ECG INTERPRETATION

Heart rate
Rhythm
The QRS axis
Intervals: PR, QRS, and QT
The P wave amplitude and duration
The QRS amplitude
ST-segment and T-wave abnormalities
Abnormal findings: hypertrophy, abnormal rate, conduction
abnormalities, metabolic disturbances
INTERVALS AND COMPLEXES

PR interval

Varies with age and heart rate

Measured in lead II
QRS complex

<0.10 sec

Increase with age, independent of rate

Measured in V5

Low voltage is 5mm or less in limb leads and 8mm or less in chest
leads

P wave

For the diagnosis of atrial hypertrophy

Normal P wave amplitude: <3 mm
Duration of P wave:
< 0.09 second in children
< 0.07 second in infants

QRS complex

important in the diagnosis of ventricular hypertrophy

vary with age

R waves: taller in the right precordial leads (i.e., V4R, V1, V2)

S waves: deeper in the left precordial leads (i.e., V5, V6) in infants
and small children
ST segment

Isoelectric

elevation or a depression of the ST segment is judged in relation to the

PR segment as the baseline

Early repolarization is a normal finding in adolescents and young adults

in whom the ST segment is elevated and concave in leads with upright
T waves

Abnormal: pericarditis, myocardial ischemia or infarction, digitalis effect

T waves

Tall peaked T waves

hyperkalemia and LVH (of the volume overload type)

Flat or low T waves

normal newborns or with hypothyroidism, hypokalemia,
pericarditis, myocarditis, myocardial ischemia
P wave

P waves are typically best reviewed in leads II or V1.

It is bullet shape.

If the cardiac rhythm originates from the sinus node, the expected
vector of depolarization will be from right to left and superior to inferior.
Thus, the P wave deflection should be positive (upward) in leads I, II,
and aVF.

RIGHT ATRIAL ENLARGEMENT

sometimes referred to as P pulmonale
is defined as a tall, broad, and peaked P wave in lead II, with elevations
greater than 3.0 mm in infants 0 to 6 months and those greater than 2.5
mm in others marking the upper limits of normal
leads to delayed activation of the right atrium. This delay causes activation
and the subsequent polarization of the atria to occur simultaneously. The
simultaneous polarization is reflected in a P wave that is peaked and
narrower than usual.
The peak in the P wave is the result of the increased amount of depolarized
tissue. Although depolarization is prolonged in an enlarged right atrium,
the P wave appears narrower because depolarization of the right atrium is
hidden by depolarization of the left atrium. Enlargement of the right atrium
may cause the vector of atrial depolarization to shift to the right and
exceed 20, causing the tallest P wave to appear in the ECG tracing for
lead III or aVF rather than the tracing for lead II.
RAE is also known as P pulmonale because it is often a result of severe lung
disease like pulmonary hypertension.
The ECG is diagnostic of it.

 Other causes are Atrial septal defect, tricuspid regurgitation, Tricuspid

stenosis, Ebstein anomaly
LEFT ATRIAL ENLARGEMENT
P mitrale
criteria include a widened and deeply notched P wave in lead II or a deep
biphasic P wave in lead V1
leads to delayed activation of the left atrium and thus prolonged
depolarization and a prolonged P wave. The increased tissue mass will
cause the terminal, or negative, portion of the P wave in lead V1 to
increase in amplitude by at least 1 mm
also known as P mitrale because it is associated with mitral valve disease
Diagnosis is based on the following ECG findings:
1. A notched P wave in lead II
2. Amplitude of the terminal component of the P-wave that descends
at least 1 mm below the isoelectric line in lead V1
3. Increased duration of the P wave; terminal portion of the P wave
must span at least one small box (40 msec)
4. No significant axis deviation because the left atrium is normally
electrically dominant

Evaluate the PR interval

P-R interval
Time interval for impulse to go from the SA to the
AV node
From the beginning of the P wave to the beginning
of the QRS complex
Normal 0.12-0.20 secs
If the PR interval is short (less than 3 small squares) it
may signify that there is an accessory electrical pathway between
the atria and the ventricles, hence the ventricles depolarise early
giving a short PR interval. One example of this is Wolff-ParkinsonParkinson

P-WAVES MORPHOLOGY

Q wave

If the PR interval looks as though it iswidening every beat and

then a QRS complex is missing, there is 2nd degree heart
block, Mobitz type I
If the PR interval is constant but then there is a missed QRS
complex then there is 2nd degree heart block, Mobitz type II
If there is no discernable relationship between the P waves and
the QRS complexes, then 3rd degree heart block is present . The
VR is low and the Atrial rate is normal
Normal Q waves, when present, represent depolarization of
the interventricular septum. For this reason, they are referred to
as septal Q waves and can be appreciated in the lateral leads I,
aVL, V5 and V6.

Pathologic Q wave
Pathologic Q waves occur when the electrical signal passes
through stunned or scarred myocardium; as such, they are usually
markers of previous myocardial infarcations, with subsequent fibrosis.
A pathologic Q wave is defined as having a deflection amplitude
of 25% or more of the subsequent R wave, or being > 0.04 s (40 ms) in
width and > 2 mm in amplitude. However, diagnosis requires the presence
of this pattern in more than one corresponding lead.
Pathological Q waves may be seen with ventricular hypertrophy
(right or left), left bundle branch block, or after myocardial infarction
Except in the newborn, the q wave is absent in V4R and V1.
The amplitude should be less than 6 mm in leads aVF and V5,
less than 5 mm in lead V6, and not more than 25% of the amplitude of the
associated R wave in any lead.
The duration does not normally exceed 0.03 s.
Pathological Q waves may be seen with ventricular hypertrophy
(right or left), left bundle branch block, or after myocardial infarction.
In congenitally corrected transposition of the great arteries, the
septum is depolarised from right to left, resulting in q waves in the right
precordial leads and their absence from the left precordial leads (Fig. 10).
In conditions with a single functional ventricle (e.g. Hypoplastic
left heart syndrome) there may be no q waves in the precordial leads.

QT Intervals

Varies with rate

Measured in Lead II

QTc using Bazetts formula

Normal: <0.44s

Prolonged in: hypocalcemia, myocarditis, diffuse

myocardial diseases, head injury, severe malnutrition, antiarrhythmics,
antipsychotic phenothiazines, tricyclic antidepressants, antibiotics (e.g.,
ampicillin, erythromycin, trimethoprim-sulfa)

Shortened in: digitalis toxicity, hypercalcemia

Corrected QT interval

The most important interval is the QT or the QTc; csignifies

corrected for heart rate. As with the previous intervals, lead II or
the lead with the least artifact should be used.

The QTc is calculated using the Bazett formula . The Bazett

formula requires values in sec rather than in msec for
calculating the QTc, but the result may be expressed in sec or
msec.

A long QTc of > 0.44 sec is usually abnormal and requires

interpretation by a pediatric cardiologist. An abnormal QTc can
result in sudden death; therefore, the QTc must be checked
closely in every EKG.

Right Ventricular Hypertrophy

For determining the presence or absence of right ventricular

hypertrophy (RVH), use only lead V1.

The 4-step method has 3 rules for RVH:

1. Upright T waves in V1 after about 7 days of age.
2. An RSR pattern in V1 in which the R is taller than the R
3. A pure R wave in V1 after about 6 months of age
Other RVH Criteria

R-wave height greater than the 98th percentile for age on lead V1

S wave depth greater than the 98th percentile for age in lead V6

R/S ratio inappropriately high for V1 or low for V6

T-wave deflection abnormality

persistence of neonatal pattern of R-wave progression in

children in adolescence in which there are tall R waves in the
right precordial leads (V1, V2, V3) with small S waves that
progress to small R waves and large S waves in the
left precordial leads (V4, V5, V6).

Right axis deviation alone should not be used as a

criterion for RVH, particularly in infants and young
children

Left Ventricular Hypertrophy

Voltage criteria for LVH in children consist of an R-wave height

greater than the 98th percentile for age in lead V6 and an S-wave
depth greater than the 98th percentile for age in lead V1.

The R-wave progression pattern across the precordial leads may

also provide helpful information.

In newborns, one expects large R waves and small S waves in

the right precordial leads.

Presence of the inverse pattern (adult-type R-wave progression)

is indicative of LVH.

Inversion of T waves in leads II, III, aVF, V4, V5 , and V6 is

commonly called a strain pattern and is highly suggestive of
LVH.

Additional electrocardiographic markers of LVH include tall R

waves in aVF, left axis deviation, and Q waves in leads V4, V5,
and V6.
Right Ventricular Enlargement
1. RAD for the patient's age
2. Increased rightward and anterior QRS voltages;
a. R waves in V1, V2, or aVR > upper limits for age
b. S waves in I and V6 > upper limits for age
3. Abnormal R/S ratio in favor of the RV
a. R/S ratio in V1 and V2 > upper limits for age
b. R/S ratio in V6 < 1 after 1 month of age
4. Upright T waves in V1 (>7 days old), provided that the T is upright
in the left precordial leads (V5, V6); upright T waves in V1 are not
abnormal in patients older than 6 years.
5. A q wave in V1 (qR or qRs patterns) suggests RVH
6. In the presence of RVH, a wide QRS-T angle with T axis outside
the normal range (in the 0 to 90 degree quadrant) indicates a
strain pattern. A wide QRS-T angle with the T axis within the
normal range suggests a possible strain pattern.
ST segment

The ST segment is the flat, isoelectric section of the ECG

between the end of the S wave (the J point) and the beginning of
the T wave.

It represents the interval between ventricular depolarisation and

repolarisation.

The ST segment may be elevated or depressed by either

ischemia or infarction.

Neonates
1.
2.
3.
4.
5.
6.

S waves in lead I > 12 mm

Pure R waves (with no S waves) in V1 > 10 mm
R waves in V1 > 25 mm or R waves in aVR > 8 mm
A qR pattern seen in V1
Upright T waves seen in V1 after 7 days of age
RAD with the QRS axis greater than +180 degrees

4.

a.
b.

Left Ventricular Hypertrophy

1. LAD for the patient's age
2. QRS voltages in favor of the LV
R waves in leads I, II, III, aVL, aVF, V5, or V6 > upper limits for age
S waves in V1 or V2 greater than the upper limits of normal for age
3.
Abnormal R/S ratio in favor of the LV: R/S ratio in V1 and V2 <
lower limits for age
4.
LV diastolic overload: Q waves in V5 and V6, >5 mm; tall
symmetrical T waves in the same leads
5.
In the presence of LVH, a wide QRS-T angle with the T axis
outside the normal range indicates a strain pattern; this is manifested
by inverted T waves in lead I or aVF. A wide QRS-T angle with the T
axis within the normal range suggests a possible strain pattern.
Biventricular Hypertrophy
1. Positive voltage criteria for RVH and LVH in the absence of
bundle branch block or preexcitation
2. Positive voltage criteria for RVH or LVH and relatively large
voltages for the other ventricle
3. Large equiphasic QRS complexes in two or more of the limb leads
and in the mid-precordial leads called the Katz-Wachtel
phenomenon (with normal QRS duration)

Ventricular Conduction Disturbances

1. Bundle branch block, right and left
2. Preexcitation (e.g., WPW-type preexcitation)
3. Intraventricular block
Right Bundle Branch Block

During a right bundle branch block, the right ventricle is not

directly activated by impulses travelling through the right bundle
branch. The left ventricle however, is still normally activated by the
left bundle branch. These impulses are then able to travel through
the myocardium of the left ventricle to the right ventricle and
depolarise the right ventricle this way. As conduction through the
myocardium is slower than conduction through the Bundle of HisPurkinje fibres, the QRS complex is seen to be widened. The
QRS complex often shows an extra deflection which reflects the
rapid depolarisation of the left ventricle followed by the slower
depolarisation of the right ventricle.

Delayed conduction through the right bundle branch prolongs the

time required for a depolarization of the RV

Produces prolongation of the QRS duration

Criteria
1. RAD, at least for the terminal portion of the QRS complex
2. QRS duration longer than the upper limit for age: greater
than 0.10 sec in children ages 4 to 16 years, and greater
than 0.90 sec in children less than 4 years of age
3. Terminal slurring of the QRS complex directed to the right
and usually, but not always, anteriorly:
- Wide and slurred S waves in leads I, V5, and V6

- Terminal, slurred R in aVR and the right precordial leads

(V4R, V1, and V2)
ST-segment shift and T-wave inversion are common in
adults but not in children

Right Bundle Branch Block

Commonly associated conditions:
1. Atrial Septal Defect
2. Conduction disturbances after open heart surgery involving right
ventriculotomy
3. Ebstein's anomaly
4. COA in infants younger than 6 months
5. AV Canal type of defect
6. Partial Anomalous Pulmonary Venous Return
Left Bundle Branch Block

Left bundle branch block (LBBB) is a cardiac conduction

abnormality seen on the electrocardiogram (ECG).

In this condition, activation of the left ventricle is delayed, which

causes the left ventricle to contract later than the right ventricle.
LBBB criteria

The heart rhythm must be supraventricular in origin

The QRS duration must be 120 ms]

There should be a QS or rS complex in lead V1

There should be a RsR' wave in lead V6.

The T wave should be deflected opposite the terminal deflection

of the QRS complex. This is known as appropriate T wave
discordance with bundle branch block. A concordant T wave may
suggest ischemia or myocardial infarction.

Left Bundle Branch Block

The duration of the QRS complex is prolonged for age and the slurred
portion of the QRS complex is directed leftward and posteriorly
A Q wave is absent in V6
A prominent QS pattern is seen in V1 and a tall R wave is seen in V6
Commonly associated conditions
1. Cardiac disease or surgery in the LV outflow tract
2. Septal myomectomy
3. Replacement of the aortic valve

Prognosis depends on associated disease

A mnemonic to remember the ECG changes is WiLLiaM MaRRoW, i.e.

with Left bundle branch block there is a W in V1 and a M in V6 and with
a RBBB there is a M in lead V1 and a W in lead V6
Intraventricular Block

Prolongation is throughout the duration of the QRS complex

Bundle Branch Blocks

Ventricular Hypertrophy VS Ventricular Conduction Disturbances

The ST segment is the flat, isoelectric section of the ECG

between the end of the S wave (the J point) and the beginning of
the T wave.
It represents the interval between ventricular depolarisation and
repolarisation.
The ST segment may be elevated or depressed by either
ischemia or infarction.
In electrocardiography, the ST segment connects the QRS
complex and the T wave and has a duration of 0.080 to 0.120 sec
(80 to 120 ms).
It starts at the J point (junction between the QRS complex and ST
segment) and ends at the beginning of the T wave. The typical ST
segment duration is usually around 0.08 sec (80 ms). It should be
essentially level with the PR and TP segment.

Interpretation

The normal ST segment has a slight upward concavity.

Flat, downsloping, or depressed ST segments may

indicate coronary ischemia.

ST elevation may indicate myocardial infarction. An elevation of

>1mm and longer than 80 milliseconds following the J-point. This
measure has a false positive rate of 15-20% (which is slightly
higher in women than men) and a false negative rate of 20-30%.[1]

ST depression may be associated with hypokalemia or digitalis

toxicity.[2]

ST-SEGMENTS AND T-WAVE CHANGES

T-wave changes
Myocardial Infarction

Limb Leads
Lateral

I, aVL

Anterior

V5, V6
V1, V2, V3

Anterolateral

I, aVL

Diaphragmati
c

II, III, aVF

Posterior

Precordial Leads

V2V6

HYPERKALEMIA

The ECG changes make their appearance when K level rises

beyond 6 meq

It is not necessary to have ECG changes in all patients with

hyperkalemia

At K levels of 6 meq/L there peaking of T wave and shortening of

QT interval

At K levels of 6.5 meq/L and above there is increase duration of

the QRS complex

The ECG changes make their appearance when K level rises

beyond 6 meq

It is not necessary to have ECG changes in all patients with

hyperkalemia

At K levels of 6 meq/L there peaking of T wave and shortening of

QT interval

At K levels of 6.5 meq/L and above there is increase duration of

the QRS complex

Where K levels of exceeds 7 meq/L the amplitude of P wave

decreases and the duration decreases

At K levels of 8 meq/L the P waves are not usually seen but QRS
complex are seen

The secondary ST T wave changes may be seen due to delayed

intraventricular conduction

V1V3

ELECTROLYTE DISTURBANCES
Common ELECTROLYTE disturbances which interferes with ECG changes
are
1. Hypokalemia
2. Hyeprkalemia
3. Hypocalcemia
4. Hypercalcemia
5. Hypomagnesemia
6. Hypermagnesemia
Potassium

THE ECG CHANGES IN HYPERKALEMIA

1.
prolongation of the PR interval
2.
prolongation of the QRS complex
3.
shortening of the QTc interval
4.
flattening or loss of the P wave
5.
ST T segment changes
Mark ST depression with upright T waves (called secondary
ST T wave changes and do not indicates ischemia)
6.
increase amplitude and peaking of T waves
7.
Arrhythmias
8.
Atrial standstill
9.
Ventricular arrhythmias extrasystoles, tachycardia, flutter
fibrillation
10.
At very high levels, cardiac standstill
PLASMA CALCIUM

Normal Plasma calcium lelvel is 4.0 4.5 meq/L or 9

10.5 mg/dl

Plasma level of ionized calciumis 2.3 2.8 meq/L or 4.5 5.6

mg/dL

Symptoms generally appear at Calcium level above 11.4 mg/dL

But some patiemts are asymptomatic even at this level

Severe hypercalcemia is serum calcium level at or above 15

mg/dl

Levels of Hypokalemia

Normal level of K = 3.5 5.5 meq/L

ECG changes appear at level less than 3 meq/L

Mark at less than 2 meq/L

ECG CHANGES IN HYPOKALEMIA
1. increase amplitude and with of the P wave
2. prolongation of the PR interval
3. first degree AV block as well as 2 degree AV block Wenkebach
type is common
4. slight depression of the ST segment
depression may be horizontal or concave upwards
5.
prolongation of the QTc interval
6.
flattening and inversion of the T wave
7.
increase prominence of the U wave
8.
premature beats and tachyarrhythmias
9.
Torsade de Pointes can occur in severe hypokalemia

HYPOCALCEMIA

lenthening of the QT interval in the range of 0.50 to 0.60 seconds

HYPERALCEMIA

Above 12 mg/dl shortness of the QT interval

Shortening is inversely proportional to serum calcium levels

At levels 16 mg/dl and above T waves become prolonged or

widen, even become inverted or flattened

In extreme hypercalcemia an increase in the amplitude of QRS

complex , biphasic T waves an Osborn waves has been described
HYPOMAGNESEMIA

ECG manifestation are similar to hypokalemia

If K supplementation fails to normalize the the QTc interval,

hypomagnesemia must be suspected

HYPERMAGNESEMIA

Similar to hyperkalemia

No definite criteria differentiating the two

In summary, the ECG is an inexpensive noninvasive test that provides much

information regarding suspected cardiac pathology in both children and
adults.
In infants and children, appreciation for the rapidly changing parameters
within the ECG will aid the clinician in formulating the correct diagnosis.

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