BASIC ECG

module
 ECG fundamentals

I. ECG Recording

II. The Cardiac Cycle and the ECG

III. Leads and Planes

IV. Waveforms, Segments and Intervals

V. Basic ECG interpretation

VI. Skills testing

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 Section 1

ECG Recording
The ECG shows the precise sequence of the electrical events of the heart. These electrical
activities produce currents that radiate through the surrounding tissue to the skin. The
electrodes of the ECG, attached to the skin of the patient, sense the heart’s electrical
signals and transmits them to the ECG machine. The electrical currents are recorded as
waveforms on the ECG that represent the heart’s depolarization and repolarization cycle or
the cardiac cycle. By interpreting these waveforms, one can identify arrhythmias,
abnormalities in the heart’s conduction and even electrolyte imbalance. The ECG
waveforms are also invaluable in the diagnosis of acute coronary syndromes and
pericarditis.

ECG recording
To record an ECG there must be a complete system comprising the electric circuit
between the heart and the electrocardiogram. Electrodes are placed on specific parts on
the body surface and connected to the electrograph by means of cables. The whole
system of the ECG consists of the ECG machine, electrodes, cables and leads.

parts of the ECG:

1. ECG machine

2. electrode

3. cable

4. leads - can be defined as a pair of

terminals with designated polarity, each of
which is connected either directly or via
passive-active network to recording
electrodes.

To b e a b l e t o a c q u i r e a n
electrocardiograph, attach the soft, sticky
patches called electrodes to the skin of
the patient’s chest, arms, and legs. The
patches are the size of a peso coin.
Sometimes, metal clamps or suctions are
placed instead of patches.

Usually, there are 10 electrodes attached

to the skin that will detect the heart’s electrical signals. The patient must lie still on the

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examining table during this time. The ECG machine will record these signals on the graph
paper or display them on the screen. The entire test should last less than 10 minutes.

The appearance of the ECG can vary depending on the position of the body at the time of
examination. A recumbent or lying flat position is recommended for proper ECG recording.
Any variation to this position must be noted on the printed ECG. The patient must be lying
comfortably and relaxed to minimize artifacts and achieve clinically accurate readings.

ELECTRODE PLACEMENT

The following electrode sites should be correctly identified and the placement of the
electrodes must conform to AHA recommendations.

Each lead wire is generally color coded and labeled to aid identification of the electrodes.
However, the color may differ depending on the ECG machine manufacturer.

Limb Leads

It is recommended that the limb electrodes be attached on both arms and legs, slightly
proximal to the wrist and ankle. It is important to check and verify the electrode label and
the position where it is attached so the results will not be erroneous.

• Right arm limb lead (RA, red) - right forearm, proximal to wrist

• Left arm limb lead (LA, yellow) - left forearm, proximal to wrist

• Left leg limb lead (LL, green) - left lower leg, proximal to ankle

• Right leg limb lead (RL, black) - right lower leg, proximal to ankle

Electrode Position

V1 fourth intercostal space at the right sternal border

V2 fourth intercostal space at the left sternal border (just across V1)

V3 midway between V2 and V4

V4 fifth intercostal space in the mid-clavicular line

V5 left anterior axillary line at same horizontal level as V4

V6 left mid-axillary line at same horizontal level as V4 and V5

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Precordial (Chest) leads

The correct anatomical positions for placing the precordial leads have been defined and
should always be used. Each position have been specified to correspond to an area of the
heart.

Locating chest positions:

• Care should be taken when counting the intercostal spaces down from the
clavicle that the small space between the clavicle and the first rib is not mistaken for the
first intercostal space.

• To avoid this mistake, the sternal angle (or the angle of Louis) should be used as
the main reference point. This anatomical landmark denotes the position of the sternal
angle at the manubriosternal joint.

To locate the sternal angle, a finger should run down from the
sternum, from the notch at the top until a bony horizontal ridge,
the sternal angle, is met. With the finger on this ridge, sliding
down and to the side will locate the second intercostal space.

• From the sternal angle, with the finger on the ridge, sliding down and to the side,
locate the second intercostal space. Then count down to the third and fourth space.
Locate the very edge of the sternum on the right side and place V1 there. Repeat this to
the other side (left side) to correctly position V2.

• Next the position for V4 should be located. This should be placed in the fifth
intercostal space in line with the mid point of the clavicle.

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 • Once the V4 electrode is placed then the location for V3 can be identified,
directly mid-way between V2 and V4.

• V5 and V6 are then positioned, taking care not to follow the line of the ribs, but
to follow a horizontal line from V4. V5 is placed with the anterior axilla and V6 in line with
the mid-axilla.

• When recording an ECG from female patients by convention the lateral chest
electrodes (V4, V5, and V6) are placed beneath the left breast.

Recording the ECG

• To acquire a good quality ECG the patient must be comfortable and relaxed. If
these conditions are not satisfied the ECG will record somatic (body) muscle potentials as
well as the heart’s activity. This will make ECG interpretation difficult. Some patients will
not be able to relax fully because of severe pain or may have neurological condition like
tremors from Parkinson’s disease. Make them as comfortable as possible and take note of
the condition on the ECG recording.

• Patient details (name and a second unique qualifier like a hospital number or
birthdate) should be entered into the ECG machine after it has been verified by the patient
directly (or by a companion speaking on their behalf).

• Before recording the ECG, check that the patient’s limbs are still and appear
relaxed. If the patient has clenched fists or stiff arms, or is shivering or chewing gum, it will
not be possible to get a high quality ECG.

• Press the appropriate button on the machine to start recording. (start or auto).

STANDARDIZATION OF THE ECG

• Standard calibration of the ECG is 10mm/mV.

➡ at this calibration, 1 mV signal is expected to produce a rectangle of 10mm height and

5 mm width

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 • The filter button should not be used in the initial recording

When to use the filter button:

If despite all efforts to make the patient relax and comfortable, somatic muscle
potentials appear in the ECG recording, switch on the filter and repeat the recording.
It should be noted that the filter has been switched on to the ECG recording.

The filter will reduce the interference from the somatic muscle potential. However, it
may also distort the ECG recording. It should only be used if all attempts to eliminate
the interference have failed.

• If the ECG complexes are of high voltage then the gain should be adjusted (5mm/mV) to
enable them to be measured accurately. Any alteration in the gain settings should be
noted on the ECG recording.
10 mm/mV 5 mm/mV

• If the rhythm is noted to be irregular, a rhythm strip (from lead II) should be
recorded for a minimum of 10 seconds.

• If the ECG recording is technically correct and with good quality, re-check the
label to ensure it is correct and full, then the electrodes may be removed from the patient
and the electrode patches must be disposed off as clinical waste. Lastly, wipe the patient’s
skin clean.

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Types of ECG recording (cardiac monitoring)

12 lead ECG
Rhythm strip
- This type of ECG recording shows continuous information about the heart’s
electrical activity by monitoring its rhythm, rate, and appearance of waveforms. The
continuous monitoring can be done using one or several leads simultaneously. Lead
II is the most commonly used lead in monitoring; others are V1 and V6.
There are two types of ECG monitoring system - the hardwire monitoring and
the telemetry. The hardwire monitoring system are commonly seen in critical care
units, mounted on shelves or walls beside the patient and is usually equipped with
a defibrillator. The electrodes are directly connected to the monitor limiting patient
movement. The monitor displays the continuous cardiac rhythm and transmits the
ECG to a console at the nurses station. Both the monitor and the console have
alarms and can print rhythm strips when the monitor detects abnormalities in
rhythms and rates. This type of cardiac monitoring sometimes have modules to
monitor oxygen saturation, blood pressure and other hemodynamic measurements
and parameters. This kind of monitoring is used in critically-ill patients.

The telemetry monitoring, on the other hand, is a more mobile type of

monitoring. The electrodes attached to the patient are connected to a small,
battery-powered transmitted that sends the heart’s electrical signals to a monitor
screen usually in the nurses station. This type of monitoring is especially helpful for
detection of irregular rhythms during rest, exercise, sleep, or stressful situation.
Most telemetry systems can only monitor the heart rate and rhythm.

Patient preparation and attaching electrodes and lead wires.

Just like recording the 12 lead ECG, it is important to reassure your patient
before attaching the electrodes. Explain that you are attaching the electrodes to
monitor your patient’s heart rate and rhythm, not controlling them. Reassure that the
cardiac monitor is equipped with an alarm that may go off to detect abnormalities in
heart rate and rhythm, or if there is a problem with the monitoring system like when a
lead wire become loose, the signal detected is poor, or the battery is running low.
Again, explain how the procedure is done, respect patient privacy, and wash your
hands before attaching the electrodes. Bare the patient’s chest, and select the sites
where the electrodes will be attached. Choose areas on the chest with soft tissue
and near the bones. Do not place electrodes over bony prominence, thick muscles or
skin folds as these areas can produce ECG artifacts.

Skin preparation. If possible, wash the patient’s chest with soap and water, and
then dry it thoroughly with a dry washcloth. Ensure that the patient’s skin is clean by
briskly rubbing with a dry washcloth or gauze pad until the skin reddens. Brisk
rubbing will help improve electrical contact by removing dirt, oil and dead skin cells.

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Hair may interfere with acquiring a good cardiac recording. It may sometimes be
necessary to clip or shave the area of hair before attaching the electrodes. If the
patient has oily skin, wipe clean the area with an alcohol pad and allow to air-dry.
This procedure allows good adhesion and prevents alcohol becoming trapped
beneath the electrode which can cause skin irritation and breaking.

Attaching the electrode pads and lead wires. Usually a three, sometimes five,
-lead wire system are used for bedside monitoring. The lead wires and the cable
connections need to be connected to the monitor. Then connect the lead wires to the
electrodes. Lead wires are usually snap on or sometimes it may be clip on. If they are
snap on, better to attach the lead wires on the electrodes prior to attaching them on
the patient.
To apply the electrode, remove the backing and make sure that the pregelled
electrode is still moist. Discard electrode pads that are dry. Dry electrode pads will
not have a good electrical contact with the skin and will interfere with the waveforms.
Place the electrode on the specified prepared site of the leadwire. Making sure that
the electrode pads are sticking properly to the skin by pressing down on its adhesive
edge around the outside of the electrode to the patient’s skin. Repeat the procedure
for all electrode patch and leadwire. The electrode patch may have to be replaced
every 24 hours depending on your institution’s protocols.

Cardiac monitoring. After attaching the leadwires to the electrode pads, make
sure the cables are connected properly to the monitor, then check the display on the
screen. It should show the patient’s ECG waveform. Some monitors may need
adjustment on the size of the waveforms by adjusting the gain control. If the ECG
waveforms are off the baseline (too high or too low on the screen)- adjust the
position dial. Other leads can also be selected to get a different view of the heart.
This is done by selecting the leads with the lead selector button or dial.
Always verify the that the monitor is able to detect each heartbeat by comparing
the patient’s pulse by palpating central pulses or listening for the apical heart beat.
Set the upper and lower limit of the heart rate alarm depending on the patient’s
condition or attending physician’s instructions. Heart rate alarms are usually set
10-20 beats/minute higher or lower than the patient’s heart rate.
The cardiac monitor can be set to automatically print out rhythm abnormality
that it detects. Printing can also be done manually. Select the rhythm strip that needs
to be printed in the record or history box on the monitor then press print selection.
Just like a 12 lead ECG recording, printed rhythm strip must always have the
patient’s name, date, time, and if a medication has been administered, presence of
chest pain, or patient’s activity during ECG acquisition.

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COMMON 12 LEAD ECG AND CARDIAC MONITORING ARTIFACTS

Examples of common ECG artifacts:

1. Somatic (muscle) tremors or noise. This can be seen if the patient is not relaxed,
moving his fingers or toes, or shivering from cold. Reassure and advise the patient to
keep still and relax; if the patient is shivering due to cold, cover with a warm blanket.

2. AC interference - tight rapid oscillations that may be caused by power cords,

lighting or electrical wires in the walls, ceiling and floor. When an ECG machine is
poorly grounded or not equipped to filter this interference, the ECG lines will have a
thick baseline. In cases like this, try to move the power cord or sometimes move the
bed to a 45 degree angle from the source of the electrical power. Check if the patient
does not have a cellphone or wearing any other electronic device and that the patient
cables are within the confines of the patient.

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3. Wandering baseline - the isoelectric line changes in position. It can be caused by
moving cables during recording, patient movement, dirty lead wires/ electrodes, or
loose electrodes.

4. Reversed leads or misplaced leads - an ECG recording with wrong lead

placements will cause abnormal waves or complexes directions. The rhythm being
viewed comes from a totally different lead or direction. In the example below, the P
waves are upside down and the rhythm may be erroneously read as other than the
normal sinus rhythm.

example of left arm and right arm reversal electrodes

Key ECG findings in reversed right/arm arm electrodes:

- inverted P-QRS-T waves in lead I

- “normal” appearance of lead aVR (upright P-QRS-T) as opposed

to the expected inversion of these waveforms in a normal ECG
tracing

- QRS vector in lead I will not have the same vector as lead V6

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after the left and right arm electrodes are placed correctly in their proper positions,
the ECG recording will look like this:

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 Section 2

cardiac cycle and ECG

Over a hundred years ago, Willem Einthoven invented

the first electrocardiogram. He developed a mechanism
that would allow the studying of the electrical activity of
the heart graphically. Professor Einthoven used a string
galvanometer that required telephonic transmission of
the ECG from the physiology laboratory at the University
of Leiden, The Netherlands, to a clinic in the Academic
Hospital about a mile away, naming his recordings as
“telecardiogramme.” His report contained many ECG
patterns and arrhythmias. He likewise developed a
system of electrocardiographic standardization that is
still being used around the world today. Professor
Einthoven was able to recognize the great potential
importance of the ECG as a diagnostic and investigative tool, thus he was named the
founder of the modern electrocardiography. He was awarded the Nobel Prize in 1924 in
physiology and medicine, “for the discovery of the mechanism of the electrocardiogram.”

Einthoven hypothesized that the body is a homogenous conductor. Electric signals from
the specialized conduction system of the heart can therefore be recorded at the body
surface as the electrocardiogram. Simple as it may sound, the ECG is actually the final
outcome of a complex series of mechanical and electrical events that occur in a single
heart beat, or cardiac cycle.

how the ECG works

First, ionic currents are developed in the cardiac myocytes and travel from cell and
between adjacent cells. The electrical field generated will have to pass other structures
that perturb the cardiac electrical field, like the lungs, blood, and skeletal muscle before it
can be recoded through the body surface.

The current reaching the skin are then detected by electrodes placed in specific locations
on the extremities and chest that are made to produce leads, representing the difference in
potentials sensed by pairs of electrodes or electrode combination. These electrical outputs
are amplified, filtered and displayed to produce an ECG recording.

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how the heart works: the cardiac cycle

The electrical signal originates from a

specialized conduction system tissue
that controls the heart rate. It is
influenced by a variety of factors but
most especially by the parasympathetic
and sympathetic stimulation. This
specialized conduction system provides
the normal sequence of activation of the
cardiac chambers that will produce
efficient and maximizing contraction and
filling (relaxation). It possess general
properties to undergo spontaneous
depolarization and function as
pacemakers that controls the beating of the heart. Inside the cardiac myocytes, electrical
excitation consists of transmission of a membrane-based depolarizing and depolarizing
currents called the ACTION POTENTIAL that spreads throughout the heart via the
specialized conduction system.

Anatomically, the specialized conduction system of the heart starts from the sinus node or
the sino-atrial node (SA node). It is a spindle-shaped tissue that is located in the right
atrium near the superior vena caval junction. It has the fastest
spontaneous depolarization rate among the components of the
conduction system of the heart. The SA node provides the
normal control of the heart rate. It is under the direct influence of
the autonomic nervous and the neuroendocrine systems
(which modulates the beat-to-beat and longer-term
variations in heart rate.

The electrical signal or The signal traverses the specialized conduction system
action potential (AP) starts
in both atria simultaneously spreading to the atrial myocytes producing atrial
in the SA node.
contraction. This produces the P wave on the surface ECG.

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 take a closer look.... at the AV junction

AV node The AV node has a slow

Bundle of His
conduction time that is responsible
This region comprises of the atrioventricular
The atrial conduction system will node (AV node) and the distal His bundle.
to the normal delay of the atrial and
then meet at the atrio-ventricular This junction is located just where the atrial ventricular contraction. This delay
region. and ventricular myocardial fibers converge. is displayed as the PR interval.

At the AV junction area, electrical excitation of the

His bundle spreads to the large intraventricular
fascicles. This fascicles comprise of the right bundle
and the large bi-branched left bundle. The left
bundle will further branch into the anterior and
posterior fascicles.

Both bundle branches will ramify

within the ventricular myocardium into The electrical signal in the Purkinje fibers will be transmitted to individual
the smallest branches of the
ventricular myocytes causing ventricular contraction or ventricular
specialized conduction tissue, called
Purkinje fibers. depolarization producing the QRS complex on the surface ECG.

The left ventricle, biggest cardiac chamber, is the largest

source of electrical potential difference; that is why the
voltage of the QRS complex on the surface ECG reflects
mostly the LV.
Within the ventricles, the AP spreads from myocyte to
myocyte via specialized structures called intercalated
The ST segment represents the plateau phase and is
disks.
then followed by the repolarization phase or the T
The electrical activation begins in both ventricles; the left
wave on the ECG. The repolarization phase of the
ventricle slightly before the right ventricle.
heart’s action potential triggers the ventricular diastole
and filling phase of the cardiac cycle.

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 Sinoatrial node

Bundle of His

Atrioventricular
node
Right
Left Bundle Branches
Bundle
Branch

ventricular depolarization
QRS complex

atrial
depolarization

ventricular repolarization

PR interval QT interval

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 Section 3

leads and planes

Leads and Planes

The electrodes attached on the skin at different locations in the body will give us a
total picture of the heart’s electrical activity from different perspectives called the
leads and planes.

LEADS

A lead provides a view of the heart from two points or poles. Each pole consists of a
positive or negative pole. An imaginary connecting line between two poles is called
the axis and refers to the direction of the current moving through the heart.

+ -

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The direction of the flow of current between the poles determine the appearance of
the waveform on the ECG. An electrical current that is flowing towards a positive pole
of the electrode will have a positive or upward stroke and is called a positive
deflection. A current that flows away from the positive pole, will deflect downward,
and is called a negative deflection. A current that flows perpendicular to the axis of
the two electrode poles will have a waveform that may go into both directions or may
be unusually small. An absent current or an electrical current that is too small to be
detected will have an isoelectric deflection or the line remains within the
baseline.

- +

PLANES

A plane is a cross section of the heart. A plane of the ECG will provide a view of a
particular section of the heart. There are two
planes that we can analyze thru the ECG: frontal
and horizontal planes. The frontal plane is the view
of the heart from the right and left sides. The six
limb leads gives us a view of the frontal plane of
the heart. The horizontal plane, on the other hand,
views the electrical activity from the anterior to the
posterior sections of the myocardium.

In a 12 lead ECG recording, all the 12 leads [6 limb

leads, and 6 chest or precordial leads] provide
information on 12 different views of the heart by
placing the electrodes on specific parts of the
arms, legs and chest.

The six limb leads - I, II, III, augmented vector right (aVR), augmented vector left
(aVL), and augmented vector foot (aVF)- presents information on the frontal view of
the heart. Leads I, II, and III are bipolar leads which needs a negative and a positive

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pole while the augmented leads (aVR, aVF, and aVF) only requires a positive
electrode making them a unipolar lead. The six precordial leads- V1, V2, V3, V4, V5
and V6- shows us the horizontal plane of the heart. These are also unipolar leads,
requiring only a positive electrode, just like the augmented leads. The negative pole
of the unipolar leads is calculated by the ECG machine to be in the center of the
heart.

The Standard Limb Leads

The standard limb leads are leads I, II, and III. As mentioned, these leads are bipolar
and requires a third electrode, the ground, which is placed on the chest to prevent
the appearance of interferences during ECG recording. The axis of these three limb
leads form a triangle around the heart giving us a frontal view of the heart.

• Lead I - shows the view of the heart’s electrical current moving from right
to left. The positive electrode is placed on the left arm and the negative
electrode is placed on the right arm. Lead I usually produces a positive
deflection of the waveforms on the ECG.
• Lead II - records the flow of the electrical current of the heart down and to
the left. The positive electrode is located on the left leg and the negative
electrode is on the right arm. The resultant ECG waveforms should show an
upright P, R and T waves. This lead is usually used for continuous ECG
rhythm monitoring because of the high voltage and positive deflections of
the waveforms.
• Lead III - also usually produces a positive deflection of the waveforms on
the ECG tracing. The positive electrode is placed on the left leg and the
negative electrode should be in the left arm.

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 lead I aVR
aVL

lead II lead III

the axes of the 3 limb leads form the

Einthoven’s triangle.
aVF

aVL
lead I aVR

lead III
lead II aVF

Augmented unipolar leads

The augmented leads are the aVR, aVL, and aVF. They are called as such because
the ECG will “augment” the small waveforms that these unipolar leads will produce.
These augmented leads also represent the frontal view of the heart

• lead aVR - positive electrode is located on the right arm. The waveforms
will show a negative deflection because the flow of electrical current moves
away from the lead
• lead aVL - the positive electrode is on the left arm and usually shows a
positive deflection on the ECG
• lead aVF - the positive electrode is on the left leg and usually produces a
positive deflection

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Precordial unipolar leads

The six precordial leads are placed in sequence across the chest to give a view of the
horizontal plane of the heart. These leads are unipolar, that means containing only a
positive electrode. The deflection of the waveforms are progressive, more negative R
wave at V1 and V2, then the positive and negative deflections becoming equal at V3,
and then becoming more positive and upright from V4 to V6.

So that a normal 12 lead ECG will look like this: Note the axis and the deflections of
the waveforms of each lead.

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 Section 4

Waveforms, Segments, and Intervals

In the previous section, the cardiac cycle and the have been discussed. We’ve learned that
each waveform, segment and interval coincide with a particular event in the heart’s
depolarization and repolarization cycle. The timing and duration of each component of the
ECG tracing is also represented on the surface ECG.

ECG waves and Intervals: What do they mean

WAVE & EVENT IN THE CARDIAC

INTERVAL CYCLE

P wave atrial depolarization

interval time from onset of

PR atrial depolarization to the
interval onset of ventricular
depolarization

QRS ventricular depolarization

ST
ventricular repolarization
segment
duration of ventricular
QT
depolarization and
interval
repolarization

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The ECG paper

The ECG paper consists of lines going across and going perpendicular to each other
forming a grid. The grids or squares are measurements of time and amplitude. The small
squares are grouped by 5 forming one big square.

The horizontal line determines the time measured in seconds (secs) or milliseconds. A
small square is equivalent to 0.04 sec or 4 msecs. The time duration of one big square is
0.2 of a second or 200 msecs. A second will compose of five (5) big squares ( 0.02 secs x
5).

The vertical lines will measure the amplitude of voltage. The height of one small square is
equivalent to 1 mm in amplitude or 1 millivolts (mV) in electrical voltage. The amplitude of
one big square, is therefore, 5 mm or 5mV. To measure the amplitude or voltage of a wave,
count the number of small squares starting from the base of a wave going towards its tip.

12 mm or 12 mV

0.40 sec

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P wave

The P wave is the first component of the ECG. It

represents the sequential depolarization of the
right and left atrium. This can be appreciated in
lead V1 wherein the P wave appears to be
biphasic. The initial positive deflection
represents the right atrial depolarization
immediately followed by a negative deflection
which demonstrates the left atrium’s
depolarization. (lead V1 electrode is placed on
the right parasternal border of the fourth
intercostal space. This location is nearer to the
right atrium, thus the positive deflection of the initial phase of the P wave). In all other
leads, except in lead aVR, the P waves are always upright.

The normal P wave should always precede the QRS complex. Its height is 2-3 mm or
less than small squares with a duration of 0.06 to 0.12 seconds (less than 2 small
squares to 3 small squares). The wave must be rounded and smooth.

A normal looking P wave followed by a QRS complex will assume

that the electrical impulse originated from the SA node. An
abnormally looking P wave, like if it is negatively deflected in lead
II, with a very short interval from the QRS complex, may mean
that the electrical impulse came from another structure such as
the AV node.

If the P wave also looks notched and wide or tall and peaked may also indicate
enlargement of an atrium associated in diastolic dysfunction of the left ventricle, right
heart enlargement, chronic pulmonary disease, or pulmonary embolism.

Different looking P waves within a lead ECG recording indicates different origins of
the electrical stimuli within the atria, like in atrial tachycardia or atrial flutter. A P wave
that is not followed by a QRS complex or the P wave is not associated with a
succeeding QRS complex may signify heart blocks.

PR interval

The PR interval marks the duration or the time it takes for the electrical impulse to
travel from the atrium to the ventricles. Basically, it is the time that the impulse flows
in the AV node, to Bundle of His, and then to the two bundle branches.

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 The PR segment is the isoelectric line after the P wave. The PR
interval is measured from the beginning of the P wave to the end
of the PR segment just before the start of the Q wave. The
normal duration is 0.12 to 0.20 seconds.
PR

The PR interval may be prolonged in the elderly or those taking

beta blockers. A markedly prolonged PR interval > 0.20 seconds
is a form of AV block. On the other hand, a markedly short PR
interval <0.12 second signify that the electrical stimulus originate somewhere else
like in pre-excitation syndromes or AV node arrhythmias.

QRS complex

The QRS complex represents the ventricular depolarization. Myocardial contraction

occurs immediately after the QRS complex on the
ECG. Normally, the QRS complex follows the P wave
after a slight delay, PR interval. The QRS complex is
composed of 3 waves - Q, R and S waves. The Q
wave is the initial negative deflection, followed by a
tall and upward R wave, then ending with another
negative deflection - the S wave. In the 12 lead ECG,
not all leads will have all three waves or have the
same upright configuration. The QRS complex will be
normally upright in lead I, II, III, aVL, aVF, V4 to V6. It
will be biphasic in lead V3. In aVR, V1 and V2, it will
be deflected downwards.

The height or amplitude of the QRS complex differ from

each lead but may range from 5 mm (1 big square) to 30
mm (6 big squares). It has a duration of less than 0.12
second or 3 small squares. The duration must be
measured from the beginning of the Q wave to the end of
the S wave. If there is no Q wave, the measurement must
start at the beginning of the R wave.

It is important to note the duration of the QRS complex.

An abnormally prolonged QRS complex (>0.12 sec)
represents ventricular conduction delay. And a markedly
widened QRS without a preceding P wave may mean that
the electrical impulse originated from the ventricles itself.

Also, a very deep Q wave (let’s say, >25% of the height of the R wave) may mean
myocardial infarction. A notched and wide R wave may signify bundle branch block.

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ST segment
The ST segment shows the end of the ventricular
depolarization to the start of the ventricular repolarization.
The duration of the ST segment starts from the S wave
J point until the beginning of the T wave. An important point of the
ST segment is the J point. This point marks the end of the
QRS complex and the beginning of the ST segment.
ST segment The J point and the ST segment is normally isoelectric,
meaning it is along the baseline but there may be slight
variation of less than 1 small square especially in the
precordial leads.

A negatively displaced ST segment may indicate myocardial ischemia while an

elevated ST segment may indicate ongoing myocardial injury.

T wave

The T wave represents the relative refractory period of

the myocardial repolarization or recovery. The normal T
wave is upright, rounded and smooth (except in aVR
and V1, variable in III) and follows the ST segment.

An abnormally peaked or tenting T wave may indicate

myocardial injury or electrolyte imbalance.

QT interval

The QT interval is the entire duration of the ventricular depolarization and

repolarization. The normal QT interval is 0.36 to 0.44 second; the QT interval should
not be more than half of the duration of two consecutive R waves (R-R interval).

It is important to measure the QT interval because it determines the time for the
ventricles to depolarize then repolarize. Prolonged QT intervals may indicate that the
relative refractory period is slow or conduction abnormalities are present. This
condition is seen in some congenital conduction system defect or those taking

25
 anti-arrhythmic drugs. Short PR intervals arise in some electrolyte
abnormalities or in digoxin toxicity.

To accurately measure the QT interval, the following formula is used:

computed QT = actual QT
R-R interval

The Joint Report of the AHA, the American College of Cardiology (ACC), and other
professional organizations, has suggested that the upper limit for QTc be set at 460
msecs (0.46 sec) for women and 450 msec (0.45 sec) for men, and that the lower
limit be set at 390 msec (0.39 sec).

26
 Section 5

Basic ECG Interpretation

Trying to interpret an ECG is a daunting task. Its value as a diagnostic tool for cardiac
conditions is high. A systematic and simplified approach in ECG interpretation will help
make this task less challenging. One must remember that ECG interpretation and analysis
is a skill that needs to be learned and practiced. Thus, frequent practice with a systematic
approach will aid you in the practice of ECG interpretation.

This is a 12 lead ECG of a 40 year old woman with chest discomfort.

Our task is to analyze this ECG as a diagnostic tool.

Determine the Rhythm

Determining the ECG rhythm is the primary and important step in ECG analysis. Basically,
you want to know if the heart’s electrical impulse originate in the SA node. A normal
impulse conduction will generally have regular rhythm, with a fixed P-P and R-R intervals,
and that all P waves are followed by a QRS complex. It is important to determine if the
atrial rhythm (P-P interval) and the ventricular rhythm (R-R interval) are regular and the
same.

To determine this regularity, you can use a caliper or simply with a pen and paper.

To determine the rhythm, measure the distance between two consecutive waves. Then
compare the distance between other consecutive waves; the interval should be consistent
throughout the strip. If it is, then the rhythm is regular. There may be slight variations of

27
0.04 to 0.12 sec (1 to 3 small square) between intervals but you can still consider as
normal.

Let us start by determining the ventricular rhythm.

Then do the same for the atrial rhythm by analyzing the P-P intervals.

After measuring the regularity, next step is to identify the origin of the heart’s electrical
impulse. The normal conduction begins in the SA node. This will be evident in the ECG
with a normal looking P wave and is followed by a normally-timed QRS complex. The
following algorithm will guide you in identifying the origin of the electrical impulse:

Rhythm?

1. Is the rhythm regular or irregular?

2. What is the rate?

P wave before every QRS
AND 3.Are there P waves? If there are P
waves, are they normal looking P
P wave is positive (upright) in lead II NO
waves?

4. Are the P waves associated with

YES the QRS complexes?

5. Is the QRS complex wide or

narrow?
SINUS RHYTHM

28
Determine the RATE

The normal heart rate is 60 to 100 beats per minute. When analyzing the heart rate of an
ECG strip, verify if the standard paper speed is 25 mm/sec. There are several methods in
determining the heart rate of an ECG tracing:

a. Count the number of large boxes in between two consecutive waves and divide
into 300.
1 2 3 1/2
Rate = 300 / # of big boxes

= 300/ 3.5

= 85.7 or 86 bpm

b. Count the number of small boxes between two consecutive waves and divide
into 1500.
16 small boxes Rate = 1500 / # of small boxes

= 1500/ 16

= 93.7 or 94 bpm

c. Box rule: Using the large boxes as a guide, memorize the heart rate associated
between the number of large boxes as:

# of large box heart rate # of large heart rate

between (bpm) box between (bpm)

1 300 4 75

2 150 5 60

3 100 6 50

29
3 big boxes in between QRS complexes --> heart rate is estimated at 100 bpm

d. If the rhythm is irregular, count the number of complexes on an ECG strip over a 6
second period (30 big boxes) then multiply by 10.
6 seconds strip (30 big boxes)

1 2 3 4 5 6 7 8 9 10 11 12

There are 12 QRS complexes within a 6 second strip in an irregularly irregular rhythm.
Multiply by 10 (to make 60 seconds= 1 minute) to get the heart rate in a minute.

12 x 10 = 120 bpm

Determine the axis

The QRS axis in a 12 lead ECG represents the major vector of the ventricular activation. It
is important to be determined because abnormality of an axis can be a clue to cardiac
diseases. The normal ECG axis is -30 to +105º in persons aged 40 years old and
younger; -30 to +90º for those aged over 40 years old.

Axis deviation to the left is an axis deviated to -30 to -90º, and right axis
deviation is those with an axis of +110 to +180º.

To determine the axis, measure the net QRS voltage (positive minus the negative
deflection of the QRS) of two leads perpendicular (an X and Y axis), for example,
lead I and aVF. Then plot the net QRS voltage against each other.

30
 aVF
- +
lead I
-
+
lead I
has a net
QRS voltage of + 5 (The QRS complex is upright with no negative deflection). Lead aVF

- lead I
+
45º NORMAL AXIS

has a net voltage of +5.

+aVF

The QRS axis of the 12 lead ECG is +45º and is within the normal range.

Another method to determine the QRS axis is by measuring the net QRS voltage in the
leads I, II and aVF. Then use the following table as a guide in determining the axis.

31
 Lead I (net QRS aVF (net QRS Lead II (net QRS
AXIS
voltage) voltage voltage

+ + 0 to 90º Normal

+ - + 0 to -30º Normal

-30 to -90º left axis

+ - -
deviation

- + > 105º right axis deviation

-90 to +180º right superior

- -
(indeterminate) axis

Possible causes of axis deviation:

Right Axis Deviation (RAD) Left Axis Deviation (LAD)

1. Right Ventricular Hypertrophy 1. Left Anterior Fascicular Block

(RVH)
2. Left Ventricular Hypertrophy
2. Lateral wall infarction
3. Inferior wall infarction
3. Pulmonary embolism
4. Left Bundle Branch Block (LBBB)
4. Chronic Lung Disease
5. Atrial Septal Defect (ostium
5. Left Posterior Fascicular Block primum)

6. Dextrocardia 6. Severe Hyperkalemia

7. BAD DATA - left/right arm 7. Other mechanical shifts (e.g. left

electrodes are reversed lung resection)

8. Atrial Septal Defect (ostium

secundum)

9. Vertical Heart

10. Normal Variant

32
Measure the Intervals

A systematic approach in measuring the intervals of the ECG tracing is to

measure them one after each other, noting for any abnormalities as you go along.

I. PR interval
The normal PR interval is 0.12 to 0.20 sec or 3 to 5 small squares from the
start of the P wave to the end of the PR segment just before the R or Q wave begins.
Example 1.

PR

The PR interval measured is 4

small squares or 0.16 sec

Example 2

The PR interval
measured is 9 small
squares or 0.36 sec

In example 2, the PR interval is markedly prolonged.

Example 3

The PR interval measured is

PR less than 3 small squares or
less than 0.12 sec

Example 3 shows an ECG tracing with a very short PR interval (less than 3 small
squares or <0.12 sec).

33
 II. QT interval
The normal QTc (corrected QT) interval is 0.30 to 0.44 sec. The actual QT
interval is measured from the beginning of the Q (or R wave if Q wave is not
present) wave to the end of the T wave.
The QT interval vary inversely with the heart rate. Therefore, we determine
the corrected QT interval by using the Bazett’s formula which factors in the
heart rate:

Let’s practice: Heart rate = 54 bpm

R-R interval = 22 small corrected QT interval

squares or 1.08 sec
= 0.40 / ⎷1.08

= 0.38 sec
actual QT= 0.40 sec

another example:

corrected QT interval

= 0.42 / ⎷0.64

= 0.52 sec

This example shows an ECG tracing with a prolonged corrected QT

interval. Prolonged QT interval increases the risk for polymorphic ventricular
tachycardia which is potential fatal.

Some medications can increase the QT interval.

- Class IA and III anti-arrhythmics - quinidine, procainamide,
amiodarone, sotalol
- tricyclic antidepressants
- some antibiotics like erythromycin and some fluoroquinolones
Some electrolyte abnormalities like hypocalcemia, hypomagnesemia, and
hypokalemia. Other conditions are intracranial hemorrhage (ICH), myocarditis,
myocardial ischemia, hypothermia, myxedema, starvation, and severe bradycardias
(like complete heart block). There are known inherited conditions that include

34
prolonged QT interval as part of the syndrome like Romano-Ward syndrome, and
Jervell and Lange-Nelson syndrome.

Check the waves and segments morphology

WAVES & ABNORMAL

NORMAL MORPHOLOGY
SEGMENTS MORPHOLOGY

duration amplitude POSSIBLE CAUSES

<2.5 mm (2 1/2 small May indicate atrial enlargement

boxes) in limb leads
- tall, peaked in lead II and tall
0.08 - 0.12 sec positive in V1: right atrial
P wave (< 3 small biphasic wave in V1 enlargement

squares) with <1.5mm positive

- notched in lead II and deep
deflection then <1 mm negative deflection in V1: left
negative deflection atrial enlargement

depression from baseline may be

PR segment isoelectric seen in pericarditis

- prolonged and widened QRS

duration: intraventricular
conduction delay and bundle
less than 0.12 branch blocks
QRS sec (< 3 small variable
- ventricular hypertrophies
squares)
- deep Q waves may indicate old
infarcted myocardium

- slight elevation (<1mm): early

repolarization pattern

ST segment - elevation from baseline: acute

isoelectric
(J point) myocardial injury

- depression > 1.5mm: myocardial

ischemia

- deeply inverted: myocardial

ischemia, ventricular
upright (except in aVR and V1), rounded hypertrophies, stroke, WPW,
T wave
and smooth myocarditis

- Tall and tented: hyperkalemia

35
U waves

The T wave may be followed by a low amplitude wave known

as the U wave. This is very small, usually 0.1 mv (less than 1
small square) with the same polarity as the preceding T wave. It
is most likely to be seen in V1 and V2 and most often is seen in
slow heart rates. Its origin is still uncertain but is though to be
caused by the late repolarization of the Purkinje fibers.

Prominent U waves can be seen in hypokalemia, hypothermia, bradyarrhythmias, and

some cardiac drugs like digoxin and amiodarone.

Q waves

The Q wave is the initial negative wave that precedes the R wave of the QRS. It has a
negative polarity and may be deep or small. However, the Q wave is not always present.
And sometimes, the presence of Q waves can be pathologic or abnormal.

It is normal to see small Q waves in most leads. Deeper Q waves, > 2mm or 2 small boxes,
may be seen in leads III and aVR as a normal variant. Q waves are not seen in the right
sided leads (V1 to V3) under normal circumstances. The loss of small Q waves in lead V5
and V6 should be considered abnormal and this is most commonly due to left bundle
branch block.
normal Q wave

Q waves are considered pathologic or abnormal if they are:

- > 0.40 sec or (1 small box) wide

- > 2 mm (2 small boxes) deep OR

- > 25% of the depth of the QRS complex

- seen in leads V1-V3

normal Q wave abnormal Q wave

36
Possible conditions associated with pathologic Q waves are myocardial infarction,
cardiomyopathic conditions, extreme clockwise or counter-clockwise rotation of the heart,
or lead placement errors like the upper and lower limb leads are reversed.

Note the deep Q waves in leads V1 to

V4. This is part of the ECG of a
patient who had recent anteroseptal
myocardial infarction. There are still
small initial negative deflection in V5
and V6 which are considered normal
Q waves.

The red arrows show the abnormal or pathologic Q waves. Note that they are deep, >
2mm, and appear on the leads that localizes on the lateral wall of the myocardium. This
ECG is from a patient with an old lateral wall wall infarction.

37
Things to check when analyzing the waves and segments:

☐ Are P waves present?

☐ Do the P waves have a normal configuration?
☐ Do all the P waves have a similar size and shape?
☐ Is there one P wave for every QRS complex?
☐ Does the PR interval duration fall within the normal range?
☐ Is the PR interval constant?
☐ Are all QRS complexes the same size and configuration?
☐ Does the duration of the QRS complex fall within normal limits?
☐ Does a QRS complex appear after every P wave?
☐ Are there any pathologic Q waves?
☐ Are T waves present?
☐ Do all T waves have a normal shape?
☐ Do all T waves have a normal amplitude?
☐ Are the ST segments within the isoelectric baseline?

Evaluate other components

Note the presence of escape beats or other abnormalities.

8 steps in interpreting the ECG

First, note the origin of the rhythm. For example, sinus rhythm

Secondly, note the rate: normal if the heart rate is 60-100 bpm), bradycardia (less
than 60 bpm), or tachycardic ( more than 100 bpm)

Thirdly, note the axis; if its normal, or if there is left or right axis deviation

Fourthly, measure the intervals

Fifth, check the waves and segments

Sixth, note if there is presence of any cardiac chamber abnormality

Seventh, if there is ischemia and infarction. Don’t forget to localize the area of the
myocardium that is affected.

Lastly, check for other abnormalities.

38
References:

1. Guidelines for recording a standard 12-lead electrocardiogram. British

Cardiovascular Society. https://www.bcs.com/documents/consensus_guidelines.pdf

2. Harrigan, et al. Electrocardiographic Electrode Misplacement, Misconnection, and

Artifact. Journal of Emergency Medicine. 2012; 43(6):1038-1044.

2. Barold, SS. Willem Einthoven and the birth of clinical electrocardiography a

hundred years ago. Cardiology Electrophysiology Review. 2003 January; 7(1)
99-104 http://www.ncbi.nlm.nih.gov/pubmed/12766530

3. Hurst’s The Heart Manual of Cardiology. 12th edition.

4. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 10th edition.

5. Wagner GS, Macfarlane P, Wellens H, Josephson M, Gorgels A, Mirvis DM, Pahlm

O, Surawicz B, Kligfield P, Childers R, Gettes LS. AHA/ACCF/HRS
recommendations for the standardization and interpretation of the
electrocardiogram: part III: intraventricular conduction disturbances: 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. Circulation. 2009;119

39
 Section 6

Let’s practice...

1. Indicate which electrode lead must be placed on the specific parts of the limbs and
torso for recording a standard 12 lead ECG.

V1 V2 V3 V4 V5 V6

2. The surface ECG is a graphical representation of the heart’s entire cardiac cycle: TRUE
or FALSE?

3. What is the primary pacemaker of the heart? ______________________________

4. Give at least 3 indications for recording an ECG: 1. ________________________

2.___________________________________________
3.___________________________________________

40
5. The following are examples of wrong ECG recordings. Can you identify the mistake or
problem of the recording?

_______________________________________

___________________________

___________________________

____________________________________________________________

41
6. Match the waveforms, segment, or interval on the left with the corresponding event of
the cardiac cycle on the right.

WAVEFORM, SEGMENT or INTERVAL CARDIAC CYCLE

ventricular depolarization and

P wave
repolarization

PR interval atrial depolarization

interval of electrical current from the

QRS complex atria to the ventricles; at the AV
junction

QT interval ventricular depolarization

7. Identify the normal duration of the corresponding waveform, segment or interval.

QRS complex: ________________ sec

QT interval: __________

PR interval: ______________________ sec

8. What is the formula for the corrected QT interval?

corrected QT interval= _____________________________

42
9. Interpret the 12 lead ECG tracing:

Rhythm: PR interval: ______ computed QT Impression:

_____________ sec interval:______sec normal ECG
abnormal ECG
Rate: normal normal
________________ abnormal abnormal

QRS complex: ____ do the waveforms

Axis:
sec and complexes all
normal
normal look normal?
left axis deviation
right axis deviation abnormal normal
abnormal

43
10. Interpret the 12 lead ECG tracing:

Rhythm: PR interval: ______ computed QT Impression:

_____________ sec interval:______sec normal ECG
abnormal ECG
Rate: normal normal
________________ abnormal abnormal

QRS complex: ____ do the waveforms

Axis:
sec and complexes all
normal
normal look normal?
left axis deviation
right axis deviation abnormal normal
abnormal

44
12. Interpret the 12 lead ECG

What is the axis? ________º

normal

deviated to the left

deviated to the right

Rhythm: PR interval: ______ computed QT Impression:

_____________ sec interval:______sec normal ECG
abnormal ECG
Rate: _______ bpm normal normal
abnormal abnormal

QRS complex: ____ do the waveforms

sec and complexes all
normal look normal?
abnormal normal
abnormal

45
 13. Interpret the rhythm strip in the cardiac monitor:

Rate: _______ bpm ★ are all the P waves wide? (narrow QRS
followed by a QRS approximates < 0.12
Rhythm? complex? sec): ____________
★ are there P waves? [] yes [] no Impression:
[] yes [] no ★is the R-R interval normal sinus rhythm
regular? abnormal
★ is the P-P interval
regular? [] yes [] no

[] yes [] no ★ are the QRS

complexes narrow or

14. Interpret the rhythm strip:

Rate: _______ bpm

Rhythm?

★ are there P waves?

★ is the P-P interval regular? [] yes [] no
★ are all the P waves followed by a QRS
complex? [] yes [] no
★is the R-R interval regular? [] yes [] no
★ are the QRS complexes narrow or
wide?

IMPRESSION: ____________________

46
15. Interpret the 12 lead ECG:

Rhythm: PR interval: ______ computed QT Impression:

_____________ sec interval:______sec normal ECG
abnormal ECG
Rate: _______ bpm normal normal
abnormal abnormal

QRS complex: ____ do the waveforms

sec and complexes all
normal look normal?
abnormal normal
abnormal

47
 Chapter 2
Abnormal ECG
I. Intraventricular Conduction Delays and Blocks

I. FASCICULAR BLOCKS

I. LEFT ANTERIOR FASCICULAR BLOCK

II.LEFT POSTERIOR FASCICULAR BLOCK

II.BUNDLE BRANCH BLOCKS

I. RIGHT BUNDLE BRANCH BLOCK

II.LEFT BUNDLE BRANCH BLOCK

II. Chamber Enlargement and Hypertrophy

I. ATRIAL ABNORMALITY

I. LEFT ATRIAL ABNORMALITY

II.RIGHT ATRIAL ENLARGEMENT

II.VENTRICULAR HYPERTROPHY

I. LEFT VENTRICULAR HYPERTROPHY

II.RIGHT VENTRICULAR HYPERTROPHY

III. Myocardial Ischemia and Infarction

I. ACUTE MYOCARDIAL INJURY (INFARCTION) PATTERN

II.MYOCARDIAL ISCHEMIA

48
 Section 1

Intraventricular Conduction Disturbances

atria Intraventricular conduction disturbances refers to
abnormalities in the intraventricular current that
will form the shape and/ or the duration of the
QRS complex. These changes may be
permanent in the ECG or may be intermittent that
AV will manifest only during episodes of tachycardia
node or bradycardia. It can be due to structural
abnormalities in the His Purkinje conduction
system or in the ventricular myocardium. These
abnormalities may be due to necrosis, fibrosis,
His calcification, infiltrative lesions, or impaired
Bundle vascular supply, or they may be functional like a
supraventricular impulse arriving during the
relative refractory period (aberrant ventricular
conduction) or an abnormal conduction that
RBB LBB bypasses the AV node resulting in pre-excitation.

Intraventricular Conduction disturbances or

blocks occur in the conduction system of the
heart. We know that there are two main bundles
of conducting fibers wherein the electrical signals
LPF
LAF flow through the ventricles - the right bundle and
the left bundle branches. The left bundle has two
branches - the anterior fascicle and the posterior
fascicle.

Intraventricular Conduction Abnormalities are:

ventricle
- Right bundle branch block (RBBB)

- Left bundle branch block (LBBB)

- Anterior Hemi-block or anterior fascicular block

- posterior hemi-block or posterior fascicular block

- Bifascicular block (RBBB and left anterior hemi

block)

49
 Fascicular Blocks
A SHORT REVIEW ...
Disturbance in the conduction in one fascicle
NORMAL QRS DURATION of the left bundle (fascicular block) results in
The QRS duration depends in the method of
the abnormal sequence of the left ventricular
measurement, age and gender. QRS duration should activation leading to characteristic ECG
be measured from the onset to the last point of patterns. The delay in the conduction may be
offset of the complex. (See blue line in the figure on
absolute or relative but even a slight delay
the left).
may be enough to cause an alteration in the
Several considerations must be taken into account ventricular activation and produce ECG
when measuring the QRS complexes:
changes.
1. QRS durations may increase with increasing
heart size. Left Anterior Fascicular Block
(LAFB)
2. QRS complexes are wider in the precordial than
in the limb leads.
Normally, the left anterior fascicle activates
3. In children less than 4 years old, QRS complex the uppermost portion of the septum, the
should be less than 90 msec. Those 4 to 16
antero-superior portion of the left ventricle,
years old, a QRS complex of 100 msec or more
is considered prolonged.In adult males, the and the left anterior papillary muscle during
normal QRS complex may be up to 110 msec. the early part of the QRS complex. In LAFB,
these regions are activated later than usual;
The current AHA recommendation states that a QRS
complex duration of greater than 110 msec in the inferior and posterior become activated
subjects older than 16 years of age is regarded as earlier and the antero superior forces are later
abnormal. The mean frontal axis recommendation is during the QRS complex. The unbalanced
described in the table below:
activation causes the ECG changes of LAFB
with the most characteristic finding is marked
QRS
Axis
left axis deviation.
Age Abnormal 1.frontal plane QRS axis: -45 to -90 degrees
Normal Description
Values
Values 2.small Q in lead I and aVL, small R in II, III
and aVF
-30º to left axis
Adult < -30º 3.normal QRS duration
90º deviation

moderate left 4.late intrinsicoid defection R wave in aVL >

-30º to 0.045 sec
axis
-45º
deviation 5. increased QRS voltage in the limb leads
marked left LAFB also produce prominent changes in the
-45º to
axis precordial leads. Leads V4 through V6 will
-90º
deviation show deep S waves. In some cases, a small q
wave may appear in the right precordial leads.
The overall QRS duration is not prolonged.
Fascicular block alters the sequence but NOT
the duration.

50
 I aVR

II aVL

aVF
III

LAFB is the most common cause of left axis deviation but it is not the same. Extreme left
axis deviation (-45 to -90 degrees) reflect other conditions like left ventricular hypertrophy
(LVH) even without damage to the conduction system.

LAFB is common because the structure of the fascicle is delicate. However, this ECG
pattern is also common even in persons without overt cardiac disease and in a variety of
cardiac conditions.

LAFB can hide or mimic ECG changes from other conditions. The rS pattern in leads II, III
and aVF in LAFB can hide the Q wave in inferior wall infarction. The larger R waves in
leads I and aVL but small R with deep S waves in leads V5 and V6 also make LVH criteria
relying on R wave voltage difficult.

Example:

51
Left Posterior Fascicular Block (LPFB)

LPFB is less common. The left posterior fascicle is less prone to damage because of its
thicker structure and its location (near the left ventricular out flow tract. Damage that
causes conduction delay in this tract will have an opposite effect that of the LAFB - early
unopposed activation of the antero superior left ventricle followed by the late activation of
the inferoposterior left ventricle. This marked ECG characteristic pattern in LPFB is right
axis deviation.

1.Frontal plane between 90 and 180

degrees in adults.

2.rS pattern in leads I and aVL

3.qR pattern in leads III and aVF

4.QRS duration less than 120 msec.

5.exclusion of other factors causing right

axis deviation (like right ventricular
hypertrophy, lateral wall infarction).

I aVR

II
aVL

III aVF

52
Bundle Branch block

Bundle branch block occurs when a delay or a block happens along the specialized
conduction fibers in the bundle branches of the heart's right or left ventricle. The delay can
occur in a part or the entire branch of the pathway where the electrical signals flow.

A bundle branch block can sometimes alter the heart's ability to pump effectively.

Bundle branch blocks are not treated specifically. But the underlying cause of the bundle
brach block, e.g. Coronary heart disease, will need to be treated.

Right Bundle Branch Block (RBBB)

RBBB is caused by a conduction delay in any portion of the right intraventricular

conduction system. The block is most common in the main right bundle branch or in ints
distal branches.

MECHANISM OF THE ECG COMMON DIAGNOSTIC CRITERIA FOR

ABNORMALITIES (nice to know): COMPLETE RIGHT BUNDLE BRANCH BLOCK

The delay or block in the right 1. QRS duration of more than or equal to 120
bundle branch system will cause a sec
delay and slowed activation of the
right ventricle. The activation of 2. rsr', rRs', or RSR' patterns in leads V1 and V2
the RV will happen after the
depolarization of the septum and 3. S waves in leads I and V6 are > 40 sec wide
the left ventricle occurred. The LV (wide, slurred S waves in the lateral leads - I,
is activated normally so the initial aVL, V5-V6)
QRS remains unchanged. The
4. Normal time to peak R wave in leads V5 and
delayed RV activation produces a
V6 but > 50 sec in V1
secondary R wave (r' or R') in
leads V1-V3 and a slurred S wave
in lead I and V6. The delayed
activation of the RV also causes
the prolongation of the QRS
complexes and secondary
depolarization abnormalities like
ST -T wave inversion in the
precordial leads.

53
RBBB is a common ECG finding in the general population. Many persons will have an
ECG finding of RBBB and have no clinical evidence of structural heart disease. These
patients do not have an associated increased risk of mortality or morbidity. On the other
hand, patients with heart disease the coexistence of RBBB suggests advanced disease.

Example of CRBBB:
rsR' pattern

Slurred S wave

Left Bundle Branch Block (LBBB)

A conduction delay or block in any of the parts of the intraventriclular conduction system,
including the main left bundle brach, each of the two major fascicles (anterior and
posterior), distal conduction of the LV, and the fibers if the His bundle that become the
main left bundle brach, or in the ventricular myocardium, will result in LBBB.

MECHANISM OF ECG ABNORMALITIES IN COMPLETE LEFT BUNDLE CRITERIA FOR COMPLETE

BRANCH BLOCK
LEFT BUNDLE BRANCH
LBBB causes diffuse alteration in the activation and recovery of the left BLOCK
ventricle resulting in widened QRS complex and ST-T wave changes.

In LBBB, the spread of septal depolarization is reversed (becoming right 1. QRS duration of > 120 sec
to left), the impulse then spreads from the RV via the right bundle branch
then to the LV via the septum. This causes prolongation of activation to 2. Dominant S wave in V1
more than 120 sec and removes the normal septal Q waves in the lateral
leads. The overall direction of depolarization (R --> L) will produce tall R
waves in the lateral leads (I, V5-V6) and deep S waves in the right 3. Absence of Q waves in the
precordial leads (v1-V3), and usually with left axis deviation. lateral leads
The altered activation of the ventricles to sequential (rather than
simultaneously) causes the formation of a broad or notched (M) R wave 4. Prolonged R wave peak
in the lateral leads time > 6m0sec in V5-V6

54
LBBB occurs in 1% of the general population. LBBB occurs in more than 1/3 of patients
with heart failure and as many as 70% of persons with LBBB have ECG evidence of LVH
before. However, approximately 10% of people with LBBB have no clinical evidence of
heart disease.

! in persons with LBBB, with or without overt heart disease, LBBB is associated with
higher-than normal risk for mortality or morbidity from myocardial infarction, heart failure,
and arrhythmias including high grade AV block. In patients with CAD, the presence of
LBBB is associated with severe multi-vessel disease, more severe left ventricular
dysfunction, and reduced survival rates.

Example of CLBBB:
Deep S in V1 - V3

Wide, notched R wave in V5 and V6

55
Practice ECG: Name or specify the intraventricular conduction abnormality in the following
ECGs:

1.________________________________________

2. _____________________________________

1. Complete Right Bundle Branch Block 2. Complete Left Bundle Branch Block

Answer:

56
 Section 2

Chamber Hypertrophy

The ECG is a valuable traditional tool in the identification of cardiac chamber enlargement
or hypertrophy. Even with the advancement in imaging technologies in cardiology, the ECG
remains to be key instrument in identifying structural abnormalities in the heart and
provides a simple screening tool, up to this day, for clinical and prognostic data.

Atrial Enlargement

Atrial depolarization is represented in the 12

lead ECG by the P wave. Any abnormality in
any of the two atria will, therefore, manifest in
the shape and size of the P wave.

Electrical impulse of the heart

starts in the sinus node moving across the
atria to depolarize these chambers. In the
surface ECG, the P wave reflects the
depolarization of the two atrial chambers.
Since the sinus node is located at the
superior and lateral portion of the right
atrium, the initial deflection of the P wave
reflects the activation of the right atrium,
while the terminal end will reflect the left
atrium. The atrial muscles are relatively thin (compared to the ventricular muscle mass) so
that the voltage of the P wave in the ECG is also small, usually 0.1-0.2 mV or 1-2 small
squares.

The term "atrial abnormality" may be used instead of "atrial enlargement" because the
latter term suggests a particular underlying pathophysiology.

57
Right Atrial Abnormality

Right atrial abnormality is typically manifested in the ECG as an abnormal increase in the
height of the P wave in the limb and right precordial leads. A tall upright P wave in lead II
of > 2.5 mm or two and a half small squares, is characteristic of right atrial enlargement.
The appearance of a more upright or more positive P wave in leads V1 or V2 also suggest
right atrial enlargement.

Criteria:

LA 1.Peaked P waves with amplitudes in lead

II > 0.25 mV ("P pulmonale")

RA 2.Prominent initial positivity in lead V1 or

V2 > 0.15 mV (more than one and a half
small square

3. Widened initial positive deflection of

the P wave in lead V1

4.Rightward shift of mean P wave axis to

more than +75 degrees

V2
V1 The presence of P pulmonale in the ECG of
patients with chronic obstructive pulmonary
Normal Right Left disease are associated with more severe
pulmonary dysfunction, with significantly
reduced survival.
RA LA

II
Left Atrial Abnormality

Increase in left atrial mass or chamber size

will cause an increase in the P wave height
RA LA
and duration. Because the left atrium is
V1 located posterior of the chest and the
activation occurs after the right atrium,
changes in the normal structure of the left
atrium will manifest in the latter half of the P
wave. Structural abnormalities that can alter

58
the P waves include atrial dilation,
atrial muscle hypertrophy, and
elevated intra-atrial pressures.

These anatomical and

physiologic changes will manifest
in the ECG as prolonged P wave
duration, notching of the P wave
in the inferior leads (lead II), and Biatrial Abnormality
increased amplitude of the terminal P
wave in V1. Patients with abnormalities in both atria
can have ECG changes that manifest each
Criteria:
abnormality. Suggestive findings include
1. Prolonged P wave duration to > 120 large biphasic P waves in lead V1, and tall
msec in lead II broad P wave in leads II, III and aVF.

2. Prominent notching of P wave, usually Ventricular Hypertrophy

most obvious in lead II, with the interval
Main ECG changes associated with
between notches of >0.40 msec or 1
ventricular hypertrophy are increases in
small square ("P mitrale")
QRS height and duration, changes in the
3. Ratio between the duration of the P QRS vectors, abnormalities in the ST
wave in lead II and duration of the PR segment and T waves, and abnormalities
segment is > 1.6 in the P waves.

4. Increased duration and depth of Right Ventricular Hypertrophy

terminal negative P wave in V1 (P (RVH)
terminal force) so that area subtended
by it > 0.04 mm-sec Because of the larger muscle mass of the
bigger left ventricle, ECG changes is often
5. Leftward shift of mean P wave axis to seen with moderate to severe concentric
between -30 and -45 degrees RVH. Common ECG findings include
abnormal, tall R waves in the anterior and
The presence of left atrial abnormality in
right- directed leads such as aVR, V1 and
the ECG are associated with more severe
V2, and deep S waves and abnormally
left ventricular dysfunction in patients with
small r waves in the leftward-directed
ischemic heart disease and with more
leads (I, aVL, and lateral precordial leads).
severe valve damage in patients with mitral
These changes will alter the normal
or aortic disease. Current evidence have
progression of the R wave in the precordial
shown that patients with left atrial
leads, shift the frontal plane QRS to the
abnormalities have higher risk to develop
right and the presence of S waves in leads
atrial tachyarrhythmias, including atrial
I, II, and III (S1S2S3 pattern).
fibrillation.

59
If the RVH is not as marked, the ECG changes may be subtle or limited to rSr' pattern in
V1 and persistence of s (or S) waves in the left precordial leads. This pattern is typical off
right ventricular overload like that in atrial septal defect.

Common Diagnostic Criteria for RVH:

1. R in V1 > 0.7mV (7 small squares)

2. QR in V1

3. R/S in V1 with R > 0.5 mV

4. R/S in V5 or V6 <1

5. S in V5 or V6 . 0.7 mV

6. R in V5 or V6 > 0.4 mV with S in V1 < 0.2

mV

7. Right axis deviation (>90 degrees)

8. S1Q3 pattern
V1 V2
9. S1S2S3 pattern

10.P pulmonale

Left Ventricular Hypertrophy

(LVH)

The most characteristic finding of LVH in

the ECG is increased amplitude of the
QRS complex. The R waves in the leftward
leads (I, aVL, V5 and V6) are taller than
normal, and the S waves on the opposite
side are deeper than normal. There are
other QRS changes in LVH like widening of V6
the QRS complex > 11msec, delayed V5
intrinsicoid deflection (the ventricular
activation time), and notching of the QRS V1 V2
complex and evidence of left atrial
abnormality. The ST -T waves patterns
vary in patients with LVH. The most typical
There are many sets of diagnostic criteria
is a downward ST sloping with the J point
currently available. Only the most common
depressed and the T wave asymmetrically
criteria are listed below.
inverted.

60
Measurement CRITERIA

Sv1 + Rv5 > 3.5 mV

Sokolow-Lyon voltages
RaVL > 1.1 mV
✴ Any limb lead R wave or S wave > 2.0
mV (3 points)

✴ or SV1 or SV2 > 3.0 mV (3points)

✴ or RV5 to RV6 > 3.0 mV (3 points)

✴ ST-T wave abnormality, no digitalis

Romhilt-Estes point score system
therapy (3 points)
= probable LVH is diagnosed with total of 4
✴ ST-T wave abnormality, on digitalis
points
therapy (1 point)
= definite LVH is diagnosed with 5 or more
✴ Left atrial abnormality (3 points)
points
✴ Left axis deviation >-30 degrees (2
points)

✴ QRS duration > 90 msec (1 point)

✴ Intrinsicoid deflection in V5 or V6 >50

msec (1 point)
SV3 + RaVL > 2.8 mV (for men)
Cornell voltage criteria
Sv3 + RaVL > 2.0 mv (for women)

The presence of LVH in the ECG of a patient with hypertension is associated with
significant increased risk for cardiovascular morbidity and mortality. Also, hypertensive
patients with additional repolarization (ST-T wave abnormalities) have more severe degrees
of structural LVH, and a greater risk for future cardiovascular events.

An accurate diagnosis of LVH is important to identify ventricular hypertrophy, assess

prognosis and monitor progression or regression of hypertrophy during treatment.

61
Practice ECGs:

Right Atrial abnormality

Tall or peaked P wave in lead II, III

and aVF

Positive P wave in lead V1 and V2

Left Atrial Abnormality

Notched with prominent terminal P wave

in lead II

Deep and wide terminal P wave in lead V1

62
Right Ventricular Hypertrophy

Right axis
deviation

Tall and
wide R wave
in V1 and V2

Deep S
wave in the
leftward leads
- I, AVL,
V5-V6

Left Ventricular Hypertrophy

R in lead I + S in lead III >25 mm

S in V1 + R in V5 >35 mm

ST-Ts in left leads

R in aVL >11 mm

Left axis deviation > -30 degrees

63
Practice on your own. Identify the hypertrophied chambers in the following ECGs:

1. _________________________________________________

2. _________________________________________________________________

64
 65
Answers: 1. Sinus rhythm, normal axis, Probable LVH 2. Sinus rhythm, right atrial enlargement, probable RVH; 3. Sinus rhythm, left axis
deviation, LVH with strain pattern 4. Sinus rhythm, first degree AV block, left axis deviation, left atrial abnormality.
4. ___________________________________________________
3. ____________________________________________________________
66
 Section 3

Myocardial Ischemia & Infarction

Even in this era of modern and high technology in medicine, the ECG remains to be one of
the most important tools in the diagnosis of myocardial ischemia and infarction. In fact, the
ECG persists to be a critical tool in the diagnosis and management of acute coronary
syndrome. Therapeutic decision in this life-threatening condition rely on distinguishing
between ST-segment elevation myocardial infarction (or ischemia) (STEMI) and non-STEMI
(or ischemia).

ECG findings of ischemia and infarction differ depending on four major factors:

1. Duration of the ischemic process (if acute, evolving or chronic)

2. Extent of injury (size of infarct and if the injury is transmural or subendocardial)

3. Topography or area of injury

4. Presence of underlying abnormalities that may alter characteristic features of ischemia

and infarction in the ECG. Examples are presence of left bundle branch blocks,
Wolff-Parkinson-White Syndrome, or pacemaker patterns.

The Coronary Arteries and Veins The heart's blood supply comes from the
aorta thru an opening near the aortic root,
The heart, like any organ in the body, the coronary ostium. During ventricular
needs adequate supply of blood in able to contraction, while the aortic valve is open,
survive and function normally. The the coronary osmium is partially covered
coronary arteries supply the heart muscle by an aortic cusp. When the aortic valve
with blood and oxygen. Understanding closes during ventricular relaxation, the
coronary blood flow is important in the coronary ostium opens, enabling it to fill
diagnosis and care of patients with the coronary artery with blood.
o n g o i n g m y o c a rd i a l i n f a rc t i o n ( o r
ischemia). The ECG of the patient with From the aorta, the two major (left main
ongoing acute coronary syndrome (ACS) and right coronary arteries) branch off
or blockage of the coronary artery will aid from a single branch called the Sinus of
in determining the temporality (timing - if Valsalva.
acute or ongoing), extent of heart muscle
injury, and localization of the site of
myocardial infarction.

67
Sudden reduction or obstruction of the blood supply to the heart's muscles will cause a
series of events that will lead to myocardial injury (ischemia) and ultimately (if not treated in
the appropriate period of time) to myocardial infarction (MI) or muscle cell death. The
rupture of an atherosclerotic plaque followed by clot formation within the coronary lumen
causes acute coronary syndrome
(ACS).

The ECG will show changes that

reflect the sequence of events of this
critical condition. Also, the ECG will
Left main
LCx reflect the severity of the MI that will
RCA be invaluable in the diagnosis and
LAD treatment decisions. Sudden complete
occlusion of the lumen of a coronary
RA LV will show characteristic ST elevation
on the leads that represent the are of
the heart that it subserves. On the
RV other hand, if there is only partial
occlusion of the coronary, the ECG will
show no ST elevation.

The right coronary atrium and will usually that help supply blood to
artery (RCA) supplies branch into two - the left both ventricles.
blood to the right atrium anterior descending (LAD)
the right ventricle, and part and the left circumflex The left circumflex artery
of the inferior and (LxC) arteries. The LAD will circles around the LV to
posterior surfaces of the run down the anterior give our blood supply to
left ventricle. In about 60% surface of the LV towards the lateral portion of the
of the population, the RCA the apex supplying blood left atrium, lateral wall of
will supply blood to the to the anterior wall of the the LV, and the posterior
sion-atria (SA) and LV, the interventricular fascicle of the left bundle
atrioventricular (AV) nodes, septum, the right bundle branch.
including the bundle of branch, and the anterior
His. fascicle of the left bundle
branches. Along down the
The left main LAD are septal perforators
coronary artery runs along and diagonal branches
the surface of the left

68
St segment ELEVATION and myocardial ischemia/ infarction

The earliest and most consistent finding during

acute severe ischemia (reduced or inadequate
blood flow) is deviation of the ST segment.
Normally the ST segment is isoelectric because
Coronary all healthy myocardial cell attain approximately
artery the same electrical potential during the initial
lumen phases of repolarization which corresponds to

STEMI

the ST segment in the ECG. It is

proposed that the ST segment
deviations during acute ischemia are
produced by the differences in voltage
between ischemic and non-ischemic
cardiac muscle cells during the
repolarization phase.

In the ECG, transmural (meaning entire

myocardial layer) injury will show ST
elevation on the positive lead(s) over
Subendocardial Injury: ST Depression
the area of injury. On the contrary, if
the injury is limited in the
subendocardial layer or
non-transmural, the flow of current is
towards the subendocardium. This will
manifest in the ECG as ST depression
because the flow of current is away
from the positive lead(s) over the area
of the heart.

ST segment changes can happen in

those with stable angina and may be
precipitated by treadmill or bicycle exercise testing, or any form of stress. ST depression
can also occur in unstable angina - symptoms even at rest, and is associated with severe
multi-vessel or left main coronary artery disease.

69
 ST elevation in the ECG is any upward deviation of the ST
V6
segment from the baseline or isoelectric line. It is usual to see
some ST elevation of 1 mm (or 1 small box) in leads V1-V3.
Significant J-point or ST elevation (especially in the setting of
ACS) is defined as >1 mm elevation in the limb leads and >
2mm rise in the precordial leads. The current recommendation
are listed in the box below. The ST elevation usually distorts
the shape of the T wave. In the initial minutes to hours of an
acute injury, the T waves are tall and peaked, called the hyper
acute T waves. The T wave appears to be incorporated within
> 2 mm or 2 small boxes in
the ST elevation. There will also be reciprocal changes in the
upward deviation in the
precordial leads leads opposite the area of acute injury. This will manifest as
deep ST depressions.

After several hours to days of

persistent myocardial injury,
the T waves start to become
inverted and the Q wave
develops. This is the
pathologic Q wave, meaning
they are significant and are
associated with infarcted
myocardium.

Q waves are considered

pathologic if it is wider than
40 msec or deeper than a
third of the height of the
entire QRS complex.

AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the

ECG 2009: Recommendations for threshold in ST elevation:
1. for males aged > 40 yrs, abnormal J point elevation should be 0.2 mV (2mm) in
leads V2 and V3, and 0.1 mV (1mm) in all other leads
2. for males aged < 40 yrs, abnormal J point elevation should be 0.25 mV (2.5
mm) in leads V2 and V3, and 0.1 mV (1mm) in all other leads
3. For females, abnormal J point elevation is 0.15 mV (1.5 mm) in leads V2 and
V3, and 0.1 mV (1mm) in all other leads

70
This ECG is from a man suffering from acute myocardial infarction. Note the ST elevation
with peaked T waves circled and the reciprocal changes with ST depression noted by the
arrows.

The magnitude and extent of the ECG changes depend on the size and location of the
ischemic or infarcted depend on the coronary artery involved, the site of occlusion within
the artery, and the presence or absence of collateral circulation. Studies have shown that
localization of the culprit artery thru ECG have similar findings with coronary angiography.
ECG is capable of providing a more accurate correlation of the waveform changes to the
involved vessel and to the site of occlusion within the vessel.

The positions of the 12 leads of the ECG refer to anatomic locations on the body surface
that determines the positive pole of the
lead.

71
So that in the 12 lead ECG, the heart will look like this:

In ST elevation MI, the upward deviation of the ST segment typically results from the acute
occlusion in leads whose positive poles are located over the injured region and with
reciprocal ST depression in leads whose positive poles are oriented in the opposite
direction.

This ECG shows ST elevation in leads I, aVL, V1-V6. This reflects acute infarction in the
anterolateral walls of the LV. Note the reciprocal ST depression in leads II, III and aVF
which describes the inferior LV whose positive leads are opposite the anterolateral region
of the heart.

72
This ECG shows ST elevation in leads II, III and aVF. This signify acute inferior wall
infarction. The reciprocal ST segment depression is seen in lead I and aVL.

An important thing to remember is that ST elevation of the inferior wall may extend to the
the right ventricle (RV). Getting the right sided chest leads (V4R, V5R and V6R - placed on
specified locations on the right anterior chest) is very important to determine RV
involvement.

The current AHA/ACC recommendation states that right sided chest leads V3R and V4R
be recorded in all patients presenting with ECG evidence of acute inferior wall ischemia or
infarction. For male and females, the threshold for abnormal J-point elevation in V3R and

73
V4R should be 0.05 mV (0.5mm) except for males less than 30 years wherein 0.1 mV or
1mm is more Appropriate in the diagnosis of acute RV infarction.

Determine the regions involved in the acute injury as described by this ECG.
Is there RV involvement?

Diagnosis of myocardial infarction in certain underlying conditions

STEMI is more difficult to diagnose if the baseline ECG shows a bundle branch block
pattern or when a patient has pacemaker rhythm (wherein the ECG will show a similar
pattern to a CLBBB).

RIGHT BUNDLE BRANCH BLOCKS

In right bundle branch block (RBBB), the criteria for ST elevation MI diagnosis is the same
as those with normal conduction.

This ECG shows complete RBBB in the setting of acute MI. There is ST elevation in leads I, aVL and V1-V6 with
reciprocal ST depression in II, III and aVF.. The wall affected with acute injury is the anterolateral wall.

74
LEFT BUNDLE BRANCH BLOCK OR PACEMAKER RHYTHM

The diagnosis of MI is more confusing in left bundle branch block (LBBB) because this
conduction abnormality alters the early and late phases of ventricular repolarization (ST
segment and T wave) and produces ST-T changes that will look like a STEMI.

If the LBBB is presumed to be new, meaning the patient had a normal conduction or
different conduction defect before the event, this is considered to be an equivalent of a
STEMI. However, more often than not, most cases of LBBB are "not known to be old
LBBB" because old ECGs are not available for comparison.

Because of this difficulty, a diagnostic criteria has been proposed to diagnose STEMI in
patients with LBBB or if with pacemaker rhythm in their ECG. The 2013 ACC/AHA STEMI
guidelines has recommended the Sgarbossa criteria for this.

Sgarbossa Criteria

CRITERION SCORES

ST elevation > 1 mm &

concordant with QRS 5
complex
ST segment depression >
3 ST elevation ST ST elevation
1 mm in lead V1, V2 or V3
> 1mm with depression >5 mm with
ST elevation > 5 mm &
concordant discordant
discordant with QRS 2
QRS QRS
complex

a score > 3 is more diagnostic (98% specificity) for ischemia in the setting of LBBB

a score of 0 does not rule out STEMI

Example of criteria 1:
concordant ST
elevation of > 1 mm
(5 points)

75
Criteria 2: ST depression in
V1, V2 or V3

Criteria 3: discordant ST elevation > 5 mm

ST T WAVE changes in myocardial ischemia

ECG abnormalities particularly in ST T wave segments can occur in association with

symptoms of angina but without any signs of acute injury or infarction. Myocardial
ischemia can cause STT wave changes without causing any change on the QRS complex.
The characteristic change associated with ischemia are ST segment depression or T wave
inversion. Clinically, these changes are significant because it is associated with risks for
severe angina, MI or death within 12 months from their initial presentation.

However, the presence of changes of the ST segments and T waves are not specific for
ischemia, especially if these ECG findings occur without a clinical history of the patient
and angina. These changes can also occur with other disease process like LVH,
hypokalemia and digoxin therapy.

ST SEGMENT DEPRESSION

Typically, ST segment depression or downward deviation from the baseline is a sign of

myocardial ischemia. ST segment depression is considered significant if there is > 2mm
downward depression and it is widespread, occurring in > 2 leads. The presence of this

76
significant ST depression is associated with grave prognosis and implies extensive
coronary artery disease.

The red arrows indicate significant ST depression. Note that the deviation is deep >
2mm with slow upsloping and is widespread in leads II, III, aVF and I, aVL and V5-V6.

77
T WAVE CHANGES

Myocardial ischemia changes the T wave. But detecting an abnormal T wave may be
confusing. Firstly, there is no set criteria for a normal T wave and T wave changes may not
be appreciated if there is no baseline comparison. Secondly, flattened T waves are often
seen in patients wth myocardial ischemia but this is very non specific. Lastly, T wave
inversion can also occur but this can also be "normal." An inverted can be normally seen
in leads III, aVR, and V1 - V2. However, deep and symmetrically inverted T waves in
contiguous leads will strongly suggest myocardial ischemia.

Note the deep and symmetrical T waves in leads I, aVL, V5- V6 which strongly suggest
myocardial ischemia.

78
Try interpreting the following 12 lead ECG by identifying the myocardial injury present and
its location in the heart.

1. Sinus rhythm, normal axis, ___________________________________________________

interpret the ECG: What is your complete ECG diagnosis?

Rhythm? ______ Rate: ______ bpm
Axis? normal or with left/right axis deviation?
signs of chamber enlargement?
ST segment or T wave deviation? Is the myocardial injury acute or old?

2. __________________________________________________________________________

interpret the ECG:

What is your complete ECG diagnosis?
Rhythm? ______ Rate: ______ bpm
Axis? normal or with left/right axis
deviation?
signs of chamber enlargement?
ST segment or T wave deviation?
Is the myocardial injury acute or old?

3.

79
 _____________________________________________________________________

interpret the ECG: What is your complete ECG diagnosis?

Rhythm? ______ Rate: ______ bpm
Axis? normal or with left/right axis deviation?
signs of chamber enlargement?
ST segment or T wave deviation?

4. _______________________________________________________________________

interpret the ECG: What is your complete ECG diagnosis?

Rhythm? ______ Rate: ______ bpm
Axis? normal or with left/right axis deviation?
signs of chamber enlargement?
ST segment or T wave deviation?

80
 ABNORMAL RHYTHMS
I. BRADYARRHYTHMIAS

• SINUS BRADYCARDIA

• SINUS ARRHYTHMIA

• ESCAPE RHYTHMS

• SINUS PAUSE AND SINUS EXIT BLOCK

• ATRIOVENTRICULAR BLOCKS

• FIRST DEGREE AV BLOCK

• SECOND DEGREE AV BLOCKS

• TYPE I

• TYPE II

• THIRD DEGREE AV BLOCK

• PACEMAKER RHYTHM

• COMMON PACING MODES

• PACING MALFUNCTION

II. SUPRAVENTRICULAR TACHYARRHYTHMIAS

I. SINUS TACHYCARDIA

II.ATRIAL TACHYCARDIAS

I. FOCAL ATRIAL TACHYCARDIA

II.MULTIFOCAL ATRIAL TACHYCARDIA

III.ATRIAL FLUTTER

IV.ATRIAL FIBRILLATION

III. AV NODAL TACHYCARDIA (PAROXYSMAL SUPRAVENTRICULAR

TACHYCARDIA)

III.VENTRICULAR TACHYARRHYTHMIAS

81
 1

Bradyarrhythmias
Bradyarrhythmia is defined as a heart rhythm with a rate below 60 beats per minute.
Frequently, bradyarrhythmias are physiologic like in well-conditioned athletes and during
sleep. However, these can occur in pathologic conditions as well. Disturbances in the
sinus or atrioventricular nodes can produce abnormal slowing of the heart rate and
produce symptoms that will require intervention.

SINUS BRADYCARDIA

Sinus Bradycardia is diagnosed in adults when the heart rate is less than 60 bpm
and the rhythm normally originates from the sinus node. The P waves are normal in
shape and occurs before a QRS complex, and the PR interval is normal and
constant.

Sinus bradycardia (SB) can occur with excessive vagal or decreased sympathetic
tone, effect of a medication, or from anatomic changes in the sinus node. In most
cases, this is a benign arrhythmia and asymptomatic. This is frequently seen in
healthy young adults, particularly well-trained athletes, and decreases in prevalence
with advancing age. SB can also be physiologic like during sleep when the heart
rate falls down to 39 to 40 bpm. It can also occur during vomiting or vasovagal
syncope, or during carotid massage stimulating the vagal baroreceptor.
Administration of parasympathetic drugs (e.g. Lithium, amiodarone, beta-blockers,
clonidine, ivabradine, or calcium channel blockers), medical conditions or
procedures (eye surgery, meningitis, intracranial tumors, increased intracranial
pressure, cervical & mediastinal tumors, severe hypoxia, myxedema, hypothermia,
fibrodegenerative changes, convalescence from some infections, sepsis, or mental
depression), and conjunctival instillation of beta-blockers for glaucoma, especially in
the elderly, can produce sinus bradycardia.

Rhythm strip showing sinus bradycardia. Heart rate is less than 60 beats per minute (40 bpm), normal looking P waves
occurring before a QRS complex , normal PR interval.

82
SINUS ARRHYTHMIA

Sinus Arrhythmia (SA) is characterized by a phasic variation in the cyclic length, with
the variation of cycle do not exceed 0.12 sec or the difference between the shortest
and longest P-P intervals do not exceed 3 small squares. This is the most common
form of arrhythmia and is considered to be a normal variation.

SA typically has two basic forms: respiratory and non respiratory. The respiratory
form, the P-P interval shortens with inspiration and becomes longer with expiration.
The non respiratory form is characterized with phasic variation of the P-P interval not
related to respiration and may be due to inferior wall infarction, advanced age, use of
digoxin or morphine, and conditions involved increased intracranial pressure.

This rhythm strip shows sinus arrhythmia. The rhythm originates from the sinus node as characterized by a normal
looking P wave that occurs before the QRS complex. Note the slightly varied P-P interval that is characteristic of sinus
arrhythmia.

SA occur as the heart's normal response to respirations. The vagal tone increases during
inspiration when there is an increase blood flowing back to the heart (venous return),
increasing the heart rate (shortened P-P interval). While during expiration, there is
decreased venous flow into the heart which lengthens the P-P interval.

SINUS ARREST or SINUS PAUSE

Sinus arrest or sinus pause is a disorder of impulse formation. The sinus node fails
to generate enough electrical impulse to produce any myocardial contraction. In the
ECG this will be a prolonged absence of any PQRST complex of more than 3
seconds.

83
The ECG remains usually normal except for the missing Pacemaker cells are
found at different
complex or pause. The term sinus pause is applied if one or
sites throughout the
two beats are not formed, and sinus arrest if three or more conducting system of
beats are missing. the heart. Each site
has the capability to
Sinus arrest may result from degeneration of the sinus node,
independently sustain
increased vagal tone during Valsalva, medications (digoxin, the heart rhythm and
quinidine, procainamide, and salicylate if given in toxic levels), has an intrinsic firing
heart diseases, and acute inferior wall infarction. rate.

ESCAPE RHYTHMS • Sinus node: 60-100

bpm

Escape rhythms occur when the inherent faster pacemakers • AV node: 40-60 bpm
fail and the latent slower pacemaker take over. Note that
these rhythms are not considered as arrhythmias but as • Ventricular
escape mechanisms. pacemaker: 20-40
bpm
JUNCTIONAL RHYTHM
The predominant
Junctional rhythm is a rhythm that originates from the
pacemaker is the one
atrioventricular (AV) node that occurs when there is a the fires fastest.
prolonged delay in the atrial conduction or the sinus node Under normal
(the higher pacemaker) did not fire. This is the first conditions, the
"back-up" system of the heart to prevent ventricular slower pacemaker is
standstill when the sinus node fails. The intrinsic firing rate suppressed by the
of the AV node is 40 to 60 bpm. more rapid impulses
from a higher
The ECG rhythm strip of a junctional escape will show: pacemaker - that is
- regular rhythm (constant and persisting R-R interval) the sinus rhythm from
- Rate of 40 to 60 bpm the sinus node.
- Inverted P waves in leads II, III and aVF; Junctional &
normal-looking QRS complex, T wave and QT interval ventricular escape
In junctional rhythms, the atrial depolarization rhythms arise when
come after the AV nodal discharge by means of the rate of impulses
retrograde (going back) conduction. Thus, the P from the sinus node
waves are inverted. The conduction to the or atrium arriving at
ventricles remains normal. the AV node is less
than the intrinsic rate
of the ectopic
pacemaker.

The rhythm strip shows a junctional escape rhythm, Note that the rate is
50 bpm with a short PR interval. Note the characteristic inverted P wave.

84
VENTRICULAR ESCAPE RHYTHM

This rhythm, also known as idioventricluar rhythm, is an escape mechanism that occurs
when all the supraventricular (SA node, atrial, AV node) pacemakers fail to generate
impulses to produce a myocardial contraction. The rate is very slow, around 30 bpm, and
the characteristic ECG pattern is a wide QRS, regular bradycardia.

This rhythm strip shows a sinus rhythm that converted to ventricular escape rhythm when the sinus beat failed
to continue regular wide QRS bradycardia with a rate of 42 bpm, typical of a ventricular escape rhythm. There is
no visible P wave.

ATRIOVENTRICULAR BLOCK (HEART BLOCK)

Atrioventricular (AV) block refers to abnormality in the electrical conduction between

the atria and ventricles. The term heart block has also been used. The term degree
is used to indicate the severity of the AV block. First degree is a minor disturbance
describing a delay in conduction, second degree describes a moderate severity -
some impulses fail to conduct to the ventricles, and lastly the most severe, third
degree or complete, when no impulse is conducted at all.

First Degree AV Block

First degree AV Block is defined as a prolongation of AV conduction time (PR

interval) to > 0.20 sec.

In this bradyarrhythmia, the conduction time of the atrial impulse is prolonged but all
the impulses are conducted to the ventricles. The ECG will show a regular rhythm,
with a prolonged PR interval of more than 5 small squares. Since all atrial impulses
are conducted to the ventricles, all P waves are followed by a QRS complex with a
regular ventricular rate.

In healthy middle-aged men, a prolonged PR interval in the presence of a normal

QRS complex does not affect the prognosis and is not related to ischemic heart
disease.

85
 First degree AV block. Note the
consistent prolonged PR interval
(line) followed by a narrow QRS
complex of regular ventricular rate.
P P
P

Second Degree AV Block

Second degree AV Block is present if one or more, but not all, of the atrial impulses
fail to reach the ventricles because of impaired impulse conduction. The block may
be intermittent or persistent, and there may be more P waves than QRS complexes.

Second degree AV Block usually occurs in the AV node and is associated with
reversible conditions such as acute inferior MI or rheumatic fever, or treatment with
digitalis, a beta-blocker, or a calcium channel blocker. Generally, second degree AV
Block is a transient rhythm and rarely progresses to complete heart block except for
high degree type II AV block. Chronic second degree AV block may occasionally
occur in many conditions including aortic valve disease, atrial septal defect,
amyloidosis, Reiter's syndrome, and mesothelioma of the AV node.

Second degree AV Block type I

The more common form of second degree AV block begins with the PR interval
having a normal or near-normal PR interval. With each succeeding beats, the PR
interval gradually lengthens progressively until an impulse completely fails to
conduct and the QRS complex is dropped. Following the dropped QRS, the PR
interval goes back to normal or near-normal again, and the cycle or sequence is
repeated. The terms Mobitz type 1 or simply type 1 are used to describe a second
degree AV block when there is PR interval variation.

This gradual and progressive lengthening of the PR interval occurs because each
successive atrial impulse arrives earlier and earlier in the refractory period of the AV
node making it harder for the atrial impulse to penetrate the AV node and reach the
ventricles.

This ECG strip shows the characteristic type 1 second degree AV Block prolongation of the PR interval
before a P wave with a dropped beat (arrow) occurs.

86
Second degree AV Block type II

Mobitz type II or simply type

II second degree AV Block is
characterized by a lack of PR
interval lengthening
preceding the nonconducted
P wave and a lack of
shortening of the PR interval in the next cycle. So, the pattern is constant PR interval until
a sudden dropped beat occurs. Fortunately, this type of AV block is less common but
much more serious.

The impulse disturbance in type II AV block occurs infranodal or within the Purkinje
system. The conducted beats will almost always have a bundle branch block pattern and
an intermittent block in one of the bundle branches will cause the dropped beat to occur.
This type of block can suddenly progress to complete or third degree AV block, or
ventricular standstill. Since the level of block occurs in the distal part of the conduction
and pacemaking system of the heart, no escape rhythm may occur and may experience
syncope (Stokes-Adams attacks), cardiac arrest, or sudden death.

Another example of type II second degree AV Block. Sudden nonconducted P waves (red arrows)
occur with the preceding and succeeding cycles having a constant PR interval. No PR interval
variation is seen.

This is another type II second degree AV

block; note that there are 2 P waves not
conducted to the ventricles then the 3rd P
(blue arrow) is conducted describing a 3:1 (red
arrows) AV conduction and is a harbinger of
high grade of AV Block.

This example of type II AV block shows an

alternating conducted (blue arrows) and
nonconducted (red arrows) P wave. This is
an example of 2:1 high grade AV Block.

87
Third Degree AV Block or Complete Heart Block

The third and most serious heart block occurs when no atrial impulses are
conducted to the ventricles and the intrinsic pacemaker of the ventricles fires to
produce a ventricular escape rate (around 20-40 bpm). This independent atrial and
ventricular activation is termed AV dissociation and is characteristic of complete
heart block. The dissociation of the atrial and ventricular activation is recognized in
the ECG by the slow wide QRS (ventricular) complexes and the more frequent P
(atrial) waves. Each maintains its own rhythm without regard for the other.

The conduction block in all Purkinje fascicles is usually the cause of permanent
complete AV block. Idiopathic fibrosis, termed either Lev's disease or Lengere's
disease, is the most common cause of chronic complete heart block. Acute third
degree AV block results from inferior MI, digitalis intoxication, and rheumatic fever.
Complete AV block may also be congenital.

R R R This is an example of
Complete AV block. The two
leads of a rhythm strip
P P P P P P P P showing the P waves and
QRS complexes are
independent, with an atrial
rate of 113 bpm and a
ventricular rate of 38 bpm.

R R R Three examples of third degree or

complete AV block. All showing AV
P P P P P P P P P
dissociation with higher atrial rate and
much slower ventricular rate.

Try plotting the P and R waves,

determine their rate and regularity. The
first one has been done for you.

88
 Pacemaker system
ARTIFICIAL CARDIAC PACEMAKERS

Artificial cardiac pacemakers are the

most commonly used management for
symptomatic bradycardia caused by
abnormal cardiac impulse formation or
conduction.

This illustrates the components of an artificial

pacemaking system. Electronic impulses are
formed in a device called the pulse generator,
which may be located inside or outside the
patient's body. The impulses from the pulse
When the heart rhythm is initiated by an generator flows through the leads to the pacing
artificial pacemaker, pacemaker spikes electrodes that touches the ventricular
(red arrow) can usually be detected on endocardium. Usually the endocardial electrodes
an ECG recording. The amplitude of are placed in the right ventricular endocardium
these spikes varies among ECG leads near the apex. This produces a sequential right
and may not be apparent on a single then left ventricular activation. In the ECG, a
ECG recording. complete left bundle branch block pattern is
seen.
The assessment of the normal function
The pacing system is chosen to meet the
of artificial pacing system on the ECG
particular needs of the patient. During the initial
recording is dependent on the following:
years of the artificial pacemakers, in the 1960s, all
of the units were programmed with a single
1. The patient's rhythm at the time of fixed-rate mode to pace the ventricles. The
ECG recording. demand mode with sensing to prevent
2. The type of artificial pacing system. interference with the patient's own rhythm.
3. How the pacing system has been Subsequently, modern cardiac medicine
programmed. developed artificial pacemakers that will include
4. The myocardial location of the pacing external programmability, interaction with the
electrode. patient's intrinsic rhythm, sensing of the patient's
physiological status, AV sequential stimulation,
and incorporation of antitachycardia functions.
Assessment of whether the pacing system is
functioning normally requires knowledge of the
specific unit implanted.

89
The pacemakers are classified by the nature of their pacing mode. The classification
follows the pacemaker code developed by the North American Society of Pacing and
Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG).
The NASPE/BPEG Generic (NBG) Pacemaker Code was last revised in 2002. This coding
system was developed to use and understand pacemakers. The code has five positions
and is used for pacing nomenclature.

I II III IV V

Chamber(s) Chamber(s) Mode(s) of Programmable Antitachycardia

Paced Sensed Response Functions Functions
R = rate
V= ventricle V= ventricle T= triggered O = none
modulated
C=
A= atrium A= atrium I = inhibited P = paced
communicating
D = dual triggered/ M = multi
D= dual (A&V) D= dual (A&V) S = shocks
inhibited programmable
P = simple
O = none O = none O = none D = dual (P &S)
programmable

O = none

Position I - refers to chambers being paced.

Position II: Chambers sensed - refers to the location where the pacemaker senses
intrinsic cardiac activity.

Position III: Response to sensing - refers to the pacemaker's ability to respond to the
intrinsic cardiac activity of the patient. This mode is directly tied to the sensing mode
(position II). The pacemaker will only respond to the intrinsic heart activity if it will be able
to sense. The inhibited (I) response will pulse an electrical activity to the chamber unless it
senses an intrinsic electrical activity. T or the triggered mode is rarely seen and is
generally used for device testing.

The first three letter codes are usually sufficient to describe current pacemakers. The
fourth position in the code refers to rate modulation, if any. This is an adjustment in the
pacemaker's target heart rate based on the patient's changing cardiovascular demands.
It may be programmable (P), or be based on the metabolic or other sensors that can
detect the need for increased heart rate like in exercise. The fifth letter generally refers to
the antitachycardia function of the pacemaker, if there are any.

90
Common Pacing Modes

AAI

This pacing mode refers to a pacemaker that will pace and sense the atrium. If an
intrinsic electrical activity is sensed then pacing is inhibited but if there is no intrinsic atrial
activity sensed for a pre-determined time then atrial pacing is initiated. This type of
pacing is usually used for patients with sinus node dysfunction with intact AV conduction.

In atrial pacing, the pacemaker

blips will occur just before the P
wave and show a normal QRS
duration.

VVI

In VVI pacing, the ventricle is the chamber paced and sensed. This is similar to the
AAI mode but this type involves the ventricles. This is usually used in patients with
chronic atrial impairment like those with atrial fibrillation or flutter.

This ECG strip shows a ventricular (single)

chamber paced and sensed pacing. The
intrinsic rhythm is atrial fibrillation.

DDD

This pacing mode is capable of pacing and sensing both atrium and ventricle. This is
the most common pacing mode. Atrial pacing occurs if no intrinsic atrial activity is sensed
for a set time; and ventricular pacing occurs if no intrinsic ventricular activity is sensed for
a predetermined time.

This ECG strip shows

pacemaker blips before
the P wave and the
QRS complex
indicating that both the
atrium and ventricle are being paced.

91
COMMON PACEMAKER MALFUNCTION

Failure to Pace

This is detected in the ECG when a pacing spike (blip) is not immediately followed by
the appropriate cardiac waveform. Failure to pace early after insertion of the pacemaker
can be due to high pacing threshold of the ventricular endocardium than the programmed
output of the pulse generator, or the pacing electrode migrated away from its position on
the endocardium. If this pacing malfunction occurs late after implantation, fracture of the
electrode should be suspected.

This ventricular- paced rhythm

shows several noncaptured
pacemaker spikes (red arrow), as
depicted by the pacemaker blips
without the appropriate cardiac
waveform.

Failure to Sense

Failure of the pacemaker to sense an intrinsic or native cardiac electrical activity is

commonly caused by either alteration of the position of the endocardial pacemaker
electrode or there is scar formation between the electrode and the myocardium. This
pacing problem will result in asynchronous pacing. ECG findings may be minimal but this
is suspected if pacing spikes are seen embedded within a QRS complex.

This ECG strip shows a ventricular-paced rhythm with failure to sense (undersensing). Note that there are
persistent pacemaker blips (black dots) even with an intrinsic ventricular activity has occurred. Note that
the blips are within the QRS duration.

92
PRACTICE ECG STRIPS.

1. ____________________________

2. ____________________________

3. ____________________________

4. ___________________________

5. _________________________

6. ___________________________

7. __________________________

93
9. ______________________________

10. ___________________________

11. ____________________________

12. _____________________________

13. _____________________________

14. ____________________________

15. ____________________________

Answers: 1. Second degree AV Block type 1 (2.) Second degree AV Block type 2 (3.) Sinus Bradycardia (4.) second
degree AV block type 2 or High Degree AV Block (5.) Complete or 3rd degree AV Block (6.) First degree AV Block (7.)
ventricular paced rhythm (9.) Ventricular paced rhythm with non capture (10.) 3rd degree AV block (11.) 3rd degree AV
block (12.) Sinus bradycardia (13.) first degree AV block (14.) 2nd degree AV block type 2 (15.) 2nd degree AV block type 2

94
 Section 2

SUPRAVENTRICULAR
TACHYARRHYTHMIAS
Tachyarrhythmia is considered for all cardiac rhythms that has a rate of > 100 beats per
minute. Two important aspects of arrhythmias that are basic in understanding them are:
(1.) their mechanism, and (2.) the site of origin.

An increase in rate (tachycardia) can be produced by two different alterations of impulse

formation (automaticity): accelerated automaticity or triggered activation. In accelerated
automaticity, the maximal rate of impulse formation is limited to the inherent pacemaker
cells, and will rarely cause clinically significant tachyarrhythmias (e.g. Sinus tachycardia).
While the latter mechanism is usually the result of prolongation of the depolarization state
of the pacemaker cell and can produce clinically important reentrant tachyarrhythmias, like
in paroxysmal supraventricular tachycardia.

Sinus Tachycardia

The rate of impulse of the sinus node is regulated by the balance of the parasympathetic
and sympathetic nervous system. Increased sympathetic stimulation will cause an
increase in heart rate. The resultant sinus tachycardia is actually the body's physiologic
response to the body's needs rather than a pathologic cardiac condition. Maximal
sympathetic stimulation can increase the rate of impulses in the sinus node up to 200 -
220 beats per minute. In non-exercising adults, the heart rate rarely exceeds 160 bpm.

In sinus tachycardia, there is normally one P wave for every QRS complex. Because of the
increased sympathetic tone, this also speeds up AV nodal conduction showing a short PR
interval during the tachycardia. The QRS complex is usually normal in appearance. A

Sinus Tachycardia with a rate of 136 beats per min. There is a normal P wave with every QRS complex.

characteristic feature of sinus tachycardia is the gradual onset and termination of the
tachycardia. If the beginning or ending is not available for evaluation, a simple vagal
maneuver can aid in the diagnosis. Increased vagal tone will not abruptly cease the

95
tachycardia, instead, this will only cause transient slowing of the heart rate. This maneuver
may also be used in differentiating sinus tachycardia with other tachyarrhythmias.

If there are discrete P waves that precedes each QRS complex, short PR interval, and a
normal QRS duration are present, then the diagnosis of sinus tachycardia is most likely.
Another important note: the ventricular rate in adults during sinus tachycardia rarely
exceeds 150 bpm.

A 12 lead ECG that shows sinus tachycardia with a rate of 150 bpm. There is a short PR interval with normal looking
QRS complexes.

PREMATURE SUPRAVENTRICULAR BEATS

Premature complexes are among the most common causes of an irregular pulse and
palpitations. The premature beats can originate from anywhere in the heart - most
frequently in the ventricles, less often from the atria and the junctional area. These
premature beats are common in normal hearts and increases in frequency with age.

Premature atrial contractions (PAC)

The diagnosis of premature atrial contractions is made on the ECG by the presence
of a premature P wave with a normal PR interval. The P wave morphology generally
have a different morphology from the sinus P wave. Depending on the timing of the
onset of the premature beat on the cardiac cycle, a compensatory pause after the
PAC may occur, the premature P wave may not conduct to the ventricles, or if it

96
occurs during ventricular repolarization phase - the P wave will be buried in the T
wake and just distort the T wave.

The first red arrow head demonstrate the premature P wave buried in the T wave, distorting it, and is not conducted
to the ventricles explaining the dropped QRS complex. The second PAC occurs just after the T wave followed by a
compensatory pause. The last arrow head is embedded within the QRS complex.

ATRIAL TACHYARRHYTHMIAS

Focal Atrial Tachycardia

This rhythm strip shows atrial tachycardia

with a rate of 130 bpm. The P wave
morphology is not the normal sinus P wave.
It appears to be inverted but remains in the
isoelectric baseline.

Focal atrial tachycardias generally have rates of 150 to

200 beats per minute, with the P waves looking
different from the normal sinus P wave. Frequently,
atrial tachycardia occur in short, recurrent bursts with
spontaneous terminations. If the atrial rate is not
excessive, each P wave can conduct to the ventricles.

In focal atrial tachycardia, the impulses originate from

an ectopic focus from the atria instead normally from
the sinus node. Because of the ectopic origin, the P
wave is distorted or different looking from the normal
sinus P wave. Since the impulse conduction is supraventricular in origin, the QRS complex
is normal looking unless the tachyarrhythmia is accompanied by a bundle branch block
problem. Common causes include digoxin toxicity, atrial scarring, congenital heart
disease, or it may be idiopathic.

More often than not, the rhythm of focal atrial tachycardia is regular. However, as in cases
of digitalis toxicity, an AV block can accompany this atrial tachyarrhythmia. In this
condition, the atrial rate becomes excessive and the normal physiologic response of the
AV node is to suppress some of the atrial impulses to travel down the ventricles. In nearly
half of the cases of atrial tachycardia with block, the rhythm is irregular.

97
Multifocal Atrial Tachycardia

Multifocal (sometimes called chaotic) atrial tachycardia is

characterized by rate between 100 to 130 beats per minute
that is accompanied by different looking P waves and
irregularly irregular P-P intervals. In general, at least 3
different variations of P waves are noted and often the PR
intervals are also variable. Severe pulmonary disease is the
most common cause of the irregular atrial tachycardia. MAT
is typically known to be a transitional arrhythmia between
frequent premature atrial beats and
atrial flutter/ fibrillation.

This ECG strip shows at least 9 different

varieties of P wave with irregular P-P intervals
and different PR intervals.

Atrial Flutter

Atrial flutter is the prototype of macroreentrant atrial rhythm. There is a continuous reentry
of electrical impulse within the atrial myocardium. The typical reentering impulse goes
around the atrium in a single circuit in a counterclockwise manner. This produces regular
uniform "sawtooth-like" ♒︎ waves (F waves). The F waves are best seen in the inferiorly
oriented leads (II, III, aVF) and are may not be evident in the opposite leads (I, aVL).

F F F F F F F F F F F F F F F F F

Atrial Flutter with varying A:V conduction resulting in irregularly irregular rhythm.

The F waves of atrial flutter has rates of 220 and 350 beats
per minute. The ventricular rhythm varies from being regular
to irregularly irregular. The conduction of atrial beats to
ventricular beats may vary from 1:1 to 2:1 to 6:2 to 4:1 so that
the ventricles may or may not have a rapid rate. This ratio
depends on the slowly conducting AV node capability to
carry the electrical impulses to the ventricles. When the ratio
of 1:2, 2:1 or 4:1 remain constant, the ventricular rhythm will
be regular.

When the ratio is 6:2, the ventricular rhythm is regularly irregular; when the ratio becomes
variable, the ventricular rhythm becomes irregularly irregular.

98
The onset of atrial flutter is abrupt
and may be triggered by a
properly-timed premature atrial
contraction.

Atrial flutter is less common than

atrial fibrillation. Its incidence is
This atrial flutter rhythm strip shows almost regular R-R interval with
only one-twentieth that of atrial 4:1 conduction.
fibrillation. It is most often seen in
patients with ischemic heart disease
and those with atrial dilatation from septal defects, tricuspid valve stenosis or
regurgitation, heart failure, previous atrial ablation, or aging.

Atrial Fibrillation

Atrial fibrillation is characterized by the irregular undulation of the baseline with an

irregularly irregular ventricular rhythm. The undulations (f waves) may be gross and
distinct, intermediate in form, or barely perceptible.
Like in atrial flutter, the mechanism of atrial
fibrillation is the continuing reentry of impulse within
the atrium. In contrast to atrial flutter wherein the
continuous reentry goes around in a single circuit,
the reentering electrical impulse in atrial fibrillation
proceeds around multiple circuits producing the f
waves or fibrillatory baseline.

Atrial fibrillation may complicate any cardiac

condition and may be seen even in those without
structural heart disease (lone AF). The five most
common conditions that produce atrial fibrillation
are: rheumatic heart disease, ischemic heart

This is a 12 lead
ECG of a patient
with atrial fibrillation
with a ventricular
rate of 80 bpm. The
ventricular rhythm is
notably irregularly
irregular. The
fibrillatory (f) waves
are best appreciated
in leads II, III, aVF.

99
 disease, hypertensive heart disease,
heart failure of any cause, and
thyrotoxicosis. Advancing age and
dilation of the left atrium are also
related to the development of AF.
Chronic AF once established usually
will last the life time except for those
with mitral valve disease. The chronic AF may revert to normal sinus rhythm after mitral
valve surgery.

The atrial rate in atrial fibrillation is approximately 350 to 650 beats per minute. Fortunately,
not all atrial impulses are conducted to the ventricles. Some of the electrical impulses from
the atrium are suppressed by the AV node. Thus, the ventricular rate becomes variable
and conducted impulses that are carried to the ventricular level are irregular. Remember,
atrial fibrillation is not capable of producing regular ventricular rhythm. If this occurs, there
can be concomitant complete heart block or ventricular escape rhythm, or may be a sign
of digitalis toxicity.

JUNCTIONAL TACHYARRHYTHMIA

Paroxysmal Supraventricular Tachycardia

Tachycardia involving the AV node is characterized by a narrow QRS complex

(supraventricular in origin), sudden onset and termination with rates of 150 to 250
beats per minute, or faster in children. The P waves are generally buried in the QRS
complex (retrograde).The P wave might just be right before or just after the end of the
QRS complex. This type of tachycardia begins abruptly, usually after a premature
supraventricular beat.

P P P This illustration shows the common path

of reciprocating impulses that reenter the
AV node causing the tachyarrhythmia.
Illustration A shows the reentry is thru the
AV node itself producing inverted P waves
just before each QRS complex. In
illustration B, the reentry utilizes an
accessory pathway so that the atrial
activation is retrograde such that the P
P P P wave occurs after the QRS complex. The
QRS complex in both types are notably
narrow with normal shape.

100
PSVT is a reentrant tachycardia. The electrical impulse originate from the AV node.
The reentry of the impulse can be through the AV node itself, the atrium, ventricles, or
with the use of an accessory pathway.

This
rhythm strip shows the abrupt onset and termination of the PSVT. The tachyarrhythmia is precipitated by a premature
beat (arrow). The rate of the PSVT is around 160-170 bpm. The P wave during the tachycardia is buried within the T

Basically in PSVT, a premature beat causes the activation of the AV node to produce
an electrical impulse. Since the AV node is distal to the atria, the activation of the
atria proceeds in a retrograde manner, producing inverted P waves just before or just
at the end of the QRS complex. And because the electrical impulse is formed in the
AV node, which is proximal to the ventricular level, the QRS complex maintains to be
narrow and normal-looking. Unless the impulses formed are associated with aberrant
conduction in the ventricles.

This is another example of a PSVT without the onset and termination periods. The ventricular rate is very fast (188 bpm)
with regular, narrow QRS complexes. The P waves are not visible in this rhythm strip.

This is a 12 lead
ECG of a
supraventricular
tachycardia. The
ventricular rate is
approximately 170
bpm, regular, and
with a narrow QRS.
The P waves
occurred after the
QRS complex,
buried within the T
wave. These are
characteristics of
paroxysmal
supraventricular
tachycardia.

101
IDENTIFY THE SUPRAVENTRICULAR TACHYARRHYTHMIAS IN THE FOLLOWING
RHYTHM STRIPS:

1. ________________________________________________________________________

2. ______________________________________________________________

3. ________________________________________________________________

4. ________________________________________________________________

5. _______________________________________________________

102
6. ___________________________________________________________________

7. __________________________________________________________________

8.________________________________________________________________

9.________________________________________________________________

10. ____________________________________________________________________

103
104
1. Sinus Tachycardia
2. Atrial flutter
3. Multi focal Atrial Tachycardia
4. Sinus rhythm converting to PSVT
5. Atrial fibrillation
6. PSVT
7. Sinus Tachycardia
8. Atrial Flutter 1:1 conduction
Answers:
 3

VENTRICULAR TACHYARRHYTHMIAS

Premature Ventricular Complex

A premature ventricular complex, beat or contraction is characterized by the

premature occurrence of a wide, bizarre-looking QRS complex. The T wave usually is
large as well and has the opposite direction of the QRS deflection. The premature
QRS is not preceded by a premature P wave but is usually followed by a
compensatory pause.
PVC Compensatory pause
PVCs can occur alone, like an isolated
occurrence, or it can occur
occasionally, with several premature
beats within a certain amount of time.
Frequent occurrence of PVCs, for
example alternating with a normal
sinus beat is termed bigeminy, a trigeminy will have a premature beat followed by 2
normal sinus beats, a premature beat followed by three normal sinus beats is called
quadrigeminy, and so on. PVCs can also be grouped; two successive PVCs are
known as a pair or a couplet, but three or more successive PVCs are termed
ventricular tachycardia. PVCs can have a uniform appearance, or different shapes
often called multifocal.

The ECG strip on the left shows alternating PVC with a

normal sinus beat, termed PVCs in bigeminy; the strip on
the right shows a pattern of 3 normal sinus beat followed
by a PVC, called PVCs in trigeminy.

2 PVCs = couplet 3 successive PVCs = nonsustained ventricular tachycardia

105
Ventricular Tachycardia

Ventricular Tachycardia (VT) is a very serious tachycardia. It is never taken lightly

especially in the presence of structural heart disease, especially in ischemic heart
disease or cardiomyopathy, because the risk for sudden death increases in these
patients presenting with ventricular tachycardia. But for those without structural heart
disease, patients with VT and PVCs is generally good.

By definition, ventricular tachycardia consists of at least three consecutive QRS

complexes origination from the ventricles and recurring at a rapid rate, over 100
bpm. It is considered sustained or non sustained depending on whether it persists
over 30 seconds or not. The rhythm is regular or slightly irregular. During VT, the atria
can have an independent activity from the ventricular rhythm, or the atrial activity be
conducted retrograde.

The QRS complex in VT is wide, over 0.12 secs, with the ST-T waveforms pointing
the opposite direction of the main QRS vector. Because of the fast ventricular rate,
the dissociated or retrograde P waves, may be buried in the wide bizarre-looking
QRS complexes. Sometimes these P waves may be recognized as bumps or notches
within the QRS, ST-T complexes.

The Diagnosis of Ventricular Tachycardia

It would be easier if all wide-complex tachycardia can be considered as ventricular

tachycardia. But some supraventricular tachyarrhythmias can also present as a
regular wide-QRS tachycardia. Clues to the diagnosis of VT are outlined as follows:

1. Look for AV dissociation. If there is AV dissociation with wide QRS tachycardia,

the diagnosis of VT is highly probable. In VT, the origin of the impulse arise from
the ventricular conduction fibers. The ectopic focus (or foci) continue to discharge
impulses with disregard with the sinus node impulses. The sinus P wave occurs
independently and regularly, and is much slower than the rate of VT.

P P P P P

106
2. Look for fusion beats or capture beats. Fusion beat is an atrial beat that fused
with a ventricular beat; while a capture beat is an atrial impulse occurring before a
ventricular beat begins. If either a fusion or capture beat is proven to be present,
the diagnosis is almost certain VT.

F F C

A 12 lead ECG of ventricular tachycardia with a rate of 220 bpm. The QRS complexes have the same morphology.
Note the presence of fusion beats (F) and capture beats (C) best seen in lead V1.

3. Check for concordance. Concordance of the predominant direction of the wide

precordial QRS complexes is another useful clue. Concordance means that all the
QRS complex from lead V1 to V6 are deflected the same way - either positive
concordance or negative concordance, the diagnosis is most likely VT.

107
But if there is an RS pattern in the precordial NICE TO KNOW!!!
leads, measure the interval from the onset of the
QRS to the nadir of the S wave, it should be > Finding any of these clues will help in aiding the
diagnosis of VT. But the findings of some of these
0.10 sec (> 2 small squares) for the clues, e.g. presence of capture or fusion beats,
diagnosis of VT. are not readily present in a single ECG recording.
Other ECG findings that may differentiate VT from
SVT with aberrancy are listed below.

The following findings are more suggestive of

SVT with aberration in an ECG with regular wide
> 0.10 sec QRS tachycardia:

1. Consistent onset of the tachycardia with

a premature P wave (the onset of
Lets take a QRS complex in lead V1 from the 12 tachycardia is reproducible)
2. Very short PR interval
lead ECG we used for criteria #2: 3. QRS morphology has the same
morphology as during supraventricular
conduction at similar rates
4. The P wave and QRS are associated; the
R rhythm suggests that ventricular
activation depends on atrial activation
5. There is slowing or termination of the
tachycardia with vagal stimulation.
S

0.16 sec

Try analyzing this ECG and determine if the regular wide QRS complex is a
ventricular tachycardia or not,

see
answer at the next page...

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The 12 lead ECG is a Ventricular Tachycardia; ventricular rate of approximately 260 bpm with wide bizarre looking
QRS. There is concordance in the precordial leads ( the 6 leads are all deflected downwards) with presence of
fusion beats (encircled).

Polymorphic Ventricular Tachycardia (Torsades de Pointes)

Torsades de pointes is a French phrase for "twisting of points" which characterizes

polymorphic ventricular tachycardia (see rhythm strip below). This tachyarrhythmia is
often thought of as an intermediate between ventricular tachycardia and ventricular
fibrillation. In polymorphic VT, there is a continuous alternating undulations of the
QRS waveforms above and below the baseline. The rate varies from 180 to 250 bpm.
The ventricular waveforms does not look like the usual QRS or T waves. Torsades
most often is nonsusutained: but it may also last > 30 seconds satisfying the criteria
for a sustained VT. It has a high likelihood of evolving into ventricular fibrillation.

Polymorphic Ventricular Tachycardia or Torsades de Pointes. Note the twisting pattern of the alternating
undulations of the QRS waveforms above and below the baseline forming a "party banner"-like pattern.

Polymorphic VT almost always occurs in the presence of prolongation of the corrected QT

interval. Causes of prolongation of the QTc include use of proarrhythmic drugs like

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quinidine, procainamide, amiodarone, sotalol, phenothiazine, and tricyclic antidepressants.
It can also occur in the setting of electrolyte abnormalities like hypomagnesemia and
hypokalemia, insecticide poisoning, subarachnoid hemorrhage, ischemic heart disease,
bradyarrhythmias, and congenital prolongation of the QTc.

Another example of Torsades de Pointes:

Ventricular Fibrillation

Ventricular fibrillation is the irregular undulation of the ventricles that produces no

discernible QRS nor T waves. The ECG will show irregular wide fibrillatory waves; the
rhythm will look similar if it is viewed right side up or upside down.

Ventricular fibrillation is the most common cause of sudden death. VF was found to
follow a properly-timed PVC that occurs on the T wave of a QRS compels (R-on-T
phenomenon), monomorphic VT persisting for more than 100 beats, monomorphic
VT with a rate of > 180bpm, and polymorphic VT.

This illustration shows a

continuous rhythm strip of
ventricular fibrillation (VF). The
first strip shows coarse VF with
large irregular waveforms; the
bottom strip has fine fibrillatory
waves that terminates into
asystole.

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This rhythm strips starts with monomorphic VT that evolved into fine VF.

Give the ECG diagnosis of the following rhythm strips:

1._________________________________________________

2. _______________________________________________

3. ___________________________________________________

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4. ____________________________________________________

5.________________________________________________________

6. __A. _____________________________________B. ______________________________

A. B

7. ______________________________________________________________________

8. ________________________________________________________________________

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9. ___________________________________________________________

10. A. _______________________________________________________________

10.B. _________________________________________________________

Answers: 1. Coarse ventricular fibrillation 2. Monomorphic VT 3. Sinus Tachycardia with occasional PVC's 4.
Monomorphic VT (note the capture beat - first and third beat) 5. Sinus rhythm with occasional PVC evolving to
polymorphic VT 6a. PVC's in couplet 6b. Nonsustained VT 7. Monomorphic VT 8.Ventricular Fibrillation 9. Sinus
rhythm with PVC's converting to monomorphic VT 10A.fine VF 10B. Asystole

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 References

1. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 10th edition.

2. Marriott's Practical Electrocardiography 10th edition.

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