Download Clinical Examination: ECG library

Clinical Examination: ECG library
Like the chest X-ray, the electrocardiograph (ECG) is often considered an extension of the physical
examination of the heart. Even better than an X-ray, it can be performed at the bedside and the
tracing is available immediately for interpretation.
Medical students need some familiarity with important ECG changes and the variations of
normal findings. It is important to remember that, like any test, the ECG is best interpreted in the
context of the patient’s symptoms and physical examination findings.
The following is not a comprehensive guide to ECG interpretation, but gives some advice on
basic ECG interpretation and contains a collection of common ECGs, each with a brief
commentary.
Basic ECG interpretation
Method
Students should usually begin their ECG interpretation by following a number of steps in order; in a
way like examining a system of the body. The following is one suggested method.
1 Calculate or measure the heart rate.
2 Work out the cardiac rhythm.
3 Measure the intervals and durations—PR interval; QRS duration; QT interval.
4 Decide if there is a bundle branch block present—based on the QRS duration, among other
things.
5 Decide if the QRS axis is normal or if there is right or left axis deviation.
6 Look for pathological Q waves and at the ‘R wave progression’.
7 Look for ST segment elevation or depression.
8 Look for T wave changes.
9 Look for QRS voltage abnormalities.
10 Look for P wave abnormalities.
((case 1))
Case 1 The basic components of the ECG
Interpretation of findings
1 The heart rate can be worked out using an ECG ruler, or estimated by dividing the number of
large squares between two R waves into 300. For example, if there are three large squares
between the R waves the heart rate is 300 ÷ 3 = 100. By definition, rates of 100 or more
represent tachycardia and those below 50 bradycardia.
((case 2))
Case 2 A normal 12-lead ECG
In this example the rhythm strip is not synchronous with the channels above, but in the other leads the QRS
complexes underneath each other represent the same heartbeat (arrows). The calibration marker can be seen
(open arrows). There are just over 4 large squares between complexes so the heart rate is about 70 beats per
minute.
Leads L1, L2, L3, aVR, aVL and aVF are called the limb or standard leads; the ‘a’ stands for augmented.
These are constructed from different combinations of the electrodes attached to the four limbs. The V leads
(V1 to V6) are the praecordial leads. They are derived from electrodes are placed across the chest.
• L2, L3 and aVF are called the inferior leads. They ‘look’ at the inferior wall of the left ventricle.
• V1 and V2 are the anteroseptal leads. They look at the anterior wall and septum.
• V3 and V4 are called the anterior leads.
• V5 and V6 are called the anterolateral leads.
• L1 and aVL are called the high lateral leads.
2 The ECG in Case 2 shows sinus rhythm: each QRS complex is preceded by a P wave which
represents atrial contraction. Examples of other cardiac rhythms are shown later.
3 The PR interval is measured from the beginning of the P wave to the beginning of the QRS
complex. The upper limit of normal is 20 ms, or one large square.
• The QRS duration is normally less than 100–120 ms (three small squares).
• The QT interval is measured from the Q or R wave to the end of the T wave. The length
depends on the heart rate, but an interval of more than 400 ms or of more than 50% of the R–
R interval is usually abnormal.
4 Widened QRS complexes may be a result of:
• conduction delay within the ventricles as a result of failure of the left or right bundles (left
bundle branch block, LBBB, or right bundle branch block, RBBB);
• a rhythm that originates in the ventricle (ventricular ectopic beats, ventricular tachycardia or
idioventricular rhythm);
• or ‘pre-excitation’ of the ventricle as a result of an accessory pathway (Wolff-ParkinsonWhite conduction).
5 The QRS axis is the mean direction of depolarisation of the ventricles. In general, the axis is
normal if leads L1 and L2 are both upright (the R wave is taller than the S wave is deep). Left
axis deviation means that L2 is predominately negative, and right axis that L1 is negative.
6 Q waves are normally present in lead aVR and often in lead V1. Small q waves (less than 1/3 the
height of the following R wave) are normal in the inferior leads. Small q waves may also be
present in the lateral leads. Otherwise Q waves suggest previous myocardial infarction.
7 Deviation of the ST segment from the isoelectric line (usually taken to be the PR interval) may
be a sign of ischaemia. ST-segment elevation may represent acute myocardial infarction or
pericarditis. ST depression may represent ischaemia or be associated with left ventricular
hypertrophy, among other things. ST depression during exercise suggests myocardial ischaemia.
8 T waves are normally upright except in leads aVR and V1, and sometimes V2 and V3.
Otherwise T-wave inversion may be a sign of ischaemia.
9 Increase in the QRS size (voltage) may be a sign of left or right ventricular hypertrophy. Low
voltages may be a sign of previous infarction, a large pericardial effusion or an over-expanded
chest (chronic obstructive pulmonary disease, COPD).
10 The normal P-wave duration is less than 100 ms (2.5 mm) long and less than 2.5 mm tall. It is
normally inverted in lead aVR. Tall P waves are called right atrial abnormality, RAA (previously
called P pulmonale). Wide P waves are called left atrial abnormality, LAA (previously P
mitrale).
Common ECG observations
Rate
((case 3))
Case 3 Sinus bradycardia
Each P wave is followed by a QRS complex, but the rate is only 35 beats a minute.
((case 4))
Case 4 Sinus tachycardia
The heart rate is 106. There is flattening of the T waves in the inferior and lateral leads. These are ‘nonspecific’ changes and not diagnostic of ischaemia.
Rhythm
((case 5))
Case 5 Atrial bigeminy
Every second beat is not preceded by a P wave. All the QRS complexes are narrow. The abnormal beats arise
in the atrium or atrioventricular node from an ectopic focus and are conducted normally once they reach the
ventricles (complexes are not wide). When every second beat is abnormal the rhythm is called bigeminal. If
every third beat is abnormal the rhythm is trigeminal.
((case 6))
Case 6 Ventricular bigeminy
Every second beat is wide and not preceded by a P wave. These ectopic beats arise in the ventricles, they are
wide, and their T waves are in the opposite direction to those of the sinus beats.
((case 7))
Case 7 Sinus arrhythmia
The heart rate varies as the patient breathes in and out—it accelerates during inspiration. This is a normal
variant.
((case 8))
Case 8 Atrial fibrillation with ventricular response rates varying from 65 to 170
The heart is beating irregularly and quickly. There are no P waves but the baseline is irregular (fibrillation
waves). The QRS complexes are narrow, which means that the rhythm arises above the ventricles.
((case 9))
Case 9 Atrial fibrillation with ventricular response rate is between 60 and 80
The heart beat is irregular but not fast. Always comment on the ventricular response rate when the patient is
in atrial fibrillation.
((case 10))
Case 10 Atrial flutter with ventricular response rate of 150
There is a ‘saw-tooth’ pattern visible in L2. The rate of the flutter waves is 300/minute and every second one
is conducted to the ventricles. Atrial flutter is a common cause of a regular narrow complex tachycardia with
a rate of 150; the differential diagnosis is sinus tachycardia. The saw-tooth pattern makes the diagnosis here.
Note a number of ventricular ectopic beats (wide complexes) towards the end of the tracing.
((case 11))
Case 11 Supraventricular tachycardia (SVT)
The heart rate is over 200. The complexes are narrow. These palpitations began very suddenly in a well 18year-old.
((case 12))
Case 12 Ventricular tachycardia
The heart rate is 170. The complexes are very wide.
((case 13))
Case 13 A rhythm strip showing the onset of ventricular fibrillation
The patient has chronic atrial fibrillation. The ventricular fibrillation is associated with no QRS complexes
and of course no cardiac output.
((case 14))
Case 14 Sinus tachycardia
The heart rate is 138. P waves are visible before all the complexes except the widened ones, which are
ventricular ectopic beats (VEBs).
((case 15))
Case 15 Accelerated junctional rhythm
The heart rate is 67. No P waves are visible but the complexes are narrow (of normal width). The rhythm
arises in the area around the atrioventricular (AV) node rather than from the sinus node. Although there are
cells in the AV node with spontaneous activity, these do not usually produce impulses at rates over about 45
times a minute and are thus prevented from pacing the heart by the faster intrinsic rhythm of the sinus node.
There is also widespread ST segment elevation. This is a post coronary artery surgery patient and the ST
changes probably represent pericardial inflammation.
((case 16))
Case 16 A 2:1 atrioventricular block
Only every second P wave is conducted and the ventricular rate is only about 30. Note that the QRS
complexes are wide—left bundle branch block (LBBB)—which is further evidence of conduction disease.
((case 17))
Case 17 Ventricular pacing
There are ‘pacing spikes’ visible before the QRS complexes. The complexes are wide and have an LBBB
pattern. This is ventricular pacing with an electronic pacemaker; the pacing electrode is in the right ventricle.
The underlying rhythm is atrial fibrillation.
((case 18 a&b))
Case 18 (a) Dual chamber pacing. Atrial and ventricular pacing spikes are seen. The distance between the
atrial and ventricular spikes is an artificial PR interval and is called the AV interval. It can be adjusted by
reprogramming the pacemaker. For all modern pacemakers, pacing is inhibited if the intrinsic atrial or
ventricular rate rises above the rate set for electronic pacing.
(b) When the pacemaker is inserted because of AV nodal disease, there may be atrial sensing (a normal P
wave is seen, followed by a ventricular pacing spike and paced beat—a sensing V pacing). In this ECG the
pacing spikes are followed by complexes that are narrow, and in some cases the pacing spikes occur after the
start of the QRS complex. These are ‘fusion’ beats; partly paced and partly conducted normally. The
pacemaker need to be reset to a longer AV interval to allow atrioventricular conduction to occur without
pacing.
Intervals
((case 19))
Case 19 The PR interval is short: 105 ms; the QRS complexes are of normal width but the QRS
voltages are high—unrelated left ventricular hypertrophy
This short PR interval is not usually of any consequence unless the patient has had fast palpitations. In this
case it may indicate an accessory pathway within the atrioventricular (AV) node that conducts more rapidly
than the normal pathway, and means the patient may have episodes of re-entrant AV nodal tachycardia—
supraventricular tachycardia (SVT).
((case 20))
Case 20 The PR interval is short and there is some widening of the QRS complexes
This is due to the slurred upstroke of the R waves, and is called a δ wave. It is a result of an accessory
pathway (the bundle of Kent) which connects the atria with the left ventricle directly, bypassing the
atrioventricular node. The ventricle is stimulated early (pre-excitation). This is an example of Type A WolffParkinson-White conduction. These patients are also at risk of developing supraventricular tachycardia
(SVT).
((case 21))
Case 21 The PR interval is 232 ms (the upper limit of normal is 200 ms)
A long PR interval means first-degree heart block. It is a sign of slowing of conduction in the atrioventricular
node. It is often of no significance.
((case 22))
Case 22 The QRS complexes are wide (152 ms) but preceded by P waves—sinus rhythm. There is an
rSR’ pattern in V1
This is right bundle branch block (RBBB). The ventricles are being depolarised through the left bundle.
((case 23))
Case 23 The QRS complexes are wide (146 ms) but preceded by P waves. The complexes are negative
in V1 and positive in V6
This is left bundle branch block (LBBB). The left bundle is much larger than the right, and LBBB so distorts
the shape of the QRS complexes that further interpretation (e.g. for the presence of pathological Q waves or
ST segment changes) is usually not possible. It is therefore important to make the diagnosis of LBBB before
embarking on attempts to make these interpretations.
((case 24))
Case 24 Prolonged QT interval
In this case, an interval of 500 ms from the beginning of the QRS complex to the end of the T wave. The
corrected QT (QTc)—corrected for rate—is also long at 487 ms. These patients may be at risk of ventricular
arrhythmias and of sudden death. There are many causes including anti-arrhythmic drugs, hypothermia and
inherited conditions.
Axis
((case 25))
Case 25 The QRS complexes in L2 point downwards—left axis deviation (LAD)
This is often due to left anterior fascicular (hemi-) block. The anterior fascicle of the left bundle is not
working and the direction of depolarisation is changed to the left.
((case 26))
Case 26 The QRS complexes in L1 are just negative and there is right bundle branch block (RBBB)
This is right axis deviation (RAD). It is a result of left posterior bundle block (left posterior hemi-block). In
combination with RBBB it is called bifascicular block (right bundle and left posterior bundle) and indicates
conduction system disease. If there is also first-degree heart block, the changes amount to trifascicular block.
These patients are at risk of syncopal episodes as a result of episodes of complete heart block. RAD can be
the result of changes to the right ventricle resulting from chronic lung disease and is associated with
congenital heart disease.
Q waves and R-wave progression
((case 27))
Case 27 Normal R-wave progression
The height of the R waves in the praecordial leads usually increases steadily from lead V1 to V5. Loss of R
wave height can be a sign of previous anterior infarction, but may represent rotation of the heart in the chest.
In this ECG there are also small q waves in leads V5 and V6 and in standard leads 2 and 3. These are not
abnormal because they are small in relation to the following R waves.
((case 28))
Case 28 Reduced R-wave progression
The R waves are small until lead V3 but no Q waves are present.
((case 29))
Case 29 Early transition
The R waves are tall even in lead V1. This is usually due to rotation of the heart, but tall R waves in V1 can
be a result of right ventricular hypertrophy (where usually there is also right axis deviation); or ‘true’
posterior infarction where there are also Q waves in the inferior leads).
((case 30))
Case 30 There is a Q wave in L3; there are no Q waves in L2 or aVF (although the voltages are low in
aVF)
This Q wave is probably not pathological.
((case 31))
Case 31 Q waves are present in the three inferior leads: L2, L3 and aVF
This is an old inferior infarct. Pathological Q waves form when an area of infarction leaves an electrically
inactive scar on the ventricle. Electrodes which ‘look’ at this part of the heart see through this ‘window’ to
the myocardium on the opposite wall of the heart. Here electrical activity will be directed away from the
electrode as conduction occurs from the endocardial to the epicardial surface. The normal electrical activity
of the infarcted wall which would have been towards the electrode (from endocardial to epicardial surface—
producing an R wave) is gone.
((case 32))
Case 32 Q waves are present in all the praecordial leads
This represents an anterior infarct. The persisting ST changes suggest that it may be recent (within a few
days of the tracing).
ST segment changes
((case 33))
Case 33 The ST segments are depressed in V2 to V5; there is about 2.5 mm of horizontal depression
This is strongly suggestive of anterior wall ischaemia.
((case 34))
Case 34 There is ST elevation in the anterior leads (V1 to V5); the maximum elevation is 2.5 mm
This is associated with loss of septal R waves and symmetrical T-wave inversion. These are the changes of a
recent anterior infarct. It is likely to be due to occlusion of the left anterior descending coronary artery.
((case 35))
Case 35 There is inferior and lateral ST elevation which is extensive—up to 2 mm in height
This may represent acute myocardial infarction involving a large circumflex coronary artery.
((case 36))
Case 36 There is early transition and the T waves are tall in the praecordial leads; the ST segments in
these leads appear elevated
In fact, this pattern is a normal variant called early repolarisation. The T waves begin close to the end of the
QRS complex and the upstroke of the T wave occurs early. It resembles ST elevation.
((case 37))
Case 37 Massive anterior ST elevation in an acute anterior infarct; there are also inferior lead changes
ST depression in the leads opposite those with ST elevation are called reciprocal changes.
((case 38))
Case 38 Widespread ST elevation
When ST elevation occurs in too many leads to be explained by occlusion of a single coronary artery,
pericarditis should be suspected. The patient’s chest pain will be pleuritic.
T-wave changes
((case 39))
Case 39 There are T-wave changes (inversion) in the inferior and lateral leads
These are not specific for ischaemia but are very suggestive of it, especially if the patient has chest pain.
((case 40))
Case 40 Widespread T-wave changes; the T waves in the anterior leads are symmetrically inverted
This is quite specific for a stenosis of the left anterior descending coronary artery.
((case 41))
Case 41 There is widespread flattening of the T waves
This is a non-specific abnormality but may represent ischaemia.
((case 42))
Case 42 Atrial fibrillation with lateral ST ‘sagging’—leads V5 and V6
This may be a result of treatment with digoxin—the ‘digoxin effect’; it does not indicate digoxin toxicity.
There are also prominent U waves in leads V2 and V3.
Voltages
((case 43))
Case 43 The sum of the R wave in V5 and the S wave in V2 is about 8 large squares or 4 volts
This suggests left ventricular hypertrophy (LVH). An increase in the thickness of the ventricular wall
produces larger QRS voltages. There are also ST changes in the lateral leads. This is called a ‘strain pattern’.
It may represent sub-endocardial ischaemia caused by LVH.
((case 44))
Case 44 Right ventricular hypertrophy with tall R waves in V1
This patient has pulmonary stenosis. There is also right axis deviation and the P waves are taller than 2.5
mm—showing right atrial abnormality (RAA).
P waves
Case 44 shows RAA (P waves taller than 2.5 mm).
((case 45))
Case 45 In L2 the P waves are broad—wider than 2.5 mm
This represents left atrial abnormality. It can be a sign of mitral valve disease which is a cause of left atrial
enlargement.
Recording problems
((case 46))
Case 46 ‘Baseline wander’ in V3
Usually a result of poor contact between the electrode and the skin. In this tracing, leads V2 and V3 have
been transposed: the R wave cannot get smaller in V3 and then larger again in V4. This is the most common
technical error made during ECG recording. Incorrect limb lead placement is also common. It should be
suspected when the axis appears strange (L1 and L2 both negative) and aVR appears upright. This lead
should always have downgoing P waves, a negative QRS complex and inverted T waves.
((case 47))
Case 47 This patient has a tremor which causes the abnormal appearance of the baseline in the lateral
leads