Download Basic principles in ECG

BASIC PRINCIPLES IN ECG
INTRODUCTORY PRINCIPLES
Basic Cardiac Electrophysiology
Lam Kam Bick
What is an electrocardiogram
Registered Nurse
Department of Medicine, TWH
Acute Myocardial Infarction
7.3.2014
BLOOD FLOW THROUGH THE HEART
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Deoxygenated blood from the systemic circulation
on
enters the RA and then travels through the TV to
the RV.
Pulmonary
arteries
Lung
Deoxygenated blood is pumped from the RV
through the PV, into the L and R pulmonary
arteries, and then into the lungs.
While in the lungs, the blood becomes oxygenated
ed
and then travels through the pulmonary veins too
the LA.
THE ELECTRICAL CONDUCTION SYSTEM OF THE HEART
Pulmonary
Veins
LA
Aorta
RA
RV
LA
RA
RV
LV
LV
Oxygenated blood form the LA travels through the
e
e
MV to the LV, then through the AV, and into the
n.
aorta, where it travels to the systemic circulation.
y
The cardiac stimulus is generated in the SA node, which is located in the RA. The stimulus
then spreads through the RA and LA.
This blood flow is affected by the electrical
conduction systems of the heart, which provides
he
the “electrical energy” so the heart can pump the
blood
y
Next, it spreads through the AV node and the bundle of His (which comprise the AV
junction.
y
The stimulus then passes into the LV and RV by the way of the left and right bundle
branches, which are continuations of the bundle of His.
y
Finally, the cardiac stimulus spreads to the ventricular muscle through the Purkinje fibers.
SINOATRIAL (SA) NODE
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The intrinsic pacing rate of the
SA node is 60 to 100
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The heart prefers the natural
pacemaker of the heart, the SA
node, to assume pacemaker
control
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Under normal conditions the SA
node fires and transmits an
impulse that causes atrial
contraction. This atrial
contraction causes the blood to
leave the atria and to enter
ventricle.
THE BUNDLE OF HIS
AV NODE
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It allows the atria to complete
their contractions and to fill the
ventricles with blood.
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The AV node can assume
pacemaker control of the heart if
the SA fails to fire. The intrinsic
pacing rate of the AV node is
40 – 60
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When the AV node assumes
pacemaker control of the heart,
the rhythm is called a junctional
rhythm.
RIGHT BUNDLE
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Is a connective tissue sheet, that
connects the upper and low
chambers of the heart
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It transmit the electrical
impulse from tshse bundle of
His down to the RV
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It receives the electrical impulse
from the AV node and speedily
transmits the electrical impulse
downward to the right and left
bundle branches
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Abnormal condition of the
right bundle:RBBB
A delay in the transmission of
the electrical impulse down
the right bundle is referred to
as a right bundle branch block.
LEFT BUNDLE
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It transmit the electrical
impulse from tshse bundle of
His down to the LV
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It separates into two: the
anterior and the posterior
fascicle. These fascicles
transmit the electrical impulse
to different areas of the LV.
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It needs more electrical
circuits is because the muscle
on the left side of the heart is
bigger.
PURKINJE FIBERS
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The Purkinje fibers transmit the
electrical impulse from the ends of
the bundle branches to the ventricles,
from the endocardium to the
epicardium, to initiate
depolarization
The Purkinje fibers can assume
pacemaker control of the heart if the
SA node and the AV node fail to fire.
The intrinsic rate of the Purkinje
fibre is 20 -40
When the Purkinje fibers in the
ventricle assume pacemaker control
of the heart, the rhythm is called an
idioventricular rhythm
ANTERIOR FASCICLE AND
POSTERIOR FASCICLE
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The anterior fascicle transmits the electrical impulse to the
anterior superior endocardial surface of the LV
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The posterior fascicle transmits the electrical impulse toe the
posterior inferior region of the left ventricle’s endocardial
surface
PROPERTIES OF CARDIAC CELL
Two basic types of cardiac cell
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Myocardial working cells
1. Contain contractile filaments
2. Contract when electrically stimulated
3. Form he muscular layers
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Pacemaker cells (conduction)
1. Cannot contract
2. Spontaneously generate and conduct electrical
impulses
Cardiac Conductivity and
Automaticity
Type of
cardiac cells
Primary
characteristics
Pacemaker cells
Automaticity
Conductivity
SA node,
AV junction,
Purkinje
network fibers
Contractility
Myocardium
Myocardial
cells
Location
CARDIAC ACTION POTENTIAL
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Generation and
conduction of
electrical impulses
Cell membranes contain membrane channels. These channels
are pores through which specific icons or other small, water
soluble molecules can cross the cell membranes from outside to
inside.
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Contraction and
relaxation
A series of events causes the electrical charge inside the cell to
change from its resting state (-ve) to its depolarized state (+ve)
and back to its resting state (-ve)
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The cardiac action is an illustration of these events in a single
cardiac cell during polarization, depolarization, and
repolarization. The stimulus that alters the gradient across the
cell membrane may be electrical, mechanical, or chemical
Function
Polarization
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Cardiac cells are in a
resting state
No electrical flow or
contractions occurring.
Positive charge is
outside cell membrane
DEPOLARIZATION
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Polarization (resting)
Movement of ions (Na+ K+ Ca+) cross cell membrane causing
inside of cell to become more positive; an electrical event which is
expected to result in a contraction, a mechanical event
Depolarization
(stimulated)
Polarization (inside negative)
K+
Negative charge is
inside cell membrane
Potassium (K+)
Na+ Sodium (Na +)
Depolarization
(inside positive)
K+
Potassium (K+)
Na+
Sodium (Na +)
Anions
Anions
WHAT IS AN ELECTROCARDIOGRAM
(ECG OR EKG)
REPOLARIZATION
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Movement of ions cell membrane in which in inside of the
cell is restored to its negative charge
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An electrocardiogram (ECG) is
graph that records cardiac
electrical activity by means of
electrodes placed on the surface
of the body.
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These metal electrodes are placed
on the arms, legs and chest wall
(precordium).
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It records only the currents
produced by the working heart
muscle.
Repolarization (resting)
K+
Na+
Potassium (K+)
Sodium (Na +)
Repolarization (inside negative)
Anions
FUNCTIONS OF ECG
Monitoring
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Heart rate and rhythm
Evaluate the effects of disease or injury on the heart function
Evaluate pacemaker function
Evaluate the response to medications (e.g. antidysrhythmics)
Obtain a baseline recoding before, during and after a medical
procedure.
LIMITATIONS OF THE ECG
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b). Not all heart attacks can be detected by ECG. Angina, a
common heart disorder, cannot usually be detected by a routine
ECG.
Provide information
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Orientation of the heart in the chest
Conduction disturbance
Electrical effects of medications and electrolytes
Ischemic damage of cardiac muscle
Non cardiac disease diagnostic e.g. pulmonary embolism,
hypothermia
Provide information on physical condition of the heart e.g. LVH, MS
A normal ECG does not rule out serious heart disease. For example:
a). An irregular heart rhythm that 'comes and goes', and the
recording can be normal between episodes.
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It does not provide information about the mechanical (contractile)
condition of the myocardium.
LEADS (1)
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Lead is a record of electrical activity between two electrodes. Each lead
records of average current flow at a specific time in a portion of the heart
Two different planes for viewing of the heart’s electrical activity :
1. Frontal (coronal)
2. Horizontal (transverse)
12 lead ECG provides view of heart in both the frontal and horizontal
planes and views the surfaces of the heart from 12 different angles
Three types of leads: Standard limb leads
Augmented leads
Precordial lead (chest)
LEADS (3)
LEADS (2)
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FRONTAL PLANES LEADS VIEW
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A.The wave of depolarization moves toward the positive electrode, the waveform
recorded on the ECG graph paper will be upright
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B. the wave of depolarization moves toward the negative electrode, the waveform
produced will be inverted
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C. A biphasic (partly positive, partly negative) waveform is recorded when the wave
of depolarization moves perpendicularly to the pos1tive electrode
Each lead has positive and negative electrode (pole). The
position of the positive electrode on the body determines
the portion of the heart “seen” by each lead.
View the heart from the front of the body.
Directions in the frontal plane are superior, inferior, right and left.
Include of six limb leads
1. Standard Limb Leads (Three bipolar limb leads):
- Lead I: R arm (-ve) to left arm (+ve)
- Lead II: R arm (-ve) to L leg (+ve)
- Lead III: L arm (-ve) to L leg (+ve)
2. Augmented Leads (Three Unipolar limb leads):
- aVR
- aVL
- aVF)
SUMMARY OF FRONTAL PLANES
LEADS
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Standard limb leads
Lead
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Positive electrode Negative electrode Heart surface viewed
Lead I
Left arm
Right arm
Lateral
Lead II
Left leg
Right arm
Inferior
Lead III
left keg
Left arm
Infeior
Augmented leads
Augment Lead
Positive electrode
Heart surface viewed
Lead aVR
Right arm
none
Lead aVL
Left arm
lateral
Lead aVF
Left leg
Inferior
HORIZONTAL PLANE LEADS
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STANDARD LIMB LEAD & AUGMENTED LEAD
View the heart as if the body were
sliced in half horizontally
Directions in the horizontal plane
are anterior, posterior, right and
left
There are six precordial unipolar
leads: V1 to V6 , whose axes span
from the positive electrodes on the
chest wall to the indifferent
reference point in Einthoven’
triangle
LEFT PERCORDIAL LEADS SUMMARY
Lead
Positive electrode position
Heart surface
viewed
Lead V1
R side of sternum, fourth intercostal space
Septum
Lead V2
L side of sternum, fourth intercostal space
Septum
Lead V3
Midway between V2 and V4
Anterior
Lead V4
L midclavicular line, fifth intercostal
space
Anterior
Lead V5
L anterior axillary line at same level as
V4
Lateral
Lead V6
L midaxillary line at same level as V4
Lateral
THE MEAN P VECTOR
VECTORS
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Leads have a negative and positive electrode that senses the magnitude
and direction of the electrical force caused by the spread of waves of
depolarization and repolarization throughout the myocardium.
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A vector is a (arrow) symbol representing this force
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Leads that face the tip or point of vector record a positive deflection on
ECG paper
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A mean vector identifies the average of depolarization in one portion of
the heart
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The average direction of a mean vector is called the main axis and is
only identified in the frontal plane
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An imaginary line joining the positive and negative electrodes of a lead
is called axis of the lead
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Electrical axis refers to determining the direction in which the main
vectgor of depolarization is pointed
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The mean P vector
THE MEAN QRS VECTOR
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Represents the average magnitude and direction of both
right and left ventricular depolarization
The mean QRS vector
Represents the average magnitude and direction of both
right and left atrial depolarization
AXIS (1)
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The mean QRS vector points down
inferior and to the left
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The axes of leads I, II, and III form an
equilateral triangle with the heart at the
centre (Einthoven’s triangle). If the
augmented limbs leads are added to this
configuration and the axes of the six
leads moved in a way in which they
bisect each other, the result is the
hexaxial reference system
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The hexaxial reference system represents
all of the frontal plane (limb) leads with
the heart in the centre and is the means
used to express the location of the frontal
plane axis.
ELECTRICAL AXIS DETERMINATION:
AXIS (2)
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Forms a 360 degree circle
surrounding the heart
The positive end of lead I is
designated at 0 degrees,
The six frontal plane leads divide the
circle into segments, each
representing 30 degree
Upper hemisphere are labeled as
negative degrees, and all degrees in
the lower hemisphere are labeled as
positive degrees.
ECG PAPER
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The chart will help quickly determine the direction of a patient’s electrical
axis. Observe the deflections of the QRS complexes in leads 1 and aVF.
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Lead 1 indicate whether impulses are moving to the right or left, and lead
aVF indicates whether they are moving up or down.
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Through the chart to determine whether the patient’s axis is normal, or
has a left, right, or extreme right deviation.
Axis
Normal
Left
Right
Indetermi
nate
Lead 1
QRS
Direction
Positive
Positive
Negative
Negative
AVF
QRS
Direction
Positive
Negative
Positive
Negative
SPEED OF THE ECG
0.20
sec
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Normal international speed
(25mm/second)
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Tachycardia
Speed 50mm/second is used to extend the ECG wave
complex twice as much
5 mm
0.04
sec
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3.0
seconds
Is graph paper made up of small and large boxes. The smallest boxes are 1mm wide and
1mm high
Dark lines show every 5th block
Counting horizontally measures time (intervals measured in seconds)
Counting vertically measures amplitude (height measured in millimeters)
Each small block measures 0.04 sec,
5 small blocks equal one big block=0.2 sec,
25 small blocks equals = 1 second = 5 big blocks,
1500 small locks = 1 minute,
300 big blocks = 1 minute
INTERNATIONAL CALIBRATION
ECG WAVEFORM AND INTERVAL
COMPONENTS
1 STD = Normal
1 mV electrical signal will produce a deflection measuring
exactly 10 mm tall.
| ½ STD = used if amplitude of QRS is high
| 2 STD = used if the amplitude of QRS is low
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1 Standard
½ Standard
2 Standard
THE P WAVE
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Mechanism – Represents atrial depolarization
Characteristics
Location:
precedes QRS complex
Amplitude:
not exceed 2 to 2.5mm in height
Duration:
0.06 to 0.11 second
Configuration: usually rounded and upright
Defection:
upright (positive) in leads I, II, aVF and V2 to V6; inverted
(negative)
in aVR; biphasic (positive and negative) lead III, aVL, and V1
P wave abnormalities
1. Peaked P waves : R atrail hypertrophy (e.g. COPD)
2. Broad notched P wave : L atrial hypertrophy (e.g. Mitral valve disease)
3. Inverted P waves : junctional dysrhythmia
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A series of waveform that
correspond to the heart’s
depolarization and
repolarization
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An upward defection is
positive and a downward
deflection is negative as a
result of the directional
flow of the heart’s
electrical impulse
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A straight (isoelectric) line
when there is no electrical
activity
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Components: P wave, PR
interval, PR segment, QRS
complex, J point, ST
segment, T wave, QT
interval and sometimes
present U wave
J point
THE PR SEGMENT
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Mechanism – His Purkinje system is activated (not seen on the surface
ECG)
Characteristics
Location:
end of the P wave to the beginning of QRS complex
Duration:
depends on the duration of the P wave and impulse
conduction through the AV junction
Deflection:
isoelectric
THE PR INTERVAL
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Mechanism
An interval is a waveform and a segment. The P wave plus PR segment
equals the PR interval. The PR interval reflects depolarization of the R
and L atria and the spread of the impulse through the AV node, bundle
of His, right and left bundle branches, and the Purkinje fibers.
Characteristics
Location:
from the beginning of the P wave
to the first QRS
Amplitude: not applicable
Duration: 0.12 to 0.2 sec
Clinical significance of PR interval abnormalities
Shortened: sinus tachycardia, preexcitation syndromes, AV junctional
rhythms, or HT
Prolonged: sinus bradycardia, 1st degree AV block, drug induced by
beta blocker, digitals toxicity, or hypothyroidism
PATHOLOGICAL Q WAVES
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Q waves are usually absent from most of the leads of a normal ECG.
However, small q waves are normal in leads that look at the heart from
the left: I, II, aVL, V5 and V6.
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They result from septal depolarization, which normally occurs from left to
right, the hence are referred to as ‘septal’ Q waves
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Q waves in other leads are likely to be abnormal or ‘pathological’
particularly if they are:
- > 2 small squares deep
- > 1/3 of the height of the following R wave in depth
- > 1 small square wide
Normal
THE QRS COMPLEX (1)
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Mechanism – represents ventricular depolarization
Characteristic
THE QRS COMPLEX (2)
|Deflection:
Location :
Flows the PR interval
Amplitude:
Differs in each of the 12 leads
Duration:
is 0.06 to 0.10 sec. The QRS complex is measured from the
beginning of the QRS complex to the end of the QRS
complex
Configuration: consists of the Q wave, R wave, S wave if the first deflection
in the QRS complex is negative, it’s called a Q wave. The R
wave is the first positive deflection. The S wave appears as
the negative deflection after the R wave. Because the
ventricles depolarize quickly, the QRS complex appears
thinner than other ECG components.
QRS complex may appear in various forms
Abnormal
- will be either positive or negative depending upon the
lead.
- Lead I, II, III and aVF, V4 to V6 : positive
- aVR, V1 and V2: negative
- V3 and V4 may be biphasic
- In precordial leads not less than
6mm in V1 and V6,
8mm in V2 and V5,
10mm in V3 and V4
upper limit of normal is 25 to 30 mm.
THE QRS COMPLEX (3)
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Importance for ECG strip interpretation
its importance in reflecting ventricular myocardial cell activity. The QRS
complex represents ventricular depolarization. Ventricular contraction
results in blood being pumped from the heart to the rest of the body(cardiac
output).The QRS complex duration represents intraventricular conduction
time.
THE JOINT POINT
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The J point marks the end of the QRS complex
and the beginning of the ST segment.
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It is used as a marker for measuring QRS
complex segments and ST segment shifts
Clinical significance of QRS abnormalities
1. Excessive width: intraventricular conduction problem e.g bundle branch
block
2. Excessive height: ventricular hypertrophy or enlargement
3. Low voltage:
diffuse coronary disease, cardiac failure, pericardial
effusion emphysema, obesity, generalized edema.
THE ST SEGMENT (1)
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J
Point
THE ST SEGMENT (2)
Mechanism
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represents the end of ventricular depolarizartion and the beginning of
ventricular repolarization
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Characteristics
Location:
extends from the end of the S wave to the beginning of
ventricular repolarization
Deflection: usually isoelectric, may vary slightly but not usually more
than 1mm
Importance for ECG interpretation
is representative of part of the repolarization process
Clinical significance of ST displacement
1. ST segment elevation 1mm or > the base line, may indicate MI or
muscle injury
2. ST segment depression > 1mm, may indicate myocardial
ischemia
3. ST segment changes may also be seen with pericarditis,
myocarditis, LVH, pulmonary embolism, electrolyte disturbances,
medication alter depolarization and repolarization, e.g.
antiarrhythmics such as aminodarone
THE T WAVE (1)
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Mechanism: represents repolarization of the ventricles.
Characteristics
Location : follows the QRS complex and the ST segment
Amplitude: 5mm or less in standard leads I, II, and III;
10mm or less in precordial leads V1 to V6,
less than 0.5mm in height in leads I and II is abnormal
Duration: not measured
Configuration : rounded and smooth
Deflection: normally it is upright in leads I, II, V2 to V6;
inverted in lead aVR,
variable in leads III, aVL, aVF, V1 to V2
THE QT INTERVAL (1)
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Mechanism : represents the time required for ventricular depolarization
and repolarization to take place
Characrteristics
Location: from the beginning of the QRS complex to the end of the T wave,
includes the QRS complex , ST segment and T wave
Amplitude: not applicable
Duration: “rule of thumb” is less than half the preceding RR interval,
usually lasts, The most commonly used method for correcting
the QT interval for rate is the formula : QTc= QT/ square root
of RR, normal limit:0.36 – 0.44 sec
THE T WAVE (2)
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Importance for ECG strip interpretation
The peak of the T wave represents the “vulnerable” period
of repolarization – the time during which the ventricles are
especially vulnerable to extra stimuli
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Clinical significance of T wave abnormalities
1. Inverted T waves may indicate myocardial ischemia
2. Peaked (tented) T waves usually indicate hyperkalemia
3. Heavily notched T waves may indicate pericarditis in
adults, but usually normal in children
THE QT INTERVAL (2)
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Importance for ECG strip importance
represents the ventricular refractory time
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Clinical significance of QT abnormalities
1. Prolonged QT: reflects dispersion of repolarization within
the myocardium, predisposing to a malignant polymorhous
ventricular tachycardia – torsades de pointes. May be cause
by the medication e.g. quinidine, amiodarone
2. Shortened QT interval may be a result of hypercalcemia or
digitals.
3. A shortened QT interval may occur with sinus tachycardia
THE U WAVE
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Mechanism:
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Characteristics
represents repolarization of the HisPurkinje fibers. May or may not be seen on the ECG
DETERMINING RATE (1)
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Location: follows the T wave
Amplitude: not measured
Duration: not measured
Configuration: upright, rounded
Method 1: Times ten (the 6-second method)
Obtain a six second tracing (30 five mm boxes) and count the number of R
waves that appear within that 6 second period and multiply by 10 to obtain
the HR/min
Example : If there are 7 five mm boxes in a 6 second tracing then the heart
rate would be : 7 x 10 = 70 bpm
Deflection: upright
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Clinical significance of U wave abnormalities
may be caused by hypokalemia
DETERMINING RATE (2)
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Method 2 : The 300 Method
Count the number of large boxes between 2 R waves and divide this
number into 300 to obtain the HR/min
Example: If there were 2.5 large 5mm boxes between two successive R
waves, then the HR would be: 300/2.5 large boxes=120bpm
Method 3: The 1500 Method
Count the number of small boxes between two R waves and divide this
number into 1500 to obtain the HR/min
Example: If there were 12.5 small boxes between two successive R
waves, then the heart rate would be:1500/12.5 small boxes = 120bpm
DETERMINING RATE (3)
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Method 4:The cardiac ruler method
Place the beginning point of a cardiac ruler over and R wave.
Look at the number on which the next R wave falls and that
becomes the heart rate for that patient, use the following
numbers to indicate what the HR is between two successive R
waves: 300, 150, 100, 75, 60, 43, 37, 33, 30
NORMAL CORONARY ARTERIES
Coronary arteries are vessels that provide oxygen-rich blood and other
nutrients to the heart muscle. The two main coronary blood vessels, which
branch from the body''s main artery (aorta), are the right coronary artery
(RCA) and the left coronary artery (LCA).
ACUTE MYOCARDIAL
INFARCTION
PATHOPHYSIOLOGY(1)
Pathophysiology(2)
Atherosclerosis
Normal artery
Mild
Atherosclerosis
Severe
Atherosclerosis
Normal Coronary Artery
㬋ⷠⅈ䉨≽傰
Atherosclerosis
埨䭉䱍㧋慵䠔⊾
Atherosclerosis
With blood clot
≽傰䱍㧋䠔⊾
Ờ㚱埨ↅ⟲
Atherosclerosis, sometimes called “hardening of the arteries,” occurs
when cholesterol, calcium, and other substances build up in the inner
lining of the arteries, forming a material called plaque. Over time, plaque
buildup narrows the artery and blocks blood flow through it.
Spasm
埨䭉㉥㎸(䖁㓋)
ACUTE CORONARY SYNDROMES
Is a term used to refer to patients presenting with ischemia
chest pain.
| Consist of three major syndromes that are related:
- ST-elevation MI
- Non-ST-elevation MI
- Unstable angina
|
ECG PATTERN OF STEMI AND NSTEMI
Illustration of normal ECG as well
as STEMI and NSTEMI
In STEMI patients the ST segment is
elevated; in NSTEMI patients the ST
segment is not elevated, and instead
other patterns are seen. The most
common characteristics of NSTEMI
ECGs are ST depression and T
inversion.
ISCHEMIA, INJURY, AND INFARCTION
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The sudden occlusion of a
coronary artery because of a
a,
thrombus may result in ischemia,
injury, and necrosis of the area off
the myocardium supplied by thee
affected artery.
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The area supplied by the
obstructed artery goes through a
characteristic sequence of events
ts
identified as “zone” of ischemia,
a,
injury, and infarction. Each zonee
is associated with characteristic
ECG changes.
ISCHEMIA
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Myocardial ischemia results when the heart’s demand for oxygen
exceeds its supply from the coronary circulation. Myocardial ischemia
can occur because of a decrease in myocardial oxygen demand. This
imbalance may be caused by decreased coronary artery blood flow
because of blood vessel obstruction, decreased filling time, or decrease
filling pressure in the coronary arteries.
Symmetrically
inverted T waves
ST segment
depression
INJURY
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INFARCTION
Myocardial injury occurs when the period of ischemia is
prolonged more than just a few minutes. This period is a
time of severe threat to the myocardium because injured
myocardial cells can live ore die. If blood flow is
restored to the affected area, no tissue death occurs.
However, without rapid intervention, the injured area will
become necrotic.
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Is the actual death of injured myocardial cells, MI occurs when there
is a sudden decrease or total cessation of blood flow through a
coronary artery to an area of the myocardium. This most commonly
occurs because of the blockage of a coronary artery by a thrombus.
Normal
ST elevation >1mm
NORMAL ECG
MYOCARDIAL INFARCTION “EVOLVES”
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Three phases of whole process, each phase has its own clear ECG
characteristics
Phase
Before Heart
attack
1st Stage
Acute injury
2nd Stage
Necrosis
ECG
Change
s
Times
Before
infarction
Minutes hours
Hours – 1 day
3rd Stage
Resolution
3rd Stage
Resolution
Persistent Q’s
and may be
flipped T’s
Q’s and T’s
back to upward
1 week
months
2 small squares deep
> 1/3 of the height of the
following R wave in depth
ANTERIOR MI
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ECG changes V1 –V6, I, AVL
ANTEROSPETAL MI
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ECG changes V1 – V4
The QS complexes, resolving ST segment elevation and T wave
inversions in V1-2 are evidence for a fully evolved anteroseptal MI.
The inverted T waves in V3-5, I, aVL are also probably related to
the MI.
Inferior MI
Leads with ECG changes:
ST elevation in II, III, aVF,
ST depression in V1, V2, V3, V4 and I, aVL
INFERIOR MI WITH LBBB
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ECG Changes II III aVF, Poor R-wave progress in
V1-V3, QRS > 0.12 sec
INFERIOR MI WITH RV INFARCTION
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INFERIOR MI WITH RV INJURY
ECG Changes II, III, aVF, V3R – V6R
A 12 lead ECG obtained using the right-sided precordial leads. Inferior
infarction with evidence of right ventricular injury (V5R, V6R)
EXTENSIVE ANTEROLATERAL MI
ECG changes: ST elevation in V1 –V6, I, AVL ST depression in II III AVF
EXTENSIVE ANTEROLATERAL MI
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ECG Changes V1 – V6, I, & aVL
Significant pathologic Q-waves (V2-V6, I, aVL) plus marked ST
segment elevation are evidence for this large
anterior/anterolateral MI.
SITE OF INFARCTION
INFERIOR MI WITH LBBB
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The ECG has been used to localize the site of ischemia and infarction
Area of infarct
ST elevation in II III aVF, Poor R-wave progress in V1-V3, QRS >
0.12 sec
ANALYZING THE 12 LEAD ECG
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Use a systematic method
Findings suggestive of an acute MI are considered significant if viewed in two
or more leads looking at the same area of the heart.
If these findings are viewed in leads that look directly at the affected area,
they called indicative changes.
If findings are observed in leads opposite the affected area, they are called
reciprocal changes.
Rate: atrial and ventricular
Rhythm: atrial, junctional and ventriuclar
Intervals: PR interval, QRS duration, QT interval
Waveforms: P waves, Q waves, R waves (R-wave progression), T waves, U
waves
ST segment: elevation, depression
Axis
Chamber enlargement/Hypertrophy
Myocardial ischemia, injury, infarction
Effects of medications and electrolyte imbalances
Intraventricular conduction delays : RBBB, LBBB
Leads with ECG changes
Usually associated
with Cornary artery
Anterior
ST elevation in V3, V4
ST depression in II, III, aVF
LAD
Inferior
ST elevation in II, III, aVF,
ST depression in V1, V2, V3, or I, aVL
RCA
Lateral
ST elevation in I, aVL, V5, V6
ST depression in II, III, aVF
LCx
Septal
ST elevation in V1, V2
LAD
Posterior
Tall and wide R waves and ST depression
in V1,V2
RCA and or LCx
Anteroseptal
ST elevation in V1- V4
LAD
Anterolateral
ST elevation in V3 – V6, I, aVL
LAD and LCx
Extensive
anterior
ST elevation in I, aVL, V1 – V6
Proximal LAD
RV
ST elevation in V4R, V5R, V6R
Proximal RCA
NORMAL ECG
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Sinus rhythm
P wave rate 60-100 bpm ( rate <60 is sinus bradycardia , >100 is
sinus tachycardia)
P waves height,2.5mm in lead II, width<0.11 sec in lead II
P-R interval 0.12 to 0.20 sec
QRS complex <0.11 sec duration, In precordial leads not less than
6mm in V1 and V6, 8mm in V2 and V5, 10mm in V3 and V4,
upper limit of normal is 25 to 30 mm.
QT interval – 0.36 to 0.43 sec
ST segment – no elevation or depression
T wave - 5mm or less in limbs leads I, II, and III; 10mm or less in
precordial leads V1 to V6
Axis : - 0 to + 90 degrees in the frontal plane
REFERENCES
1.
Ary L. Goldberger, (2006), Clinical Electrocardiography, Seventh
Seventh Edition, Mosby, U.S.A.
2.
Barbara A., (2002), ECG made easy –Chapter 2: Basic Electrophysiology,
2nd Edition, Mosby, U.S.A.
3.
Diane S., (1992) EKG workbook How to interpret EKGs correctly, 1st
Edition, Springhouse, England.
4.
Mary B.C, 1998, Pocket guide series Electrocardiography- chapter 1 & 2:
The 12 Electrocardiogram Leads And Normal Electrical Activation of the
Heart, 4th Edition, Mosby, U.S.A.
5.
http://www.ecglibrary.com/ecgs/norm.gif
6.
http://www.geocities.com/Athens/4656/ecg3.html?200527
7.
http://Jan.ucc.nau.edu/-daa/lecture/EKGl.html