ECG
Dr. Bernhard Arianto Purba, M.Kes., AIFO
Textbooks
•
•
•
•
•
•
Guyton, A.C & Hall, J.E. 2006. Textbook of Medical
Physiology. The 11th edition. Philadelphia: ElsevierSaunders: 918-930, 961-977.
Brooks, G.A. & Fahey, T.D. 1985. Exercise Physiology.
Human Bioenergetics and Sts Aplications. New York : Mac
Millan Publishing Company: 122-143.
Foss, M.L. & Keteyian, S.J. 1998. Fox’s Physiological Basis
for Exercise and Sport. 4th ed. New York : W.B. Saunders
Company: 471-491.
Astrand, P.O. and Rodahl, K. 1986. Textbook of Work
Pysiology, Physiological Bases of Exercise. New York :
McGraw—Hill.
Braunwald, Pauci, et al.2008. Harrison's PRINCIPLES OF
INTERNAL MEDICINE. Seventeenth Edition. New York :
McGraw—Hill: Chapter 332, 333, 338.
Jardins, Terry Des. 2002. Cardiopulmonary Anatomy &
Physiology. The 4th edition. USA: Delmar, A Division of
Thomson Learning Inc.
ELECTROCARDIOGRAPHY
(ECG)
ECG
A Brief introduction to ECG
•
•
The electrocardiogram (ECG) is a time-varying signal
reflecting the ionic current flow which causes the cardiac
fibers to contract and subsequently relax. The surface ECG
is obtained by recording the potential difference between
two electrodes placed on the surface of the skin. A single
normal cycle of the ECG represents the successive atrial
depolarisation/repolarisation and ventricular
depolarisation/repolarisation which occurs with every heart
beat.
Simply put, the ECG (EKG) is a device that measures and
records the electrical activity of the heart from electrodes
placed on the skin in specific locations
What the ECG is used for?
•
•
•
•
•
•
•
Screening test for coronary artery disease,
cardiomyopathies, left ventricular hypertrophy
Preoperatively to rule out coronary artery disease
Can provide information in the precence of metabolic
alterations such has hyper/hypo calcemia/kalemia etc.
With known heart disease, monitor progression of the
disease
Discovery of heart disease; infarction, coronal
insufficiency as well as myocardial, valvular and cognitial
heart disease
Evaluation of ryhthm disorders
All in all, it is the basic cardiologic test and is widely
applied in patients with suspected or known heart disease
Each small box = 1 mm
= .04 Sec.
5 small boxes = 1 large
box = 0.2 Sec.
MEASURING ECG
 ECG
commonly measured via 12
specifically placed leads
Lead Configurations for ECG Measurement
n
Bipolar Leads
Augmented Leads
n
Chest (V) Leads
n
Bipolar Leads: lead I
+
_
+
vo
_
Bipolar Leads: lead II
+
_
+
vo
_
Bipolar Leads: lead III
+
_
+
vo
_
ECG Limb Leads
Augmented Leads: aVR
+
_
+
vo
_
Augmented Leads: aVL
+
_
+
vo
_
Augmented Leads: aVF
+
_
+
vo
_
ECG Augmented Limb Leads
Unipolar Chest Leads
v1
v2
v4
v3
v5 v6
v1: fourth intercostal space, at right
sternal margin.
v2: fourth intercostal space, at left
sternal margin.
v3: midway between v3 and v4.
v4: fifth intercostal space, at mid
clavicular line.
v5: same level as v4, on anterior
axillary line.
v6: same level as v4, on mid
axillary line.
Unipolar Chest Leads (cont.)
+
_
+
_
ECG Precordial Leads
Current Lead Placement Conventions
(22 Electrodes)
H
M
V9
V8
V7
V3R
V6R
V5RV4R
I
E
6R
I
5R
3R
E
Current clinical conventions may use 22 different leads
ECG Lead Color Codes
C (brown)
RA (white)
RL (green)
LA (black)
LL (red)
Surface Cardiac Potentials
taken at t = to suggests an equivalent
dipole located within the heart
Eindhoven’s Triangle
-very crude solution to inverse problem using bipolar
limb leads:
_
lead I
+
RA
_
LA
_
lead II
lead III
+
+
LL
NORMAL HEARTBEAT AND ATRIAL
ARRHYTHMIA
Normal rhythm
Atrial arrhythmia
AV septum
Ventricular
depolarization
Ventricular
depolarization
(cont’d)
Ventricular
depolarization
(cont’d)
Ventricular
repolarization
- +
- +
+
-+
+
-
- + - + - + - +- + - + - + - + +
-+
+
+
+
+
+
Lead I
Lead II
Lead III
Limb
Leads
Lead I
(bipolar)
Lead II
Lead III
aVR
aVL
aVF
Unipolar
Lead
aVR
aVL
aVF
Normal
values
Intrinsicoid
deflection
< 0.05”
QT segment
Men < 0.39”
Wo < 0.40”
ST segment
Std: > 1mm
Pre : > 2mm
PR interval
0.12-0.20”
P wave
00.8-0.11”
U wave
QRS duration
0.06-0.10”
T wave
Precordial
leads
V6
V1
V2
V3
V4
V5
Horizontal
vs
Vertical
heart
Horizontal
vs
Vertical
heart
Clockwise
vs
Counter
clockwise
rotation
3
4
2
Viewed from below the heart looking towards the apex in vertical heart
P wave
V1
Atrial
Enlarge
ment
Left atrial
enlargement
P mitral
Wide and notch
Biphasic with
(-) terminal
component
V1
Atrial
Enlarge
ment
(cont’d)
Right atrial
enlargement
Tall and peaked
P wave
Tall and peaked
P wave
V1
Electrical
axis
qRS = +3
Lead I
qRS = +1
aVF
The
QRS
Bundle of His
LBB
Anterosuperior
division
Posteroinferior
division
RBB
The
QRS
QRS vectors:
• Initial depolarization
• Terminal depolarization
• S-T segmen
• Re-polarization
4
2
1
3
V1
V6
Myocardial
injury
Electrical forces are directed away from a injured area
A
Normal
B
Minimal
C
Subendocard
D
Transmural
E
Subepicard
Myocardial
injury
ST segment deviated towards the surface of injured tissue
A
Normal
B
Minimal
C
Subendocard
D
Transmural
E
Subepicard
Myocardial
infarction
Zones of myocardial infarction:
• Necrosis
• Injury
• Ischaemia
4
3
2
1
3
1
22
1
3
4
Myocardial
infarction
(cont’d)
ECG parameters of myocardial infarction:
• Necrosis
• Injury
• Ischaemia
4
2
1
3
V1
V6
Myocardial
infarction
(cont’d)
Phases of myocardial infarction:
• Hyperacute phase
- Slope elevation of the ST sement
- Tall widened T wave
- Increased ventr. activation time
• Fully evolved phase
- Pathological Q wave
- Coved, elevated ST segment
- Inverted symetrical T wave
• Old infarction
- Pathological Q wave
- ST segment and T wave return to normal
Myocardial
Localization of infarcted areas
infarction
(cont’d)
2
1
V1
V2
V3
3
II, III, aVF
I
aVL
V4
V5
V6
Right
ventri
cular
hyper
trophy
4
2
3
V1
1
V6
Left
ventri
cular
hyper
trophy
Diatolic overload
4
2
3
V1
1
V6
Left
ventri
cular
hyper
trophy
Systolic overload
4
2
3
V1
1
V6
RBBB
LBBB
1b
QT
interval
Prolonged QTc
• Hypocalcemia
•Acute rheumatic carditis
Shortened QTc
• Hypercalcemia
• Digitalis effect
• Hyperthermia
• Vagal stimulation
Normal QT does not exclude the diagnosis of
QTc=
QT
R-R
• Acute myocardial infarction
• Acute myocarditis of any causes
• Sympathetic stimulation
• Procain effect
Atrial
Septal
Activation
Disturbances of impulse formation
Sinus rhythms
• Sinus arrythmia
• Sinus tachycardia
• Sinus bradycardia
Ectopic atrial rythms
• Atrial extrasystole
• PAT
• Atrial fibrilation
• Atrial flutter
AV nodal rythms
• AVn extrasystole
• Paroxysmal AVn tachycardia
• Idionodal tachycardia
Ventricular rhytms
• V-extrasystole
• V-tachycardia
• V-flutter
• V-fibrilation
• Idioventricular tachycardia
Arrhyth
mias
Disturbances of impulse conduction
A-V block
S-A block
Reciprocal rythms
WPW syndrome
(Wolf-Parkinson-White)
LGL syndrome
(Lawn-Ganong-Levin)
Arrhyth
mias
2nd disorders of rythms
A-V dissociation
Atrial escape
Aberrant ventricular
conduction
AVn escape
Ventricular
escape
Arrhyth
mias
Diagnostic approach
To be
continued
next week
Insyaa Allah
Arrhyth
mias
4
2
3
V1
1
V6
Arrhyth
mias
4
2
3
V1
1
V6
Arrhyth
mias
4
2
3
V1
1
V6
Arrhyth
mias
4
2
3
V1
1
V6
Arrhyth
mias
4
2
3
V1
1
V6
Electrocardiogram
The Waves
P wave
atrial
depolarization
duration 0.11s
amplitude <
3mm
detects atrial
function
SA node
Electrocardiogram
The Waves
QRS Complex
ventricular depolarization
duration 0.10s
detects ventricular function
Q wave
first downward stroke
R wave
first upward stroke
S wave
any downward stroke
preceded by an upward
stroke
T wave
ventricular repolarization
Intervals and Segments
PR segment
end of P wave to start of QRS
measures time of
depolarization through AV
node
PR interval
start of P wave to start of QRS
measures time from start of
SA conduction to end of AV
node conduction
normal 0.12-0.20s
Intervals and Segments
ST segment
end of QRS complex to start of T
wave
measures start of ventricular
repolarization
elevated in MI’s
ST interval
end of QRS to end of T wave
represents complete time of
ventricular repolarization
QT interval
start of QRS to end of T wave
duration of ventricular systole
< 1/2 of the RR interval
Intervals and Segments
Intervals
the timing for depolarizations/repolarizations
can be interpreted from the EKG
P-R 0.12-0.2 sec
measures the time between the start of
atrial depolarization and the start of
ventricular depolarization
a long P-Q interval is a sign of AV node
dysfunction
QT interval, about 0.4 sec
start of QRS to end of T wave
QRS 0.08-0.1 sec
wider with ventricular dysfunction
ST segment (don’t worry about time)
elevated with acute MI
Electrocardiogram
The waves
more on the QRS
note that the Q or the R or the S
wave is not always present
name according to direction of
first deflection, second, etc
Q waves are often absent
lead V1
no Q
small R
large S
lead V2
no Q
large R
small S
Heart Rate
Heart Rate
defined as beats per minute
easy way to estimate rate
find an R wave on a thick
line
count off on the thick lines
300, 150, 100, 75, 60, 50
until you reach another R
wave
75
100
150
300
in our example the middle R
wave falls on the dark line
the next R falls just before
the 75, so estimate about 80
bpm
Heart Rate
Normal Sinus Rhythm
heart rate between 60-100
bpm
pacing by SA node.
QRS after every P wave
rhythm is regular
Sinus Tachycardia
heart rate > 100 bpm
p wave is there but hidden by
the T wave
regular QRS rhythm
Sinus Bradycardia
heart rate < 60 bpm
QRS after every P wave
regular rhythm
Wave Abnormalities
ST segment elevation
ischemia
Q wave
in some leads may
indicate ischemia
and necrosis
T wave inversion
late sign of necrosis
and fibrosis
Rhythm Abnormalities
Atrial Fibrillation
multifocal areas in atria firing
no p waves and irregular heart rate
Rhythm Abnormalities
Complete (3rd degree) AV Block
AV node cannot conduct impulse
p waves and QRS not connected
irregular heart rate
Rhythm Abnormalities
Premature Ventricular Contractions
ventricles pace early
early heart beat
large QRS
Rhythm Abnormalities
Ventricular Tachycardia
rapid ventricular pacing
rapid, regular rate
wide QRS
Rhythm Abnormalities
Ventricular Fibrillation
multifocal ventricular
beats
irregular
won’t last long
Axis
-90
QRS AXIS
+
—
180
0
another name for the vector of
depolarization
an axis is measured in degrees
the axis is measured by adding the
positive deflection and subtracting
the negative deflection
overall + is left axis direction
overall - is right axis direction
for lead one most of the QRS is
positive, therefore it has a leftward
axis
if an MI caused the QRS to be
mostly negative the lead would
have a rightward axis
+90
Axis
-90
—
180
0
+
+90
QRS AXIS
lead II
positive on left leg
negative on right arm
looking at the tracing we see
that the QRS is mostly
positive
what does this mean?
Axis
-90
—
180
0
+
+90
QRS AXIS
lead III
positive on left leg
negative on left arm
looking at the tracing we see
that the QRS is mostly
positive
what does this mean?
Axis
-90
QRS AXIS
lead I
leftward axis
lead II
downward axis
from this we can see that a normal
QRS axis lies somewhere in between
0 and +90 degrees
+
—
180
0
+
+90
remember that infarction will cause
the axis to shift rightward (>+90)
and that hypertrophy will shift the
axis upward (between 0 and -90)
The Anatomy of the Heart
The Blood Supply to the Heart
• Coronary circulation meets heavy demands
of myocardium for oxygen, nutrients
• Coronary arteries (right, left) branch from
aorta base
• Anastomoses (arterial interconnections)
ensure constant blood supply
• Drainage is to right atrium
• Great, middle cardiac veins drain capillaries
• Empty into coronary sinus
Blood Supply to the Heart
• Arteries include the right and left
coronary arteries, marginal arteries,
anterior and posterior interventricular
arteries, and the circumflex artery
• Veins include the great cardiac vein,
anterior and posterior cardiac veins, the
middle cardiac vein, and the small
cardiac vein
SA node activity and atrial
activation begin.
SA node
Time = 0
Stimulus spreads across the atrial
surfaces and reaches the AV node.
AV node
Elapsed time = 50 msec
There is a 100-msec delay at the
AV node. Atrial contraction begins. AV bundle
Bundle branches
Elapsed time = 150 msec
The impulse travels along the interventricular
septum within the AV bundle and the bundle
branches to the Purkinje fibers.
Elapsed time = 175 msec
The impulse is distributed by Purkinje fibers
and relayed throughout the ventricular
myocardium. Atrial contraction is completed,
and ventricular contraction begins.
Elapsed time = 225 msec
Purkinje fibers
Coronary Circulation
Coronary Circulation
Coronary Circulation
Figure 20.9a, b
Coronary Circulation
Figure 20.9c, d
HOLTER MONITOR
Technology
•
•
•
•
•
•
5 electrodes
2-3 leads
Derived 12 lead available
Digital or analog recording
Digital transmission to analyzer
Requires removal of Holter monitor to
scan recording
HOLTER MONITOR
Uses:
• Patients experiencing daily symptoms
• Precise quantification of arrhythmias
Positives:
• 24-48 hours full disclosure available
• Heart rate and AF burden graphs
• Arrhythmia counts (ex., 10 PVCs per
hour)