Section 1. ECG Basics 1. TP Segment.: ECG Reviews and Criteria Brugada Syndrome

Section 1.
ECG Basics
1. TP Segment.
The TP segment is the portion of the ECG from the end of the T wave to the
beginning of the P wave. This segment should always be at baseline and is used
as a reference to determine whether the ST segment is elevated or depressed, as
there are no specific disease conditions that elevate or depress the TP segment.
During states of tachycardia, the TP segment is shortened and may be difficult
to visualize altogether. It is good to examine the TP segment closely for the
presence of U waves or atrial activity that could indicate pathology.
2. ST Segment.
The ST segment is the portion of the ECG from the end of the QRS complex to
the beginning of the T wave. The ST segment normally remains isoelectric, thus
ST segment depression or ST segment elevation can indicate cardiac pathology.
The ST segment is scrutinized (xem xét kỹ lưỡng) on the ECG for the detection
of myocardial ischemia. This can be done in the setting of either exercise or
pharmacologic stress testing. Abnormal ST segments are reviewed based on the
causes outlined in the relevant ECG Reviews and Criteria sections and include
anterior, posterior and inferior myocardial infarctions, left ventricular
hypertrophy, pericarditis and Brugada syndrome.
3. QT Interval.
The QT interval is the time from the beginning of the QRS complex,
representing ventricular depolarization, to the end of the T wave, resulting from
ventricular repolarization. The normal QT interval is controversial (tranh cãi),
and multiple normal durations have been reported. In general, the normal QT
interval is below 400 to 440 milliseconds (ms), or 0.4 to 0.44 seconds. Women
have a longer QT interval than men. Lower heart rates also result in a longer
QT interval. A quick way to distinguish a prolonged QT interval is to examine
if the T wave ends beyond the halfway point between the RR interval. If the T
wave ends past the halfway point of the RR interval, it is prolonged.
4. T Wave.
The T wave occurs after the QRS complex and is a result of ventricular
repolarization. T waves should be upright in most leads; the exceptions are aVR
and V1. Further, T waves should be asymmetric in nature. The second portion
of the T wave should have a steeper decline when compared with the incline of
the first portion. If the T wave appears symmetric, cardiac pathology such as
ischemia may be present.
Many abnormal T wave patterns exist and are reviewed in more detail in the
relevant ECG Reviews and Criteria sections. These include hyperkalemia,
Wellens’ syndrome, left ventricular hypertrophy with repolarization abnormalities,
pericarditis (stage III), arrhythmogenic right ventricular dysplasia or ARVD, and
hyperacute T waves during myocardial infarction.
5. QRS Complex
A combination of the Q wave, R wave and S wave, the “QRS complex” represents
ventricular depolarization. This term can be confusing, as not all ECG leads
contain all three of these waves; yet a “QRS complex” is said to be present
regardless.
For example, the normal QRS complex in lead V1 does not contain a Q wave —
only a R wave and S wave — but the combination of the R wave and S wave is
still referred to as the QRS complex for this lead.
The normal duration (interval) of the QRS complex is between 0.08 and 0.10
seconds — that is, 80 and 100 milliseconds. When the duration is between 0.10
and 0.12 seconds, it is intermediate or slightly prolonged. A QRS duration of
greater than 0.12 seconds is considered abnormal. The QRS duration will lengthen
when electrical activity takes a long time to travel throughout the ventricular
myocardium. The normal conduction system in the ventricles is called the His-
Purkinje system and consists of cells that can conduct electricity quite rapidly.
Thus, normal conduction of an electrical impulse through the atrioventricular, or
AV, node, then to the ventricles via the His-Purkinje system, is fast and results in a
normal QRS duration. When electrical activity does not conduct through the His-
Purkinje system, but instead travels from myocyte to myocyte, a longer time is
necessary, and the QRS duration is widened. A widened QRS duration occurs in
the setting of a right bundle branch block, left bundle branch block, non-specific
intraventricular conduction delay and during ventricular arrhythmias such as
ventricular tachycardia — all of which are discussed in detail inside their
respective sections in ECG Reviews and Criteria.
6. S Wave
The S wave is the first downward deflection of the QRS complex that occurs after
the R wave. However, a S wave may not be present in all ECG leads in a given
patient.
In the normal ECG, there is a large S wave in V1 that progressively becomes

smaller, to the point that almost no S wave is present in V6. A large slurred S wave
is seen in leads I and V6 in the setting of a right bundle branch block. The presence
or absence of the S wave does not bear major clinical significance. Rarely is the
morphology of the S wave discussed. In the setting of a pulmonary embolism, a
large S wave may be present in lead I — part of the S1Q3T3 pattern seen in this
disease state. At times, the morphology of the S wave is examined to determine if
ventricular tachycardia or supraventricular tachycardia with aberrancy is present;
this is discussed elsewhere.
7. R Wave
The R wave is the first upward deflection after the P wave and part of the QRS
complex. The R wave morphology itself is not of great clinical importance but can
vary at times.
The R wave should be small in lead V1. Throughout the precordial leads (V1-V6),
the R wave becomes larger — to the point that the R wave is larger than the S
wave in lead V4. The S wave then becomes quite small in lead V6; this is called
“normal R wave progression.” When the R wave remains small in leads V3 to V4
— that is, smaller than the S wave — the term “poor R wave progression” is used.
Both types of wave progression are depicted below.

Recall that the R wave is usually quite small in lead V1; if the R wave is large in
V1 — that is, greater in amplitude than the S wave — significant pathology may
be present.
The causes for a R/S wave ratio greater than 1 in lead V1 include right bundle
branch block, Wolff-Parkinson-White syndrome, an acute posterior myocardial
infarction, right ventricular hypertrophy and isolated posterior wall hypertrophy,
which can occur in Duchenne muscular dystrophy.
If a right bundle branch block is present, there may be two R waves, resulting in
the classic “bunny ear” appearance of the QRS complex. In this setting, the second
R wave is termed “R’” or “R prime.”
8. Q Wave
The Q wave is the first downward deflection after the P wave and the first element
in the QRS complex. When the first deflection of the QRS complex is upright, then
no Q wave is present. The normal individual will have a small Q wave in many,
but not all, ECG leads.
Abnormalities of the Q waves are mostly indicative of myocardial infarction and

discussed further inside the relevant sections of ECG Reviews and Criteria. The
terms “Q wave myocardial infarction” and “non-Q wave myocardial infarction”
are earlier designations of different types of MIs ultimately resulting in,
respectively, Q wave development or the absence of Q wave development.
9. PR Segment
The PR segment is the portion of the ECG from the end of the P wave to the
beginning of the QRS complex. The PR segment is different from the PR interval,
which is measured in units of time. Remember that segments are different than
intervals. The important factor in analyzing segments on the ECG is their change
from the isoelectric line — that is, elevation or depression — whereas the
important thing in analyzing intervals is their duration. Although abnormalities of
the PR segment are not very common, they can indicate certain cardiac disease
states. PR segment depression can be a signal for pericarditis or atrial infarction.
PR segment elevation occurs in lead aVR in the setting of pericarditis.
10.P Wave
The P wave indicates atrial depolarization. The P wave occurs when the sinus
node, also known as the sinoatrial node, creates an action potential that depolarizes
the atria.
The P wave should be upright in lead II if the action potential is originating from
the SA node. In this setting, the ECG is said to demonstrate a normal sinus rhythm,
or NSR. As long as the atrial depolarization is able to spread through the
atrioventricular, or AV, node to the ventricles, each P wave should be followed by
a QRS complex.
Multiple abnormalities of the P wave are discussed in detail in ECG Reviews and
Criteria. Atrial enlargements can widen the P wave or increase the P wave
amplitude. Ectopic atrial rhythms can alter the normal morphology of the P waves.
There are many heart rhythms in which the P waves are not able to be identified,
including atrial fibrillation and sometimes junctional rhythms. At times, the P
waves can be buried at the end of the QRS complex, causing a “short RP” scenario,
as seen in atrioventricular reentrant tachycardia, or AVNRT.
11.Determining Axis.
The axis of the ECG is the major direction of the overall electrical activity of the
heart. It can be normal, leftward (left axis deviation, or LAD), rightward (right axis
deviation, or RAD) or indeterminate (northwest axis). The QRS axis is the most
important to determine. However, the P wave or T wave axis can also be measured.
To determine the QRS axis, the limb leads (not the precordial leads) need to be
examined. The depiction of the standard leads and their relationship to the cardiac
axis is below.
Note that lead I is at zero degrees, lead II is at +60 degrees, and lead III is at +120
degrees. Lead aVL (L for left arm) is at -30 degrees and lead aVF (F for foot) is at
+90 degrees. The negative of lead aVR (R for right arm) is at +30 degrees; the
positive of lead aVR is actually at -150 degrees.
Although memorizing the above picture is crucial to accurately determining axis,

some shortcuts to quickly determine the axis are outlined below.
The normal QRS axis should be between -30 and +90 degrees. Left axis deviation
is defined as the major QRS vector, falling between -30 and -90 degrees. Right
axis deviation occurs with the QRS axis and is between +90 and +180 degrees.
Indeterminate axis is between +/- 180 and -90 degrees. This is summarized in the
image below.
LAD = Left Axis Deviation
RAD = Right Axis Deviation
NW = Northwest axis, or indeterminate axis
The fastest non-specific method to determine the QRS axis is to find the major
direction of the QRS complex — positive or negative — in leads I and aVF.
Normal QRS Axis
If the QRS complex is upright (positive) in both lead I and lead aVF, then the axis
is normal. The image below demonstrates this example, with the electrical vector
heading towards the positive of lead I and the positive of lead aVF, as indicated by
the arrows. The QRS axis is thus between these two arrows, which falls within the
normal range.
Left Axis Deviation
If the QRS is upright in lead I (positive) and downward in lead aVF (negative),
then the axis is between 0 and -90 degrees. However, recalling that left axis
deviation is defined as between -30 and -90, this scenario is not always technically
left axis deviation. In this scenario, the QRS axis could fall between 0 and -30,
which is within normal limits. To further distinguish normal from left axis
deviation in this setting, look at lead II. If lead II is downward (negative), then the
axis is more towards -120, and left axis deviation is present. If the QRS complex in
lead II is upright (positive), then the axis is more towards +60 degrees, and the
QRS axis is normal.
The causes of LAD are listed below. Note that the first three account for almost
90% of ECG tracings with LAD.
1. Normal variant
2. Left anterior fascicular block
3. Left ventricular hypertrophy (rarely with LVH; usually axis is normal)
4. Left bundle branch block (rarely with LBBB)
5. Mechanical shift of heart in the chest (lung disease, prior chest surgery, etc.)
6. Inferior myocardial infarction
7. Wolff-Parkinson-White syndrome with “pseudoinfarct” pattern
8. Ventricular rhythms (accelerated idioventricular or ventricular tachycardia)
9. Ostium primum atrial septal defect
Below is an example of LAD to help visualize the above explanation.
Right Axis Deviation
If the QRS is predominantly negative in lead I and positive in lead aVF, then the
axis is rightward (right axis deviation). The causes of RAD are listed below.
1. Normal variant
2. Right bundle branch block
3. Right ventricular hypertrophy
4. Left posterior fascicular block
5. Dextrocardia
6. Ventricular rhythms (accelerated idioventricular or ventricular tachycardia)
7. Lateral wall myocardial infarction
8. Wolff-Parkinson-White syndrome
9. Acute right heart strain/pressure overload — also known as McGinn-White
Sign or S1Q3T3 that occurs in pulmonary embolus
Below is a pictorial example of RAD.
Indeterminate Axis
If the QRS is downward (negative) in lead I and downward (negative) in lead aVF,
then the axis is indeterminate and sometimes referred to as “northwestern axis.”
This finding is uncommon and usually from ventricular rhythms; however, it can
also be from paced rhythms, lead misplacement and certain congenital heart
diseases.
12.Determining Rhythm
The rhythm is either sinus rhythm or not sinus rhythm. Sinus rhythm refers to the
origination of the electrical activity coming from the sinus node — also known as
the sinoatrial node, or SA node. This results in an upright P wave in lead II on the
ECG.
If there is a P wave before every QRS complex, and it has a sinus morphology,
then normal sinus rhythm, or NSR, is said to be present. A sinus morphology is an
upright P wave in lead II and biphasic (up and down) P wave in lead V1.
The first ECG strip below shows a P wave with sinus morphology, thus normal
sinus rhythm. If the P wave has a morphology different from the typical sinus
morphology, it is termed ectopic, meaning coming from somewhere other than the
sinus node. The second ECG strip below shows an ectopic atrial rhythm. Note that
the P wave is down in lead II and only up (not biphasic) in lead V1.
Ectopic atrial rhythms including atrial tachycardia, multifocal atrial

tachycardia and junctional rhythms all have P waves that are not of sinus
morphology and will be reviewed in detail later.
If there is sinus rhythm, and the heart rate is less than 60 beats per minute,
then sinus bradycardia is present. If there is sinus rhythm, and the heart rate is
greater than 100 bpm, then sinus tachycardia is present. The links below take you
to examples of each of these.
If there are no P waves present, or the P wave morphology is not normal, then the
exact rhythm must be determined. Various arrhythmias — including atrial
fibrillation, atrial flutter, and ventricular rhythms such as ventricular tachycardia or
ventricular fibrillation — are discussed in detail in their respective sections in ECG
Reviews and Criteria.
Below are three more examples of rhythms other than sinus rhythm: atrial
fibrillation, atrial flutter and multifocal atrial tachycardia.
Note that when atrioventricular, or AV, dissociation is present (complete heart

block or VT), as previously described, there may not be a P wave before every
QRS complex. However, as long as the P wave is upright in lead II, sinus rhythm is
still said to be present.
13.Determining Rate
There are two different rates that can be determined on an ECG. The atrial rate is
indicated by the frequency of the P waves. The ventricular rate is indicated by the
frequency of the QRS complexes.
In the absence of disease, the atrial rate should be the same as the ventricular rate.
However, certain conditions including third-degree atrioventricular nodal
block or ventricular tachycardia can alter this normal relationship, causing “AV
dissociation.” In this setting, the atrial rate (P waves) and ventricular rate (QRS
complexes) are at different heart rates.
One quick and easy way to measure the ventricular rate is to examine the RR
interval — that is, the distance between two consecutive R waves — and use a
standard scale to find the rate. If two consecutive R waves are separated by only
one large box, then the rate is 300 beats per minute. If the R waves are
separated by two large blocks, then the ventricular rate is 150 bpm. Continuing
down the scale, if two consecutive R waves are separated by eight large boxes,
then the rate is 37 bpm. The pictorial explanation of this method is shown here.
Another quick way to calculate the rate is based on the entire ECG being 10
seconds. By counting the number of QRS complexes and multiplying by six,
the number per minute can be calculated — because 10 seconds times six
equals 60 seconds, or 1 minute. This is a better method when the QRS
complexes are irregular, as during atrial fibrillation, in which case the RR
intervals may vary from beat to beat.
Below are examples using each method.
Example #1
Note that the QRS complexes are about 5 1/2 large boxes apart. Referencing the
above image, it can be determined that the ventricular heart rate is between 50 and
60 bpm. This is a full 10-second rhythm strip, and there are nine QRS complexes
total. Multiply the number of QRS complexes by six, and the exact heart rate is 54
bpm. There is one P wave for each QRS complex, thus the atrial rate is the same.
Example #2
These QRS complexes are exactly three large boxes apart; therefore, the
ventricular heart rate is 100 bpm. Now, multiply the number of QRS complexes
on this strip by six. This would be 17 x 6 = 102. There is one P wave for each
QRS complex, thus the atrial rate is the same.
Example #3
These QRS complexes are less than two large boxes apart, thus the heart rate is
between 150 and 300 bpm. Multiply the number of QRS complexes by six for
the ventricular rate — that is, 29 x 6 = 174 bpm. There is likely one P wave for
each QRS complex (difficult to see on this strip), thus the atrial rate is likely the
same.
Example #4
The below ECG strip shows the irregularly irregular QRS complexes present
during atrial fibrillation. Using the first method to determine heart rate would
not be accurate because the RR intervals vary significantly. The best way to
determine the ventricular heart rate would be to simply count the QRS
complexes and multiply by 6, which would be 15 x 6 = 90 bpm. The P waves
are not able to be identified in atrial fibrillation, and it is assumed that the atrial
rate is between 400 and 600 bpm.
Example #5
This ECG strip shows AV dissociation, meaning the P waves (indicating atrial
activity) are at a different rate than the QRS complexes (indicating ventricular
activity), as explained earlier. This rhythm is actually an accelerated
idioventricular rhythm, or slow ventricular tachycardia. The atrial rate is
indicated by the P waves. There are almost exactly five large boxes between P
waves, indicating an atrial rate of 60 bpm. There are a total of ten P waves on
this strip (difficult to see some of them, as they are intermittently buried in the
QRS complexes) and 10 x 6 = 60. This confirms the first method. There are just
more than four big boxes between each QRS complexes, thus the ventricular
rate is between 60 and 75. Because there is a total of eleven QRS complexes in
this full 10-second strip, the calculation for the actual ventricular rate is 11 x 6
= 66 bpm.
Section 2. ECG Reviews and Criteria

PI. Atrial Arrhythmias
1. Atrial Fibrillation ECG Review

Atrial fibrillation occurs when action potentials fire very rapidly within the
pulmonary veins or atrium in a chaotic manner. The result is a very fast atrial
rate — about 400 to 600 beats per minute. Because the atrial rate is so fast, and the
action potentials produced are of such low amplitude, P waves will not be seen on
the ECG in patients with atrial fibrillation.
At times, the P wave activity may be observed as “coarse fibrillatory waves,” and
the term “coarse atrial fibrillation” is used, though there is no clinical significance
to this finding.
The atrial action potentials all attempt to conduct through the atrioventricular node;
however, the AV node becomes intermittently refractory and will only allow a
certain number of atrial action potentials to reach the ventricles. This is the reason
the ventricular rate is not also 400 to 600 bpm, but rather around 100 to 200 bpm.
The degree to which action potentials can cross the AV node to the ventricles is
variable and reduced by AV blocking medications.
Because the AV node is intermittently (not regularly) refractory, the QRS

complexes that are produced when an atrial action potential does reach the
ventricles will occur in an “irregularly irregular” manner, as there is no pattern to
their frequency. This is commonly described as varying RR intervals.
The only two other rhythms that are irregularly irregular are atrial flutter with
variable conduction and multifocal atrial tachycardia, or MAT. Atrial flutter has
the typical “sawtooth pattern,” whereas multifocal atrial tachycardia requires three
distinct P wave morphologies in one 12-lead ECG tracing. Note that there are quite
a few arrhythmias that are regularly irregular, such as second-degree AV block
type I (Wenkebach).
This means an ECG showing atrial fibrillation will have no visible P waves
and an irregularly irregular QRS complex. The ventricular rate is frequently
fast, unless the patient is on AV nodal blocking drugs such as beta-blockers
or non-dihydropyridine calcium channel blockers. Fibrillatory waves may or
may not be detected.
Ex 1. Atrial Fibrillation with Bradycardia ECG

ECG finding:
1. Atrial Fibrillation with a slow ventricular response

2. Left Ventricular Hypertrophy
3. Poor R Wave Progression
Ex2. Atrial Fibrillation with Normal Ventricular Rate ECG

Ex3. Atrial Fibrillation with Rapid Ventricular Rate ECG
ECG findings:
1. Atrial Fibrillation with a rapid ventricular response (RVR)

2. Left Ventricular Hypertrophy
3. ST abnormality - consider ischemia

ECG findings:
1. Atrial Fibrillation with a rapid ventricular response (RVR)
2. Premature Ventricular Contraction (PVC)
2. Atrial Flutter ECG Review

Atrial flutter occurs when a “reentrant” circuit is present, causing a repeated loop
of electrical activity to depolarize the atrium at a rate of about 250 to 350 beats per
minute; remember the atrial rate in atrial fibrillation is 400 to 600 bpm. This
produces a characteristic “sawtooth” pattern of the P waves — different from atrial
fibrillation, in which the atrial rate is so fast that the P waves are not identifiable,
or only coarse fibrillatory waves are seen.
Just as in atrial fibrillation, not all of the P waves are able to conduct through the
atrioventricular node, and thus the ventricular rate will not be as fast as the atrial
rate. Typically, the atrial rate will be about 300 bpm, and only every other atrial
depolarization will be conducted through the AV node. In this situation, the
ventricular (QRS) rate will be exactly 150 bpm and regular.
CLINICAL PEARL: A narrow complex tachycardia at a ventricular rate of exactly

150 bpm is very commonly atrial flutter.
The regularity of the QRS complexes frequently present with atrial flutter helps to

distinguish it from atrial fibrillation, though atrial flutter with variable conduction
of the P waves can also occur. In this situation, there may be three P waves to one
QRS complex, then a quick change to two P waves to one QRS complex, and so
on; any combination of P waves to QRS complexes can occur. This results in the
rhythm becoming “irregularly irregular.” There are only two other rhythms that are
commonly irregularly irregular, including atrial fibrillation and multifocal atrial
tachycardia, or MAT.
When the heart rate is significantly elevated — that is, greater than 150 bpm — it
is often difficult to determine atrial flutter from atrial fibrillation, atrial tachycardia
or atrioventricular nodal reentrant tachycardia, or AVNRT. In this situation,
giving adenosine will transiently slow the ventricular rate, unmasking the atrial
flutter waves and allowing a more definitive diagnosis to be made.
Atrial flutter can described as “typical” (type I) or “atypical” (type II) based on the
anatomic location from which it originates. Also, atrial flutter can be described as
“clockwise” or “counterclockwise” depending on the direction of the circuit.
Typical atrial flutter rotates counterclockwise in direction, from a reentrant circuit

around the tricuspid valve annulus and through the cavo-tricuspid isthmus. This
results in negatively-directed flutter waves in the inferior leads.
At times, the direction of the circuit can reverse, causing clockwise atrial flutter
from the same anatomical location. This appears as positively-directed flutter
waves in the inferior leads. Atypical atrial flutter originates from the left atrium or
areas in the right atrium, such as surgical scars, and has a variable appearance on
ECG in regards to the flutter waves.
Ex1. Atrial Flutter with 1:1 Conduction ECG

ECG findings:
1. Atrial Flutter with 4:1 Conduction

2. Old Septal Myocardial Infarction
ECG findings:
2. Right Bundle Branch Block
3. Left Anterior Fascicular Block
4. Bifascicular Block
Ex5. Atrial Flutter with Variable Conduction ECG

3. Atrioventricular Nodal Reentrant Tachycardia (AVNRT) ECG
Review
Atrioventricular nodal reentrant tachycardia is the most common form of
paroxysmal supraventricular tachycardia, or PSVT, in adults. AVNRT occurs
when a reentrant circuit is present within the AV node itself. In this situation, there
are two separate conduction pathways within the AV node instead of just one
(present in about 5% of the general population).
This is sometimes termed “dual AV nodal physiology.” One pathway is slower and
has a short refractory period, while the other is faster and has a long refractory
period. Normal conduction occurs through the faster pathway with the long
refractory period.
If a premature atrial contraction, or PAC, or less commonly a premature

ventricular contraction, or PVC, occurs at the right time, the normal conduction
pathway will still be refractory; thus, the action potential will conduct through the
fast AV nodal pathway with the shorter refractory period instead. After this action
potential reaches the ventricles or atrium, it will conduct back through the normal
AV nodal conduction pathway, as it will no longer be refractory and a reentrant
circuit will be created.
Initiation of AVNRT with a PVC
Findings on ECG include the following:
1. Narrow complex tachycardia

2. A P wave that occurs after the QRS complex (a short RP interval)
3. Tachycardia that quickly terminates with AV blocking maneuvers (carotid
massage or adenosine)
Ex 1. AV Nodal Reentrant Tachycardia (AVNRT) ECG
4. Atrioventricular Reentrant Tachycardia (AVRT) ECG Review
Atrioventricular reentrant tachycardia occurs when a reentrant circuit is present
outside of the AV node through an abnormal conduction pathway that connects the
atrium to the ventricles. This pathway is termed an “accessory pathway” or
a “bypass tract.” The presence of this congenitally abnormal accessory pathway is
seen in Wolff-Parkinson-White (WPW) syndrome.
If an action potential is able to traverse the accessory pathway and then return
retrograde through the AV node ― or vice versa ― a reentrant circuit can be
created, resulting in AVRT.
Findings on ECG include the following:
 a narrow complex tachycardia; and

 variable findings, depending on the direction of the circuit and location of
the accessory conduction pathway.
5. Ectopic Atrial Rhythms ECG Review

Atrial tachycardia and other ectopic atrial rhythms occur when a site outside of
the sinus node, but within the atria, creates action potentials faster than the sinus
node. This ectopic focus becomes the predominant pacemaker of the heart.
When the atrial rate is greater than 100 beats per minute, the rhythm is atrial
tachycardia. If less than 100 beats per minute, then the term “ectopic atrial
rhythm” is used.
Because the origination of this electrical activity is not from the sinus node, the P
wave would not have its normal sinus appearance ― that is, upright in lead II and
biphasic in V1. However, it would have a different morphology depending on
exactly where it originates. This is referred to as an “ectopic atrial rhythm” or
“ectopic P wave.”
Ectopic P waves are also commonly seen in multifocal atrial tachycardia, or

MAT, wandering atrial pacemaker, and premature atrial contractions, or PACs.
Atrial tachycardia is quite common. The causes of atrial tachycardia include

chronic hypertension, congestive heart failure, valvular heart disease and simply
aging of the heart. Brief atrial tachycardia is seen very commonly on ambulatory
ECG monitoring in the elderly and is frequently asymptomatic.
Symptoms of atrial tachycardia depend on the ventricular rate and the duration of
the tachycardia, and include palpitations from the rapid heart rate. If hypotension
ensues, dizziness and weakness can occur. The shortened diastolic filling time
during tachycardic states can lead to decreased cardiac output and symptoms of
congestive heart failure.
Atrial tachycardia is best treated with AV blocking medications such as beta-

blockers or nondihydropyridine calcium channel blockers. Adenosine can
terminate the rhythm at times, but not always. Ablation of atrial tachycardia is also
an option, especially when medical therapy fails.
Special Situations – Ectopic Atrial Rhythms: Atrial Tachycardia with 2:1
Block. When atrial tachycardia occurs with a 2:1 conduction block, digoxin
toxicity should be considered.
Ex1. Atrial Tachycardia
Ex2. Atrial Tachycardia with 2:1 AV Block ECG

ECG findings:
1. Atrial Tachycardia with 2:1 conduction
2. Left Bundle Branch Block

Ex3. Ectopic Atrial Bradycardia ECG
ECG findings:
1. Ectopic Atrial Bradycardia
2. Prolonged QT Interval
3. Wellen's Sign
6. Multifocal Atrial Tachycardia (MAT)

Multifocal atrial tachycardia is a tachycardic version of wandering atrial
pacemaker in which the atrial rate is greater than 100 beats per minute. Multifocal
atrial tachycardia occurs when multiple areas, or ectopic foci, within the atrium
generate consecutive action potentials that are all conducted to the ventricles.
Thus, each QRS complex will be preceded by a P wave; however, each P wave
will have a different morphology because they originate from different areas. By
definition, multifocal atrial tachycardia must have at least three distinctly different
P wave morphologies and a ventricular rate of greater than 100 beats per minute.
Multifocal atrial tachycardia frequently occurs in the setting of severe lung disease
and, more specifically, during an exacerbation of lung disease. This rhythm is
benign, and once the underlying lung disease is treated, it should resolve. If rate
control is needed, the historical treatment (without much evidence to support it)
has been verapamil. There is no thromboembolism risk in MAT, such as seen
in atrial fibrillation or atrial flutter, as the atrium are contractile in MAT. If the
heart rate is less than 100 beats per minute, then the rhythm is wandering atrial
pacemaker, or WAP.
The differential diagnosis of an irregularly irregular rhythm includes atrial

fibrillation, atrial flutter with variable conduction and MAT or WAP.
ECG findings:
1. Multifocal Atrial Tachycardia (MAT)
2. Aberrantly conducted supraventricular beats
7. Premature Atrial Contractions (PACs)

A premature atrial contraction occurs when a focus in the atrium (not the sinoatrial
node) generates an action potential before the next scheduled SA node action
potential.
There are four main characteristics of PACs:
1. Premature, occurring earlier than expected if measured against previous P-P

intervals.
2. Ectopic, originating outside of the SA node, and thus, the P wave
morphology would be different from the normal sinus P wave morphology.
3. Narrow complexes; because they come from the atrium, they will eventually
travel through the AV node and use the normal conduction system to spread
to the ventricles. Unlike premature ventricular contractions, or PVCs, which
are wide-complexed because they do not use the normal ventricular
conduction system. Less commonly, PACs can conduct aberrantly in a right
or left bundle pattern, which can make it challenging to differentiate them
from PVCs.
4. Compensatory pause following the contraction; the extra atrial action
potential causes the SA node to become refractory to generating its next
scheduled beat, and thus it must “skip a beat” and will resume exactly 2 P-P
intervals after the last normal sinus beat.
When every other QRS complex is a premature atrial contraction, then the rhythm
is referred to as “atrial bigeminy” as seen in this strip above.
If a PAC occurs when the AV node has not yet recovered from the refractory
period, it will fail to conduct to the ventricles; this means there will not be a QRS
complex following, or the ectopic PR interval will be prolonged. The ECG will
show a premature, ectopic P wave and then no QRS complex afterward. When this
occurs in a pattern of bigeminy, the interpreter may be fooled into thinking that
sinus bradycardia is present, because every other beat is a nonconducted PAC, and
the QRS rate is quite slow.
Ashman’s Phenomenon, also known as the Ashman Beat, occurs when a PAC or

supraventricular beat occurs before the right bundle branch has recovered from its
refractory period. This results in the premature beat displaying a right bundle
branch block pattern and can be confused with a premature ventricular contraction.
Ex1. Atrial Bigeminy ECG

ECG findings:
1. Normal Sinus Rhythm
2. Premature Atrial Contractions (PACs) in a pattern of atrial bigeminy
Ex2. Non-conducted or Blocked Premature Atrial Contractions

ECG findings:
2. Non-conducted Premature Atrial Contractions (Blocked PACs)
Ex3. Premature Atrial Contractions (PACs)

8. Sinoatrial (SA) Exit Block
Sinoatrial exit block occurs when the action potential initiated by the sinoatrial
node is inhibited or completely blocked before it is able to leave the SA node and
reach the atrium, and thus no P wave will appear on the ECG.
First-degree sinoatrial exit block occurs when there is a delay from the time the SA
node creates an action potential and the time the atrium is actually depolarized.
This is not recognizable on the 12-lead ECG because the time that SA node fires is
not able to be determined. The ECG may simply show sinus rhythm or sinus
bradycardia. This is different than a first-degree atrioventricular, or AV,
block, which shows a prolonged PR interval.
Second-degree sinoatrial exit block is categorized into type I and type II.
Second-degree SA exit block type I (Wenkebach) demonstrates progressive

shortening of the RR or PP intervals until a P wave is blocked in the SA node,
which would not appear on the ECG. A “sinus pause” ensues afterward and would
be shorter than two of the preceding RR intervals. Here is an example:
Second Degree Type I Sinoatrial Exit Block (Wenckebach)
Second-degree SA exit block type II occurs when there are consistent RR and PP
intervals, then a P wave is blocked in the SA node, also not seen on the ECG. The
subsequent sinus pause here is an exact interval of the preceding RR intervals,
usually two times.
Second Degree Type II Sinoatrial Exit Block
Third-degree sinoatrial exit block occurs when no SA nodal action potentials are
able to leave the SA node. No P waves are seen on the ECG. When a junctional
escape ensues, the rhythm may be confused with a junctional rhythm. If no
junctional escape rhythm is present, a long pause resulting in asystole and cardiac
arrest can occur.
9.Sinus Arrhythmia
Sinus arrhythmia refers to a changing sinus node rate with the respiratory cycle, on
inspiration and expiration. This is quite common in young, healthy individuals and
has no clinical significance. The heart rate increases with inspiration, due to
the Bainbridge reflex, and decreases with expiration.
The ECG criteria to diagnose sinus arrhythmia is a variation of the P-P interval,
from one beat to the next, of at least 0.12 seconds, or 120 milliseconds. Sinus
arrhythmia ― if not in a young person and not occurring with respiration may be a
sign of ― sick sinus syndrome, or SSS.
3 ECGs findings: ECG findings: Normal Sinus Rhythm with Sinus Arrhythmia
10.Sinus Bradycardia
Sinus bradycardia occurs on an ECG when there is a normal upright P wave in lead
II ― sinus P wave ― preceding every QRS complex with a ventricular rate of less
than 60 beats per minute.
The causes of sinus bradycardia include the following:
 AV blocking medications (beta-blockers, nondihydropyridine calcium

channel blockers, digoxin)
 Heightened vagal tone (i.e. well-trained athlete)
 Sick sinus syndrome
 Hypothyroidism
 Hypothermia
 Obstructive sleep apnea
 Hypoglycemia
Sinus bradycardia is frequently asymptomatic. Heart rates in the 40s and 50s can
be tolerated well. When symptoms arise, they manifest as fatigue, dizziness and
dyspnea on exertion (including chronotropic incompetence). Severe sinus
bradycardia is a form of sick sinus syndrome, and a pacemaker would relieve any
associated symptoms.
11.Sinus Tachycardia
Sinus tachycardia is recognized on an ECG with a normal upright P wave in lead II
preceding every QRS complex, indicating that the pacemaker is coming from the
sinus node and not elsewhere in the atria, with an atrial rate of greater than 100
beats per minute.
The ventricular rate (indicated by the QRS complex rate) is usually also greater
than 100 bpm because, in most cases, the P wave conducts through the
atrioventricular node to the ventricles to produce a QRS complex in a 1:1 fashion.
On occasion, the sinus rate can be different rom the ventricular rate ― known as
AV dissociation ― such as in ventricular tachycardia or third-degree AV block.
Treatment is aimed at the primary cause.
The differential diagnosis for sinus tachycardia includes the following:

1. Exercise
2. Anemia
3. Dehydration or shock
4. Fever/sepsis/infection
5. Hypoxia
6. Chronic pulmonary disease
7. Hyperthyroidism
8. Pheochromocytoma
9. Medications/stimulants
10.Decompensated congestive heart failure
11.Pulmonary embolus
Sinus tachycardia is rarely a primary cardiac arrhythmia and almost always caused
by one of the above conditions. The syndrome of inappropriate sinus tachycardia
has been described and is a form of autonomic dysfunction. Sinus node
modification or ablation procedures can be done; however, they pose a risk of
causing significant sinus node dysfunction, necessitating pacemaker implantation.
12.Wandering Atrial Pacemaker (WAP)

Wandering atrial pacemaker is similar to multifocal atrial tachycardia except
the heart rate is normal ― that is, less than 100 beats per minute.
Wandering atrial pacemaker occurs when multiple areas (ectopic foci) within
the atrium generate consecutive action potentials that are all conducted to the
ventricles. Thus, each QRS complex will be preceded by a P wave ― though
each P wave will have a different morphology, as it is originating from a
different area.
By definition, WAP must have at least three distinctly different P wave

morphologies and a ventricular rate of less than 100 bpm.
The differential diagnosis of an irregularly irregular rhythm includes atrial

fibrillation, atrial flutter with variable conduction and multifocal atrial
tachycardia or wandering atrial pacemaker.
13.
PII. Chamber Enlargements
1. Left Atrial Enlargement (LAE)

When left atrial enlargement occurs, it takes longer for cardiac action potentials to
travel through the atrial myocardium; thus, the P wave also lengthens. Therefore,
the criteria for diagnosing LAE on a 12-lead ECG is as follows:
1. The length of the P wave in lead II is greater than 120 milliseconds

OR
2. The downward deflection of the P wave in lead V1 is greater than 40
milliseconds in length, with greater than 1 millimeter negative deflection (<
-1 mm in amplitude)

P-mitrale occurs when the depolarization of the right atrium and left atrium are
both visible in the P wave. This is seen as a notch in the P wave and occurs when
the left atrium is markedly enlarged, such as in mitral valve stenosis.
Note that left atrial enlargement is not able to be diagnosed in the presence of atrial
fibrillation because this rhythm is defined by erratic atrial activity and no visible P
wave on the ECG. Also, LAE is a significant risk factor for developing atrial
fibrillation.
Ex1.
ECG findings:
1. Sinus Tachycardia
2. Left Atrial Enlargement
Ex2.
ECG findings:
Ex3.
ECG findings:
2. Left Atrial Enlargement with P-mitrale pattern
4. First Degree AV Block
5. Premature Ventricular Contractions
2. Left Ventricular Hypertrophy (LVH)

Left ventricular hypertrophy can be diagnosed on ECG with good specificity.
When the myocardium is hypertrophied, there is a larger mass of myocardium for
electrical activation to pass through; thus the amplitude of the QRS complex,
representing ventricular depolarization, is increased.
Likewise, when the myocardium is abnormally thickened, and electrical activity

takes longer to traverse throughout the whole heart, the duration of the QRS
complex may be widened. This is referred to as “LVH with QRS widening.” Also,
repolarization may be affected via similar mechanisms that can result in abnormal
ST segments or T waves. This is referred to as “LVH with strain” or “LVH with
repolarization abnormality.”
At times, these repolarization abnormalities can mimic ischemic ST changes, and

distinguishing them from those during a myocardial infarction is important, though
often difficult. The typical pattern with LVH includes deviation of the ST segment
in the opposite direction of the QRS complex (discordance), and a typical T wave
inversion pattern is present, as seen in the image here:
Left Ventricular Hypertrophy ECG Criteria
Through many studies, multiple criteria have been developed to diagnose LVH on
an ECG; they are listed below.
Cornell criteria: Add the R wave in aVL and the S wave in V3. If the sum is
greater than 28 millimeters in males or greater than 20 mm in females, LVH is
present.
Modified Cornell Criteria: Examine the R wave in aVL. If the R wave is greater

than 12 mm in amplitude, LVH is present.
Sokolow-Lyon Criteria: Add the S wave in V1 plus the R wave in V5 or V6. If

the sum is greater than 35 mm, LVH is present.
Romhilt-Estes LVH Point Score System: If the score equals 4, LVH is present
with 30% to 54% sensitivity. If the score is greater than 5, LVH is present with
83% to 97% specificity.
 Amplitude of largest R or S in limb leads ≥ 20 mm = 3 points

 Amplitude of S in V1 or V2 ≥ 30 mm = 3 points
 Amplitude of R in V5 or V6 ≥ 30 mm = 3 points
 ST and T wave changes opposite QRS without digoxin = 3 points
 ST and T wave changes opposite QRS with digoxin = 1 point
 Left Atrial Enlargement = 3 points
 Left Axis Deviation = 2 points
 QRS duration ≥ 90 ms = 1 point
 Intrinsicoid deflection in V5 or V6 > 50 ms = 1 point
EX1.
EX2.
ECG findings:
2. Left Ventricular Hypertrophy (LVH)
EX3.
EX4.
ECG findings:

2. Left Ventricular Hypertrophy (LVH) with repolarization abnormalities
ECG findings:
2. Left Ventricular Hypertrophy (LVH) with repolarization abnormalities
3. Poor R Wave Progression (PRWP)

Poor R wave progression refers to the absence of the normal increase in size of the
R wave in the precordial leads when advancing from lead V1 to V6.
In lead V1, the R wave should be small. The R wave becomes larger throughout
the precordial leads, to the point where the R wave is larger than the S wave in lead
V4. The S wave then becomes quite small in lead V6.
Note that an old anterior myocardial infarction can cause poor R wave progression.
In this setting, there is no R wave in the anterior precordial leads and instead Q
waves are present; see Anterior Myocardial Infarction Topic Review.
The causes of PRWP are as follows:
1. Old anterior myocardial infarction

2. Lead misplacement (frequently in obese women)
3. Left bundle branch block or left anterior fascicular block
4. Left ventricular hypertrophy
5. Wolff-Parkinson-White syndrome
6. Dextrocardia
7. Tension pneumothorax with mediastinal shift
8. Congenital heart disease
4.Right Atrial Enlargement (RAE)
When right atrial enlargement occurs, it does not take longer for cardiac action
potentials to travel through the atrial myocardium (similar to left atrial
enlargement). However, the amplitude of the P wave is exaggerated due to the
close proximity of the hypertrophied right atrial myocardium to the SA node. This
is referred to as p-pulmonale since lung disease can cause severe right heart strain
and right atrial enlargement. Thus, the P wave height becomes larger. The ECG
criteria for diagnosing right atrial enlargement (RAE) are as follows:
1. The P wave amplitude in lead II > 2.5 mm, or

2. The upward deflection of the P wave in lead V1 > 1.5 mm in amplitude.
EX1.
ECG findings:
2. Right Atrial Enlargement
3. Incomplete Right Bundle Branch Block

EX2.
ECG findings:
2. Right Atrial Enlargement (RAE)
3. Right Ventricular Hypertrophy (RVH)
EX3.
ECG findings:
2. Right Atrial Enlargement (RAE)
EX4.
5. Right Ventricular Hypertrophy (RVH)
Right ventricular hypertrophy occurs when the right ventricular wall thickens due
to chronic pressure overload, similar to that of left ventricular hypertrophy.
RVH is diagnosed on ECG in the presence of a R/S ratio of greater than 1 in lead
V1 in the absence of other causes, or if the R wave in lead V1 is greater than 7
millimeters tall. The strain pattern occurs when the right ventricular wall is quite
thick, and the pressure is high, as well. Strain causes ST segment depression and
asymmetric T wave inversions in leads V1 to V3.
Other causes of an R/S ratio of greater than 1 in lead V1:
1. Posterior wall myocardial infarction (also causes ST segment depression in

V1-V3, but T waves are symmetrically inverted, and the patient would be
presenting with chest pains)
2. Right bundle branch block
3. Wolff-Parkinson-White Type A
4. Lead misplacement (if V1 is placed too high)
5. Isolated posterior wall hypertrophy (occurs in Duchenne’s muscular
dystrophy)
EX1.
ECG findings:
2. Right Ventricular Hypertrophy
3. Right Atrial Enlagement

Note the R:S ratio > 1 in lead V1 as well as right axis deviation.
EX2.
ECG findings:
2. Right Ventricular Hypertrophy with strain or repolarization abnormalities
PIII. Conduction Abnormalities
1.2:1 Atrioventricular (AV) Block

2:1 atrioventricular block is a form of second-degree AV nodal block and occurs
when every other P wave is not conducted through the AV node to get to the
ventricles, and thus every other P wave is not followed by a QRS complex.
2:1 AV block can possibly be from either second-degree AV nodal block type I
(Wenkebach) or second-degree AV nodal block type II. This distinction is crucial,
as the former is usually benign, whereas the later requires implantation of a
permanent pacemaker.
A general rule to remember is that if the PR interval of the conducted beat is

prolonged and the QRS complex is narrow, then it is most likely second-degree
AV nodal block type I (Wenkebach). Alternatively, if the PR interval is normal and
the QRS duration is prolonged, then it is most likely second-degree AV nodal
block type II, and a pacemaker is probably warranted.
Recall that second-degree AV nodal block type I (Wenkebach) is an issue in

the AV node itself, which is subject to sympathetic and parasympathetic tone,
whereas second-degree AV nodal block type II is an “infranodal” conduction
disease of the His-Purkinje system, meaning that altering AV nodal conduction
would have no effect.
Various maneuvers can be employed to distinguish between the two potential

rhythms when an ECG reveals 2:1 AV nodal block:
Carotid sinus massage or adenosine: This slows the sinus rate, allowing the AV
node more time to recover, thus reducing the block from 2:1 to 3:2 and unmasking
any progressing prolonged PR intervals that would indicate second-degree AV
nodal block type I (Wenkebach).
Atropine administration: This enhances AV nodal conduction and could eliminate

second-degree AV nodal block type I (Wenkebach), as it is due to slowed AV
nodal conduction.
Exercise ECG testing: This enhances AV nodal conduction and could also
eliminate second-degree AV nodal block type I (Wenkebach), as it is due to
slowed AV nodal conduction.
EX1.
ECG findings:
2. 2nd Degree AV Block - 2:1 Block
EX2.
EX3.
ECG findings:

2. 2nd Degree AV Block - 2:1 Block
A bifascicular block on ECG is defined by the combination of a right bundle
branch block and either a left anterior fascicular block or left posterior fascicular
block. When these occur in combination, significant conduction disease is usually
present, and there is a risk for higher degrees of atrioventricular block in the future
causing symptomatic bradycardia and requiring pacemaker implantation.
Note: A bifascicular block is related to a trifascicular block, which also includes

a first-degree AV block. Even though technically incorrect, the AV node in this
situation is considered the third fascicle.
A bifascicular block can occur as a part of the ischemic heart disease or as a part of
the normal degeneration of the conduction system (Lev's disease). Although the
2009 American College of Cardiology/American Heart Association scientific
statement on ECG interpretation does not recommend the use of the
terms “bifascicular” or “trifascicular,” they are quite commonly used.
EX1.
ECG findings:
EX2.
ECG findings:
EX3.
ECG findings:
5. Short PR Interval
EX4.
ECG findings:
EX5.
ECG findings:
EX6.
ECG findings:
3. Left Posterior Fascicular Block
3. First-Degree Atrioventricular (AV) Block

A first-degree atrioventricular node block occurs when conduction through the AV
node is slowed, thereby delaying the time it takes for the action potential to travel
from the sinoatrial node through the AV node, and to the ventricles.
A first-degree, or 1st degree, AV block is indicated on the ECG by a prolonged PR

interval, as seen below.
Recall that the P wave indicates atrial depolarization, initiated by firing of the SA
node. The atrial depolarization eventually spreads to the AV node, where there is a
slight delay before the electrical impulse is conducted to the ventricles. If the AV
nodal conduction (dromotropy) is decreased, it will take longer for the impulse to
reach the ventricles, meaning there will be a greater distance between the P wave
and the QRS complex. Remember the QRS complex indicates ventricular
depolarization; thus the PR interval will be prolonged.
The PR interval is normally between 0.12 and 0.20 seconds. A PR interval

consistently longer than 0.20 seconds, or greater than five small boxes, indicates a
first degree AV block.
There is a 1/1 ratio between P waves and QRS complexes in first-degree AV block,
unlike second-degree, or 2nd degree, and third-degree, or 3rd degree, AV nodal
blocks.
In general, a first-degree AV block is a benign finding that does not require any
treatment. However, it may be an indicator of higher-degree AV block in the future
and, depending on the PR interval, AV blocking medications may be avoided.
Note: A first-degree AV block is also part of a trifascicular block, as the AV node

is sometimes considered the third fascicle.
EX1:
ECG findings:
4. Poor R Wave Progression
EX2
ECG findings:
5. Trifascicular Block
EX3.
ECG findings:
EX4.
ECG findings:
6. Premature Ventricular Contraction
4. Left Anterior Fascicular Block (LAFB)

A left anterior fascicular block, also known as left anterior hemiblock, occurs when
the anterior fascicle of the left bundle branch is no longer able to conduct action
potentials.
The criteria to diagnose a LAFB, or LAHB, on ECG include the following:
1. Left axis deviation of at least -45 degrees

2. The presence of a qR complex in lead I and a rS complex in lead III
3. Usually a rS complex in lead II and III (sometimes aVF as well)
A very quick way to diagnose a left anterior fascicular block on ECG is to first
identify the left axis deviation; see image below. If the QRS complex is up in lead I
and down in lead aVF while also down in lead II, then left axis deviation is
present. Then look at lead III. If there is an rS complex, then you have a LAFB on
ECG. This method should take just a few seconds.
Note: An old inferior wall myocardial infarction is not able to be diagnosed in the
setting of a left anterior fascicular block due to the inferior Q waves present from
the LAFB.
A left anterior fascicular block can also occur in the setting of a bifascicular or
trifascicular block. Below is a bifascicular block with a LAFB on ECG. Note there
is also a right bundle branch block.
EX1.
ECG findings:
EX2.
ECG findings:

EX3.
ECG findings:
5. Short PR Interval
EX4.
ECG findings:
EX5.
ECG findings:
EX6.
ECG findings:
2. Left Anterior Fasicular Block
EX7.
ECG findings:
EX8.
ECG findings:

4. Left Bundle Branch Block (LBBB)
The ECG criteria for a left bundle branch block include:
1.QRS duration greater than 120 milliseconds

2.Absence of Q wave in leads I, V5 and V6
3.Monomorphic R wave in I, V5 and V6
4.ST and T wave displacement opposite to the major deflection of the QRS
complex
A simple way to diagnose a left bundle branch in an ECG with a widened QRS
complex (> 120 ms) would be to look at lead V1. If the QRS complex is widened
and downwardly deflected in lead V1, a left bundle branch block is present. If the
QRS complex is widened and upwardly deflected in lead V1, a right bundle branch
block is present. The image below shows the typical findings of a left bundle
branch block in the precordial ECG leads.
Note: If the QRS duration is 100 to 119 ms with criteria 2, 3 and 4 of the above, an
incomplete LBBB is present.
A rate-dependent LBBB can occur at times of fast heart rates. This may be caused
by myocardial ischemia or refractoriness of the left bundle at faster heart rates.
When occurring at heart rates greater than 100 beats per minute, a rate-dependent
LBBB can at times be difficult to distinguish from ventricular tachycardia because
both cause a wide complex QRS complex. The Brugada Criteria for diagnosing
ventricular tachycardia is helpful to make this distinction.
The ECG strip below shows normal sinus rhythm, then atrial fibrillation with a
rapid ventricular response develops. With the faster heart rate, the QRS complex
morphology changes to that of a LBBB. As sinus rhythm restores, and the
ventricular rate slows, the QRS morphology returns to normal.
Sgarbossa Criteria
The Sgarbossa criteria is used in the diagnosis of an acute myocardial infarction

when a LBBB is present.
Traditionally, it has been taught that MI is not able to be diagnosed via ECG in the
presence of a LBBB. However, Sgarbossa et al described in 1996 some ECG
changes seen in patients with LBBB and concomitant MIs and devised a point
scoring system. This is called the Sgarbossa criteria, and they are listed below.
1. ST segment elevation > 1 mm and in the same direction (concordant) with

the QRS complex = 5 points
2. ST segment depression > 1 mm in leads V1, V2 or V3 = 3 points
3. ST segment elevation > 5 mm and in the opposite direction (discordant) with
the QRS = 2 points
A score of 3 points is required to diagnose an acute MI. Criteria #3 is under debate
as to its usefulness; therefore, either criteria 1 or criteria 2 are essentially required.
This patient just made 1 mm ST segment elevation in lead V5 and about 0.5 mm
ST elevation in V6 — an ECG indeed from a patient with an acute left anterior
descending thrombosis.
Note: Cabrera’s sign and Chapman’s sign have also been used to diagnose acute

MI in the setting of a LBBB. Examining the T wave in leads V5 to V6 can be
helpful, as well. In the Sgarbossa study, there was a 26% sensitivity to detect acute
MI when the T wave was upright rather than inverted.
EX1.
ECG findings:
2. Incomplete Left Bundle Branch Block (LBBB)
EX2.
ECG findings:
3. Cabrera's Sign
EX3.
ECG findings:
3. Chapman's Sign
EX5.
ECG findings:
2. Rate Dependant Left Bundle Branch Block (LBBB)
3. Paroxysmal Supraventricular Tachycardia
5. Left Posterior Fascicular Block (LPFB)

A left posterior fascicular block ― also known as a left posterior hemiblock, LPHB ―
occurs on the ECG when the posterior fascicle of the left bundle branch is no longer
able to conduct action potentials. This is much less common than a left anterior
fascicular block, or LAFB, as the posterior fascicle is much more sparsely distributed;
thus, a large amount of myocardial tissue must be damaged to block the posterior
fascicle.
The criteria to diagnose a LPFB on a 12-lead ECG include the following:
 Right axis deviation of 90-180 degrees

 Presence of a qR complex in lead III and a rS complex in lead I
 Absence of right atrial enlargement, or RAE, and/or right ventricular hypertrophy, and
RVH
Note: The above pattern can appear similar to the S1Q3T3 pattern sometimes present in
patients with a pulmonary embolus.
A LPFB can occur in the setting of a bifascicular block as well.
EX1.
EX2.
ECG findings:
3. Left Posterior Fascicular Block
6. Right Bundle Branch Block (RBBB)

The ECG criteria for a right bundle branch block include the following:
1. QRS duration greater than 120 milliseconds

2. rsR’ “bunny ear” pattern in the anterior precordial leads (leads V1-V3)
3. Slurred S waves in leads I, aVL and frequently V5 and V6
Remember that T wave inversions and ST segment depression are normal in leads V1
to V3 in the presence of a right bundle branch block; thus, myocardial ischemia
technically cannot be easily determined in these leads. However, unlike in the presence
of a left bundle branch block, myocardial ischemia and infarction can easily be detected
on ECG when a RBBB is present.
Below is an ECG displaying a right bundle branch block with an anterior ST segment
elevation MI, followed by some other examples.
 Anterior Wall ST Segment Elevation Myocardial Infarction (MI) with RBBB ECG
(Example 1)
 Anterior Wall ST Segment Elevation Myocardial Infarction (MI) with RBBB ECG
(Example 2)
 Inferior Wall Myocardial Infarction (MI) with RBBB ECG (Example 1)
 Inferior Wall Myocardial Infarction (MI) with RBBB ECG (Example 2)
Some variations of right bundle branch blocks can occur. There are times when a QRS
complex may appear in a RBBB pattern intermittently. This is the case in premature
ventricular contractions that arise from the left ventricle, which take time to travel to the
right ventricle, thereby resulting in a RBBB QRS morphology. This may also occur in the
setting of an Ashman beat, a premature atrial contraction or supraventricular beat that
occurrs when the right bundle is refractory, causing the beat to conduct with a RBBB
pattern. Here is an example:
A typical “bunny ear” pattern is not always present in a RBBB, as the R or the R’ may be
very small; therefore, do not rely on identifying “bunny ears” to diagnose a RBBB. Here
is an example of a QRS complex with a RBBB pattern, but without the typical rsR’
pattern:
A “rate-dependent” right bundle branch block can also occur during times of fast heart
rate. When the heart rate slows, the narrow QRS complex returns. A rate-dependent
RBBB can, at times, be mistaken for ventricular tachycardia. The Brugada Criteria can
be helpful in distinguishing these two entities.
Lastly, VT itself can sometimes have a RBBB pattern if it arises from the left ventricle. If
tachycardia is present — that is, heart rate greater than 100 beats per minute — in a
RBBB pattern, VT should be considered.
The QRS morphology criteria to diagnose VT with a RBBB include the following:
1. A monophasic R or biphasic qR complex in V1

2. An RSR’ or “bunny ear” pattern present in V1 or V2, with the R peak higher in amplitude
than the R’ peak (see image below)
3. A rS complex in lead V6 (favors VT)
EX1.
ECG findings: Incomplete RBBB

EX2.
ECG findings:
1. Atrial Fibrillation with an uncontrolled ventricular response
2. Rate Dependent Right Bundle Branch Block (RBBB)
7. Second-Degree Atrioventricular (AV) Block

Type I (Wenkebach)
In second-degree atrioventricular nodal block — also known as Wenckebach block or
Mobitz Type I AV block — varying failure of conduction through the AV node occurs,
such that some P waves may not be followed by a QRS complex. Unlike first-degree AV
nodal block, a 1:1 P-wave-to-QRS-complex ratio is not maintained. Second-degree type
I AV block is specifically characterized by an increasing delay of AV nodal conduction
until a P wave fails to conduct through the AV node. This is seen as progressive PR
interval prolongation with each beat until a P wave is not conducted. There is an
irregular R-R interval. Sometimes when the block is consistent, the QRS complexes are
said to demonstrate "group beating."
A second-degree type I AV block occurs when conduction within the AV node itself is
delayed in this progressive manner. It does not necessarily indicate intrinsic conduction
disease, and rarely requires a pacemaker to be implanted. A second-degree type I AV
block can be caused by AV blocking medications or increased vagal tone. AV nodal
ischemia during an inferior MI can cause AV nodal blocks, as well.
Note that if every second P wave is not conducted, there will not be enough time to see
PR prolongation. This is called 2:1 AV block, as depicted below:
When 2:1 AV block is present, the rhythm may be second-degree type I or second-
degree type II AV block. Exercising the patient will increase AV nodal conduction and
help distinguish these two. If second-degree type I AV block is present, then the heart
rate will increase and the progressive prolongation of PR intervals prior to a non-
conducted P wave will be apparent. If second-degree type II AV block is present, there
may be no change with exercise.
Ex1.
ECG findings:
2. Second Degree AV Block Type I (Wenkebach)
3. Inferior ST Elevation Myocardial Infarction
EX2.
8.Second-Degree Atrioventricular (AV) Block
Type II (Mobitz type II AV Block)
In second-degree type II AV nodal block (a.k.a. Mobitz Type II AV block), the AV node
becomes completely refractory to conduction on an intermittent basis. For example,
three consecutive P waves may be followed by a QRS complex, giving the ECG a
normal appearance, then the fourth P wave may suddenly not be followed by a QRS
complex since it does not conduct through the AV node to the ventricles.
The PR interval may be normal or prolonged, however it is constant in length unlike

second-degree AV block Mobitz Type I (Wenckebach) in which the PR interval
progressively lengthens until a P wave is not conducted. A second-degree type II AV
block indicates significant conduction disease in this His-Purkinje system and is
irreversible (not subject to autonomic tone or AV blocking medications). This is a very
important distinguishing factor compared to second-degree type I AV block. Because of
this, a permament pacemaker is indicated in every patient with second-degree type II
AV block.
9.Third-Degree Atrioventricular (AV) Block
10. Third-degree atrioventricular nodal block, also known as third-degree heart block
or complete heart block, occurs when no action potentials conduct through the
AV node. This results in the P waves (atrial depolarizations) being completely
unrelated to the QRS complexes (ventricular depolarizations) ― meaning the P
waves occur at one rate and the QRS complexes at another. This is termed “AV
dissociation.”
11.
12. In this situation, the ventricles never see action potentials originating from the
atria and compensate by making action potentials of their own. However, the
ventricles are unable to create action potentials at a fast rate. This means the
ventricular rate (QRS complexes) is slow (around 30 to 40 bpm), and the atrial
rate (P waves) is faster than the ventricular rate (around 60 to 100 bpm).
13. “High grade AV nodal block,” a type of 3rd degree heart block, occurs when there
is AV dissociation similar to complete heart block, but occasional P waves do
conduct through the AV node to produce a QRS complex.
14. Complete heart block is usually symptomatic from the slow ventricular rates.
These symptoms include fatigue, dyspnea, dizziness and syncope. Because
intrinsic conduction disease of the His-Purkinje system is the cause of 3rd degree
AV block (not autonomic tone or AV blocking medications), the rhythm is usually
irreversible and a permanent pacemaker is indicated.
Ex2.
ECG findings:
2. Third Degree AV Block (Complete Heart Block)
Ex3.
ECG findings:
Ex4.
ECG findings:
4. Left Anterior Fascicular Block (LAFB)
Ex5.
ECG findings:

A trifascicular block is the combination of a right bundle branch block, left anterior or
posterior fascicular block and a first-degree AV block (prolonged PR interval). The term
“trifascicular block” is a misnomer, since the AV node itself is not a fascicle. A
trifascicular block is a precursor to complete heart block. While a trifascicular block itself
does not require any treatment, high doses of AV blocking agents likely should be
avoided. Some series report a 50% lifetime need for a permanent pacemaker in the
setting of a trifascicular block.
EX1.
ECG findings:
Ex2.
ECG findings:
Ex3.
ECG findings:
PIV. Ischemic Heart Disease
1.Anterior Wall ST Segment Elevation MI

An anterior wall myocardial infarction — also known as anterior wall MI, or AWMI, or
anterior ST segment elevation MI, or anterior STEMI — occurs when anterior
myocardial tissue usually supplied by the left anterior descending coronary artery
suffers injury due to lack of blood supply. When an AWMI extends to the septal and
lateral regions as well, the culprit lesion is usually more proximal in the LAD or even in
the left main coronary artery. This large anterior myocardial infarction is termed an
extensive anterior.
The ECG findings of an acute anterior myocardial infarction wall include:
1. ST segment elevation in the anterior leads (V3 and V4) at the J point and sometimes in
the septal or lateral leads, depending on the extent of the MI. This ST segment elevation
is concave downward and frequently overwhelms the T wave. This is called
“tombstoning” for obvious reasons; the shape is similar to that of a tombstone.
2. Reciprocal ST segment depression in the inferior leads (II, III and aVF).

According to the American College of Cardiology/American Heart Association guidelines

for STEMI, there must be “new ST segment elevation at the J point in at least two
contiguous leads of ≥ 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads
V2-V3 and/or of ≥ 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.”
This means 1 millimeter in any two contiguous leads, except leads V2 or V3, where the
elevation must be 2 mm in men or 1.5 mm in women.
See the full 12-lead ECG example below and a few more at the bottom.
The ECG findings of an old anterior wall MI include the loss of anterior forces, leaving Q
waves in leads V1 and V2. This is a cause of poor R wave progression, or PRWP.
Here is an example of an old anterior wall MI:
Note: To distinctly say that an old anterior wall MI is present on the ECG, there must be
no identifiable R wave in lead V1 — and usually V2, as well. If there is an R wave in V1
or V2, the term poor R wave progression, but not old anterior wall MI, can be used.
On rare occasions, persistent ST segment elevation may be seen in V1 and/or V2,

indicating a ventricular aneurysm — a known complication of a myocardial infarction.
Visit Left Ventricular Aneurysm ECG Review or Left Ventricular Aneurysm Topic
Review. An example of an old anterior myocardial infarction with a left ventricular
aneurysm is below.
EX1.
ECG findings:
2. Anterior ST Elevation Myocardial Infarction

2. Inferior Wall ST Segment Elevation
Myocardial Infarction (MI)
n inferior wall myocardial infarction — also known as IWMI, or inferior MI, or inferior ST
segment elevation MI, or inferior STEMI — occurs when inferior myocardial tissue
supplied by the right coronary artery, or RCA, is injured due to thrombosis of that
vessel. When an inferior MI extends to posterior regions as well, an associated posterior
wall MI may occur.
The ECG findings of an acute inferior myocardial infarction include the following:
1. ST segment elevation in the inferior leads (II, III and aVF)

2. Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL, V5 and
V6)
Note: If the reciprocal ST segment depressions are not present, consider alternative
causes of ST segment elevation, such as pericarditis.
An inferior MI can have multiple potential complications and can be fatal. See
the STEMI Topic Review for more detail on these complications and a detailed
discussion on treatment.
Ex1.
ECG findings:
3. Posterior Wall Myocardial Infarction (MI)

The ECG findings of a posterior wall myocardial infarction are different than the typical
ST segment elevation seen in other myocardial infarctions. A posterior wall MI occurs
when posterior myocardial tissue (now termed inferobasilar), usually supplied by the
posterior descending artery — a branch of the right coronary artery in 80% of
individuals — acutely loses blood supply due to intracoronary thrombosis in that vessel.
This frequently coincides with an inferior wall MI due to the shared blood supply.
The ECG findings of an acute posterior wall MI include the following:
1. ST segment depression (not elevation) in the septal and anterior precordial leads
(V1-V4). This occurs because these ECG leads will see the MI backwards; the
leads are placed anteriorly, but the myocardial injury is posterior.
2. A R/S wave ratio greater than 1 in leads V1 or V2.
3. ST elevation in the posterior leads of a posterior ECG (leads V7-V9). Suspicion
for a posterior MI must remain high, especially if inferior ST segment elevation is
also present.
4. ST segment elevation in the inferior leads (II, III and aVF) if an inferior MI is also
present.
Ex1.
ECG findings:
2. Inferior Wall Myocardial Infarction

3. Posterior Wall Myocardial Infarction
Ex2.
ECG findings:
EX3.
ECG findings:
PV. Ventricular Arrhythmias
1.Asystole
Asystole occurs when no electrical activity of the heart is seen. This may be a fatal
arrhythmia when it occurs related to a severe underlying illness (ie, septic shock,
cardiogenic shock or post-pulseless electrical activity arrest). Emergent implementation
of Advanced Cardiac Life Support is crucial in this situation.
Asystole can also be related to intrinsic conduction system disease. In this situation, the
pause of electrical activity may be brief (ie, a few seconds) and result in syncope;
however, spontaneous recovery of sinus rhythm may occur. Treatment for this form of
asystole is permanent pacemaker implantation.
2.Idioventricular Rhythms
An idioventricular rhythm is very similar to ventricular tachycardia except the ventricular
rate is less than 60 beats per minute. All other characteristics of VT apply; this includes
the presence of atrioventricular dissociation, as seen in the ECG and strip below, and
the Brugada Criteria. An idioventricular rhythm is frequently referred to as a “slow
ventricular tachycardia” for this reason.
When the ventricular rate is between 60 and 100 bpm, it is referred to as an accelerated
idioventricular rhythm. This is a hemodynamically stable rhythm that occurs commonly
after myocardial infarction and no treatment is needed.
Example #1
This ECG displays an accelerated idioventricular rhythm. This has a left bundle branch
block pattern and is a good example of the AV dissociation that occurs. Now, look at the
rhythm strip at the bottom in lead V1 to see the AV dissociation. This ECG also meets
the Brugada Criteria for concordance. In this LBBB pattern, all the QRS complexes are
negative in the precordial leads.
Example #2
In this ECG example of AIVR, note the right bundle branch block pattern and upward
concordance, with all the QRS complexes up in the precordial leads V1 to V6 during the
wide complex rhythm. Recall that the morphology of the QRS complex (right or left
bundle) depends on from where the focus of the ventricular rhythm originates (right or
left ventricle). If the rhythm starts in the left ventricle, then the electrical activation takes
longer to get to the right ventricle, and a RBBB pattern will occur. Likewise, if the rhythm
originates in the right ventricle, then the left ventricle will take longer to depolarize, and
the QRS complex pattern will appear similar to a LBBB.
Ex1.
ECG findings:
2. Accelerated Idioventricular Rhythm (AIVR)
Ex2.
ECG findings: Accelerated Idioventricular Rhythm (AIVR) – Slow VT
ECG findings: Accelerated Idioventricular Rhythm (AIVR) – Slow VT

3.Junctional Rhythms
A junctional rhythm occurs when the electrical activation of the heart originates near or
within the atrioventricular node, rather than from the sinoatrial node. Because the
normal ventricular conduction system (His-Purkinje) is used, the QRS complex is
frequently narrow. A junctional rhythm is normally slow — less than 60 beats per
minute. When faster, it is referred to as an accelerated junctional rhythm.
Because the electrical activation originates at or near the AV node, the P wave is
frequently not seen; it can be buried within the QRS complex, slightly before the QRS
complex or slightly after the QRS complex. The morphology of the P wave will not be
similar to the sinus P wave, which is normally upright in lead II and biphasic in lead V1.
Often, the P wave is inverted in lead II, if it can be seen at all. A pacemaker may be
needed to relieve symptoms when no reversible cause — i.e. AV blocking medications
or electrolyte disturbances — is found.
The strip below shows a junctional rhythm with retrograde P waves seen just before the
QRS complex. The second rhythm strip shows retrograde P waves just after the QRS
complex.
EX1.
ECG findings: Accelerated Junctional Rhythm
Ex2.
ECG findings: Accelerated Junctional Rhythm
EX3.
ECG findings: Junctional Bradycardia
Ex4.
ECG findings: Junctional Tachycardia
4.Premature Ventricular Contractions (PVCs)

A premature ventricular contraction occurs when a focus in the ventricle generates an
action potential before the next scheduled sinoatrial nodal action potential.
There are four main characteristics of premature ventricular contractions:
1. Premature, occurring earlier than expected if measured against previous R-R intervals.
2. Ectopic, originating outside of the SA node, and thus the QRS morphology would be
different from the normal morphology when the action potential travels through the
normal conduction system.
3. Wide complexes; because they come from the ventricles and do not use the normal
ventricular conduction system, action potentials need to travel from myocyte to myocyte,
which is much slower, creating a wide QRS complex. Unlike premature atrial
contractions, or PACs, usually narrow-complexed because they use the normal
ventricular conduction system (unless a baseline right or left bundle branch block is
present).
4. Compensatory pause following the contraction; the extra action potential causes the SA
node to become refractory to generating its next scheduled beat, and thus it must “skip a
beat” and will resume exactly two P-P intervals after the last normal sinus beat.
Ventricular bigeminy occurs when every other beat is a PVC.
No treatment is necessary for PVCs. If symptomatic, beta-blockers or antiarrhythmic

drugs can be effective. Rarely, ablation of PVCs is needed.
5.Ventricular Fibrillation (VF)

Ventricular fibrillation is often a fatal arrhythmia. It occurs when the ventricular rate
exceeds 400. In this setting, virtually no forward cardiac output occurs. Advanced
Cardiac Life Support (ACLS) should be instituted immediately, including emergent
electrical cardioversion. This is frequently accomplished using an automated external
defibrillator (AED). Ventricular fibrillation is the main cause of sudden death in patients
with myocardial infarction. Implantable cardioverter defibrillators (ICDs) are
recommended in certain situations to abort sudden cardiac death from ventricular
fibrillation.
6.Ventricular Tachycardia (VT)

Ventricular tachycardia refers to a wide QRS complex heart rhythm — that is, a QRS
duration beyond 120 milliseconds — originating in the ventricles at a rate of greater than
100 beats per minute. This can be hemodynamically unstable, causing severe
hypotension, and can thus be life-threatening. Ventricular fibrillation, asystole and
sudden cardiac death can occur soon after ventricular tachycardia if action is not taken
immediately.
Ventricular tachycardia can occur with many variations of the QRS morphology,
depending on where the arrhythmia originates, which sometimes makes diagnosis on
ECG challenging. Below are two examples of ventricular tachycardia with different QRS
morphologies — one with a right bundle branch block morphology and one with a left
bundle branch block morphology. VT can also occur with QRS morphologies anywhere
in between. You can find links to many more examples of VT at the bottom of this
review.
Ventricular tachycardia can be classified as sustained or non-sustained VT, or NSVT.

Sustained VT is any ventricular tachycardia that lasts for more than 30 seconds or is
symptomatic. Non-sustained VT lasts for less than 30 seconds and is asymptomatic.
Ventricular tachycardia should be described by type (monomorphic or polymorphic),

duration (sustained or non-sustained) and heart rate — i.e. monomorphic VT non-
sustained at a heart rate of 220 bpm or sustained polymorphic VT at a heart rate of 250
bpm.
Electrophysiologists may also describe the location within the ventricles from where the
VT is originating. This can be determined by the morphology of the QRS complex. For
example, VT that has a LBBB morphology must come somewhere from the right
ventricle; this is because the electrical potential takes a long time to reach the left
ventricle, similar to what occurs with a simple LBBB.
Polymorphic VT (Torsades de Pointes) is a form of VT with multiple QRS morphologies.

Polymorphic VT is best treated with intravenous magnesium. Patients with a prolonged
QT interval have a higher risk for developing polymorphic VT. Removing offending
drugs that prolong the QT interval and correcting potassium or calcium imbalances is
crucial. Here is an example of polymorphic VT:
Ventricular tachycardia can be difficult to distinguish from supraventricular tachycardia,

or SVT, with aberrancy. The Brugada Criteria are most commonly used to differentiate
between these two entities — a clinically important distinction. Similar rules are provided
in the American College of Cardiology/American Heart Association Guidelines. If
present, “fusion beats” and “capture beats” can also be helpful to diagnose VT.
A fusion beat — also known as Dressler’s beat — occurs when sinus node activity (P
wave) begins to conduct through the normal conduction pathway during an episode of
VT. The abnormal ventricular impulse then conducts retrograde (backward) across the
atrioventricular node, colliding with the sinus impulse. The resulting QRS is a fusion of
the normal QRS morphology and the ventricular morphology from the VT.
A capture beat is similar to a fusion beat, except the QRS morphology looks completely
like the normal QRS complex, as the sinus node impulse conducts to the ventricles
before the retrograde ventricular activation occurs.
A few general rules apply to diagnosing ventricular tachycardia:

1. If there is any question regarding diagnosis, treat the patient as if the rhythm is VT.
2. The rhythm is much more likely to be VT in patients with ischemic heart disease or
systolic congestive heart failure.
3. VT is more likely with advancing age. Some references state that in patients aged older
than 40 years, assume the rhythm is VT — though this is not 100% accurate.
The Brugada criteria/algorithm is outlined below.
1. Do you see concordance present in the precordial leads (V1-V6)?
Sometimes explained as the absence of a “RS complex,” concordance simply means

“all up” or “all down.” A simple way to think of this would be to ask the question: Are all
QRS complexes completely upright (positive) or completely downward (negative) in the
precordial leads? If the answer is yes, then VT is the diagnosis. The images below show
positive and negative concordance during VT.
2. Is the R to S interval greater than 100 ms in any one precordial lead?
If the R to S interval exceeds 100 ms in any one precordial lead, then VT is the

diagnosis. Simply use calipers to measure the distance between the R wave and S
wave in each precordial lead. An example is below.
3. Do you see atrioventricular dissociation?
If AV dissociation is present, the diagnosis is VT. AV dissociation occurs when P waves,

representing atrial depolarization, are seen at different rates than the QRS complexes.
This is present in only a small percentage of VT ECG tracings, but it is diagnostic of VT.
Frequently, this is difficult to see due to the fast rate of the QRS complex. Below is an
ECG strip of a patient with VT. See the PP interval when in sinus rhythm then march out
the P waves within the wide QRS complex to find the AV dissociation that is present,
confirming the diagnosis of VT.
4. Examine the morphology of the QRS complex to see if it meets the specific

criteria for VT.
VT is frequently either in a right bundle branch block (upright in V1) or a left bundle
branch block pattern (downward in V1).
If upward in lead V1 (RBBB pattern), then VT is present in the following situations:
 A monophasic R or biphasic qR complex in V1

 A rS complex in lead V6 favors VT
 A RSR’ or “bunny-ear” pattern present in V1, with the R peak being higher in amplitude
than the R’ peak (see image below)
If downward in lead V1 (LBBB pattern), then VT is present in the following situations:
 The presence of any Q or QS wave in lead V6 favors VT

 A wide R wave (≥ 40 ms) in lead V1 or V2 favors VT; see image below
 Slurred or notched downstroke of the S wave in V1 or V2 favors VT
 Duration of onset of QRS complex to peak of QS or S wave greater than 60 ms favors
VT
Note that rhythms can, at times, originate in the ventricles but have a heart rate less
than 100 bpm. These rhythms — called “idioventricular rhythms” — are sometimes
referred to as “slow ventricular tachycardia” or “slow VT” because they meet the
diagnostic criteria for VT, but the heart rate is below 100 bpm. When the heart rate is
less than 60 bpm, and the rhythm originates in the ventricle, it is simply called an
“idioventricular rhythm.” When the heart rate is between 60 and 100 bpm, it is referred
to as an “accelerated idioventricular rhythm,” or AIVR; this is a common
hemodynamically stable rhythm that occurs after myocardial infarction and requires no
treatment. Some examples of both VT and idioventricular rhythms are below.
Ex1.
ECG findings:
2. Accelerated Idioventricular Rhythm (AIVR) – Slow VT
EX2.
ECG findings: Bidirectional Ventricular Tachycardia
Bidirectional ventricular tachycardia is quite rare, but pathognomonic for digoxin toxicity.

This ECG has two distinct QRS morphologies alternating every other beat. The QRS
complex duration is prolonged (wide). Both morphologies meet criteria for a ventricular
origin. They are both in a right bundle branch block pattern since they are upright in lead
V1. One of the QRS complexes is upward concordant in the precordial leads (all
upward) indicating a ventricular origin. The other morphology has an R larger than the
R' in lead V1 indicating a ventricular origin. Note the pause, one sinus beat, then the
resumption of the bidirectional ventricular tachycardia.
Ex2.
ECG findings:
2. Non-sustained Monomorphic Ventricular Tachycardia
Ex3.
ECG findings: Monomorphic sustained VT
Ex4.
ECG findings: Ventricular Tachycardia with Anti-Tachycardia Pacing (ATP)
Ex5.
ECG findings: Polymorphic Non-sustained Ventricular Tachycardia
Ex6.
ECG findings: Polymorphic sustained Ventricular Tachycardia

PVI. Miscellaneous
1.Arrhythmogenic Right Ventricular

Dysplasia (ARVD)
The classic ECG findings in arrhythmogenic right ventricular dysplasia are inverted T
waves in the right precordial leads (V1-V3) with an “epsilon wave” just after the QRS in
lead V1, representing early afterdepolarizations or “late potentials.” The epsilon wave is
frequently described as having a “grassy knoll” appearance. This can also be seen on a
signal-averaged ECG.
ECG findings: Arrhythmogenic Right Ventricular Dysplasia (ARVD) with Epsilon Waves

2.Atrial Septal Defect (ASD)
An atrial septal defect should show a right bundle branch block, or RBBB ― sometimes
incomplete ― on ECG. This is partially due to the right ventricular volume and pressure
overload that occurs. When an ostium primum atrial defect is present, the ECG reveals
left axis deviation. When an ostium secundum atrial septal defect is present, the ECG
reveals right axis deviation.
3.Brugada Syndrome
Brugada Syndrome is a genetic disorder that results in sudden cardiac death from
polymorphic ventricular tachycardia or ventricular fibrillation in the setting of a
structurally normal heart. This most commonly results from a mutation in the sodium
channel ― gene SCN5A. Unlike other genetic syndromes that result in sudden cardiac
death, the QT interval is normal in Brugada Syndrome.
There are three types of ECG findings in Brugada syndrome patients:
Type I: Lead V1 has a “coved” ST segment elevation of at least 2 millimeters, followed

by a negative T wave.
Type II: There is a “saddleback” appearance of the ST segment in lead V1 with ST
segment elevation of at least 2 millimeters; this can be present in normal individuals as
well.
Type III: Features of type I (coved) or type II (saddleback) with less than 2 millimeters of
ST segment elevation.
These ECG changes can be provoked in the electrophysiology lab by

infusing ajmaline or procainamide. The treatment for Brugada Syndrome is
an implantable cardioverter defibrillator, or ICD.
4.Dextrocardia
Dextrocardia occurs when the heart is positioned in the right side of the chest instead of
the left.
The ECG findings include:
1. Predominantly negative P wave, QRS complex, and T wave in lead I.

2. Low voltage in leads V3-V6 (since these leads are placed on the left side of the
chest).
ECG findings:
1. Atrial Flutter with a rapid ventricular response

2. Dextrocardia
5. Digoxin Effect
Digoxin can cause many different ECG abnormalities when supratherapeutic levels
occur.
The classic digoxin effect appears as a downsloping ST segment depression, also

known as the "reverse tick" or "reverse check" sign.
Digoxin toxicity can induce literally every arrhythmia except for rapidly conducted atrial
arrhythmias (atrial fibrillation and atrial flutter). The classic arrhythmias seen during
digoxin toxicity include atrial tachycardia with a 2:1 conduction, bidirectional ventricular
tachycardia and atrial fibrillation with a slow ventricular response.
ECG findings: AT with 2:1 conduction
ECG findings:
1. Atrial Tachycardia with 2:1 conduction
ECG findings: Bidirectional Ventricular Tachycardia
Bidirectional ventricular tachycardia is quite rare, but pathognomonic for digoxin toxicity. This
ECG has two distinct QRS morphologies alternating every other beat. The QRS complex
duration is prolonged (wide). Both morphologies meet criteria for a ventricular origin. They are
both in a right bundle branch block pattern since they are upright in lead V1. One of the QRS
complexes is upward concordant in the precordial leads (all upward) indicating a ventricular
origin. The other morphology has an R larger than the R' in lead V1 indicating a ventricular
origin. Note the pause, one sinus beat, then the resumption of the bidirectional ventricular
tachycardia.
6.Early Repolarization
Early repolarization is a common finding in young, healthy individuals. It appears as mild
ST segment elevation that can be diffuse; however, it is more prominent in the
precordial leads. The ST elevation in this setting appears like an elevated “J point.”
While this is thought to be a benign finding, it needs to be distinguished from pathologic
ST elevation that can be seen during acute myocardial infarction and pericarditis.
Note: The ECG changes of pericarditis must be distinguished from those of early
repolarization. The ST elevation seen in early repolarization is very similar: diffuse and
concave upward.
Three things may help to distinguish pericarditis from early repolarization:
1. The ratio of the T wave amplitude to the ST elevation should be > 4 if early repolarization
is present. In other words, the T wave in early repolarization is usually 4 times the
amplitude of the ST elevation. Another way to describe this would be that the ST
elevation is less than 25% of the T wave amplitude in early repolarization.
2. The ST elevation in early repolarization resolves when the person exercises.
3. Early repolarization, unlike pericarditis, is a benign ECG finding that should not be
associated with any symptoms.
7.Hypercalcemia
The ECG findings of hypercalcemia include:
1. A shortened QT interval
2. A shortened ST segment
3. Osborne Waves
8.Hypokalemia
The typical ECG findings of hypokalemia (low potassium level) include:
1. U wave that occurs just after the T wave and is usually of smaller amplitude than
the T wave.
2. flattening of the T wave.
3. ST depression on occasion, which can mimic ischemia.
9.Hyperkalemia
Hyperkalemia can cause life-threatening arrhythmia, and thus recognizing related
patterns on the ECG is crucial. The ECG findings of hyperkalemia change as the
potassium level increases, from slightly high levels to very high levels. The ECG
findings include:
1. Peaked T waves best seen in the precordial leads, shortened QT interval and, at times,
ST segment depression
2. Widening of the QRS complex (usually potassium level ≥ 6.5 mEq/L). This frequently
appears as “non-specific intraventricular conduction delay,” characterized by a widened
QRS complex of greater than 120 milliseconds that does not meet the criteria for a left or
right bundle branch block. Frequently, an IVCD will look like a LBBB in lead V1 with a rS
complex or monomorphic S wave, and it appears like a RBBB in leads I and V6 with a
broad, slurred S wave.
CLINICAL PEARL: If you see an IVCD, think of hyperkalemia.
3. Decreased amplitude of the P waves, an increase in the PR interval and bradycardia in

the form of atrioventricular blocks occur as the potassium level exceeds 7.0 mEq/L
CLINICAL PEARL: Supportive measurements like fluids, pacing and pressors do not
work in the setting of hyperkalemia. You must treat the hyperkalemia first.
4. Absence of the P waves and eventually a “sine wave” pattern, as seen below, which is
frequently a fatal rhythm
CLINICAL PEARL: Giving intravenous calcium is “cardioprotective” in the setting
of hyperkalemia. Frequently, instant reversal of all hyperkalemic ECG changes
within seconds of administration is experienced; see relevant example below.
Calcium does not decrease the potassium levels; therefore, other therapy such
bicarbonate or insulin is needed to do this. Calcium administration can be fatal
when digoxin toxicity is causing hyperkalemia and should be avoided.
EX1.
ECG findings:
1. Junctional Rhythm
2. Hyperkalemia
EX2.
ECG findings:
2. Hyperkalemia
EX3
ECG findings:
2. Hyperkalemia
Note the time stamp in the lower right corner of the ECG. Calcium is given to reverse the
electrical effects of hyperkalemia (although it does not lower the potassium level). Click here to
see the ECG of the same person only 2 minutes after calcium is given.
10. Hypokalemia
The typical ECG findings of hypokalemia (low potassium level) include:
1. U wave that occurs just after the T wave and is usually of smaller amplitude than
the T wave.
2. flattening of the T wave.
3. ST depression on occasion, which can mimic ischemia.
11.Hypertrophic Obstructive Cardiomyopathy

(HOCM)
Hypertrophic obstructive cardiomyopathy is a pathologic cardiac condition in which the
interventricular septum is abnormally thickened.
The classic ECG finding in hypertrophic obstructive cardiomyopathy is large dagger-like

“septal Q waves” in the lateral — and sometimes inferior — leads due to the abnormally
hypertrophied interventricular septum. Criteria for left ventricular hypertrophy is usually
present. Wolff-Parkinson-White, or WPW, syndrome can be associated with HOCM as
well.
The apical variant of HOCM, known as “Yamaguchi Syndrome,” does not result in

septal Q waves, as the septum is normal in thickness in this conduction. The cardiac
apex is abnormally thickened, resulting in diffuse T wave changes throughout the
precordial leads. This is sometimes referred to as “giant T Wave Inversion.”
ECG findings:
1. Apical Hypertrophic Cardiomyopathy

3. 3rd Degree AV Block (Complete Heart Block)
12.Hypothermia
The ECG findings of hypothermia include:
1. An "Osborne wave" characterized by a notch in the downward portion of the R

wave in the QRS complex.
2. Low voltage.
3. Bradycardia: This can be sinus bradycardia, junctional bradycardia, atrial
fibrillation with a slow ventricular response or higher grade AV blocks.
4. Baseline artifact from shivering
ECG findings:
2. 3rd Degree AV Block (complete heart block)
3. Osborne waves consistent with hypothermia
4. Non-specific ST-T wave abnormalities
13. Limb Lead Reversal

If the limb lead that was supposed to be attached to the right arm is put on the left arm
— and vise-versa — a characteristic appearance will be seen on ECG that includes:
1. Predominantly negative P wave, QRS complex and T wave in lead I.

2. Predominantly upward P wave, QRS complex and T wave in aVR.
This is opposite of what is seen in a normal ECG. The above findings are similar to that
seen in a person with dextrocardia; however, if the heart is located in the right side of
the chest instead of the left, the voltage in leads V3-V6 will be very low. This would not
be seen in simple limb lead reversal.
ECG findings:
2. Limb Lead Reversal

3. Old Inferior Myocardial Infarction
4. T Wave Abnormality - Consider Ischemia
14. Low Voltage

Low voltage on the ECG is defined as a peak-to-peak QRS amplitude of less than 5
millimeters in the limb leads and/or less than 10 millimeters in the precordial leads.
Low voltage may be present in the following situations:
1. Obesity
2. Chronic obstructive pulmonary disease, or COPD
3. Pericardial effusion
4. Severe hypothyroidism
5. Subcutaneous emphysema
6. Massive myocardial damage/infarction
7. Infiltrative/restrictive diseases such as amyloid cardiomyopathy
Note: If the gain indicated at the left of the ECG is turned down accidentally, the voltage
will be falsely low (pseudo low voltage). The indicator should be set to 10 mm
amplitude.
ECG findings:
1. Atrial Fibrillation
2. Low Voltage
3. Incomplete Right Bundle Branch Block
4. Premature Ventricular Contractio

ECG findings:
2. Low Voltage
3. Old Anterior Myocardial Infarction
4. Old Inferior Myocardial Infarction
14. Lown-Ganong-Levine Syndrome

The Lown-Ganong-Levine (LGL) syndrome occurs when an accessory pathway is
congenitally present that directly connects the atria to the ventricles, bypassing the AV
node similar to the Wolff-Parkinson-White (WPW) syndrome. Thus, when the sinus
node fires, the electrical activation does not need to travel through the AV node like in a
normal person (which usually delays the impulse from getting to the ventricles). Instead,
the action potential can travel down the accessory pathway and activate the ventricles
rapidly. This short duration between the sinus node firing and the ventricles being
depolarized results in a short PR interval on the ECG.
The main distinguishing feature between LGL and WPW syndromes is that the
accessory pathway in LGL syndrome connects distally to the normal conduction
pathway (bundle of His), and in WPW the accessory pathway connects to the
ventricular myocardium. Thus, both disease states can have a short PR interval,
however LGL syndrome will not have a delta wave or widened QRS complex as seen in
WPW syndrome. This is because ventricular activation occurs normally in LGL
syndrome instead of occurring from myocyte to myocyte as seen in WPW.
Similar arrhythmias occur with LGL syndrome and WPW syndrome,

including atrioventricular reentrant tachycardia (AVRT) and rapidly conducting atrial
fibrillation. Treatment is similar to WPW and procainamide is frequently utilized. Ablation
of the accessory pathway is more difficult in LGL syndrome compared to WPW
syndrome since it is located very close to the AV node and there is risk of causing
complete heart block necessitating permanent pacemaker implantation.
ECG findings:
2. Lown-Ganong-Levine
3. Premature Atrial Contractions

ECG findings:
2. Lown-Ganong-Levine
15. Left Ventricular (LV) Aneurysm

A left ventricular aneurysm can be diagnosed on ECG when there is persistent ST
segment elevation occurring 6 weeks after a known transmural myocardial infarction
(usually an anterior MI). Without knowing the past medical history, the ECG changes of
an aneurysm may mimic an acute anterior MI.
With an anterior or apical aneurysm, the persistent ST elevation is in lead V1 and V2

with associated Q waves indicating the old anterior MI. In an inferior aneurysm it would
be in lead II, III and aVF, although this is less common. The only way to be sure that the
ECG changes present are from an LV aneurysm (not ST elevation from an acute MI) is
to have the patient’s history of a prior MI and cardiac imaging to document the presence
of an aneurysm. The shape of the ST elevation is also relatively unique and has been
described as “coving” as seen below:
ECG findings:
2. Old Anterior Wall Myocardial Infarction
3. Left Ventricular Aneurysm

16. Neurologic Insult
Most commonly seen in the setting of acute stroke or cerebrovascular accident,
intracranial hemorrhage, subarachnoid hemorrhage, or after carotid endarterectomy,
neurologic injury can result in the following ECG changes:
1. Diffuse deeply inverted T waves

2. Prolonged QT interval
These changes may mimic ischemia. There is debate regarding the risk for
the prolonged QT interval leading to polymorphic ventricular tachycardia in this setting.
ECG findings:
2. Prolonged QT Interval and T wave abnormality consistent with Neurologic Injury
This patient had an intracranial hemorrhage (ICH).

ECG findings:
This patient had just underwent carotid endarterectomy and had a normal ECG 1 day
prior.
ECG findings:
17. Pericarditis ECG

Pericarditis, or inflammation of the pericardium, has typical ECG findings. These
findings occur in progressive stages, all of which are seen in about 50% of cases of
pericarditis.
Stage I (acute phase): Diffuse concave upward ST segment elevation in most leads,

PR depression in most leads (may be subtle) and sometimes notching at the end of the
QRS complex.
Stage II: ST segment elevation and PR depression have resolved and T waves may be
normal or flattened.
Stage III: T waves are inverted, and the ECG is otherwise normal.
Stage IV: T waves return to the upright position, and thus the ECG is back to normal.
Note: The ECG changes with pericarditis must be distinguished from those of early
repolarization. The ST segment elevation seen in early repolarization is very similar ―
diffuse and concave upward. However, three things may help to distinguish pericarditis
from early repolarization:
1. The ratio of the T wave amplitude to the ST elevation should be greater than 4 if
early repolarization is present, meaning the T wave in early repolarization is
usually 4 times the amplitude of the ST segment elevation. Another way to
describe this would be that the ST segment elevation is less than 25% of the T
wave amplitude in early repolarization.
2. The ST segment elevation in early repolarization resolves when the person
exercises.
3. Early repolarization, unlike pericarditis, is a benign ECG finding that should not
be associated with any symptoms.
17. Prolonged QT Interval
A prolonged QT interval has a variety of causes and can be a very serious ECG finding,
as it may lead to the potentially fatal arrhythmia polymorphic ventricular
tachycardia (Torsades de Pointes). See the ECG Tutorial section on QT interval to learn
how this is measured.
Multiple medications, electrolyte abnormalities (hypocalcemia, hypomagnesemia and
hypokalemia) and certain disease states (ie, intracranial hemorrhage) can prolong the
QT interval. Prolonged QT genetic syndromes exist and include Romano-Ward
syndrome, Jervell-Lange-Nielsen syndrome and long-QT 1-13 syndrome.
18. Pulmonary Embolism
The most common ECG finding in the setting of a pulmonary embolism is sinus
tachycardia. However, the “S1Q3T3” pattern of acute cor pulmonale is classic; this is
termed the McGinn-White Sign.
A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together
indicate acute right heart strain. This pattern only occurs in about 10% of people with
pulmonary embolisms and is similar to the ECG findings of a left posterior fascicular
block, or LPFB. Recall that sinus tachycardia is actually the most common ECG finding
during a pulmonary embolus.
ECG findings:
2. Pulmonary Embolism with S1Q3T3 pattern
3. Interventricular Conduction Delay

20. Wellens’ Syndrome
Wellen's phenomenon occurs when biphasic T waves are seen in leads V1-V3, or deep
symmetric inverted T waves are seen in the precordial leads. Both of these ECG
findings are indicative of a severe proximal left anterior descending stenosis (acute or
chronic).
Note that there is no ST segment elevation that occurs with Wellen's ECG changes.
21. Wolff-Parkinson-White (WPW) Syndrome
Wolff-Parkinson-White is characterized by the presence of an “accessory pathway” or a
“bypass tract.” This connects the electrical system of the atria directly to the ventricles,
allowing conduction to avoid passing through the atrioventricular node.
In normal individuals, when the sinus node creates an action potential, it must pass
through the AV node to get to the ventricles. When an accessory pathway is present,
the sinus node action potential can pass through the bypass tract before the AV node,
resulting in the ventricles becoming rapidly depolarized. This is termed “pre-excitation”
and results in a shortened PR interval on the ECG.
The typical ECG finding of WPW is a short PR interval and a “delta wave.“ A delta wave
is slurring of the upstroke of the QRS complex. This occurs because the action potential
from the sinoatrial node is able to conduct to the ventricles very quickly through the
accessory pathway, and thus the QRS occurs immediately after the P wave, making the
delta wave.
The combination of WPW and atrial fibrillation can potentially be fatal, especially if AV
blocking agents are given (remember “ABCD” for adenosine or amiodarone, beta-
blockers, calcium channel blockers and digoxin). The medical treatment is procainamide
― though electrical cardioversion is reasonable, especially with hemodynamic
instability.
In patients with WPW and atrial fibrillation, the erratic atrial action potentials (occurring
at 400-600 bpm) can conduct through the accessory pathway very quickly ― faster than
through the AV node. Therefore, patients with WPW who develop atrial fibrillation have
higher ventricular rates than those without WPW.
If an AV blocking agent is given, fewer atrial action potentials will pass through the AV
node, and more will pass through the accessory pathway. This paradoxically increases
the ventricular rate, potentially causing the fatal, hemodynamically unstable
rhythm ventricular fibrillation. Procainamide or electrical cardioversion is recommended
in these situations.
ECG findings:
2. Wolff-Parkinson-White Syndrome with Alternans

When every other beat conducts through an accessory pathway causing a short PR interval and a
delta wave, the term WPW alternans is used. The accessory pathway that is exists is refractory
on an alternating basis creating this appearance. This is a relatively rare ECG finding.

Section 1. ECG Basics 1. TP Segment.: ECG Reviews and Criteria Brugada Syndrome

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Section 1. ECG Basics 1. TP Segment.: ECG Reviews and Criteria Brugada Syndrome

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Section 1.

In the normal ECG, there is a large S wave in V1 that progressively becomes

Both types of wave progression are depicted below.

Abnormalities of the Q waves are mostly indicative of myocardial infarction and

Although memorizing the above picture is crucial to accurately determining axis,

Normal QRS Axis

Right Axis Deviation

Ectopic atrial rhythms including atrial tachycardia, multifocal atrial

Note that when atrioventricular, or AV, dissociation is present (complete heart

Below are examples using each method.

Section 2. ECG Reviews and Criteria

1. Atrial Fibrillation ECG Review

Because the AV node is intermittently (not regularly) refractory, the QRS

Ex 1. Atrial Fibrillation with Bradycardia ECG

1. Atrial Fibrillation with a slow ventricular response

3. Poor R Wave Progression

Ex2. Atrial Fibrillation with Normal Ventricular Rate ECG

1. Atrial Fibrillation with a rapid ventricular response (RVR)

3. ST abnormality - consider ischemia

1. Atrial Fibrillation with a rapid ventricular response (RVR)

2. Premature Ventricular Contraction (PVC)

2. Atrial Flutter ECG Review

CLINICAL PEARL: A narrow complex tachycardia at a ventricular rate of exactly

The regularity of the QRS complexes frequently present with atrial flutter helps to

Typical atrial flutter rotates counterclockwise in direction, from a reentrant circuit

Ex2. Atrial Flutter with 2:1 Conduction ECG

1. Atrial Flutter with 4:1 Conduction

2. Right Bundle Branch Block

3. Left Anterior Fascicular Block

Ex4. Atrial Flutter with 6:1 Conduction ECG

Ex5. Atrial Flutter with Variable Conduction ECG

If a premature atrial contraction, or PAC, or less commonly a premature

Findings on ECG include the following:

1. Narrow complex tachycardia

Findings on ECG include the following:

 a narrow complex tachycardia; and

5. Ectopic Atrial Rhythms ECG Review

Ectopic P waves are also commonly seen in multifocal atrial tachycardia, or

Atrial tachycardia is quite common. The causes of atrial tachycardia include

Atrial tachycardia is best treated with AV blocking medications such as beta-

Ex1. Atrial Tachycardia

Ex2. Atrial Tachycardia with 2:1 AV Block ECG

2. Left Bundle Branch Block

6. Multifocal Atrial Tachycardia (MAT)

The differential diagnosis of an irregularly irregular rhythm includes atrial

1. Multifocal Atrial Tachycardia (MAT)

2. Aberrantly conducted supraventricular beats

7. Premature Atrial Contractions (PACs)

There are four main characteristics of PACs:

1. Premature, occurring earlier than expected if measured against previous P-P

Ashman’s Phenomenon, also known as the Ashman Beat, occurs when a PAC or

Ex1. Atrial Bigeminy ECG

2. Premature Atrial Contractions (PACs) in a pattern of atrial bigeminy

Ex2. Non-conducted or Blocked Premature Atrial Contractions

2. Non-conducted Premature Atrial Contractions (Blocked PACs)

Ex3. Premature Atrial Contractions (PACs)

Second-degree SA exit block type I (Wenkebach) demonstrates progressive

Second Degree Type II Sinoatrial Exit Block

 AV blocking medications (beta-blockers, nondihydropyridine calcium

The differential diagnosis for sinus tachycardia includes the following:

12.Wandering Atrial Pacemaker (WAP)

By definition, WAP must have at least three distinctly different P wave

The differential diagnosis of an irregularly irregular rhythm includes atrial