Basic ECG Lecture - New
Basic ECG Lecture - New
Basic ECG Lecture - New
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
CONDUCTION SYSTEM
OF THE HEART
ELECTROPHYSIOLOG
Y
4 Electrophysiologic Events Involved
in the Genesis of the ECG:
Impulse
Transmission
fibers)
Depolarization
Repolarization
CONDUCTION SYSTEM
OF THE HEART
SA Node
Atrial Muscles
AV Node
Bundle of His
Bundle Branches
Purkinje Fibers
Ventricular Muscles
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
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
LEAD
PLACEMENT
Limb Leads
RA
LA
LL
RL
Red
Yellow
Green
Black
Right arm
Left arm
Left leg
Right leg
Chest Leads
V1
Red
V2
Yellow
V3
Green
V4
Brown
V5
Black
V6
Violet
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
Atrial Fibrillation
QRS complexes in 6-sec strip X 10
ANALYZING AXIS
Normal: 0 (+90)
Left axis: 0 (-90)
Right axis: (+90) (+180)
Extreme axis: (-90) (-180)
AVL
AVR
AVF
ANALYZING 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)
Paroxysmal
Paroxysmal
Supraventricular
Supraventricular
Tachycardia
Tachycardia (PSVT)
(PSVT)
AVN Conduction
with unilateral block
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
Atrio-Ventricular
Blocks (AVB)
R
T
P
Q
S
First Degree
Atrio-Ventricular
Block
R
T
P
Q
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
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
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
HIGH
HIGH GRADE
GRADE
A-V
A-V BLOCK
BLOCK
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
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
Intraventricular
Conduction Delay
h Supraventricular rhythm with
associated BBB
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)
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
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 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
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
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
Changes during
Infarction
First day
R wave amplitude
diminishes
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
Infarcted myocardium
Localization of Injury
I, AVL
AVL
High lateral
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)
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 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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