Ecg fundamentals

ECG fundamentals
Dr. Emad Efat
Shebin El kom Chest hospital
July 2016

What is an ECG?
 The electrocardiogram (ECG) is a representation
of the electrical events of the cardiac cycle.
 Each event has a distinctive waveform
 the study of waveform can lead to greater insight
into a patient’s cardiac pathophysiology.

With ECGs we can identify
 Arrhythmias
 Myocardial ischemia and infarction
 Pericarditis
 Chamber hypertrophy
 Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
 Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)

Depolarization
• Contraction of any muscle is associated with
electrical changes called depolarization
• These changes can be detected by electrodes
attached to the surface of the body

Pacemakers of the Heart
• SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
• AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker with
an intrinsic rate of 20 - 45 bpm.

Height
• 10mm = 1mV
• Look for a reference pulse
which should be the
rectangular looking wave
somewhere near the left of
the paper. It should be
10mm (10 small squares)
tall
Electrical impulse that travels
towards the electrode produces
an upright (“positive”)
deflection
Calibration

Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

The “PQRST”
P wave - Atrial depolarization
T wave - Ventricular repolarization
QRS - Ventricular depolarization

The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)

The ECG Paper
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box
0.5 mV ( 5 mm )

The 12-leads include:
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
–6 Precordial leads
(V1- V6)
ECG Leads ( The 12-Leads ):

ECG Leads
Bipolar Leads: Two different points on the
body (I, II, III)
Unipolar Leads: One point on the body
and a virtual reference point with zero
electrical potential, located in the center of
the heart (aVR, aVL, aVF)

Arrangement of Leads on the ECG

Anatomic Groups
(Anterior Wall)

Anatomic Groups
(Lateral Wall)

Anatomic Groups
(Inferior Wall)

Determine regularity
 Look at the R-R distances (using a caliper
or markings on a pen or paper).
 Regular (are they equidistant apart)? And
presence of same number of P waves and
QRS complexes
 Occasionally irregular? Regularly
irregular? Irregularly irregular?
Interpretation? Regular
R R

Determining the Heart Rate
Rule of 300/1500
6 Second Rule

Rule of 300
Count the number of “big boxes” between two
QRS complexes, and divide this into 300. (smaller
boxes with 1500)
for regular rhythms.
300/R-R interval ( big boxes) or 1500/R-R
interval (smaller boxes )

What is the heart rate?
(300 / 6) = 50 bpm

6 Second Rule
Number of QRS in 6 seconds ( 30 large squares ) x 10
For irregular rhythms.
This method can be used also with regular rhythm.
the heart rate 9 x 10 = 90 bpm
3 sec 3 sec

The QRS Axis
The QRS axis represents
overall direction of the heart’s
electrical activity.
Normal QRS axis from -30° to
+90°.
-30° to -90° is referred to as a
left axis deviation (LAD)
+90° to +180° is referred to
as a right axis deviation
(RAD)

Normal QRS axis from -30° to +90°.
QRS up in I and up in aVF = Normal

QRS up in I and
up in aVF = Normal

Example
Negative in I, positive in aVF  RAD

Causes of left axis deviation include:
• Normal variation (physiologic, often with age)
• Mechanical shifts, such as expiration, high diaphragm
(pregnancy, ascites, abdominal tumor)
• ventricular hypertrophy
• Left bundle branch block
• left anterior fascicular block
• Congenital heart disease (e.g. atrial septal defect)
• Emphysema
• Hyperkalemia
• Ventricular ectopic rhythms
• Preexcitation syndromes
• Inferior myocardial infarction
• Pacemaker rhythm

Causes of right axis deviation include:
• Normal variation (vertical heart with an axis of 90º)
• Mechanical shifts, such as inspiration and emphysema
• Right ventricular hypertrophy
• Right bundle branch block
• Right ventricular load, for example Pulmonary Embolism
or Cor Pulmonale (as in COPD)
• Left posterior fascicular block
• Dextrocardia
• Ventricular ectopic rhythms
• Preexcitation syndromes
• Lateral wall myocardial infarction

P wave
• Always positive in lead I and II
• Always negative in lead aVR
• < 3 small squares in duration
• < 2.5 small squares in amplitude
• Commonly biphasic in lead V1
• Best seen in leads II

Right Atrial Enlargement
• Tall (> 2.5 mm), pointed P waves (P Pulmonale)
• Causes : pulmonary diseases (pulmonary embolism and
pulmonary hypertension) - Congenital e.g. PS,ASD

• Wide more than 0.12 sec in duration (3 small
squares) & Notched in ( II,I) or biphasic in ( V1)
P wave (P ‘mitrale’ )
• Causes: Valvular e.g.: MR,AR,AS – HTN - Dilated cardiomyopathy
Left Atrial Enlargement

• Inversion :
A-V junctional rhythms
-ve in lead II
+ve in lead aVR
• Absent : in some of A-V junctional rhythms.
• Replaced : by fibrillatory or flutter waves ( AF
and Atrial flutter respectively)
Other abnormalities of P wave

• the PR interval is the period, measured from the
beginning of the P wave (the onset of atrial
depolarization ) until the beginning of the QRS complex
(the onset of ventricular depolarization)
• it is normally between 0.12 – 0.20 sec in duration ( 3-5
small squares).
The PR interval

Short PR Interval
1. Low atrial or junctional
rhythms.
2. WPW (Wolff-Parkinson-
White) Syndrome:
Accessory pathway (Bundle
of Kent) allows early
activation of the ventricle
(delta wave, wide QRS
and short PR interval)

Long PR Interval
• First degree Heart Block

QRS Complexes
• Comment on: ( axis, voltage, interval and abnormal Q )
• A) Voltage:
• Normally : The amplitudes of all the QRS complexes in
any of the six limb leads is > 5 mm
• low voltage when: The amplitudes of all the QRS
complexes in the limb leads is < 5 mm

QRS Complexes
• Specific causes of low voltage include:
 Pericardial effusion
 Pleural effusion
 Obesity
 Emphysema
 Pneumothorax
 Constrictive pericarditidis
 Previous massive MI
 End-stage dilated cardiomyopathy
 Infiltrative myocardial diseases — i.e. restrictive cardiomyopathy due
to amyloidosis, sarcoidosis, haemochromatosis
 Scleroderma
 Myxoedema

QRS Complexes
• High Voltage ( Ventricular hypertrophy):
A. Left Ventricular Hypertrophy (LVH) (Exaggeration of
normal)
• S wave depth in V1 + tallest R wave height in V5-V6 > 35
mm or > 7 large squares ( Voltage criteria )
• (±) the left ventricular ‘strain’ pattern : ST segment
depression and T wave inversion in the left-sided leads
• Concomitantly : left atrial enlargement may be present
• N.B. LVH can be diagnosed if S in V1 > 5 large squares
or R in V5 or V6 > 5 large squares ( Voltage criteria )

QRS Complexes
• Causes of LVH:
 Hypertension (most common cause), Aortic stenosis, Aortic
regurgitation, Mitral regurgitation, Coarctation of the aorta,
Hypertrophic cardiomyopathy

QRS Complexes
• Right Ventricular Hypertrophy (RVH) (opposite
normal)
 Right axis deviation of +110° or more.
 Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
 Dominant S wave in V5 or V6 (> 7mm deep or R/S
ratio < 1).
 Right atrial enlargement (P pulmonale) may be present.
 Right ventricular strain pattern = ST depression / T
wave inversion in the right precordial (V1-4)

QRS Complexes
 Causes of Right Ventricular Hypertrophy (RVH) :
Pulmonary hypertension, Mitral stenosis, Pulmonary embolism,
Chronic lung disease (cor pulmonale), Congenital heart disease (e.g.
Tetralogy of Fallot, pulmonary stenosis), Arrhythmogenic right
ventricular cardiomyopathy

QRS Complexes
 B) Interval (duration):
The width of the QRS complex should be less than 3 small squares
(0.12 seconds )
Wide QRS Complex:
• Bundle branch block
• Hyperkalaemia
• Pre-excitation (i.e. Wolff-Parkinson-White syndrome)
• Hypothermia
• Poisoning with sodium-channel blocking agents (e.g. tricyclic
antidepressants)
• Ventricular pacing

QRS Complexes
Right Bundle Branch Block ( R.B.B.B )
 Criteria:
• Broad QRS ≥ 0.12 sec ( 3 small squares )
• rsR’ with prominent final R in V1-3 (‘M-shaped’ QRS complex)
• Wide final S wave in the lateral leads (I, aVL, V5-6)
• ST depression and T wave inversion in the right precordial leads
(V1-3)

QRS Complexes
Right Bundle Branch Block ( R.B.B.B )
 Causes of RBBB:
( Right ventricular hypertrophy / cor pulmonale, Pulmonary
embolus, Ischaemic heart disease, Rheumatic heart disease,
Myocarditis or cardiomyopathy, Degenerative disease of the
conduction system, Congenital heart disease (e.g. atrial
septal defect)
 R.B.B.B is also called RSR pattern
 Can occur in healthy people with normal QRS width
( partial RBBB )

QRS Complexes
Left Bundle Branch Block( L.B.B.B )
 Criteria:
• Broad QRS ≥ 0.12 sec ( 3 small squares )
• Dominant S wave in V1
• Prominent (often notched ) R wave (M shaped ) in lateral leads
(I, aVL, V5-V6)
• the ST segments and T waves always go in the opposite
direction to the main vector of the QRS complex

QRS Complexes
Left Bundle Branch Block( L.B.B.B )
 Causes :
( Aortic stenosis, Ischaemic heart disease, Hypertension, Dilated
cardiomyopathy, Anterior MI, Primary degenerative disease
(fibrosis) of the conducting system (Lenegre disease),
Hyperkalaemia, Digoxin toxicity )
 New onset LBBB with chest pain consider Myocardial
infarction
 Not possible to interpret the ST segment.

Q wave
• The Q wave represents the normal left-to-right
depolarisation of the interventricular septum
• Non-pathological Q waves: Small ‘septal’ Q waves are
typically seen in the left-sided leads (I, aVL, V5 and V6)
• A Q wave can be pathological if it is:
Deeper than 2 small squares (0.2mV) and/or Wider than 1 small
square (0.04s) and/or In a lead other than III or one of the leads
that look at the heart from the left (I, II, aVL, V5 and V6) where
small Qs (i.e. not meeting the criteria above) can be normal
• Pathological Q waves usually indicate current or prior
myocardial infarction.

Poor R Wave Progression
• R wave height ≤ 3 mm ( 3 small squares ) in V3.
• The R wave height normally becomes progressively
taller from leads V1 through V6.

Poor R Wave Progression
• Causes:
 Anterior MI
 Left ventricular hypertrophy
 Dilated cardiomyopathy
 Inaccurate lead placement (e.g. transposition of V1
and V3)
 WPW syndrome
 LBBB, Left anterior fascicular block
 Chronic lung disease, Left sided pneumothorax
 May be a normal variant

ST Segment
• The ST segment is the flat, isoelectric section of the ECG
between the end of the S wave (the J point) and the
beginning of the T wave.
• It represents the interval between ventricular
depolarization and repolarization.
• Elevation or depression of ST segment by 1 mm or
more
Variable Shapes Of ST Segment Elevations in AMI

ST Segment
• Abnormalities:
• ST Segment Elevation :
• Acute myocardial infarction
• Coronary vasospasm (Printzmetal’s angina)
• Pericarditis
• Ventricular aneurysm
• Benign early repolarization
• Left bundle branch block
• Left ventricular hypertrophy
• Brugada syndrome
• Ventricular paced rhythm
• Raised intracranial pressure

ST Segment
• Acute ST elevation myocardial infarction (STEMI):
There is usually reciprocal ST depression in the electrically
opposite leads.
Anterolateral STEMI
elevation
reciprocal ST depression

ST Segment
Inferior MI
elevation reciprocal ST depression

ST Segment
• Pericarditis:
• Widespread concave ST elevation and PR depression
throughout most of the limb leads (I, II, III, aVL, aVF) and
precordial leads (V2-6).
• Reciprocal ST depression and PR elevation in lead aVR (± V1).
• Sinus tachycardia due to pain and/or pericardial effusion.

ST Segment
Pericarditis
elevation reciprocal ST depression

ST Segment
Coronary Vasospasm (Prinzmetal’s angina):
• ST elevation that is very similar to acute STEMI occurring during
episodes of chest pain.
• the ECG changes are transient, reversible with vasodilators and
not usually associated with myocardial necrosis. It may be impossible
to differentiate these two conditions based on the ECG alone.

ST Segment
• Left Ventricular Aneursym:
• ST elevation seen > 2 weeks following an acute MI.
• Most commonly seen in the precordial leads.
• May exhibit concave or convex morphology.

ST Segment
• ST Depression:
• Acute Coronary Syndrome (ACS): Unstable angina (UA) & Non-
ST-elevation MI (NSTEMI) ( subendocardial ischaemia )
• Reciprocal change in STEMI
• +ve stress E.C.G test
• Strain pattern with LVH or RVH ( asymmetrical )
• 2ry ST-T changes with BBB & WPW pattern
• Drugs e.g. Digoxin effect
• Hypokalaemia
• Posterior MI
• Variant of normal

ST Segment
• Subendocardial ischaemia:
• ST depression is usually widespread — typically present in leads
I, II, V4-6 and a variable number of additional leads.
• ST depression localised to a particular territory (esp. inferior or
high lateral leads only) is more likely to represent reciprocal
change due to STEMI. The corresponding ST elevation may be
subtle and difficult to see, but should be sought.

ST Segment
• Digoxin Effect:
• Down-sloping ST depression with a characteristic “sagging”
appearance (see below).
• Flattened, inverted, or biphasic T waves.
• Shortened QT interval.

T wave
• It represents part of ventricular repolarisation.
• Generally follow the direction of the main deflection of QRS
• Upright in all leads except aVR and V1
• Amplitude < 5 mm in limb leads, < 10 mm in precordial leads
• T wave abnormalities:
• Prominent T wave inversion
• Tall +ve T wave
• Biphasic T waves

T wave
• Prominent T wave inversion ( or flat T wave ):
• Strain pattern with LVH or RVH
• 2ry ST-T changes with BBB & WPW pattern
• Hypertrophic cardiomyopathy
• subendocardial ischaemia
• Evolving phase of MI
• Pulmonary embolism
• Drugs e.g. Digoxin effect
• Normal finding in children
• Hypokalaemia
• Raised intracranial pressure

T wave
• Tall +ve T wave:
• The early stages of ST-elevation MI (STEMI)
• Hyperkalaemia
• Normal variant

T wave
• Biphasic T waves:
• There are two main causes of biphasic T waves:
Myocardial ischaemia
Hypokalaemia
• The two waves go in opposite directions:
Ischaemic T waves go up then down
Hypokalaemic T waves go down then up

QT interval
 Total duration of Depolarization and Repolarization
 Measured from the start of the QRS complex to the end of the T
wave.
 QT interval decreases when heart rate increases
 QT interval should be 0.36–0.44 (9–11 small squares)
 Should not be more than half of the interval between adjacent R
waves (RR interval).

QT interval
1. A prolonged QT:
( Hypokalaemia, Hypomagnesaemia, Hypocalcaemia, Hypothermia,
Myocardial ischemia, Post-cardiac arrest, Raised intracranial pressure,
Congenital long QT syndrome, DRUGS )
2. A short QT:
1. familial/genetic:
(short Q-T syndrome)
1. Digoxin toxicity
2. Hypercalcemia
3. Hyperthermia

U wave
• The U wave is a small deflection immediately following the
T wave, usually in the same direction as the T wave.
• It is best seen in leads V2 and V3.They are thought to be
due to repolarisation of the atrial septum
• Prominent U waves can be a sign of hypokalaemia,
hyperthyroidism

E.C.G sequence of MI
1. Acute phase:
 ST segment elevation in 2 or more consecutive leads with
reciprocal changes (Sometimes tall positive T wave )
 At least 1mm ST elevation in limb leads and 2mm in precordial
leads to be significant.
 Pathological Q appear in leads that show ST elevation (8-48 h )
2. Evolving phase:
ST segment returns to the baseline with development of deep T wave
inversion hours to days later in the same leads that show ST elevation
3. Chronic phase:
Regression of ST-T changes pathological Q wave without ST-T
changes that usually persists for months to years (old MI )

Again localization of leads in STEMI
1. Septal (V1-2)
2. Strict anterior (V3-4)
3. Anteroseptal ( V1 V4 )
4. Lateral (I , aVL, V5-6)
5. Anterolateral
( V3 V6 ,I,aVL )
6. Extensive anterior
(V1 V6, I,aVL )
7. Inferior (II, III, aVF)

Inferior Wall MI
This is an inferior MI. Note the ST elevation in
leads II, III and aVF.

Inferior Wall MI
Now how about the
inferior portion of the
heart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF

Anterolateral MI
This person’s MI involves both the anterior wall
(V2-V4) and the lateral wall (V5-V6, I, and aVL)

Lateral MI
So what leads do you think
the lateral portion of the
heart is best viewed?
Leads I, aVL, and V5- V6

Anterior MI
Remember the anterior portion of the heart is
best viewed using leads V1- V4.

E.C.G Signs of Pulmonary embolism
1. Sinus tachycardia: 8-73%.
2. RBBB (complete/incomplete): 6-67%.
3. Rightward axis shift : 3-66%.
4. P Pulmonale : 6-33%.
5. Inverted T-waves in right chest leads: 50%.
6. S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%).
7. Clockwise rotation:10-56%.
8. AF or A flutter: 0-35%.
9. No ECG changes: 20-24%.

E.C.G Signs of Pulmonary embolism
Heart rate of 100/min & S1Q3T3 & inverted or
flattened T waves in leads V1 through V3.

Hyperkalemia (according to K serum level )

Arrhythmias
1. Regular Tachyarrhythmias ( HR >100 beats/minute ):
 Sinus tachycardia ( S.T )
 Paroxysmal supraventricular tachycardia (PSVT)
 Ventricular tachycardia ( VT) Wide QRS
 Atrial flutter ( usually regular tachycardia but may be with normal
or slow regular HR, or irregular HR with variable heart block )
2. Regular Bradyarrhythmias (HR < 60 beats/minute ):
 Sinus bradycardia ( SB )
 Nodal rhythm
 Partial heart block
 Complete heart block

Arrhythmias
3. Irregular rhythm ( with tachycardia, bradycardia or
within normal HR ):
 Atrial fibrillation ( A.F ) may be irregular tachycardia,
irregular bradycardia or with controlled ( within normal ) rate.
 Premature beats ( may occur with sinus tachycardia, sinus
bradycardia or with normal rate.
 Partial irregular ( variable ) heart block ( bradycardia ).
 PSVT & Atrial flutter with variable heart block ( usually
tachycardia ).
 Ventricular Fibrillation
N.B. all arrhythmias are arrow QRS complex except with ventricular
origin (Ventricular premature beats , Ventricular tachycardia and
sometimes with complete heart block ) Wide QRS complex.

Arrhythmias
Regular Tachyarrhythmias :
1. Sinus tachycardia ( S.T ) ( like normal but rapid ):
Regular sinus rhythm.
Each normal P is followed by a normal QRS complex.
Rapid HR ( 100-180 beats/m )

Arrhythmias
2. Paroxysmal supraventricular tachycardia (PSVT) :
( Very rapid > 140/ min ), usually no P wave )
 Rapid HR ( 100-250 beats/m ), regular QRS complexes of
normal morphology
 P wave are either a) Abnormal (deformed or has different
shape) atrial tachycardia or b) Inverted ( retrograde ) or
usually absent ( buried in QRS ) junctional tachycardia

Arrhythmias
3. VT ( ventricular tachycardia ) : ( wide rapid regular )
 QRS complexes are wide ( usually > 0.14 sec ), bizarre
shaped with rapid HR ( 120-250 beats/m )
 P wave are of normal ( 60-100/m) rate and usually obscured
by QRS complexes but sometimes may be superimposed on
QRS complexes with A-V dissociation.

Arrhythmias
4. Atrial flutter : ( Saw-tooth appearance, usually regular
tachycardia, exclusion. DD from AF )
 P wave is replaced by flutter waves (“saw-tooth” pattern)
best seen in leads II, III, aVF . may be more easily
spotted by turning the ECG upside down!
 Atrial rate = 250-350/m with a ventricular rate that is often
fraction of the atrial rate ( 1/2, 1/4 , etc )
 Atrial rate = 1500/ F-F interval ( small squares ) or simply
( no of F waves before QRS +1) X HR ( ventricular rate )

Arrhythmias
Regular Bradyarrhythmias :
1. Sinus bradycardia ( like normal but slow ):
Regular sinus rhythm.
Each normal P is followed by a normal QRS complex.
Slow HR (< 60 beats/m)

Arrhythmias
2. Nodal ( junctional ) rhythm :
( Slow, no or retrograde P wave ).
QRS complexes are regular, narrow, slow ( usually 40-60 beats/m )
of normal morphology.
P wave is either : a) absent b) Inverted (retrograde)

Arrhythmias
3. Heart block :
a) First degree HB: constant prolongation of P-R interval >
0.20 sec (> 5 small squares )
b) Second degree HB 2 subtypes:
Mobitz type I HB ( Wenckebach ):
Progressive prolongation of the PR interval from beat to beat
until a dropped or non conducted beat then the sequence is
repeated.

Arrhythmias
Mobitz type II HB :
 Intermittent non-conducted P waves without progressive
prolongation of the PR interval (compare this to Mobitz I).
 The PR interval in the conducted beats remains constant.
 The block may be fixed ( 2:1, 3:1 ) or variable.

Arrhythmias
c) Third degree HB ( complete HB ): ( No relation
between QRS and P waves)
 QRS may be normal width or abnormally wide of slow
regular rate ( 30- 60 beats/m)
 P waves are of normal regular rate and may be
superimposed on QRS complex and T wave. Atrial rate is
almost always faster than ventricular rate. P-R interval is
constantly changing. There is complete A-V dissociation.

Arrhythmias
 1St & 2nd degree HB are considered incomplete or partial HB.

Arrhythmias
3. Irregular rhythm :
1) A.F.: ( irregular)
• Irregularly irregular rhythm. No P waves.
• Variable ventricular rate. QRS complexes usually rapid ( 100-
200 beats/m) but may be slow from drug toxicity e.g. digitalis
or disease of A-V junction or controlled by drugs e.g. digitalis.
• Fibrillatory waves may be present and can be either fine
(amplitude < 0.5mm) or coarse (amplitude >0.5mm).
• Fibrillatory waves may mimic P waves leading to misdiagnosis.

Arrhythmias
2. Premature beats = Extrasystole:
• Comes prematurely followed by compensatory pause.
• Premature peats may occur with sinus tachycardia, sinus
bradycardia or with normal heart rate.
Atrial premature beats ( APB )
( Like normal but comes early followed by slight compensatory pause )
A premature abnormal ( deformed or has different shape ) P
wave with different PR interval followed by normal QRS complex
followed by slight compensatory pause.

Arrhythmias
Ventricular premature beats ( VPB )
( wide, bizarre, comes early and followed by full compensatory pause)
Abnormal ( Wide > 0.12 sec, bizarre ) premature QRS complex
not preceded by P wave followed by full compensatory pause.
The T wave is of opposite direction to QRS . ( uniform VPBs :
the same shape in a single lead, multiform VPBs : different shapes
in the same lead ).

Arrhythmias
N.B.
When a VPB occurs regularly after each normal beat
Ventricular bigemini ( common with digitalis toxicity )

Arrhythmias
When the rhythm is two normal beats followed by a VPB
ventricular trigemini

Arrhythmias
When two VPBs in a row ventricular couplet

Arrhythmias
1. When a APB occurs regularly after each normal beat Atrial
bigemini
2. When the rhythm is two normal beats followed by a APB
Atrial trigemini
3. When two APBs in a row Atrial couplet
1
2
3

Arrhythmias
none• Rate?
• Regularity? irregularly irregular
none
wide, if recognizable
• P waves?
• PR interval? none
• QRS duration?
Ventricular Fibrillation

ECG RULES
• Professor Chamberlains 10 rules of a normal
ECG, a foundation to ECG interpretation used all over the
world to this date.

RULE 1
PR interval should be 120 to 200 milliseconds
or 3 to 5 little squares

RULE 2
The width of the QRS complex should not exceed
110 ms, less than 3 little squares

RULE 3
The QRS complex should be dominantly upright in
leads I and II

RULE 4
QRS and T waves tend to have the same
general direction in the limb leads

RULE 5
All waves are negative in lead aVR

RULE 6
The R wave must grow from V1 to at least V4
The S wave must grow from V1 to at least V3
and disappear in V6

RULE 7
The ST segment should start isoelectric
except in V1 and V2 where it may be elevated

RULE 8
The P waves should be upright in I, II, and V2 to V6

RULE 9
There should be no Q wave or only a small q less
than 0.04 seconds in width in I, II, V2 to V6

RULE 10
The T wave must be upright in I, II, V2 to V6

Ecg fundamentals

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