a large part of the ventricular

myocardium is damaged in the infarction the ejection
fraction of the heart may decrease to the point that the

83 | P a g e
patient develops cardiogenic shock. This is difficult to
treat. Other causes of cardiogenic shock include the
'mechanical' complications such as left ventricular free
wall rupture as listed below. Patients may require
inotropic support and/or an intra-aortic balloon pump.

Chronic heart failure: As described above, if the patient

survives the acute phase their ventricular myocardium
may be dysfunctional resulting in chronic heart failure.
Loop diuretics such as furosemide will decrease fluid
overload. Both ACE-inhibitors and beta-blockers have
been shown to improve the long-term prognosis of
patients with chronic heart failure.

Tachyarrhythmias : Ventricular fibrillation, as

mentioned above, is the most common cause of death
following a MI. Other common arrhythmias including
ventricular tachycardia.

Bradyarrhythmias : Atrioventricular block is more

common following inferior myocardial infarctions.

Pericarditis : Pericarditis in the first 48 hours following

a transmural MI is common (c. 10% of patients). The
pain is typical for pericarditis (worse on lying flat etc), a
pericardial rub may be heard and a pericardial effusion
may be demonstrated with an echocardiogram.

Dressler's syndrome tends to occur around 2-6 weeks

following a MI. The underlying pathophysiology is
thought to be an autoimmune reaction against antigenic
proteins formed as the myocardium recovers. It is

84 | P a g e
characterised by a combination of fever, pleuritic pain,
pericardial effusion and a raised ESR. It is treated with
NSAIDs.

Left ventricular aneurysm : The ischemic damage

sustained may weaken the myocardium resulting in
aneurysm formation. This is typically associated with
persistent ST elevation and left ventricular failure.
Thrombus may form within the aneurysm increasing the
risk of stroke. Patients are therefore anticoagulated.

Left ventricular free wall rupture : This is seen in

around 3% of MIs and occurs around 1-2 weeks
afterwards. Patients present with acute heart failure
secondary to cardiac tamponade (raised JVP, pulsus
paradoxus, diminished heart sounds). Urgent
pericardiocentesis and thoracotomy are required.

Ventricular septal defect : Rupture of the

interventricular septum usually occurs in the first week
and is seen in around 1-2% of patients. Features: acute
heart failure associated with a pan-systolic murmur. An
echocardiogram is diagnostic and will exclude acute
mitral regurgitation which presents in a similar fashion.
Urgent surgical correction is needed.

Acute mitral regurgitation : More common with infero-

posterior infarction and may be due to ischemia or
rupture of the papillary muscle. An early-to-mid systolic
murmur is typically heard. Patients are treated with
vasodilator therapy but often require emergency surgical
repair.

85 | P a g e
ECG CHANGE FROM DAY 1 TO YEAR LATER

86 | P a g e
 ST SEGMENT CHANGES FROM ISCHEMIA TO MI

ST Segment elevates as heart progresses toward

infarction.

Treatment : Medical therapy with aspirin, heparin,

nitrates, and beta blockers is indicated in patients who
have had a myocardial infarction and have ongoing
ischemic symptoms. Calcium channel blockers are
contraindicated for acute coronary syndrome , but as
drug of choice in Prinzmetal angina.

87 | P a g e
An intra-aortic balloon pump (IABP) should be
inserted promptly in patients with hemodynamic
instability or severe LV systolic dysfunction. Coronary
angiography should be performed in patients who are
stabilized with medical therapy, but emergency
angiography may be undertaken in unstable patients.
Revascularization, percutaneous or surgical, is
associated with improved prognosis.

ST SEGMENT ELEVATION & DEPRESSION

A normal ST segment represents early ventricular

repolarization. Displacement of the ST segment can be
caused by various conditions listed below :

88 | P a g e
Primary causes of ST segment depression

Myocardial ischemia
Left ventricular Hypertrophy
Intraventricular conduction defects
Medication (eg digitalis)
Reciprocal changes in leads opposite the area of
acute injury

Primary Causes of ST Elevation :

ST elevation > 1mm in the limb leads and >2mm in the

chest leads indicates an evolving acute MI until there is
proof to the contrary.

Early repolarization (normal variant in young

adults)

Pericarditis

Ventricular aneurysm

Pulmonary embolism

Intracranial Hemmorrhage

89 | P a g e
Lead aVR is a non diagnostic lead and does not show any
change in an MI

An MI may not be limited to just one region of the heart ,

for example, if there are changes in leads V3 , V4
(anterior) and in l , aVL , V5 & V6 (lateral) , the resulting
MI is called as anterolateral infarction.

90 | P a g e
 INFERIOR WALL MI

Results from occlusion of the right coronary artery

Posterior descending branch

ECG Changes : ST segment elevation in leads ll , lll , and

aVF

Be alert for symptomatic sinus bradycardia , AV blocks ,

hypotension and hypopersion which can lead this MI.

91 | P a g e
 ANTERIOR WALL MI

Occlusion of the left coronary artery Left anterior

descending branch

ECG changes : ST segment elevation with tall T waves &

taller than normal R waves in lead V3 & V4

92 | P a g e
 LATERAL WALL MI

Occlusion of left coronary artery Circumflex branch

ECG Changes : ST segment elevation in leads l, aVL , V5 &

V6

Lateral MI is often associated with anterior or inferior

wall MI. Be alert for the changes that may indicate
cardiogenic shock or congestive heart failure.

93 | P a g e
 CHAPTER 6 : JUNCTIONAL ARRYTHMIA S

JUNCTIONAL RHYTHM

The atria and SA node do not perform their normal

pacemaking function. A junctional escape rhythm begins

Rate : 40-60 bpm

Rhythm : Regular
P Waves : Absent , inverted , buried or retrograde
PR interval : None , short or retrograde
QRS : Normal

Junctional arrhythmias originate in the atrioventricular

(AV) junctionthe area around the AV node and the
bundle of His.
The arrhythmias occur when the sinoatrial (SA) node, a
higher pacemaker, is suppressed and fails to conduct
impulses or when a block occurs in conduction.

Electrical impulses may then be initiated by pacemaker

cells in the AV junction. AV node fires at the rate of 40-60
bpm.
Treatment : For asymptomatic : No treatments . In
patients with complete AV block, high-grade AV block, or
symptomatic sick sinus syndrome (ie, sinus node
dysfunction), a permanent pacemaker may be needed.

94 | P a g e
 ACCELERATED JUNCTIONAL RHYTHM

Rate : 60-100 bpm

Rhythm : Regular
P waves : Absent , inverted , buried or retrograde
PR interval : None , Short or retrograde
QRS : Normal

Moniter the patient , not just the ECG , for clinical

improvement.

An accelerated junctional rhythm is caused by an

irritable focus in the AV junction that speeds up to take
over as the hearts pacemaker (AV dissociation).

The atria are depolarized by means of retrograde

conduction, and the ventricles are depolarized normally.
The accelerated rate is usually between 60 and 100
beats/minute.

Conditions Responsible for AJR are :

Digoxin toxicity
Hypokalemia
Inferior or posterior wall MI
Rheumatic heart disease
Valvular heart disease.

Treatment : Same as in Junctional Rhythm.

95 | P a g e
 JUNCTIONAL ESCAPE BEATS

A junctional escape beat is a delayed heartbeat

originating not from the atrium but from an ectopic focus
somewhere in the AV junction..An escape complex comes
later than the next expected sinus complex

Rate : Depends on the rate of underlying rhythm

Rhythm : Irregular , whenever an escape beat occurs
P waves : None , inverted , buried , or retrograde in the
escape beat
PR interval : None , short , or retrograde
QRS : Normal

A junctional escape rhythm is a string of beats that

occurs after a conduction delay from the atria. AV node
junction firing rate is 40 to 60 beats/minute.
A junctional escape rhythm can be caused by any
condition that disturbs SA node function or enhances AV
junction automaticity.

Causes of the arrhythmia include:

Sick sinus syndrome
Vagal stimulation , Digoxin toxicity
Inferior wall MI
Rheumatic heart disease.
Junctional rhythms (if a bradycardia), can cause
decreased cardiac output. Therefore, the person may

96 | P a g e
exhibit signs and symptoms similar to other bradycardia
such as lightheadedness, dizziness, hypotension, and
syncope. Usually this rhythm can be tolerated if the rate
is above 50 bpm

Treat the underlying cause , Atropine may be given to

increase the heart rate, or a temporary or permanent
pacemaker may be inserted if the patient is symptomatic.

WOLF-PARKINSON WHITE SYNDROME

In WPW , an accessory conduction pathway is present

between the atria and the ventricles. Electrical impulse
are rapidly conducted to the ventricles

These rapid impulses create a slurring of the initial

portion of the QRS called the Delta wave

Rate : Depends on rate of underlying rhythm

Rhythm : Regular unless associated with A-fib
P waves : Normal , unless A-fib is present
PR interval : Short (<0.12 sec) if p wave is present
QRS : Wide (>0.10sec) , Delta wave present

97 | P a g e
Clinical Note : WPW is associated with narrow complex
tachycardias , including A-Flutter and A-Fib

Usually not treated till patient remains asymptomatic ,

this syndrome must be treated if tachyarrythmias, such
as atrial fibrillation and atrial flutter occurs .

First, electrophysiology studies are done to determine

the location of the conduction pathway and evaluate
specific treatments.

Pharmacologic treatment : Block Accessory pathway by

Use of Procainamide or Quinidine (Class la
antiarythmic). DONT SLOW AV CONDUCTION (AVOID
DIGOXIN , B-BLOCKERS , CA+ CHANNEL BLOCKERS ,
ADENOSINE)

Radiofrequency ablation may be used with resistant

tachyarrhythmias.

PREMATURE JUCTIONAL CONTRACTIONS

Enhanced automaticity in the AV junction produces PJCs

98 | P a g e
Rate : Depends on the rate of underlying rhythm
Rhythm : Irregular whenever a PJC occurs
P waves : Absent. Inverted , buried , or retrograde in
PJC
PR interval : None, short or retrograde
QRS : Normal
Before deciding that isolated PJCs may be insignificant ,
consider the cause.

PJCs may be caused by

Toxic levels of digoxin (level greater than 2.5

ng/ml)
Excessive caffeine intake
Inferior wall myocardial infarction (MI)
Rheumatic heart disease, valvular disease
Hypoxia, heart failure, or swelling of the AV
junction after heart surgery.

Patient Presentation depends upon the underlying Cause

.

Usually dont require treatment till symptoms develops ,

Treat underlying cause.

SINGLE CHAMBER PACEMAKER RHYTHM -

VENTRICULAR

A pacemaker (or artificial pacemaker, so as not to be

confused with the heart's natural pacemaker) is a
medical device that uses electrical impulses, delivered by
electrodes contracting the heart muscles, to regulate the
beating of the heart. The primary purpose of a

99 | P a g e
pacemaker is to maintain an adequate heart rate . there
are many methods of pacing like : Percussive pacing ,
Transcutaneous pacing , Epicardial pacing (temporary) ,
Transvenous pacing (temporary) , Permanent pacing. It
can be place in atrium or in ventricles or both .

SINGLE CHAMBER PACEMAKER RHYTHM -

ATRIAL

DUAL CHAMBER PACEMAKER RHYTHM ATRIAL

& VENTRICULAR

100 | P a g e
 CHAPTER 7 : PREMATURE VENTRICU LAR
CONTRACTIONS

A premature ventricular contraction (PVC) is an ectopic

beat that may occur in healthy people without causing
problems.
PVCs may occur singly, in clusters of two or more, or in
repeating patterns, such as bigeminy or trigeminy (See
ECG below

PVCs are usually caused by electrical irritability in the

ventricular conduction system or muscle tissue.

This irritability may be provoked by anything that

disrupts normal electrolyte shifts during cell
depolarization and repolarization.
Conditions that can disrupt electrolyte shifts include:

Electrolyte imbalances, such as hypokalemia,

hyperkalemia, hypomagnesemia, and
hypocalcemia , Metabolic acidosis, Hypoxia
Myocardial ischemia and infarction
Drugs (cocaine, amphetamines, and tricyclic
antidepressants)
Enlargement of the ventricular chambers
Increased Sympathetic firing , Caffeine or
alcohol ingestion , Tobacco use.

PVCs may be perceived as a skipped heart beat, a strong

beat, or a feeling of suction in the chest. They may also
cause chest pain, a faint feeling, fatigue, or
hyperventilation after exercise

The P wave is usually absent. Retrograde P waves may

be stimulated by the PVC and cause distortion of the ST
segment.

101 | P a g e
The PR interval and QT interval arent measurable on a
premature beat, only on the normal beats Increase in
Duration of QRS complex , T wave deflect in opposite
direction of QRS complex.
Treatment : Usually not treated , If severe & symptomatic
consider B-Blocker or amiodarone

PVC : UNIFORM VS MULTIFORM

Uniform PVCs : PVC that look similar to each other arise

from same site with abnormal waves

Multiform PVCs : PVCs that look different from one

another arise from different sites or from the same site
with abnormal . Multiform PVCs may indicate increased
ventricular irritability.

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 PVC : VENTRICULAR BIGEMINY VS TRIGEMINY

Bigeminy and trigeminy :PVCs that occur every other beat

(bigeminy) or every third beat (trigeminy) : indicates
increased in ventricular irritability.

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 PVC : VENTRICULAR QUADRIGEMINY VS
COUPLETS

Paired PVCs : Two PVCs in a row are called a paired . A

pair can produce ventricular tachycardia because the
second depolarization usually meets refractory tissue. A
salvothree or more PVCs in a rowis considered a run
of ventricular tachycardia

104 | P a g e
COMPONENTS OF PAUSE & QRS COMPLEX GROUPING

105 | P a g e
 CHAPTER 8 : MISCELLA NEOUS

HYPERKALEMIA VS HYPO KALEMIA

106 | P a g e
Potassium level must be regulary moniter on all patients
who are on Digoxin & Diuretics.

The major causes of hyperkalemia are

Renal insufficiency
Diseases of the adrenal gland like Addisons
disease , Aldosterone deficiency
Acidosis , Rhabdomyolysis : potassium shifting
out of cells into the blood circulation
Drugs : ACE inhibitors , NSAIDs , K+ Sparing
Diuretics (Spironolactone) , Digoxin
Low Insulin

Symptoms : Symptoms are fairly nonspecific and

generally include malaise, palpitations and muscle
weakness; mild hyperventilation may indicate a
compensatory response to metabolic acidosis, which is
one of the possible causes of hyperkalemia. Often,
however, the problem is detected during screening blood
tests for a medical disorder, or it only comes to medical
attention after complications have developed, such as
cardiac arrhythmia or sudden death.

When potassium levels exceed 6.5 mmol/l, emergency

lowering of potassium levels is mandated.(Normal : 3.5
5.0 mmol/l).

Immediate Treatment is necessary : Control

underlying Cause + Calcium Gluconate (decreases
myocardial excitation) , & Insulin + 50% Glucose to
shift Potassium into the cell by Na-K ATPase

Major Causes of HypoKalemia are :

107 | P a g e
 Starvation
Gastro-Intestinal Problems like : Diarrhoe
Potassium wasting diuretics like Loops
(furosemide) and Thiazide
(hydrocholorothiazide)
Alkalosis (Shifts the Potassium from plasma into
the cells)

Symptoms :

Mild hypokalemia : Asymptomatic , although it may

cause a small elevation of blood pressure and can
occasionally provoke cardiac arrhythmias.

Moderate hypokalemia : Serum potassium

concentrations of 2.5-3 mEq/L (Nl: 3.5-5.0 mEq/L), may
cause muscular weakness, myalgia, and muscle cramps
(owing to disturbed function of the skeletal muscles),
and constipation (from disturbed function of smooth
muscles).

Severe hypokalemia : flaccid paralysis and hyporeflexia

may result. Rhabdomyolysis will occur if potassium is
less than 2 mEq/L .

Treament : Usually , treat the underlying cause.

K+ Spaing diuretics like Spirinolactone ,Amiloride,

Triampterene , Increase K+ in blood by blocking Na+
reabsorbtion in collecting duct (Normally , under action
of aldosterone Na is reabsorbed & H+ & K+ are
excreted)

108 | P a g e
 HYPERCALCEMIA VS HYPOCALCEMIA

HyperCalcaemia will have Osborn Wave (Positive

Deflection at junction between QRS complex and ST
segement) . Such wave is also seen in Hypothermia
(<32C) 90 F.

Main Causes of HyperCalcemia :

HyperParathyroidism
Malignancies
HyperVitaminosis D
Hyperthyroidism
Renal failure
Presentation : The neuromuscular symptoms of
hypercalcemia are caused by a negative
bathmotropic effect due to the increased
interaction of calcium with sodium channels.
Since calcium blocks sodium channels and
inhibits depolarization of nerve and muscle
fibers, increased calcium raises the threshold for
depolarization.

109 | P a g e
Mnemonic for remembering the effects of
hypercalcaemia: "Stones, Bones, Groans, Thrones and
Psychiatric Overtones" where 1) Stones (renal or biliary)
2) Bones (bone pain) 3) Groans (abdominal pain, nausea
and vomiting) 4) Thrones (sit on throne - polyuria) 5)
Psychiatric overtones (Depression 30-40%, anxiety,
cognitive dysfunction, insomnia, coma) . Other
symptoms can include fatigue, anorexia, and pancreatitis

HypoCalcaemia will Show Prolonged QT time.

Main Causes of Hypocalcemia :

Hypoparathyroidismm
Hypovitaminosis D
Alkalosis
CalcitoninTreatment is mainly concerned in
treating underlying causes.

Presentation : The neuromuscular symptoms of

hypocalcemia are caused by a positive bathmotropic
effect due to the decreased interaction of calcium with
sodium channels . Since calcium blocks sodium channels
and inhibits depolarization of nerve and muscle fibers,
diminished calcium lowers the threshold for
depolarization .

The symptoms can be recalled by the mnemonic "CATS

go numb"- Convulsions, Arrhythmias, Tetany and
numbness/parasthesias in hands, feet, around mouth
and lips.

110 | P a g e
Treatment :

Hypercalcemia : Initiall Therapy : Fluids & Diuretics

(Except Thiazides Group of diuretics which will be
contraindicated)

Additional therapy : Bisphosphonate & Calcitionin.

Hypocalcemia : Intravenous Calcium Gluconate 10%

111 | P a g e
CHAPTER 9 : P & Q W A VE R ELATIONSHIPS

Atrial depolarisation proceeds sequentially from

right to left, with the right atrium activated
before the left atrium.

The right and left atrial waveforms summate to

form the P wave.

The first 1/3 of the P wave corresponds to right

atrial activation, the final 1/3 corresponds to left
atrial activation

the middle 1/3 is a combination of the two.

In most leads (e.g. lead II), the right and left

atrial waveforms move in the same direction,
forming a monophasic P wave.

However, in lead V1 the right and left atrial

waveforms move in opposite directions.

This produces a biphasic P wave with the initial

positive deflection corresponding to right atrial
activation and the subsequent negative
deflection denoting left atrial activation.

This separation of right and left atrial electrical

forces in lead V1 means that abnormalities
affecting each individual atrial waveform can be
discerned in this lead.

Elsewhere, the overall shape of the P wave is

used to infer the atrial abnormalit

112 | P a g e
 P MITRALE/P SINISTROCARDIALE (MITRAL
STENOSIS)

The presence of broad, notched (bifid) P waves in lead

II is a sign of left atrial enlargement, classically due to
mitral stenosis.

Mitral stenosis is a valvular heart disease characterized by

the narrowing of the orifice of the mitral valve of the heart.
Patient might be asymptomatic , but on later stage of
development .

Symptoms of mitral stenosis include:

-Heart failure symptoms, such as dyspnea on exertion

orthopnea and paroxysmal nocturnal dyspnea

- Palpitations, Chest pain , Hemoptysis

- Ascites , edema and hepatomegaly (if right-sided heart

failure developed)

Symptoms increase with exercise and pregnancy

Fatigue , Wasting (weakness)

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Most common cause is Rheumatic Heart Disease and in
some cases Calcification .

P PULMONALE (COR PULMONALE)

The presence of tall, peaked P waves in lead II is a sign of

right atrial enlargement, usually due to pulmonary
hypertension (e.g. COR PULMONALE from chronic
respiratory disease).

RIGHT ATRIAL ENLARGEMENT

Right atrial enlargement causes increased height (>

114 | P a g e
1.5mm) in V1 of the initial positive deflection of the P
wave.

In right atrial enlargement, right atrial

depolarisation lasts longer than normal and its
waveform extends to the end of left atrial
depolarisation.

Although the amplitude of the right atrial

depolarisation current remains unchanged, its
peak now falls on top of that of the left atrial
depolarisation wave.

The combination of these two waveforms

produces a P waves that is taller than normal (>
2.5 mm), although the width remains unchanged
(< 120 ms)

LEFT ATRIAL ENLARGEMENT.

LEFT ATRIAL ENLARGEMENT LEAD V1

115 | P a g e
Left atrial enlargement causes widening (> 40ms wide)
and deepening (> 1mm deep) in V1 of the terminal
negative portion of the P wave.

In left atrial enlargement, left atrial

depolarisation lasts longer than normal but its
amplitude remains unchanged.

Therefore, the height of the resultant P wave

remains within normal limits but its duration is
long. A notch (broken line) near its peak may or
may not be present (P mitrale).

MECHANISM OF Q WAVE

116 | P a g e
 ACUTE PERICARDITIS

Acute Pericarditis must be differentiated from

Myocardial Infarction.

In Pericarditis , ST Elevation does not confine to a

Coronary territory ( Diffuse ST Elevation is seen). The ST
Elevation usually shows concavity upwards (In this ECG
it mimics STEMI)

117 | P a g e
 C AR D IA C PH AR M AC OL OG Y

ANTI-ARRYTHMIC DRUGS

Some arrhythmias are asymptomatics , which usually

does not require any treatment.

For symptomatic arrhythmias : treatment is choosen

based on the type of arrhythmia, the severity of
symptoms being experienced, and the presence of other
conditions (such as, diabetes, kidney failure, or heart
failure) which can affect the course of the treatment.

Class I drugs : Sodium Channel blockers

Class Ia antiarrhythmics : Quinidine , Procainamide
hydrochloride

Act on open or activated state Na+ Channel

On ECG : Prolongs QRS comples & QT interval ----
if associated with syncope then called as Torsade
(Twisting Rhythm) . No effect on SA/AV node.
Quinidine also blocks Muscarinic & Alpha
receptors , so typical side effect caused by them
is called as Cinchonism (Gastro intestinal
problem Constipation/diarrhoe , Tinnitus ,
ocular dysfunction , CNS excitation , hypotension
, Torsades)
Procainamide Less Muscarinic block compared
to quinidine , No alpha block. But, it acts like
Hapten , and adverse side effect is SLE (systemic
lupus erythematous) like syndrome in slow
acetylators , Hematotoxicity , Torsades

Class Ib antiarrhythmics : Lidocaine hydrochloride ,

Mexiletine ,Tocainide

118 | P a g e
 Blocks inactivated Na+ channel
On ECG : Decrease QT interval , Increases Heart
Rate , No effect on SA/AV node .
Use is Post MI , Digoxin toxicity works best in
Hypoxic tissues
Tocainide side effect : Agranulocytosis

Class Ic antiarrhythmics : Flecainide, Propafenone ,

Moricozine

Blocks Fast NA+ channel , especially of His-

Purkinje Tissue
Highly proarrythmogenic , Last choice drugs
when all other option fails.
On ECG : Prolongs QRS , Heart rate is variable

Class ll : B-Blockers : Acebutalol , propranolol , Sotalol ,

Esmolol

Decreases SA & AV nodal activity

On ECG Slight increase in PR interval and
decreases Heart rate

Use : Post MI , Anigna (except Prinzmetal angina ) ,

Anti hypertensive and in Supraventricular tachycardia ,
thyrotoxicosis (Propranolol) , migraine prophylaxis ,
anxiety

Esmolol (IV) is use in acute SVTs

Carvedilol : Beta1 & Alpha 1 blocker (Vasodilates +

decrease Heart rate)

Side-effect :bronchospasm , cold peripheries , fatigue ,

sleep disturbances, including nightmares

119 | P a g e
 Contraindications: uncontrolled heart failure , asthma
, sick sinus syndrome , concurrent verapamil use: may
precipitate severe bradycardia

Class lll : Potassium Channel Blockers : Amiodarone ,

Sotalol

Amiodarone : half life is more than 80 Days ,

High tissue binding ( Decrease metabolism of
Warfarin). Act like class l , ll ,lll ,lV antiarrythmic
drugs .

Side effects : Blue pigmentation of skin ,

Pulmonary fibrosis , Corneal deposits ,
hepatotoxic , Thyroid dysfunction ,
thrombophlebitis (because ideally given I.V) ,
Peripheral Neuropathy , Prolongs QT interval
(Torsades ).

Use : Any arrhythmia

Sotalol : Potassium + B-Blocker , so decreases
Heart rate , decreases AV conduction.
Use : Life threaning Ventricular arrhythmias.

Class lV : Calcium Channel Blockers : Verapamil ,

Diltiazam
Blocks cardiac calcium channel , decreases SA
and AV nodal activity
Use : SVTs , Angina , Anti-hypertensive
Side effects are : Heart failure, constipation,
hypotension, bradycardia
B-blockers , Ca+ channel blocker , digoxin have
additive AV node block effect. If given in
combination there is high risk for AV nodal
blockage.

120 | P a g e
 dihydropyridines (eg Nifedipine , Amlodipine)
family of calcium channel blockers have more
action on vasculature (vasodilation) than on the
heart and so use as a antihypertensive agents ,
Angina & Reynauds Phenomenon . They will
cause reflex tachycardia . Side effects are :
Flushing, headache, ankle swelling.

Unclassified : Adenosine , Atropine , Digoxin ,

Epinephrine , Magnessium Sulphate

Adenosine : Decreases SA & AV nodal activity by

decreasing cAMP (Hyperpolarize the cell by Potassium
efflux) , Duration of action is 10 Sec only .

Drug of choice in Paroxysmal Supraventricular

tachycardia & AV nodal arrythimia.

Effects of adenosine are enhanced by dipyridamole

(anti-platelet agent) and blocked by theophyllines. It
should be avoided in asthmatics due to possible
bronchospasm.

Adverse effects : chest pain ,bronchospasm , can

enhance conduction down accessory pathways resulting
in increased ventricular rate (e.g. WPW syndrome)

Magnessium : Use in Torsades .

Digoxin : is a cardiac glycoside , increases intracellular

Ca+ by inhibiting cardiac Na-K+ ATPase , increases
contractile force and blocks AV node by indirectly
increasing vagal activity (by inhibiting neuronal Na-K+
ATPase).

121 | P a g e
Use : Congestive Heart failure , SVTs (except Wolf
Parkinson White Syndrome). Moniter Potassium level
when patient is on Digoxin .

Digoxin toxicity : lethargy, nausea & vomiting, anorexia,

confusion, yellow-green vision , arrhythmias (e.g. AV
block, bradycardia) .

Precipitating factors are : Hypokalaemia (Classic)

Increasing age , Renal failure , Myocardial ischemia ,
hypomagnesemia, hypercalcemia, hypernatremia,
acidosis , hypoalbuminemia , hypothermia ,
hypothyroidism . Drugs ike amiodarone, quinidine,
verapamil, diltiazem, spironolactone (compete for
secretion in distal convoluted tubule therefore reduce
excretion). Also drugs which cause hypokalaemia e.g.
thiazides and loop diuretics

In Toxicity use Digibind (Fab antibodies toward

digoxin) and supportive electrolyte therapy + lidocaine.

Atropin As a antimuscarinic Increases Heart Rate .

useful to pace up the heart

Epinephrine :
Low dose : increases Heart Rate and Vasodilates (Beta 1
, Beta 2 action)
Medium dose : Increases Heart Rate only (Alpha-1 , Beta
1 , Beta 2 action . Alpha-1 & B-2 action cancel each other
High Dose : Alpha 1 action predominates , so
vasoconstrict and increase Blood pressure (useful in
Shock , Hemorrage and many other condition . Please
Read adrenergic-noradrenergic receptor pharmacology
for more detail)

122 | P a g e
Nesiritide : Recombinant form of Human Beta-type
Natriuretic Peptide. BNP is synsthesize in right atrium
when there is overload/stretch on atrium and will help
to get rid of extra volume by diuresis.Used in
Decompensated Congestive Heart Failure.

Angina pectoris: Drug management

The management of stable angina comprises lifestyle

changes, medication, percutaneous coronary
intervention and surgery.
Medication :
1) All patients should receive aspirin and a statin in
the absence of any contraindication.
2) Sublingual glyceryl trinitrate to abort angina
attacks
3) A beta-blocker or a calicum channel blocker is
generally used first-line
4) If a calcium channel blocker is used as
monotherapy a rate-limiting one such as
verapamil or diltiazem should be used. If used in
combination with a beta-blocker then use a long-
acting dihydropyridine calcium-channel blocker
(e.g. modified-release nifedipine). Remember
that beta-blockers should not be prescribed
concurrently with verapamil (risk of complete
heart block)
5) If there is a poor response to initial treatment
then medication should be increased to the
maximum tolerated dose
6) If a patient is still symptomatic after
monotherapy with a beta-blocker add a calcium
channel blocker and vice versa
7) If a patient is on monotherapy and cannot
tolerate the addition of a calcium channel

123 | P a g e
 blocker or a beta-blocker then consider one of
the following drugs: a long-acting nitrate,
ivabradine, nicorandil or ranolazine
8) If a patient is taking both a beta-blocker and a
calcium-channel blocker then only add a third
drug whilst a patient is awaiting assessment for
Percutaneous Coronary Intervation or Coronary
Artery Bypass Grafting

Nitrates : Have vasodilating effects : Dilate the coronary

arteries and also reduce venous return which in turn
reduces left ventricular work, reducing myocardial
oxygen demand.

Mainly use is in the management of angina and the acute

treatment of heart failure. Sublingual Glyceryl trinitrate
is the most common drug used in patients to relieve
angina attacks .

Side-effects : hypotension , tachycardia , headaches

Nitrate tolerance : Some patients who develop

tolerance should take the second dose of isosorbide
mononitrate after 8 hours, rather than after 12 hours.
this effect is not seen in patients who take modified
release isosorbide mononitrate

Ivabradine : A new class of anti-anginal drug which

works by reducing the heart rate , acts on the If ('funny')
ion current which is highly expressed in the sinoatrial
node, reducing cardiac pacemaker activity

Adverse effects: visual effects, particular luminous

phenomena, are common. Bradycardia, due to the
mechanism of action, may also be seen.

124 | P a g e
 ANTIHYPERTENSIVE DRUGS

Beta Blockers (Atenolol , Acebutolol , Propranolol ,

Metaprolol )

Calcium channel blockers (Nifedipine , Amlodipine)

Diuretics (Loops , Thiazides )

Vasodilators : Hydralazine , Isosorbide Dinitrate ,

nitroprusside , nitroglycerin , ACE- inhibitors , ARBs are
other Antihypertensive and antianginal agents

Hydralazine : used for hypertension in pregnancy and

for severe hypertension, act by increasing cGMP leading
to arterial smooth muscle relaxation

Contraindication : Systemic lupus erythematous ,

ischemic heart disease

Side effect : tachycardia , palpitations , flushing , fluid

retention , headache , drug-induced lupus

Diuretics (Furosemide , Ethacrynic acid ,Thiazides ,

Spironolactone etc)

Loop diuretics (Furosemide and bumetanide,

Ethacrynic Acid)

Inhibiting the Na-K-Cl cotransporter in the thick

ascending limb of the loop of Henle, reducing the
absorption of NaCl

125 | P a g e
 Uses in : heart failure: both acute (usually
intravenously) and chronic (usually orally) ,
Resistant hypertension, particularly in patients
with renal impairment
Adverse effects : Hypotension , Hyponatremia ,
Hypokalemia , Hypochloremic Alkalosis ,
Ototoxicity (Except Ethacyninc Acid) ,
Hypocalcemia , Renal impairment (from
dehydration + direct toxic effect) ,
Hyperglycemia (less common than with
thiazides) , Gout.

Thiazides (Hydrocholorothiazide , Indapamide) :

Inhibit Na+/Cl- transporter on distal tubules ,

Increases Calcium (+ve charge) absorbtion by
inhibiting Sodium (+ve Charge )

Uses : Hypertension , CHF , Nephrolithiaisis (Calcium

stone) ,Nephrogenic Diabetic Insipedus .

Side effects : Sulfonamide hypersensitivity ,

Hypokalaemia & Alkalosis, Hypercalcemia ,
Hyperuricemia , Hyperglycemia , Hyperlipidemia .
Avoid in Patients with Diabetes.

Potassium Sparing Diuretics (Spirinolactone ,

Amiloride, Triampterene)

Spirinolactone : Aldosterone Receptor Antagonist

(On collecting duct) .

Uses : Hyperaldosteronic state , Adjunct to

Potassium wasting diuretics , Antiandrogenic uses ,
CHF

126 | P a g e
 Side effect : Hyperkalaemia & Acidosis , Anti
androgenic (Gynaecomastia in males, hirsuitism ,
acne in female)

Amiloride & Triampterene : Na+ Channel blocker

(on collecting duct)

Use : Adjunt to K+ wasting diuretics , lithium induced

Diabetes insipedus. Side effect : Hyperkalaemia ,
acidosis .

Other diuretics like Carbonic Anhydrase inhibitors

(Acetazolamide , dorzolamide- Use : Glaucoma ,
Acute Mountain Sickness , Metabolic Alkalosis ) &
Osmotic diuretics (Mannitol - use to decrease
intraocular pressure in Glaucoma , to decrease
intracerebral pressure , Oliguric states eg
Rhabdomyolysis) are not typically use in Cardiology.

Angiotensin-converting enzyme (ACE) inhibitors : Act

by inhibiting the conversion angiotensin I to angiotensin
II in Lungs.

Uses : Hypertensive (Young patients ) , heart failure ,

Diabetic nephropathy They are less effective in treating
hypertensive black patients and have a role in secondary
prevention of ischemic heart disease.

Side-effects: Cough (due to increased bradykinin levels) ,

Angioedema , hyperkalemia (because of decreased
aldosterone) , first-dose hypotension: more common in
patients taking diuretics

Contraindications : pregnancy and breastfeeding (Class

127 | P a g e
IV drug) , Bilateral Renal artery stenosis , Aortic stenosis
- may result in hypotension , patients receiving high-dose
diuretic therapy - significantly increases the risk of
hypotension due to hypovolemia , Hereditary of
idiopathic angioedema

Monitor : Urea and electrolytes should be checked before

treatment is initiated and after increasing the dose , a
rise in the creatinine and potassium may be expected
after starting ACE inhibitors. Acceptable changes are an
increase in serum creatinine, up to 30% from baseline

ARBs (Angiotensin Receptor Blockers) are used when

patient develops side effects of ACE inhibitors arises .
They blocks AT1 Receptors , Same mechanism & Uses as
ACEIs & do not interfere with bradykinin degeneration .

ANTIHYPERLIPIDEMIC DRUGS

Atherosclerosis which is the main cause of

Cardiovascular & Cerebrovacular diseases is associated
with Hypercholesterolemia .

HMG-CoA Reductase Inhibitors : Statins

(Atorvastatin , Lovastatin , - statins)

Inhibit HMG-CoA Reductase which results in Decrease in

Liver Cholesterol Production , Increase in LDL Receptor
expression and decrease in Plasma LDL. Also decreases
Triglyceride synthesise. Myalgia , Rhabdomyolysis ,
Hepatotoxic are common side effects . Increase risk of
Rhabdomyolysis if combined with other
antihyperlipidemic like Gemfibrozil (use to decrease
Triglyceride).

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Bile Acid Sequetrants : Cholestyramine & Colestipole:
Binds to the Bile salts in the gut , which results in
decrease entero hepatic circulation of bile salts , which
leads to increase in new bile salts by the liver by the use
of cholesterol , thus decreasing Liver cholesterol, which
leads to increase in LDL Receptor expression and thus
Decreases Blood Cholesterol.

Side effect : Increase VLDL and so , Triglyceride.,

Malabsorbtion of Lipid Soluble vitamins and so related
problems . Contraindication - Hypertriglyceridemia.

Niacin : Inhibit VLDL synthesis so , decreases VLDL &

LDL , while main effect is Increase in HDL . Side effect :
Flushing , Rashes , which are controlled by use of Aspirin
before taking Niacin.

Gemfibrozil : Induction of Lipoprotein Lipases -

Decreases VLDL , LDL so Use in Hypertriglyceridemia ,
and not in HyperCholesteremia. Side effect : Gallstone ,
myositis (on combination with Statins) ,
Thromboenbolism

Ezetimibe : Prevent intestinal absorption of Cholesterol ,

so , decrease in LDL ,Nowadays , it is mostly replaced by
Statins .

129 | P a g e
 NON PHARMACOLOGICAL TREATMENTS

For symptomatic arrhythmias : treatment is choosen

based on the type of arrhythmia, the severity of
symptoms being experienced, and the presence of other
conditions (such as, diabetes, kidney failure, or heart
failure) which can affect the course of the treatment.

Lifestyle modification : Elimination of caffeine, alcohol,

or any other substances believed to be causing the
problem, stress-reduction measures, such as meditation,
stress-management classes, an exercise program, or
psychotherapy.

Cardioversion. In this procedure, an electrical shock is

delivered to the heart through the chest to stop certain
very fast arrhythmias such as atrial fibrillation,
supraventricular tachycardia, or atrial flutter. The
patient is connected to an ECG monitor which is also
connected to the defibrillator. The electrical shock is
delivered at a precise point during the ECG cycle to
convert the rhythm to a normal one.

Ablation. This is an invasive procedure done in the

electrophysiology laboratory, which means that a
catheter (a very thin, flexible hollow tube) is inserted
into the heart through a vessel in the groin or arm. The
procedure is done in a manner similar to the
electrophysiology studies (EPS) described above. Once
the site of the arrhythmia has been determined by EPS,
the catheter is moved to the site. By use of a technique,
such as radiofrequency ablation (very high frequency
radio waves are applied to the site, heating the tissue
until the site is destroyed) or cryoablation (an ultra-cold
substance is applied to the site, freezing the tissue and

130 | P a g e
destroying the site), the site of the arrhythmia may be
destroyed.

Pacemaker. A permanent pacemaker is a small device

that is implanted under the skin (most often in the
shoulder area just under the collar bone), and sends
electrical signals to start or regulate a slow heart beat. A
permanent pacemaker may be used to make the heart
beat if the heart's natural pacemaker (the SA node) is not
functioning properly and has developed an abnormal
heart rate or rhythm or if the electrical pathways are
blocked. Pacemakers are typically used for slow
arrhythmias such as sinus bradycardia, sick sinus
syndrome, or heart block.

Implantable cardioverter defibrillator. An

implantable cardioverter defibrillator (ICD) is a small
device, similar to a pacemaker, that is implanted under
the skin, often in the shoulder area just under the
collarbone. An ICD senses the rate of the heartbeat.
When the heart rate exceeds a rate programmed into the
device, it delivers an electrical shock to the heart in order
to correct the rhythm to a slower more normal heart
rhythm. ICDs are combined with a pacemaker to deliver
an electrical signal to regulate a heart rate that is too
slow. ICDs are used for life-threatening fast arrhythmias
such as ventricular tachycardia or ventricular fibrillation.

Surgery. Surgical treatment for arrhythmias is usually

done only when all other appropriate options have
failed. Surgical ablation is a major surgical procedure
requiring general anesthesia. The chest is opened,
exposing the heart. The site of the arrhythmia is located,
the tissue is destroyed or removed in order to eliminate
the source of the arrhythmia.

131 | P a g e
 REFERENCES

www.Wikipedia.org Robins Pathology 8th

edition

ECG Interpretations : Brocherts Crush Step 2

Lippincott Williams and
Wilkins

Some ECG images freely Dr Najeebs

available on Internet (If you Electrocardiogram lectures
own that image , please let us
know from our website) USMLE First AID step 3

USMLEstat Secret Pathology Notes

USMLE High yields.
www.mayoclinic.org
ECG Made Easy
www.heart.org

If you didnt liked anything inside the book and want us to

change something , please Message us through our Website

www.medicaids22.info

Dr. Chirag Navadia

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 Kindle book available on Amazon for Just $4.99

ECG Short Rapid Review : Edition 2.2

New Inclusions to this Edition :

- Cardiology Summary

- 20 ECG Practice Strips

- Book Size Increased to 6*9

- 15 Clinical USMLE Style Q&A

- 150+ Super High Yield Points for USMLE STEP 1 & 2.

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