ANALYSIS AND INTERPRETATION OF THE NORMAL VALUES

ELECTROCARDIOGRAM Heart rate 60 - 100 bpm

PR interval 0.12 - 0.20 s
INTRODUCTION QRS interval ≤ 0.12 s
The electrocardiogram (ECG) is one of the most useful QT interval < half RR interval
diagnostic tests in emergency medicine. It is an easy and (males < 0.40 s;
inexpensive test that is used routinely in the assessment of females < 0.44 s)
patients with chest pain. The ECG is the cornerstone for P wave amplitude (in lead II) ≤ 3 mV (mm)
making the diagnosis of cardiac ischemia and is used for P wave terminal negative ≤ 1 mV (mm)
making decisions about eligibility for thrombolytic therapy. deflection (in lead V1)
Q wave < 0.04 s (1 mm) and < 1/3 of R
THE 12 LEAD ECG wave amplitude in the same
The 12 lead ECG is made up of the three standard limb leads lead
(I, II and III), the augmented limb leads (aVR, aVL and aVF)
and the six precordial leads (V1, V2, V3, V4, V5 and V6).
APPROACH TO THE ECG
Developing a systematic approach to the interpretation of the
ECG is a critical skill for all clinicians. The following outlines
one such approach.
Step 1: Determine the heart rate
There are a number of strategies for determining the heart
rate. A simple, quick technique is to find a QRS complex that
falls on a major vertical grid-line (1), then count the number of
large squares to the next QRS complex (2). Dividing this
number into 300 gives you the heart rate. In the ECG below,
there are 2 large squares between QRS complexes. 300/2
gives a heart rate of 150 beats per minute.

WAVES AND COMPLEXES

Step 2: Measure important intervals

The measurement of important electrocardiographic intervals
usually includes the PR interval, the QRS interval and the QT
interval. At a standard paper speed of 25 mm/second, the
width of each small square (1mm) represents 0.04 seconds.
One large square (5mm) represents 0.2 seconds.

INTERVALS AND SEGMENTS

PR Interval: From the start of the P wave to the start of the
QRS complex
PR From the end of the P wave to the start of the
Segment: QRS complex
The junction between the QRS complex and the
J Point: ST segment
From the start of the QRS complex to the end of
QT Interval: the T wave
QRS
Interval: From the start to the end of the QRS complex
ST From the end of the QRS complex (J point) to
Segment: the start of the T wave

Step 3a: Calculate the electrical axis

The mean QRS axis refers to the average orientation of the
heart's electrical activity. In most cases, an approximation of
the axis will be sufficient for the ECG interpretation. There are
many different approaches to axis determination, but this
discussion will be limited to a simple technique which uses the
leads I and aVF to calculate an approximate axis.
 Step 5: Inspect P waves for atrial enlargement
• Recall that the axis can be considered in terms of The P waves in leads I, II, III and V1 should be inspected for
four quadrants, with lead I oriented at 0°, and aVF evidence of right or left atrial enlargement. Usually, lead II will
oriented at +90°. An ECG with the QRS axis oriented have the clearest P wave.
to the quadrant between 0° and 90° is said to be
normal. • P wave amplitude should not exceed 3 small squares
(3 mm or 0.3mV). If it does, this represents right atrial
• An ECG with the QRS axis oriented to the quadrant enlargement.
between -1° and -90° is said to have left axis
deviation. • In lead V1, the terminal negative deflection of the P
wave represents left atrial depolarization and should
• An ECG with the QRS oriented to the quadrant not exceed 1 mm (0.1mV). If it does, this is indicative
between +91° and 180° is said to have right axis of left atrial enlargement.
deviation.
• An ECG with the QRS oriented to the quadrant
between -91° and -180° is said to have an
indeterminate axis because one cannot tell if it
represents right or left axis deviation.
Step 3b: Calculate the electrical axis
The mean QRS axis is oriented towards the lead with the
greatest net QRS deflection. To calculate the net QRS
deflection, add up the number of small squares that
correspond to the height of the R wave (positive deflection),
and subtract the number of small squares that correspond to
the height of the Q and S waves (negative deflection).

In actual fact,
the net QRS
deflection
can be
approximate
d without Step 6: Inspect QRS complexes for ventricular hypertrophy or
resorting to low voltage
counting
squares. In In the setting of Left Ventricular
the example Hypertrophy (LVH), the left
shown here, ventricle enlarges and so the
one can leads oriented to the left ventricle
easily see (V5, V6, aVL) will "see" more
that the net electrical activity moving towards
deflection is them. As well, the leads oriented
slightly more away from the left ventricle (V1,
positive than V2) will "see" more activity moving
negative. away from them. In LVH therefore,
leads V5, V6 and aVL will have tall
R waves, while leads V1 and V2
Step 3c: Calculate the electrical axis will have deep S waves. (The
Approximate the net QRS deflection for leads I and aVF. arrow in the diagram on the right
Remember that the mean QRS axis will be oriented towards shows the direction of the net
the lead with the greatest positive net QRS deflection. If the electrical activity in LVH.)
net deflection is positive for both, the axis lies between leads I
and aVF (0-90°) and is therefore normal. V1 or V2 V5, V6 or aVL The voltage criteria for
LVH are satisfied if the
Step 4: Evaluate the cardiac rhythm sum of the amplitude of
If the rhythm is regular, the RR interval should be constant the deepest S wave in V1
throughout the ECG. This can be checked using calipers, or or V2, and the amplitude
more simply by marking on a piece of paper the distance of the tallest R wave in
between two R waves, and comparing this distance between V5 or V6, is equal to or
pairs of QRS complexes on the ECG. Next, check to see if a P greater than 35 mm (3.5
wave is present before each of the QRS complexes. mV). The voltage criteria
are also satisfied if the
amplitude of the R wave
in lead aVL is equal to or
greater than 12 mm
(1.2mV).
Step 7a: Inspect QRS complexes for bundle branch block or
fascicular block
The normal QRS interval is 0.12 seconds (3 mm or 3 small
squares) on the ECG. To correctly determine the QRS interval,
use the lead with the widest QRS complex. If the QRS
complex is less than or equal to 0.12 seconds, then no further
analysis is necessary. If it is greater than 0.12 seconds, then
you should try to determine the reason for the abnormally long
QRS interval.
A simple approach is to consider the following three possible
causes for QRS widening:

Step 7e: Inspect QRS complexes for bundle branch block or

fascicular block
If the ECG cannot be characterized as a typical RBBB or a
typical LBBB, then it can be categorized as an intraventricular
conduction delay. This will not be addressed in any more
detail at this time.
Step 8: Assess Q waves and determine significance
The Q waves should be assessed and their significance
determined, particularly in regard to the diagnosis of
The type of bundle branch block can usually be determined myocardial infarction. Small Q waves are commonly a normal
from the examination of three key leads: I, V1 and V6. finding in the inferior leads III and aVF, and in the anterolateral
Step 7b: Inspect QRS complexes for bundle branch block or leads aVL, I, V5 and V6. Q waves of 0.04 seconds (1 mm)
fascicular block duration and greater than one third the R wave's amplitude in
In the normal heart, at the beginning of ventricular the same lead may be pathological.
depolarization, the QRS axis is oriented to the right because of
left-to-right depolarization of the septum. This produces a
small R wave in lead V1. Immediately following septal
depolarization, the left and right ventricles depolarize. The size
of the left ventricle results in a predominantly leftward axis for
the remainder of the QRS complex.

The pathological Q waves seen in V1 - V6 indicate that this

patient has had an anterior MI in the past. This patient also
has evidence of an acute inferior MI as shown by the ST
segment elevation in leads III and aVF.
Step 9: Assess ST segments and T waves
Step 7c: Inspect QRS complexes for bundle branch block or Assess the ST segment for the presence of elevations or
fascicular block depressions, together with T wave abnormalities. ST elevation
In the setting of RBBB, the initial part of the ECG is unchanged can indicate the presence of conditions such as acute
because septal depolarization and depolarization of the left myocardial injury, Prinzmetal's (variant) angina, pericarditis,
ventricle are unaffected. However, the right ventricle ventricular aneurysm or myocardial ischemia.
depolarizes in a delayed and slow fashion. This results in a
widening of the terminal part of the QRS complex and
orientation of the axis of the terminal part of the QRS complex
to the right.

This ECG is from a patient with an acute inferior MI. Note the
ST elevation in the inferior leads (II, III and aVF). The ECG also
shows ST depression in leads V1, V2 and V3 - likely a result of
reciprocal changes associated with the MI.
Step 7d: Inspect QRS complexes for bundle branch block or
fascicular block Step 10: Measure QT interval for specific diagnoses
In the setting of LBBB, the septum is activated in a right to left The QT interval can be prolonged secondary to metabolic
direction, and then there is depolarization of the right and left disorders and drug effects. It must be corrected for heart rate
ventricles through the right bundle. The result is that the QRS since it is rate dependent. The corrected QT interval is
axis has a predominantly left orientation throughout and is calculated using the following formula:
wide secondary to the slow activation of the left ventricle. • QTI corrected = (QTI observed) / (square root of RR
interval)
The QTI corrected is often reported with computerized ECG
interpretation.
 5. T wave:
• T wave deflection should be in the same direction as
the QRS complex in at least 5 of the 6 limb leads
• normally rounded and asymmetrical, with a more
gradual ascent than descent
• should be upright in leads V2 - V6, inverted in aVR
• amplitude of at least 0.2 mV in leads V3 and V4 and
at least 0.1 mV in leads V5 and V6
• isolated T wave inversion in an asymptomatic adult is
generally a normal variant
6. QT interval:
• Durations normally less than or equal to 0.40
seconds for males and 0.44 seconds for females.
This ECG is from a male patient with familial prolonged QT
syndrome. The QTI corrected is approximately 0.52 seconds. Acute anterolateral MI
Normal QTI corrected: 0.40 seconds for males; 0.44 seconds Acute anterolateral MI is recongnized by ST segment elevation
for females. in leads I, aVL and the precordial leads overlying the anterior
and lateral surfaces of the heart (V3 - V6). Generally speaking,
ECG index the more significant the ST elevation , the more severe the
The following represent common ECG findings that the infarction. There is also a loss of general R wave progression
clinician should be familiar with. across the precordial leads and there may be symmetric T
wave inversion as well. Anterolateral myocardial infarctions
Normal ECG frequently are caused by occlusion of the proximal left anterior
descending coronary artery, or combined occlusions of the
LAD together with the right coronary artery or left circumflex
artery. Arrythmias which commonly preclude the diagnosis of
anterolateral MI on ECG and therefore possibly identify high
risk patients include right and left bundle branch blocks,
hemiblocks and type II second degree atrioventricular
conduction blocks.

A normal ECG is illustrated above. Note that the heart is

beating in a regular sinus rhythm between 60 - 100 beats per
minute (specifically 82 bpm). All the important intervals on this
recording are within normal ranges.
1. P wave:
• upright in leads I, aVF and V3 - V6
• normal duration of less than or equal to 0.11 seconds Acute inferior MI
• polarity is positive in leads I, II, aVF and V4 - V6; Leads II, III and aVF reflect electrocardiogram changes
diphasic in leads V1 and V3; negative in aVR associated with acute infarction of the inferior aspect of the
• shape is generally smooth, not notched or peaked heart. ST elevation, developing Q waves and T wave inversion
2. PR interval: may all be present depending on the timing of the ECG
relative to the onset of myocardial infarction. Most frequently,
• Normally between 0.12 and 0.20 seconds. inferior MI results from occlusion of the right coronary artery.
3. QRS complex: Conduction abnormalities which may alert the physician to
• Duration less than or equal to 0.12 seconds, patients at risk include second degree AV block and complete
amplitude greater than 0.5 mV in at least one heart block together with junctional escape beats. Note that
standard lead, and greater than 1.0 mV in at least the patient below is also suffering from a concurrent posterior
one precordial lead. Upper limit of normal amplitude wall infarction as eveidenced by ST depression in leads V1
is 2.5 - 3.0 mV. and V2.
• small septal Q waves in I, aVL, V5 and V6 (duration
less than or equal to 0.04 seconds; amplitude less
than 1/3 of the amplitude of the R wave in the same
lead).
• represented by a positive deflection with a large,
upright R in leads I, II, V4 - V6 and a negative
deflection with a large, deep S in aVR, V1 and V2
• in general, proceeding from V1 to V6, the R waves
get taller while the S waves get smaller. At V3 or V4,
these waves are usually equal. This is called the
transitional zone.
4. ST segment:
• isoelectric, slanting upwards to the T wave in the
normal ECG
• can be slightly elevated (up to 2.0 mm in some
precordial leads)
• never normally depressed greater than 0.5 mm in any
lead
Acute posterior MI Atrial fibrillation
When examining the ECG from a patient with a suspected Atrial fibrillation represents disorganized atrial activity without
posterior MI, it is important to remember that because the contraction or ejection. The electrocardiogram demonstrates
endocardial surface of the posterior wall faces the precordial an irregular baseline where the normal P waves are replaced
leads, changes resulting from the infarction will be reversed with rapidly quivering small deflection of variable amplitude (f
on the ECG. Therefore, ST segments in leads overlying the waves - outlined below). An irregularly irregular ventricular rate
posterior region of the heart (V1 and V2) are initially demonstrating narrow QRS complexes is established between
horizontally depressed. As the infarction evolves, lead V1 100 - 160 bpm. Atrial fibrillation is common in patients with
demonstrates an R wave (which in fact represents a Q wave in rheumatic heart disease, pulmonary emboli, cardiomyopathy,
reverse). Note that the patient below is also suffering from an pericarditis, ischemic heart disease and thyrotoxicosis. It
inferior wall myocardial infarction as evidenced by ST causes minimal hemodynamic compromise and often the
elevation in leads II, III and aVF. patient presents complaining of palpitations as the only
symptom. Although hemodynamic compromise is minimal,
atrial fibrillation is an important risk factor for the development
of thromboembolic complications, such as strokes and
transient ischemic attacks.

Acute right ventricular MI

In patients presenting with acute right ventricular MI,
abnormalities in the standard 12 lead ECG are restricted to ST
elevation greater than or equal to 1 mm in lead aVR. Although
isolated right ventricular MI is usually seen in patients suffering Atrial flutter
from chronic lung disease together with right ventricular The electrocardiogram in atrial flutter is typically characterized
hypertrophy, it can occur in patients suffering a transmural by its "sawtooth" flutter waves (F waves - arrows below) best
infarction of the inferior-posterior wall which extends to involve demonstrated in the inferior leads (II, III, aVF and V1). A rapid
the right ventricular wall as well. Right ventricular MI is most regular atrial rhythm is generally demonstrated between 250
commonly caused by obstruction of the proximal right and 350 bpm, and the qRS rate is determined by the ratio of
coronary artery and is frequently associated with right bundle atrioventricular conduction. Although the usual ratio of AV
branch block. Furthermore, only 5% - 10% of patients suffer conduction is 2:1 (as illustrated below), 1:1, 3:1, 4:1, 6:1 and
from hemodynamic symptoms. other variable ratios are also demonstrated, albeit less
frequently. Typically, this results in a ventricular heart rate
between 150 and 170 bpm. Atrial flutter is relatively
uncommon and is most often seen in patients presenting with
acute ischemic heart disease or pulmonary embolism.
Nevertheless, it can present as a chronic condition in patients
who suffer from organic heart disease.

Acute septal MI
Acute septal MI is associated with ST elevation, Q wave
formation and T wave inversion in the leads overlying the
septal region of the heart (V2 and V3).
Complete heart block
Complete heart block refers to a form of atrioventricular
dissociation where no P wave produces a QRS complex. A
sinus or ectopic atrial rhythm develops that fires
independently of the ventricles. This rhythm may be junctional
(as illustrated below) or ventricular in origin. The rhythm is
usually regular, but may present irregularly as a result of
intermittent premature ventricular beats. Patients presenting
with complete heart block complain of symptoms resembling
profound bradycardia (loss of atrial kick) and reduced cardiac
output (syncope, angina, presyncope).
 Hypokalemia
Hypokalemia is associated with progressive ST depression,
progressive flattening or inversion of the T waves, the
development of U waves, increased amplitude and duration of
the P waves and QRS complexes as well as a slight increase
in the duration of the PR interval. Furthermore, hypokalemia
affects automaticity of the pacemaker cells and leads to
multiple arrhythmias such as sinus bradycardia,
atrioventricular block, atrial flutter and Torsades de Pointes.
Most commonly, hypokalemia results from thiazide diuretic
misuse, diarrhea, renal or adrenal disease. Other causes
include infusion of large amounts of glucose or alkali
substances, liver cirrhosis and diabetic coma.

Digitalis effect
These glycosides can cause ST sagging and shortening, best
seen in leads V4, V5 and V6 (see below).

Left atrial enlargement

Left atrial enlargement is typically characterized by an
Dual chamber pacemaker increase in the terminal portion of the P wave. Best seen in
This electrocardiogram demonstrates an artificial cardiac lead II, this terminal deflection is often demonstrated as a
pacemaker which is responsible for initiating contractions distinct second peak within the P wave (arrow below). In some
within the atria as well as the ventricles. Note the double leads, this second peak gives the P wave an "m-like" shape.
pacemaker spikes associated with each complete cycle of This deflection does not usually affect the amplitude of the P
contraction. The first spike indicates stimuli to the atria, while wave, but may increase its duration to greater than 0.12
the second pacemaker spike indicates initiation of ventricular seconds. In addition to this increased P wave deflection in
contraction. lead II, LAE results in a terminal negative deflection within the
P wave best seen in lead V1 (see below). With extreme LAE,
the amplitude of the P wave may be increased, and terminal
negativity may be demonstrated in leads II, III and aVF (see
below). Left atrial enlargement may result from left atrial
dilatation, pressure overload (ie. from mitral valve disease) or
abnormal intra-atrial conduction. Other terms frequently used
to describe LAE include left atrial hypertrophy, left atrial
overload and left atrial abnormality.

Hyperkalemia
Potassium overdose is frequently seen in patients with renal
failure or those on K sparing diuretics. In mild hyperkalemia
(serum levels less than 6.5 mEq/l), leads II, V2 and V4
demonstrate tall, tented, symmetrical T waves with a narrow
base. The P wave remains normal, as does the QRS complex.
With moderate K overdose (6.5 mEq/l - 8.0 mEq/l) the QRS
complex broadens and the S wave is widened in leads V3 -
V6. This S wave become continuous with the tented T waves
and eventually the ST segment disappears. Furthermore the Left ventricular hypertrophy
duration of the P wave is increased, while the amplitude is Electrocardiograms from patients presenting with LVH
decreased. At K levels greater than 8.0 mEq/l (see below), the demonstrate variably increased R wave voltage and duration
P wave duration and PR interval duration both increase, until in leads over the right ventricle (V5 and V6 - circled below). In
the P wave eventually disappears entirely. The QRS complex 35% - 90% of the cases, there is a delay between the onset of
is diffusely broadened and continuous with the tall, tented T the QRS complex and the R wave. This intrinsicoid deflection
wave in all leads. may extend to greater than 0.05 seconds. Furthermore,
delayed repolarization as a result of ventricular hypertrophy
generally produces ST depression and T wave inversion in the
same leads. Enlargement of the left ventricle is commonly
associated with left atrial enlargement as well as incomplete
LBBB. Leads V2 and V3 commonly demonstrate increased S
wave amplitude (arrow below), while leads V5 and V6 show
increased R wave amplitude. Left ventricular hypertrophy may
be associated with conditions giving rise to pressure or
volume overload of the left ventricle such as aortic stenosis or
systemic hypertension. Furthermore, LVH increases patient
risk of other cardiovascular diseases including myocardial
infarction, congestive heart failure, stroke, arrhythmia and
sudden death.
 individuals, PAC's may arise from various stimuli including
tobacco, caffeine and alcohol as well as strong emotions.
Other situations which may lead to the development of PAC's
include myocardial infarction, various drugs, infections,
hypokalemia and hypomagnesemia.

Left bundle branch block

In left bundle branch block, activation of the intraventricular
septum is reversed and electrical impulses to the left ventricle
are delayed. These altered electrical forces produce a wide
QRS complex (greater than 0.12 seconds in duration) with an
abnormal morphology. In leads I and V6, abnormal initial
forces fail to produce any Q wave or S wave, and the resultant Premature ventricular complex
R wave is steep and often notched (circled below). Premature ventricular complexes (circled below) may arise in
Furthermore, a deep rapid S wave is generated in lead V1 normal individuals as well as patients suffering from nearly
(arrow below). The ST segment is slightly elevated in multiple every form of structural heart disease. Premature ventricular
leads and the T wave polarity is diffusely opposite to the complexes are recognized as single or paired unifocal beats,
ventricular complex. with no preceding P wave, a wide QRS complex of increased
amplitude characteristically lasting greater than 0.14 seconds,
and a T wave demonstrating polarity opposite to that of the
PVC. They arise early in the cardiac cycle and are more likely
to occur during periods of bradyarrhythmia. Although no P
waves precede the wide QRS complex, retrograde activation
of the atria may produce P waves which occur after the PVC or
are buried in their T waves. Premature ventricular beats may
arise from excessive catecholamines, myocardial ischemia or
injury, electrolyte imbalances, certain medications including
digitalis and class IA and IC antiarrhythmic agents.

Pericarditis
Patients presenting with acute pericarditis demonstrate diffuse
ST segment elevation in all leads except aVR and V1 (see
below). These ST changes are sometimes associated with
concurrent PR segment depression in the same leads and an
increased sinus heart rate (above 138 bpm). At 2-5 days after
the acute presentation, the ST segments return to baseline.
Following this return to baseline, the T waves in all leads
except aVR become inverted, eventually returning to their
previously normal polarity and amplitude over the following
couple of weeks. Prolonged QT interval
The QT interval represents the time between the beginning of
the Q wave until the end of the T wave. This interval is best
measured in lead II and represents both the depolarization
and repolarization phases of the ventricles. It is significantly
influenced by many factors including heart rate, various
medications (especially quinidine, procainaminde and
disopyramide), hypokalemia, hypomagnesemia and athletic
training. Therefore, tables or formulas are often needed to
calculate the corrected QT interval (ATc) to determine if the
QT interval on a particular electrocardiogram is appropriate for
its demonstrated heart rate. One accepted calculation in
determining this QTc is a modified version of Bazett's formula.
This formula states that the QTc = QT + 1.75(ventricular rate -
60). Normal values for this corrected QT interval are found to
Premature atrial complex approximate 0.41 seconds, although this value is slightly
Premature atrial complexes (circled below) are recognized by longer in females and in patients of increasing age. If this
three distinct features: calculation is applied to the ECG demonstrated below, the
1. a premature and unusually shaped P wave QTc is measured as 0.52 seconds [QTc = 0.52 + 1.75 (60 -
(designated P') 60)]
2. a QRS complex resembling a normal sinus beat
3. a following cardiac cycle that is less than
compensatory in duration
PAC's originate from a focus outside the SA node. Hence the
irregular shape of the P' wave, irregular duration of the PP
interval and extended duration of the P'R interval to greater
than 0.12 seconds. It is important to remember that if this PAC
fires very early in the cycle, ventricular activation may not
occur, or a reentrant atrial tachycardia may develop. In normal
 and V6. Triphasic complexes are identified as the late
intrinsicoid "m-shaped" RSR' complex in lead V1, and the early
intrinsicoid qRS complex in lead V6.

Pulmonary embolism
Electrocardiogram abnormalities can be observed in a Single chamber pacemaker
minority of patients presenting with pulmonary embolism. Artificial cardiac pacemakers are most commonly used in the
These changes are rarely diagnostic unless greater than 50% management of symptomatic bradycardias. These
of the pulmonary vascular compartment is occluded. pacemakers provide electrical stimuli to the atria or ventricles
Pulmonary embolism increases resistance to blood flow to the or both at a desired rate to cause them to contract regularly at
right side of the heart, commonly resulting in cor pulmonale that rate. On the electrocardiogram, these electrical impulses
involving right atrial enlargement and right ventricular dilation are seen as "pacemaker spikes" identified by their abrupt
or hypertrophy. Lead III demonstrates ECG changes which vertical spike (arrows below), preceding the atrial or
mimic acute inferior myocardial infarction (circled below). ventricular complex, depending on which chambers the
These changes include an increase in the normal Q wave pacemaker is responsible for. In this example, a pacemaker
amplitude, minimal ST segment elevation, and often shallow T has been inserted which is responsible for providing a regular
wave inversion. Pulmonary embolism is differentiated from ventricular rhythm (wide, bizarre QRS complex - circled
acute inferior MI by the absence of these changes in the other below). No atrial contractions are present.
inferior leads (II and aVF). Elevated ST segments, increased S
wave amplitude and inverted T wave polarity may sometimes
be seen in the precordial leads.

Supraventricular tachycardia - AV reentry

Supraventricular tachycardia commonly presents in two forms
- AV reentry and AV nodal reentry. In AV reentry (below), the
Right atrial enlargement SVT presents as a regular tachycardia originating outside the
Patients presenting with RAE demonstrate an ECG pattern in ventricular myocardium. In this type of SVT, the AV node is
which the P wave duration is unaffected, but its shape is used for impulse conduction to the ventricles, while an
peaked and its amplitude is increased to greater than 2.5 mm accessory pathway is used to return electrical conduction
in leads II, III, aVF (arrows below) and sometimes V1. With back to the atria. The heart rate is usually regular, at a rate of
extreme enlargement of the right atrium, the P wave may 170 to 250 bpm (below = 188 bpm). In this type of SVT, P
demonstrate terminal negativity in lead V1, resembling LAE. waves are always present outside of the QRS complex, while
Right atrial enlargement is commonly associated with their polarity depends on the atrial insertion of the accessory
congenital heart disease, tricuspid valve disease, pulmonary pathway. The QRS complex is narrow with a duration less that
hypertension and diffuse lung disease. Furthermore, patients 0.2 seconds and an atrioventricular conduction ratio of 1:1. In
presenting with RAE often demonstrate ECG changes 25% - 30% of patients demonstrating AV reentry, QRS
associated with right ventricular hypertrophy as well. alternans is present (varying amplitudes of the QRS complex
in all leads except V4). AV reentry is not usually associated
with structural heart disease and commonly presents as a
variety of symptoms including palpitations, nervousness,
anxiety, syncope or heart failure.

Right bundle branch block

As illustrated in the electrocardiogram below, right bundle
branch block presents with delayed activation of the right
ventricle, leading to a wide QRS complex lasting greater than
0.12 seconds. Altered terminal QRS forces produce a terminal
R wave in lead aVR and terminal S waves in leads I, aVL, V5
Supraventricular tachycardia - AV nodal reentry
AV nodal reentry is a form of SVT that establishes its
atrioventricular circuit entirely within the AV node. The heart
rate is usually regular, between 150 to 250 bpm (below = 186
bpm). The QRS complex is narrow with a duration less than
0.2 seconds and a conduction ratio of 1:1. P waves are buried
within the QRS compelx (as illustrated below), although they
may be visible at the end of the complex as a distortion of the
terminal forces. Due to the fact that atrial activation originates
from the inferior aspect of the right atrium, P wave polarity is
negative in leads II, III and aVF. This form of SVT is usually
benign and is easily converted to sinus rhythm by vagal
maneuvers.

Wolff-Parkinson-White syndrome
Electrocardiograms from patients presenting with WPW
demonstrate a group of characteristic findings frequently
associated with paroxysmal tachycardias and atrial fibrillation.
In WPW, accessory pathways of accelerated ventricular
impulse formation lead to the development of delta waves.
These waves resemble pathological Q waves and represent
initial slurring of the QRS complex as a result of early
ventricular depolarization through this accessory pathway (see
lead II, V1 and V6 - arrow below). As a result, the PR interval is
shortened to less than 0.12 seconds and the QRS direction is
altered (lead III), while its duration is extended to greater than
V1/V3 interchanged 0.10 seconds. Secondary T wave anomalies resulting from
Accurate electrocardiogram interpretation can only be abnormal ventricular repolarization are often demonstrated
achieved if all 12 leads are placed in their appropriate (leads II, III, V2, V3 and V4).
positions. One of the more common errors involving lead
placement involves reversal of the positioning of leads V1 and
V3 (demonstrated below). This mistake produces an ECG
pattern in which the normal R and S wave progressions in the
precordial leads V1 to V3 is lost.

Ventricular tachycardia
Ventricular tachycardia is defined as three or more ventricular
complexes in succession at a rate greater than 100 bpm.
Patients presenting with ventricular tachycardia often present
with a regular heart rate between 100 and 250 bpm (HR below
= 146 bpm), in which the QRS morphology is constant and
abnormally wide (greater than 0.12 seconds). Frequently,
these ECG's demonstrate AV dissociation in which the
ventricular rate is greater than the atrial rate. P waves are
frequently hidden within the broad ventricular complexes,
although they can sometimes be identified as bumps or
notches in the ventricular cycles. Although patients without
heart disease may develop paroxysmal non-sustained
ventricular tachycardia, chronic sustained VT is most
commonly associated with coronary artery disease, dilated
cardiomyopathy and prior myocardial infarction or severe
heart disease.
 Lead 1 Lead aVF Description Interpretation Axis
ECG#1 Leads I and aVF Normal axis ~ 40°-
equally positive. The 50°
axis will be midway
between 0° and 90°.

ECG#2 Leads I and aVF Normal axis ~ 20° -

both positive. Lead I 40°
more positive than
aVF. The axis will
therefore be
oriented more
toward 0°.

ECG#3 Lead I positive. Normal axis ~ 0°

Lead aVF almost
equiphasic.
Therefore, the axis
will be approaching
0°. (Note: when a
lead is equiphasic,
the axis will be 90°
to that lead.)

ECG#4 Lead I positive. Left axis deviation ~

Lead aVF -30°
negative.The axis
will be oriented
negatively past 0°.

ECG#5 Lead I negative. Right axis deviation

Lead aVF positive. ~ -120°
The axis will be
oriented positively
past 90°.

ECG#6 Both leads I and Indeterminate axis

aVF negative. The ~ -135°
axis will be oriented
between -90° and -
180°.