Technical aspects:

• The ECG is a plot of voltage on the vertical axis against time on the horizontal axis.
• The machine used to record an ECG is called the electrocardiograph. The process of
recording an ECG is called electrocardiography.
• The standard ECG is a 12 lead ECG, composed of 6 limb leads and 6 chest leads. Such
an ECG is recorded using 4 limb and 6 chest electrodes.
o The limb electrodes are color-coded. Knowing which electrode goes where is
important as putting them on the wrong way will result in technical errors
and an incorrect interpretation. The limb leads are I, II, III, aVR, aVF, and aVL.
▪ Red → right arm
▪ Yellow → left arm
▪ Green → left foot
▪ Black → right foot (this is a grounding electrode)
A mnemonic you can use is “Ride Your Green Bike”. R is for Red and
Right arm. Start at the right arm, and go clockwise, ending with the black
electrode for the right foot.
o The 6 chest leads are V1-6, also called C1-6. Putting them in their correct
position is important, as misplacing them makes you unable to interpret R
wave progression and clockwise/counterclockwise rotation.
▪ V1: right 4th intercostal space, to the right of the sternum
▪ V2: left 4th intercostal space, to the left of the sternum
▪ V3: between V2 and V4
▪ V4: left 5th intercostal space, midclavicular line
▪ V5: left 5th intercostal space, anterior axillary line
▪ V6: left 5th intercostal space, midaxillary line

o Additional leads:
▪ V4R: done by putting the V4 electrode in its usual position but on
the right side of the chest (5th right intercostal space in the mid-
clavicular line). Used to check for RV infarction (see if there's ST

1
 segment elevation[1]). This is important as in RV infarction, nitrates
are contraindicated (they may develop severe hypotension and
shock).
▪ Posterior leads: Leads extended further round the chest – V7, V8
and V9. These are placed on the posterior chest wall in the following
manner:
• V7 – Left posterior axillary line, in the same horizontal plane
as V6.
• V8 – Tip of the left scapula, in the same horizontal plane as
V6.
• V9 – Left paraspinal region, in the same horizontal plane as
V6

• These are used for posterior MI, which can occur with left
circumflex occlusion. With a posterior infarct, anterior chest
leads show ST depression. No lead looks directly at the
posterior wall of the heart. V1 (and V2, V3) look through the
middle of the heart directly at the endocardial surface of the
posterior wall. These leads see the ECG signs of infarction,
but reversed (as they examine this part of the heart from
the inside, not the outside). So, acutely, instead of ST
elevation occurring, ST depression in seen. Posterior
infarction is diagnosed based on the presence of ST segment
elevation in leads V7-9.

2
• Standardization:
o A standardization mark is seen the start of each lead. This mark should be
two large squares tall (10 mm/mV), and one large square wide (25 mm/s)[1].
The paper speed and voltage standardization are also written on the ECG
paper.

▪ If the voltage standardization is too low (short mark), then this may
lead to incorrect interpretation of a low voltage QRS complex (e.g.,

3
 hypothyroidism, pericardial effusion, emphysema, pneumothorax,
etc.)
▪ If the voltage standardization is too high (tall mark), it may lead to
an incorrect interpretation of tall QRS complexes (e.g., ventricular
hypertrophy)
▪ With a standardization of 10 mm/mV and 25 mm/s:
• Large square: 5 mm, 0.2 seconds (200 ms), 0.5 mV
• Small square: 1 mm, 0.04 seconds (40 ms), 0.1 mV
• When depolarization is directed towards a lead, it results in a positive deflection in
that lead. The mean direction electrical activity (depolarization wave) of the
ventricles is represented by the cardiac axis. The same principle applies to atrial
depolarization, hence, the p wave in aVR is negative.

• Artifacts may be seen in the baseline tracing (which may be mistaken for an
arrhythmia, e.g., the random electrical activity of atrial fibrillation). These can result
from patient movement, tremors (e.g., Parkinson’s disease), or a bad machine with a
bad filter for the artifacts

4
• ECG machines may have autoanalysis software that interprets and calculates things
like rate, cardiac axis, periods and intervals, etc. and may even give a diagnosis (e.g.,
description of rhythm and of QRS and T patterns). While using the other ones is fine,
you shouldn’t rely on the diagnosis given by the machine; ECG findings should be
correlated with clinical findings obtained from history and examination to reach a
diagnosis (note: ECG recorders tend to “over-report” and describe abnormalities
where none exist)
• An ECG may also provide a “long strip”, usually of Lead II, for rate, rhythm, heart
block dx.
• The ECG is now widely used. Indications for using an ECG include:
o Chest pain
o SOB
o Syncope
o Palpitations
o Any suspicion of cardiovascular disease.
ECG is important for myocardial ischemia, particularly ACS, and arrythmias
(tachy- and brady-arrhythmias)
• Modes of ECG:
o Resting ECG
o Ambulatory ECG:
▪ ECG recording for a prolonged period of time. This can be done with
a Holter monitor or a cardiac memo. Loop recorder, a device
implanted subcutaneously, can be used for longer recording periods
(it can record heart rhythm for up to 3 years)
▪ This is mainly used to diagnose paroxysmal arrythmia, with a normal
ECG in-between attack, e.g., SVT, sick sinus syndrome, atrial
fibrillation. The duration of the ambulatory ECG recording depends

5
 on the frequency of the attacks. With infrequent episodes, a loop
recorded is used.
▪ Ambulatory ECG is also used to diagnose angina. The ECG may
normal in between episodes of chest pain, but show ST or T changes
during attacks.
o Stress ECG
Two types:
▪ Exercise stress ECG
• Treadmill
• Ergometer bicycle
▪ Pharmacological stress ECG
• Positive inotropic agents, e.g., dobutamine
• Vasodilator agents, e.g., adenosine, dipyridamole
(persantine)
Used to assess and diagnose:
▪ Coronary artery disease and angina
▪ Exercise-induced arrythmia
▪ Valvular heart disease, particularly aortic stenosis and mitral
stenosis
▪ Some occupations require it, e.g., pilots

6
Interpretation
1) Assess technical aspects:
• Patient name, gender, and age
• Date and time
• Paper speed and voltage measurement calibration
• Correct placement of limb leads – check lead I and aVR:
o The most common mistake in electrode positioning is reversal of the right
and left arm leads (3% of ECGs recorded in a hospital setting)
o Normally, all complexes are positive in lead I and negative in aVR
o If they’re all negative in lead I and positive in aVR, it could either be that the
arm leads have been reversed or the patient has dextrocardia.
▪ To distinguish them, look at V1 and V6
• With reversal of arm leads, the progression of R waves is
normal (negative V1, positive V6)
• With dextrocardia, the progression is reversed (positive V1,
negative V6) (dextrocardia can also be detected with clinical
examination, e.g., auscultation or apex beat)

7
2) Rhythm
• Regularity:
o Regular: completely fixed RR interval
o Irregular: variable RR interval
▪ Regularly irregular: RR interval variable but with a pattern, e.g.,
normal and ectopic beats (atrial or ventricular) grouped together
and repeating over and over.
▪ Irregularly irregular: RR interval variable with no pattern, totally
irregular. Causes include:
• Atrial fibrillation (VIP)
• Multifocal atrial tachycardia
• Atrial flutter with variable block (not atrial flutter alone;
atrial flutter alone produces a regular rhythm)
• Sinus rhythm or not? Look for P waves in Lead II and V1; the normal P wave is
positive in II and aVF and biphasic in V1[1]
o A negative P wave means the rhythm is not sinus; it could be atrial[1] or
nodal/junctional[1]
Arrythmias: bradyarrhythmia and tachyarrhythmia:
• Bradyarrhythmias:
o Sinus bradycardia
o Sick sinus syndrome: consists of 5 components [Dr. Abdulstar]
▪ Sinus arrest (pause > 3 seconds): temporary cessation of sinus node
discharges; there are no P waves and associated QRS-T during sinus
pause. This pause is sometimes followed by an escape rhythm, but
the absence of escape rhythms results in asystole, which can lead to
hypotension and fainting; the syncope results from the transient
ventricular asystole causing a steep decline in stroke volume and
cerebral perfusion. Such episodes are known as Strokes-Adams
attacks - A typical episode is characterized by a sudden loss of
consciousness, which frequently occurs without warning and may
result in a fall. There is pallor and a death-like appearance during

8
 the attack and the patient has no pulse, but when the heart starts
beating again there is a characteristic flush. In contrast to epilepsy,
recovery is rapid. Sinus pause less than 3 seconds usually needs no
investigation and may be seen in normal people; however, longer
pauses (≥ 3 seconds) are significant, requiring further investigation
and treatment.
▪ Sinoatrial block: similar ECG presentation to sinus pause. In SA exit
block, sinus node depolarization is normal, but it fails to conduct to
surrounding atrial tissues.
▪ Tachy-brady syndrome (episodes of paroxysmal tachycardia):
bradycardia alternating with paroxysmal supraventricular
tachyarrhythmias
▪ Atrioventricular block
▪ Atrial fibrillation
Patients may have one or more of these arrhythmias [Dr. Abdulstar]
These may not be seen on a regular ECG. An ambulatory ECG is needed
to diagnose SSS.
(extra) Sinus arrest and block: The SA node consists of two main groups of cells: A central core of
pacemaking cells (P cells) that produce the sinus impulses, and an outer layer of transitional cells (T
cells) that transmit the sinus impulses out into the right atrium. Sinus node dysfunction can result
from either: Failure of the P cells to produce an impulse (this leads to sinus pauses and sinus arrest),
or failure of the T cells to transmit the impulse (this leads to sino-atrial exit block). The patterns of
conduction in SA exit block are identical to the different types of AV block. However, as the initial
sinus impulse is not visible on the ECG, the relationship between impulse generation and transmission
must be inferred from the P waves alone (analogous to examining only the R waves in AV block). Only
second degree SA block (types I and II) can be diagnosed from the 12-lead ECG. With first degree SA
block, there is delay between impulse generation and transmission to the atrium. Second degree SA
block has 2 types: Type I (Wenckebach), where there is Progressive lengthening of the interval
between impulse generation and transmission, culminating in failure of transmission, which leads to
successive P waves being pushed closer together (grouping of P-QRS complexes, with the P-P interval
progressively shortening) until a pause occurs due to dropped P waves at the end of each group; and
type II, where there are Intermittent dropped P waves with a constant interval between impulse
generation and atrial depolarisation, which is equivalent to Mobitz II – there is no clustering of P-QRS
complexes, there is no clustering of P-QRS complexes, and intermittent P waves “drop out” of the
rhythm with subsequent P waves arriving “on time”. With third degree SA block, None of the sinus
impulses are conducted to the right atrium, and there is a complete absence of P waves. This is
indistinguishable from sinus arrest due to pacemaker cell failure on 12 lead ECG. Rhythm may be
maintained by a junctional escape rhythm, but the onset of 3rd degree SA block may produce long
sinus pauses or sinus arrest, which may lead to fatal asystole.

9
o Heart block (atrioventricular block): characterized by an interrupted or
delayed conduction between the atria and the ventricles. There are three
degrees:
▪ First degree heart block: prolonged PR interval (larger than 1 large
square/5 small squares/200 ms)
▪ Second degree heart block: dropped beats occur because some
impulses from the atria fail to conduct to the ventricles
intermittently. Two types:
• Mobitz type I (Wenckebach phenomenon): progressive
lengthening of successive PR intervals, culminating in a
dropped beat. The cycle then repeats itself.
• Mobitz type II: the PR interval of the conducted impulses
remains constant but some P waves are not conducted.
Every other beat could be conducted (2:1 block, twice as
many P waves as there are QRS complexes), every other 2
beats could be conducted (3:1 block), etc.
o (extra) There may be no pattern to the conduction
blockade, or alternatively there may be a fixed
relationship between the P waves and QRS
complexes, e.g., 2:1 block, 3:1 block.
▪ Third degree heart block (complete heart block): no beats are
conducted from the atria to the ventricles; there is complete AV
dissociation. When this occurs, the ventricles are excited by a slow
‘escape mechanism’, from a depolarizing focus within the
ventricular muscle.
• No relationship between P waves and QRS complexes
• Regular, slow rate
• Wide, abnormally shaped QRS complexes.

Note: a pacemaker may be needed, but you should exclude

reversible causes first.

10
Complete heart block:

11
• Tachyarrhythmias: either supraventricular tachycardia or ventricular tachycardia
o Sinus tachycardia
o Supraventricular tachycardias: atrial, nodal/junctional
▪ Atrial:
• Atrial ectopics/extrasystoles: the morphology of the P wave
is different from that of sinus beats, followed by a QRS
complex (early) that’s the same as those of the sinus beats,
then there’s a compensatory pause (extra: since the
myocardium is its refractory period and does not respond to
the sinus impulse that reaches it). After this, normal
conduction resumes.
• Atrial tachycardia: frequent atrial ectopics
• Multifocal atrial tachycardia: multiple arrhythmic foci within
the atria.
o Irregularly irregular
o QRS complexes are normal (assuming no BBB or
Wolf-Parkinson-White syndrome [WPW])
o Multiple different P wave morphologies; by
definition, multifocal atrial tachycardia must have at
least three distinctly different P wave morphologies
• Atrial fibrillation:
o Irregularly irregular
o No P waves
o Fibrillation waves (absence of isoelectric baseline;
irregular baseline)
o QRS complexes are normal (assuming no BBB,
WPW)

12
 • Atrial flutter:
o Regular
▪ Unless there’s atrial flutter with variable
block, in which case it’s irregularly irregular
o Saw-tooth-like flutter waves
▪ Nodal: atrioventricular nodal reentry tachycardia (ANVRT), very
common type of supraventricular tachycardia (SVT). This is
commonly, but inappropriately, called SVT.
• No p waves
• Regular, tachycardia
• QRS complexes are normal (assuming no BBB, WPW)
o Ventricular:
▪ Ventricular ectopics/extrasystoles (common)
• No P waves
• Wide, bizarre QRS complexes (early)
• The direction of the T wave is usually opposite that of the
QRS complex[1]
• Retrograde P wave: the ectopic impulse is conducted
retrogradely through the AV node, producing atrial
depolarization, producing an inverted P wave, usually
occurring after the QRS complex; this is an indicator the
beat is ventricular in origin. This is not always seen.
• These can occur in single beats but can be repetitive:
o Bigeminy: every other complex is a ventricular
ectopic
o Trigeminy: every third complex is a ventricular
ectopic
o Quadrigeminy: every fourth complex is a ventricular
ectopic
o Couplet: 2 ventricular ectopics in a row
o Triplets: 3 ventricular ectopics in a row
o More than 3 ventricular ectopics in a row →
ventricular tachycardia[1]
▪ Ventricular tachycardia: multiple ventricular extrasystoles in a row
• Less than 30 seconds → nonsustained VT
• More than 30 seconds → sustained VT
• Criteria in support of VT:

13
 o Extreme left axis deviation
o QRS complex larger than 3 small squares
o Complete AV dissociation
o Concordance – in VT, all QRS complexes in V1-6 are
either all negative or all positive
o Fusion and capture beats: In ventricular tachycardia,
there is independent atrial and ventricular activity.
Occasionally, a P wave is conducted to the ventricles
through the AV node, producing a normal sinus beat
in the middle of the tachycardia (a capture beat);
more commonly, however, the conducted impulse
fuses with an impulse from the tachycardia (a fusion
beat). This can occur only when there is
atrioventricular dissociation and is therefore
diagnostic of ventricular tachycardia.
• Differential diagnosis (of broad-complex tachycardia):
o VT
o SVT with BBB
o SVT with WPW

If in doubt, treat as VT, as it can be life threatening.

▪ Ventricular fibrillation: sinusoidal waves, where P, QRS and T waves

cannot be differentiated (?? Dr. Abdulstar). This is fatal if
cardioversion is not done.

14
15
16
 Note – causes of cardiac arrest:

Shockable • Ventricular fibrillation

rhythms; you • Pulseless VT: very rapid but ineffective contractions, leading to a dramatic decrease
should cardiovert in cardiac output and no pulse being present
• Asystole: isoelectric flat line
o Not shockable
o Management: atropine, adrenaline, CPR
• Electromechanical dissociation (EMD) (also called pulseless electrical activity): the
presence of discernible electrical complexes (excluding ventricular tachycardia and
ventricular fibrillation) and the absence of palpable pulses. This is also not
shockable. Causes include:
o Ventricular wall rupture (e.g., after MI) (rapidly fatal)
6 Hs:
o Hypovolemia
o Hypoxia
o Hypothermia
o Hypoglycemia
o Hydrogen ions (acidosis)
o Hyperkalemia or hypokalemia

6 Ts:
o Tablets or toxins
o Tamponade
o Tension pneumothorax
o Thrombosis (e.g., myocardial infarction, pulmonary embolism)
o Tachycardia
o Trauma (e.g., hypovolemia from blood loss)

Note: these causes are potentially treatable

3) Rate
• May be provided by the ECG machine
• Rate estimation depends on rhythm regularity:
o Regular rhythm: count the number of squares between R waves
▪ 1500/no. small squares = rate
▪ 300/no. large squares = rate
o Irregular rhythm:
▪ Choose 15 successive large squares (= 3 seconds)
▪ Count the number of R waves in this interval
▪ No. of R waves * 20 = rate
4) Cardiac axis: the normal cardiac axis lies between -30° and +110°

17
The negative and positive poles of the leads lie within 30° increments of each other:

Methods of assessing the cardiac axis:

• Quadrant method: Look at the QRS complex in Lead I and aVF. Normally, both are
positive.
o Compare the negative and positive deflections in the QRS complex and
determine net direction:

18
 aVF
+ -
+ Normal cardiac axis Left axis deviation
Lead I Extreme axis deviation
- Right axis deviation (opposite axis??), e.g., in
dextrocardia

• The isoelectric lead:

o Examine the 6 six limb leads to find one that is isoelectric (positive
deflection = negative deflection); this occurs when the cardiac axis is
perpendicular (at a 90° angle to it) to a particular lead, e.g., if lead I (0°) is
isoelectric, then the cardiac axis is +90° or -90°; if lead II (+60°) is isoelectric,
then the cardiac axis is -30° or +150°.
o Find the positive leads; this lets you determine the direction in which the
cardiac axis
o The QRS axis is at 90° to the isoelectric lead, pointing in the direction of the
positive lead

19
Example: aVL is isoelectric, so the cardiac axis is perpendicular to aVL (-30°), meaning it
could be +60° or -120°. Lead I, II, and III are positive, so the cardiac axis is pointing in their
direction. The cardiac axis is thus +60°.
• Graph method: this method uses lead I and aVF, which are perpendicular. Draw
these two perpendicular leads, and mark on each lead equidistant lines to represent
a ruler-like marking or draw them on graph paper.
o Examine lead I and aVF to determine the negative or positive deflection of
the QRS complex in each lead. Net deflection is the larger of the two
deflections (R or S) minus the smaller deflection. For example:
▪ The positive deflection in lead aVF is 12 mm (1 small square = 1 mm
= 1 mV), and the negative deflection is 2 mm, so the net deflection is
+10.
▪ The positive deflection in lead I is 7, while the negative deflection is
4, so the net deflection is +4.
▪ Mark these on the graph
o Draw perpendicular lines from each line at the point of net deflection, and
the two lines will intersect. The QRS vector (cardiac axis) will be the line
traversing the point of intersection of I and aVF to the point of the two
drawn lines intersecting.
o An exact measurement will require a protractor; however, it is easy to
estimate with a mere glance.

20
5) Assess the periods:
• PR-interval: start of P wave to start of QRS complex; normally 120-200 ms (3-5 small
squares)
o Prolonged → heart block (see above)
o Short → preexcitation, e.g., Wolf-Parkinson-White (WPW) syndrome, Lown–
Ganong–Levine (LGL) syndrome
o Can’t be assessed if no P waves can be seen, e.g., atrial fibrillation.
• QRS complex width: normally less than 120 ms (< 3 small squares)
o More than 3 small squares → wide QRS complex, e.g., right or left bundle
branch block, WPW syndrome, ventricular ectopics or rhythms
• QT interval: start of Q wave to end of T wave. This interval varies with heart rate; it’s
shorter when the heart rate is faster. To assess the QT interval, you have to correct
it for heart rate (corrected QT interval, cQT); The corrected QT interval (QTc)
estimates the QT interval at a standard heart rate of 60 bpm
𝑄𝑇 𝑜𝑛 𝐸𝐶𝐺
𝑐𝑄𝑇 =
√𝑅𝑅 − 𝑖𝑛𝑡𝑒𝑟𝑣𝑎𝑙 𝑖𝑛 𝑠𝑒𝑐𝑜𝑛𝑑𝑠

o Normal cQT: 340-430 ms

o If the rhythm is irregular, take 5 cardiac cycles and use the average QT and
the average RR interval[1]

21
 o If RR = 5 LS (heart rate = 60 bpm), the cQT = QT. If the RR interval is close to
5 LS, calculating cQT is not necessary
o The QT interval is important, as a prolonged QT interval and shortened QT
interval are both arrhythmogenic conditions. The latter has fewer causes.
▪ There are many causes of prolonged QT interval:
• Electrolyte abnormalities: hypokalemia, hypocalcemia,
hypomagnesemia
• Drugs (common): class Ia anti-arrhythmic drugs (e.g.,
disopyramide), class Ic anti-arrhythmic drugs (e.g.,
flecainide), class III antiarrhythmic drugs (e.g., amiodarone),
amitriptyline and other TCAs, erythromycin and other
macrolides, Chlorpromazine and other phenothiazines
• Congenital syndromes: type 1, 2, and 3. Romano–Ward
syndrome is the most common form of congenital Long QT
syndrome; there is no hearing loss. Jervell and Lange-
Nielsen syndrome (JLNS) is a rare type of long QT syndrome
associated with severe, bilateral sensorineural hearing loss.
• Hypothermia
• Cardiomyopathy[1]
▪ Causes of short QT interval[1]:
• Congenital
• Digoxin overdose
• Hypercalcemia
• Hyperthermia
• (extra) hyperkalemia, effects of catecholamine, acidosis
6) Assess the:
6.1. P wave: represents the depolarization of the atria, and hence, an abnormality in the P
wave reflects an abnormality of the atria. Atrial depolarization proceeds sequentially from
right to left, with the right atrium activating before the left atrium. The right and left atrial
waveforms summate to form the P wave; The first 1/3 of the P wave corresponds to right
atrial activation, the final 1/3 corresponds to left atrial activation; the middle 1/3 is a
combination of the two.
Look at lead II and V1 to assess the P wave:
• Normally:
o Lead II:
▪ the P wave is positive (note: always negative in aVR)
▪ ≤ 3 small squares wide
▪ ≤ 3 small squares tall[1]
o V1:
▪ In most leads (e.g., lead II), the right and left atrial waveforms move
in the same direction, forming a monophasic P wave. However, they
move in opposite directions in V1
▪ The P wave is biphasic, with similar sizes of the positive and negative
deflections.
• Positive deflection → right atrium
• Negative deflection → left atrium
• Right atrial enlargement:

22
 o Lead II: more than 3 small square in height, but normal duration (width)[1] (P
pulmonale)
o V1: positive component much larger than negative component[1]
• Left atrial enlargement:
o Lead II: more than 3 small squares in length, normal height; frequently M-
shaped (bifid P-wave; P mitrale)
o V1: negative component larger than the positive component.
• P wave more than 3 small squares wide AND tall → bi-atrial enlargement

✓ The P wave may not be seen at all, e.g., in atrial fibrillation and atrial flutter (where
it’s replaced by saw-tooth shaped flutter waves.
✓ An abnormally shaped P wave is seen with ectopic atrial rhythms.
✓ A clear P wave is needed for it to be analyzed
6.2. QRS complex: represents the depolarization of the ventricles (note: the QRS complex,
which represents the depolarization of both ventricles, is influenced mainly by the large bulk
of myocardium of the left ventricle, the electrical forces of which swamp those arising from
the right ventricle)
❖ Used for the diagnosis of right and left bundle branch block (RBBB and LBBB), and
left and right ventricular hypertrophy (LVH and RVH)
❖ Normal duration: less than 3 small squares wide
• More than 3 small squares in width → wide QRS complex, could be due to BBB
Look at leads V1 and V6 to detect BBB
o Normally:
▪ V1: small R wave, deep S wave
▪ V6: small Q wave, tall R wave, usually no S wave[1]
o RBBB:

23
 ▪ V1: RR’ or RSR’ complex (a second R wave is formed); M-shaped
(either the first or second R wave could be larger [Dr. Abdulstar]; the
R waves are taller than they should be) (a tall, wide and frequently
notched R wave [RR’] or rSR’ complex instead of normal rS in lead
V1[1])
▪ V6: deep, slurred S wave; W-shaped
• Mnemonic: MaRRoW (M in V1, W in V6, and R for RBBB)
▪ T wave inversion in right sided leads: II, III, aVF, V1, V2[1]

Example:

o LBBB:
▪ V1: R wave remains, wide slurred S wave[1]; W-shaped
▪ V6: M-shaped R wave[1]; M-shaped
• Mnemonic: WiLLiaM (W in V1, M in V6, L for LBBB)
▪ T wave inversion in left-sided leads: I, aVL, V5, V6

24
Example:

• Ventricular hypertrophy: the voltage criteria are the most sensitive way to detect
hypertrophy [?? Dr. Abdulstar]
o LVH:

25
 ▪ The QRS complexes have the same configuration, but the depth of
the S wave in V1 + the height of the R wave in V6 ≥ 7 large squares.
▪ Left axis deviation
▪ ST depression and T-wave inversion in I, aVL, V5, V6 (LV strain
pattern)
• Note: the mechanism responsible for this “strain” pattern is
uncertain, but “strain” is related to the increased pressure
(overload) in the left ventricular cavity[1].
o RVH:
▪ Tall R wave in V1, deep S wave in V6.
▪ Right axis deviation
▪ ST depression and T-wave inversion in II, III, aVF, V1, V2 (RV strain
pattern)
o Causes of ventricular hypertrophy:
▪ LVH: hypertension, aortic valve disease (stenosis and regurgitation),
hypertrophic cardiomyopathy, mitral regurgitation, coarctation of
aorta
▪ RVH: pulmonary HTN, pulmonary embolism, pulmonary stenosis
• Note – transition point, clockwise rotation, and counterclockwise rotation: the QRS
complex in the precordial leads shows a progression from V1, where it is
predominantly negative, to V6, where it is predominantly positive. The “transition
point” is where the R and S waves are equal, and indicates the position of the
interventricular septum. This is normally at V3/V4. In some conditions, it’ll be moved
to V4/V5 or even V5/V6; seen from below, the heart can be thought of as having
rotated in a clockwise direction, hence this is called “clockwise rotation”. This can
occur if the right ventricle is enlarged, thus occupying more of the precordium than
is normal, and clockwise rotation is characteristic of chronic lung disease. If the
transition occurs earlier, it’s known as counterclockwise rotation.
• Note – low voltage QRS:
o Damping of the electrical signal due to excess air (emphysema, COPD), fluid
(pericardial effusion, pericardial constriction, pleural effusion), edema
(anasarca), fat (obesity), or amyloid cardiomyopathy
o Electrically inert myocardium due to a loss of viable myocardium such as in
myocardial infarction and Chagas disease
o Infiltration of the myocardium (myxedematous, Chagas disease)
6.3. ST segment: normally isoelectric; abnormalities of this segment are either elevation or
depression
• ST segment elevation: important for the diagnosis of STEMI (should be excluded)
o Shape (very important):
▪ Dome → acute pericarditis; Biconcave → STEMI [???? Dr. Abdulstar]
▪ The ST elevation of pericarditis is described as concave upwards or
“saddle shaped”[1]
▪ The ST elevation is STEMI is convex (dome-shaped)[1]
o STEMI causes localized elevation, according to the site affected (e.g., if there
is an inferior MI, there will be ST elevation in inferior leads – III, aVF). In
contrast, there is diffuse (in most leads) ST segment elevation in acute
pericarditis.
o In STEMI, the ECG evolves over time[1]:

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 1. Hyperacute (tall) T waves (due to localized hyperkalemia; These
changes are rarely seen as they are transient and frequently occur
prior to hospital arrival)
2. ST elevation
3. Q waves
4. T wave inversion

• More than one of these changes may be seen on the same ECG (e.g.,
ST elevation and T wave inversion)
• This would not be seen with acute pericarditis; in
pericarditis, T wave inversion usually occurs only after the
ST segments have returned to baseline. In infarction, T wave
inversion usually precedes normalization of the ST
segments[1]
• Q waves are typically permanent, and give no indication to the age
of the MI (old MI)
• In pericarditis, Q wave formation does not occur. PR depression may
be seen.

• ST segment depression:
o Up-sloping (usually not significant[1])
o Down-sloping
o Horizontal Pathological

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 o Causes of ST depression:
• Angina
• NSTEMI
• Strain pattern
• BBB
• Electrolyte abnormality, e.g., hypokalemia, hypomagnesemia
• Reciprocal ST depression in STEMI, where there is usually reciprocal
ST depression in the electrically opposite leads, e.g., STE in the high
lateral leads I + aVL typically produces reciprocal ST depression in
lead III. This is one of the features of STEMI that distinguishes it from
other causes of ST elevation[1].
• Digoxin effect (down-sloping ST depression)
Reciprocal ST depression:

6.4. T wave: normally positive except in aVR, where it’s negative. Abnormality occurs in the
form of either tall T waves or inverted T waves

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 • Tall T waves: MI (“hyperacute T waves”; fat and wide, with a more blunted peak),
hyperkalemia (tented T wave, sharp peak, narrow base)

• Inverted T waves:
o Symmetrical: down slope and up slow have the same angle, common in
coronary disease
o Asymmetrical: downslope is much shallower (gentler) than the up slope
(which is rapid), resulting in a “reverse tick” appearance, common in LVH,
BBB, coronary disease and digoxin.

o Causes of T inversion:
▪ Ischemia
▪ Electrolyte abnormalities
▪ BBB
▪ Ventricular hypertrophy (strain pattern)
▪ Chronic pericarditis[1]
▪ Hypothyroidism
▪ Hypothermia
▪ Myocarditis
▪ Digoxin
These should be interpreted within clinical context.
6.5. Additional waves:

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• U wave: a small (0.5 mm) deflection immediately following the T wave, usually in
the same direction as the T wave, coming between the T wave and the P wave of the
next cardiac cycle.
o Normally seen in the precordial leads
o Diffuse U waves are a feature of hypokalemia

• Delta waves: slurred upstroke in the QRS complex due to preexcitation of the
ventricles, associated with a shortened PR interval and widened QRS Complex. Seen
in Wolf-Parkinson-White syndrome (common condition).

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 • J wave or Osborn wave: The Osborn wave (J wave) is a positive deflection (notch)
seen at the J point (QRS-ST junction) in precordial and true limb leads. It is most
commonly associated with hypothermia.

Thus, to interpret an ECG, approach it systemically as mentioned above, collect the ECG
findings and correlate them with the patient’s clinical findings to reach a diagnosis.

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 Summary
1. Technical aspects:
• Patient name, gender, age
• Date, time
• Paper speed, voltage measurement calibration
• Correct placement of limb leads → I and aVR
2. Rhythm
• Regularity
• Sinus rhythm or not? Check P wave
• Arrhythmias
3. Rate
• Regular rhythm:
• No. of small squares/1500
• No. of large squares/300
• Irregular rhythm: no. of R waves in an interval of 15 large squares X 20
4. Cardiac axis: check I and aVF
5. Periods
• PR interval: 120-200 ms (3-5 large squares)
• Prolonged → heart block
• Shortened → preexcitation
• QRS complex width: <120 ms (< 3 small squares)
• Widened QRS → ventricular rhythm or ectopics, BBB, WPW
• QT interval
6. Assess:
• P wave: Left and right atrial enlargement
• QRS complex:
• BBB
• Ventricular hypertrophy
• Transition point and rotation
• ST segment: elevated, isoelectric (normal), or depressed
• T wave:
• Tall T waves
• Inverted T waves
• Additional waves:
• U wave
• Delta wave
• J or Osborn wave

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