The EMpret EKG book

Andreas Engelbrecht and Vidya Lalloo

2019
Contents
Disclaimer................................................................................................................................................ 2
Introduction ............................................................................................................................................ 3
Approach to the EKG ............................................................................................................................... 4
Standardisation of the EKG ................................................................................................................. 5
Rate ..................................................................................................................................................... 7
Rhythm ................................................................................................................................................ 7
Axis ...................................................................................................................................................... 9
R Wave progression .......................................................................................................................... 11
The P-wave ........................................................................................................................................ 12
The PR segment and interval ............................................................................................................ 14
The QRS complex .............................................................................................................................. 15
The ST segment and J-point .............................................................................................................. 17
The T-wave ........................................................................................................................................ 23
The QT-interval ................................................................................................................................. 25
The U-wave ....................................................................................................................................... 26
EKG interpretation ............................................................................................................................ 27
Conclusion ............................................................................................................................................. 27

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Disclaimer

The authors disclaim responsibility for any adverse effects resulting directly or indirectly from
information presented in this manual, undetected errors or misunderstandings by the
readers.

2
Introduction

This book is written by emergency physicians, Professor Andreas Engelbrecht and Dr Vidya Lalloo. It is
intended to accompany the EMpret EKG course and is targeted towards clinicians working in an
emergency unit (EU).

The EKG has become an invaluable bedside investigation in nearly every patient in the EU. EKGs are
critically important in our daily practice because it saves lives! Acquiring a fancy ECMO machine or
ultrasound requires years of tactful motivation. An EKG machine, however, is available and cheap!

But how often have you done an EKG and looked at it wondering what you are missing? Knowing how
to interpret an EKG will help you achieve legend status in your EU! Once the word gets out that you
have a reasonable clue about EKGs, you will be the go-to person in your EU. The more you do it, the
more you learn to love the challenge and that allows you to make some incredible diagnoses.

A very hands-on, practical advantage of EKG knowledge in the emergency setting is that it is an
additional tool in triage. It assists in the decision of where to place patients in the EU. The ominous
diagnosis of a STEMI is a clear indication for moving a patient into a resuscitation bed. However more
subtle conditions like gastroenteritis may well be left in the ambulant area of the emergency unit
unless an EKG was obtained, and a long QT was picked up. The hypokalaemia / hypomagnesemia with
resulting prolonged QT is an unstable rhythm which could deteriorate into a torsade de pointes at any
moment. This is a subtle find which will allow you to rather triage that patient into a resuscitation bed
and save a life.

We trust that this book will be of value to you in your preparation for the EMpret EKG course. EKG is
not learnt in a day. As with all good things in life, practice makes perfect!

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Approach to the EKG

The first principle in EKG interpretation is that the EKG must never be interpreted without pertinent
clinical information. This includes the age and gender of the patient, the history and physical findings
including the vital signs. This information will direct the clinician to the most appropriate EKG
diagnosis. Once it is obtained, a systematic approach should always be used to interpret the EKG.

The EKG is loaded with information. Without the above-mentioned systematic approach, it is easy to
be distracted by the most obvious abnormality. This may lead to the error of premature closure. This
is an error which occurs when a diagnosis is made prior to obtaining all the relevant information.

There are many systems advocated in the literature and by various experts. The EMpret team have
reviewed many of these methods and based on our research, designed a system that we now teach.
This system is illustrated in figure 1.

Scan – Standard. Hyperacute STE / life threating arrhythmia

Rate

Rhythm

Axis and R-wave progression

Waves, segments and intervals

EKG interpretation (compare) and sign off

Figure 1: The EMpret system of EKG interpretation

Using the system above, you may notice that the first step is to scan the EKG for standardisation and
obvious life-threatening conditions. This may be likened to the primary survey (ABC) that all
emergency clinicians are accustomed to. If a life-threatening condition is identified on the EKG, the
patient should be moved to the resuscitation area where emergency treatment can be initiated. A
common scenario may be that of a patient with a STEMI or a life-threatening dysrhythmia such as a
ventricular tachycardia. Remember to go back to the EKG and complete the system once the patient
is stable.

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If no life-threatening conditions are identified, we move on to complete our system. Assess the rate,
rhythm, axis and R-wave progression. Then move to the waves, segments and intervals. Finally, put
the clinical picture of the patient together with the information that you have gathered from the EKG
to make a final EKG diagnosis. Remember to compare your diagnosis with the EKG analyser to ensure
that you have not missed anything that the computer algorithm may have picked up. The analyser is
often incorrect. Thus, a pitfall is starting with this step, leading to anchoring on the wrong diagnosis.
The last step is to sign and date your EKG.

Let’s take a closer look at this system and how it can help you to gather the information that you need.

Standardisation of the EKG

Patient details: Ensure that the EKG in front of you is that of the correct patient. In busy EUs, it may
happen that another patient’s EKG inadvertently finds its way into your patient’s file. This may have
serious medicolegal implications if either a diagnosis is missed, or incorrect therapy is administered.

Paper speed: Our brains are equipped with powerful pattern recognition software. This software is
based on a paper speed set at 25 mm/sec. If this speed has been altered (faster or slower), our pattern
recognition becomes flawed. On rare occasions, increasing the paper speed to 50 mm/sec may be
necessary. An example of this is to identify the presence or absence of P-waves in tachyarrhythmias
such as suspected fast atrial fibrillation. If you choose to alter the paper speed, it is very important to
return the settings back to 25 mm/sec. This prevents the next user from misinterpreting the EKG.

Voltage: The standard voltage must be set at 10 mm/ 1 mV electrical stimulus. This means that that
the standardisation block on the ECG must be 10 mm (2 big blocks) in height. See figure 2.

Figure 2: Standardisation block showing a voltage of 10 mm/mV

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Filters: The EKG machine has several filters that that can be set to optimise the recording. See figure
3.

Figure 3: Filter settings on the EKG

The baseline drift suppression filter prevents the baseline from drifting by locking it into one position
at the start of the recording. The most common cause of a drifting baseline is body movement or chest
movement caused by breathing. It can either be set on strong (D), weak (d) or None (off).

The AC filter is set to match your AC powerline frequency. In South Africa this is 50 Hz.

The high-cut filter. All electrical impulses above this frequency setting will be cut out of the EKG
tracing. The electronic frequency of the EKG ranges between 0,05 and 150Hz. The ideal setting for
diagnostics includes the full range up to 150 Hz. However, setting the high-cut filter at 150 Hz will
allow interference from various other electrical sources including electro-encephalographs (EEG)
impulses and electromyography (EMG) impulses. For this reason, the high-cut filter is generally set at
100 Hz. The high-cut filter setting for EKG monitoring is set at 40 Hz. This high-cut setting is not
sensitive enough for diagnostics.

The EMG suppression filter filters out interference to the EKG from muscle movement. The filter is
only necessary if there is interference on the EKG from muscle activity. See figure 4. This includes
shivering, tensing of the muscles or the bed being too narrow or short to support the limbs
comfortably.

Figure 4: EMG interference on an EKG

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Rate

Calculating the heart rate on an EKG gives the first clue to the type of pathology that we are dealing
with. The normal heart rate ranges between 60 and 100 beats per minute. The patient has a
bradycardia when the heart rate is below 60 beats per minute. Bradycardia may be physiological in
young, healthy, fit patients. It may also be a clue to more ominous diagnosis such as conduction blocks
and escape rhythms. A tachycardia is defined as a heart rate above 100 beats per minute. It is often
the body’s response to stress. It may be from pain, anxiety, hypovolemia, sepsis, pulmonary embolism
etc.

The rate in sinus tachycardia seldom goes above 220 minus the age of the patient. This is a useful
pearl to help distinguish sinus tachycardia from supraventricular tachycardia.

Calculating the heart rate

1. 6 X method. Count the number of QRS complexes in a 10 second rhythm strip and multiply it
by 6. This method is preferred for patients with irregular rhythms. Premature ventricular
complexes must also be counted.
2. 10 X method. Use a 6 second rhythm strip by counting out thirty large boxes (30 X 0.2
seconds = 6 seconds). Count the number of QRS complexes in that 6 second strip and
multiply by 10.
3. 300 method. Count the big squares between two QRS complexes and divide into 300.
4. 1500 method = count the small squares between two QRS complexes and divide into 1500.
5. Sequence method: Only used in regular rhythms. Identify 2 consecutive QRS complexes.
Each block will correlate with a heart rate from a memorized a sequence of numbers. 300;
150; 100; 75; 60; 50. See table 1.

Blocks between Heart rate

QRS complexes
1 300
2 150
3 100
4 75
5 60
6 50
Table 1: The sequence method for calculating heart rate

Rhythm

A normal sinus rhythm originates in the sino-atrial (SA) node in the right atrium. A sinus rhythm
implies that there is one P wave married to each QRS complex. The heart rhythm is seldom perfectly
regular, even when the impulse is initiated in the sinus node. Sinus rhythm typically fluctuates with
the respiratory cycle. This is called a sinus arrhythmia.

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When assessing the rhythm, consider the following:

• Sinus vs. non-sinus

• P before every QRS
• Regular vs. irregular

- Is the space between each QRS the same?

The rhythm is best analysed by looking at a rhythm strip. On a 12 lead EKG this is usually a 10 second
recording from Lead II. Confirm or corroborate any findings in this lead by checking the other leads.

Irregular rhythms:

A regularly irregular rhythm has a pattern that repeats itself. For example, a patient may have a
second-degree heart block where every third beat is dropped creating a regularly irregular rhythm.

An irregularly irregular rhythm has no pattern at all. All the intervals are haphazard and do not
repeat themselves. There are 3 common narrow complex irregularly irregular rhythms. These should
be memorized. They are:

• Atrial fibrillation (AF)

• Atrial flutter with a variable AV conduction block
• Multifocal atrial rhythm / tachycardia (MAT)

Irregular rhythms are summarised in table 2 below.

EMpret classification of irregular rhythms

Regularly irregular Irregularly irregular
Narrow Sinus arrhythmia AF
(QRS complex < 100 ms) PAC (premature atrial complexes) Atrial flutter with variable block
PJC (premature junctional MAT
complexes) Wandering atrial pacemaker
Supraventricular escape beats
High 2nd Degree blocks
Narrow and wide PVC, Bigeminy, Trigeminy, Multifocal PVC
Quadrigeminy

Wide Low 2nd degree Mobitz II blocks Ventricular Fibrillation

(QRS complex > 100 ms) Polymorphic ventricular
tachycardia
Torsades de pointes
AF with WPW (Wolff-
Parkinson-White syndrome) or
aberrant conduction
Table 2: Irregularly irregular rhythms

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Axis

The axis is the dominant vector (orange arrow in figure 5) of electricity in the heart that flows from
the SA node in the right atrium (RA), downward and to the left, towards the apex of the left ventricle
(LV). A change in the cardiac axis can be a valuable clue to certain pathological conditions. The axis
may be deviated to the left or the right. The limb leads (I, II, III, aVL, aVR and aVF) on the 12-lead EKG
are used to estimate the axis.

Figure 5: The cardiac axis

In order to estimate the axis, one must understand some simple electrophysiological principles. When
electricity flows towards a lead, an upward / positive deflection is recorded on the EKG (the deflection
is above the baseline). When electricity flows away from a lead, a downward / negative deflection is
recorded (the deflection is below the baseline). In figure 5, the dominant vector is flowing in the
general direction of lead II (between 0 and 90°- normal axis). It is also flowing away from lead aVR. For
that reason, we expect to see positive deflections of the waves in lead II and negative deflections of
the waves in lead aVR. When this vector is between + 90° and + 180°, it is considered a right axis
deviation (RAD). When this vector is between 0° and – 30°, it is still considered normal. Between - 30°
and - 90°, the cardiac axis is deviated to the left, i.e. left axis deviation (LAD). An extreme axis deviation,
aka northwest axis is when the main cardiac vector is between - 90° and - 180°.

Simple methods of estimating the axis:

1. Lead I, II, III method

Look at leads I, II and III.

Which QRS complex is the most positive (tallest)?

Lead I Lead II Lead III

Left axis Normal axis Right axis
Table 3: the simple I, II, III method for estimating the cardiac axis

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 2. Rule of thumb

Look at leads I and aVF. Lead I correlates with your left thumb, while lead aVF correlates with
your right thumb. Thumbs up = upward QRS deflection; thumbs down = downward QRS
deflection. See table 4 below.

Axis Lead I Lead aVL

Normal

Left axis
deviation

Right axis
deviation

Extreme axis
deviation
Table 4: Rule of thumb method for estimating the cardiac axis

Causes of a LAD

• Obesity / left elevated diaphragm (normal variant)

• Left bundle branch block (LBBB)
• Inferior myocardial infarction
• Ventricular pre-excitation (WPW)
• Hyperkalemia
• Cardiac pacing
• Left ventricular hypertrophy (LVH) -common association
• Left anterior fascicular block (LAFB)
• Congenital:
o tricuspid atresia
o ostium primum atrial septal defect

Causes of a RAD

• Normal variation (tall thin patient)

• Chronic Obstructive Pulmonary Disease (COPD)
• Right ventricular hypertrophy (RVH)
• Right bundle branch block (RBBB)
• Left posterior fascicular block (LPFB)
• Wolf-Parkinson-White Syndrome (WPW Syndrome)

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Causes of an extreme AD

• Misplaced leads (limb leads swapped around)

• Ventricular rhythms
o Ventricular tachycardia (VT)
o Accelerated idioventricular rhythms
o Ventricular escape rhythms
• Dextrocardia
• Ventricular paced rhythms
• Hyperkalemia
• Severe RVH

R Wave progression

In a horizontal plane V1 looks at the right side of the heart and V6 at the left side. In lead V1, a small
R-wave (upward deflection) and big S-wave (downward deflection) are usually recorded. The small R-
wave represents septal depolarisation. This is followed by depolarisation of the ventricles which is
dominated by left ventricular depolarisation and manifests as the large S-wave.

V6 looks at the heart from the opposite direction to V1. Thus, V6 records a small Q-wave (downward
deflection; septal depolarisation) followed by a large R-wave (upward deflection; left ventricular
depolarisation). When one follows the progress of the height of the R-waves from V1 to V6, you will
notice that the R-wave gets progressively larger while the S-wave becomes progressively smaller.
Good R-wave progression is present when the height of the R-wave in lead V3 is greater than 3 mm.
We call the lead in which the R-wave and S-wave are approximately the same size, the transitional
zone. The normal transitional zone is between V3 and V4.

Transition at V1 and V2 implies early transition, rightward transition or counter-clockwise rotation. (as
if the heart has turned to the right).

Transition at V5 and V6 implies late transition, leftward transition or clockwise rotation. (As if the heart
is turned or rotated to the left.)

Poor R-wave progression is an indication of damage to the left ventricle. This may be acute or long-
standing. It is commonly present in patients with an acute or previous large anterior myocardial
infarction. It is also seen in patents with LV failure, LV aneurysms and cardiomyopathies of various
origins.

False positives are seen when the precordial leads electrodes are placed too high on the chest wall. A
common scenario is when V1 and V2 are placed in the second intercostal space (instead of the 4th
intercostal space) and the rest of the precordial leads are also placed too high.

Causes of late transition

• Anterior myocardial infarction

• Dilated cardiomyopathy
• Chronic COPD with cor-pulmonale causing rotation of the RV

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Causes of early transition

• RVH
• PE (acute dilation)
• Left-to-right shunt
• RBBB
• HCM (hypertrophic cardiomyopathy)
• WPW
• Dextrocardia
• Posterior MI

The P-wave

The P-wave represents atrial depolarisation. Depolarisation originates in the SA node in the RA. Thus,
the right atrium depolarises before the left atrium. This records on the EKG as a combined wave (the
P-wave). The first third of the P-wave represents the initial right atrial depolarisation. The middle third
of the P-wave represents the end of RA depolarisation and the beginning of LA depolarisation. The
final third of the P-wave represents the end of LA depolarisation. These 3 phases of atrial
depolarisation merge to form a symmetrical round P-wave. It may be normal to find a notch in the
middle third of the P-wave. The duration of a typical P-wave is < 0.12 seconds (3 small blocks). In the
limb leads, the height of the P-waves are less than 2.5 mm, while they are less than 1.5 mm in the
precordial leads.

Figure 6: The typical rounded symmetrical P-wave; as seen in lead II

When searching for P-waves, leads II and V1 are usually scrutinised first. Since lead II looks most
directly at the vector of atrial depolarisation, P-waves are most prominent here. Lead V1 however,
looks at the atrium from the right side. It records a biphasic P-wave (first up, then down). The initial
deflection is upward and represents right atrial depolarisation. The subsequent deflection is
downward, representing left atrial depolarisation moving away from lead V1. This is useful since it
allows us to differentiate right and left atrial pathology.

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 Figure 7: A biphasic P-wave as seen in lead V1

P wave pathology

1. P–pulmonale = right atrial enlargement

A tall, peaked P-wave is called a P–pulmonale. These P-waves are > 2.5 mm in height (limb
leads) but have a normal duration (< 120m). In lead V1 there is increased height of the initial
positive deflection (>1.5mm). This is a summation of the prolonged RA depolarisation with
normal LA depolarisation. P-pulmonale is often seen in respiratory conditions as a result of
increased pressure in the right side of the heart, e.g. COPD and asthma. Other causes include
pulmonary embolism, idiopathic pulmonary hypertension, dilated cardiomyopathies,
hyperthyroidism and sympathetic overdrive.

Figure 8: P-pulmonale as seen in lead II (A) and lead V1 (B)

2. P-mitrale = left atrial enlargement

When an atrium is enlarged, it takes longer to depolarise. The LA depolarises after the RA and
therefore creates a P-wave with a notch and a longer duration (>120 ms). In lead V1, the
terminal negative portion of the P-wave is wider (> 40 ms) and deeper (> 1 mm). P-mitrale is
classically seen in mitral valve stenosis. It is also seen in other conditions that cause LA
enlargement such as dilated cardiomyopathies, mitral valve incompetence, etc.

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 Figure 9: P-mitrale as seen in lead II (A) and lead V1 (B)

3. Inverted P-waves
Normal P-waves originating in the SA node are upright, except in lead aVR (inverted) and V1
(biphasic). Inverted P-waves suggest a source other than the SA node (i.e. an ectopic source).
The ectopic focus can be identified by analysing the PR interval. When the PR interval is < 120
ms, the origin is in the AV node / junction. This is known as a junctional rhythm. The inverted
P-wave is due to retrograde conduction from the AV junction to the atria. When the PR
interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm).

4. P-waves of different sizes

When there is chronic irritation of the right atrium (e.g. hypoxia or increased pressure from
COPD), the SA node malfunctions.
• When this manifests as multiple small re-entry circuits, many fibrillatory waves
develop in the atria (400 – 800 per minute). This records on the EKG as atrial
fibrillation.
• If multiple foci develop from the irritable atria. The result is that atrial depolarisation
originates from multiple different foci. This records on the EKG as a multifocal atrial
rhythm (MAR). These P-waves have different shapes, sizes and morphologies. If the
heart rate is > 100 beats per minute, it is known as multifocal atrial tachycardia (MAT).

The rule of 3’s for MAR / MAT

• 3 different p-wave morphologies

• 3 different PR-intervals
• 3 different RR intervals

Table 5: The rule of 3’s

The PR segment and interval

The PR interval is from the beginning of the P-wave till the beginning of the QRS-complex. It represents
the time that it takes for the electrical impulse to travel from the SA node to the ventricles. This
includes the delay in the AV-node.

The normal PR interval is 0.12 – 0.2 seconds (3-5 small blocks).

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Causes for a short PR interval (<0.12s)

• Accessory pathway (WPW and LGL)

• Atrial or junctional ectopics
• Drugs e.g. steroids and phenytoin

Causes for a long PR interval (>0.2s)

• First and second-degree heart blocks

• Atrial enlargement (P-mitrale)
• AV nodal blocking drugs
o A- Amiodarone and adenosine
o B- Beta blockers
o C- Calcium channel blockers
o D- Digoxin
• Hypercalcaemia
• Sick sinus syndrome

The PR segment is the segment on the EKG between the end of the P-wave and the beginning of the
QRS complex. It may be elevated or depressed. This elevation or depression should be assessed in
comparison to the baseline formed by the T-P segment.

• PR segment depression is most often seen in pericarditis. It may also be present in patients
with atrial ischemia.
• PR segment elevation is seen in atrial infarction. It is a poor prognostic sign in acute myocardial
infarction as it indicates extensive myocardial damage

The QRS complex

The QRS-complex represents ventricular depolarization.

Nomenclature. The first negative deflection after the P-wave is called the Q-wave. If it is written with
a small letter q, it implies that it is < 5mm deep. A capital Q implies that it is > 5mm deep. The first
positive deflection is called the R-wave. The first negative deflection after the R-wave is called the S-
wave. If there is a second positive deflection after the S-wave, it is known as the R’-wave.

Normal Q-waves are found in the lateral leads (I, aVL, V5 and V6). Q waves should not be seen in the
right-sided leads (V1-3). Pathological Q-waves are a sign of a recent / previous MI, hypertrophic
cardiomyopathy, rotation of the heart or misplaced leads. They are as follows:

o > 40 ms (1 small block) wide

o > 2 mm deep
o > 25% of the depth of QRS complex
o Seen in leads V1-3

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The normal duration of a QRS complex is ≤ 0.10 seconds (2½ small blocks). A QRS complex is
considered wide when it is ≥ 0.12 seconds (3 small blocks). When analysing the QRS complex, one
should consider both the voltage (height) and the duration (width).

Causes of a wide QRS complex

• Abnormal impulse conduction:

o Left and right bundle branch blocks
o WPW syndrome
o LVH with strain pattern
o An atrial septal defect (ASD) causes a notch in the R wave. This is known as a
crochetage pattern
• Ventricular site of origin
o Paced rhythm
o Ventricular ectopics
• Disruption of the cardiac action potential
o Acidosis
o Hyperkalaemia
o Sodium channel blockers

Causes of increased QRS amplitude

Physiological causes of increased QRS amplitude:

• Younger age
• Male
• Thin chest wall
• Axis directly towards lead II (60°)

Pathological causes of increased QRS amplitude:

• Left ventricular hypertrophy. See diagnostic criteria in table 6 below.

Voltage criteria for LVH

Precordial Leads Limb Leads
S-wave in V1 or V2 + R-wave in R-wave in lead aVL > 11 mm
V5 or V6 (small blocks)
≥ 35 mm S-wave in lead aVR > 14 mm
(Sokolov-Lyon criteria)
Biggest R-wave + biggest S-wave R-wave in lead aVF > 20 mm
≥ 45 mm

R-wave in lead V5 or V6 ≥ 26 mm
Non-voltage criteria for LVH
• Broad QRS complex
• LV strain pattern (ST-depression and T-wave inversions in the
lateral precordial leads – I, aVL, V4-V6)

Table 6: LVH criteria

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 Figure 10: Left ventricular hypertrophy with a strain pattern

• Biventricular hypertrophy. Associated with large biphasic QRS complexes in V2-V5. This
finding is known as the Katz-Wachtel phenomenon.

Causes of decreased QRS amplitude

Physiological causes of a decreased QRS amplitude

• Thick chest wall (obese patients)

Pathological causes of a decreased QRS amplitude

• Hyperinflation of the lungs (COPD, asthma)

• Pericardial effusion
• Left-sided pleural effusion

The ST segment and J-point

The ST-segment is the segment between the QRS complex and the T-wave. The starting point of the
ST-segment, at the end of the QRS complex, is called the J-point. This is an important landmark to note
as the amount of ST-segment deviation (elevation or depression) is calculated at the J-point.

The ST-segment is most famous for its role in the life-threatening ST-elevation myocardial infarction
(STEMI). There are, however, many other causes for ST-elevation, as well as many EKG features of

17
myocardial infarction that does not fit in with the official definition of STEMI. Hence the ST-segment
is a topic of great nuance.

Causes of ST-segment elevation

1. STEMI: The American Heart Association (AHA) has devised strict criteria defining a STEMI. This
is as follows: ST-segment elevation at the J-point in 2 or more contiguous leads (see figure 11),
with the following specific criteria:
a. In men < 40 years of age: ST-elevation must be ≥ 2.5 mm in V2-V3 and 1 mm in all
other leads
b. Men > 40 years of age: ST-elevation must be ≥ 2 mm in V2-V3 and 1 mm in all other
leads
c. Women of any age: ST-elevation must be ≥ 1.5 mm in V2-V3 and 1 mm in all other
leads

Figure 11: Contiguous leads on a 12-lead EKG

The morphology of the ST-segment in a STEMI has no boundaries. It may be saddle-shaped,

flat, tomb-stone shaped or have the appearance of a checkmark. STEMIs have other features
including poor R-wave progression, late transition, the development of Q-waves and
reciprocal changes. STEMIs also evolve with time. See figure 12.

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 Figure 12: The evolution of a STEMI

Figure 13: An inferior STEMI

2. Pericarditis: This condition causes global upwardly concave (saddle-shaped) ST-elevations.

Any other morphology of ST-segment should alert one to the possibility of a STEMI.
Pericarditis (especially if viral) may also have widespread PR-depressions. These ST-elevations
and PR-depressions occur with reciprocal ST-depression and PR-elevation in leads aVR and V1
(the right sided leads). An additional EKG sign to support the diagnosis of pericarditis is a
down-sloping TP-segment. This is known as “Spodick’s sign”. Since a STEMI may also produce
saddle-shaped ST-elevations, one must ensure that there are no ST-depressions other than in
leads aVR and V1. The amount of ST-elevation in limb lead III must be less than that in lead II.
If these last 2 criteria are not met, suspect a STEMI.

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 Figure 14: Pericarditis. Notice the widespread saddle-shaped ST-elevations, PR-depressions
and Spodick’s sign

3. Benign Early Repolarisation (BER): Also known as high uptake or high take-off. This EKG finding
is the most common cause of ST-elevation seen in young patients in the emergency unit. As
the name suggests, it is a benign cause of ST-elevation. ST-elevation may only be attributed
to BER in patients younger than 50yrs of age. The typical features of BER include saddle-
shaped ST-elevations predominant in leads V2-V5. The T-waves are asymmetrical with a
longer up-slope and sharper decline giving the ST-T complexes a “smiley-face” appearance. J-
waves or “fish-hooks” are often present. BER does not produce reciprocal changes or Q waves.
If these are present, suspect a STEMI.

Differential diagnosis of J-
waves

• Benign early repolarisation

• Hypothermia
• Hypercalcaemia
• Occult cardiac injury*

Table 7: The J-wave

* A controversial article was published in 2013 in Injury supporting the J-wave as a new EKG
sign suggestive of occult cardiac injury following penetrating injuries to the heart. The mean
age of the patients in this study was 28 years and 96% were male. A significant number of
patients with these demographics would have BER at baseline.

4. LV aneurysm: Sometimes, after a massive myocardial infarction, the scarred, weakened LV

myocardium balloons out and forms a LV aneurysm. On EKG, it manifests as a persistence of
ST-elevation > 2 weeks following an acute myocardial infarction. In this condition, Q-waves
are always present. There are no reciprocal changes or evolution of the EKG picture with time
(both of which would suggest an acute MI). The main clincher of the diagnosis, however, is

20
 the clinical picture of the patient. They should not be having any current ischemic symptoms
to suggest an acute MI.

5. Hyperkalemia: An elevated potassium (K+) causes several EKG changes. Some experts go as far
as recommending a K+ level on any bizarre looking EKG that cannot be explained. Tall, broad
or peaked T-waves are typical. However, as the K+ increases, other changes such as a
prolonged PR interval, broad QRS complex and sine waves with bizarre broad QRS morphology
and ST-elevations occur.

6. Subarachnoid haemorrhage: Raised intracranial pressure may cause neurogenic myocardial

stunning resulting in EKG changes. In some cases, it may even produce echocardiographic
evidence of regional ventricular wall motion abnormality. Much like hyperkalaemia, raised
intracranial pressure can present with any EKG pattern and that includes ST-elevations and
depressions. The classic description of EKG findings with raised intracranial pressure is
widespread giant T-wave inversions (“cerebral T waves”). In this scenario, the clinical state of
the patient will be a crucial guide. It is seldom that a patient with a neurogenic stunned
myocardium will be awake and alert.

Figure 15: Bradycardia, ST-elevations and cerebral T-waves in a patient with a subarachnoid
haemorrhage

7. Left bundle branch block (LBBB): LBBB is characterised by a QRS duration of >120 ms, a
dominant S-wave in V1 and a broad monophasic or notched R-wave in the lateral leads (I, aVL,
V5-V6). Another normal feature of LBBB is ST-QRS discordance. This means that when the QRS
complex is predominantly positive, there will be ST-depression. Similarly, when the QRS
complex is negative, there will be discordant ST-elevation. The amplitude (height) of
discordant ST-elevation is normally less than 25% of the QRS amplitude. If there is
concordance (ST-elevation in the presence of a positive QRS-complex) or if the discordant ST-
elevation is ≥ 25% of the QRS amplitude, then a STEMI is present (Smith-Modified-Sgarbossa
criteria).

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 Figure 16: ST-elevations in an EKG with LBBB

8. Paced rhythms: Paced rhythms present as a LBBB on the EKG. The above ST-changes in LBBB
also apply to paced rhythms. The original Sgarbossa’s criteria has been validated in paced
rhythms, however the Smith-Modified-Sgarbossa changes have not been validated.

9. Left ventricular hypertrophy (LVH): In addition to the voltage and non-voltage criteria
mentioned above when discussing the QRS complex, LVH also normally produces discordant
QRS-ST changes. Appropriate discordance of the ST-segment to the QRS complex is when the
ST segment is elevated < 17% of the depth of the QRS complex. If there is excessive
discordance > 17%, or any concordance or reciprocal changes, consider a STEMI in the
presence of LVH. A general guide is to be suspicious of STEMI if the ST-elevation is ≥ 3 mm.

Figure 17: Normal discordant ST-elevations associated with LVH

10. Brugada syndrome: Brugada syndrome is an inherited sodium channelopathy. It is a cause of

unexpected sudden death or syncope in a young patient. The typical EKG pattern is found in
leads V1-V3. Type 1 Brugada pattern is the presence of a RBBB QRS morphology (i.e. an RSR’
pattern in V1-V3), followed by a coved ST-segment elevation > 2mm in amplitude and an
inverted T-wave. A type 2 Brugada pattern is the presence of a RBBB QRS morphology, saddle-

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 back ST-elevation > 2mm in amplitude and either an upright or biphasic T-wave. Type 3 follows
either type 1 or 2 pattern, but the ST-elevation is < 2mm. The significance of these Brugada
patterns are unclear and only considered significant in conjunction with clinical findings. These
include:
• Documented ventricular fibrillation or polymorphic ventricular tachycardia
• Family history of sudden cardiac death at <45 years old
• Coved-type ECGs in family members
• Inducibility of VT with programmed electrical stimulation
• Syncope
• Nocturnal agonal respiration

Figure 18: Type 1 Brugada pattern in lead V2

11. Aortic dissection: A proximal thoracic aortic dissection may extend into the coronary vessels
and present with ST-elevations just like a STEMI. The most common extension is into the right
coronary artery mimicking an inferior and / or posterior STEMI.

Causes of ST-depressions

• Ischaemia / NSTEMI
• Reciprocal changes of a STEMI
• LBBB and paced rhythms
• Posterior myocardial infarction- ST-depressions in V1-V4 (we are essentially seeing the
reciprocal change in the anterior leads)
• Digoxin effect- reverse-tick shaped ST-depressions
• Hypokalaemia
• SVT (discordant ST changes to the QRS complex)
• RVH
• LVH- strain pattern in the lateral leads includes ST-depression and T-wave inversion

The T-wave

The T-wave represents ventricular repolarization. Normal T-waves are asymmetrical with a gradual
upward slope and a steeper downward slope. T-waves are upright except in aVR and V1. A persistent
juvenile pattern with inverted T-waves in V1 to V3 may be seen in adolescents.

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T wave abnormalities
• Inverted
• Peaked
• Hyperacute

T wave-inversions

Pathological T-wave inversion are usually symmetrical and deep (>3mm). They are found in the
following conditions:

• Myocardial ischaemia and infarction (including Wellen’s syndrome)

• Left bundle branch block (inverted T-waves follow discordant ST-depressions when
the QRS is positive)
• Ventricular hypertrophy (strain patterns)
• Pulmonary embolism (Inverted T-waves in the anterior and inferior leads are the most
specific EKG sign of PE)
• Hypertrophic cardiomyopathy
• Raised intracranial pressure (cerebral T-waves)

Wellen’s syndrome
It is indicative of critical proximal LAD occlusion. The patient is pain free at the time
of the EKG recording as spontaneous reperfusion has occurred. Wellen’s syndrome
is considered a STEMI equivalent as re-occlusion may occur at any time.

• Type 1: Biphasic T-waves (first up then down) in V1-V4

• Type 2: Deep symmetrical inverted T-waves in V1-V4

Table 8: Wellen’s syndrome

Peaked T-waves

Peaked T-waves are caused by hyperkalaemia. They are tall and pointed like a steeple. The evolution
of EKG changes in hyperkalaemia is referred to as the “String theory”. Imagine that the EKG tracing is
formed by a piece of string. The changes occur as you hold onto the T-wave of the tracing and pull in
an upward and outward direction. As the EKG stretches out, the PR-interval prolongs, P-wave flattens,
the QRS-complex broadens, and the T-wave becomes increasingly tented. Any conduction block may
develop. At higher K+ levels, a sine wave develops. This is a sign that the patient is peri-arrest. See
figure 12.

Figure 19: The hyperkalaemia string theory

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Hyperacute T-waves

Hyperacute T-waves are often seen in patients that present very early after the onset of ischemic
symptoms. It is a large, broad-based, symmetrical T-wave. They are most frequently found in the
septal and anterior precordial leads (V1-V4) as they are associated with left anterior descending (LAD)
occlusion. Hyperacute T-waves dominate the preceding QRS complex (approaching the height of the
QRS complex) or may even be larger than the QRS complex. See figure 13. True hyperacute T-waves
evolve into STEMIs over a short period of time. Serial EKGs and checking the serum K+ level helps to
differentiate hyperkalaemia and BER from an ischemic hyperacute T-wave.

Figure 20: Hyperacute T-waves

The T-wave in lead V1 is negative. A new tall T-wave in V1 (NTTV1) is abnormal. It is often an early sign
of infarction. If the amplitude of the T-wave in V1 is > V6, it further supports the possibility of early
infarction. Note the changes in V1 and V6 in figure 13 above.

De-Winter’s ST-T complex is a form of hyperacute T-wave. It is the combination of a deeply depressed
ST segment (> 1mm) followed by a large hyperacute T-wave. It is a sign of proximal LAD occlusion /
critical stenosis. It is considered a STEMI equivalent and mandates urgent angiography for
percutaneous intervention (PCI). The De-Winter’s ST-T complex does not always evolve into a STEMI.

The QT-interval

The QT-interval represents the entire duration of ventricular depolarisation and repolarisation. This
interval is of critical importance since it represents the time during which the heart is highly sensitive
to the development of life-threatening dysrhythmias. There is an increased risk for dysrhythmias to
occur when the QT-interval is prolonged or shortened. See table below. The QT-interval is measured
from the beginning of the QRS-complex (ventricular depolarisation) to the end of the T-wave
(ventricular repolarisation). The QT-time varies depending on the heart rate of the patient. To
standardise the QT-value, it is corrected for a rate of 60 beats per minute. This may be done using
many formulae, the most common being Bazette’s formula.

Bazette’s formula = QT interval in milli-seconds / √RR interval in seconds.

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 Corrected QT-times
Normal range in males 350 – 440 ms
Normal range in females 350 – 460 ms
High risk for torsade-de-pointes ≥ 500 ms
High risk for ventricular tachycardia ≤ 300 ms
Table 9: Corrected QT-times

The eyeball method for estimating the QT-interval

With a heart rate between 60 and 100, the T-wave must be completed before half the R-R interval

Table 10: Eyeball method

Causes of a prolonged QTc

“Anti”-drugs

• Anti-malarials
• Anti-biotics
• Anti-psychotics
• Anti-depressants
• Anti-histamines
• Anti-arrhythmics
• Anti-cholinergics

“Hypo”-electrolytes

• Hypo-kalaemia
• Hypo-magnesaemia
• Hypo-calcaemia

Congenital long QT syndrome

Causes of a short QTc

• Hypercalcaemia
• Digoxin effect
• Congenital short QT syndrome

The U-wave

The U-wave signifies repolarisation of the His-Purkinje fibres. U-waves are normally in the same
direction as the T-wave and < 25% in height. They become visible when the heart rate slows down.

Abnormal U-waves are larger than 25% of the T-wave or in the opposite direction to the T-wave.

Causes of abnormally large U-waves

• “Hypo”- electrolytes (K+, Mg++)

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 • Drugs- digoxin

Inverted U-waves

• Early marker of unstable angina and myocardial infarction

• Hypertension
• Valvular disease
• Congenital heart disease
• Cardiomyopathies
• Hyperthyroidism

EKG interpretation

The final step in the interpretation of the EKG is putting it all together. Although the components of
the EKG were assessed individually, the final step requires a consolidation of the information.
Remember to correlate the patient history and physical examination to the EKG findings. This will
guide you towards the most likely diagnosis. Remember that all the waves and intervals on the EKG
should be in proportion to each other. When one wave is too large or out of proportion, or if an
interval is too short or too long, it gives you a clue that pathology may be present.

Always take a moment before you sign off the EKG, to compare the diagnosis that you have made to
that of the EKG analyser. Although the EKG analyser is often inaccurate, it has happened in the past
that the analyser algorithm has picked up pathology that was missed by the treating physician. Don’t
let this happen to you!

Conclusion

We hope that you have enjoyed this overview of the EMpret EKG system. We hope to include more
of the various pathologies discussed in the EMpret EKG course in future editions of this book.

Remember, to become an EKG legend you need to practice, practice, practice!

Regards,

Andreas Engelbrecht and Vidya Lalloo

The EMpret EKG team

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