Systematic Approach to ECG

Adopting a systematic approach to ECG assessment is crucial in helping to develop your

interpretation skills. It is important to standardise your approach for every ECG and practice,
practice, practice to improve your speed and accuracy.

Below is a brief outline of one approach which may be helpful:

• Rate
• Rhythm
• Axis
• P wave and PR interval
• QRS
• ST segment
• T wave
• QT interval
• Additional waves

Rate
Rate is fairly easy to quantify given the ECG paper speed is standardised
at 25mm/s.
o Rate = 300/number of large squares of RR interval or
o Rate = 1500/number of small squares of RR interval
If the rhythm is very irregular you should quote a range. If the atrial and
ventricular rates differ, you should calculate both.
Bradycardia is defined as < 60 bpm. Tachycardia is defined as > 100bpm.

Rhythm
This is best appreciated by looking at the rhythm strip at the bottom of the ECG which is
typically lead II.

Sinus Rhythm

Sinus Arrhythmia

1st degree AV block

2nd degree AV block (type 1)

2nd degree AV block (type 2)

3rd degree AV block

Junctional rhythm

AVRT

Atrial fibrillation

Atrial flutter

Idioventricular rhythm
VT

Torsades de Pointes

VF

Axis

A rapid method to assess axis is to look at leads I & II. If the

QRS in both of these leads are predominately positive, the axis
is normal. If it is positive in lead I, but negative in lead II the
axis is leftward. If it is negative in lead I the axis is rightward.

It is important to appreciate what has caused the access deviation.

Causes of leftward deviation:

• LAFB
• LBBB
• LV hypertrophy
• Inferior MI
• WPW syndrome
Causes of rightward deviation:
• LPFB
• Lateral MI
• RV hypertrophy
• Lung disease
• Sodium channel blocker toxicity
• Normal variant in children or slim adults

P wave
The P wave is best examined in the inferior leads. Its duration should be < 0.12s and
amplitude < 0.25mV. A normal P wave is upright through all leads except for V1 where it is
biphasic and aVR where it is inverted.

PR interval
The normal PR interval is 0.12 to 0.2 seconds. A prolonged interval signifies a degree of AV
blockade. A short interval suggests the presence of an accessory pathway and pre-
excitation or can be seen in some junctional rhythms.

QRS
The normal QRS duration is less than 0.1s. Broader complexes are due to aberrant
conduction or are ventricular in origin.

LAFB

• L axis
• Prominent R waves I, aVL
• Prominent S waves II, III &
aVF
 LPFB

• R axis
• Prominent S wave I, aVL
• Prominent R wave III (and
often II & aVF)

LBBB

• QRS > 0.12s

• Leftward axis
• Prominent S wave V1-3
usually with STE
• Prominent R wave with
inverted T wave 1, aVL and
V6

RBBB

• QRS > 0.12s

• Normal or rightward
axis
• RSR’ in V1
• Wide S wave in V6 & I
• Deemed incomplete if
0.1 – 0.12s

Q waves are considered pathological if they are more than 25% of the depth of the QRS
complex or if they are present in V1 to V3. Pathological Q waves usually represent
myocardial infarction, but can be seen in HOCM.

R wave progression throughout the praecordial leads typically transitions at V3, such that
there are small R waves in V1-2 and large R waves in V5-6. Poor R wave progression is a
feature of ischaemia, LVH, right heart strain or imprecise lead placement, although it can be
a normal variant.

ST segment
Normally, the ST segment is isoelectric. It represents the period between ventricular
depolarisation and repolarisation.
 Causes of ST elevation:
• Myocardial infarction
• Pericarditis
• BER
• LBBB
• Ventricular aneurysm
• Brugada syndrome
• Paced rhythm

Localisation of STE to specific territories can be helpful to confirm myocardial ischaemia.

Reciprocal Coronary artery

Localisation ST elevation
changes involved
Anterior MI V1 to V6 None LAD

Septal MI V1 to V4 None LAD

Lateral MI I, aVL, V5-6 II, III, aVF Cx

Inferior MI II, III, aVF I, aVL RCA (80%) Cx (20%)

Posterior MI V7-9 V1-3 RCA or Cx

RV MI V1, V4R I, aVL RCA

T wave
T waves represent ventricular depolarisation and should be upright in all leads except V1 and
aVR, although T wave inversion can also be a normal variant in lead III.

Causes of T wave inversion:

• Ischaemia
• LVH
• BBBs
• R heart strain
• HOCM
• Normal finding on paediatric ECG
• Persistent Juvenile T wave pattern

Hyperacute T waves with ischaemia

Peaked T waves with hyperkalaemia

QT interval
The QT interval is measured from the start of the Q wave to the end of the T wave. It is
affected by many things such as the heart rate, where the QT interval shortens as the heart
beat increases. There are multiple formulas which correct the QT for heart rate, the most
popular of these currently is Bazett’s formula;

A normal QTc is considered < 440ms for men and < 460ms for women.

A prolonged QT interval puts you at risk of Torsades. More recent research investigating the
association between Torsades and a prolonged QT interval plots the QT data into clouds
from which they developed the QT nomogram – above which a person is much more likely to
develop Torsades. The nomogram roughly correlates with a QTc of 500ms.

For the purposes of ECG interpretation, calculate the QT interval and use Bazett’s formula to
correct.

A quick way to determine if the QT is normal for rates of 60 to 100 bpm, can be to see if the
QT interval is less than half the preceding RR interval.
 Causes of long QT
• Congenital long QT syndromes
• Ischaemia
• Drugs/Toxins
• Hypokalaemia
• Hypocalcaemia
• Hypomagnesaemia
• Hypothermia

Additional waves

U wave
• The U wave is a small wave seen
immediately after the T wave
• Seen in bradycardia, hypokalaemia,
hypothermia, and following some
antiarrhythmics

Obsorne or J wave
• The Osborne wave refers to a
rounded positive deflection at the J
point
• Seen classically in hypothermia but
can be a normal variant or 2ndry to
medications

Delta wave
• The delta wave is a slurred upstroke to
the QRS seen in WPW

Epsilon wave
• The epsilon wave is a small blip buried
in the end of the QRS complex seen in
arrhythmogenic RV dysplasia
Special ECG scenarios

Benign Early Repolarisation

Characteristic findings:
1. Upward concave STE
2. Notching at J point
3. Large amplitude T
waves

Hypothermia

Characteristic findings:
1. AF
2. Bradycardia
3. Prolonged QRS &
QT
4. Obsborne waves

Pericarditis

Characteristic findings:
1. Widespread
concave STE
2. Widespread PR
depression
3. Reciprocal STD &
PR elevation aVR

R heart strain

Characteristic findings:
1. STD V1-3
2. TWI V1-3
Sodium channel blockade

Characteristic findings:
1. Prolonged QRS
2. Terminal R wave
>3mm in aVR

Paediatric ECG

Characteristic findings:
1. Rightward axis due
to dominance of RV
2. Tachycardia
3. TWI in V1-3 “juvenile
pattern”
4. Shorter PR & QRS
intervals due to less
cardiac mass
5. QTc 490 normal <
6months

Brugada pattern

Characteristic findings:
1. RBBB or incomplete
RBBB
2. STE right
praecordial leads
LVH

Characteristic findings:
1. Largest R + largest S
waves in chest leads >
45mm
2. ST depression and TWI in
V4-6
3. Leftward axis
4. LAE

HOCM

Characteristic findings:
1. LVH
2. Deep Q waves laterally &
inferiorly
3. LAE

WPW

Characteristic Findings:
1. Short PR interval <
0.12s
2. Broad QRS > 0.1s
3. Delta wave
Other considerations:

VT v SVT with aberrancy

Practically this can be difficult to differentiate. The clinical state of the patient is paramount,
if in doubt treat as VT.

Features of VT:
• Extreme axis
• Very broad complex >160ms
• AV dissociation
• Fusion beats
• Capture beats
• Concordance throughout chest leads (either all negative or all positive)
• RSR’ with a taller left peak (compared to RBBB with a taller right peak)

Performing a Right sided ECG

A right sided ECG is particularly important to
identify an RV infarct. In essence it is a mirror
image of the left sided ECG. V4R is the most
sensitive lead for infarction.

Performing a Posterior ECG

Again a posterior ECG is required to identify
posterior involvement in a STEMI. It is
suggested if there is ST depression anteriorly.
The posterior leads are V7, V8 and V9 which
continue posteriorly from V6.