Year 2 Semester 1 2013 James Rodway

What is an ECG and how is it interpreted?

Year 2 Semester 1 2013 James Rodway
Year 2 Semester 1 2013 James Rodway

NB:

 Slow conduction through the AV node is carried by Ca2+ ions. The myocardium, Purkinje
fibres and bundle of His use fast-moving Na+ ions for the conduction of depolarisation.
 Atrial and ventricular contractions last longer than the P wave and QRS complex,
respectively

‘Lead’

 A ‘view’ of the heart from the position where the ‘wire’ is attached
 Impulse towards an electrode gives a positive deflection
 Impulse away from an electrode gives a negative deflection
 Impulse perpendicular to an electrode gives a biphasic deflection

Bipolar limb leads

 Lead I
• Records the voltage between the (positive) left arm (LA) electrode and right arm (RA)
electrode
• Views the heart from 0o
 Lead II
• Records the voltage between the (positive) left leg (LL) electrode and the right arm
(RA) electrode
• Views the heart from +60o
 Lead III
• Records the voltage between the (positive) left leg (LL) electrode and the left arm
(LA) electrode
• Views the heart from +120o

These leads “view” the heart in the coronal plane.

Year 2 Semester 1 2013 James Rodway

The right leg (RL) electrode functions solely as a ground to prevent alternating-current interference.

Unipolar leads – augmented limb leads

 Two of the limb electrodes are connected together to form the indifferent (negative)
electrode, representing an electrical potential of zero in the centre of the heart
 The third lead is the exploring (positive) electrode, recording the heart’s electrical activity
from its particular limb
 aVR
o The electrodes on the left arm and leg are combined to form the negative electrode,
while the electrode on the right arm is the positive electrode, viewing the heart
from the right shoulder
o Views the heart from -150o
 aVL
o The electrodes on the right arm and left leg are combined to form the negative
electrode, while the electrode on the left arm is the positive electrode, viewing the
heart from the left shoulder
o Views the heart from -30o
 aVF
o The electrodes on the left and right arms are combined to form the negative
electrode, while the electrode on the left leg is the positive electrode, viewing the
heart from the left leg
o Views the heart from +90o
Year 2 Semester 1 2013 James Rodway

Leads aVL, and I look at the left lateral surface of the heart.

Leads II, aVF, and III look at the inferior surface of the heart.

Lead aVR looks at the right atrium.

Year 2 Semester 1 2013 James Rodway
Year 2 Semester 1 2013 James Rodway

Chest leads

 The chest leads are unipolar leads, with the indifferent or negative electrode being due to a
combination of the limb electrodes on the arms and left leg; the exploring or positive
electrode is the electrode on the chest
 Look at the heart in the horizontal plane I.e. From back (negative) to front (positive), with
the AV node the intersecting point of the negative to positive direction
 V1
o 4th intercostal space at the right sternal margin
o Looks at the right ventricle
 V2
o 4th intercostal space at the left sternal margin
o Looks at the right ventricle
 V3
o Midway between leads V2 and V4
o Looks at the apex of the heart at the bottom of the septum (the inter-ventricular
septum and at the anterior wall of the left ventricle)
 V4
Year 2 Semester 1 2013 James Rodway

o At the intersection of the mid-clavicular line and the left 5th intercostal space
o Looks at the apex of the heart at the bottom of the septum (the inter-ventricular
septum and at the anterior wall of the left ventricle)
 V5
o At the intersection of the left anterior axillary line and the horizontal line through V4
o Looks at the anterior and lateral walls of the left ventricle
 V6
o At the intersection of the left mid-axillary line and the horizontal line through leads
V4 and V5
o Looks at the anterior and lateral walls of the left ventricle

ECG paper

 Little squares
o 1mm x 1mm
o 0.04 sec (1/20 sec)
 Big squares
o 5x5 little squares
o 5mm x 5mm
o 0.2 sec (1/5 sec)
 Machine speed
o 25mm/sec

Reading the ECG

1. Rate
a. HR = 1500/no. of little squares between R waves; OR
b. HR = 300/no. of big squares between R waves
c. HR = cycles/6 second strip x 10
d. 60< or = HR < or = 100 is normal
2. Rhythm
a. Regular or irregular?
Year 2 Semester 1 2013 James Rodway

b. If irregular
i. Regularly irregular? OR
ii. Irregularly irregular?
3. P waves
a. Atrial depolarisation
b. Present or not?
c. Duration should be < or = 2.5 little squares
d. Amplitude should be < or = 2.5 little squares
e. P-R interval (beginning of P to beginning of QRS complex) should be 3-5 little squares
 Longer duration indicates left atrial enlargement
 Longer amplitude indicates right atrial enlargement
 Shorter PR interval duration implies an abnormal tract of conducting tissue that by-
passes the AV valve
 Longer PR interval duration implies AV block due to disease in the normal
conducting system
4. QRS complex
a. Ventricular depolarisation – mostly left ventricle
b. Axis – is this a normal axis?
i. Normal from -30° to 90°
ii. To determine:
1. Look for the lead with the most biphasic QRS complex
2. Identify the lead most perpendicular to this lead
3. Is the impulse travelling towards or away from this lead?
4. What roughly is the angle of the direction in which the impulse is
travelling?
5. The cardiac axis may move to either the right or the left due to
abnormalities or changes in the
a. Position of the heart
b. The musculature of the ventricles
c. The conduction of the ventricles
6. Left axis deviation can be due to
a. Left anterior fasicular block
b. Ostium primum atrial septal defect
c. LV hypertrophy
d. Some cases of inferior infarction
7. Right axis deviation can be due to
a. Left posterior fascicular block
b. Ostium secundum atrial septal defect
c. RV hypertrophy
d. Pulmonary embolus
c. Pathological Q waves
i. Q wave is septal activation, with bundle of His running in left side, so goes
from left to right
ii. Should be <1mm wide
iii. Should be <2mm deep
Year 2 Semester 1 2013 James Rodway

iv. Pathological are indicative of full-thickness myocardial infarction, with the

leads in which they appear overlying the damaged myocardium (e.g. in V3-
V5 would be indicative of infarction of the anterior wall of the left ventricle)
1. Look at lead 2 in particular
Year 2 Semester 1 2013 James Rodway

^ Q wave because the septum depolarises left-to-right because depolarisation of the septum is
induced by terminal filaments of the LBB in the septum, which the RBB doesn’t have

d. R wave progression across chest leads

i. Lack of R-wave progression may be indicative of RV enlargement or of an old
anterior infarct
e. Duration of QRS complex should be < or = 2.5 little squares
i. Pathology
1. Bundle branch block
a. Manifested by ‘M’ shaped complexes
i. Best seen in leads V1-V2 in RBBB
ii. Best seen in leads V5-V6 in LBBB
iii. REMEMBER
1. WiLLiaM
a. W in V1
b. M in V6
c. Occurs in LBBB
2. MoRRoW
a. M in V1
b. W in V6
c. Occurs in RBBB
Year 2 Semester 1 2013 James Rodway

2. Ventricular ectopic focus

3. Anomalous atrio-ventricular pathway
4. Non-specific interventricular conduction defect
f. Amplitude
i. Depends on amount of muscle generation QRS complex, with the further the
heart is from the electrodes, the smaller the QRS complex
ii. Can determine LV hypertrophy
1. Sokolow-Lyon criteria:
a. S-wave in lead V1 + R-wave in either lead V5 or V6 > 35 mm
2. Cornell criteria:
a. Males: S-wave in lead V3 + R-wave in lead aVL > 28 mm
b. Females: S-wave in lead V3 + R-wave in lead aVL > 20 mm
iii. Can determine RV hypertrophy
1. Lead V1: positive deflection > negative deflection (in the presence
of a normal QRS duration).
2. Right precordial leads: ST-segment depression and T-wave inversion.
3. Right axis deviation
5. ST segments
a. Occur between QRS complex and T wave
b. J point usually on isoelectric line – should not deviate more than 1mm from
isoelectric line
c. Often has a gentle upward slope
d. Depression
i. Subendocardial ischaemia
ii. Digoxin
e. Elevation
i. Full-thickness ischaemia
ii. Pericarditis
6. T waves
a. Amplitude should be
i. >1/8 of R wave in limb leads
ii. <2/3 of R wave in chest leads
Year 2 Semester 1 2013 James Rodway

b. Polarity should be within 45° QRS complex

NB: the U wave represents the final phase of Purkinje repolarisation, which may terminate a little
later than the rest of the myocardium

Cardiac axis explanation

 Deploarisation of the ventricles occurs in three dimensions. Initially, the wave of

depolarisation travels down the septum in the Bundle of His, but then spreads via the right
and left bundle branches into their respective ventricles. In the right ventricle, the impulse
spreads to the right of the heart, anteriorly, posteriorly, while in the left ventricle, the
impulse spreads to the left, anteriorly (through the left anterior fasciculus), posteriorly
(through the left posterior fasciculus), and finally upwards towards the left atrium. To
complicate matters, the larger mass of the left ventricle generates a larger current, which
tends to “obscure” the depolarisation of the right ventricle
 Despite the above, the differing magnitudes and directions of the various depolarisation
currents can be “summed” to form a resulting electrical vector, which is known as the
cardiac axis
 Abnormalities or changes in the position of the heart, in the musculature of the ventricles, or
in their conduction, can lead to changes in the cardiac axis, which may move to either the
right or the left

QT interval

 Clinically significant, as systole lasts from the beginning of the QRS until the end of the T
wave (I.e. The QT interval)
 Length varies with rate, so are corrected for rate I.e. QTc
 As a rule of thumb, normal when <0.5 R-R interval at normal rates

Pathologies

Atrial enlargement

 Right
o P wave amplitude > 2.5mm in the inferior leads II, III and aVF
 Left
o P wave duration > 2.5mm

Ventricular hypertrophy

 Right
o Right axis deviation
o Lack of R wave progression
 In lead V1, the R wave is larger than the S wave
 In lead V6, the S wave is larger than the R wave
o [common causes]
Year 2 Semester 1 2013 James Rodway

 [pulmonary disease]
 [congenital heart disease]
 Left
o Sokolow-Lyon criteria:
 S-wave in lead V1 + R-wave in either lead V5 or V6 > 35 mm
o Cornell criteria:
 Males: S-wave in lead V3 + R-wave in lead aVL > 28 mm
 Females: S-wave in lead V3 + R-wave in lead aVL > 20 mm
 Both
o The effects of the usually dominant LV obscure those of the RV
 NB
o There may also be secondary repolarisation abnormalities of ventricular
hypertrophy
 ST depression
 T wave inversion
Year 2 Semester 1 2013 James Rodway
Year 2 Semester 1 2013 James Rodway

Arrhythmias

 Usually result from alterations in

o Impulse formation
o Impulse conduction
 Junctional escape rhythm
o Results from slowing of discharges from the SA node
o Pacemaker in the AV node (junctional automaticity focus)
o Simultaneous activation of atria and ventricles
 Retrograde activation of atria
 Normal activation of ventricles
o Ventricular rate < 60 bpm
o Retrograde P waves
 Often located within or very close to the QRS complex
o Normal QRS complex
 Ectopic atrial rhythm
Year 2 Semester 1 2013 James Rodway

o Results from increased vagal tone, suppressing SA and AV nodes, with a pacemaker
in the atrial wall taking over, as the cells of the atria are less sensitive to
parasympathetic stimulation
o Pacemaker low in R atrium
o Simultaneous activation of atria and ventricles
o Characterised by
 Ventricular rate: slow to normal
 Retrograde P waves close occurring prior to QRS complexes, and having a
shortish PR interval
 Normal QRS complexes
o Usually asymptomatic
 Wandering atrial pacemaker
o Characterised by an atrial pacemaker that shifts from the sino-atrial node to another
part of the atria, and then back to the sino-atrial node again. As it does, the
morphology of the resulting P waves changes.
o When rate is >100, is called multifocal atrial tachycardia
 The atrial automaticity foci show early signs of parasystole (entrance block),
developing a resistance to overdrive suppression
 Atrial fibrillation
o Caused by multiple, parasystolic (suffering entrance block) atrial foci
o Ventricular response is ALWAYS irregular
 Atrial flutter
o Originates in an atrial automaticity focus
o 250-350/min rate
o Saw-tooth appearance
o Vagal manoeuvres can be a diagnostic aid
 Ectopic beats
o Premature depolarisations resulting from abnormal automaticity of cardiac cells
o Supraventricular (arising in the atria or AV node)
 Abnormal P waves (due to ectopic focus)
 Normal QRS complex
o Ventricular
 QRS complex abnormal (His-Purkinje system is not involved – ventricular
deposarisation occurs more slowly and in a different pattern; T wave
polarity opposite to that of the QRS complex)
 P waves absent
 SA node exit block
o Pacemaker cells in the SA node depolarise, but the resulting impulse is blocked from
activating the atria
o Manifested on the ECG as
 Dropped P wave
 P-P inberval is a multiple of normal
 AV block
o First degree
 A sinus rhythm where
Year 2 Semester 1 2013 James Rodway

 Every P wave is followed by a QRS complex, but

 The PR interval is prolonged (PR > 0.2 secs)
 A.K.A. PR interval prolongation
 Due to impairment in conduction of the AV node
 The impulse is not really blocked, but delayed
o Second degree
 Sinus rhythm where not every P wave is followed by a QRS complex
 Mobitz type I (Wenchebach)
o Results from ‘fatigue’ of the AV node
o The PR interval gradually lengthens with each beat until an
impulse is completely blocked, such that a P wave is not
followed by its QRS complex for one beat
o Following the dropped beat, conduction is restored and the
cycle repeats itself
 Mobitz type II
o There is a sudden, intermittent loss of AV conduction -> P
waves not being followed by their QRS complexes
o The PR interval of the conducting beats remains constant,
but not every P wave is followed by a QRS complex
o There may be no pattern to the conduction blockade, but
there is usually a fixed relationship between the P waves
and QRS complexes e.g. 2:1 block, 3:1 block, etc.
o Usually due to failure of conduction at the level of the His-
Purkinje system (i.e. below the AV node)
o Usually implies significant disease in the specialised
conduction system
o Often associated with haemodynamic compromise, severe
bradycardia, and progression to complete heart block. The
onset of haemodynamic instability may be sudden and
unexpected, causing syncope (Stokes-Adams attacks), or
sudden cardiac death. The risk of an asystolic event is
around 35% per year. Requires the implantation of a
pacemaker, even in asymptomatic patients
o Third degree (a.k.a. complete heart block)
 Present when there is a complete failure of conduction between the atria
and ventricles
 No relationship between atrial depolarization and ventricular depolarization
 Due to failure of conduction at the level of the AV node or below
 The ventricles are driven by a latent pacemaker below the level of the block
and exhibit an escape rhythm
 Bundle branch blocks
o R or L bundle blockage due to ischaemic or degenerative changes in the affected
bundle
o The affected ventricle does not depolarise in the normal sequence, instead relying
on the relatively slow myocyte-to-myocyte spread of electrical activity travelling
Year 2 Semester 1 2013 James Rodway

from the unaffected ventricle -> prolonged depolarisation -> widened QRS complex
(>0.12 sec)
o RBBB
 Characterised by
 Broad QRS complex: duration > 0.12 secs;
 “M-shaped” complex in right-sided chest leads (V1, V2, V3);
 Wide, slurred S waves in the lateral leads (I, aVL, V6);
 T waves having the opposite polarity to the terminal vector of the
QRS (secondary changes).
 MoRRoW
 M in V1
 W in V6
o LBBB
 Characterised by
 Broad QRS complex: duration > 0.12 secs;
 Loss of the septal r wave in V1 and the septal q wave in V6 (in LBBB,
the septum is activated from right-to-left by the right bundle
branch);
 “M-shaped” complex in lateral leads (I, aVL,V6);
 Wide, deep QS waves in the right-sided chest leads (V1, V2, V3);
 T waves having the opposite polarity to the terminal vector of the
QRS (secondary changes).
 WiLLiaM
 W in V1
 M in V6
 Fascicular blocks
o Left anterior
 Characterised by
 Left axis deviation (axis > -45o);
 Q-wave in aVL & r-wave in III & aVF;
 QRS duration <0.12
o Left posterior
 Right axis deviation (axis > 120o);
 R-wave in aVL & q-wave in III & aVF;
 QRS duration <0.12
o Bifascicular
o Trifascicular

Ventricular escape rhythms (pacing from a ventricular focus) -> decreased blood flow to the brain ->
unconsciousness (syncope) = Stokes-Adams Syndrome

Escape rhythm vs escape beat – pacing vs transient escape of one beat

Premature atrial, junctional and ventricular beats are similar but don't require SA block or arrest, as
escape beats and rhythms do, respectively
Year 2 Semester 1 2013 James Rodway

Premature atrial beats

 May lead to aberrant ventricular conduction due to one BB not having completely
repolarised before the premature beat
 May be non-conducted (doesn't lead to depolarisation of the AV node, but does of the SA
node, leading to a pause)
 May lead to atrial bigeminy or trigeminy

Premature ventricular contractions

 > 6/min is considered pathological

 When occurring on the peak of a T wave can cause R on T phenomenon and lead to
dangerous arrhythmias

Paroxysmal tachycardias

 Can be atrial, junctional or ventricular

Paroxysmal supraventricular tachycardia

 Includes both paroxysmal atrial tachycardia and paroxysmal junctional tachycardia

Torsades de Pointes

 A form of rapid ventricular rhythm

 Due to low potassium or congenital abnormalities e.g. Long QT syndrome
 250-350/min rate
Year 2 Semester 1 2013 James Rodway
Year 2 Semester 1 2013 James Rodway
Year 2 Semester 1 2013 James Rodway

Ischaemia

 The inferior leads (II, III, aVF) usually reflect ischaemia in the distribution of the RCA;
 The chest leads (V1 – V4) usually reflect ischaemia in the distribution of the LAD;
 The lateral leads (aVL, I, V5,6) usually reflect ischaemia in the distribution of the Cx.

STEMI

 To be significant, these changes need to occur in two or more adjacent leads:

o Persistent ST-segment elevation of 1mm in two contiguous limb leads;
o Persistent ST-segment elevation of 2mm in two contiguous chest leads.
 If reperfusion is not accomplished and infarction occurs, the ST-segment elevation persists
for a couple of days before returning to baseline
 After 24 hrs, the T-waves start to become symmetrically inverted, and remain that way for
months
Year 2 Semester 1 2013 James Rodway

NSTEMI

 ST-segment depression, with may be either horizontal or down-sloping

Year 2 Semester 1 2013 James Rodway

RV hypertrophy

 In the presence of a normal QRS duration

o Lead V1 dominant R wave
o Lead V5/6 dominant S wave
o Right axis deviation
 Supportive features
o RA enlargement
o RV strain pattern: Right precordial and inferior (especially lead III) leads -> ST-
depression and T wave inversion
o S1S2S3 pattern: far right axis deviation with dominant S waves in leads I, II and III
o Deep S waves in lateral leads (I, aVL, V5-6)
 Causes
o Pulmonary HTN
o Mitral stenosis
o PE
o Cor pulmonale (chronic lung disease)
o Congenital heart disease
o Arrhythogenic RV cardiomyopathy

T waves

 Should be > 1/8 but < 2/3 the size of the preceding R wave
Year 2 Semester 1 2013 James Rodway

 Its axis should be within 45 degrees of that of the QRS complex