EKG/ECG Interpretation

Everything You Need to Know About the

12-Lead EKG/ECG Interpretation and
How to Diagnose and Treat Arrhythmias

SECOND EDITION

S. MELONI M.D.
M. MASTENBJÖRK M.D.
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 CONTENTS
INTRODUCTION

1. THE BASICS
ECG Procedure
ECG Tools
Calipers
ECG Ruler
Axis-wheel Rulers
Straight Edge
Calibration
Exercises

2. THE HEART
Electrical Conduction
SA Node
Internodal Pathways
The AV Node
The Bundle of His
The Left Bundle Branch
The Right Bundle Branch
The Left Anterior Fascicle (LAF)
The Left Posterior Fascicle (LPF)
The Purkinje System
Electrolytes
Phase 4 (Resting Potential)
Threshold Potential
Phase 0
Depolarization
Phase 1
Phase 2
Phase 3
Exercises

3. THE ECG COMPLEX

Prime Waves
The P Wave
The TP Wave
 The PR Segment
The PR Interval
The QRS Complex
Q Wave
Intrinsicoid Deflection
The ST Segment
The T Wave
The QT Interval
The U Wave
The R-R Interval
The P-P interval
Baseline
Exercises

4. MAKING INTERPRETATIONS
Heart Rate
Rhythm
Measuring Rhythm
Using a piece of paper and pencil
Using calipers
Bradycardia
Tachycardia
Narrow QRS Complex Tachycardia/ Supraventricular Tachycardia
Broad QRS Complex Tachycardia
Electrical Axis
Electrode Placement
Einthoven’s Triangle
Augmented Leads
The Hexaxial System
Precordial System
Normal Sinus Rhythm (NSR)
Exercises

5. ECG DIAGNOSIS
A
Accelerated Idioventricular Rhythm
Accelerated Junctional Rhythm
Anterior STEMI
Arrhythmogenic Right Ventricular Dysplasia
Atrial Flutter
Atrial Fibrillation
Atrial Fibrillation in WPW
Atrial Ectopic Beat/Atrial Premature Beat
Atrial Tachycardia
AV block: 1st degree / First-Degree Heart Block
AV block: 2nd degree, Mobitz 1 (Wenckebach)
AV block: 2nd degree, Mobitz II / Mobitz II Second-Degree Heart Block
AV block: 3rd degree (complete heart block) / Third-Degree Heart Block
AVNRT (AV-nodal re-entry tachycardia) / Supraventricular Tachycardia (SVT)
Atrial
Atrioventricular
AVRT (Atrioventricular Re-Entry Tachycardia)
B
Benign Early Repolarization / High Take Off / J-Point Elevation
Beta-Blocker Toxicity
Bidirectional VT
Bifascicular Block
Biventricular Enlargement
Biatrial Enlargement
Brugada Syndrome
C
Calcium-Channel Blocker Toxicity
Carbamazepine Cardiotoxicity
Cardiomyopathy, Dilated
Cardiomyopathy, Hypertrophic
Cardiomyopathy, Restrictive
Chronic Obstructive Pulmonary Disease (COPD)
D
De Winter’s T waves
Dextrocardia
Digoxin Effect
Digoxin Toxicity
E
Ectopic Atrial Tachycardia
Electrical Alternans
F
Fascicular VT
H
High Take-Off
Hypercalcemia
Hyperkalemia
Hyperthyroidism
Hypocalcemia
Hypokalemia
Hypomagnesemia
Hypothermia
Hypothyroidism
I
Interventricular Conduction Delay (QRS Widening)
Intracranial Haemorrhage
Intrinsicoid Deflection/ R Wave Peak Time
J
J-point Elevation
Junctional Ectopic Beat / Junctional Premature Beat / Premature Junctional
Contraction
Junctional Escape Beat
Junctional Rhythm
L
Lateral STEMI
Lead reversals: Limb Lead Reversals (overview)
Lead Reversal: Left Arm/Right Arm
Lead Reversal: Right Arm/Left Leg
RA/RL(N) Reversal
Bilateral Arm-Leg Reversal (RA-RL and LA-LL)
LL/RL(N) Reversal
Left Atrial Enlargement / Left Atrial Hypertrophy
Left Anterior Fascicular Block / Left Anterior Hemiblock
Left Axis Deviation
Left Bundle Branch Block
Left Bundle Branch Block – How to Diagnose Myocardial Infarction (Sgarbossa
Criteria)
Left Main Coronary Artery Occlusion (ST Elevation In aVR)
Left Posterior Fascicular Block / Left Posterior Hemiblock
Left Ventricular Aneurysm
Left Ventricular Hypertrophy
Lown Ganong Levine Syndrome
Low QRS Voltage
M
Movement Artefact
Multifocal Atrial Tachycardia
Myocardial Ischemia
Myocarditis
N
Non-Paroxysmal Junctional Tachycardia
P
Pericardial Effusion/Tamponade
Pericarditis
Persistent ST Elevation (LV Aneurysm Morphology)
Polymorphic Ventricular Tachycardia (PVT)
Poor R Wave Progression (PRWP)
Posterior STEMI
Preexcitation
Premature Ventricular Contraction (PVC)
Q
QRS Widening
Quetiapine Toxicity
R
Right Atrial Enlargement/ Right Atrial Hypertrophy
Right Axis Deviation
Right Bundle Branch Block
Incomplete RBB
Right Ventricular Hypertrophy
Right Ventricular MI
Right Ventricular Outflow Tract (RVOT) Tachycardia
Right Ventricular Strain
R-Wave Peak Time
S
Shivering Artefact
Short QT Syndrome
Sinus Arrhythmia
Sinus Bradycardia
Sinus Pause / Arrest
Sinus Tachycardia
Sodium Channel Blocker Overdose/Tricyclic Overdose
ST Elevation In AVR (Lmca/3vd)
STEMI
STEMI, Anterior
STEMI, High Lateral
STEMI, Inferior
STEMI, Lateral
STEMI (old)
STEMI, Posterior
STEMI, right ventricular
Subarachnoid Haemorrhage
T
Tako Tsubo Cardiomyopathy
Torsades de Pointes
Tremor Artefact
Tricyclic Overdose (Sodium-Channel Blocker Toxicity)
Trifascicular Block
Incomplete
Complete
V
Ventricular Aneurysm
Ventricular Escape Beat
Ventricular Escape Rhythm / Idioventricular Rhythm
Ventricular Fibrillation (Vfib)
Ventricular Flutter
Ventricular Tachycardia (VTach)
Fusion Beats
Capture Beats
Brugada’s Sign
Josephson’s Sign
Ventricular Tachycardia: Fascicular VT
Ventricular tachycardia: Monomorphic VT
W
Wellens Syndrome
Wolff-Parkinson-White Syndrome
 Exercises

REFERENCES

ANSWERS TO EXERCISES

CONCLUSION
 Introduction
earning the ECG is a valuable skill for both medical practitioners and
L non-practitioners. Knowing how to interpret ECG readings will help with
understanding how specific features of a person’s heart can affect him or her.
This knowledge will guide appropriate care, and prevent undesirable
complications from happening.
This book is intended to be a beginner’s guide that will provide a mental
framework for more advanced topics. Reading this is enough for you to
comprehend ECG readings, but you need to know as much as you can so that
you can provide the best care.
Study this book and other materials thoroughly. If there is something you do
not understand, seek clarification before moving on to something else, to
minimize your confusion. The more you understand something, the better
you will be able to respond to it – especially during emergencies.
Aside from this, reading from an introductory book may not prepare you
enough for the diversity of ECG readings. You need to practice reading as
many ECG strips as possible while knowing the patients’ symptoms and
diagnosis. This will consolidate everything you will learn from this book and
other learning materials.

Each chapter includes exercises. The answers for these are found at the end of
the book. Answering these will serve as your review for the chapter.
With that being said, let us begin with the basics of ECG – what it is, what it
does, and what you need to prepare for it.
 CHAPTER 1

The Basics
he electrocardiogram (ECG or EKG) is a device that detects the
T electrical activity of the heart in order for heart problems to be
diagnosed. It displays this as line tracings that are printed on paper.

An ECG and an EKG is one and the same. The German translation for
electrocardiogram is elektro-kardiographie, which is shortened to EKG.
An ECG/EKG has numerous uses:

It determines the heart’s electrical activity

It finds the cause/s of pressure or pain within the chest
It uncovers the reasons for heart disease symptoms
It checks whether the heart chamber walls are abnormally thick
It evaluates the effects of medicines and heart implants
It examines heart health

When combined with special algorithms (calculations), this device can study
numerous biometrics (measurements related to a person’s biology), as
follows:

Heart rate
Heart rate variability
Heart age
Breathing index
Fatigue
Stress

Although the ECG gives us several details about the heart, it cannot predict if
the person will have a heart attack or when it will happen. It may not
adequately pick up heart problems; someone with heart disease may have a
normal EKG. Because of this, the doctors will also look at other factors such
as the medical history, other symptoms present, physical examinations, and
additional tests.
Sometimes, a problematic EKG output only registers during exercise,
scenarios when the heart is stressed, or while the patient is currently
experiencing the symptoms. For these instances, ambulatory (walking) and
stress EKGs are done.

An EKG done while a person is having a heart attack may seem normal or the
same as his/her previous EKGs. When this happens, the EKG is repeated
over a period of time, such as over several hours or a few days to detect
significant changes. These are labelled as serial EKGs.
ECG PROCEDURE
Before taking an ECG/EKG, the patient will be asked to do the following:

Report all medicines taken – these may affect how the tests will turn
out.
Take off all jewellery from the neck, the arms, and the wrists.
Refrain from moving or talking.
Breathe normally and relax.
Avoid removing the electrodes before the test is done.

During the procedure, the patient will lie on the table or bed. The chest, arms,
and legs may be shaved to obtain suitable surfaces for the electrodes.
The electrodes are attached to the patient’s skin, at specific points on the
body where cardiac electrical activity is detected. These are linked to the
machine that prints the output.
The device will then record the activity for a few minutes. The patient is
asked to refrain from moving too much or talking, to prevent interfering with
the readings.
When the reading is obtained, the electrodes are removed from the body and
the paste is wiped off from the skin. The patient then gets up from the bed or
table.
ECG TOOLS
There are certain instruments that help with ECG interpretation:
Calipers
Calipers are perhaps the most important tool in ECG interpretation. To use
one, put one pointed edge against one end of what you are measuring, and the
other edge at the other end. The caliper will maintain this position. You can
then move on to a blank area of the ECG strip. Count the number of boxes to
get your measurements (example: 1 small box = 0.04 seconds, 1 big box =
0.20 seconds, and so on).
You can use calipers to check whether the distance between complexes is
equal. Measure the complex with the two pins. Hold the right pin down and
gently swing the left pin to the next complex. If they are the same, the next
complex will coincide with the pin. This technique is called “walking”, and it
is useful for determining complex regularity and detecting ECG
abnormalities.
Aside from width, calipers can also measure wave heights. You can likewise
“walk” the caliper, so that you will know the biggest or smallest complexes
and see whether a wave is more positive or more negative.
ECG Ruler
This helps with measuring ECG, but it is not that necessary, since a caliper
can do what this does.
Axis-wheel Rulers
Axis-wheel rulers are used to calculate waves and segments’ true axis. This
ruler has a red line and a perpendicular arrow.
Straight Edge
It evaluates the baseline, and can determine elevations and depressions.
At first, you may be dependent on these instruments, which can enable you to
make accurate diagnoses. After a lot of practice, you will be able to quickly
make measurements without having to use them.
Calibration
The end of an ECG strip will usually have a calibration box, which is 10 mm
high and 0.20 seconds wide. This says that the ECG follows the standard
format. This has a rate of 25 mm/sec.
There are ECGs that have a half-standard calibration, especially when the
complexes are so large that they overlap. When this is the case, the
calibration box will have a stair-like design.
The third calibration is set at 50 mm/sec. The calibration box is 0.40 seconds
in width.
It is important to check the calibration of the ECG, in order to evaluate the
tracings correctly.
These are some of the basic things you need to know before diving into the
details of ECG interpretation.

The next chapters will tackle the heart and the mechanisms of the heartbeat
so that you will understand how they affect the ECG readings.
 EXERCISES

1. What does ECG mean?

a. Electric Cardiology Gadget
b. Electrocardiogram
c. Electrocartographer
d. Electrode Cardiograph
2. All of these are uses of ECG except one, which is it?
a. Monitors the heart’s electrical activity
b. Finds the cause of chest pain
c. Predicts heart attacks
d. Evaluates heart health
3. True or False: Stress and ambulatory tests are done to know how the
heart behaves while in its normal state.

4. A device that has pointed edges and can be used to get

measurements by “walking”
a. ECG ruler
b. straight edge
c. axis-wheel ruler
d. caliper
5. A calibration box 10 mm high and 0.20 seconds wide has a rate of _
mm/sec

6. A _ calibration has a stair-like design.

7. The third calibration is set at _ mm/sec and is .40 seconds in width.

 8. It is important to check the calibration of the ECG to determine the
_ of the tracings.
a. height
b. voltage
c. rate
d. form
9. Several ECGs done over a period of time are called _ ECGs
a. multiple
b. comparative
c. serial
d. secondary
10. True or false: The patient needs to be sedated during the procedure
to get a clear reading.
 CHAPTER 2

The Heart
o understand the ECG better, it is helpful to study the heart itself.
T Without this foundational knowledge, the ECG may become
undecipherable.

The heart is in the center of the chest, slightly tilting downwards to the left. It
is nearer the front of the body than the back.
The heart functions as a pump with four main chambers, with two atria
(plural for atrium) and two ventricles. The left ventricle releases blood into
the peripheral circulatory system (the blood vessels of the body), while the
right ventricle pumps blood into the pulmonary system (lungs).
Oxygen-rich blood from the heart passes through the arteries, while oxygen-
depleted blood from the body returns to the heart through the veins.
After oxygen is used by the body cells, the blood is returned to the heart. The
right ventricle pushes this through the pulmonary artery and into the lungs,
where it is infused with oxygen again. This flows into the left ventricle,
which pumps the blood through the aorta and into the blood vessels of the
entire body.
The right ventricle takes up most of the front part of the heart, but the left
ventricle is the one that produces most of the electricity.
ELECTRICAL CONDUCTION
The heart has cells that are designed to conduct electricity – some of them are
responsible for setting a pace, while others transmit electrical impulses. This
is an electro-chemical process that happens in the myocardium (heart
muscles) found in the walls of the heart.
The atrial myocytes (heart muscle cells) activate each other in sequence. The
internodal pathways carry the impulse from the sino-atrial (SA) node to the
atrioventricular (AV) node, reaching the Purkinje system, which goes around
the ventricles and energizes the myocardial cells.
These cells set the pace at which the heart beats. All cells in the conduction
system can create a pace, but the rate of each cell type is slower than the rate
of those that came before it. Thus, the SA node has the fastest pace; the AV
node has the second fastest, and so on, with the last component having the
slowest pace. The node with the fastest rate establishes the rate because it
resets all the paces of those that come after it. If it malfunctions, the next
fastest will serve as its backup, ensuring that the heart beats at near the
normal rate.
These are the approximate rates of each component:

SA node cells: 60-100 BPM (beats per minute)

Atrial cells: 55-60 BPM
AV node: 45-50 BPM
Bundle of His cells: 40-45 BPM
Bundle branch cells: 40-45 BPM
Purkinje cells: 20-40 BPM
SA Node
Found in the wall of the right atrium, the SA node is the main pacemaker.
Internodal Pathways
The anterior, middle, and posterior pathways (located in the right atrium and
inter-atrial septum - the wall separating the two atria) send the pacing
impulses from the SA node towards the AV node. This pathway also consists
of the Bachmann bundle, which carries impulses through the inter-atrial
septum.
The AV Node
Within the right atrium and near the coronary sinus, the AV node slows down
the conduction of the atria to the ventricles, to enable atrial contraction to
occur. Slowing down the pace enables the atria to fill the ventricles, and
maximizes the output of the heart.
The Bundle of His
The Bundle of His begins at the AV node, and splits into the left and right
bundle branches. It is partially located in the right atrium walls and in the
interventricular septum, which is the partition between the ventricles. This
allows for transmission of impulses between the ventricles and atria.
The Left Bundle Branch
The LBB originates from the end of the His bundle, traverses the
interventricular septum, and ends at the start of the left anterior and left
posterior fascicles (LAF and LPF). This innervates the left ventricle, and the
left part of the interventricular septum.
The Right Bundle Branch
This also begins at the His bundle, but it innervates the right ventricle and
right part of the interventricular septum. It ends at the Purkinje fibres.
The Left Anterior Fascicle (LAF)
The LAF goes through the left ventricle, and reaches the Purkinje cells that
energize the front and top parts of the left ventricle. This consists of a single
strand.
The Left Posterior Fascicle (LPF)
The LPF is composed of many strands that lead to the Purkinje cells, that
innervate the back and bottom part of the left ventricle.
The Purkinje System
This is composed of cells beneath the inner layer of the heart (myocardium).
These directly innervate the cells of the myocardium, and start the ventricular
depolarization cycle.
ELECTROLYTES
Electrolytes enable cells to generate electricity. They affect how the heart
beats, so you need to have an idea of how they work to interpret an ECG
well.
Each cell of the heart (myocardial cell/myocyte) is made of two parts that
glide over each other. These partitions are linked to the outside of the cells,
and they are made up of myosin molecules that are distributed between actin
molecules.
The cells are linked together to create long bands called myofibrils, which in
turn are linked together by connective tissue to create fluid-covered sheets.
The bands expand and contract according to the electrical impulse that
reaches them.

When one or all of the bands in a sheet contract, the sheet shortens. It returns
to its original size when all of the bands expand. These sheets form the
chambers of the heart: the 2 atria on top and the 2 ventricles at the bottom.
The atria are smaller and thinner than the ventricles below them.
Each cell has fluid inside and outside of it – this contains water, proteins, and
salts. When the salts interact with fluid, they break down into particles that
have either a positive and negative charge – these are called ions. The
positively charged ions, or cations, are potassium, sodium, and calcium while
the negatively charged ions (anions) are mostly chloride.
 Figure 1. Impulse transmission in heart muscle cells

A living cell maintains a difference between the concentrations of the ions,

and charges within the cell and outside it. Normally, the inside of the cell has
a higher concentration of potassium, while the outside environment has a
higher sodium concentration. There is a negative charge within the cell as
compared to outside, because calcium, a positively charged ion, also floats
outside the cell.
The difference between electrical charges within and outside of the cell wall
is considered as the cell’s electrical potential. Because ions and chargers tend
to maintain neutrality, sodium tends to enter the cell wall and potassium tends
to exit. In order to maintain its electrical potential, the cell has mechanisms
that control these ions in ways that do not allow them to follow their natural
tendency.
Phase 4 (Resting Potential)
The sodium-potassium ATPase pump facilitates the movement of ions around
the cell, to protect the electrical charge and concentration. It uses ATP to
push out three sodium ions, and pull in two potassium ions. This results in a
greater positive charge existing on the outside of the cell as compared to the
inside. Because of this, the resting myocyte’s electrical potential is
maintained from between -70 to -90 millivolts.
After a while, the ions begin to overload the pump, and the cell’s interior
becomes less negative because more sodium ions are entering.
Threshold Potential
Gradually, the cell becomes positively charged, and this opens up a new
batch of channels – the fast sodium channels. These are one-way valves that
permit only ions such as sodium to enter the cell.
Phase 0
When these valves open, sodium ions rapidly enter the cell and cause a surge
of positive charge inside it. This impulse stimulates the cell, and passes on to
the cells near it, until all cells have been activated.
Depolarization
When the cell is no longer negatively charged or polarized, it is now said to
be depolarized, and it is also positive like the fluids outside it.
Phase 1
When the cell reaches its maximum positive charge, it enters phase 1 of the
action potential. This triggers chloride ions (negative charge) to enter the cell,
which slows down the entrance of sodium ions (positive charge).
Phase 2
The rapid sodium channels close down at this point, while the slow sodium
channels and the calcium channels open. The slow sodium channels let
sodium ions slowly enter the cell, while the calcium channels let calcium
enter. Since calcium has two positive charges, it helps maintain the cell’s
depolarized state.
Calcium helps cells contract by triggering actin and myosin proteins to move
against each other. When there is more calcium, the proteins clamp faster and
contract longer.
Phase 3
A few potassium channels open to make potassium ions exit the cell, causing
rapid repolarization. The negative charge of the cell returns as positively
charged potassium leaves it. This leads to the resting potential (phase 4) and
the cycle begins again.

Each cell of the heart has these action potential cycles, and can polarize and
depolarize 70-100 times in one minute. Even though there are millions of
cells in the heart, they all act together because of the electrical conduction
system. These electrical discharges come together and create one large
current or electrical axis. The ECG picks up these electrical potentials and
transforms them into patterns.
It is better if you understand what has been discussed in this chapter before
you move on to the next ones. Doing so will help you integrate the
information more easily.
 EXERCISES

1. The _ pumps blood through the aorta and into the blood vessels of
the body.
a. Left atrium
b. Right atrium
c. Left ventricle
d. Right ventricle
2. The _ takes up most of the front part of the heart.
a. Left atrium
b. Right atrium
c. Left ventricle
d. Right ventricle
3. The _ produces most of the electrical activity of the heart.
a. Left atrium
b. Right atrium
c. Left ventricle
d. Right ventricle
4. The main pacemaker of the heart is:
a. SA Node
b. AV Node
c. Bundle Branches
d. Ventricles
5. The secondary pacemaker of the heart is:
a. SA Node
b. AV Node
c. Bundle Branches
d. Ventricles
6. Which of the following transmits electrical impulses between the
SA and AV nodes?
a. SA Node
b. AV Node
c. Bundle Branches
 d. Ventricles
7. The SA node has a rate of _.
a. 120 - 200 BPM
b. 60 - 100 BPM
c. 40 – 60 BPM
d. 20 – 40 BPM
8. The main negative ion is:
a. Sodium
b. Potassium
c. Chloride
d. Calcium
9. There is a high concentration of _ inside a cell and a high
concentration of _ outside it.
a. Potassium, Sodium
b. Sodium, Potassium
c. Calcium, Magnesium
d. Magnesium, Calcium
10. The ion that enables the troponin and tropomyosin in heart tissue to
clamp together.
a. Potassium
b. Sodium
c. Magnesium
d. Calcium
 CHAPTER 3

The ECG Complex

Figure 2. Components of the ECG complex

he ECG records waves, intervals, and segments. These have particular

T morphologies (forms), axes, durations, and amplitudes when normal.
When the ECG readings are different from these traits, there may be
something wrong with the heart.
A wave represents a cardiac event, such as atrial depolarization, atrial
repolarization, ventricular depolarization, ventricular repolarization, and His
bundle transmission.
A wave is a deflection from a baseline, which is the line from one TP
segment to another one next to it. It can be single, positive, negative,
biphasic, isolated, or have multiple parts that can be positive or negative.

An interval is the time distance between two cardiac events. A segment is a

specific part of a complex on an ECG. A segment is different from an
interval.
This is the normal sequence of the waves:

The P wave is the first positive (upward) deflection that shows up on

the ECG
The Q wave is the first negative (downward) wave, which appears
after the P wave
The R wave is the first positive wave after the Q wave
The S wave is the first negative wave after R wave
The T wave is a positive wave that appears after the S wave.

Tall waves are given big letters, while small waves are labelled with small
letters
PRIME WAVES
Waves are called prime when they cross the baseline, or change directions.

When there are extra waves where they aren’t supposed to be, they are
labelled as prime waves.
A wave can be a double prime when it occurs twice.
THE P WAVE
The P wave is normally the first wave on the TP segment. It represents the
atria’s electrical depolarization. The wave begins when the SA node fires,
and it embodies the impulse transmission through the internodal pathways,
the Bachmann bundle, and the atrial myocytes.
Since the P wave represents atrial depolarization, P wave abnormalities
signify atrial abnormalities. Check the inferior leads (II, III, and aVF), and
precordial lead V1 for this.

The wave duration is between 0.08 – 0.11 seconds, or less than 120 ms. Its
axis is commonly directed downwards, and to the left (Axis: 0 to 75 degrees),
since it goes through the atrioventricular node and atrial appendages.
The first one third of the wave embodies the right atrial activation, the last
third represents the left atrial activation, and the middle is the blend between
the two.
P waves are normally upright in leads I and II and inverted in lead aVR. They
are monophasic in lead II and biphasic in V1.
In V1, the P wave is biphasic and begins with a positive deflection, showing
right atrial activation, and ends with a negative deflection, which reflects left
atrial activation. Because of this, the state of each individual atrium can be
determined by looking at each part of this waveform.
These are some things that can be known from P waves:

Tall and prolonged P waves can indicate atrial enlargement.

Bifid P waves (broad and notched) are associated with left atrial
enlargement, while peaked P waves are linked to right atrial
enlargement.
Inverted P waves indicate ectopic atrial and junctional rhythms.
Variable P wave forms hint to multifocal atrial rhythms.

THE TP WAVE
The TP wave symbolizes the repolarization of the atria. This moves in the
opposite direction of the P wave.
This is not commonly obvious because it coincides with the more prominent
QRS wave.
The TP wave appears when the QRS is absent, such as in the case of AV
dissociation or non-conducted beats. This also shows up in PR depression, or
in the ST segment depression during sinus tachycardia.

It shows as ST depression because the QRS arrives earlier and the TP wave
draws the ST segment down.
THE PR SEGMENT
The PR segment is found when the P wave ends, and the QRS complex
begins. It normally lies along the baseline, but can be depressed or elevated
by up to 0.8 mm. PR segment abnormalities indicate atrial
infarctions/ischemia and pericarditis.
The PR segment shows the transmission of the electrical depolarization
impulse through the AV node, bundle of His, bundle branches, and Purkinje
system.
THE PR INTERVAL
The PR Interval is the time period from the P wave’s beginning to the QRS
complex’s beginning. It consists of the P wave and the PR segment.
The PR interval involves events from the start of the electrical impulse in the
SA node to ventricular depolarization. (Beginning of impulse, atrial
depolarization and repolarization, stimulation of AV node, His bundle,
bundle branch, and Purkinje System).
This normally lasts from 0.12 – 0.20 seconds.
If it’s longer than 0.20 seconds, it is a sign of a first-degree AV block.
It can also be called as PQ interval when a Q wave begins the QRS complex.
THE QRS COMPLEX
The QRS complex reflects ventricular depolarization. It usually lasts 0.06 –
0.11 seconds with an axis of -30 to +105 degrees, going downward and to the
left.
It has two or more waves which have their own name.
The Q wave is usually the first negative deflection after the P wave, but it can
sometimes be absent.
The R wave is the first positive deflection after the P wave. It can be the
starting wave of the QRS complex if the Q is not around.
The first negative deflection following the R wave is the S wave.
Q WAVE
A Q wave is considered significant if it lasts for 0.03 seconds or longer, or if
it is as tall or taller than 1/3 of the R wave. When these conditions are
present, there is a myocardial infarction (MI).
Insignificant Q waves are traditionally found in I, aVl and V6, and these are
caused by septal innervations. These are usually called septal Qs.
INTRINSICOID DEFLECTION
This begins from the start of the QRS complex to the start of the downward
slope of the R wave, in leads that begin with an R wave and do not have a Q
wave. It symbolizes the time taken for the electrical impulse to traverse the
Purkinje system from within the inner layer to outer layer of the heart.
It is shorter in the right precordial leads (V1-V2) because the right ventricle is
thinner than the left.
The intrinsicoid deflection will be longer if the myocardium is thicker than
normal (eg. Ventricular hypertrophy), or when the electrical system conducts
slower in that area because of a delay (eg. Left bundle branch block).
These are the upper normal limits for intrinsicoid deflection:
Left precordials = 0.045 seconds

Right precordials = 0.035 seconds

THE ST SEGMENT
The ST segment is the electrically neutral period in between ventricular
depolarization and repolarization. In this phase, the myocardium is
maintaining its contraction to push the blood from the ventricles. Its axis is
normally inferior and to the left.
This is the section from the QRS complex’s end to the T wave’s start. It is
usually found on the baseline, but can deviate up to 1 mm from it in normal
patients’ limb leads, and 3 mm in the right precordials. This may be caused
by left ventricular hypertrophy or an early repolarization pattern.

The J point marks the spot where the QRS complex stops and the ST segment
begins.
When the ST segment is elevated, it should be considered as significant, as it
can reveal a myocardial infarction or injury.
THE T WAVE
The T wave signifies ventricular repolarization. This is the next positive or
negative deflection after the ST segment. It is expected to begin in the same
direction as that of the QRS complex. The axis is downward and to the left
for this wave as well.
The T wave is asymmetrical, with the first part dropping or rising slowly and
the last part moving rapidly.
To check whether the T wave is symmetrical or not, draw a perpendicular
line from the wave’s peak to the baseline and compare the two sides.
Symmetric Ts usually signify problems.
THE QT INTERVAL
The QT interval comprises of the QRS complex, ST segment, and T wave.

It involves cardiac events of ventricular systole, that is, from the start of
ventricular depolarization until the end of the repolarization cycle.
The QT interval depends on the patient’s age, sex, heart rate, and electrolyte
condition.
A prolonged QT can mean arrhythmias.
QTc means QT corrected interval. This is adjusted according to the heart rate.
As heart rate increases, the QT interval shortens, and as the heart rate
decreases, so the QT interval would lengthen as well.
To obtain QTc, add QT + 1.75 * (ventricular rate -60)
The QTc interval normally lasts 0.410 seconds, and anything longer than .419
is considered prolonged.
THE U WAVE
The U wave is the small wave commonly seen after the T wave and before
the following P wave. This has low voltage, and has the same direction as the
T wave.

It is not clear as to what it symbolizes, but it is theorized that it stands for

ventricular depolarization and endocardial repolarization.
It is seen in normal individuals especially those with bradycardia (slow
heartbeats). It is also evident in hypokalemia or low potassium in the blood,
thus there is no hyperkalemia (high levels of potassium) when a U wave
exists.
THE R-R INTERVAL
The R-R interval is the distance between two identical points or peaks of two
consecutive QRS complexes.
This is used to determine whether the rhythm is regular or irregular. Those
with regular rhythms have consistent R-R intervals.
THE P-P INTERVAL
This is the distance between two identical points on a P wave, and the next
one. This is used to assess rhythm abnormalities such as atrial flutter,
Wenckeback second-degree heart block and third-degree heart block.
BASELINE
The baseline of the ECG is the line from the TP of one complex to the TP of
another one.
The PR segment should be on this line, but there are times when it is
elevated.
 EXERCISES

1. Which of the following represents atrial depolarization

a. P Wave
b. TP Wave
c. QRS Complex
d. T Wave
e. U Wave
2. Which of the following represents atrial repolarization
a. P Wave
b. TP Wave
c. QRS Complex
d. T Wave
e. U Wave
3. Which of the following represents ventricular depolarization
a. P Wave
b. TP Wave
c. QRS Complex
d. T Wave
e. U Wave
4. Which of the following represents ventricular repolarization
a. P Wave
b. TP Wave
c. QRS Complex
d. T Wave
e. U Wave
5. Which of the following is theorized to represent endocardial
repolarization
a. P Wave
b. TP Wave
c. QRS Complex
d. T Wave
e. U Wave
 6. A line between a TP segment of one complex to the TP segment of
the following complex is called:
a. Baseline
b. P-P Interval
c. Q-T Interval
d. ST Segment
7. Interval representing all cardiac events of ventricular systole.
a. Baseline
b. P-P Interval
c. Q-T Interval
d. ST Segment
8. A Q wave with a height that is one third or greater of the R wave,
and lasts longer than 0.03 seconds is:
a. Normal Sinus Rhythm
b. Benign Arrhythmia
c. A Myocardial Infarction sign
d. Bradycardia
9. Which of the following symbolizes the time it takes for the
electrical impulse to traverse the Purkinje system that runs along the
inner to the outer layer of the heart.
a. P-P interval
b. R-R interval
c. ST segment
d. Intrinsicoid Deflection
10. The distance between two identical peaks of consecutive QRS
complexes is known as:
a. P-P interval
b. R-R interval
c. ST segment
d. Intrinsicoid Deflection
 CHAPTER 4

Making Interpretations
nterpreting the ECG take some practice, because there’s a lot going on in
I the graph. It is important that you understand everything you read here.
You don’t have to memorize everything, but do keep notes, or this book
handy.
When you have an ECG to interpret, look at it broadly and take note of any
outstanding features. Do not dwell on the tiny details at this point, but try to
form a general impression about it. Does it seem like a case of arrhythmia,
ischemia, etc.? Keep your tentative conclusion in mind as you go through the
next steps.
An ECG gives a lot of information that is only unlocked if you know what
each part of the tracings mean. In general, a normal reading has the following
characteristics:

The heart beat is somewhere from 60 to 100 beats per minute (for
adults)
It shows a regular rhythm
The tracing follows the normal pattern (this will be discussed later)

A reading is considered abnormal when these are present:

The heart beat is faster than average (above 100 BPM)

It is slower than normal (below 60 BPM)
It displays an irregular rhythm
The tracing deviates from the expected outline

After gaining an overview, go over the ECG sequentially. Determine where

the normal and abnormal beats are. For the normal ones, evaluate the axis,
intervals, blocks, and other things you need to find out. For the abnormal
beats, think about what may be causing them.

Before anything else, you must know that the above features are just general
indicators of normality and abnormality.
If you want to get useful insights, you have to consider other features. Read
on to know how to get specific information from ECG readings.
HEART RATE

The ECG paper has tiny boxes that measure 1 mm each, and these are
grouped together to form bigger boxes. It runs under the pen at 25 mm/sec,
thus each box on the graph represents 1/25 of a second, or 0.04 seconds).
th

The large boxes have 5 small boxes each. Each one represents 5 x 0.04
seconds = 0.2 seconds.
5 large boxes mean 5 x 0.2 seconds, which is equal to 1 second.
In summary:

1 small box (1 mm) = 0.04 seconds

1 large box (5 mm) = 5 small boxes = 0.2 seconds
5 large boxes (25 mm)= 1 second
The ECG is traditionally 10 seconds long, with each lead covering 2.5
seconds. The paper has three to four strips. The top three strips have 12 leads.

Bear in mind that the vertical height of a segment or wave is measured by

millimetres, while the width is measured in milliseconds. This is because the
width of the tracing reveals the duration of the electrical activity, while the
height shows its voltage.
Some ECG devices calculate the heart rate on their own, but they may be
inaccurate, especially when the waveforms are abnormal. It is always better
to know how to make calculations manually.
There are many ways to compute for the rate of the heartbeat:

For regular rhythms, count the number of large squares in one R-R
interval. Divide 300 by the number of squares.
For fast rhythms, count the small squares in one R-R interval, and
divide 1,500 by that number.
For slow or irregular rhythms, multiply the number of complexes by 6
to obtain the average rate of the heartbeat for every 10 seconds.

Check: is the heart rate faster or slower than expected? Again, the normal
heart rate is 60-100 beats per minute, but this may vary according to the
patient’s age and other health conditions.

You can already make a diagnosis based on heart rate:

For adults, the normal rate is at 60 – 100 beats per minute (BPM). If the rate
is greater than 100 BPM, tachycardia is present. If it is less than 60 BPM,
there is bradycardia.
Children normally have faster heart rates than adults, because of their smaller
body sizes. Anything faster than the values given below counts as
tachycardia; if slower, then it is bradycardia.

Newborn babies: 110 – 150 BPM

 2 years old: 85 – 125 BPM
4 years old: 75 – 115 BPM
6 years old and older: 60 – 100 BPM

RHYTHM
The heartbeat rhythm is more easily studied by using a rhythm strip, which is
most often a 10 second recording from Lead II (if you used a 12 lead ECG).
Look into the other leads as well, to make a more accurate diagnosis about
the rhythm.
One of the easiest things to determine from the rhythm is whether it is slow
or fast (bradycardia or tachycardia), and whether it’s irregular or regular.
MEASURING RHYTHM
There are two ways to measure rhythm:
Using a piece of paper and pencil
Place the paper along the baseline. Move it up so that the edge is near the R
wave’s peak. On your paper, mark the R waves of two consecutive QRS
complexes to get the R-R interval. Transfer the paper across the ECG tracing
and see whether the following R-R intervals line up with your marks. If yes,
you can say that the ventricular rhythm is regular. If not, it is irregular. Do
the same for the P waves (P-P intervals), to know whether the heart’s atrial
rhythm is regular or irregular.
Using calipers
Place one point of your caliper on the peak of an R wave. Adjust the calipers
so that the other point lands on the next R wave. This gives you the R-R
interval. Swivel the calipers to check whether it falls on the third R wave’s
peak. If they do, the R-R (ventricular) rhythm is regular. If not, it is irregular.
You can also determine the atrial rhythm this way, by measuring the P-P
interval.
If the heartbeat has a regular rhythm, count how many complexes there are
on the rhythm strip. This is usually 10 seconds long. Multiply 6 to this
number to get the average number of complexes per minute.
An irregular heart rhythm may be regularly irregular, with a recurring pattern
of irregularity, or irregularly irregular, which means that the rhythm is totally
disorganized.
Is the rhythm grouped or ungrouped? Abnormal heart rhythms have grouped
beats.
Check whether the rhythm is wide or narrow. This means observing the
average width of the QRS complexes. If it is wide, there may be a conduction
problem coming from the ventricles, or from the supraventricular region
(above the ventricles). If narrow, the abnormality may be located in the sinus
node, atria, or junctional region.
Look for P waves – if you can’t find them, the patient may be experiencing
atrial fibrillation or sinus arrest.
If they are present, check the ventricular and atrial rate. Are all P waves
similar to each other? They are expected to be the same if there is a 1:1
conduction to the QRS complexes.
Abnormal ratios between P waves and QRS complexes may indicate
atrioventricular dissociation (AV dissociation). In complete AV dissociation,
the atrial and ventricular electrical activities always occur separately. In
incomplete AV dissociation, capture beats show up infrequently.
If there is an abnormality in P wave shape and PR interval, this suggests that
there is something wrong in the conduction of the sinus, atria, junction or
ventricles. You will know the location depending on which leads the
abnormalities show up.
If the heartbeat is irregular, compute for the range. Inspect the PR, QRS,
QTc, PP, and RR intervals. Observe if there are irregularities in the intervals.
Consider onsets and terminations. If they are abrupt, a re-entrant process may
be causing them. If gradual, it is possible that an area of the heart has
increased automaticity (ability to conduct impulses).
There are a lot of heart problems that can be diagnosed by heart rhythm type:
P waves Each P wave is followed by QRS Sinus Node Dysfunction:
Present complex Sinus bradycardia
Sinus node exit block
Sinus pause/arrest

Not every P is wave followed by a AV Node Dysfunction:

QRS complex AV block: 2nd degree, Mobitz I
(Wenckebach)
AV block: 2nd degree, Mobitz II
AV block: 2nd degree, “fixed ratio
blocks” (2:1, 3:1)
AV block: 2nd degree, “high grade AV
block”
AV block: 3rd degree (complete heart
block)

P waves Broad complexes Ventricular Escape Rhythm

Absent
Narrow complexes Junctional Escape Rhythm

BRADYCARDIA

Figure 3. Sinus bradycardia: Note that the rate is about 45 bpm

TACHYCARDIA
 Figure 4. Sinus tachycardia: Note that rate is more than 100 bpm

NARROW QRS COMPLEX TACHYCARDIA/ SUPRAVENTRICULAR

TACHYCARDIA
Regular Rhythm Irregular Rhythm

Atrial Atrial Flutter Atrial fibrillation

Atrial Tachycardia Atrial flutter with variable
Inappropriate Sinus Tachycardia block
Sinus Tachycardia Multifocal atrial tachycardia
Sinus node re-entrant Tachycardia

Atrioventricular Automatic Junctional Tachycardia

Atrioventricular re-entry Tachycardia
(AVNRT)
AV nodal re-entry tachycardia (AVRT)

BROAD QRS COMPLEX TACHYCARDIA

Regular Rhythm Irregular Rhythm

Ventricular Tachycardia Ventricular fibrillation

Antidromic atrioventricular re-entry Polymorphic VT
tachycardia (AVRT) Torsades de Pointes
Any regular supraventricular tachycardia AF with Wolff-Parkinson-White syndrome
with aberrant conduction Any irregular supraventricular tachycardia
with aberrant conduction

ELECTRICAL AXIS

The electrical impulses are vectors which have energy and direction.
Vectors add up when they head towards the same direction, decrease in
energy and change their direction when they are going in opposite locations,
and add or subtract energy and change directions when they meet at an angle.
The heart has numerous vectors, but as mentioned, they all combine to
produce major currents. All these vectors together are referred to as the
electrical axis.
There are a number of vectors detected by the ECG’s electrodes: the P-wave
vector, T-wave vector, ST segment vector, and QRS vector.

Electrodes pick up electrical activity. When a positive electrical impulse

moves away from an electrode, the ECG registers it as a negative or
downward wave. When a positive wave approaches an electrode, the ECG
transforms it into a positive or upward wave. When the electrode sits at the
middle of a wave, the ECG demonstrates a positive wave for the energy
coming towards it, and a negative wave for the energy retreating from it.

These electrodes are placed at specific angles to the main axis, in order to get
a three-dimensional view of the heart’s electrical activity.
Just like with heart rate and rhythm, the electrical axis is affected by
abnormalities. This is why electrical axis is studied in the ECG.
As you may recall, the QRS complex stands for ventricular depolarization.
This is the strongest impulse in the heart, and thus the QRS complex
determines the heart’s main axis.
The degree of the QRS axis will tell you whether it is normal or deviated:
 Normal: between -30 to +90 degrees
Left Axis Deviation (LAD): less than -30 degrees
Right Axis Deviation (RAD): greater than +90 degrees
Extreme Axis Deviation (EAD): between -90 and 180 degrees

These are some ways to determine the axis:

The quadrant method involves looking at leads I and aVF.
Lead I Lead aVF Quadrant Axis
Positive Positive Left Lower Normal

Positive Negative Left Upper Possible LAD

Negative Positive Right Lower RAD
Negative Negative Right Upper EAD

The Isoelectric Lead Method is more precise than the method above, and
involves finding the isoelectric/equiphasic lead. This is the frontal lead that
has zero net amplitude, meaning a QRS that is a flat line or biphasic, with R
wave height that is equal to Q or S wave depth.
After finding the isoelectric lead, the next step is to find the positive leads –
those with the highest R waves or biggest R to S ratios.
When this is done, the QRS axis is calculated by going 90 degrees to the
isoelectric lead and pointing towards the positive leads.
Later on in this book, you will know how to diagnose heart problems based
on axis deviations.
ELECTRODE PLACEMENT
Where the electrodes are placed depends on whether there are 3, 5, or 12
leads used. This book will concentrate on 12-lead ECG.
Electrodes or leads are positioned at these areas:
Limbs: Also known as extremity leads, limb leads are stationed at least 10 cm
from the patient’s heart. When you are using the three-lead system, it is
recommended to place the leads on areas on the chest that are equally distant
from the heart, instead of the limbs. The arm leads can be placed on the
shoulder, at 10 cm distance from the heart..

Right arm (RA)

Left arm (LA)
Right leg (RL)
Left leg (LL)

Precordial leads: Otherwise called as chest leads, these are attached at precise
points on the patient’s chest.
Position V1 and V2 are located on each side of the sternum (flat bone in front
of the chest) at the fourth intercostal space, or the fourth space that exists
between the ribs.
To find this space, feel the Angle of Louis or the bump along the top 1/3rd
portion of the sternum. This is positioned beside the second rib, and the space
right below it is the second intercostal space. To find the fourth one, count
two more spaces below the second.
Right after this lead is V4, placed at the fifth intercostal space. This is found
at the intersection of this space and the mid-clavicular line, an imaginary line
that extends downwards from the middle of the nearest clavicle (collarbone).
V3 sits in the middle of V2 and V4.
To find V5, go down, and to the right of V4. Find the intersection of this
position and the anterior axillary line, or the line that extends from the front
part of the armpit. Imagine a line going down from the middle of the armpit
to get the mid-axillary line. This is where you place V6. .
The ECG scans the positive and negative poles of the limb electrodes to
create lead I, II, and III.
Limb Leads: I, II, III, IV (aVR), V (aVL), VI (aVF)
Chest leads: V1, V2, V3, V4, V5, V6
Einthoven’s Triangle
The Einthoven’s Triangle is formed by the three bipolar limb leads (leads I,
II, and III).

Lead I’s axis runs from one shoulder to another, with the right arm (RA) lead
being negative and the left arm (RA) lead being positive. Lead II’s axis goes
from the negative RA lead to the positive left leg (LL) lead. Lead III’s axis
goes from the negative left arm (LA) lead to the positive left leg (LL) lead.
Augmented Leads
Augmented leads are composed of leads aVR, aVL, and aVF. They pick up
the electrical activity coming from one limb lead and one electrode. Lead
aVL records input from the heart’s lateral (side) wall, while lead aVF
monitors input from the heart’s inferior (bottom) wall. The lead aVR does not
give a view to the heart but can still be useful at times.
The Hexaxial System
Hexaxial means six axes. This consists of 6 leads: I, II, III, VR, VL, and VF.
The leads are 30 degrees apart from each other, thus, all 6 together
encompass 180 degrees.
This system divides the heart into a back half and a front half. The positive
pole of Lead I is at the right of an imaginary circle that spans this axis, while
the negative pole of Lead I is at the left. The other leads also have their
opposite poles on the opposite side.
Precordial System
The precordial leads on the chest are on a plane perpendicular to the hexaxial
or limb leads. This system splits the heart into top and bottom parts.
All these leads provide a 3-D view of the heart. Example:

Anterior (front): V3 and V4

Lateral (sides): I, aVl, V5, V6
Septum: V1 and V2
Bottom of the heart: V1, V2, aVF

NORMAL SINUS RHYTHM (NSR)

This rhythm is present when the SA node is functioning normally as the lead
pacer. The intervals should be consistent and fall within normal ranges. The
rate is 60-100 BPM and regular. There is a P wave, and the P to QRS ratio is
1:1. The PR interval and QRS width are both normal. There is no grouping,
and no dropped beats.
The next chapter is all about ECG abnormalities, and what to do about them.
To make a diagnosis, put all of your observations together. Don’t forget to
include the following important details:

Rate
Rhythm
Axis
Hypertrophy
Interval abnormalities
Blocks
T and ST wave abnormalities

Compare the ECG findings with the patient’s symptoms. Do these make
sense? Is the ECG the reflection of a problem or the cause of another pre-
existing health condition?
As you can see, the more you know about health, the better you can diagnose
a person based on his or her ECG readings.
 EXERCISES

1. The normal heart rate of adults is 80 - 120 BPM (True/False)

2. A normal axis is:

a. less than -30 degrees
b. between -90 and 180 degrees
c. -30 to +90 degrees
d. greater than +90 degrees
3. Limb Leads are V1 to V6 (True/False)

4. Chest leads are I, II, III, aVR, aVL and aVF (True/False)

5. A normal sinus rhythm has a P to QRS ratio of _

a. 2:1
b. 2:2
c. 1:2
d. 1:1
6. Anterior view is measured by leads _ and _.

7. Lateral view is monitored by leads _, _, _, and _.

8. The septum is monitored by leads _ and _.

9. The bottom of the heart is monitored by leads _, _, and _.

10. V4 lead is placed at the _ intercostal space.
a. Third
b. Fourth
c. Fifth
d. Sixth
 CHAPTER 5

ECG Diagnosis
This is a list of ailments that can be diagnosed from ECG readings.
 A
ACCELERATED IDIOVENTRICULAR RHYTHM
Accelerated Idioventricular Rhythm occurs when the ectopic ventricular
pacemaker works faster than the sinus node.
This kind of rhythm is most commonly observed during the reperfusion phase
of acute STEMI (ST-Elevation Myocardial Infarction). It may be triggered by
certain substances such as cocaine, anaesthetics, and beta-sympathomimetics
(ex. Adrenaline and isoprenaline). Illnesses such as cardiomyopathy,
myocarditis, congenital heart disease and electrolyte abnormalities may cause
this rhythm. Return of spontaneous circulation (ROSC) after cardiac arrest or
post thrombolysis (blood clot breakdown) may lead to this rhythm as well.
However, athletic hearts may beat in this fashion but this is not usually a
problem.
Accelerated Idioventricular Rhythm is a faster type of Idioventricular rhythm.
It has a regular rhythm at 40-100 BPM. QRS is wide and deformed,
measuring 120 ms or more. It has no P waves. In AV dissociation or third-
degree heart block, accelerated idioventricular rhythm may contain P waves.
It may include fusion and capture beats.
Treatment
AIVR is usually mild and does not need treatment most of the time. Like
IVR, it is self-limiting, and normalizes when the sinus rate exceeds the
ventricular rate. It is more important to treat the underlying causes, in order to
improve prognosis. In some situations, however, AIVR may need to be
inhibited, as it can worsen prognosis. This is seen in cases of loss of atrial-
ventricular synchrony, relative rapid ventricular rate, and ventricular
tachycardia or fibrillation. In these cases, atropine is used to increase the
heart rate. Anti-arrhythmic agents are not used because this may lead to
precipitous hemodynamic deterioration. Low cardiac output patients may be
given atropine to increase AV conduction and sinus rate.
ACCELERATED JUNCTIONAL RHYTHM

This occurs in an AV junctional pacemaker that fires faster than the normal
pacemaker (sinus node). The AV node experiences an increased automaticity,
while the sinus node has decreased automaticity.
The classic cause of AJR is digoxin toxicity, but beta-agonists can also
contribute to it. Heart ailments such as myocarditis and myocardial ischemia
can sometimes provoke this rhythm. It is also an infrequent side-effect of
cardiac surgery.
AJR has an above-average pace of 60-100 BPM; if beyond that, it is
recognized as junctional tachycardia. If slower than 60 BPM, it is considered
as junctional escape rhythm.
It is classified according to cause:

Automatic Junctional Rhythms, that are caused by increased

automaticity in the cells of the AV node.
Re-entrant Junctional Rhythms, which are caused by a re-entrant loop
in the AV node.
The QRS duration is narrow, usually measuring less than 120 ms except for
cases of pre-existing bundle branch block or other conduction abnormalities.
Ventricular rate is usually at 60-100 BPM. P waves may be retrograde and
show up during, before, or after QRS complexes. They are usually inverted in
the inferior leads (II, III, and aVF) and upright in aVr and V1.
If the ventricular rate is greater than the atrial rate, AV dissociation may be
involved.
Rapid AJR (Automatic Junctional Tachycardia) is similar to re-entrant
junctional tachycardias such as AVRT and AVNRT. The distinguishing
factor of AJR is heart rate variability and rhythm irregularity. It does not
usually respond to vagal stimulation – ventricular rate may temporarily slow
down, but the sinus rhythm will not normalize.
Junctional tachycardia is around 115 BPM. P waves are retrograde and
upright in V1 and aVr, while inverted in leads II, III, and aVF. The short PR
interval measuring less than 120 ms implies a junctional focus.
AJR with aberrant conduction is similar to accelerated idioventricular
rhythm. If there are fusion or capture beats, it is ventricular and not
junctional.
Treatment
Management of accelerated junctional rhythm depends on the condition of
the patient and the underlying cause of the abnormal rhythm. Asymptomatic
patients, if the cause is normal physiological response, may not need
treatment, especially if the rhythm is caused by a normal increase in vagal
tone. However, patients in whom heart block is the cause must be treated.
Those with AV blocks or sinus node dysfunction may benefit from having a
pacemaker implanted. AJR caused by digoxin toxicity may be counteracted
by medication such as Digibind and atropine.
For severe cases, radiofrequency ablation may be done to correct the rhythm.
ANTERIOR STEMI

Figure 5. Acute anterior myocardial infarction, showing ST elevation in anterior leads (V1-6,
I and aVL) and reciprocal ST depression in inferior leads.

Anterior STEMI (ST elevated myocardial infarction) is the blockage of the

left anterior descending artery. This condition is considered the worst of all
infarct cases.
Anterior STEMI is recognizable by ST segment elevation with Q waves in
the precordial leads (V1 to V6) and/or high lateral leads (I and aVL). There is
a reciprocal ST depression in the inferior leads (usually III and aVF).
The infarct patterns are based on the leads that display the most ST elevation:

Septal = V1 to V2
Anterior = V2 to V5
Anteroseptal = V1 to V4
Anterolateral = V3 to V6, I and aVL
Extensive anterior/anterolateral = V1 to V6, I and aVL

These are other things to look for:

Left main coronary artery occlusion: general ST depression with ST

elevation in aVR, that is greater or equal to V1
 Anterior-inferior STEMI caused by occlusion of left anterior
descending artery: ST elevation in both precordial and inferior leads,
because the blocked LAD wraps around the cardiac apex to supply the
left ventricle’s anterior and inferior walls
Wellen’s syndrome: deep T wave inversions in the precordial leads or
biphasic T waves in V2 to V3, implying proximal LAD stenosis that
may immediately lead to anterior infarction
De Winter’s T waves: upsloping ST depression, with symmetrical T
waves in the precordial leads; a sign of acute LAD occlusion

Treatment
The mainstay of any MI is to establish reperfusion quickly, in order to
salvage the myocardium. This may be done surgically or medically.
Percutaneous coronary intervention, or coronary artery bypass grafting are
the surgical techniques used. If this cannot be done immediately, medications
that disintegrate clots (fibrinolytics) are used, such as streptokinase, along
with blood thinners and platelet inhibitors. Oxygen is given to provide
oxygenation to the blood in the absence of a properly functioning heart.
ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA

Arrhythmogenic right ventricular dysplasia (enlargement or proliferation of

abnormal cells) is a kind of cardiomyopathy (heart muscle disease) that does
not involve blockages. It is also called as arrhythmogenic right ventricular
cardiomyopathy (ARVC).
ARVC is an inherited disease of the right ventricular myocardium, where the
normal muscle is replaced by fibrous fat. This is said to be the second most
common reason for sudden cardiac death in young people below the age of
35. Those with a family history of sudden cardiac death may have ARVC.
ARVC is diagnosed with a combination of ECG and other imaging devices
such as MRI, CT scans, and right ventricular contrast angiography.
The characteristics of ARVC are:

Sustained ventricular tachycardia with LBBB morphology

Ventricular ectopic beats
Accompanied by syncope, palpitations, or cardiac arrest
 Can lead to right ventricular failure, severe biventricular failure,
and/or dilated cardiomyopathy

The tell-tale sign of ARVC in an ECG is the Epsilon wave but it is only seen
in around 1/3 of patients. Almost all, however have prolonged S-wave
upstrokes of 55 ms in V1 to V3, as well as T wave inversions in V1 to V3.
There is localized widening of the QRS complexes, measuring 110 ms in V1
to V3. Ventricular tachycardia with LBBB morphology comes in paroxysms.
Treatment
ARVC is treated by anti-arrhythmic medication such as sotalol, amiodarone,
or conventional beta-blockers such as metoprolol. Those with urgent
symptoms can benefit from an implantable cardioverter-defibrillator (ICD)
which is very effective in preventing sudden cardiac death. Patients with
persistent ARVC can be given radiofrequency ablation of the conduction
pathways.
If this progresses to heart failure, ACE inhibitors, diuretics, and anti-
coagulants are given. Heart transplant may also be done for extensive damage
which cannot be treated with pharmacological intervention.
ATRIAL FLUTTER

Figure 6. Atrial flutter showing ‘sawtooth’ or ‘picket-fence’ appearance.

Atrial flutter is a form of supraventricular tachycardia, that is triggered by a

re-entry circuit in the right atrium.

The atrial rate is dependent on the atrium size, and is usually 250-350 BPM,
while ventricular rate is determined by the AV conduction ratio or the degree
of the AV block, and is often around 125-175 BPM.
The AV ratio is often 2:1, but medications or heart disease can result into
lower rates.
1:1 conduction may be caused by sympathetic stimulation, or an accessory
pathway, such as when AV-nodal blocking agents were given to a WPW
patient. It is also linked to severe hemodynamic instability and may progress
to ventricular fibrillation.
F waves manifest in a saw-tooth pattern. The QRS rate is often regular and
complexes appear at some multiple of the P-P interval. There may be 2 F
waves for every QRS complex. The ventricular response may have 3:1 or
higher rates. It may also be irregular.
Treatment
The first choice of treatment for atrial flutter is radiofrequency ablation,
which is believed to be superior to medical therapy because it has a decreased
risk of associated complications. Synchronized electrical cardioversion is
done for flutters of short duration (< 48 hours). Patient must be immediately
started on anticoagulation therapy, to prevent thromboembolic complications.
In cases where ablation is not feasible, anti-arrhythmic agents, such as
dofetilide, or ibutilide are used. If the heart function is normal, beta-
adrenergic blockers or calcium channel blockers are given concurrently.
ATRIAL FIBRILLATION

Figure 7. Atrial fibrillation depicting typical irregularly irregular ventricular rhythm.

Atrial fibrillation happens when atrial pacemaker cells fire randomly. This is
the most common form of sustained arrhythmia. It is caused by several
factors: ischemic or valvular heart disease, pericardial disease, dilated or
hypertrophic cardiomyopathies, hypertension, pulmonary embolus, acute
infections, thyrotoxicosis, phaeochromocytoma, electrolyte imbalances
(hypomagnesaemia, hypokalemia), acid-base imbalance, and certain drugs.
Atrial fibrillation has an irregularly irregular pattern with a ventricular rate of
about 110-160 BPM in general. It is categorized as a “rapid ventricular
response” if it is over 100 BPM and “slow” if it is below 60 BPM. Slow AF
is caused by sinus mode dysfunction, hypothermia, digoxin toxicity, and
some medications.
There are no P waves, and the QRS complexes are usually less than 120 ms,
unless there is an accessory pathway, bundle branch block, or other
conduction problem. There is no set P:QRS ratio or PR interval.
This may contain fibrillatory waves that may sometimes resemble P waves.
ATRIAL FIBRILLATION IN WPW

Figure 8. Wolf-Parkinson-White syndrome with atrial fibrillation and an irregularly irregular,

wide complex tachycardia.

Wolff-Parkinson-White syndrome is a congenital condition in which there are

abnormal conductive pathways between the atria and ventricles. 1/5 of people
with WPW will tend to have atrial fibrillation because the accessory pathway
directs conduction to the ventricles without passing the AV node. Rhythm is
irregular, and rates exceed 200 BPM. QRS complexes are wide and erratic
because of abnormal ventricular depolarization. Axis remains stable though,
unlike in Polymorphic VT.
Treatment
Treatment in a hemodynamically stable individual include either medical
methods, such as ibutilide or procainamide, or DC cardioversion. In a
hemodynamically unstable one, urgent synchronized DC cardioversion is
recommended. Anticoagulants such as warfarin or heparin should be used to
prevent stroke in almost all patients suffering from AF, except those who are
at a higher risk of bleeding.

Cryoablation or radiofrequency ablation is the recommended surgical mode

of treatment in younger patients where rhythm cannot be controlled by
pharmacological intervention or cardioversion.
AF should not be treated with AV nodal blocking drugs (beta-blockers,
calcium channel blockers, adenosine) because these may increase the
conduction through the accessory pathway, which will speed up ventricular
rate and degenerate to VF or VT.
In Wolff-Parkinson-White syndrome, therapy is aimed at removing the
accessory pathway, which is usually achieved by radiofrequency ablation of
that pathway. Anti-arrhythmic drugs, as described above, can also be used to
slow conduction.
ATRIAL ECTOPIC BEAT/ATRIAL PREMATURE BEAT

Figure 9. Atrial Premature Beat (APB) characterized by an abnormal P wave and a small
compensatory pause.

In this, the ECG shows an abnormal P wave leading the ectopic beat and a
small compensatory pause following it. This is also known by other terms,
such as atrial premature depolarizations, Premature Atrial Contraction (PAC).
This condition does not usually require treatment, however, in those that have
other heart problems, a PAC may lead to re-entrant tachydysrhythmia.
All these terms that are defined as a premature beat originate from an ectopic
focus in the atria.
PAC happens when another pacemaker cell in the atria fires faster than the
SA node. This causes the complex to arrive earlier than normal. The
premature beat resets the SA node, thus the rhythm is disturbed.
The rhythm is irregular. The P wave exists but is abnormal.
P: QRS ratio is 1:1 but the PR interval varies. QRS is normal. There may
sometimes be grouping but there are no dropped beats.
PAC may be provoked by diverse things: excess caffeine intake, anxiety,
beta-agonists, sympathomimetics, digoxin toxicity, myocardial ischemia,
hypokalemia, or hypomagnesaemia.
Treatment
Since most of these premature beats are benign, they do not need treatment.
Sometimes, PAC may require treatment, especially if it is associated with an
underlying disease. In these cases, either beta blockers or anti-arrhythmic
agents may be prescribed.
ATRIAL TACHYCARDIA

Atrial tachycardia is also known as ectopic atrial tachycardia, paroxysmal

atrial tachycardia (PAT), unifocal atrial tachycardia, and multifocal atrial
tachycardia.
It is a fast beat originating from the atria but outside the sinus node.
This is commonly due to one ectopic focus but there can also be several foci.
Causes may be idiopathic, or due to digoxin toxicity, catecholamine excess,
atrial scarring, or congenital defects.
As with tachycardia in general, atrial tachycardia has an atrial rate of greater
than 100 BPM. Because the P wave is ectopic, it looks different from normal.
Atrial tachycardia has at least 3 consecutive ectopic P waves that are
identical. The inferior leads (II, III, aVF) show an inverted P-wave axis. The
QRS complexes are often normal.
Atrial tachycardia can be distinguished from atrial flutter because the former
has an isoelectric baseline, while the latter does not.
Treatment
The primary goal during an episode of atrial tachycardia should be rate
control by using AV nodal blocking drugs. Many episodes of atrial
tachycardia can terminate if the cause is addressed. If it persists, however, the
episode may be terminated by the use of agents that block the AV node (beta
blockers and calcium channel blockers). Carotid sinus massages or
Valsalva’s manoeuvres may also be performed to correct atrial tachycardia. If
the patient is unstable, such as a child with complex congenital heart disease,
urgent synchronized electrical cardioversion is given.
Surgical ablation should be performed in patients with complex congenital
heart disease.
AV BLOCK: 1ST DEGREE / FIRST-DEGREE HEART BLOCK

Figure 10. AV node block showing long PR interval

This happens when the AV node experiences a prolonged block because of

vagal stimulation, medication (eg. AV nodal blocking drugs), and health
conditions such as inferior MI, myocarditis, and electrolyte imbalances, or as
a side-effect of mitral valve surgery. Athletes may also experience this. This
does not require treatment and does not cause hemodynamic problems.

The PR interval is greater than 200 milliseconds. If greater than 300 ms, it is
considered as a marked first degree block.
The rhythm is regular. The P wave is normal and has a 1:1 ratio to the QRS.
The QRS width is likewise normal, and there are no dropped beats or
groupings.
Treatment
The treatment depends on the underlying cause of the block. If asymptomatic,
usually no treatment is required. However, if the block is marked (PR
interval> 300 ms), cardiac pacemakers may be beneficial. Pharmacological
therapy may also be used, including atropine and isoproternerol. Use of AV
node blocking agents must be avoided, and discontinued. Any electrolyte
imbalances must be identified and corrected. Hospitalization may be required
in first-degree heart block patients presenting with associated myocardial
infarction.
AV BLOCK: 2ND DEGREE, MOBITZ 1 (WENCKEBACH)

Figure 11. 2 to 1 AV block where every other P wave is conducted; cannot be labeled as a
Mobitz type I or II pattern

A diseased AV node, with a prolonged refractory period causes this

condition. The conduction block is reversible, however. This is usually
benign; those without symptoms don’t need treatment while those who do
often get better with atropine.
Causes of Mobitz I are increased vagal tone, myocarditis, inferior MI, post
cardiac surgery (example repair of mitral valve or Tetralogy of Fallot), and
some drugs.
The PR interval lengthens between beats until a beat is dropped, then the
cycle restarts. The P-P interval is relatively consistent, but the R-R interval
shortens with every beat.
The rhythm is regularly irregular. The P wave is present, but the P:QRS ratio
varies (2:1, 5:4, 4:3, etc.) such as in Wenkebach.
The PR interval is variable and is at its longest before a dropped beat and
shortest after it. The QRS width is normal. Grouping may exist and may be
variable. There are dropped beats.
Treatment
This does not require specific therapy if the patient is asymptomatic. The
cause of the AV block is identified and managed. Drugs such as digoxin, beta
blockers, and calcium channel blockers may be discontinued, or the dose may
be reduced. Atropine, isoproterenol, and transcutaneous pacing may be given
for symptomatic cases, until the arrhythmia is gone.
AV BLOCK: 2ND DEGREE, MOBITZ II / MOBITZ II SECOND-
DEGREE HEART BLOCK

This is more commonly caused by conduction failure of the His-Purkinje

system because of structural damage (ex. Fibrosis, infarction, necrosis). This
is more serious than Mobitz I because it can lead to complete heart block.
Those with LBBB or bifascicular block tend to have Mobitz II. There are
several causes: idiopathic fibrosis, anterior MI, infiltrative myocardial
disease, autoimmune, cardiac surgery, hyperkalemia, and drug toxicity.
There are grouped beats with a beat dropped between groupings. The PR
interval is the same for all of the conducted beats.
Like Mobitz I, the rhythm is also regularly irregular. There are P waves that
have variable P:QRS ratios.
PR interval is normal.
QRS may be wide when the conduction block occurs distal to the His Bundle,
and narrow when it’s in the His Bundle.
Groupings are present and may vary. Dropped beats are observable.
Treatment
As with Mobitz 1 block, agents that can block AV node must be avoided or
reduced. Transcutaneous cardiac pacing is the treatment of choice and must
be done as soon as possible. Dopamine, epinephrine, or a combination of
both may be given through I.V. infusion.

For serious cases, a permanent pacemaker may be necessary.

AV BLOCK: 3RD DEGREE (COMPLETE HEART BLOCK) / THIRD-
DEGREE HEART BLOCK

Figure 12. Complete Heart Block showing no correlation between P waves and QRS
complexes

This is a total block of the AV node, where the atria and ventricles are firing
on their own. The sinus rhythm may be normal, or faster or slower than
expected. The escape beat can be junctional or ventricular.
Sinus rhythm and escape rhythm have their own rates, and are dissociated
from each other. Rhythm is regular but P and QRS rate are dissimilar. P
waves are there but P:QRS ratio is variable. PR interval is variable and has no
discernible pattern. QRS width may be wide or normal. There are no dropped
beats or grouping.
Remember: when there are the same number of P waves and QRS complexes,
but they are dissociated, it is AV dissociation and not third-degree heart
block.
Treatment
As with the previous heart blocks, transcutaneous pacing is the treatment of
choice. Any causative medications must be withdrawn, and I.V. infusion of
epinephrine and/or dopamine may be given. Installation of a permanent
pacemaker or an implantable cardioverter defibrillator (ICD) may also be
considered in patients with complete heart block. Atropine is indicated when
the patient is hemodynamically unstable, however, atropine is contraindicated
when there are wide-complex ventricular escape beats.
AVNRT (AV-NODAL RE-ENTRY TACHYCARDIA) /
SUPRAVENTRICULAR TACHYCARDIA (SVT)

AVNRT and SVT are one and the same, however they can be used to
describe any tachydysrhythmia (fast abnormal beat) originating above the His
Bundle.
AVNRT/SVT is the most common cause of palpitations among those with
normally structured hearts. It is provoked by caffeine, physical exertion,
alcohol, beta-agonists, or sympathomimetics. This is generally non-fatal,
even among those with heart disease.

This is produced by the AV node or atria, and usually results into tachycardia
(140-280 BPM) with narrow complexes (less than 120 ms), unless there are
other problems present. P waves may be visible and display inversion
(retrograde conduction) in leads II, III, and aVF, positioned after the QRS
complex, or at rare times, before it. It can also be hidden in the QRS
complex.

SVTs are categorized according to origin and regularity:

Atrial

Regular rhythm: Atrial flutter, Atrial tachycardia, Sinus tachycardia,

Sinus node re-entrant tachycardia, Inappropriate sinus tachycardia
Irregular rhythm: Atrial flutter with variable block, Atrial fibrillation,
Multifocal atrial tachycardia
Atrioventricular

AV nodal re-entry tachycardia (AVNRT)

Atrioventricular re-entry tachycardia (AVRT)
Automatic junctional tachycardia
Treatment
The treatment of AVNRT depends on the patients’ cardiac history and
previous ECGs. AVNRT management includes vagal maneuver, such as
carotid sinus massage and Valsalva maneuver, preferably with the patient in
Trendelenberg position. However, these are contraindicated if hypotension is
present. Pharmacological therapy may be used to terminate an attack by
slowing down conduction through the AV node, including medication, such
as adenosine. Recurrence is avoided by use of calcium-channel blockers,
beta-blockers, and amiodarone. Asthmatic patients should be closely
monitored as adenosine and beta-blockers can cause congestion of the
airways. If the patient does not respond to pharmacotherapy, or has
hemodynamic compromise, DC synchronized cardioversion may be applied.
Those who do not respond to regular treatment may be given catheter
ablation.
AVRT (ATRIOVENTRICULAR RE-ENTRY TACHYCARDIA)

This is a tachyarrhythmia caused by a re-entry circuit in the normal

conduction system, or a direct conduction from the atria to ventricles through
an accessory pathway, as is seen in Wolff-Parkinson White syndrome.
This is often provoked by premature atrial or ventricular beats.
Treatment
Treatment is similar to AVNRT. Vagal maneuver may be attempted before
starting drug treatments, but should not be done if the patient has low blood
pressure. Direct current synchronized cardioversion may terminate the attack
if the patient is hemodynamically compromised or if the drug treatment does
not work. Competitive atrial or ventricular pacing may be used if
cardioversion is not permitted.
 B
BENIGN EARLY REPOLARIZATION / HIGH TAKE OFF / J-POINT
ELEVATION

Benign early repolarization is seen among healthy individuals who are less
than 50 years old. Although benign, this resembles acute MI or pericarditis.
BER is recognizable by widespread concave elevation of the ST segments,
especially in the mid to left precordial leads (V2 to V5). The J-points have
notches. The T-waves are prominent and slightly asymmetrical and points at
the same direction as the QRS complexes.
The ST elevation is usually less than ¼ of the height of the T wave in V6. It
is generally less than 2 mm in the precordial leads and less than 0.5 mm in
the limb leads.
Treatment
Asymptomatic patients may not need to be treated, as the name indicates that
the condition is benign. Symptoms that may manifest are given remedies. If
the patients has experienced ventricular fibrillation, or sudden cardiac arrest,
an implantable cardioverter defibrillator may be placed.
BETA-BLOCKER TOXICITY
This rhythm is caused by excessive intake of beta-blockers such as atenolol,
propranolol, metoprolol, and sotalol and some cardioselective calcium-
channel blockers like diltiazem and verapamil.
The ECG shows bradycardia (sinus, ventricular, and/or junctional), and/or
1 /2 /3 degree AV block.
st nd rd

Treatment
The goal of treatment is to increase the cardiac output, by increasing the heart
rate and improving myocardial contractility. Hypotension, bradycardia, and
seizures should be prepared for. Charcoal (not Ipecac syrup) may be
indicated to help flush out the substance via gastric decontamination.
If the patient is hypotensive, 20ml/kg of isotonic intravenous fluids may be
given while he/she is in the Trendelenburg position.
The following protocol is recommended if the patient does not respond to
above mentioned measures.

Glucagon
High-dose insulin
Inotropes and chronotropes
Benzodiapenes (for seizures)
Hemodialysis
Extracorporeal membrane oxygenation
Cardiac pacing and/or resuscitations
BIDIRECTIONAL VT

This is a rare type of ventricular dysrhythmia that shows beat-to-beat

alternation along the frontal QRS axis. This can signify an alternating left and
right bundle-branch lock.
Bidirectional VT is most commonly observed in cases of severe digoxin
toxicity, but also among those with herbal aconite poisoning. Individuals with
familial catecholaminergic polymorphic ventricular tachycardia (CPVT) also
have this rhythm.
Treatment
If bidirectional VT is caused by digoxin, Digibind is used (2 – 20 ampoules,
depending on severity). If caused by AV block, atropine 0.6 mg bolus is
given intravenously. Intravenous lignocaine can also treat the arrhythmia.
Hyperkalemia is counteracted by insulin, dextrose, and sodium bicarbonate,
but not with calcium given intravenously.
Bidirectional VT may cause cardiac arrest; patients may need continuous
CPR until Digibind becomes available. DC cardioversion is ineffective for
this condition.
Catecolaminergic Polymorphic Ventricular Tachycardia is treated by beta-
blockers, electrical cardioversion or defibrillation, and an implantable
cardioverter-defibrillator.
BIFASCICULAR BLOCK

A bifascicular block is RBBB (right bundle branch block), coinciding with

LPFB (Left Posterior Fascicular Block) or LAFB (Left Anterior Fascicular
Block). This implies an extensive conducting system disorder, but rarely
progresses to complete heart block. The conduction arriving at the ventricles
is done through the remaining fascicle.

The main causes of this kind of block are ischemic heart disease,
hypertension, anterior MI, aortic stenosis, congenital heart disease,
degenerative disease of the conductive system, and hyperkalemia.
The ECG displays RBBB traits and a deviation to the left or right axis.
Treatment
Management depends on the cause of the bifascicular block. The underlying
cause must be analyzed and treated appropriately. Those with no symptoms
do not usually need treatment; those who do (e.g. repeated episodes of
syncope) may benefit from a pacemaker, which will regularize the rhythm.
Patients with renal disease or structural heart disease also have higher risk of
progressing to trifascicular block. Hence, this group requires continuous
monitoring, and pacemaker insertion may also be considered in these
patients.
BIVENTRICULAR ENLARGEMENT
This is the hypertrophy or enlargement of both ventricles.
The main ECG features of this condition are a combination of LVH and RVH
indicators; however, it may be hard to detect since LVH and RVH often
negate each other. A more obvious sign is the Katz Wachtel phenomenon,
where large biphasic QRS complexes are witnessed in V2 to V5.
In case of confirmed LVH, additional signs to look out for to confirm
Biventricular Enlargement are right axis deviation, right atrial enlargement
(as seen in other imaging studies), deep S waves in V5 to V6, and tall
biphasic QRS complexes in several leads.
In case of confirmed RVH, indicators for biventricular enlargement are QRS
complexes that are greater than 50 mm, tall R waves and deep S waves in
leads V2 to V5.
Treatment
Treatment focuses on addressing the cause. In cases of systemic
hypertension, medication that lowers blood pressure may help with
normalizing the size of the ventricles. These include ACE inhibitors, ARBs,
beta/calcium channel blockers, and diuretics. Digoxin may be administered to
enhance the pumping function of the heart. If the enlargement is caused by
stenosis, surgery may be done to repair or replace the faulty valve. Patients
with coronary artery disease need to undergo removal of blockages, to
improve blood flow by performing coronary bypass surgery. Heart transplant
is the last option if all of the above treatment modes fail to respond.
BIATRIAL ENLARGEMENT

This is enlargement of both atria that may be caused by pulmonary

hypertension, hypertension, congenital heart disease, aortic or tricuspid
stenosis, hypertrophic cardiomyopathy, mitral incompetence, mitral/aortic
valve disease, or chronic lung disease.
Biatrial enlargement is diagnosed when there are indicators of both left and
right atrial hypertrophy on the ECG.
In Lead II, the bifid P wave is equal to or greater than 2.5 mm and equal to or
greater than 120 ms.
In V1, biphasic P waves has an initial positive deflection measuring 1.5 mm
or greater and has a terminal negative deflection 1mm deep or greater and 40
ms or greater in duration.
Combination criteria includes P wave positive deflection 1.5 mm and above
in leads V1 or V2 and notched P waves greater than 120 ms in limb leads and
V5 or V6.
Treatment
As with biventricular enlargement, the cause of the condition is addressed.
Enlarged atria may be treated by controlling hypertension through ACE
inhibitors, beta blockers, and diuretics. Anticoagulants and anti-arrhythmics
should also be administered along with these medications. Potassium
supplements may be given to correct heart conduction problems. Implantable
cardioverter-defibrillator (ICD) may be recommended for patients at risk of
developing serious arrhythmias. Surgery is required for correcting structural
abnormalities, such as faulty valves, which would require replacement.
BRUGADA SYNDROME

Brugada syndrome is named after the Brugada brothers who first described
the condition.
This is linked to Sudden Unexplained Nocturnal Death Syndrome (SUNDS).
It is due to a genetic mutation in the cardiac sodium channel, also known as
sodium channelopathy.
Conditions accompanying it are fever, hypothermia, ischemia, hypokalemia,
drugs (pharmaceutical and recreational), and post DC cardioversion.
This condition is diagnosed by the Brugada sign, an ST segment elevation of
greater than 2 mm in more than 1 lead of V1 to V3 and followed by a
negative T wave.
To confirm this diagnosis, the following criteria must be met:

Presence of polymorphic ventricular tachycardia or ventricular

fibrillation.
Inducible VTs with electrical stimulation
Family history of sudden cardiac death while aged below 45 years old
Family members also have coved ECGs
Syncope (loss of consciousness)
Difficulty in breathing during sleeping
Treatment
The best way to treat Brugada syndrome is with the implantation of a
cardioverter-defibrillator (ICD). Patients with Brugada syndrome, who have
survived cardiac arrest, are candidates for ICD implantation, while
asymptomatic patients do not require it, but must be monitored closely.
Family history of sudden cardiac death is another reason to consider ICD
implantation.
No medications have been proved to be effective in preventing sudden death
in patients with Brugada syndrome.
 C
CALCIUM-CHANNEL BLOCKER TOXICITY
This is a lethal condition that causes the heart to collapse, but the patient can
be saved by providing thorough treatment and circulatory support.
The most toxic overdoses come from diltiazem and verapamil. Since these
two and other channel blockers like them prevent the influx of calcium to the
heart cells, too much of them can interfere with the heartbeat and dilate the
blood vessels.
Symptoms are chest pains, palpitations, difficulty breathing, vomiting,
seizures, sweating, dizziness, and fainting. Blood pressure is low and heart
rate is slow.
In the ECG, this manifests as bradycardia, AV block, bundle branch block,
and ST segment and T wave abnormalities.
Treatment
Managing this condition involves life support protocol; manage the airway,
breathing and circulation of the patient, while correcting electrolyte and acid-
base imbalances. Crystalloid fluid boluses are given to flush out the drug.
Bradycardia is treated with atropine. Activated charcoal given orally may
help absorb and flush out the toxic substance if taken within an hour of
poisoning. Ipecac syrup is strongly contraindicated as it may increase the risk
of seizures.
Specific medications used are calcium to overcome the channel blockade,
lipid emulsion therapy agents, high-dose insulin and glucagon to promote
calcium entry into cells, and vasopressors.
CARBAMAZEPINE CARDIOTOXICITY
Carbamazepine overdose (greater than 50 mg/kg) creates this condition
because of fast sodium channel blockade.
Symptoms of carbamazepine overdose or toxicity includes hallucinations,
blurred eyesight, nausea, vomiting, seizures, tremors, loss of control of body
movements (ataxia) and rapid unintentional movement of eyes (nystagmus).
Urine output is reduced because of the alteration of sodium levels in the
blood.

Heart rate is fast and blood pressure is dangerously low. This causes QRS
widening or sometimes 1st degree AV block. There may be a small
secondary R wave in the lead aVR.
Treatment
As with most poisoning cases, charcoal may be given to remove the
carbamazepine from the body, for as long as he/she is still conscious and the
airway is clear. Do not induce vomiting, in order to prevent CNS depression
and seizures. In case seizure results, diazepam or other benzodiapenes will
help to control them.
IV fluids may be administered, especially if the patient is hypotensive.
Whole-bowel irrigation should be performed. The guidelines recommend 1.5-
2 litres/hour of polyethylene glycol lavage solution for adults, whereas,
children should be treated with 0.5 litres/hour. If the QRS is wider than 100
ms, give sodium bicarbonate to counter sodium channel blockade.
CARDIOMYOPATHY, DILATED
This is a fatal heart disease involving dilatation of the ventricles, and overall
heart dysfunction. It has two common types: ischemic, following a massive
anterior MI, and non-ischemic/genetic. Others causes include viral
myocarditis, toxins, autoimmune disease, pregnancy, and alcoholism.
Dilated cardiomyopathy has no specific indicator, unlike Brugada syndrome
but the ECG looks abnormal in general. It shares common signs with
hypertrophy (atrial, biatrial, ventricular, biventricular). There are
intraventricular delays because of cardiac dilatation.

QRS complexes have reduced voltage in the limb leads because of

myocardial fibrosis. Abnormal Q waves are observed in V1 to V4, and may
resemble an MI pattern.
Treatment
Dilated cardiomyopathy is treated similar to chronic heart failure. This is
treated with antihypertensives, including vasodilators, diuretics, cardiac
glycosides, ACE inhibitors, and beta-blockers. Anti-coagulants are given to
thin blood and prevent clots. If arrhythmias are present, anti-arrhythmic drugs
are given. Surgical options include left ventricular assist devices, implantable
cardioverter-defibrillators, biventricular pacing, ventricular restoration
surgery, and heart transplants.
CARDIOMYOPATHY, HYPERTROPHIC

Hypertrophic cardiomyopathy (HCM) was previously called as hypertrophic

obstructive cardiomyopathy (HOCM) and idiopathic hypertrophic subaortic
stenosis (IHSS).
This is one of the most prevalent inherited disorders of the heart, and is the
leading cause of mortality in athletes.
This manifests as a dynamic obstruction of the left ventricular outflow tract
(LVOT). The left ventricle’s diastole is abnormal, because of its inability to
relax and fill up sufficiently. The intramural coronary arteries have thick
walls and narrowed passageways. There is a disorganized transmission of
electrical impulses, which can lead to arrhythmia.
The effects of this condition are syncope, chest pain, palpitations, and
pulmonary congestion. It can sometimes lead to cardiac death.

The ECG shows signs of left atrial hypertrophy, left ventricular hypertrophy
(abnormal T waves and ST segments), deep and narrow Q waves in the
inferior and lateral leads, huge T wave inversions in the precordial leads,
signs of WPW (delta waves and short PR), and other dysrhythmias.
Treatment
This is treated by medication (beta blockers, calcium channel blockers, anti-
arrhythmic agents, blood thinners). Surgery may be done to remove tissue
overgrowth, for example, septal myectomy. Septal ablation involves
destroying the thickened heart muscle, by injecting alcohol through a
catheter. For life-threatening conditions, an implantable cardioverter-
defibrillator is implanted.
CARDIOMYOPATHY, RESTRICTIVE

Restrictive cardiomyopathy occurs during advanced myocardial infiltrative

disease.
Ventricular arrhythmias and atrial fibrillation tend to accompany this
condition.
There are low-voltage QRS complexes and unusual Q waves.
T waves and ST segments are abnormal.
Indicators of bundle branch blocks are present. AV block may also be
involved, and in the case of sarcoidosis, may manifest as a 3rd degree AV
block.
ECG may show atrial and ventricular dysrhythmias
Treatment
The treatment for restrictive cardiomyopathy is targeted to its particular
causes. Symptomatic treatment can be given to reduce congestion, lower
filling pressure, and prevent embolism. This is achieved by use of
vasodilators, diuretics, and ACE inhibitors. If not contraindicated, anti-
coagulants may also help in preventing thromboembolism. Permanent pacing,
LVAD therapy, and heart transplantation may be done on certain patients,
who do not respond to pharmacotherapy.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

COPD affects the heart rhythm, and causes ECG changes. When the lungs
over expand, the heart becomes compressed and the diaphragm lowers,
causing the heart to become longer and to be vertically oriented. It can rotate
clockwise, with the right ventricle moving slightly forwards and left ventricle
moving slightly backwards.

Because of the new position and an excess of air surrounding the heart, the
electrical signals may become weakened. The QRS complexes will show this
and have reduced amplitude.
Other ECG traits are as follows:
The P wave axis shifts to the right, with P waves prominent among the
inferior leads and inverted or flat in leads I and aVL.

The QRS wave axis also shifts to the right. QRS voltages are low especially
in the left precordial leads (V4 to V6).
Atrial depolarization is amplified, resulting to ST and PR segments that dip
below the baseline.
The R waves may be totally gone in leads V1 to V3.
COPD effects may also include signs seen in RBBB, and multifocal atrial
tachycardia.
Treatment
The primary goal of treatment should be to optimize the lung function, reduce
severity of symptoms, and prevent recurrence. The cause/s of the COPD is
treated. Medications that reduce shortness of breath, control coughing fits,
and prevent the recurrence of the condition are used. Beta-2 agonists and
anticholinergic drugs are used to provide vasodilatation. Inflammation is
managed by using oral or inhaled steroids. If infection sets in, doxycycline is
preferred. Long-term antibiotics such as erythromycin may be recommended
in patients with two or more than two episodes of COPD per year. Mucolytic
agents such as n-acetyl cysteine can be used to reduce secretions. Oxygen is
given to assist with the patient’s breathing. Refractory cases might require
lung transplantation.
 D
DE WINTER’S T WAVES

This rhythm gets its name from de Winter and Wellens, who observed it
among patients with acute LAD blockages. It is now known that this ECG
pattern can predict the condition quite accurately.
This is an anterior STEMI equivalent, but without an apparent elevation of
the ST segments.

The most noticeable features are peaked and symmetrical T waves and
depressed ST segments in the precordial leads. The ST depression measures
greater than 1 mm at the J-point, and 0.5 – 1 mm in aVR. There is no ST
elevation in the precordial leads.
Treatment
When a patient has De Winter’s T waves, it means that he/she is experiencing
STEMI.. Oxygen, morphine, nitroglycerin and aspirin are given primarily, as
necessary. Fibrinolytic therapy is started to lyse the blood clot. PCI or CABG
must be done to reestablish reperfusion.
DEXTROCARDIA

This is a rare condition where the heart’s apex is at the right side of the body
(instead of the normal left).

The ECG reflects a right axis deviation with positive QRS complexes and
upright P and T waves in the lead aVR.
In Lead I, the complexes are all inverted.
S waves are dominant in the chest leads, and R wave progression is
noticeably absent.
Take note that the reversal of the right and left electrodes may cause this
pattern. Check whether the leads are placed correctly.
Treatment
Dextrocardia may cause complications such as frequent infections, and
intestinal obstructions. These are treated by antibiotics and surgery.

Heart abnormalities are sometimes associated with holes in the septum,

which can be remedied by surgical correction and pacemakers.
DIGOXIN EFFECT

Figure 13. Digoxin effect showing characteristic ‘reverse tick’ appearance (down sloping ST
depression, visible here in leads V5 and V6), dysrhythmias, and shortened QT interval.

Digoxin is a cardiac stimulant. It affects ECG readings.

Digoxin shortens the refractory period of the atrium and ventricles, and
increases the vagal effects in the SA node.
It creates ST depressions that appear to sag, as well as shortened QT
intervals. It makes the T waves become inverted, flat, or biphasic.
Other indicators of digoxin effect are big U waves, peaked terminal parts of T
waves, slight PR interval prolongation of up to 240 ms, and J point
depression mainly in leads with tall R waves.
Treatment
Digoxin effect is not treated unless it produces unpleasant symptoms (see the
following section).
DIGOXIN TOXICITY
Digoxin toxicity results when too much digoxin is taken, and the body reacts
adversely.
Symptoms include nausea, vomiting, diarrhoea, blurred and abnormal vision,
palpitations, difficulty breathing, confusion, dizziness, and fainting.
Several types of dysrhythmias may result because of increased automaticity
and decreased AV conduction.

The classic sign of digoxin toxicity is a mixture of supraventricular

tachycardia and slow ventricular response.
There may be frequent PVC and ventricular bigeminy or trigeminy. Sinus
rhythm may be slow and there may be slow AF.
AV blocks may exist.

Ventricular tachycardia may also be there especially polymorphic and

bidirectional VT.
Treatment
For acute overdose, activated charcoal is given to help eliminate the digoxin.
Digoxin Immune Fab is the most effective medication for this kind of
toxicity. Electrolyte imbalances are corrected, while dysrhythmias are treated
with medication such as beta-blockers, lidocaine, phenytoin, and atropine.
Calcium channel blockers are contraindicated because they can enhance
digoxin levels. Magnesium sulfate can help stop dysrhythmias but it is
prohibited among those with AV block, bradycardia, or renal failure.
Cardioversion should be attempted cautiously because this can lead to
ventricular fibrillation and asystole.
 E
ECTOPIC ATRIAL TACHYCARDIA
This condition takes place when the ectopic atrial focus fires faster than the
sinus rate. The P waves and PR intervals are dissimilar, because the rhythm is
created by a pacemaker other than the normal SA node. This usually occurs
only briefly. Because of the faster rate, some ST and T wave abnormalities
may appear temporarily.

The rate is at 100-180 BPM but has a regular rhythm. The P wave‘s ectopic
focus has a different form. The P:QRS ratio is 1:1. In the PR interval, the
ectopic focus has a different interval. The QRS width may be normal or not.
There are no groupings or dropped beats.
Treatment
Patients not having cardiac failure may be given intravenous class Ia and Ic
anti-arrhythmics, such as quinidine or propafenone. Those with abnormal
ventricular function are prescribed intravenous amiodarone. Class III anti-
arrhythmic drugs do not always correct ectopic atrial tachycardia, but they
help with maintaining normal sinus rhythm after conversion. Digoxin and
beta-blockers may also be recommended to control heart rate.
Radiofrequency ablation is also curative for ectopic atrial tachycardia.
ELECTRICAL ALTERNANS

This is a condition caused by the heart swinging to-and-fro in a huge

pericardium filled with fluid. This creates normally conducted QRS
complexes that have alternate heights. It occurs in cardiac tamponade and
severe pericardial effusion.
Treatment
The immediate goal is to rule out cardiac tamponade. If tamponade is present,
emergency pericardiocentesis needs to be performed. In cases of pericardial
effusion without tamponade, drainage will still be required for large
effusions. For smaller pericardial effusions, medications targeting the
underlying cause are administered, such as antibiotics for infection and
NSAIDs for inflammation.
 F
FASCICULAR VT
This is the most prevalent idiopathic ventricular tachycardia. Healthy people
may experience this when stressed, while exercising, after taking beta-
agonists, or sometimes even during rest

The first treatment done is usually administering of Verapamil.

ECG signs are:

RBBB indicators with a left axis deviation (posterior fascicular VT)

RBBB indicators with a right axis deviation (anterior fascicular VT)
RBBB that may resemble LBBB, with narrow QRS complexes and
normal axis arising from upper septum region (upper septal fascicular
VT)
Treatment
Verapamil is fascicular VT’s first line of treatment for stable patients with
moderate symptoms, given at a dose of 120-480 mg/day. If the patient has
severe symptoms, or is intolerant or resistant to anti-arrhythmias, catheter
ablation should be performed. For emergency cases, electrical cardioversion
is done.
 H
HIGH TAKE-OFF
(See Benign Early Repolarization)
HYPERCALCEMIA
Hypercalcemia is an excess of calcium in the blood. Because calcium is
involved with the action potential of cells, an excess of it will result in
conduction abnormalities of the heart.

Causes of hypercalcemia are:

Hyperparathyroidism
Sarcoidosis
Paraneoplastic syndromes
Bony metastases
Milk-alkali syndrome
Excess vitamin D

This condition appears in the ECG as strange-looking QRS complexes,

extremely short QT intervals, and J waves (notches in the terminal QRS
complex especially in V1)
Treatment
Fluid volume loss associated with hypercalcemia is treated with isotonic
sodium chloride solution. When the volume has normalized, loop diuretics
are given to block sodium and calcium reabsorption. Bisphosphonates may be
used to prevent osteoclastic activity.
If the hypercalcemia is caused by hyperparathyroidism, surgical intervention
may be necessary to remove the parathyroid gland.
HYPERKALEMIA

Figure 14. Hyperkalemia is characterized by tall and tented T waves, small or absent P
waves and ST segments, wide QRS, as well as atrial and ventricular fibrillation

Potassium is an important key in maintaining the heart’s normal electrical

activity. When there is a greater than normal level of potassium in the blood,
the myocardial excitability becomes reduced, resulting into weakened
reaction of the conducting and pacemaking heart tissues.
When this condition worsens, the SA node’s impulses become suppressed,
and the AV node and His-Purkinje reduce conduction activities. This
ultimately leads to conduction blocks, bradycardia, and even cardiac arrest.
The earliest sign of hyperkalaemia is peaked T waves. This implies
repolarization aberrations.
When the atria become paralyzed, the P wave becomes wider and more flat,
and the PR segments lengthen until they disappear altogether.
When the condition progresses, QRS intervals become prolonged and QRS
complexes take on bizarre shapes. There may be high-grade AV blocks,
accompanied by slow ventricular and junctional escape rhythms. Conduction
blocks may also be present.
Slow AF or sinus bradycardia may be observed.
The ECG may develop a sine wave pattern, which is a danger sign. If this
leads to cardiac arrest, ventricular fibrillation and asystole may occur.
Treatment
Limiting dietary intake and increasing excretion by using diuretics is
sufficient for patients with moderate hyperkalemia without any ECG
abnormalities. It is necessary to be vigilant with patients that have an AV
block or bradyarrhythmia, especially those who have renal failure or on
haemodialysis and taking potassium-sparing diuretics, ACE inhibitors, and
potassium supplements. These things may cause a spike in potassium in the
blood.
Hyperkalemia is treated by infusing calcium, in order to prevent cardiac
arrest. Insulin-glucose infusion is given to drive potassium into cells. Loop
diuretics are used to remove excess potassium. Metabolic acidosis, if present,
is corrected by bicarbonate infusion.
HYPERTHYROIDISM
The thyroid produces hormones that regulate how cells use energy. When it is
hyperactive, it makes too much of these hormones, which creates unpleasant
symptoms such as irregular heartbeat, fatigue, insomnia, and weight loss.

In the ECG, hyperthyroidism creates the following changes because of the

increased responsiveness of the sympathetic nervous system and
overstimulation of the myocardium:

Sinus tachycardia
Atrial fibrillation
Rapid ventricular response
High voltage from left ventricles
Supraventricular arrhythmias
Ventricular extra systoles
T wave and ST abnormalities
Treatment
Hyperthyroidism is treated by anti-thyroid medications, radioactive therapy,
or thyroidectomy. Anti-thyroid medication includes propylthiouracil and
methimazole, which inhibit the conversion of T4 to T3. Radioactive iodine
(I131) is administered orally, and it is preferentially taken up by the thyroid
gland, where it causes fibrosis and destruction of cells. Surgery can also be
done for thyroid hormone-producing tumors.
HYPOCALCEMIA

For the normal functioning of the cells, calcium must be present in

appropriate levels in the blood. If there is a low amount of it, it will affect the
way the cells work, including those in the heart.
The causes of hypocalcemia may be hypoparathyroidism (underactive
parathyroid), vitamin D deficiency, hypomagnesemia, hyperphosphatemia,
acute pancreatitis, diuretics, certain congenital diseases such as DiGeorge
syndrome, and sepsis.
Symptoms are seizures, neuromuscular excitability, tetany, carpopedal
spasm, Trousseau’s sign, and Chvostek’s sign.
ECG reflects prolonged QTc segments, specifically on the ST segments. The
T wave is usually normal. Dysrhythmias are usually uncommon, but atrial
fibrillation may sometimes occur. Torsades de pointes may also happen, but
it is less likely as with hypomagnesaemia or hypokalaemia.
Treatment
Calcium and magnesium are given orally and intravenously. Mild
hypocalcemia requires oral supplementation. Severe forms require IV
infusion. Magnesium aids in calcium absorption. If seizures present, they are
managed with benzodiazepines. If it is caused by other conditions such as
hypoparathyroidism, these are treated.
HYPOKALEMIA

Figure 15. Hypokalemia is associated with small or absent T waves,

prominent U waves, AV block, and slight ST depression.

Potassium regulates the electrical conduction of the heart. Decreased levels of

potassium in the blood cause hyper-excitability of the heart cells, which leads
to the development of re-entrant arrhythmias. This is often linked to
hypomagnesaemia.
The effect of early hypokalaemia on the ECG causes the following features:

Bigger and longer P waves

Prolonged PR intervals
Flat and inverted T waves
Depressed ST segments
Prominent U waves especially in the precordial leads
 Fusion of the T and U waves, causing what seems to be longer QT
intervals

When it worsens, the ECG reflects these:

Frequent supraventricular and ventricular ectopic beats

Supraventricular tachyarrhythmias
Ventricular arrhythmias
Treatment
Intravenous potassium is infused slowly at a rate of 10 mEq per hour.
Continuous ECG monitoring is essential. The cause for hypokalemia must be
diagnosed and addressed; this may involve stopping diuretics and replacing
with potassium sparing diuretics, and prevention of nausea, vomiting and
polyuria.
Surgical intervention is required only in case of renal artery stenosis,
intestinal obstruction, and adrenal adenoma.
HYPOMAGNESEMIA
Hypomagnesemia is the condition of having low levels of magnesium in the
blood. This can happen because of malnutrition, alcoholism, diarrhoea,
digestive disorders, excessive sweating, antibiotic and diuretic side effects.
The main sign of hypomagnesaemia in an ECG is a prolonged QTc segment.
Other than that, there is ectopy in the atria and ventricles, torsades de pointes,
and tachyarrhythmia in the atria.
Treatment
Treating this involve correcting the serum magnesium levels. Intravenous
magnesium is given at the rate of 50 mEq over 8 to 24 hours. Calcium and
potassium levels must also be monitored and corrected if required. In case of
torsades de pointes, 2mg magnesium rapid IV bolus is given.
HYPOTHERMIA
Hypothermia is body temperature that is below acceptable levels, usually
below 35 degrees Celsius.

ECG clues of hyperthermia include shivering artefact (fuzzy ECG baseline),

bradyarrhythmias (sinus bradycardia, slow junctional rhythms, atrial
fibrillation with slow ventricular response, and AV blocks), ventricular
ectopic beats, prolonged PR, QT, and QRS intervals, and Osborn waves
(positive deflection at the J point in most leads except in aVr and V1, where
they are negative). If unmanaged, it may trigger VT or VF. Sometimes, this
can also lead to cardiac arrest.
Treatment
The hypothermic patient is warmed, using hot water bottles or chemical
warmers, to regain normal body temperature. Lignocaine can be used to
prevent cardiac dysrhythmias. If ventricular fibrillation occurs, chemical
conversion could be attempted with intravenous bretylium, and supported by
CPR when necessary. Defibrillation should be done when the patient’s body
temperature is above 30 degrees celsius to be effective.
HYPOTHYROIDISM

An underactive thyroid or myxoedema causes the body to produce minimal

amounts of a hormone called thyroxin, which affects the ability of the heart
to function properly.

In an ECG reading, hypothyroidism may be diagnosed with bradycardia, low

QRS voltage, and widespread T-wave inversions, often without ST segment
deviations.
Other supporting indicators are first degree AV block, QT segment
prolongation, and intraventricular conduction delay.
These ECG abnormalities may be due to gelatinous connective tissue
deposits in the myocardium, decreased sympathetic nervous system activity,
and decreased chronotropy and inotropy of the heart.
Treatment
Synthetic thyroid hormone such as levothyroxine is given orally to treat
hypothyroidism, at a starting dose of 50-75 µg per day. . Once the levels have
been stabilized, patients should be carefully monitored for the signs of
overdose such as palpitations, tachycardia, headache, fatigue, tremors, or
angina.
 I
INTERVENTRICULAR CONDUCTION DELAY (QRS WIDENING)

This is when the duration of the QRS complexes exceed 100 ms, and there is
a supraventricular rhythm.
This is most often caused by left ventricular hypertrophy or a bundle branch
block.

Hyperkalaemia and TCA poisoning are the most significant causes of this
condition.
Other causes include the following: Left anterior/posterior fascicular branch
block, left/right bundle branch block, bifascicular block, trifascicular block,
left ventricular/right ventricular hypertrophy, biventricular hypertrophy,
dilated cardiomyopathy, Wolff—Parkinson-White syndrome, arrhythmogenic
right ventricular dysplasia (AVRD), and Brugada syndrome.
Treatment
The cause of the interventricular conduction delay must be ascertained by
thorough cardiac evaluation. Treatment is given according to the underlying
cause. Treatments of the various causes are described in their respective
sections.
INTRACRANIAL HAEMORRHAGE
Intracranial haemorrhage is bleeding within the skull, which can cause
increased intracranial pressure. This is a dangerous condition that affects
several parts of the body, including the heart’s conduction system.

This is caused by traumatic brain injury, cerebral metastases, and massive

ischemic stroke.
This is associated with bradycardia (Cushing reflex –warns of likely
herniation of the brainstem), QT prolongation, widespread huge T-wave
inversions (aka cerebral T waves).

Other ECG signs are:

ST depression or elevation
Increased amplitude of U waves
Rhythm disturbances – atrial fibrillation, premature ventricular
contractions, sinus tachycardia
Treatment
Intracranial haemorrhage requires intensive care in a medical facility.
Endotracheal intubation is done to protect the airway, and hypotension is
induced to a mean arterial pressure less than 130 mm Hg. Emergency CT
scan should be performed after the vital signs have been stabilized.
Intracranial pressure is monitored. Mannitol can be administered to control
intracranial pressure. Normotonic fluids should be used to maintain brain
perfusion without causing edema. Large hematomas must be evacuated
surgically.
INTRINSICOID DEFLECTION/ R WAVE PEAK TIME
This is the time from the beginning of the earliest Q or R wave, up to the
peak of the R wave in the lateral leads (V5 to V6, aVL),
This represents the time that it takes for the impulse to spread from
endocardium to epicardium of the left ventricle.
The intrinsicoid deflection is said to be prolonged if it exceeds 45 ms.
Causes of this include left ventricular hypertrophy, left anterior fascicular
block, and left bundle branch block.
Treatment
Intrinsicoid deflection is a symptom of an underlying condition.
This must be determined by thorough cardiac evaluation, and treated
according to the cause as described in the individual sections.
 J
J-POINT ELEVATION
(See Benign Early Repolarization)
JUNCTIONAL ECTOPIC BEAT / JUNCTIONAL PREMATURE BEAT
/ PREMATURE JUNCTIONAL CONTRACTION

It is a premature beat in the AV node. It appears rarely, but can have a regular
grouped pattern, such as in cases of supraventricular bigeminy or trigeminy.
This causes an irregular rhythm. The P wave is variable – it may be absent or
be antegrade (appearing before the QRS complex) or retrograde (appearing
after it). The PR interval is very short and the P-wave axis is abnormal or
inverted in leads II, III, and aVF).
Treatment
No treatment is required if the patient is asymptomatic. If the patient presents
with symptoms, the underlying cause is managed. The primary goal should
be to decrease the rate by treating acidosis or electrolyte imbalances. Anti-
arrhythmic medications such as amiodarone may be recommended. If it
occurs because of digoxin, the drug is discontinued and counteracted.
Caffeine may cause this as well. If so, caffeine intake is reduced.
JUNCTIONAL ESCAPE BEAT
An escape beat results when the normal pacemaker does not fire, and the next
pacemaker activates. The distance of the escape beat is always longer than
the normal P-P interval.
This has an irregular rhythm. The P wave may be variable – it may be absent,
antegrade, or retrograde. If it exists, it has a P-QRS ratio of 1:1. The PR
interval may be non-existent, short, or retrograde. If it exists, it does not
signify the atrial stimulation of the ventricles. QRS width is normal. There
are no groupings but there are dropped beats.
Treatment
Treatment depends on the underlying cause/s of the junctional escape beat. If
asymptomatic, this does not require treatment. If the beat is greater than 60
BPM, beta blocker such as esmolol may be used. Atropine or digoxin
immune Fab may be used if junctional escape beat is caused due to digitalis
toxicity. A permanent pacemaker may be indicated in patients presenting
with complete AV block or sick sinus syndrome to speed up the ventricular
rate and help normalize the arrhythmia.
JUNCTIONAL RHYTHM
A junctional rhythm is created as an escape rhythm, when the SA node and
the atria’s pacemaker do not function. It can occur during AV dissociation or
third-degree AV block.

The rate is 40-60 BPM and regular. The P wave may be variable (absent,
retrograde, or antegrade). The P:QRS ratio may be absent or 1:1. The PR
interval may be non-existent, brief, or retrograde – if present, it does not
represent the atrial stimulation of the ventricles. QRS width is normal and
there are no grouping or dropped beats.
Treatment
The underlying cause of the junctional rhythm is corrected. Generally this
condition may be physiological, and may not require treatment. However, if
it is accompanied by dizziness and syncope, or it is associated with systemic
comorbidities such as coronary artery disease, a pacemaker can be used to
normalize the rhythm. If the junctional rhythm is due to digitalis toxicity
atropine and digibind may be given. The junctional rhythm should not be
suppressed though, because doing so may cause the ventricles to stop.
 L
LATERAL STEMI

Lateral STEMI is ST segment elevation myocardial infarction of the lateral

portions of the heart.
This is recognizable by the ST elevation in the lateral leads (leads I, aVl, and
V5 to V6) and corresponding ST depression in the inferior leads (leads III
and aVF).
Treatment
Treatment for Lateral STEMI is the same as with myocardial infarctions. The
first line of treatment for patients with STEMI is reperfusion by either
mechanical (primary percutaneous intervention) or pharmacological
interventions. Initial therapy is done with aspirin, morphine, and
nitroglycerin. Intravenous access and supplemental oxygen should be
provided immediately. Fibrinolytic therapy is started and surgery may be
carried out for reperfusion.
LEAD REVERSALS: LIMB LEAD REVERSALS (OVERVIEW)
This is simply the unintentional misplacement of limb lead electrodes. This
may produce wrong readings that resemble heart diseases such as myocardial
infarction/ischemia, chamber hypertrophy, and ectopic atrial rhythm.
LEAD REVERSAL: LEFT ARM/RIGHT ARM
LA/RA reversal may copy dextrocardia, but in contrast to the genuine illness,
reversal has a normal R wave progression within the precordial leads.
Because the Einthoven’s triangle are rotated 180 degrees, the Wilson’s
central terminal sends a zero signal, and the limb leads may look like other
leads or become a flat line.
This results into the following disruptions:

Lead I is inverted
Leads II and III take each other’s place
Lead aVR and aVL switch
Lead aVF is unchanged

To determine RA/LL reversal, check the following:

Lead aVR is upright

Leads I to III and aVF are inverted (inverted P and T waves and QRS
complexes)
LEAD REVERSAL: RIGHT ARM/LEFT LEG
Switching the RA and LL electrodes rotates the Einthoven’s triangle 180
degrees vertically around the aVL axis.

This causes the following ECG effects:

Inverted Lead II
Inverted and reversed Lead I and III
Switched aVF and aVR
Unchanged aVL

To determine RA/LL reversal, look for these:

Inversion of Leads I to III and aVF

Upright aVR

RA/RL(N) REVERSAL
Reversing the RA and RL(N) electrodes causes Einthoven’s triangle to
become a narrow triangle with the LA electrode at the apex.
The LL and LA leads record near identical voltages and makes their
differences non-significant. The lead aVR faces opposite the lead II. Because
the neutral electrode is displaced, aVF and aVL becomes identical and
appears the same, but it will still be different to the baseline ECG.

So again, these are the indicators of RA/RL(N) reversal:

Lead III is a flat line (most obvious indicator)

Lead I = Lead II
Lead II is unchanged
Lead aVR is an inverted lead II
Lead aVL = Lead aVF

BILATERAL ARM-LEG REVERSAL (RA-RL AND LA-LL)

If the arm electrodes are switched with their associated leg electrodes (LL
with LA and RL with RA), the Einthoven narrows down to a very small
triangle with the LL electrode at the apex.
Because of this:

Lead I = flat line (most obvious indicator)

Lead II = inverted lead III
Lead III becomes inverted
aVR = aVL
aVF = negative lead III

LL/RL(N) REVERSAL
When the lower limb electrodes are reversed, Einthoven’s triangle remains
the same because the electrical signals from each leg are almost alike. This
results to an unchanged ECG reading.
Treatment
Lead reversals do not require treatment. The position of the electrodes is
verified, and if incorrect, electrodes are simply placed in their correct
positions.
LEFT ATRIAL ENLARGEMENT / LEFT ATRIAL HYPERTROPHY

Figure 16. Left atrial abnormality (enlargement or hypertrophy) showing abnormal P waves
(terminal negative components in lead V1)

The enlargement of the left atrium is caused by volume overload or pressure

in it. This often causes atrial fibrillation.
This is often seen with mitral stenosis, and left ventricular hypertrophy
(hypertrophic cardiomyopathy, aortic stenosis, mitral incompetence, and
systemic hypertension).
This creates broad and bifid (M-shaped) P waves in lead II and bigger
terminal negative portions of P waves in V1.
In particular:

Lead II shows bifid P waves greater than 40 ms between two wave

peaks, with total duration of greater than 110 ms.
 V1 shows biphasic P waves with terminal negative portions greater
than 40 ms in duration and deeper than 1 mm.

Treatment
Left atrial enlargement is treated by addressing the underlying cause. Blood
pressure should be managed through medications and dietary interventions.
Beta blockers, ACE inhibitors, and diuretics can all help to control
hypertension. Diuretics, anti-arrhythmics, and anti-coagulants should be
given if the cause of enlargement is mitral stenosis. Surgical interventions
such as mitral valve replacement should be considered only when other
conservative options fail to respond. Electrical cardioversion and pacemaker
implantation are performed if the underlying cause is atrial fibrillation.
LEFT ANTERIOR FASCICULAR BLOCK / LEFT ANTERIOR
HEMIBLOCK

Figure 17. Left anterior hemiblock: LVH, LAH and long PR interval

Left anterior fascicular block is an electrical conduction abnormality, where

impulses are carried through the left posterior fascicle and to the left
ventricle.
LAFB ECG features are:

Left axis deviation (-45 to -90 degrees)

Small Q waves with tall R waves in Lead I and aVL
Small R waves with deep S waves in Lead II, III, and aVF
 Increased QRS voltages in limb leads
Normal to slightly prolonged QRS (80-110 ms)
Prolonged R wave peak time in aVL that is greater than 45 ms

To distinguish LAFB from LVH, remember that in LAFB, the QRS voltage
in the aVL lead will have no strain pattern in the left ventricle.
Treatment
There is no specific treatment for left anterior fascicular block, but it is a
symptom of an underlying heart disorder. Therefore, a thorough cardiac
evaluation is necessary to diagnose any underlying cardiac disease. If this
disorder is causing unpleasant symptoms, treatment for the particular
condition is given.
LEFT AXIS DEVIATION
A left axis deviation is a description of QRS axis, that occurs between -30
and -90 degrees. It is caused by many conduction problems such as Wolff-
Parkinson White syndrome, ventricular ectopy, left ventricular hypertrophy,
left anterior fascicular block, left bundle branch block, inferior MI, and paced
rhythm.
The following features are present when there is a left axis deviation:

QRS is positive and has dominant R waves in I and aVL.

QRS is negative and has dominant S waves in II and aVF.
Treatment
The cause for the left axis deviation is addressed. If the patient is
asymptomatic, no treatment is required, apart from careful monitoring.
Symptomatic patients require treatment according to the cause, as described
in the respective sections.
LEFT BUNDLE BRANCH BLOCK

Figure 18. Acute myocardial infarction in the presence of left bundle branch block.

In LBBB, the septal depolarization becomes reversed (it goes from right to
left instead of the usual left to right).
This is caused by various conditions like ischemic heart disease, aortic
stenosis, anterior MI, dilated cardiomyopathy, fibrosis of the conducting
system, hypertension, hyperkalaemia, and digoxin toxicity.
This aberration is indicated by the following features:

QRS lasting longer than 120 ms

Dominant S waves in V1
Broad monophasic R waves in Leads I, avL, and V5 to V6
No Q waves in I, V5 – V6
R wave peak time is prolonged and measures greater than 60 ms in the
left precordial leads V5 to V6
ST segments and T waves go opposite the main vector of the QRS
R waves progress poorly in precordial leads
There is a general left axis deviation
In the lateral leads, the R wave takes on the following characteristics:

Monophasic
Notched
M shaped
Belongs to an RS complex

In V1, the following are observed:

Small R waves, deep S waves

Deep Q/S waves with no R wave before them

LBBB is described as incomplete when the QRS duration is less than 120 ms.
Reminder: LBBB is similar to LVH
Treatment
Treatment of this condition depends on the cause and the severity of the
block. Patients who are asymptomatic generally do not require treatment,
although they must undergo a cardiac evaluation, and be kept under
observation. Patients who experience syncope-like symptoms would benefit
from insertion of a pacemaker. If there is heart failure, cardiac
resynchronization therapy must be done, which would regularize rhythm on
both sides of the heart. A biventricular pacemaker should be considered for
patients with prolonged QRS (>150ms).
LEFT BUNDLE BRANCH BLOCK – HOW TO DIAGNOSE
MYOCARDIAL INFARCTION (SGARBOSSA CRITERIA)
The Sgarbossa criteria are standard ECG traits that are used to diagnose
myocardial infarction when there is LBBB.
These are the updated criteria that should be witnessed in one or more leads:

Concordant ST elevation measuring 1 mm or greater

Concordant ST depression measuring 1 mm or greater in leads V1 to
V3
STE elevation measuring 1 mm or greater
STE becoming more disorganized as based on 1/4 of the depth of the
th

preceding S-wave
Treatment
Treatment for myocardial infarction is given as per guidelines. This includes
initial therapy with aspirin, oxygen and nitroglycerin. Later management
includes fibrinolytic therapy and surgical procedures to remove the block
(CABG or angioplasty).
LEFT MAIN CORONARY ARTERY OCCLUSION (ST ELEVATION
IN AVR)
The following ECG readings are indicative of this condition:

ST elevation of 1mm or greater in aVR

ST elevation in aVR is equal to or greater than in V1
Widespread horizontal depression of the ST segments, most observed
in I, II, and V4 to V6

Although the most prominent feature of left main coronary occlusion is ST

elevation in aVR, this trait is also witnessed in other conditions: diffuse
subendocardial ischemia after cardiac arrest, severe triple-vessel disease, and
proximal left anterior descending artery occlusion
Treatment
This condition is considered as a STEMI equivalent, thus it is managed by
emergent reperfusion therapy. CABG is considered the gold standard of
therapy. However, percutaneous coronary interventions have also been
carried out with equal success. This can be combined with imaging methods,
such as intravascular ultrasound and optical coherence tomography, to
improve results.
LEFT POSTERIOR FASCICULAR BLOCK / LEFT POSTERIOR
HEMIBLOCK
In left posterior fascicular block, electrical impulses are carried to the left
ventricle through the left anterior fascicle. This is less common than LAFB,
because this is composed of a bundle of fibres. Remember that this condition
may occur with an RBBB if there is a bifascicular block.
This creates the following ECG traits:

Right axis deviation that is greater than +90 degrees

Small R waves with deep S waves in leads I and aVL
Small Q waves with tall R waves in leads II, III, and aVF
Normal to slightly prolonged QRS duration measuring 80-110 ms
Prolonged R wave peak time in aVF
Increased QRS voltages in the limb leads

Remember to rule out other causes of right axis deviation before you
diagnose LPFB.
Treatment
No treatment for this is given unless there are other underlying conditions,
which are given appropriate treatments. The patient must undergo cardiac
evaluation to find the extent of the condition. Physical exercise and dietary
modifications can aid in improvement. However, if the condition progresses
to a complete heart block, implantation of a pacemaker becomes essential.
LEFT VENTRICULAR ANEURYSM

An aneurysm in the left ventricle shows up as persistent elevation of the ST

segments. This usually occurs after an acute myocardial infarction. However,
it may also be caused by cardiac infections, cardiac myopathy, and congenital
abnormalities.

This is believed to be caused by the paradoxical movement of the ventricular

wall.
Key features of this are:

ST Elevation seen 2 weeks or more after an acute myocardial

infarction
May have convex or concave morphology
Q- or QS waves are well formed
T waves are small compared to the QRS complexes
These traits are more easily seen in the precordial leads.
This is distinguished from acute STEMI as follows:

In left ventricular aneurysm, the new ECG is identical to the previous ones,
the Q waves are well-formed, and there are no reciprocal ST depression and
dynamic ST segment changes. The T-wave to QRS ratio is less than 0.36 in
all precordial leads.
In acute STEMI, there are ECG changes compared to old ones, with the
degree of ST elevation worsening, there is reciprocal ST depression, and
there are STEMI symptoms such as chest pain, paleness, and hemodynamic
instability. The T-wave to QRS ratio is greater than 0.36 in any precordial
lead.
Treatment
Surgery is not necessary for majority of cases, but it is advised that the
patient limit physical activity levels to avoid complications. Sometimes
surgery may be performed for ventricular reduction. ACE inhibitors may also
reduce the risk of aneurysm formation and left ventricular remodelling. Anti-
coagulants are given to reduce the risk of thrombosis, while anti-arrhythmic
agents are used to maintain rhythm.
LEFT VENTRICULAR HYPERTROPHY

Figure 199. Left ventricular hypertrophy: increased QRS amplitudes and left axis deviation.

This is the enlargement of the left ventricle that may be caused by pressure
overload in the chamber.
This is most frequently caused by hypertension but also by aortic
regurgitation/stenosis, mitral regurgitation, hypertrophic cardiomyopathy,
and aortic coarctation.

ECG changes pointing to LVH are numerous:

Sokolov-Lyon criteria, which says that the S wave depth in V1 plus

the tallest R wave height in leads V5 to V6 is greater than 35 mm
R wave in lead I plus S wave in lead III is greater than 25 mm
R wave in aVL is greater than 11 mm while in aVF is greater than 20
mm
S wave in aVR is greater than 14 mm
R wave in V4, V5, or V6 is greater than 26 mm
R wave in V5 or V6 plus the S wave in V1 is greater than 35 mm
 The tallest R wave plus the tallest S wave in the precordial leads is
greater than 45 mm
Left axis deviation
Left atrial hypertrophy indicators
St elevation in the right precordial leads (V1 to V3) that are discordant
to deep S waves
Prominent U waves that are proportional to the increased QRS
amplitudes
Treatment
Left ventricular hypertrophy is treated depending on the cause. If the patient
is hypertensive, blood pressure reducers are used along with dietary
intervention. These include ACE inhibitors, beta blockers, calcium channel
blockers and diuretics. Sleep apnea, if present, must be treated with cPAP. If
aortic valve stenosis is the cause, surgery is undertaken to replace the aortic
valve.
LOWN GANONG LEVINE SYNDROME

Figure 20. Lown Ganong Levine Syndrome depicting short PR interval and no delta waves.

This is a theoretical pre-excitation syndrome that involves an accessory

pathway consisting of James Fibres. It is always associated with paroxysmal
tachycardia.
ECG indicators are PR intervals of less than 120 ms and a normal QRS
morphology.
Treatment
There is no particular treatment indicated for this syndrome. If there are
symptoms, treatments to manage those symptoms are given. For instance, if
the patient has tachycardia, pharmacological therapy for the same is
instituted, such as beta blockers, calcium channel blockers, and digoxin. If
medical therapy is ineffective, and patient has severe symptoms, pacemaker
implantation or radiofrequency ablation may be considered.
LOW QRS VOLTAGE
The voltage of the QRS segment is considered to be low when all amplitudes
in the precordial leads are less than 10 mm, and are less than 5 mm in the
limb leads.
These are generally caused by the loss of function in the myocardium, diffuse
infiltration in the heart, or layers of fat, fluid, or air between the heart and the
electrode.
The most significant cause is massive pericardial effusion, which causes
tachycardia and electrical alternans aside from QRS with low voltages.
Treatment
Since low QRS voltage may be caused by different factors, the origin is
determined and treated accordingly. Pericardial and pleural effusion are
treated surgically by drainage. Cardiac tamponade needs to be treated with
pericardiocentesis. COPD would require extensive medical therapy. If
needed, thyroid and pulmonary function testing must be done in addition to
cardiac workup.
 M
MOVEMENT ARTEFACT
This is caused by shivering or tremors. This is usually considered as a
hindrance to accurate diagnosis, but it can be helpful for detecting
hypothermia.
Certain conditions can cause this kind of artefact: anxiety, cerebellar disease,
Parkinson’s disease, benign essential tremor, thyrotoxicosis, drug toxicity,
and drug withdrawal. Cardiopulmonary resuscitation may also cause this
artefact.
Keep in mind that even simple talking and moving can cause the ECG to
register a movement artefact. Thus the patient should be instructed to keep
still and quiet during the procedure.
Treatment
This does not require treatment. The ECG may be repeated after some time to
ensure an artefact-free reading from which a proper diagnosis can be made.
MULTIFOCAL ATRIAL TACHYCARDIA
This is a tachycardia, Wandering Atrial Pacemaker. MAT and WAP are
frequently linked with severe lung disease. This condition needs prompt
treatment to prevent cardiovascular instability.
Heart rate is 100 BPM or higher. It has an irregularly irregular rhythm. The P
wave may present as at least 3 different kinds. The P:QRS ratio is 1:1. The
PR Interval is variable. QRS width is normal, and there are no grouping or
dropped beats.
Treatment
The primary goal should be identification and treatment of the underlying
cause. The ABCs should be stabilized and intravenous isotonic sodium
chloride should be administered immediately. Bronchodilators and oxygen
should be administered to treat COPD. Activated charcoal may be used if the
cause is theophylline toxicity and it is indicated. Valsalva manoeuvre or
carotid sinus massage may be done. Calcium channel blockers and beta
blockers may be used to help normalize arrhythmia. Radiofrequency ablation
and pacemaker implantation are considered in patients with recurrent MAT.
MYOCARDIAL ISCHEMIA
Myocardial ischemia is a dangerous condition that is caused by the
obstruction of the coronary artery.
It is considered as Non ST elevation myocardial infarction.
Major ECG signs include depression of the ST segments, and inversion (at
least 1mm deep and present in two or more leads with dominant R waves) or
flattening of T waves.

A unique ECG reading for myocardial ischemia is when the ST depression is

horizontal, or slopes downwards for 0.5 mm or more at the J-point in two or
more adjacent leads. Upsloping ST also indicates myocardial ischemia, but is
not specific to it.
Additional signs are peaked T waves or pseudo-normalization of inverted T
waves, and inversion of U waves.
The ECG signs will have some variations depending on the affected part:

Subendocardial: widespread ST depression usually in leads I, II, V4 to

V6
Left main coronary artery occlusion: widespread ST depression
Treatment
Myocardial ischemia is treated by medications that open the arteries, help
relax the heart muscle, and lower blood pressure such as aspirin, calcium
channel blockers, beta blockers, nitrates, ACE inhibitors, and ranolazine.
Anticoagulants may also be given to help remove blood clots. Surgery to
improve the blood flow may be performed, such as angioplasty, stenting, and
coronary artery bypass. Careful monitoring is essential to avoid infarction.
MYOCARDITIS

Myocarditis is inflammation of the myocardium, without the presence of

ischemia. This is usually benign but it can sometimes lead to dilated
cardiomyopathy, arrhythmias, cardiogenic shock, and cardiac failure.
This is caused by bacterial and viral infections, immune reactions, toxins, and
drugs.
ECG indicators for myocarditis are sinus tachycardia, ventricular
arrhythmias, AV conduction aberrations, QRS or QT prolongation, and
diffuse T wave inversion. This may also occur with pericarditis.
Treatment
Myocarditis is treated with medications that are commonly used for heart
failure. These include diuretics, nitroglycerin, and ACE inhibitors.
Anticoagulants may be given as a preventive measure. To reduce heart
inflammation, steroids and similar drugs are given. Ventricular assist devices,
intra-aortic balloon pump, and extracorporeal membrane oxygenation may be
performed in severe cases. For serious myocarditis complications, a
defibrillator or pacemaker may be used. It is important to withdraw the
causative agent (eg. Drugs).
 N
NON-PAROXYSMAL JUNCTIONAL TACHYCARDIA
(see accelerated junctional rhythm)
 P
PERICARDIAL EFFUSION/TAMPONADE

Pericardial effusion is a dangerous accumulation of fluid in the space

surrounding the heart. This can increase the pressure to the heart, and affect
heart function adversely.
This condition produces three effects: low voltage ECG readings,
tachycardia, and electrical alternans.
Treatment
Tamponade is an emergency case that requires pericardiocentesis. In milder
cases, pharmacotherapy may be used. Aspirin and steroids are useful for
autoimmune conditions. Colchicine and antibiotics are also used. Afterwards,
intravascular volume is expanded using blood, plasma, isotonic sodium
chloride, or dextran. Inotropic drugs may assist in increasing cardiac output.
The patient will also rest with legs elevated to help improve venous return.
PERICARDITIS
Pericarditis is the inflammation of the pericardium, or the membrane
surrounding the heart.

This causes chest pain, fast heart beats, and difficulty breathing.
ECG indicators

Widespread concave ST elevation and PR depression in most

precordial and limb leads
Reciprocal ST depression and PR elevation in the lead aVR
Sinus tachycardia
Pericardial effusion signs

It is possible to know the stage of pericarditis, based on the ECG readings:

Stage 1 – widespread ST and PR depression with reciprocal changes

in the lead aVR
Stage 2 – ST changes normalizes but there is generalized flattening of
T waves
Stage 3 - T waves become inverted
Stage 4 – ECG normalizes
Treatment
If pericarditis is accompanied with pericardial effusion, the patient’s heart is
surgically decompressed via pericardiocentesis. There are many types of
pericarditis and it is treated depending on the type:
Idiopathic/inflammatory: anti-inflammatory drugs help control heart
inflammation, while pericardectomy may be done for recurrent cases
Infectious: the infection is treated by antibiotics, anti-fungals, or
chemotherapy
Metabolic: those with renal failure are given haemodialysis, and those who
have hypothyroidism are given thyroid hormone therapy.
Cardiovascular: anticoagulants and thrombolytic medications may be given,
but these should be discontinued if pericardial effusion develops
PERSISTENT ST ELEVATION (LV ANEURYSM MORPHOLOGY)
(see Left Ventricular Aneurysm)
POLYMORPHIC VENTRICULAR TACHYCARDIA (PVT)

Figure 201. Polymorphic Ventricular Tachycardia (PVT), the rhythm strip shows the
defibrillator discharge followed by pacemaker rhythm.

This is a particular kind of ventricular tachycardia with several ventricular

foci. The most common cause of this is myocardial ischemia.
Torsades de Pointes is one form of PVT – for it to be considered as such, the
PVT and QT segments should both be prolonged. Bidirectional VT is also a
PVT type.
Treatment
Usually, this condition is self-limited. If it does not convert spontaneously,
defibrillation must be done. The condition causing PVT is treated to prevent
recurrence. Potassium and magnesium levels must be monitored and
corrected. Surgical intervention such as ventricular reduction may be done.
ACE inhibitors can also reduce the aneurysm. Lignocaine administration may
be beneficial.
POOR R WAVE PROGRESSION (PRWP)
This describes R waves that are 3mm or shorter in V3.
This feature is caused by conditions such as anteroseptal MI, left ventricular
enlargement, and dilated cardiomyopathy. This may also be the result of
misplacing V1 and V3. This may also be normal to a person.
Treatment
The condition causing the PRWP is identified and managed. These can
include left bundle branch block, left anterior fascicular block, Wolff-
Parkinson-White syndrome, and ventricular hypertrophy. The management of
these conditions follow the same principles as described in the respective
sections. If the person is asymptomatic, it may be normal and thus need not
be treated.
POSTERIOR STEMI

Figure 212. Acute posterior myocardial infarction is associated with tall R and upright T
waves in lead V1-3.

This is the ST-Elevated Myocardial Infarction of the posterior (back) areas of

the heart.
When a posterior STEMI is accompanied by lateral or inferior STEMI, the
patient is in danger of a fatal left ventricular dysfunction. Thus, if a patient
has an inferior or lateral STEMI, check for posterior STEMI as well.
To diagnose posterior STEMI, look for

Horizontal ST depression
T waves that are upright
Dominant R waves that measure greater than 30 ms and has an R to S
ratio of greater than 1 in V2
Treatment
Posterior STEMI treatment is handled like any myocardial infarction case.
Initial management is done with aspirin, oxygen, nitroglycerin, and
morphine. Fibrinolytic therapy must be instituted as soon as possible.
Coronary bypass grafting or percutaneous transluminal coronary angioplasty
is done to re-establish circulation.
PREEXCITATION
This means early activation of the ventricles, because the impulses skip the
AV node and head to the ventricles through an accessory pathway/bypass
tract. This is commonly seen in Wolff-Parkinson-White syndrome.
Treatment
Preexcitation syndrome has various manifestations. It is treated according to
the severity and particular type of condition that has manifested. Acute
tachyarrhythmias must be monitored, with oxygen supplementation and
cardioversion. Management ideally includes radiofrequency ablation of the
accessory pathway causing the pre-excitation. Anti-arrhythmic agents may be
used to lessen the severity of symptoms.
PREMATURE VENTRICULAR CONTRACTION (PVC)

PVC happens when a ventricular cell fires prematurely, or earlier than the SA
node or supraventricular pacer. This causes the ventricles to be in a refractory
state, that is, it’s not yet repolarized and not ready to fire). The ventricles do
not contract on the expected time. However, the beat after the PVC arrives on
schedule, creating a compensatory pause.
PVC has an irregular rhythm. There is no P wave or P:QRS ratio on the PVC.
There is no PR interval either. The QARS is wide (equal or greater to 0.12
seconds) and have a strange appearance. Groupings are usually absent, and
there are 0 dropped beats.
Treatment
No treatment is needed if the patient does not have symptoms. If there are,
PVC is treated according to the cause. Patients with mild symptoms can
control them by lifestyle changes such as limiting caffeine and tobacco. PVC
which has no other underlying condition is managed by medication such as
lidocaine, amiodarone, and procainamide. Patients with severe symptoms,
who do not respond to medical management, can undergo radiofrequency
ablation.
 Q
QRS WIDENING
(See Intraventricular Conduction Delay)
QUETIAPINE TOXICITY
Quetiapine is an anti-psychotic medication that can harm the heart in toxic
doses. It can cause toxic coma, anticholinergic crisis and delirium, sinus
tachycardia, and prolonged QTc.
Although the QTc is prolonged, this condition does not usually lead to
Torsades de Pointes.
Treatment
Activated charcoal therapy at 1mg/kg, is started immediately to help remove
the quetiapine. Wide bore IV access must be established, and intravenous
sodium chloride solution is given to prevent hypotension. In case of seizures,
benzodiapenes will help in controlling them. Ventricular dysrhythmias are
treated with advanced cardiac life support and medications. If hyperthermia
manifests, cooling measures must be undertaken. In order to reverse
dopamine blockade, bromocriptine or amantadine may be given.
 R
RIGHT ATRIAL ENLARGEMENT/ RIGHT ATRIAL HYPERTROPHY

Figure 223. Right atrial hypertrophy showing tall and pointed P waves (lead II).

This refers to enlargement of the right atrium. This is caused by chronic lung
disease (eg. Cor pulmonale), primary pulmonary hypertension, congenital
heart disease, and tricuspid stenosis.
Right atrial enlargement creates these ECG effects:

P waves greater than 2.5 mm in the inferior leads (II, III, aVF)
P waves greater than 1.5 mm in V1 and V2
Treatment
The condition causing the enlargement is treated. If the cause is pulmonary
hypertension, whether primary or due to lung disease, anti-hypertensive
medication is used. Surgery is indicated if the cause is a faulty tricuspid
valve. Valve replacement is indicated in these cases.
RIGHT AXIS DEVIATION

This is a deviation of the QRS axis that measures somewhere between +90
and +180 degrees.
This is implied by the following ECG signs:

QRS is positive, and has a dominant R wave in leads aVF and III
QRS is negative, and has a dominant S wave in leads aVL and I

Following are the common causes of a right axis deviation: lateral myocardial
infarction, ventricular ectopy, right ventricular hypertrophy, left posterior
fascicular block, WPW syndrome, acute or chronic lung disease, sodium
channel blocker toxicity, and hyperkalaemia.

This may also be normal for those with a horizontally-positioned heart.

Treatment
The cause of the right axis deviation must be identified and managed
accordingly. If the deviation was not noted on previous ECGs, it could
indicate exacerbated lung disease or pulmonary embolism. This requires a
ventilation-perfusion scan, and anticoagulant therapy if needed. However, if
the deviation is noted on serial ECGs, it could be a normal deviation, and
may be observed periodically.
RIGHT BUNDLE BRANCH BLOCK

Figure 234. Right Bundle Branch Block showing widened QRS as well as secondary R
waves (lead V1)

RBBB happens when the right ventricle’s activation is delayed because the
depolarization is forced to travel across the septum to reach the left ventricle.
RBBB is a side-effect of ailments such as congenital heart disease,
degenerative disease of the conduction system, ischemic/rheumatic heart
disease, right ventricular hypertrophy, cor pulmonale, pulmonary embolus,
cardiomyopathy, and myocarditis.

This abnormality causes the following ECG changes:

Broad QRS segments measuring more than 120 ms

RSR’ pattern in V1 to V3 with M-shaped QRS complexes; if not, the
R waves may be broad and monophasic in V1, forming qR complexes
Wide (slurred) S waves in the lateral leads (I, aVL, and V5 to V6)
T wave inversion and ST depression in the right precordial leads (V1
to V3)
INCOMPLETE RBB

RBBB is described as incomplete when there is a pattern of RSR’ in V1 to

V3, with the QRS measuring less than 120 ms.
If the patient is a child, this pattern is often normal. It must be noted that this
pattern may also be linked to Brugada syndrome, that is indicative of harmful
ventricular arrhythmias.
Treatment
RBBB cases may be asymptomatic; if so, this does not require treatment.
Follow up ECGs must be done every six months to assess for changes.
However, if there is a pathological condition causing the RBBB, treatment is
required to correct it. Medications that reduce high blood pressure and
minimize the complications of heart failure are given. If needed, coronary
angioplasty is done to open up a blocked artery causing the RBBB. A
pacemaker can be implanted as well.
RIGHT VENTRICULAR HYPERTROPHY

Figure 245. Right Ventricular Hypertrophy (irregularly irregular rhythm,

absent P waves, and right axis deviation).

This condition signifies enlargement of the right ventricle, that may be caused
by pulmonary embolism/hypertension, chronic lung disease, mitral stenosis,
congenital heart disease, or arrhythmogenic right ventricular cardiomyopathy.
RVH may lead to RBBB.
This is diagnosed by the following conditions:

Right axis deviation that is +100 degrees or greater

Dominant R waves in V1 measuring greater than 7 mm in height, or
with an R to S ratio of greater than 1
Dominant S waves in V5 or V6 measuring greater than 7 mm in
depth, or with an R to S ratio of less than 1
QRS duration of less than 120 ms

Other signs that support this diagnosis are:

Right atrial hypertrophy

Right ventricular strain pattern, with ST depression, and T wave
inversion in the inferior and right precordial leads
Deep S waves in the lateral leads
Far right axis deviation with dominant S waves in leads I to III
Treatment
The cause of the hypertrophy is managed. If pulmonary hypertension is
present, vasodilator drugs such as epoprostenol are used. If the cause is
systemic hypertension, ACE inhibitors, beta blockers and diuretics may be
used. Surgical intervention is recommended in cases with structural defects,
such as ventricular septal defects. Pacemakers are use in cases with rhythm
alterations..
RIGHT VENTRICULAR MI
This is myocardial infarction that occurs in the right ventricle.

In right ventricular MI, RV contractility is poor, causing a heightened

sensitivity to the preload. Because of this, preload-reducing agents can cause
severe hypotension among patients with right ventricular MI.
This condition is treated with fluid loading.
To diagnose right ventricular MI in the patient, the following are checked:

In general, the ST segments are elevated in the right leads (V3R to

V6R)
 ST elevation in V1 + ST depression in V2 is equal (this is a very
specific pattern for right ventricular MI)
ST elevation in V1
ST elevation in lead III is greater than in lead II, and it is greater in V1
than in V2
Treatment
During initial therapy, both nitroglycerin and morphine must be avoided as
they are vasodilators. Fentanyl is given instead. Inotropics and thrombolytic
therapy can help normalize right ventricular MI. Dopamine and dobutamine
are used as vasopressors, and IV normal saline is given to maintain cardiac
output. If there is a left ventricular dysfunction as well, an intra-aortic balloon
pump and/or an infusion of nitroprusside help with reducing the afterload. A
pacemaker may be installed when necessary.
RIGHT VENTRICULAR OUTFLOW TRACT (RVOT) TACHYCARDIA

This is a kind of monomorphic ventricular tachycardia, that arises from the

right ventricle’s outflow tract, and sometimes from the tricuspid annulus.
The characteristics of RVOT tachycardia are: heart rate of greater than 100
BPM, LBBB morphology, QRS duration of greater than 120 ms,
atrioventricular dissociation, and rightward or inferior axis measuring
approximately +90 degrees.
Treatment
Patients without cardiac problems may have this pattern, but it is also
witnessed among those with arrhythmogenic right ventricular dysplasia. The
clinical course of this disease is benign and usually requires no treatment. For
normal patients with mild symptoms,, this may respond to adenosine
medication. Anti-arrhythmic agents are used in patients with severe
symptoms; particularly those with arrhythmogenic RV dysplasia. Patients
who do not respond to drugs may require more intensive treatments, such as
radiofrequency ablation.
RIGHT VENTRICULAR STRAIN

This is an abnormal repolarization, because of enlargement or dilatation of

the right ventricle.
This may be caused by any of these conditions: pulmonary
hypertension/embolism, mitral stenosis, chronic lung disease, congenital
heart disease, or arrhythmogenic right ventricular cardiomyopathy.
ECG traits that are seen include ST depression and T wave inversion in the
right precordial leads and inferior leads, especially in lead III.
Treatment
The cause of the strain is managed according to the underlying condition,
treatments of which are described in the individual sections.
R-WAVE PEAK TIME
(See Intrinsicoid Deflection)
 S
SHIVERING ARTEFACT
(see movement artefact)
SHORT QT SYNDROME

This is an arrhythmogenic condition that presents with paroxysmal atrial and

ventricular fibrillation and syncope, which may trigger sudden cardiac death.
Treatment
Patients who have survived cardiac arrest, or who have ventricular
tachyarrhythmias with syncope, benefit from implantable cardioverter-
defibrillator placement. Some anti-arrhythmic agents such as quinidine and
hydroquinidine are also effective in dealing with this syndrome, as they
prolong the QT interval. Patients who present with atrial fibrillation may be
treated with propafenone.
SINUS ARRHYTHMIA

This rhythm is not that significant, and often creates no symptoms. However,
it can be detected as speeding up of the pulse while inhaling and slowing
down upon exhaling. This kind of rhythm may stop when the heart rate
increases during exercise.
Sinus arrhythmia is caused by several things such as drugs (morphine,
digoxin), increased ICP (Intra-cranial Pressure), inferior MI, and reflex vagal
activity inhibition. If it is observed during inhalation, it may be due to
increased heart rate and/or venous return, or decreased vagal tone. During
exhalations, it is possibly due to decreased heart rate and/or venous return, or
increased vagal tone.
Treatment
Since this is a normal characteristic of the heartbeat, it is normally not
treated. If the condition presents with other symptoms such as dizziness or
loss of consciousness, the treatment is directed towards the cause of the
symptoms.
SINUS BRADYCARDIA

Figure 256. Sinus bradycardia, the rate is about 45 bpm

Sinus Bradycardia is characterised by a rate slower than 60 BPM. This may

be caused by SA node or atrial pacemaker abnormalities, vagal stimulation,
or medicines. Some athletes also have a slower heartbeat because their heart
pumps blood efficiently.
The QRS complexes, PR, and QTc intervals may be normal or a bit
prolonged. They should not exceed the upper limit for the normal range,
however.

A person may have sinus bradycardia and experience no symptoms. In the

case of symptoms, the cause of the bradycardia is treated with drugs such as
epinephrine, dopamine, or atropine. A pacemaker may be inserted for severe
cases.
Treatment
If asymptomatic, sinus bradycardia does not require treatment. If
symptomatic, the underlying cause is treated, such as discontinuing drugs
(e.g. Digitalis), and correcting hypothermia. Atropine may be given to
improve perfusion. Long term prevention must be done by transcutaneous or
transvenous pacing. While the pacer is not yet ready, or if it is ineffective,
atropine or epinephrine/dopamine infusion is administered.
SINUS PAUSE / ARREST

The sinus pause is a time period when the sinus pacemaker is not working.
This may occur as a result of cardioactive drugs (digoxin, amiodarone, beta-
adrenergic blockers, calcium-channel blockers, quinidine, and procainamide),
acute infection, acute myocarditis, acute inferior-wall MI, cardiomyopathy,
CAD, hypertension, sinus node disease, and increased vagal tone.
It is important to monitor the pulse and heart sounds during this condition,
also to prepare against symptoms of decreased cardiac output such as low
blood pressure, dizziness, altered mental status, and fainting.
If the pause is caused by medication, it should be discontinued. Symptoms
are treated accordingly.
The rhythm is usually regular, except during the pauses. It is usually at 60-
100 BPM before a pause occurs. When there are many pauses which are
prolonged, the heart rate may slow down.
The pauses do not reflect the overall P-P intervals. There are dropped beats,
but there is no grouping. The P wave may be absent in areas of pause or
arrest, and QRS complexes may be missing as well. If present, it often comes
before a QRS complex.
Treatment
The cause of the sinus pause is managed. If the cause is due to increased
vagal tone, no treatment is required but the patient must be monitored. If it is
caused by drugs, these are discontinued.
Potassium levels must be monitored and corrected if needed. A pacemaker
may be inserted.
SINUS TACHYCARDIA

Figure 267. Sinus tachycardia, the rate is greater than 100 bpm

This is caused by conditions or medications that increase the output of the

heart. For example, exercise, haemorrhage, hypovolemia (low blood volume),
hypoxemia (low oxygen level in the blood), and acidosis.
The rhythm is regular. The P wave exists, and has a one to one ratio with the
QRS. PR interval and QRS width may be normal to slightly shortened. There
are no grouping or dropped beats.

The patient should be placed in a relaxed environment and be taught

relaxation techniques to prevent worsening of the condition. This rhythm is
also common after MI, and therefore an MI patient should have his/her heart
rhythm monitored.
Treatment
If asymptomatic, sinus tachycardia is not treated. Lifestyle modifications
such as avoiding caffeine and nicotine may be employed. Other triggers of
the tachycardia are identified and eliminated. If caused by cardiac ischemia,
beta-adrenergic blockers or calcium channel blockers are given.
SODIUM CHANNEL BLOCKER OVERDOSE/TRICYCLIC
OVERDOSE
Sodium channel blockers, such as tricyclic antidepressants, type Ia and type
Ic antiarrhythmics, local anaesthetics, propranolol, quinine, and
carbamazepine, are harmful if taken in large doses.

Their main effects are ventricular dysrhythmias and seizures.

Blocking the sodium channels in the myocardium and the central nervous
system results to the malfunction of the firing of cells, which will lead to
symptoms such as the following:

Low blood pressure

Broad complex dysrhythmias
Tachycardia
Anticholinergic syndrome
Sedation
Coma

The ECG effects are the following:

QRS prolongation (greater than 100 ms can lead to seizures while

greater than 160 ms can trigger ventricular arrhythmias)
Tall R waves in aVR
Qtc prolongation because of the inhibition of the potassium channels
Myocardial depression

Treatment
Caregivers need to ensure that the patient has a clear airway and can breathe
adequately. Oxygen should be delivered at a high flow rate so that the patient
is hyperventilated to maintain a ph level of 7.5-7.55. They should be ready to
resuscitate the patient when needed.
Activated charcoal may be given to absorb and flush out the toxic substance
from the body.
Seizures are treated with IV benzodiazepines, while hypotension is managed
with a crystal bolus or vasopressors.
In case of arrhythmias, sodium bicarbonate is given. When pH is greater than
7.55, lidocaine is given intravenously.

Amiodarone, beta-blockers, procainamide and flecainide are prohibited,

because they can worsen conduction problems and hypotension.
ST ELEVATION IN AVR (LMCA/3VD)
(See Left Main Coronary Artery Occlusion)
STEMI
STEMI, ANTERIOR
(See Anterior STEMI)
STEMI, HIGH LATERAL

High lateral STEMI is detected in the high lateral leads I and aVL. There is
reciprocal ST depression in the inferior leads III and aVF and V1 to V3.
T waves may be hyperacute in V5 to V6.
QS waves may have poor R wave progression in the anteroseptal leads V1 to
V4.
STEMI, INFERIOR

Figure 278. Acute inferior myocardial infarction characterized by ST elevation in inferior

leads and reciprocal ST depression in anterior leads.

Inferior ST elevated Myocardial Infarction occurs in around half of STEMI

cases. Some of them will also have a right ventricular infarction; they should
not be given nitrates, to avoid hypotension. There are a few cases who will
also have second or third degree AV block, causing them to have bradycardia
– these are high risk cases. If inferior STEMI is accompanied with posterior
infarction, there is a large area of myocardium involved, and this may be
harder to treat.

This condition is caused by the blockage of the coronary arteries – the right
coronary artery, the left circumflex artery, and/or left anterior descending
artery.
The clues for inferior STEMI are ST elevation and Q wave development in
the inferior leads (II, III, and aVF), and reciprocal ST depression in lead aVL.
To know which arteries are involved, these are considered:

The right coronary artery goes to the middle part of the heart’s bottom wall,
including the inferior septum – this creates an ST elevation in lead III that is
greater than in lead II. There will also be a reciprocal ST depression in lead I.
Indicators for right ventricular infarction are also likely to be present (ST
elevation in leads V1 and V4R).
The left circumflex artery goes to the side of the heart’s bottom wall and left
posterobasal portion – producing ST elevation in leads I, aVL, and/or V5 to
V6. The ST elevations in lead II is equal in lead III. There is no reciprocal ST
depression in lead I.
As mentioned, inferior STEMI may manifest with bradycardia and AV
blocks. This may be caused by AV node ischemia, because of impaired blood
flow within the AV nodal artery and/or the Bezold-Jarisch reflex, which is an
ischemia-related increase of vagal tone.
The blocks in inferior STEMI may begin as 1 degree AV block, linked to
st

Wenckebach and progress to second/third degree AV block or complete heart

block.
Sinus node abnormalities may show up as sinus pauses or arrests, sinus
bradycardia, or sinoatrial exit block.
It is fortunate though that AV blocks and bradyarrhythmias in inferior
STEMI are usually temporary, and can be managed with atropine.
STEMI, LATERAL

Lateral ST elevated myocardial infarction involves the lateral (side) walls of

the heart. This results from the blockage of the left anterior descending artery
and left circumflex artery.
Lateral STEMI is a significant diagnosis, and this alone is enough to indicate
emergent reperfusion.
If this exists with anterior, posterior, or inferior MI, it signifies that a large
area of the heart is in danger, and it may be more difficult to treat.
Indications of lateral STEMI are ST elevation in lateral leads I, aVL, and V5
to V6, as well as reciprocal ST depression in inferior leads III and aVF.
STEMI (OLD)
(see Left Ventricular Aneurysm)
STEMI, POSTERIOR

Figure 289. Acute posterior myocardial infarction associated with tall R waves
and upright T waves in leads V1-3.

This occurs in less than 1/5 of STEMI cases, usually along with inferior or
lateral infarction.
If there is an inferior and/or lateral infarction as well, posterior STEMI
signifies injury of a large area of the heart. This increases the risk of left
ventricular dysfunction and other fatal conditions. So, if there is a patient
with lateral or inferior STEMI, always check for posterior MI as well.
Isolated posterior infarction indicates the need for emergent coronary
reperfusion, but it is hard to diagnose, because ST elevation in this area is
hard to detect. To know whether there is posterior infarction, check the leads
V1 to V3 for the following traits:

Horizontal ST depression
Tall and wide R waves measuring greater than 30 ms and has R to S
ratios of greater than 1 in V2
 Upright T waves

STEMI, RIGHT VENTRICULAR

(see right ventricular MI)
Treatment
Treating all kinds of STEMI is similar to how myocardial infarction is
treated. Emergency management includes administration of aspirin,
nitroglycerin, and morphine, with supplemental oxygen. Fibrinolytic therapy
must be started, and the patient must be taken up for surgery to establish
reperfusion if required (CABG).
SUBARACHNOID HAEMORRHAGE
(see raised intracranial pressure)
 T
TAKO TSUBO CARDIOMYOPATHY
This is an ST elevated Myocardial Infarction, that resembles ischemic chest
pain, but it is not caused by blocked coronary arteries. This is common
among those who are experiencing emotional distress. It is called Tako Tsubo
because the left ventricle appears like a Japanese basket (tsubo) that is used to
catch octopi (tako).

This is common among emotionally distressed post-menopausal women. This

phenomenon is theorized to be caused by a surge of catecholamine, which
activates the nervous system and causes the blood vessels to spasm. Also, the
presence of LVOTO (left ventricular outflow tract obstruction) may increase
its likelihood.
Indicators:

There are new changes in the ECG readings, such as T wave inversion
or ST elevation
Troponin may rise
The left ventricle may move abnormally, specifically in the centre and
apex
There are no blockages in the coronary arteries

Although Tako Tsubo has similar ECG readings to STEMI, it is milder than
the latter, but it still needs treatment.
Treatment
There are no specific guidelines for tako tsubo cardiomyopathy. Since this
condition resembles STEMI on the first ECG, initial management would be
the same. Once differentiated, however, heart failure medication like ACE
inhibitors, beta blockers, and diuretics may help. Aspirin may also be given.
Stress management plays an important role in management of this condition.
TORSADES DE POINTES

Figure 30. Polymorphous ventricular tachycardia (Torsade de Pointes) showing wide QRS
complexes and changing R-R intervals.

Torsade de Pointes translates to twisting of points. It has an irregular rhythm

that is at 200-250 BPM. Its main feature is its wavy appearance wherein the
QRS complexes axis changes from positive to negative and back again
randomly. It can revert to a normal rhythm, or fall into ventricular fibrillation,
which can be fatal. There are no P waves, P:QRS ratios, PR Intervals, and
dropped beats. The QRS width is variable, and the grouping has a variable
sinusoidal pattern.
This is caused by several things: electrolyte imbalances, drug toxicity,
myocardial ischemia, SA node diseases, and AV blocks.
Treatment
Immediate management includes administration of magnesium, which must
be monitored carefully. Mexiletine may also be useful. Long term
management of torsades de Pointes is managed by addressing the underlying
cause. It may require cardiopulmonary resuscitation, defibrillation, and
overdrive pacing. If the patient is unstable, synchronized cardioversion may
be necessary.
TREMOR ARTEFACT
(see movement artefacts)
TRICYCLIC OVERDOSE (SODIUM-CHANNEL BLOCKER
TOXICITY)
(see sodium-channel blocker toxicity)
TRIFASCICULAR BLOCK

Figure 291. Trifascicular block (often a combination of RBBB, LAFB, and long PR interval).

This is the blockage of all three conducting fascicles of the heart:

Left anterior fascicle

Left posterior fascicle
Right bundle branch

Main causes are ischemic heart disease, aortic stenosis, anterior MI,
conducting system disease, congenital heart disease, digoxin toxicity, and
hyperkalaemia
This is classified into two:
Incomplete
This may lead to complete heart block but it’s not that likely as a complete
trifascicular block.

The most common of incomplete trifascicular block is a bifascicular block

and a 1 degree AV block.
st

A bifascicular block may occur with a 2 degree AV block as well.

nd

A right bundle branch block may have an alternating Left Anterior Fascicle
Block and Left Posterior Fascicular Block
Complete
This is a bifascicular block combined with a third degree AV block.
Treatment
The most recommended treatment for a trifascicular block is the insertion of a
pacemaker.
 V
VENTRICULAR ANEURYSM
(see left ventricular aneurysm)
VENTRICULAR ESCAPE BEAT

This is similar to the junctional escape beat, but it occurs in the ventricles.
This beat occurs when the ventricles do not receive adequate signal from the
atria; so they initiate a beat on their own to prevent arrest. The pause is non-
compensatory because the normal pacer did not fire. The pacer then resets
itself and creates a new timing, which may have a different rate than before.
The rhythm of a ventricular escape beat is irregular. There are no P waves,
thus no P:QRS ratios and PR intervals as well. The QRS width is wide (0.12
seconds or higher), and has a strange form. There are no groupings or no
dropped beats.
Treatment
Since ventricular escape beat acts to prevent a cardiac arrest, treatment is not
required. The cause of the escape beat must be identified, and that must be
treated. For instance, if the ventricular escape beat is caused by a third degree
AV block, it is treated with cilostazol, which will increase ventricular escape.
Other than that, an ouabain infusion reduces ventricular escape time and
increases ventricular escape rhythm.
VENTRICULAR ESCAPE RHYTHM / IDIOVENTRICULAR RHYTHM
This occurs when the primary pacemaker is a ventricular focus. Because it
originates from the ventricles, the QRS complexes are wide and strange
looking. This rhythm is regular and has a slow rate of 20-40 BPM. It can
occur by itself or as a result of AV dissociation or third degree heart block.
There are no P waves, P:QRS ratios, PR intervals, groupings, and dropped
beats.
Treatment
Treatment is usually aimed at addressing the cause of escape rhythm. This is
the last pacemaker, thus this is not treated with antiarrhythmics because
doing so may stop the heart altogether. Instead, atropine can be used to
increase the heart rate. A temporary or permanent pacemaker may be inserted
to correct the rhythm for prolonged periods of time.
VENTRICULAR FIBRILLATION (VFIB)

Figure 302. Ventricular fibrillation: a bizarre, irregular waveform

with no clearly discernable P waves or QRS complexes.

When many areas of the heart are firing in a disorganized manner, it results in
Ventricular Fibrillation. This has an indeterminate rate, and a chaotic rhythm.
There are no beats at all, thus no P waves, QRS complexes, and so on.
VFib causes recognizable symptoms such as loss of consciousness, and
absence of pulse. If the patient looks and acts normal, the leads may just have
fallen off.
Treatment
Since this is a life threatening emergency, ACLS protocol is followed.
Cardiopulmonary resuscitation, with defibrillation of 200 J are given for
ventricular fibrillation. Simultaneously, 1 mg of epinephrine is given every 3
to 5 minutes. One dose of amiodarone, or upto three doses of lidocaine are
also given.
In order to prevent VF in susceptible patients, implantable cardioverter
defibrillators may be used. Radiofrequency ablation may be used in selected
cases. Anticoagulant therapy is also given.
VENTRICULAR FLUTTER

This is an extreme form of ventricular tachycardia, and quickly progresses to

ventricular fibrillation. The beats come in at 200-300 BPM and there are no
discernable P waves, QRS complexes, T waves, and T segments. It forms a
regular sinusoidal pattern. There are no groupings and dropped beats.
A VFlutter at the rate of 300 BPM can indicate Wolff-Parkinson-White
Syndrome with an atrial flutter of 1:1 conduction.
Treatment
Ventricular flutter is an emergency. As per ACLS protocols, CPR must be
initiated immediately, and defibrillation must be done, using an external
electric shock of 200-400 joules. This treatment is to be continued even if the
patient progresses to ventricular fibrillation. Once the patient is stable, further
recurrences are avoided by drugs such as amiodarone, procainamide, and
lidocaine.
VENTRICULAR TACHYCARDIA (VTACH)

Figure 313. Ventricular tachycardia characterized by wide QRS complexes

and AV dissociation (independent P waves).
This is a very rapid ventricular rate that is often separate from an underlying
atrial rate. There are QRS irregularities at regular intervals, which represent
underlying sinus beats. The P wave shows a dissociated atrial rate. P: QRS
ratio is variable, and there is no PR interval. WRS width is wide and
abnormal. Rhythm is regular and clocks at a speed of 100-200 BPM. There
are no grouping or dropped beats. It is important to remember that wide QRS
tachycardia is VT until proven otherwise.
Variations:
FUSION BEATS
Sinus beats may sometimes allow the ventricle to become innervated through
the normal ventricular conduction system.
This leads to a fusion beat – a blend of an abnormal ventricular beat and a
normal QRS complex. This is created by two pacemakers working together,
the SA node and the ventricular pacer.
CAPTURE BEATS
A capture beat is completely innervated by the sinus beat, and cannot be
distinguished from a normal complex. It occurs during VTach, and by luck, it
beats at the right time to transmit through the AV node and depolarize the
ventricles.
Ventricular Tachycardia can be diagnosed when there are fusion and capture
beats. These are noticeable as a tachycardic rhythm with wide complexes,
(total QRS is greater or equal to 0.16 seconds), and negativity of precordial
leads (V1 to V6). Other indicators are as follows:
BRUGADA’S SIGN
This has an interval from the R wave to the bottom of the S wave, measuring
0.10 seconds or greater.
JOSEPHSON’S SIGN
This is a small notching near the bottom point of the S wave.
It is a common error to mistake VTach for a supraventricular tachycardia.
Consider it as VTach just to be safe.
Treatment
Ventricular tachycardia can manifest if there is no pulse; if so, ACLS
guidelines must be instituted immediately. This includes CPR and
defibrillation. If there is a pulse but the patient is unstable, synchronized
cardioversion is performed immediately. Electrolyte imbalances are corrected
if present. An ICD may be implanted for recurrent VT. Clinically stable
patients are usually treated with anti-arrhythmic drugs.
VENTRICULAR TACHYCARDIA: FASCICULAR VT
Idiopathic VT is a ventricular tachycardia condition that occurs without
structural abnormalities of the heart. Only around 10% of VT cases are
idiopathic (without pathological cause), and up to 90% of these starts from
the right ventricle.
Among idiopathic VT cases coming from the left ventricle, fascicular VT is
the most common.
This condition happens among those who are young and healthy. It can be
provoked by things that cause the heart to beat faster, such as stress,
emotional distress, exercise, and some medications, but it can also happen
while resting.
The possible cause of this is re-entrant tachycardia is an ectopic focus inside
the left ventricle.
ECG features:

Monomorphic ventricular tachycardia indicators such as capture beats,

fusion complexes, and AV dissociation
QRS duration of 100 – 140 ms (shorter than most VT forms)
Brief RS interval of 60 – 80 ms
RBBB pattern
Axis deviation

Fascicular VT is classified according to the location of the re-entry circuit

Posterior fascicular VT is the most common kind, occurring in up to 95% of
cases. It has a RBBB morphology and left axis deviation. It originates near
the left posterior fascicle.
Anterior fascicular VT: This accounts for up to 10% of cases. There is RBBB
morphology and a right axis deviation. This begins near the left anterior
fascicle.
Upper septal fascicular VT: This occurs in a minimal percentage of cases. It
can show either an RBBB or LBBB morphology with narrow QRS
complexes. The axis may also be normal. This occurs from the upper septum.

This can be misdiagnosed as SVT with a RBBB – to make a proper

diagnosis, additional features are considered, such as AV dissociation and
fusion or capture beats, which are particular in VT.
Treatment
Treatment of this condition depends on the severity of symptoms. For
patients with severe symptoms, radiofrequency catheter ablation is the
treatment of choice. In patients with mild to moderate symptoms, drug
therapy is initiated. Managing this typically involves verapamil. If it is
induced by digoxin, it is counteracted by Digoxin Immune Fab.
VENTRICULAR TACHYCARDIA: MONOMORPHIC VT
Monomorphic VT is caused by hypertrophic or dilated cardiomyopathy,
ischemic disease, and Chaga’s disease.

Indicators:

QRS complexes are very wide, measuring around 200 ms.

The axis may be indeterminate.
Fusion and capture beats may be present.
Josephson’s sign may be seen, with notching near the S wave’s nadir
(best observed in leads II, III, and aVF)
Brugada’s sign may also be seen with monomorphic VT – time from
the beginning of QRS until the S wave’s nadir is longer than 100 ms
(this is more obvious in V6).
Treatment
Treatment is based on whether the patient is hemodynamically stable or
unstable. Unstable patients would present with dyspnoea, hypotension, and
altered level of consciousness. Such patients are immediately treated with
synchronized direct current cardioversion, with a starting dose of 100 J. If the
patient is stable and asymptomatic, with normal left ventricular function, the
patient is given pharmacotherapy, which includes intravenous procainamide,
sotalol, or lidocaine.
If left ventricular function is impaired, amiodarone or lidocaine is preferred
over other medications. If it is caused by drug toxicity or electrolyte
imbalances, these are addressed.
 W
WELLENS SYNDROME

This is an ECG pattern that accurately diagnoses critical stenosis of the left
anterior descending artery. Those with this sign are at risk of experiencing
extensive anterior wall MI, even though there may be no symptoms present.
The criteria for Wellen’s Syndrome are:

Inverted or biphasic T waves in leads V2 to V3 or sometimes from V1

to V6
Minimally elevated ST segments measuring less than 1 mm
Q waves are absent in the precordial leads
R waves progress in the precordial leads

Treatment
Wellen’s syndrome must be monitored via serial ECGs because it does not
usually present symptoms, and it may lead to myocardial infarction. If ST
segment elevation is seen, treatment must be instituted immediately. This
includes supplemental oxygen, aspirin, and nitroglycerin. Laboratory studies
must be done to confirm or rule out MI. An angiography may also be done to
evaluate whether the patient may need coronary bypass surgery or
angioplasty.
WOLFF-PARKINSON-WHITE SYNDROME

Figure 324. Wolf-Parkinson-White syndrome showing short PR interval, broad QRS with a
slurred upstroke (delta wave), and secondary ST changes.

This syndrome is named after the people who discovered it: Louis Wolff,
John Parkinson, and Paul Dudley White. It is a congenital condition where
the heart has an accessory pathway that predisposes it to tachyarrhythmia.
The accessory pathway in WPW is the atrioventricular bypass tract (Bundle
of Kent).
WPW indicators:

PR interval is less than 120 ms

There is a delta wave or slow rise at the beginning of the QRS
segments
The QRS measures greater than 110 ms
The ST segment and T wave moves towards the opposite direction of
the QRS segments’ main components
There is paroxysmal tachycardia
Localizing the accessory pathway

LOCATION V1 V2 QRS AXIS

Left posteroseptal (type A) +ve +ve Left

 Right lateral (type B) -ve -ve Left

Left Lateral (type C) +ve +ve Inferior (90 degrees)

Right posteroseptal -ve -ve Left

Anteroseptal -ve -ve Normal

Treatment
There are several treatment modalities depending on the underlying cause.
The first-line treatment for symptomatic WPW is electrophysiologic study
with radio-frequency catheter ablation. This can be done in conjunction with
cryoablation. If the patient is at a high risk of ablation related complications,
drug therapy may be used to treat WPW. Agents acting on the AV node, such
as calcium channel blockers, beta blockers and digitalis may be used. Agents
that act on the accessory pathway, such as quinidine and amiodarone, may
also be used.
 EXERCISES

1. A sign of Ventricular Tachycardia that means an interval from the R

wave to the bottom of the S wave, measuring 0.10 seconds or
grater.
a. Josephson’s sign
b. Brugada’s sign
c. Capture beats
d. Fusion beats
2. A condition that has a wavy appearance on the ECG, and has an
irregular rhythm measuring 200-250 BPM.
a. Normal Sinus Rhythm
b. Bundle Branch Block
c. Torsades de Pointes
d. De Winter’s T Waves
3. This toxicity causes bradycardia and AV block.
a. Beta-blocker/calcium channel toxicity
b. Digoxin toxicity
c. Carbamazepine cardiotoxicity
d. Quetiapine toxicity
4. A deviation of the QRS axis, measuring somewhere between +90
and +180 degrees.
a. Right axis deviation
b. Left axis deviation
c. Extreme left axis deviation
d. Extreme right axis deviation
5. A condition where the duration of the QRS complexes is greater
than 100 ms and there is a supraventricular rhythm.
a. Interventricular Conduction Delay
b. Hyperkalemia
c. Electrical Alternans
d. Dextrocardia

6. The best way to treat a ventricular escape rhythm is to use anti-

 arrhythmic medications. (True/False)

7. A condition that involves a very rapid ventricular tachycardia is:

a. Ventricular escape beat
b. Ventricular flutter
c. Ventricular aneurysm
d. Ventricular hypertrophy
8. Which of the following is useful for detecting hypothermia
a. Movement artefact
b. Bradycardia
c. Tachycardia
d. Intraventricular conduction delay
9. The most obvious indicator of bilateral arm-leg reversal
a. Flat line in Lead I
b. Flat line in Lead III
c. Inverted Lead I
d. Upright aVR
10. Some ECG signs of this condition are the following: F waves in a
saw-tooth pattern, 2 F waves for every QRS complex, and
ventricular responses that have 3:1 or higher rates
a. Atrial flutter
b. AV block
c. Junctional Escape Beats
d. Bidirectional Ventricular Tachycardia
10.

References
1. Surawicz, B. and Knilans, T., 2008. Chou’s Electrocardiography in Clinical Practice E-
Book: Adult and Pediatric. Elsevier Health Sciences.
2. Khan, E., 2004. Clinical skills: the physiological basis and interpretation of the ECG.
British journal of nursing, 13(8), pp.440-446.
3. Dubin, D., 2000. Rapid interpretation of EKG’s: an interactive course. Cover Publishing
Company.
4. Garcia, T.B., 2013. 12-lead ECG: The art of interpretation. Jones & Bartlett Publishers.
5. Kusumoto, F.M., 2009.ECG interpretation: from pathophysiology to clinical application.
Springer Science & Business Media.
6. Kors, J.A., Macfarlane, P., Mirvis, D.M. and Pahlm, O., 2007. Recommendations for the
standardization and interpretation of the electrocardiogram: part I: the electrocardiogram
and its technology: a Scientific Statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed
by the International Society for Computerized Electrocardiology. Heart Rhythm, 4(3),
pp.394-412.
7. Hatala, R.A., Norman, G.R. and Brooks, L.R., 1997. The effect of clinical history on
physician’s ECG interpretation skills. In Advances in Medical Education (pp. 608-610).
Springer, Dordrecht.
8. www.ecglibrary.com. Dean Jenkins and Stephen Gerred.
 Answers To Exercises
Chapter 1
1. B
2. C
3. FALSE
4. D
5. 25
6. HALF-STANDARD
7. 50
8. C
9. C
10. FALSE

Chapter 2
1. C
2. B
3. C
4. A
5. B
6. C
7. B
8. C
9. A
10. D

Chapter 3
1. A
2. B
3. C
4. D
5. E
6. A
7. C
8. C
9. D
10. B

Chapter 4
1. FALSE
2. C
3. FALSE
4. FALSE
5. D
6. V3, V4
7. I, AVL, V5, V6
8. V1, V2
9. V1, V2, AVF
10. C

Chapter 5
1. B
2. C
3. A
4. A
5. A
6. FALSE
7. B
8. A
9. A
10. A
 Conclusion
Thank you again for buying this book!
I hope this book was able to help you to interpret the 12-Lead
EKG/ECG. The next step is to study this book and other materials
thoroughly.
You need to know as much as you can, so that you can provide the best
care possible.
If you liked our book and you want to help us reach more people, please
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Thank you and good luck with your medical career!

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You can find all of our products at this link:
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If you have any questions or concerns please contact us:

[email protected]

We want to be as close as possible to our customers,

that’s why we are active on all the main Social Media platforms.
You can find us here:
Facebook www.facebook.com/medicalcreations
Instagram www.instagram.com/medicalcreationsofficial
Pinterest www.pinterest.com/medicalcreations