Basics of

Electrocardiography

Dr.K.Subramanyam
23-3-2009
 Outline
Review of the conduction system
ECG leads and recording
ECG waveforms and intervals
Normal ECG and its variants
Interpretation and reporting of an ECG
 What is an ECG?
An ECG is the recording (gram)
of the electrical activity(electro)
generated by the cells of the heart(cardio)
that reaches the body surface.
Recording ECG

William Einthoven
 Useful in diagnosis of

Cardiac Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances
Drug effects and toxicity
Recording an ECG
 Basics
ECG graphs:
1 mm squares
5 mm squares
Paper Speed:
25 mm/sec standard
Voltage Calibration:
10 mm/mV standard
ECG Paper: Dimensions
5 mm

1 mm
Voltage
~Mass
0.1 mV

0.04 sec
0.2 sec

Speed = rate
 ECG Leads
Leads are electrodes which measure the
difference in electrical potential between either:

1. Two different points on the body (bipolar

leads)

2. One point on the body and a virtual reference

point with zero electrical potential, located in
the center of the heart (unipolar leads)
 The Concept of a Lead
Leads I, II, and III

LA
By changing the
arrangement of which
RA
- -
arms or legs are
positive or negative,
three unipolar leads RA - + LA
(I, II & III ) can be LEAD I
derived giving three
"pictures" of the
heart's electrical LEAD III +LL
activity from 3 angles.
LL
+
I
LEAD II

II III

Remember, the RL
is always the ground
 ECG Leads
The standard ECG has 12 leads: 3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads

The axis of a particular lead represents the viewpoint from

which it looks at the heart.
 ECG LEADS
Gold Berger :aV frontal leads

Wilson & co-workwers :chest leads

Standard Limb Leads
Precordial Leads
Precordial Leads
 Summary of Leads

Limb Leads Precordial Leads

Bipolar I, II, III -

(standard limb leads)

Unipolar aVR, aVL, aVF V1-V6

(augmented limb leads)
Limb Leads (Einthoven leads)

Einthoven triangle
Einthoven Rule
I+II+III==0
I+(-II)+III=0
I+III=II
Arrangement of Leads on the EKG
Anatomic Groups
(Septum)
Anatomic Groups
(Anterior Wall)
Anatomic Groups
(Lateral Wall)
Anatomic Groups
(Inferior Wall)
Anatomic Groups
(Summary)
 Localising the arterial territory

Lateral
I, AVL,
V5-V6

Anterior /
Inferior Septal
II, III, aVF V1-V4
 Standard sites unavailable
Patient pathology
Amputation or burns or bandages
should be placed as closely as possible to
the standard sites
Specific cardiac abnormalities
Situs inversus dextrocardia right & left
arm electrodes should be reversed
pre-cordial leads should be recorded from
V1R(V2) to V6
RVH & RV infarction:V3R & V4R
 Continuous monitoring
Bed side:
Holter monitoring:
TMT: Mason Likar system
 Other practical points
Electrodes should be selected for
maximum adhesiveness and minimum
discomfort,electrical noise,and skin-
electrode impedance
Effective contact between electrode and
skin is essential.
ECG :calibration
ECG :paper speed
Electrical artifacts:external or internal
external can be minimized by
straightening the lead wires
internal can be due to muscle
tremors,shivering ,hiccoughs .
Supine position
Interpretation of an ECG
 Steps involved
Heart Rate
Rhythm
Axis
Wave morphology
Intervals and segments analysis
Chamber enlargement
Specific changes
Wave forms
 Determining the Heart Rate

Rule of 300

10 Second Rule
 Rule of 300
Take the number of big boxes between
neighboring QRS complexes, and divide this
into 300. The result will be approximately
equal to the rate

Although fast, this method only works for

regular rhythms.
 The Rule of 300
It may be easiest to memorize the following table:

# of big Rate
boxes
1 300
2 150
3 100
4 75
5 60
6 50
 10 Second Rule

As most ECGs record 10 seconds of rhythm per

page, one can simply count the number of beats
present on the ECG and multiply by 6 to get the
number of beats per 60 seconds.

This method works well for irregular rhythms.

 QRS axis

Dr.K.Subramanyam
9-4-2009
 Genesis of QRS
Initially there is a small vector from left to
right through the IVS ,followed by a larger
vector from right to left through the free
wall of the LV
 Effect of left oriented lead
Small septal vector ,directed away from
the positive pole resulting in a small q
wave
Larger vector of the free wall ,directed
towards the positive pole resulting in a tall
R wave
 Effect of right oriented lead
Small septal vector which is directed
towards the positive pole,hence a small r
wave
Large vector of free LV wall which is
directed away from the lead and hence a
large s wave
 Transition zone
Transition from rS to qR pattern which is
usually seen in V3 /V4
 Rotation of the heart
Around AP axis;here the axis runs through
the IVS from the ant to post surface of the
heart
Horizontal position;main body of the LV is
oriented upwards and to the left:towards
leads I and avL(left axis)
Vertical position;main body of the LV is
oriented to leads II and avF(right and
inferior)
Around oblique axis;the axis runs through
the IVS from apex to base
Anatomical rotation clock-wise and
counter clock wise rotation
Counter clock-wise more anterior
position of LV
Results in transition zone shifting to left
Clock wise rotation;here th RV assumes a
more anterior position so that the IVS lay
parallel to the chest wall
There is a shift of the transition zone to the
right
 The QRS Axis

The QRS axis represents the net overall

direction of the hearts electrical activity.

Abnormalities of axis can hint at:

Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
 The QRS Axis
By near-consensus, the
normal QRS axis is defined
as ranging from -30 to +90.

-30 to -90 is referred to as a

left axis deviation (LAD)

+90 to +180 is referred to as

a right axis deviation (RAD)
 Determining the Axis

The Quadrant Approach

The Equiphasic Approach

 Determining the Axis

Predominantly Predominantly Equiphasic

Positive Negative
 The Quadrant Approach
1. Examine the QRS complex in leads I and aVF to determine
if they are predominantly positive or predominantly
negative. The combination should place the axis into one
of the 4 quadrants below.
 Example 1

Negative in I, positive in aVF RAD

 Example 2

Positive in I, negative in aVF Predominantly positive in II

Normal Axis (non-pathologic LAD)

Marked RAD -90
-60
-120
LAD
aVR -30
-150 aVL

180 0
I

150
30

120 II
III 60
Normal Axis
90 aVF
-30 to +100
RAD
 Example 1

Equiphasic in aVF Predominantly positive in I QRS axis 0

 Example 2

Equiphasic in II Predominantly negative in aVL QRS axis

+150
 Using leads I, II, III
LEAD 1 LEAD 2 LEAD 3
Normal UPRIGHT UPRIGHT UPRIGHT
Physiologic UPRIGHT /
UPRIGHT NEGATIVE
al Left Axis BIPHASIC
Pathological
UPRIGHT NEGATIVE NEGATIVE
Left Axis
UPRIGHT
Right Axis NEGATIVE BIPHASIC UPRIGHT
NEGATIVE
Extreme
NEGATIVE NEGATIVE NEGATIVE
Right Axis
 Common causes of LAD
May be normal in the elderly and very obese
Due to high diaphragm during pregnancy,
ascites, or ABD tumors
Inferior wall MI
Left Anterior Hemiblock
Left Bundle Branch Block
WPW Syndrome
Congenital Lesions
RV Pacer or RV ectopic rhythms
Emphysema
 Common causes of RAD
Normal variant
Right Ventricular Hypertrophy
Anterior MI
Right Bundle Branch Block
Left Posterior Hemiblock
Left Ventricular ectopic rhythms or pacing
WPW Syndrome
The Normal ECG

Dr.K.Subramanyam
30-3-2009
 Normal Sinus Rhythm
Originates in the sinus node
Rate between 60 and 100 beats per min
P wave axis of +45 to +65 degrees, ie.
Tallest p waves in Lead II
Monomorphic P waves
Normal PR interval of 120 to 200 msec
Normal relationship between P and QRS
Some sinus arrhythmia is normal
 Sinus Arrhythmia

ECG Characteristics: Presence of sinus P waves

Variation of the PP interval which cannot be
attributed to either SA nodal block or PACs

When the variations in PP interval occur in phase with respiration, this is

considered to be a normal variant. When they are unrelated to respiration,
they may be caused by the same etiologies leading to sinus bradycardia.
 Normal P wave
Atrial depolarisation
Duration 80 to 100 msec
Maximum amplitude 2.5 mm
Axis +45 to +65
Biphasic in lead V1
Terminal deflection should not exceed 1
mm in depth and 0.03 sec in duration
Normal P wave
 P wave
Results in negative wave form in leads
II,III and avF
Axis;-80 to -90
Retrograde activation of atria due to
impulse arising from or passing through
AV node
 Dome & dart p wave
Low left atrial rhythm
Initial dome-like deflexion and a terminal
sharp & spike like deflexion
 Normal QRS complex
Completely negative in lead aVR , maximum
positivity in lead II
rS in right oriented leads and qR in left oriented
leads (septal vector)
Transition zone commonly in V3-V4
RV5 > RV6 normally
Normal duration 50-110 msec, not more than
120 msec
Physiological q wave not > 0.03 sec
ECG showing qR pattern in lead III
,disappears on deep inspiration q wave
not significant
Mech:shift in the QRS axis
 QRS-T angle
The normal t wave axis is similar to the
QRS axis
Normally the QRS-T angle does not
exceed 60 deg
 Amplitude of QRS
Depends on the following factors
1.electrical force generated by the
ventricular myocardium
2.distance of the sensing electrode from
the ventricles
3.Body build;a thin individual has larger
complexes when compared to obese
individuals
4.direction of the frontal QRS axis
 Normal T wave
Same direction as the preceding QRS
complex
Blunt apex with asymmetric limbs
Height < 5mm in limb leads and <10 mm
in precordial leads
Smooth contours
May be tall in athletes
 ST segment
Merges smoothly with the proximal limb of
the T wave
No true horizontality
 Normal u wave
Best seen in midprecordial leads
Height < 10% of preceding T wave
Isoelectric in lead aVL (useful to measure
QTc)
Rarely exceeds 1 mm in amplitude
May be tall in athletes (2mm)
 QT interval
Normally corrected for heart rate
Bazetts formula
Normal 350 to 430 msec
With a normal heart rate (60 to 100), the
QT interval should not exceed half of the
R-R interval roughly
 Measurement of QT interval
The beginning of the QRS complex is best
determined in a lead with an initial q wave
leads I,II, avL ,V5 or V6
QT interval shortens with tachycardia and
lengthens with bradycardia
 Prolonged QTc
During sleep
Hypocalcemia
Ac myocarditis
AMI
Drugs like quinidine,procainamide,tricyclic
antidepressants
Hypothermia
HOCM
Advanced AV block or high degree AV
block
Jervell-Lange Neilson syndrome
Romano-ward syndrome
 Shortened QT
Digitalis effect
Hypercalcemia
Hyperthermia
Vagal stimulation
 Normal standardization

1 mV=10 mm
Will result in perfect right angles at each
corner
 overdamping
When the pressure of the stylus is too firm
on the paper so that its movements are
retarded
The ecg deflexions are inscribed more
slowly so that they become fractionally
wider
Results in diminished amplitude of
deflexions a small s wave may
disappear
 Underdamping or overshoot
When the writing stylus is not pressed
firmly enough against the paper
Results in overshoot of the upswing and
downswing of the writing stylus,resulting in
sharp spikes at the corners
Effects:deflexions are inscribed more
rapidly resulting in fractionally narrower
complexes
The ecg deflexions may be increased in
amplitude .
An s wave becomes exaggerated
Normal Variants in the ECG
Sinus arrhythmia
Persistent juvenile pattern
Early repolarisation syndrome
Non specific T wave changes
Persistent juvenile pattern
 Features of ERPS
Vagotonia / athletes heart
Prominent J point
Concave upwards, minimally elevated ST segments
Tall symmetrical T waves
Prominent q waves in left leads
Tall R waves in left oriented leads
Prominent u waves
Rapid precordial transition
Sinus bradycardia

Early Recognition Prevents Streptokinase infusion !

Reporting an ECG
1. Patient Details

Whose ECG is it ?!
2. Standardisation and lead
placement

Is it properly taken ?
3. Analysis of Rate, Rhythm and
Axis
4. Segment and wave form
analysis
5. Chamber enlargements
 Final Impression

Does the ECG correlate with

the clinical scenario ?
Thank you !