Basics of ECG

with the heart beat

1876- Irish scientist Marey analyzes the electric

given to William Einthoven for his work on EKG
1938 -AHA

of the electrical events of the cardiac cycle.
Each event has

(i.e. hyperkalemia, hypokalemia)
Drug toxicity (i.e. digoxin and drugs which prolong

electrical changes called depolarization

These changes can be detected by electrodes

intrinsic rate of 60 - 100 beats/minute.

AV Node - Back-up

produces an upright (“positive”) deflection

fibers

T wave - Ventricular repolarization

QRS - Ventricular depolarization

of His)

(delay allows time for the atria to contract

- 0.20 s
Vertically
One large box - 0.5 mV

points
1. Bipolar Leads: Two different points on the body

2.

Augmented Limb Leads
6 Precordial Leads

ECG RULES
Professor Chamberlains 10 rules of normal:-

200 milliseconds or 3 to 5 little squares

The width of the QRS complex should not exceed 110 ms, less than 3 little squares

complex should be dominantly upright in leads I and II

and T waves tend to have the same general direction

waves are negative in lead aVR

least V4
The S wave must grow from V1 to at

and V2 where it may be elevated

and V2 to V6

small q less than 0.04 seconds in width in I,

V2 to V6

in lead aVR
< 3 small squares in duration
< 2.5

Pulmonale)

Atrial Enlargement

early activation of the ventricle (delta wave and short PR

V5, and V6

R wave in lead V6 is smaller than

in V5 or V6 > 35 mm
An R wave

segment by 1 mm or more
“J” (Junction) point is the

Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006.

gradual slope than the second

Should be at least 1/8 but

heart rate increases
For HR = 70 bpm, QT

are small, round, symmetrical and positive in lead II, with

QRS complexes, and divide this into 300. (smaller boxes with

75 bpm

following table:

the number of beats present on the EKG
Multiply by 6

heart’s electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)

-90° is referred to as a left axis deviation (LAD)

+90°

if they are predominantly positive or negative.
The combination should

II is positive, the LAD is non-pathologic or the axis

 Predominantly positive in II 
Normal Axis

lies 90° away from the lead
3. QRS in this

QRS axis ≈ 0°

node and surrounding myocardium
Abscent of complete Cardiac cycle
Occures irregularly and

Block

system
Prolong P-R interval
All P waves are followed by QRS
Associated with

by AV node
Types:
Mobitz type 1 (Wenckebach Phenomenon)
Mobitz type 2

intervals until pause;
2. Pause is less than preceding 2

Mobitz type 1 (Wenckebach Phenomenon)

of the branches should be completely blocked;
most likely blocked in

escape rhythm at 45 bpm.
The PP intervals vary because

ventricular escape rhythm,
'B' the right ventricular pacemaker rhythm is

terminated by ventricular escapes;
Wider QRS morphology of the escape

AV Dissociation

a myocardial infarction. If so, where?

infarction.

is having a myocardial infarction?

elevation in leads II, III and aVF.

and the lateral wall (V5-V6, I, and aVL)!

interval?
none
QRS duration?
Interpretation?
Atrial Flutter

s
P waves?
PR interval?
0.16 s  none
QRS duration?
Interpretation?
Paroxysmal

by a PAC (not seen here) and the P waves

PR interval?
none
QRS duration?
Interpretation?
Ventricular Tachycardia

P waves, wide QRS).

PR interval?
none
QRS duration?
Interpretation?
Ventricular Fibrillation

junction
Ventricular cells

Bradycardia
Sinus Tachycardia


Sinus Tachycardia may be an appropriate
response to stress.

continuously due to a looping re-entrant circuit

Premature Atrial Contractions

looping re-entrant circuit
block impulses coming from the SA Node

Paroxysmal

s
QRS duration?
Interpretation?
Sinus Bradycardia

s
QRS duration?
Interpretation?
Sinus Tachycardia

waves?
PR interval?
0.14 s (except 2/7)
QRS duration?
Interpretation?
NSR with Premature

atria (but not in the SA node), therefore the contour

(7th wide)
P waves?
PR interval?
0.14 s
QRS duration?
Interpretation?
Sinus Rhythm

the ventricles

I

2nd Degree AV Block, Type II

3rd Degree AV Block

s
QRS duration?
Interpretation?
1st Degree AV Block

node or Bundle of His.

s
P waves?
PR interval?
lengthens
QRS duration?
Interpretation?
2nd Degree AV Block,

s
P waves?
PR interval?
0.14 s
QRS duration?
Interpretation?
2nd Degree AV

are completely blocked (P wave not followed by QRS).

s)
P waves?
PR interval?
none
QRS duration?
Interpretation?
3rd Degree AV Block

blocked in the AV junction; QRS complexes originate independently from

interval?
none
QRS duration?
Interpretation?
Atrial Fibrillation

P waves (impulses are not originating from the sinus node).
Atrial

interval?
none
QRS duration?
Interpretation?
Atrial Flutter

s
P waves?
PR interval?
0.16 s  none
QRS duration?
Interpretation?
Paroxysmal

by a PAC (not seen here) and the P waves

PR interval?
none
QRS duration?
Interpretation?
Ventricular Tachycardia

P waves, wide QRS).

PR interval?
none
QRS duration?
Interpretation?
Ventricular Fibrillation

go beyond looking at a rhythm strip and obtain a

the:

Anterior portion of the heart
Lateral portion of the heart
Inferior portion

look for elevation of the ST segment.

small box) in 2 leads is consistent with a myocardial

is best viewed using leads V1- V4.

V4 that are consistent with a myocardial infarction, you can

a myocardial infarction. If so, where?

infarction.

an anterior wall myocardial infarction let’s look at how you

of the heart.

look at different portions of the heart. The limb and

Limb Leads

Augmented Leads

Precordial Leads

to look for a lateral wall and inferior wall MI.
Limb

Augmented Leads

Precordial Leads

viewed using leads V1- V4.
Limb Leads
Augmented Leads
Precordial Leads

of the heart is best viewed?
Limb Leads
Augmented Leads
Precordial Leads
Leads

Limb Leads
Augmented Leads
Precordial Leads
Leads II, III and aVF

is having a myocardial infarction?

elevation in leads II, III and aVF.

and the lateral wall (V5-V6, I, and aVL)!

do you notice about the P waves?
The P waves are

following criteria:
II P > 2.5 mm, or
V1 or V2 P > 1.5

Remember 1 small box in height = 1 mm

A cause of RAE is RVH from pulmonary hypertension.

> 2 ½ boxes (in height)

> 1 ½ boxes (in height)

do you notice about the P waves?
The P waves in

following criteria:
II > 0.04 s (1 box) between notched peaks, or
V1 Neg.

Normal

LAE

A common cause of LAE is LVH from hypertension.

as different with the second one?
Normal
Left Ventricular Hypertrophy
Answer:

ECG.
For example:
The R wave in V5 or V6 plus

However, for now, all you need to know is that the QRS voltage increases with LVH.

you notice about the axis and QRS complexes over the

There is right axis deviation (negative in I, positive in II) and there are tall R waves in V1, V2.

following criteria:
Right axis deviation, and
V1 R wave > 7mm tall
A common

a normal ECG and one from a person with RVH.
Notice

Normal

RVH

you notice about the axis and QRS complexes over the

There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2.

The deep S waves seen in the leads over the right ventricle are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2).

criteria*:
R in V5 (or V6) + S in V1

A common cause of LVH is hypertension.

* There are several other criteria for the diagnosis of LVH.

S = 13 mm

R = 25 mm

fibers are seen as the QRS complex on the ECG.

changes on the ECG.
QRS complex widens (> 0.12 sec).
QRS

Giant Osborne waves