Ecg interpretation - Medicalbooksvn.wordpress.com

ECG Interpretation
HOANG CUONG MS-V
HaNoi Medical University
H a Noi, Octobe r 07, 2018

Contents
• Cardiac Electrophysiology
• The ECG leads
• Normal ECG, Normal Variants and
Abnormalities
• A systematic Approach to ECG Interpretation

Principles of Cardiac Electrophysiology
Cell types in Electrocardiology:
• Conduction cells: Disseminate the action potential
• Contractile myocardial cells: Carry out the actual contraction but are also
capable of transmitting the action potential, but much lower speed than the
conduction cells.
Cardiac cell architecture:
• Syncytium
• Intercalated discs: Connections between
the cells.
• The electrical connection is established
by gap junctions → proteins, forms
channels between the cell membranes.
→ action potential can spread from cell
to cell

The cardiac action potential
- Action potential: electrical stimulation created by a sequence of ion fluxes
through specialized channels in the membrane (sarcolemma) of cardiomyocytes
that leads to cardiac contraction.
- Action potential in cardiomyocytes:
Phase 4: The resting phase
• The réting potential in a cảdiomyocyte is -90 mV due to a constant outward of K+
through inward rectifier channels.
• Na+ and Ca2+ channels are closed at resting TMP.
Phase 0: Depolarization
• An action potential triggered → TMP to rise above -90mV
• Fast Na+ channels → open one by one and Na+ leaks into the cell → ↑ TMP
• TMP approaches -70mV → threshold potential → Fast Na+ channels have opened
to generate a self-sustaining inward Na+ current.
• Large Na+ current rapidly depolarizes the TMP to 0mV and slightly above 0 mV
for a transient period of time → overshoot → Fast Na+ channels close.
• L-type (‘long-opening’) Ca2+ channels open when TMP is ≥-40 mV → Ca2+ influx.

- Action potential in cardiomyocytes:
Phase 1: Early repolarization
• TMP is now slightly positive
• Some K+ channels open briefly and an outward flow of K+ returns the TMP to
approximately 0 mV.
Phase 2: The plateau phase
• L-type Ca2+ channels are still open and there is a small, constant inward current of
Ca2+ → Ventricular myocardium contracts.
• K+ leaks out down its concentration gradient through delayed rectifier K+
channels.
Phase 3: Repolarization
• Ca2+ channels are gradually inactivated.
• K+ channels open again and the exfflux of potassium repolarizes the cell.
• Normal transmembrane ionic concentration gradients → stored by returning Na+
and Ca2+ ions to the extracellular environment, and K+ ions to the cell interior. The
pumps involved include the sarcolemmal Na+-Ca2+ exchanger, Ca2+-ATPase and
Na+-K+ATPase

• Absolute refractory period (ARP): The cell is
completely unexcitable a new stimulus.
• Relative refractory period (RRP): A greater
than normal stimulus will depolarize the cell
and cause an action potential.
• The relative refractory period coincides with
the T-wave apex.
• Ventricular depolarization is superimposed
on the T-wave → R-on-T phenomenon.
Absolute and relative refractory periods:

Electrical Vectors
• The first vector: The atria
 Originate from atrial depolarization.
 During activation of the right atrium → directed anteriorly and to the left.
 The vector turns left and somewhat backwards → depolarization left atrium.
 Lead V1 detects: initial vector heading towards it → positive deflection, vector
heads away from it when the left atrium is activated → small negative
deflection on the terminal portion of the P-wave.
 Lead V5 detects: only notes vectors heading towards it throughout the course
of atrial activation → uniformly positive P-wave.
• The second vector: The ventricular (interventricular) septum
 The ventricular septum receives Purkinje fibers from the left bundle branch
→ Depolarization from left side to wards right side.
 Ventricular septum is relatively small → V1- a small positive wave (r-wave) and
V5- a small negative wave (q-wave).

Electrical Vectors
• The third vector: The ventricular free wall
 The vector resulting from activation of the right ventricle does not come to
expression. Because vector generated by the left ventricle >>>> right ventricle →
Vector during activation of the ventricular free walls is actually the vector
generated by the left ventricle.
 Activation of the ventricular free wall proceeds from the endocardium to the
epicardium. Because the Purkinje fibers run through the endocardium, where
they deliver the action potential to contractile cells.
→ spread of the action potential occur from one contractile cell to another, starting
in the endocardium and heading towards the epicardium.
→ Lead V5 detects a very large vector heading towards it → A large R-wave;
Lead V1 records the opposite → a large negative wave → A large S-wave.
• Fourth vector: Basal parts of the ventricles.
 The final vector stems from activation of the basal parts of the ventricles
 It heads away from V5 → negative wave (s-wave), Lead V1 does not detect.

Electrical Vectors
• The vector of the T-wave
 Since both (1) ion flows and (2) direction of the vector are opposite during
repolarization → The T-wave will be concordant with the QRS complex.
 The T-wave vector - directed forward and slightly to the left and down wards.
 P-wave and T-wave are smooth waves, whereas the QRS complex has sharp
spikes.
Concordance between QRS and T Discordance between QRS and T
The positive area of the QRS complex is greater
than the two negative areas combined. Thus the
QRS complex is net positive. The T-wave is also
positive.
The positive area of the QRS complex is smaller
than the negative area. Thus the QRS complex is
net negative. The T-wave, on the other hand, is
positive.

Chest leads (precordial leads)

The Limb leads
A) The limb leads and their view of the heart’s electrical activity B) Einthoven’s triangle

The four walls of the left ventricle and the ECG leads that “view” these walls

Normal ECG, Normal Variants, and Abnormalities
Overview of the normal ECG:

P-wave checklist
• The P-wave is always positive in lead II during sinus rhythm
• The P-wave is virtually always positive in leads aVL, aVF, -aVR, I, V4, V5
and V6. It is negative in lead aVR.
• The P-wave is frequently biphasic in V1 (occasionally in V2). The
negative deflection is normally <1mm.
• P-wave duration should be ≤0.12 seconds.
• P-wave amplitude should be <2,5 mm in the limb leads.
• P-pulmonale implies that the P-wave has abnormally high amplitude in
lead II (and in other leads in general).
• P-mitrale implies that the second hump of the P-wave in lead II and the
negative deflection of the P-wave in lead V1 are both enhanced.

PR interval and PR segment
• PR interval: the time interval from start of atrial depolarization to start of
ventricular depolarization.
• PR interval → not be too long nor too short.
• PR segment: flat line between the end of the P-wave and the onset of the
QRS complex.
• PR interval checklist:
 Normal PR interval: 0.12-0.22 seconds. Upper reference limit is 0,20
seconds in young adults.
 A prolonged PR interval (>0.22s) is consistent with first-degree AV-block.
 A shortened PR interval (<0.12s) indicates pre-excitation (presence of an
accessory pathway). This is associated with a delta wave.

The QRS complex (ventricular complex)
• A complete QRS complex consists of a Q-, R-, S-wave.
• All three waves may not be visible and there is always variation between the
leads.
• Some leads may display all waves, whereas others might only display one of the
waves.
• Naming of the waves in the QRS complex:
 A deflection is only referred to as a wave if it passes the baseline.
 If the first wave is negative → Q-wave; If the first wave is not negative → QRS not
possess a Q-wave.
 All positive waves → R-waves. The first → “R-wave” (R); The second → “ R-prime
wave” (R’); Third (rare) → “R-bis wave” (R”).
 Any negative wave occurring after a positive wave → an S-wave.
 Large waves → their capital letters (Q, R, S), and small waves → their lower-case
letters (q, r, s)

• Net direction of the QRS complex:
 QRS complex → net positive or net negative.
 QRS complex is net positive if the sum of the positive > negative areas.
 QRS complex is net negative if the sum of the negative > positive areas.

Inplications and causes of wide (broad) QRS complex:
• Prolongation of QRS duration implies that ventricular depolarization is
slower than normal.
• QRS duration ≥0.12 seconds → abnormally wide (broad).
• Cause of wide (broad) QRS complex:
 Bundle branch block:
 Hyperkalemia
 Drugs: Class I antiarrhythmic drugs, tricyclic antidepressants and other
medications.
 Ventricular rhythm, ventricular ectopy and pacemaker with ventricular
stimulation.
 Pre-excitation (Wolff-Parkinson-White syndrome)
 Aberrant ventricular conduction (aberrancy):

Amplitude of QRS complex:
• Ventricular hypertrophy or enlargement (or a combination of both)
• Electrical currents – proportional to the ventricular muscle mass.
• The distance between the heart and the eleactrodes → significant impact on
amplitudes of the QRS complex (ex: Slender individuals → larger QRS
amplitudes).
→ a person with COPD → diminished QRS amplitudes due to hyperinflation
of thorax.
• Circulatory collapse, low amplitudes should raise suspicion of cardiac
tamponade.

R-wave amplitude:
High amplitudes may be due to ventricular enlargement or hypertrophy
→ Checklist:
• R-wave should be <26 mm in V5 and V6
• R-wave amplitude in V5 + S-wave amplitude in V1 should be <35 mm.
• R-wave amplitude in V6 + S-wave amplitude in V1 should be <35 mm.
• R-wave amplitude in aVL should be ≤ 12mm.
• R-wave amplitude in leads I, II, and III should all be ≤20 mm.
• If R-wave in V1 is larger than S-wave in V1, the R-wave should be <5 mm.

R-wave peak time:
R-wave peak time is the interval from the beginning of the QRS-complex to the
apex of the R-wave.
This interval: the depolarization to spread from the endocardium to
epicardium.
→ Checklist: Normal values
• Leads V1-V2 (right ventricular) <0.035
seconds.
• Leads V5-V6 (left ventricular) <0.045
seconds.

R-wave progression
• R-wave progression is assess in the chest (precordial) leads.
• Normal R-wave progression: R-wave gradually increase in amplitude from
V1 to V5 and then diminishes in amplitude from V5 to V6 (S-wave
undergoes the opposite development)

Abnormal R-wave progression
• Myocardial infarction: Necrotic myocardium → not generate electrical
potentials → loss of R-wave amplitude in the ECG leads reflecting the
necrotic area.
• Cardiomyopathy: loss or gain of R-wave amplitude. Amplitudes may be
increased in hypertrophic cardiomyopathy, whereas they are typically
diminished in late stages of dilated cardiomyopathy.
• Right and left ventricular hypertrophy: LVH→ ↑ R-wave amplitudes in V4-V6
and ↓ S-wave in V1-V3. RVH → ↑ R-wave in V1-V3 and smaller R-wave in V4-
V6.
• Pre-excitation, bundle branch block and COPD → affect R-wave progression.

Dominant R-wave in V1/V2
• The R-wave in V1-V2 → smaller than S-wave in V1-V2.
• Dominant R-wave in V1/V2 → R-wave > S-wave → May be pathological.
• If the R-wave > S-wave → R-wave should be <5mm, otherwise the R-wave is
abnormally large:
 Right bundle branch block
 Right ventricular hypertrophy
 Hypertrophic cardiomyopathy
 Posterolateral ischemia/infarction.
 Pre-excitation
 Dextrocardia
 Misplacement of chest electrodes

The Q-wave
• It is crucial to differentiate normal from pathological Q-waves, particularly
because pathological Q-waves are rather firm evidence of previous myocardial
infarction.
• Pathological Q-waves must exist in at least two anatomically contiguous leads in
order to reflect an actual morphological abnormality.
• Existence of pathological Q-waves in two contiguous leads → sufficient for a
diagnosis of Q-wave infarction.
R-wave amplitude
Q-wave duration
Q-wave amplitude
Definition of pathological Q-wave
• Duration >0.03 seconds and/or
• Amplitude >25% of R-wave amplitude
Hence, the Q-wave visible here does
fulfill criteria for pathogical Q-waves.

Normal variants of Q-waves:
• Septal q-waves → small q-waves frequently seen in the lateral leads (V5, V6,
aVL, I).
• An isolated and often large Q-wave is occasionally seen in lead III. The
amplitude of this Q-wave typically varies with ventilation → respiratory Q-
wave. (must be isolated to lead III)
• The small r-wave in V1 → missing → QS-complex in V1 → norma, if V2
shows an r-wave.
• Small Q-waves (not fulfill criteria for pathology) → all limb leads as well as
V4-V6. On the other hand, shoul never display Q-waves (regardless of their
size).

Abnormal Q-waves:
• The most common cause of pathological Q-waves is myocardial infarction.
• Note that pathological Q-wave must exist in two anatomically contiguous
leads.
• Other causes of abnormal Q-waves are as follows:
 Left-sided pneumothorax
 Perimyocarditis, Cardiomyopathy, Dextrocardia
 Amyloidosis
 Bundle branch blocks, fascicular blocks, Pre-excitation
 Ventricular hypertrophy
 Acute cor pulmonale

Normal waveforms.
Adequate R-wave progression
Small (septal) q-waves in V5
and V6
Patient with STEMI 5 days
earlier. Suboptimal R-wave
progression, pathological Q-
waves in V4-V6
Patient with a history of
STEMI. Loss of R-waves in V1-
V3, which has left QS-
complexes in these leads.
Patient 1 Patient 1 Patient 1

The ST segment: ST depression & ST elevation
The plateau phase (phase 2) corresponds to
the ST segment on the surface ECG. The
membrance potential is relatively
unchanged during this phase and most
ventricular cells are in this phase
simultaneously (more or less). Therefore
there are no electrial potential differences in
the myocardiyum during phase 2, which
results in a flat and isoelectric ST segment.
Acute ischemia is virtually always confined
to a specific area, where the cell’s membrane
potentials change (due to ischemia). Thus,
electrical potential difference occurs in the
myocardium and this displasces the ST-
segment up or down.
Action potential
in contractile cell
ECG recorded
on body surface

The ST segment: ST depression & ST elevation
• ST segment extends from the J point to the onset of the T-wave.
• The reason why the ST segment is flat and isoelectric: the membrane potential
is relatively unchanged during the plateau phase and most ventricular cells are
in plateau phase simultaneously (more or less).
• Displacement of the ST segment → importance → particularly in acute
myocardial ischemia.
• MI affects a limited area and disturbs the cells’ membrane potential → electrical
potential difference in the myocardium.
• The EPD exists between ischemic and normal myocardium → displacement of
the ST segment.
• ST segment deviation → elevation and depression of the ST segment.

The following must be noted regarding the ST segment:
• The normal ST segment is flat and isoelectric. The transition from ST
segment to T-wave is smooth, and not abrupt.
• ST segment deviation ( elevation, depression) → measured as the heigh
difference between the J point and the baseline (the PR segment).
• ST segment and the T-wave are electrophysiologically related → changes in
the ST segment are frequently accompanied by T-wave changes.
At paper speed 50 mm/s the J-
60 point is located 3 small
boxes after the J-point.
At paper speed 25 mm/s the J-
60 point is located 1.5 small
boxes after the J point.

Primary and Secondary ST-T changes:
• Primary ST-T changes → abnormal repolarization: Ischemia, electrolyte
disorders (calcium, potassium), tachycardia, increased sympathetic tone,
drug side effects,…
• Secondary ST-T changes → abnormal depolarization causes abnormal
repolarization: Bundle branch blocks (left and right), pre-excitation,
ventricular hypertrophy, premature ventricular complexes, pacemaker
stimulated beats,…
ST segment depression:
• ST segment depression <0.5 mm → accepted in all leads.
• ST segment depression ≥0.5 mm → considered pathological.
• (Some expert consensus documents) any ST segment depression in V2-V3
→ considered abnormal (because healthy individuals rarely display
depressions in those leads).

A. Physiological ST-segment depressions B. Non-specific ST-segment depressions
Upsloping ST-segment depression is
a normal finding during physical
exercise. It should be considered a
normal finding, provided that T-
waves are not inverted.
Hyperventilation may cause similar
ST-segment depressions.
Hypokalemia and high
sympathetic tone causes ST-
segment depressions with
flat T-waves and more
marked U-wave.
High sympathetic tone also
causes tachycardia.
Digoxin (a drug
used to treat atrial
fibrillation and
some cases of
heart failure)
causes a curved
ST-segment
depressions.

C. ST-segment depressions caused by acute ischemia
Note
When considering myocardial
ischemia , deviations in the ST-
segment always indicates
ongoing ischemia, ST-segment
deviation may be accompanied
by T-wave changes, but it is
the ST-deviation that indicates
acute ischemia.
De Winter’s sign De Winter’s sign is an exception to
the rute that upsloping ST-segment
depressions are not ischemic. de
Winter’s sign implies the presence of
upsloping ST-segment depressions
with prominent T-waves in the
majority of the precordial (chest)
leads. This is a sign of acute ischemia,
most often caused by a proximal
occlusion of the left anterior
descending (LAD)

D. Secondary repolarization abnormalities (secondary ST- and T-wave changes)

A. Characteristics of ST-segment elevations caused by ischemia
ST-segment elevations caused by ischemia typically displays a comvex or
straight ST-segment. Such ST-segment elevations in presence of chest
discomfort are strongly suggestive of transmural myocardial ischemia. Not that
the straight downsloping varian is unusual.
Convex Straight upsloping Straight horizontal Straight downsloping

B. Typical non-ischemic ST-segment elevation
Non-ischemic ST-segment elevations are extremely common in all
populations. They are characterized by a concave ST-segment and a greater
distance between the J point and the T wave apex
Concave

C. Examples of ST-segment elevations caused by ischemia

D. Real life example (limb leads shown)
ECG from a male patient (age 61) who experienced chest pain while driving to
work. Note ST-segment elevations as well as reciprocal ST-segment depressions.
There are also pathological Q-waves (leads III, aVF and perhaps II)

• Concave ST segment elevations are extremely common in any population: ST
segment elevation in leads V2-V3 occur in 70% of all men under the age of 70.
• There is no definite way to rule out myocardial ischemia by judging the
appearance of the ST segment.
T wave:
• Assessment of the T-wave represents a difficult but fundamental part of ECG
interpretation.
• The normal T-wave in adults is positive in most precordial and limb leads.
• T-wave amplitude is highest in V2-V3.
Positive T-waves:
• Positive T-waves are rarely higher than 6 mm in the limb leads (typically
highest in lead II).
• A common cause of abnormally large T-wave is hyperkalemia → high, pointed
and asymmetric T-wave. Hyperacute T-wave → broad based, high and
symmetric, their duration is short.

Normal T-wave inversion:
• An isolated (single) T-wave inversion in lead V1 is common and normal.
• Concordant with the QRS complex (negative in lead V1).
• Isolated T-wave inversions also occur in leads V2, III or aVL.
• T-wave inversion in two anatomically contiguous leads → pathological.
T-wave inversion in myocardial ischemia:
• T-wave inversions without simultaneous ST-segment deviation are not
ischemic.
• T-wave inversions accompanied by ST-segment deviation → ischemia.
• T-wave inversions do occur after an ischemic episode → Post-ischemic T-
waves.

Secondary T-wave inversion
• Secondary T-wave inversions – Similar to secondary ST-segment depressions → caused by
bundle branch block, pre-excitation, hypertrophy, and ventricular pacemaker stimulation.

Flat T-waves:
• T-waves with very low amplitude are common in the post-ischemic period.
• Commonly seen in leads V1-V3 → stenosis/occlusion left anterior
descending artery. Leads II, aVF, and III → left circumflex artery or right
coronary artery.
Biphasic (diphasic) T-waves:
• Biphasic T-waves carry no particular significant
• A T-wave is classified as positive or inverted based on its terminal portion.
T-wave progression:
• T-wave progression follows the same rules as R-wave progression.

T-wave checklist:
• I, II, -aVR, V5 and V6: should display positive T-waves in adults.
• III and aVL: These leads occasionally display an isolated (single) T-wave
inversion.
• aVF: positive T-wave, but occasionally flat.
• V1: inverted or flat T-wave is rather common, particularly in women. The
inversion is concordant with the QRS complex.
• V7-V9: should display a positive T-wave.

QT duration and corrected QT (QTc) duration
• The QT duration → Total time for de- and repolarization.
• Measure from the beginning of QRS-complex to the end of the T-wave.
• Prolonged QT duration → life-threatening ventricular arrhythmias.
• QT duration → inversely related to heart rate → Corrected QT duration
(QTc)
• Bazett’s formula → calculate the corrected QT duration.
Normal values for QTc interval:
• Men: <0.45 seconds
• Women: <0.46 seconds
Causes of prolonged QTc duration: antiarrhythmica, psychiatric
medications; antibiotics ( macrolides, kinolones, ..); hypokalemia,
hypocalcemia, hypomagnesemia; cerebrovascular insult; myocardial
ischemia…

The electrical axis of the heart (Heart axis)
• Assessment of the electrical axis is an integral part of ECG
interpretation.
• The average direction of ventricular depolarization during ventricular
contraction.
• Normal heart axis: -30o to 90o, right axis deviation: ≥90o, left axis
deviation: ≤30o.
• The following rules apply:
 Normal axis: Net positive QRS complex in leads I and II.
 Right axis deviation: Net negative QRS complex in lead I but positive in
lead II.
 Left axis deviation: positive- lead I, negative –lead II.
 Extreme axis deviation: Net negative QRS complex in leads I and II.

Axis deviation: Right axis deviaton (RAD) and left axis deviation (LAD)
Causes of RAD:
• Normal in newborns; right ventricular hypertrophy; acute cor pulmonale
(pulmonary embolism); chronic cor pulmonale (COPD, pulmonary hypertension,
pulmonary valve stenosis); Left posterior fascicular block,…
Causes of LAD:
• Left bundle branch block; left ventricular hypertrophy; inferior infarction; Pre-
excitation,…
Causes of extreme axis deviation:
• Rare. Most likely due to misplaced limb electrodes.

Systematic approach to ECG interpretation
1. Rhythm
2. P-wave morphology and PR interval
3. QRS complex
4. ST segment
5. T-wave
6. QTc interval and U-wave
7. Compare with earlier ECG
8. The ECG in its clinical context

Rhythm
Assess ventricular (RR intervals) rate and rhythm:
• Is ventricular rhythm regular? What is the ventricular rate (beats/min)?
• Is atrial rhythm regular? What is the atrial rate (beats/min)?
• P-wave should precede every QRS complex and the P-wave should be positive
in lead II.
Common findings:
• Sinus rhythm: (1) heart rate 50-100 beats/min; (2) P-wave precedes every QRS
complex; (3) The P-wave is positive in lead II and (4) the PR interval is constant
• Causes of bradycardia: sinus bradycardia, second-degree AV block, third-
degree AV block, sinoatrial arrest/inhibition.
• Causes of tachycardia (tachyarrythmia) with narrow QRS complex (QRS
<0.12s): Sinus tachycardia, inappropriate sinus tachycardia, sinoatrial re-entry
tachycardia, atrial fibrillation, atrial flutter, atrial tachycardia, multifocal atrial
tachycaridia, AVNRT, AVRT (pre-excitation, WPW).

• Causes of tachycardia (tachyarrhythmia) with wide QRS complexes (QRS
duration ≥0.12s): Ventricular tachycardia is the most common cause and it
is potentially life-threatening.
P-wave morphology and PR interval:
• P-wave always positive in lead II (actually always positive in leads II, III and
aVF)
• P-wave duration should be <0.12s (all leads)
• P-wave amplitude should be ≤2.5mm (all leads)
• PR interval must be 0.12-0.22s (all leads)
Common finding:
• P-wave must be positive in lead II, otherwise → cannot be sinus rhythm.
• P-wave may be biphasic (diphasic) in V1 (the negative deflection should be
<1), may have a prominent second hump in the inferior limb leads
(particularly lead II).

• P mitrale: Increased P-wave duration, enhanced second hump in lead II and
enhanced negative deflection in V1.
• P pulmonale: increased P-wave amplitudes in lead II and V1.
• PR interval >0.22s: First-degree AV block.
• PR interval <0.12s: Pre-excitation (WPW syndrome).
• Second-degree AV-block Mobitz type I (Wenckeback block): repeated cycles
of gradually increasing PR interval until an atrial impulse (P-wave) is blocked
in the atrioventricular node and the QRS complex does not appear.
• Second-degree AV-block Mobitz type II: intermittently blocked atrial
impulses (no QRS seen after P) but with constant PR interval.
• Third-degree AV-block: All atrial impulses (P-waves) are blocked by the
atrioventricular node. An escape rhythm arises (cardiac arrest ensues
otherwise), narrow or wide QRS complexes, depending on its origin. No
relation between P-waves and the escape rhthm’s QRS complexes. Atrial
rhythm >escape rhythm.

QRS complex
• QRS duration must be <0.12s (normally 0.07-0.1s)
• There must be at least one limb lead with R-wave amplitude >5mm and at least
one chest (precordial) lead with R-wave amplitude >10mm; otherwise there is
low voltage.
• High voltage exists if the amplitudes are too high, i.e if the following condition
is satisfied: S-wave V1 or V2 + R-wave V5 >35mm.
• Look for pathological Q-waves. Pathological Q-waves ≥0.03s and/or amplitude
≥25% of R-wave in same lead, in at least 2 anatomically contiguous leads.
• Is the R-wave progression in the chest leads (V1-V6) normal?
• Is the electrical axis normal? Electrical axis is assessed in limb leads and should
be between -30o to 90o.

QRS complex
Common findings:
• Wide QRS complex (QRS duration ≥0.12s): Left bundle branch block. Right
bundle branch block; Hyperkalemia; Class I antiarrhythmic drugs; Tricyclic
antidepressants; Ventricular rhythms and ventricular extrasystoles (premature
complexes); Artificial pacemaker; Pre-excitation (WPW syndrome).
• Short QRS duration: no clinical relevance.
• High voltage: Hypertrophy (any lead). Left bundle branch block (leads V5, V6, I,
aVL); Right bundle branch block (V1-V3)… normal variant in younger, well-
trained and slender individuals.
• Low voltage: Normal variant; Misplaced leads. Cardiomyopathy. Chronic
obstructive pulmonary disease; Perimyocarditis; Hypothyreosis, pneumothorax,
Extensive myocardial infarction; obesity Pericardial effusion; Pleural effusion…

QRS complex
Common findings:
• Pathological Q-wave: Myocardial infarction. Left-sided pneumothorax.
Dextrocardia; Perimyocarditis; Cardiomyopathy; Bundle branch blocks; Anterior
fascicular block; Pre-excitation, ventricular hypertrophy, acute cor pulmonale.
• Fragmented QRS complexes: myocardial scarring (mostly due to infarction).
• Abnormal R-wave progression: Myocardial infarction, RVH (reversed R-wave
progression), LVH (Amplified R-wave progression), Cardiomyopathy, Chronic
cor pulmonale, LBBB, Pre-excitation.
• Dominant R-wave in V1/V2: Misplaced chest electrodes, Normal variant, Situs
inversus. Posterolateral infarction/ischemia. RVH, Hypertrophic
cardiomyopathy, RBBB, Pre-excitation.

QRS complex
Common findings:
• Right axis deviation: Normal in newborns, RVH, Acute cor pulmonale
(pulmonary embolism); Chronic cor pulmonale. Lateral ventricular infarction.
Pre-excitation, Switched arm electrodes (negatieve P and QRS-T in lead I), Situs
inversus, Left posterior fascicular block (rS complex in I and aVL + qR complex
in III and aVF)
• Left axis deviation: LBBB, LVH, Inferior infarction. Pre-excitation, LAFB (qR-
complex in AVL and QRS duration is 0.12s)

ST segment:
• The ST-segment should be flat and isoelectric. It may be slightly upsloping at
the transition with the T-wave.
• ST segment deviation (elevation and depression) is measured in the J point.
Common findings:
• Benign ST segment elevation: very common, particularly in the precordial leads
(V2-V6), concave ST-segment elevation (male/female pattern).
• ST-segement depression: uncommon among healthy individuals.
• Causes of ST-segment elevation: Ischemia, STEMI, Prinzmetal’s angina (coronary
vasospasm), Male/female pattern, Early repolarization, Perimyocarditis, LBBB,
LVH, Brugda syndrome, Takotsubo cardiomyopathy, Hyperkalemia, Post
cardioversion, Pulmonary embolism, Pre-excitation,…

T-wave:
Common findings:
• Normal variants: An isolated (single) T-wave inversion is accepted in V1 and
lead III.
• T-wave inversion without simultaneous ST-segment deviation: not a sign of
ongoing ischemia, but may be post-ischemia (wellen’s syndrome – Deep T-wave
inversions in V1-V6 in patient with recent episodes of chest pain)…
• T-wave inversion with simultaneous ST-segment deviation: Acute (ongoing)
myocardial ischaemia.
• High T-waves: Normal variant, Early repolarization, hyperkalemia, LVH, LBBB,
Hyperacute T-wave may be seen in very early phase of STEMI.

Common findings:
• Causes of ST-segment depression: Ischemia, NSTEMI, Physiological ST-segment
depression, Hyperventilation, Hypokalemia, High sympathetic tone, Digoxin,
LBBB, RBBB, Pre-excitation, LVH, RVH, Heart failure, Tachycardia.
• Causes of waves/deflections in the J point (J wave syndrome): Brugada
syndrome, Early repolarization.
T-wave:
• Should be concordant with the QRS complex. Should be positive in most leads.
• T-wave progression should be normal in chest leads.
• In limb leads the amplitude is highest in lead II, and chest leads-highest in V2-
V3.

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