ECG Rhythm Interpretation
ECG Basics
Objectives
To recognize the normal rhythm
of the heart - “Normal Sinus
Rhythm.”
Torecognize the 13 most
common rhythm disturbances.
To recognize an acute myocardial
infarction on a 12-lead ECG.
STUDY INCLUDES
ECG Basics
How to Analyze a Rhythm
Normal Sinus Rhythm
Heart Arrhythmias
Diagnosing a Myocardial
Infarction
Advanced 12-Lead
Interpretation
Normally cardiac impulse arise from the
sinuatrial node, a group of specialised cells in
the right atriam near the mouth of the
superior vena cava.
the impulse spreads from here through the
atria rapidly to reach the atrioventricular node.
Conduction through the atrioventricular node
is slower.
The impuls then travels to the ventricle by
specialised conduction tissue, the bundle of
his, which divides in to two branches – the left
and right bundle branches supplying the left
and right ventricles.
The left bundle branch in turn divides in to
superior and inferior facicles supplying
different area of left ventricle. The bundle
branch connect to perkinje fibers which lie on
endocardial surface of heart.
The impulse therefore reaches the endocardial
surface of heart nearly simultaneosly. The
exitation spread from endocardium towards
the epicardium surface travelling through
contractile muscle cells. The anatomy of
conducting tissue ensure that all part the
ventricle contract at about the same time.
Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
Impulse Conduction & the
ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
The “PQRST”
P wave - Atrial
depolarization
• QRS - Ventricular
depolarization
• T wave - Ventricular
repolarization
The “PQRST”
P wave - Atrial
depolarization
• QRS - Ventricular
depolarization
• T wave - Ventricular
repolarization
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 12-Leads
The 12-leads
–3include:
Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
–6 Precordial leads
(V1- V6)
The ECG Paper
Horizontally
◦ One small box - 0.04 s
◦ One large box - 0.20 s
Vertically
◦ One large box - 0.5 mV
The ECG Paper (cont)
3 sec 3 sec
Every 3 seconds (15 large boxes)
is marked by a line.
This helps when calculating the
heart rate.
NOTE: the following strips are not
marked but all are 6 seconds
long.
Rhythm Analysis
Step 1: Calculate rate.
Step 2: Determine regularity.
Step 3: Assess the P waves.
Step 4: Determine PR interval.
Step 5: Determine QRS duration.
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Step 1: Calculate Rate
3 sec 3 sec
Option 1
◦ Count the # of R waves in a 6
second rhythm strip, then multiply
by 10.
◦ Reminder: all rhythm strips in the
Modules are 6 seconds in length.
9 x 10 = 90 bpm
Interpretation? For more presentations
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Step 2: Determine regularity
R R
Look at the R-R distances (using a
caliper or markings on a pen or
paper).
Regular (are they equidistant apart)?
Occasionally irregular? Regularly
irregular? Irregularly irregular?
Regular
Interpretation?
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Step 3: Assess the P
waves
Are there P waves?
Do the P waves all look alike?
Do the P waves occur at a regular
rate?
Is there one P wave before each
Normal P waves with 1
QRS?
P wave for every QRS
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Interpretation? [Link]
Step 5: QRS duration
Normal: 0.04 - 0.12 seconds.
(1 - 3 boxes)
0.08 seconds
Interpretation?
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Rhythm Summary
Rate 90-95 bpm
Regularity regular
P waves normal
PR interval 0.12 s
QRS duration 0.08 s
Interpretation?
Normal Sinus Rhythm
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Electrode placement – chest electrodes
V1- fourth intercostal space rt. Sternal
border.
V2 – fourth intercostal space lt. sternal
border.
V3- fifth intercostal space midway between
v2 and v4
V4 – fifth intercostal space midclavicular line
V5 – fifth intercostal space anterior axillary
line
V6 – fifth intercostal space midaxillary line.
Lead 1 : left arm positive +
Right Arm negative –
Lead II : left leg positive +
Right Arm negative –
Lead III : left leg positive +
left arm negative –
12 lead ECG
ECG interpretation is easy if you
remember the directions from which the various
lead look at the heart.
leads I , II and VL look at the left lateral surface
of the heart, leads III and VF at the inferior surface
and leads VR look at the right atrium.
The 6 chest leads look at the heart in a
horizontal plane , from the front and left side.
V1 and V2- right ventricle
V3 and V4- septum between the ventricle and
anterior wall of left ventricle
V5 and V6- anterior and lateral wall of the left
ventricle
The 6 chest leads look at the heart in a
horizontal plane , from the front and left side.
V1 and V2- right ventricle
V3 and V4- septum between the ventricle and
anterior wall of left ventricle
V5 and V6- anterior and lateral wall of the left
ventricle
THE SHAPE OF QRS
COMPLEX
THE QRS COMPLEX IN LIMB LEADS
When depolarization wave spread towards a lead
the stylus move upwards, and when it spread
away from the lead the stylus move downwards.
if the QRS complex is predominantly upward or
positive (R wave is greater than the S wave)=
depolarization is moving towards that lead.
If predominantly downwards or negative (S wave
greater than R wave)the depolarization is moving
away from that lead.
When the depolarization wave is moving at right
angles to the lead , the R and S waves equal size.
THE CARDIAC AXIS
The depolarization
normally spread
through the
ventricale from 11 to
5 o’clock.
So the deflection in
lead VR are normally
downward and lead II
upward.
The direction of the
axis can be derived
most easily from the
QRS complex in lead
I, II and III
RIGHT AXIS DEVIATION
If the right ventricle
become hypertrophied,
the axis will swing
towards the right.
The deflection in lead I
become negative and
the deflection on lead
III will become more
positive. This is called
right axis deviation.
This is associated
mainly with pulmonary
condition bcoz of strain
LEFT AXIS DEVIATION
when the left
ventricle become
hypertrophied , the
axis may swing to
left, so that the QRS
complex become
negative in lead III.
The problem is
associated with
increase bulk of left
ventricle muscle.
The QRS complex in the V leads
In right ventricular lead
the deflection is first
upwards (R wave) as
the septum is
depolarized.
In left ventricle opposite
pattern is seen : small
downward deflection.
( septla Q wave)
In right ventricular lead
V1 and V2 there is
downward deflection (s
wave) as the main
muscle mass is
depolarized.
In left ventricular lead
there is upward deflectin
(R wave) as the
ventricular muscle is
depolarized.
When the whole of the
myocardium is
depolarized the ECG
returns to baseline.
The QRS complex shows
progressive pattern from
lead V1 to V6
( downward to upward)
CONDUCTION PROBLEM IN AV NODE AND
BUNDLE OF HIS
The time taken for the spread of depolarization from
the SA node to the ventricular muscle is shown by
the PR interval. And is not normally greater than 0.2
s. (one large square)
ECG event are usually time in milliseconds rather
than seconds, so the limit of the PR interval is 200
ms.
Interference with the conduction process causes the
ECG phenomenon called heart block.
FIRST DEGREE HEART BLOCK
Each wave of depolarization that
originate in the SA node is conducted to
ventricles, but there is delay somewhere
along conduction pathway, then the PR
interval is prolonged. This is called first
degree heart block.
One P wave per QRS complex
PR interval 360 ms
SECOND DEGREE HEART BLOCK
Some time excitation completely fail to pass
through the AV node or bundle of HIS. When this
occurs intermittently, it is called second degree
heart block.
Most beat are conducted with constant PR interval,
but occasionally there is an atrial contraction
without a subsequent ventricular contraction. (this
is called mobitz type 2 phenomenon)
There may be progressive lengthening of PR
interval and then failure of conduction of an atrial
beat, followed by shorter PR interval and than a
repetition of this cycle. (This is called wenckebach
phenomenon)
Third degree heart block
When atrial contraction is normal but no beats are
conducted to the ventricles. When this occurs the
ventricles are excited by slow ‘escape mechanism’
Sinus rhythm , but no p wave are conducted.
Right axis deviation
Broad QRS complex (duration 160 ms)
There may be only few QRS complex per lead
ECG CHANGES OF ISCHEMIA,
INJURY AND INFARCTION
ISCHEMIA
myocardial ischemia is a
temporary , reversible reduction of blood
supply to heart muscle and is the fast sign of
reduction of coronary blood flow. Ischemia is
represented by T wave changes on the ECG.
the normally upright , asymmetrical T wave
become deeply inverted and symmetrical.
the T wave inversion is usually seen during
episodes of acute ischemia but may not
show up for hours or day after the initial
event.
INJURY
myocardial injury result from an acute,
prolonged reduction in blood supply to the
myocardium. It is reversible if blood flow to
area of myocardium is restored before tissue
death occure.
injury is represented by ST segment changes
(elevation or depression ) on the ECG.
ST segment elevation occurs during
subepicardial injury (injury to outer ventricular
wall) . This appear within minute to hours after
the acute event.
the ST segment is displaced upward from
the baseline . The J point (at the beginning
of the ST segment) is also elevated.
ST segment depression occurs
during subendocardial injury (injury to the
inner ventricular wall)
If blood flow is not restore in time ,
irreversible muscle damage may occurs.
This is mark as non-Q wave .
INFARCTION
Myocardial infarction is irreversible
death of heart muscle due to prolonged
coronary artery occlusion.
The significant Q wave in lead represent
the area of damage.
Insignificant Q waves are small Q wave –
usually less than 25 % of the height of
the adjacent R wave
That may be found normally in lead 1 ,
aVL, V5,and V6. significant Q waves are
abnormal Q wave that are deeper than
25 % of R wave and greater than 0.04
ANTERIOR WALL MYOCARDIAL
INFARCTION
Damage to the anterior surface of the
left ventricle usually results from
occlusion of the left anterior descending
coronary artery.
ECG changes are observed in anterior
lead V1 –V4. the R wave voltage in chest
lead may decrease in association with
infarction.
LATERAL WALL MYOCARDIAL INFARCTION
If occlusion of the circumflex coronary
artery is present, damage to the lateral
surface of the left ventricle may be
reflected in lead 1 , aVL, V5, and V6.
Q wave and inverted T waves are
present in leads 1 and aVL.
INFERIOR WALL MYOCARDIAL
INFARCTION
Damage to the inferior surface of the heart
usually results from occlusion of the right
coronary artery.
Acute changes in inferior leads II, III, and aVF .
There is marked ST segment elevation in lead
II, III and aVF
The ST segment depression observed in lead
I , aVL, and V1 to V3.
POSTERIOR WALL MYOCARDIAL
INFARCTION
posterior all MI may be seen with inferior
wall MI and is usually caused by occlusion of
the right coronary artery. Bcoz there are no
convention lead placed directly over the
posterior wall of the heart.
ECG changes in leads V1 and V2 but these
leads are oriented opposite the area of
damage.
