A Guide on ECG Interpretation
Normal appearances in precordial leads
P waves: Upright in V4-V6 though can be biphasic (both positive an negative) in V1-V2
(negative component should be smaller if biphasic)
QRS complexes: V1 can show an rS pattern ,V6 shows a qR pattern. The size of the r wave
should increase progressively from V1 to V6
Normal appearances in limb leads
T waves: In the normal ECG, the T wave is always upright in leads I, II, V3-6, and always
inverted in lead aVR.
• At least one R wave in the precordial leads must exceed 8 mm
• The tallest R wave in the precordial leads must not exceed 27 mm
• The deepest S wave in the precordial leads must not exceed 30 mm
• Precordial q waves must never have a depth greater than one quarter of the height of
the R wave which follows them.
• ST segments: Must not deviate above or below the isoelectric line by more than 1
mm. Normal ST segment elevation occurs in leads with large S waves (e.g. V1-3),
and the normal configuration is concave upward.
ECG: A Methodical Approach
Patient and ECG Details
Read the name, date and time on the top of the ECG. Make sure they all correlate with the
patient you are dealing with.
(Number of QRS complexes in 30 squares) multiplied by 10.
Abnormalities in Heart Rate:
1. Tachycardia > 100bpm
Anaemia, anxiety, exercise, pain, increased temperature, sepsis, hypovolaemia, heart
failure, PE, pregnancy, thyrotoxicosis, beri beri (Thiamine (vitamin B1) deficiency),
CO2 retention, autonomic neuropathy, sympathomimetics (caffeine etc).
2. Bradycardia < 60bpm
Physical fitness, vasovagal attacks, sick sinus syndrome, acute MI (particularly
inferior), drugs (beta-blockers, digoxin), hypothyroidism, hypothermia, raised ICP,
cholectasis (flow of bile from liver blocked).
Here we look at the rhythm strip. NSR is of regular pattern and has following features:
• The P wave is upright in leads I and II
• Each P wave is usually followed by a QRS complex
• The heart rate is 60-99 beats/min
Young, athletic people may display various other rhythms, particularly during sleep. Sinus
arrhythmia is the variation in the heart rate that occurs during inspiration and expiration.
There is “beat to beat” variation in the R-R interval, the rate increasing with inspiration. It is a
vagally mediated response to the increased volume of blood returning to the heart during
inspiration. The most common arrythmias are outlined below:
Supraventricular Arrhythmias Ventricular Arrhythmias
1. Premature atrial complexes. 1. Abnormal VT due to abnormal tissues
in ventricle generation:
• QRS prolonged (excitation
spread through abnormal path
1. Atrial fibrillation due to
disorganised electrical signals:
• Irregularly irregular pattern
• QRS normal
• Absent P waves
2. Ventricular fibrillation:
• Irregular rhythm
• 300bpm +
• QRS not recognisable
• Absent P wave
3. Atrial flutter:
• Atrial rate 300bpm and
• P waves replaced by
(sawtooth like ) F (flutter)
4. Paroxymal SV tachycardia:
tachycardia that begins and ends
suddenly. Type of PSVT is WPW
syndrome, due to accessory pathway
between atria and ventricles causing:
• Short PR interval
• Slurred upstroke of QRS
(See diagram below)
More rhythms outlined at http://www.ambulancetechnicianstudy.co.uk/rhythms.html
An accurate estimate of the axis can be achieved if all six limb leads are examined. The axis
is determined as follows:
1. Choose the limb lead closest to being equiphasic. The axis lies about 90° to the right
or left of this lead
2. With reference to the hexaxial diagram, inspect the QRS complexes in the leads
adjacent to the equiphasic lead. If the lead to the left side is positive, then the axis is
90° to the equiphasic lead towards the left. If the lead to the right side is positive, then
the axis is 90° to the equiphasic lead towards the right.
See notes for abnormalities
1. PR interval: normal range 120 – 200 ms (3 – 5 small squares on ECG paper).
2. QRS duration: normal range up to 120 ms (3 small squares on ECG paper).
3. QT interval: normal range up to 440 ms (though varies with heart rate and may be
slightly longer in females)
The most common conduction abnormalities are outlined below:
Sinus node block is failure of the sinus node to depolarise or conduct to the atria. Seen
during anaesthesia (due to vagal reflexes); during digoxin, quinidine or phenylephrine
therapy; MI or infarction.
1. An absent P wave and often an absent QRS complex are seen.
2. Manifested by a gradual shortening of the P-P intervals until a pause occurs (i.e. the
blocked sinus impulse fails to reach the atria).
Sick sinus syndrome is a term used for a number of disorders that involve dysfunction of
Atrioventricular (AV) blocks occur at a number of points and involve lack of conduction
from atria to ventricles
1st degree AV block
This may be seen in healthy individuals. ECG features include:
1. Prolonged PR interval - i.e. PR interval >0.20 s.
2. All P waves are conducted to the ventricles.
2nd degree AV block
Here, all of the atrial impulses are not conducted to the ventricles. Divided into two types
with corresponding ECG features:
1. Mobitz Type I or Wenckebach phenomenon: the PR interval lengthens gradually until
a P wave which fails to conduct to the ventricles occurs. The block in this case is
almost always located in the AV node and may be caused by right coronary artery
occlusion causing inferior wall infarctions.
2. Mobitz Type II: Involves an intermittent block in conduction of the P wave into the
ventricles, but the PR interval in surrounding beats is unaltered. Type II AV block is
almost always located in the bundle branches and can result from anterior wall
infarctions. These blocks are generally permanent, with a greater risk of progressing
to complete heart block.
3rd degree /complete heart block
This involves total disruption of conduction between the atria and ventricles. In this situation,
life is maintained by a spontaneous escape rhythm. ECG features include:
1. Slow rate
2. QRS prolonged with unrelated P wave
Intraventricular blocks involve altered conduction of the cardiac impulse within the
Right bundle branch block (RBBB)
This involves total failure of conduction in the right bundle branch proximally. It can be seen
in a variety of disorders, including severe ischaemic heart disease, hypertension, pulmonary
embolism, cardiomyopathy, myocarditis, pericarditis, rheumatic heart disease, Chagas disease
and congenitally in association with atrial septal defect and Fallot’s tetralogy. ECG features
1. "Complete" RBBB has a QRS duration >0.12secs
2. M pattern (rSR) (form of QRS see page) in V1
3. Dominant R wave in V1
4. W (QS) pattern in V6
5. Inverted T waves V1-V3
6. Deep S wave in V6
Left bundle branch block (LBBB)
This involves total failure of conduction in the left bundle branch system. LBBB always
indicates significant cardiac disease. It is seen most commonly in severe ischaemic heart
disease (seen in angina, acute coronary syndromes, cardiac failure etc), hypertension, aortic
stenosis and fibrous degeneration of the conducting tissue. It may also occur in congestive
and hypertrophic cardiomyopathy, myocarditis, acute rheumatic fever, syphilis, cardiac
tumours, post-cardiac surgery and in congenital heart disease. ECG:
1. Total QRS duration >0.12 s
2. M pattern (rsR) V5 and W pattern V1.
3. Inverted T waves in I, V5-V5.
To differentiate between the two we have 16 William Morrows:
Bifascicular block is the combination of RBBB and LB fasicular block (hemiblock) and
manifests as an axis deviation
Trifasicular bundle branch block is combination of bifasicular block and 1st
degree heart block
Abnormalities of the P Wave
P wave height = 2.5 mm
P wave duration = 0.12 s
This waveform is best seen in leads II and V1 and its abnormalities include:
1. Peaked P wave (P Pulmonale):
Demonstrated in anything that causes the right atrium to become hypertrophied
(including tricuspid valve stenosis and pulmonary hypertension).
2. Notched (bifid) and broad P wave (P Mitrale):
Demonstrated in left atrial hypertrophy.
Abnormalities of QRS Complex
1. Right Ventricular Hypertrophy
Dominant R wave in V1 (>25mm).
This is usually accompanied by recipricol deep S wave in V6, right axis deviation,
peaked P wave (with right atrial hypertrophy) and in severe cases inverted T waves in
leads V1- V4 (ventricular hypertrophy).
A Special Case: Pulmonary Embolism
As pulmonary embolism can cause pulmonary hypertension and thus an increased afterload
on the right ventricle, the ECG may show features of right ventricular hypertrophy.
2. Left Ventricular Hypertrophy
Dominant R wave in V6 (>25mm).
Usually accompanied by recipricol deep S wave in lead V1, left axis deviation, P
mitrale possible though not as common (left atrial hypertrophy due to increased
afterload), and in severe cases inverted T waves in V5-V6.
Q Wave Abnormalities
Q waves greater than one square in width and at least 2mm deep indicate a myocardial
infarction and the leads in which these waves appear give an indication of the part of the heart
that has been damaged. The waves may appear as QR or QS.
1. Anterior surface of heart: V1-V4 (Septal V2-V3). Caused by occlusion of left
descending coronary artery.
2. Anterolateral: V1-V6, aVL. Most commonly caused by circumflex CA occlusions.
3. Lateral surface of the heart: I, aVL. Caused by occlusion of left circumflex coronary
4. Inferior surface: II, III and aVF. Commonly caused by right coronary artery.
5. Posterior surface: Not common but can produce a true posterior MI with occlusion of
right CA. When it does occur the result is a dominant R wave in approximately V1
along with a deep S wave in V1.
The presence of a Q wave gives no indication of the age of an infarction but once developed it
is usually permanent.
Abnormalities in ST Segment
1. Elevation of ST Segment is an indication of acute myocardial injury, usually due to
recent MI or pericarditis:
In myocardial infarction with ST segment elevation (STEMI), the leads in which
elevation occurs indicates which part of the heart has been damaged as above.
In addition to the primary changes that occur in the ECG leads facing the infracted
myocardium, "reciprocal changes" may occur in leads opposite to the site of
infarction. The changes are just the inverse of the primary changes.
Thus, if you have a left lateral MI (V5, V6, I, aVL), you would expect changes in
aVR, and sometimes V1 and V2 (depending on how lateral, lead placement, etc). A
right sided infarct (rV4, aVR) would show reciprocal changes to the left lateral leads.
Inferior events would show reciprocal changes in the anterior(septal) leads (V1-V4).
Here we see inferior MI with segment elevation in leads III and VF and V6
(suggesting some lateral wall involvement). There is reciprocal ST segment
depression in leads V1-V3.
Pericarditis is usually not a localised event, however, and causes ST elevation in most
2. Horizontal depression of the ST Segment is usually a sign of ischemia.
The ECG at rest is usually normal (unless severe angina) however when exerted and
ischemia thus occurs, this abnormality appears, particularly with angina (pain due to
ischemia). Commonly seen with T wave inversion (also indicator of ischemia).
3. Downsloping of ST Segment.
Caused by treatment with digoxin.
Abnormalities of the T Wave
1. Inversion of T wave occurs in the following circumstances:
• Normality: Commonly inverted in VR and V1, V2 in young people, and V3
in some black people.
• Ventricular hypertrophy.
• Bundle branch block due to abnormal path of repolarization.
• Administration of digoxin.
• No significance.
2. T Wave Abnormalities associated with Electrolyte Status:
• Low potassium level causes T wave flattening and the appearance of a hump
on the ned of the T wave called a “U” wave.
• A high potassium level or abnormal magnesium levels causes peaked T
waves, commonly with the disappearance of the ST segment and prolonged
• Low plasma calcium level causes prolongation of QT interval and high
plasma level shortens it.
3. Other T wave Abnormalities will be seen later (MI etc)
Evolution of A Standard MI
Usual ECG evolution of a STEMI; not all of the following patterns may be seen; the time
from onset of MI to the final pattern is quite variable and related to the size of MI, the rapidity
of reperfusion (if any), and the location of the MI.
1. Normal ECG prior to MI
2. Within hours of transmural infarction we see hyperacute T wave changes - increased
T wave amplitude and width; with ST elevation or new LBBB.
3. Over hours to days we see the development of pathologic Q waves with T wave
inversion (necrosis) (Pathologic Q waves are usually defined as duration >0.04 s or
>25% of R-wave amplitude)
4. T waves begin to flatten and eventually become upright T waves (fibrosis) after