Basic

ECG
Lecture
MAX GERONIMO T. BUTARDO, MD,
FPCP, FPCC
Internal Medicine - Adult Cardiology
GABRIELA SILANG GENERAL HOSPITAL

Outline:
To discuss:
Clinical uses of ECG
Electrophysiology/Anatomy
Normal ECG tracing
Common Arrhythmias
Ischemia/Infarction
Chamber Enlargement

Trekking a foreign
land!?

ELECTROCARDIOGRAM
(ECG)
one of the most frequently performed
tests in clinical medicine.
a graphic recording of the electrical
potentials produced by the cardiac
tissue.
recorded by applying electrodes to
various locations on the body surface
and connecting them to a recording
apparatus.

ELECTROCARDIOGRAM
(ECG)
Clinical Values:
Arrhythmia
Atrial and ventricular hypertrophy
Myocardial ischemia and infarction
Pericarditis
Systemic diseases that affect the heart
Determination of the effect of cardiac drugs
Disturbances in electrolyte balance
Evaluation of function of cardiac pacemakers

The Limitations of the ECG

the ECG reveals the heart rate and rhythm only during the
time that the ECG is taken. (If intermittent cardiac rhythm
abnormalities are present, the ECG is likely to miss them.)
Ambulatory monitoring is needed to record transient
arrhythmias.
The ECG can often be normal or nearly normal in patients
with undiagnosed coronary artery disease or other forms of
heart disease (false negative results).
Many abnormalities that appear on the ECG turn out
to have no medical significance after a thorough
evaluation is done (false positive results).

CONDUCTION SYSTEM
OF THE HEART

ELECTROPHYSIOLOG
Y
4 Electrophysiologic Events Involved
in the Genesis of the ECG:
Impulse

formation (SA node)

Transmission

of the impulse (conduction

fibers)
Depolarization

Repolarization

CONDUCTION SYSTEM
OF THE HEART
SA Node
Atrial Muscles
AV Node
Bundle of His
Bundle Branches
Purkinje Fibers
Ventricular Muscles

SA NODE: primary pacemaker; 60-100 beats/min

AV NODE: provides conduction delay;
protects the ventricle from excessive stimulation
HIS PURKINJE SYSTEM: right and left bundles;
provides orderly depolarization
of the ventricles

The ECG MACHINE

The ECG MACHINE

ECG PAPER

RECORDING and
MONITORING
Bipolar Leads
Two electrodes placed at 2 different sites
Register the difference in potential between
these 2 leads

Unipolar leads
Measure the absolute electrical potential at
one site
Requires a reference site
Reference site formed by the limb leads

LIMB
LEADS

FRONTAL PLANE
LEADS
The lead axes of the six
frontal plane leads
have been rearranged
so that their centers
overlay one another.
These axes divide the
plane into 12
segments, each
subtending 30
degrees.
Positive ends of each
axis are labeled with
the name of the lead.

PRECORDIAL
LEADS

UNIPOLAR
PRECORDIAL
LEADS

Electrodes and Lead

Connections
LEAD TYPE
Bipolar
Limb
Leads

Lead I
Lead II
Lead III

Aug
Unipolar
Limb
Leads

aVR
aVL
aVF

Aug
Unipolar
Chest
Leads

V1
V2
V3
V4
V5
V6
V7
V8
V9

POSITIVE INPUT

NEGATIVE INPUT

Left Arm
Left Leg
Left Leg

Right Arm
Right Arm
Left Arm

Right Arm
Left Arm
Left Leg

Left Arm + Left Leg

Right Arm + Left Leg
Left Arm + Left Leg

Right Sternal Margin, 4th ICS

Left Sternal Margin, 4th ICS
Midway between V2 and V4
Left Midclavicular line, 5th ICS
Left Anterior Axillary line, 5th ICS
Left Mid Axillary line, 5th ICS
Left Posterior Axillary line, 5th ICS
Left Posterior Scapular line, 5th ICS
Left Lateral Border of Spine, 5th ICS

Wilson Central Terminal

Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal
Wilson Central Terminal

LEAD
PLACEMENT

Limb Leads
RA
LA
LL
RL

Red
Yellow
Green
Black

Right arm
Left arm
Left leg
Right leg

Chest Leads
V1

Red

4th ICS RPSB

V2

Yellow

4th ICS LPSB

V3

Green

Midway between V2 and V4

V4

Brown

5th ICS LMCL

V5

Black

LAAL Lateral & horizontal to V4

V6

Violet

LMAL Lateral & horizontal to V4

TERMINOLOGY
Waveform
Movement away from the baseline in
either a positive or negative direction

Segment
A line between wave forms

Interval
A waveform and a segment

Complex
Consists of several waveforms

COMPONENTS OF
ECG
P wave: atrial systole
PR interval: physiologic delay in
the AV node
QRS complex: ventricular systole
T wave: ventricular repolarization

The
waves
and
interva
ls
of a
normal
ECG

NORMAL SINUS
RHYTHM

NORMAL VALUES
(ADULTS)
WAVE INTERVAL
P - wave
PR - interval
QRS complex
QT - interval

DURATION (msec)
< 120
120 - 200
< 120
440 - 550

T
Q

T
Q

T
Q

T
Q

NORMAL SINUS
RHYTHM
Look at the P-waves:
Rate: 60-100/min
Cycle length: not vary by 10%
PR-interval: 0.12-0.20 sec
Lead II

NORMAL SINUS
RHYTHM
Look at the P-waves:
Same contour in same lead
Upright in I, II, aVF & left
precordial leads
Followed by QRS complexes
Lead II

What Is The Rate?

Ventricular Rate:
1500
300

Small squares (R-R Interval)

Big squares (R-R Interval)

What Is The Rate?

Sinus rhythm

Atrial Fibrillation
QRS complexes in 6-sec strip X 10

Regular Sinus Rhythm (RSR)

Heart Rate of 75 beats
PR interval is 0.16 s QRS interval (duration) is 0.08 s
QT interval is 0.36 s mean QRS axis is about +70

ANALYZING AXIS

Normal: 0 (+90)
Left axis: 0 (-90)
Right axis: (+90) (+180)
Extreme axis: (-90) (-180)

AVL

AVR

AVF

ANALYZING AXIS

What Is The Axis?

10
AVL

Lead I

AVR

10

AVF

AVF

ARRHYTHMIA

Sinus
Sinus Bradycardia
Bradycardia
h Regularly occurring PQRST
h Rate < 60 / min

Rate = 48/min

Rate = 48/min

Sinus
Sinus Bradycardia
Bradycardia

Sinus
Sinus Tachycardia
Tachycardia
h Regularly occurring PQRST
h Rate > 100 / min

Rate = 111/min

Rate = 111/min

Rate = 111/min

Sinus
Sinus Tachycardia
Tachycardia

Sinus
Sinus Arrhythmia
Arrhythmia
h Identical but irregularly occurring
PQRST
h Longest PP or RR > the shortest
by 0.16 sec or more
Rate = 71/min
Rate = 94/min

Rate = 79/min

Rate = 94/min

Sinus
Sinus Arrhythmia
Arrhythmia

Premature
Premature Atrial
Atrial
Complex
Complex (PAC)
(PAC)
h Prematurely occurring PQRTS complex
h P wave different in configuration from the
sinus beat
h PR interval often long
h QRS narrow

Paroxysmal
Paroxysmal
Supraventricular
Supraventricular
Tachycardia
Tachycardia (PSVT)
(PSVT)

Due to REENTRY mechanism, most often

involving the AV node alone or the AV
node and an extra-AV nodal bypass tract
QRS complexes are narrow
Atrial depolarization is retrograde
inverted P-waves in leads II, III, aVF
P-waves may occur just before, during,
or after the QRS complexes

Paroxysmal
Paroxysmal
Supraventricular
Supraventricular
Tachycardia
Tachycardia (PSVT)
(PSVT)

AVN Conduction
with unilateral block

(N) AVN Conduction

pathway
pathway

pathway
pathway

AV
AVNODE
NODE

Atrial
Atrial Flutter
Flutter
h Atrial rate = 220-300/min
( P as flutter waves )
h Variable degree of AV block
( irregular RR interval )

Atrial
Atrial Flutter
Flutter

Atrial
Atrial Fibrillation
Fibrillation

h No discernible P waves
h Irregular RR interval

Atrial
Atrial Fibrillation
Fibrillation

Junctional
Junctional Rhythm
Rhythm
h Impulses from the AV node
h P wave inverted or buried w/in
QRS or follows the QRS
h Rate slow
h QRS narrow

Junctional
Junctional Rhythm
Rhythm

Junctional
Junctional
Premature
Premature Complex
Complex
h Prematurely occurring PQRST
h Inverted P wave that may precede,
be incorporated within, or may follow
the QRS complex
h QRS narrow

Normal Cardiac Depolarizatio

Atrio-Ventricular
Blocks (AVB)
R
T

P
Q
S

First Degree
Atrio-Ventricular
Block
R
T

P
Q

Do you have a normal P wave? Yes

Do you have a normal PR segment? No
Do you have a normal PR interval?
Prolonged (> 0.20 sec)
Do you have a normal QRS-T?
Yes

Criteria for First Degree

A-V Block
P waves present
QRS complexes present
P waves morphology and axis usual for the
subject
QRS complexes morphology and axis usual
for the subject
One P wave to each QRS complex
P-R interval constant
P-R interval must be prolonged
( i.e. > 0.21 sec )

FIRST
FIRST DEGREE
DEGREE
A-V
A-V BLOCK
BLOCK
h PR interval > 0.20 sec

0.28
0.28sec
sec

0.28
0.28sec
sec

0.28
0.28sec
sec

FIRST
FIRST DEGREE
DEGREE A-V
A-V
BLOCK
BLOCK

Second Degree
Atrio-Ventricular
Blocks
Do you have a normal P wave? Yes
Do you have a normal PR segment?
No
No
Do you have a normal PR interval?
Will there be intermittent P waves not
followed by QRS complex? Yes (dropped beats)

Second Degree
Atrio-Ventricular
Block

Type I - Mobitz type I or

Wenckebach
Type II - Mobitz type II

Degree
Atrio-Ventricular Block
(Wenckebach)
P waves present
QRS complexes present
P wave morphology and axis usual for the subject
QRS complexes morphology and axis usual for the
subject
Progressive prolongation of the P-R interval
with each succeeding beat until one P wave
occurs without a QRS (i.e. dropped beat)

Degree
Atrio-Ventricular Block
(Wenckebach)
Longest P-R interval is the one immediately before the
dropped beat.
Shortest P-R interval is the one associated with the
first conducted beat after the dropped beat.
P-R interval before the blocked beat increase and do
so by progressively decreasing amounts so that the
consecutive R-R intervals before the blocked beat
actually progressively shorten.

SECOND
SECOND DEGREE
DEGREE AV
AV
BLOCK
BLOCK
MOBITZ
MOBITZ II
h Progressive lengthening
of PR interval w/ intermittent
drop beats .

0.20
0.20sec
sec

0.28
0.28sec
sec

0.20
0.20sec
sec

Criteria for Type II Second

Degree Atrio-Ventricular
Block (Mobitz II)
P waves present
QRS complexes present
P waves morphology and axis usual for the
subject
QRS morphology and axis usual for the subject
P-R interval of conducted beats normal or
prolonged

Criteria for Type II Second

Degree Atrio-Ventricular
Block (Mobitz II)
Within period of observation, one P wave is
not followed by a QRS complex.
No change in P-R interval before the transient
failure of atrio-ventricular conduction.
n P waves to (n-1) QRS complexes for each
example of transient type II block. (n will be 3 or
more*)

Criteria for Type II Second

Degree Atrio-Ventricular
Block (Mobitz II)

Failure of AV conduction may occur more than

once within the period, but it is not seen in
relation to two or more consecutive P waves.
P-R interval constant for all conducted beats
QRS complexes after the block have the same
morphology as those preceding it

SECOND
SECOND DEGREE
DEGREE
AV
AV BLOCK
BLOCK
MOBITZ
MOBITZ II
II
h Fixed PR interval
w/ intermittent
drop beats .

0.18
0.18sec
sec

0.18
0.18sec
sec

BLOCK AT THE
h Bundle of His
h Bilateral bundle
branches

h Trifascicle

0.18
0.18sec
sec

SECOND
SECOND DEGREE
DEGREE A-V
A-V
BLOCK
BLOCK
MOBITZ
MOBITZ II
II

2
2 :1
:1 A-V
A-V
BLOCK
BLOCK

Grade
Atrio-Ventricular
Block

Some P waves followed by QRS complexes and

some are not
Atrio-ventricular conduction ratio is
3:1 or higher
P-R interval following a QRS is constant but may
be normal or prolonged

HIGH
HIGH GRADE
GRADE
A-V
A-V BLOCK
BLOCK

Criteria for Third Degree

(Complete) AtrioVentricular Block
No recognizable, consistent or meaningful
relationship between atrial and ventricular activity
QRS complexes often abnormal in shape,
duration and axis (occasionally normal)
QRS morphology constant
QRS rate constant ( 15-60 beats/min )
Any form of atrial activity seen (most commonly
sinus initiated)

THIRD
THIRD DEGREE
DEGREE
A-V
BLOCK
BLOCK
h CompleteA-V
atrioventricular
block
h Impulses originate at both SA node and at
the subsidiary pacemaker below the block
Do you have regularly occurring P waves and QRS complexes?
Are the P waves related to the QRST complexes?
No
Is the atrial rate < = > ventricular rate? greater
Ventricular rate = 83 BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

Ventricular rate = 83 BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

Atrial
Atrialrate
rate==100
100BPM
BPM

Yes

THIRD
THIRD DEGREE
DEGREE A-V
A-V BLOCK
BLOCK
WITH
WITH SUPRAVENTRICULAR
SUPRAVENTRICULAR
ESCAPE
ESCAPE RHYTHM
RHYTHM

THIRD
THIRD DEGREE
DEGREE A-V
A-V BLOCK
BLOCK
WITH
WITH VENTRICULAR
VENTRICULAR ESCAPE
ESCAPE
RHYTHM
RHYTHM

oo
A-V
Dissociation
w/o
3
A-V Dissociation w/o 3 AV
AV
Block
Block
h Impulses originate at both SA
node and
at a subsidiary pacemaker below that is
firing at the same rate (acchrocage) or
even faster than that of the SA node
Do you have regularly occurring P waves and QRS complexes?
Are the P waves related to the QRST complexes?
Is the atrial rate < = > ventricular rate?

Yes

Most of the time, NO

Sometimes yes
Less than or equal

Intraventricular
Conduction Delay
h Supraventricular rhythm with
associated BBB

h Wide QRS complexes

Branch Block
(RBBB)
Activation of right ventricle is delayed
Increase in QRS duration 120 msec
Large secondary R wave in leads V1/V2
giving rsR pattern
Slurred S wave in left ventricular leads
particularly lead I

Branch Block
(RBBB)
May be idiopathic, often associated with
congenital heart disease
Has a benign prognosis when present as
an isolated finding

Branch Block
(RBBB)

Left Bundle Branch

Block (LBBB)
Normal activation of ventricular septum
from L to R is lost
Small initial Q waves in left ventricular lead
are lost (I, aVL, V5, V6)
Initial activation in LV leads with positive
R wave
LV activation is delayed, producing large
secondary R wave in LV leads
QRS is prolonged 120 msec

Left Bundle Branch

Block (LBBB)

Usually associated with important

underlying heart disease
Prognosis is that of underlying disease

Left Bundle Branch

Block (LBBB)

Premature Ventricular Complex

(PVC)
h Prematurely occurring complex.
h Wide, bizarre looking QRS complex.
h Usually no preceding P wave.
h T wave opposite in deflection to the QRS
complex.
h Complete compensatory pause following
every premature beat.

Premature Ventricular Complex

(PVC)

Premature Ventricular
Complex
in Bigeminy
h Alternating normal sinus beat and
a PVC

Premature Ventricular
Complex
in Bigeminy

Premature Ventricular
Complex
in Trigeminy
h PVCs regularly occurring every
third beat

Premature Ventricular Comple

in Couplets
h Two premature ventricular
contractions occurring consecutively

Multifocal Premature
Ventricular Complexes
h PVCs coming from different foci in
the ventricle
h PVCs assuming different polarities
in a single lead
h PVCs of different morphology and
coupling interval

Multifocal Premature
Ventricular Complexes

Premature Ventricular
Complex
R on T Phenomenon
h R or Q of the PVC occurring at the
T wave of the preceding sinus beat
h Most dangerous PVC

Ventricular
Tachycardia (VT)
h At least 3 consecutive PVCs
h Rapid, bizarre, wide QRS complexes
(> 0.10 sec)
h No P wave (ventricular impulse
origin)
Rate > 140 / min

Ventricular
Tachycardia

Torsades de
Pointes

Torsades de
Pointes
A form of Ventricular Tachycardia
QRS appear to be constantly changing
twisted into a helix

Due to:

Drug toxicity
Idisyncratic reaction to antiarrhythmic agents
Hypokalemia,
Hypomagnesemia

Ventricular
Fibrillation (VF)

Ventricular
Fibrillation (VF)

Agonal Rhythm
h Extreme sinus bradycardia with irregular,
idioventricular rhythm and occasional atrial activity

Ventricular
Asystole
Represents total absence of ventricular
electrical activity
May occur as a primary event in cardiac
arrest, or may follow VF or pulseless
electrical activity

Ventricular
Asystole
Represents total absence of ventricular
electrical activity
May occur as a primary event in cardiac
arrest, or may follow VF or pulseless
electrical activity

Ventricular
Asystole

Wolf Parkinson White

(WPW) Syndrome
h Supraventricular rhythm with wide
QRS complex because of pre-excitation
h Short or no PR segment followed by a
delta wave (slurred upstroke of QRS)

Wolf Parkinson
White Syndrome

Pacemaker
Rhythm
h No P wave (ventricular impulse origin)
h Wide QRS complex (>0.10 sec)
h Pacemaker spike precede the wide
QRS complexes

Ischemia and
Infarction

Electrocardiogram
An economical and accessible tool in the
diagnosis, localization and assessing
progression of acute ischemic state

Sensitivity & Specificity

of
ECG on Ischemia & MI
INITIAL ECG
- diagnostic of acute MI in approximately
50%
- abnormal but not diagnostic in
approximately 40%
- normal in about 10%.
-

- ***Serial tracings increase the sensitivity to

near 95%

ST segment and T
wave in Ischemia
Symmetrical T wave inversion on leads
overlying involved areas
In exercise stress testing or resting
ECG
>1mm of horizontal or downsloping ST
segment depression 80msec from the J
point is considered and ischemic response

Changes in
Infarction
Development of
new Q waves on
areas overlying the
infarct which
>0.04. secs
duration
>25% of the
height of
associated R
wave

Myocardial
Infarction
ECG patterns in
Infarction
Ischemic zone
ST segment
depression

Injury zone
ST segment
elevation

Infarction zone
Large Q wave

Evolution of ST segment
Changes in Myocardial
Infarction

Normal

ST
elevation

Normal ST

Normal ST

T wave inversion

Q wave

Q wave

Q wave

Myocardial and ECG

Changes during
Infarction
Normal

Normal ECG

Normal Myocardium

Time Course of
Myocardial and ECG
Changes during Infarction
Onset and first several hours

Normal R wave
Peaked ST segment and T wave

Subendocardial injury and

myocardial ischemia, no
infarction yet

Changes during
Infarction
First day

R wave amplitude
diminishes

Ischemia and injury extend to

epicardial surface,
subendocardial muscle dying

Time Course of
Myocardial and ECG
Changes during Infarction
First and second days
R wave nearly gone
ST segment elevation decreased
T wave inverted

Transmural infarction nearly

complete, some injury may
persist at borders

Myocardial and ECG

Changes during
Infarction
After 2 or 3 days
No R wave, deep Q wave
ST segment back to
baseline
T wave inversion persists

Transmural Infarction

Myocardial and ECG

Changes during
Infarction
After several weeks or
months
Q wave persist, small R wave
may return, T wave inversion
lessens

Infarcted myocardium

Localization of Injury

I, AVL

AVL

High lateral

II, III, AVF

Inferior

AVR

AVF

Localization of Injury
V1,V2
Septal

V3,V4
Anterior

V5,V6
Apicolateral

V1-V3 or V4
Anteroseptal

V3 or V4-V6
Anterolateral

V1-V6
Extensive anterior

I,AVL,V5,V6
- Lateral

Anterior Wall MI
Occlusion of the Left Anterior Descending Artery (LAD)

ECG: AMI with prominent Q waves in V1-V4

Lateral Wall MI
Occlusion of the Left Circumflex Artery (LCx)

Inferior Wall MI
Occlusion of the Right Coronary Artery (RCA)

CHAMBER
ENLARGEMENT

Abnormality
(RAE/RAA)
Features:
Tall peaked P wave >2.5 mm and normal
width in lead II, III, or AVF
Lead V1 with large biphasic P wave with
tall initial component.

Abnormality
(RAE/RAA)
Clinical implications:
Usually seen in patients with chronic
obstructive pulmonary disease
Patients with ECG change have more
severe pulmonary dysfunction, as well as
significantly reduced survival

Enlargement/
Abnormality
(LAE/LAA)
Features:
Width of the P wave > 0.12 sec in lead II
Notched P wave
P terminal force is > 0.04 sec
Lead V1 shows large biphasic P wave
with wide terminal component.

Enlargement/
Abnormality
(LAE/LAA)
Clinical implications:
Associated with more severe left
ventricular dysfunction in patients with
ischemic heart disease
More severe valve damage with mitral or
aortic valve disease

Bi-atrial
Enlargement
Features:
Tall and broad P wave in lead II, III or AVF
Large biphasic P wave in V1 with wide
terminal component

Chamber
Abnormalities

Right atrial (RA) overload may cause tall, peaked P waves

Left atrial (LA) abnormality may cause broad, often notched P
waves in the limb leads and a biphasic P wave in lead V1 with a
prominent negative component representing delayed
depolarization of the LA

Right Ventricular
Hypertrophy (RVH)
Features:
R wave greater than S wave in V1
R wave gets progressively smaller from
V1-V6
Prominent S waves in V5 & V6

Right Ventricular
Hypertrophy
More clues:
RAD, +110 degrees or greater
R in V1 7 mm or greater
R/S ratio in V1 is 1 or greater
R in V1 + S in V6 10 mm or greater
P pulmonale (tall pointed P taller in
III than I)
S > R in V6
Incomplete RBBB

RA abnormality and
RV enlargement

Left Ventricular
Hypertrophy (LVH)
Features:
a. Precordial leads
RV5 or RV6 + SV1 or SV2 35 mm or greater
(Sokolow index) most widely used
RV5 or RV6 > 26 mm
b. Limb leads
R in AVL > 11mm
R in lead I > 14mm

Left Ventricular
Hypertrophy
Additional features:
LAD, -30 degrees (often) not sensitive
Wide QRS (0.10 sec or more)

Left Ventricular
Hypertrophy

Chamber
Abnormalities

Miscellaneous ECG
Findings

Miscellaneous ECG
Findings

Thank You!

END OF
LECTURE
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