ta

pogacse
.%%HtY*
#%9
were
nkkt
TOWTOREADAN
)

t.EE#Ea:.E***EE*EfgeEFies.

The

Electricity

Heart

the

of

SA

The

pacemaker
SA

His

automaticity

node

AV

GKg

There

innervates

{
AV

node

AV

for

Depolarisation
His

of
the
the

ocardium

end

where

terminal

may

lo

:
.

't

record

as

ions

cause

Nation

the

of
a

Repolarisation

is

septum

is

of

rest

the

purkinje

to

that

accomplished
fibers

to

the

spread
RBB

The

ventricular

by

Kt

down

than

filaments

of

just

beneath

IV

not

produce
of

the

the

to

controlled

cell

of

Kt

ions

from

the

septum

re

polarisation

depolarisation
outflow

depolarises

myocytes

ventricular

septum

contraction
-

bundles

the

does

the

of

composed
out

of

bundle

the

cell

the

at

myocardium

leaving

ions

longer

takes

at

depolarisation

right

atria

to

except

terminal

midway
.

Is

This

myocytes {

ventricles

conduction

begins

The

begins
left

So

atria

cation

branches

filaments

the

the

system

Nations

ventricular

terminal

produces
due

anterior

bundle

using

from

from

ventricles

left

fibres

myocyte

movement

( the

Bundle

's

Nqt

stimulate

contract

atrium

Bachmann

through

depolarisation

wave

to

right

the

conducting

the

the

occurs

the

outwards

atria

regular

fast

of

wave

proceed

ventricles

the

right

before

polarisation

re

the

fine

in

the

in

at

waves

Each

backflow

blood

prevent

enter

Ventricular

produces

polarisation

Re

to

the

immediately

Finally

Purkinje

filaments

occurs

tract

depolarisation

depolarise

LBB

the

conduction

ventricular

into

fibers

Purkinje

in

slows

conducting

rapidly

tracts

insulate

the

as

blood

of

divides

which

intermodal

valves

node

time

allowing

atrium

electrically

The

one

ventricular

also

the

left

the

atrio

The

Ions

specialised

posterior ) {

middle

intervals

both

three

are

known

located

is

It

depolarisation

branch

bundle

is

stimuli

Iegniriliiutmeiiiiewrea
"it"
initiates

Right

of

generating

The

pacemaking

A
ieabunaiebrancn
of

Bundle

node

dominant

's

heart

the

is

node

myocyte

Recording

the

ECG

machines

Each

The

square
deflections

electrode

standard

15mm

square

small

Positive

at

run

large

Each

ECG

is

negative

Mms

'

sec

depolarisation

-4

Wave
the

of

Contraction

Complex

Wave

Repolavisation

QRS

of

Wave

extra

Assumed

to

wave

wave

wave

QT

's

deflection

12

an

of

regardless

following

ventricular

wave

wave

regardless

of

Wave

systole

leads
The

ECG

compares

at

the

heart

12

views

of

6
-

The

lead

on

from
the

Interval

ECG

muscles

deflection

upward
any

of

deflection

downward

Represents

papillary

the

be

repolarisation
each

the

ventricles

depolarisation

Ventricular

an

away

atria

towards

advancing

is

ECG

Normal

0.04

when

travelling

'

25

sec

represents

produced

are

of
0.2

represents

1mm

rate

the

the

electrical

activity

directions

different

in

the

different

heart

limb
chest

right

leads

leads

leg

( Vi
is

11,111
-

an

Va

AVR

avl

avf )

)
earth

wire

Anterior

lateral

AVR

vi

Septal

V4

11

Interior

all

Vz

Septal

Vs

Lateral

111

Inferior

AVF

Va

lateral

electrodes

Inferior

Vs

Anterior

look

or
,~

npnatiahhiseaathe

A
==)

characteristic
.

identified

is

from

lead

whichever

the

#
W

rhythm

cardiac

The

,*EoIte )

shows

lead

usually

11

negative
arm
right
.

Skeeter

lead

is

is

"

horizontal

electrode

'T

standard

positive

ventricular

'

ventricular

lead

lead

interventricular

lead

is

one

positive

electrode

arm

kM#*#f

as

left

positive

is

is

one

is

ad

Another

"

y,

right

electrodes

left

it's

a.

two

in

of

pair

"

bipolar
negative
lead

limb

Each

more

wave

clearly

is

lead
both

AVF

The

electrodes

arm

AVF

uses

as

common

foot

left

the

ground

electrode
)

negative

AVF

is

#MtEQB
:
;
i.e.
+9cm
+i
lead

augmented

an

obtained

the

in

of

combination

same

manner

lead

both

AVR

111

limb

unipolav

are

11

leads

AVL

are

positive

electrodes

'

'

VR

VL

150

180

'

mp

+120

"

+60

because

leads

left

inferior

leads

called

each

of

inferior

leads

the

electrode

on

foot

'

it

determined

be

can

depolarisation

left

the

on

are

positive

toward

AVF

because

has

arm

11,111

leads

have

each

electrode

lateral

'

lateral

called

are

positive

leads

fftMy?
+

'

Inferior

AVL

leads

Lateral

Mrs.

}o

l{

leads

or

side

is

away

toward

if

moving
from

the

the

foot

Rat

of

parts

rate

contraction

of

depolarising
SA

The

of

SA

normally

the

the

SA

fail

the

If

focus

will

of

60

loobpm

from

discharge
lung

However

that

The

reflexes

muscle

SA

fails
or

in

through

over

give
Rates

site

node

If

At

keep

will

This

failure

it

mechanism

is

achieved

of

by

depolarisation

is

spontaneously

This

the

region
frequencies

the

provides

control

of

about

bundle

His

Atria

60

Nodal

40

both

If

~3o/min

which

of

both

ventricular

by

of

801mm

20

60

/ min

40/min

levels

separate

three

of

rate

501mm

blocked

is

node

AV

assumed

be

will

the

most

overdrive

as

around

ventricular

known

is

depolarised

of

backup

pacing

node
.

rate

abnormal

normal

frequency

depolarise

to

depolarisation

suppression

is

in

pace

protective

avoided

be

intrinsic

lower

to

that

the

between

to

is

potential

mechanism

Ventricles

SA

heart

the

competition

node

conduction
take

if

with

failsafe

depolarise

the

Pacing

Overdrive

of

{ also

nerves

heart

whichever

is

SA

atrial

if

or

the

by
this

spontaneous
,

the

normally

the

have

in

vagus

depolarisation

controlled

suppression
either

rate

to

having

node

is

frequently

inactive

sites

SA

heart

the

creates

fails

node

spontaneous

the

The

this

be

secondary

than

by

's

area

situations

of

the

by

frequency

highest

the

has

influenced

are

normally

sites

controlled

maintains

foci

emergency
must

be

will

ventricles

rhythmically

sloobpm

Automaticity
it

spontaneously

bobpm

<

Tachycardia

going

is

rhythm

Bradycardia

the

frequently

node

sinus

rest

depolarise

can

of

most

node

the

heart

the

Atrial

focus

If

failure

Nodal

focus

If

failure

Ventricular

focus

'

these

300

These

slow

when

occur

but

ftp.

is

the

acute

important

phase
to

not

called

rhythms

escape

initiating

higher
of

60

15

are

node

SA

to

response
in

in

for

sites

by

100

150

rhythms

secondary

seen

altogether

300

protective

the

are

100

150

inhibition

normal

It

rate

the

Calculating

depolarisation

rhythms

Escape

problems

their

disorders

primary

pathway

conducting

the

in

they

from

escape
not

are

because

MI

suppress

rhythm

escape

an

the

as

heart

stop

may

Rhythm
Rhythm
sequence
the

fainting
-

fast

sinus

arrhythmia
(

rhythm

is

controlling
sinus

called

activation

the

rhythm

sinus

respiration

with

are

bradycardia )

be

can

with

associated

attacks

MI

rhythm

pain
haemorrhage
thyroid

begins

hypothermia

sinus

normally

training

fear
-

rhythm

associated

rate

exercise

heart

heart

the

of

myxoedema

part

in

heart

sinus

athletic

in

slow
-

node

people

young

the

Normal

SA

Changes

to

refers

toxicosis

sinus

tachycardia

can

be

associated

with

seen

in

Irregular

Rhythms
Pacemaker

Wandering

wave
rate

atrial

atrial

begin

Can

varies

rates

node

MAT

is

to

ventricular

muscle
"

Rhythm

atrial

ventricular
Ventricular

EElt
.

hot

rhythm

sinus

"

"

"

Iedniorniciriainmatuiie
Supra

patients

COPD

Supra

atrial

the

rhythm

the

at

of

rhythm

from

foci

atrial

nearby

the

100

irregular

SA

Tachycardia

shape

wave

rhythm

100

<

Atrial

Multifocal

ventricular

Irregular

Irregular rhythm produced by

pacemaker activity wandering

varies

shape

rhythm

junction

rhythm

ventricular
-

depolarisation

The

via

normal

the

SA

node

atrial

muscle

depolarisation

slower

wide
wave

wave

is

is

abnormally
of

also

ventricular

rhythms

fibrillation

way

therefore

initiated

by

The

QRS

Is

also

complex

categorised

with
will

be

or

wide

as

beats

single

activation

complex

abnormal

abnormal

an

therefore

is

so

the

QRS

narrow

sustained

by

rhythm

QRS

be

ventricles

QRS

the

early
fast

normal

ventricular

can

slow

bradycavdig
extra
systoles
tachycardia
-

normal

was

region

al

the

Repolavisation

shape

wide

where

is

complex

junction

the

spreads through
Purkinje fibres

shaped

rhythms
-

QRS

the

in

depolarisation

the

or

abnormal

rhythms
Supra
Exception

the

via

pathway

Ventricular

Abnormal

whether

same

The

ventricles

the

Rhythm

The

Supra

branches

Ventricular

the

is

its

to

spreads

wave

bundle

His

the

al

sustained

is

totally

disorganised

BBB

or

WPW

syndrome

Sinus

arrest

absent

Atrial

the

in

Can

around

Ventricular
Most

Can

No

over

wave

normal

wave

normal

QRS

QRS

intrinsic

an

block

heart

no

of

frequency

abnormal

't

wave

faster

discharge

QRS

than

that

ventricular

idio

associated

rhythm

with

Ml

acute

Beats

originates

beat

premature

spontaneously

producing

Ventricular

fire

irritable

an

beat

foci

the

expected
02

sensitive

most

the

in

sensors

fires

rhythm

they

when

sense

of

because

than

that

focus

automaticity

earlier

are

spontaneously

irritable

become

in

automaticity

they

02

abnormal

block

often

Premature

Foci

have

accelerated

low

takes

complete

in

seen

heart

in

Delay

over

Escape

occasionally

seen

to

escapes

node

AV

so

focus

automaticity

an

Escape

the

commonly
be
single

Can

al )

Junction

Focus

in

completely

pacemaking

ceases

results

takes

atrium

singly

occur

Nodal
-

node

Escape

Focus

rhythm

escape

an

SA

the

suppression

overdrive

produce

when

occurs

adrenaline
Y

stimulation

sympathetic

stimulants

receptor

hyperthyroidism
t

Premature

atrial

beats
fires

spontaneously

produces

automaticity
stimulus

the

beat

premature
reach

not

Sometimes
one

of

temporarily

its

unusually
rhythm

dominant

PAB

bundle

can

refractory

is

to

widened

of

its

with

step

in

premature

is

re

does

that
not

ventricular

QRS

the

stimulus

pacing

reset

conduction

polarised

complex

waves

center
Every
by
depolarised
wave

completely

depolarisation

that

qberreht
not

is

than

premature
center

produce

is

resets

pacing

branches

it

activity

there

When

shaped
when

pacemaking

the
9

the

earlier

stimulus

Focus

atrial

irritable

an

depolarisation

resets

so

in

originate

premature

: Kt

,{

is

because

therefore

Extra

heart

the

of

part

systoles

Junction

al

extra

systoles

have

extra

systoles

have

Ventricular

be

can

Ventricular

However

when

have

shape

any

extra

wave

No

wave

QRS

wide

QRS

rhythm
equal

they

P
P

no

systole

waves

nodal

should

Normal
all

QRS

ectopic

the

at

wave

abnormal

common

are

in

early

Occur

extra

an

it

ectopic

ventricular

normal

than

AF

QRS

Normal

QRS

which

complexes

typically

are

systoles

thus

of

usually

are

fibrillation

ventricular

induce

of

wave

proceeding

they

beat

dangerous

potentially

are

importance

no

Analysis

ECG

QRS

Early
P

wave

junction

to

conducted

to

both

the

of

supra

beats

supra

periodicity

{
the

the

has

same

the

has

each

as

same

same

beat

from

different

each

the

same

other
other

beat

way

up

have

both

expected

time

compensatory

heartbeat

next

extra

SA

the

at

appear

ventricular

ventricular
of

the

is

normal

normal

systole

extra

ventricular

lie

excitation

as

inverted

the

before

the

as

beats

after

wave

look

up

way
ventricular

pause

beats

may

ventricles

the

as

look

beats

same

of

appearance

complex

throughout

shape

the

cause

QRS

atria

the

deflection

ventricular

the

ventricular

supra

wave

may

after

same

ventricular

Next

the

supra

wave

systole

extra

close

direction

duration
T

al

wave

complex

initial

anywhere

QRS

early

an

systole

extra

seen

follows

complex
atrial

abnormal

extra

wide

No

earlier

called

is

Atrial

waves

depolarise

can

heartbeat

accompanying

absent

Sinus

systoles

Any

present

waves

node

usually

systole
so

the

next

upsets
P

wave

the
comes

normal
late

can

's

achycgrdia
Foci

the

in

causing

atria

junction

tachycardia

sustained

paroxysmal

region

al

ventricles

intermittent

An

depolarise

may

repeatedly
is

tachycardia

called

Tachycardia
Supra

Ventricular

ventricular

complex
{
wide

Rs

Atrial

Atrial

Tachycardia
depolarise
faster

1501

AV

node

very

cannot

conduct

faster

lead

in

seen

seen

BBB

to

close
or

all

at

normal

QRS

qlso

in

seen

Qks

not

easily

be

the

most

abnormal

waves

may

waves

min

line

between

al

Tachycardia

min

flat

no

than

The

rate

32501

atria

Junction

Flutter

atrial

is

11

than

2001mm
block

TAV

node

AV

Activates

functioning
properly
prevents

reflex

SA

the

abolish
rate

arrhythmia

fast

's

the

SA

conduction
some

ventricular

ventricular

of

of

delay

in

stimulation

vagal

discharge

completely
slows

activated
a

of

increase

Can

nodes

to

leads

that

AV

reduction

being

at

Pressure

the

of

ventricles
From

Sinus

Carotid
is

in

others

an

the

AV

has

but

node

arrhythmia

ventricular

supra

in

node

no

effect

on

rate

Ventricular
I

If

Tachycardia
the

tachycardia
2

If

the

QRS

probably
3

Left

If

has

patient

axis

during

probably

will

Suprq
BBB

have

complex
deviation

atrial

small

QRS

complex

during

BBB

normal

squares

during

the

rhythm
160ms )

the
,

rhythm

is

origin

in

usual

tachycardia

than

with

the

rhythm

sinus

shape

Same

wider

is

ventricular

in

when

the

Tachycardia

ventricular

the

fibrillation

indicates
QRS

ventricular

complex
with

BBB

is

very

origin
irregular

the

rhythm

is

's

Fibrillation
Caused

the

by

Atrial

continuous

there

an

all

bundle

shape

flutter

fashion

constant

ventricles

conduction

into

there

for

waves

3s

2-

qre

AV

depolarisation

intensity

However

therefore

contract

through

the

node

is

At
in

conducts

waves

is

QRS

normal

passing

these

waves

waves

irregularly
ventricles

no

The

the

that

so

into

are

normal

Fibrillation
QRS

No

is

complex

Patient

will

present

the

consciousness

loose

disorganised

totally

ECG is

Torsades

Pointes

de

rhythm

of

form

ventricular
rapid
abnormalities
congenital
QT
the
segment
250
350
Rate
/ min (

or

no

usually

if

brief

in

lead

can

effective

to

waves

250

rate

AV

later

lengthen

pumping

ventricular

which

arrhythmia

identical

back

to

depolarisation

back

waves

tooth

saw

conduct

to

the

only

so

in

one

series

ventricles

ventricles

the

drive

period

refractory

long

at

the

rate

excessive

same

Flutter

by
exceptionally

resolves

arrhythmia
the

As

hardly

arteries

VF

occurs

VF

ventricles
fill

do

so

not
due

rapid
4

is

are

there

relieve

to

at

an

rate

series

self

rarely

min

firing

focus

automaticity

ventricular

single
rapid

250-3501

rate

produces
-

has
waves

produced

of

medications

min

cannot

Ventricular

of

identical

node

350

) all

potassium

foci

atrial

an

are

the

of

in

succession

rapid

syndrome

deadly

Flutter

originates

QT

long

low

by

caused

episodes

unresolved

Atrial
-

foci

automaticity

Rhythms
-

like

of

are

the

as

Ventricular

'

nothing

irregular

multiple

independently

contract

be

may

or

His

the

fibres

muscle

Atrial
times

Other

of

firing

Fibrillation
-

rapid

of

smooth

always

nearly

contracting

is

no

blood

hypoxic

at

so

ventricular

the

to

output
heart
.

the

rate

Therefore

has

deadly

alarming

an

foci

amplitude

similar

prelude

cardiac

in

waves

no

ventricles

the

cardiac

blood

supply

Wolff

The

only

electric

normal

bundle

accessory

The

interval

delta

wave

Clinical
This

Lown

of

AV
'

This

usually

delay

to

Levine

forms
the

on

conduction

the

of

shows

complex
QRS

the

up

Pre

side

left

in

therefore

excitation

an

direct

normal

is

slurred

early

an

upstroke

by

by

occurs

the

atrium

to

bundle

rapid

to

adjacent

the

is

's

no

Sig

rates

rate

in
,

The

AV

interval

PR

bundle

His

the

reasonable

there

QRS

to

tract

ventricular

supra
at

so

intermodal

directly

ventricles

the

James

the

anterior

the

filters

node

AV

of

depolarisation

atrial

the

are

extension

an

conducts

waves

tachycardia

sustained

depolarisation

the

reactivate

the

down

spread

can

to

pathway

accessory

Ordinarily

Depolarisation

syndrome

'

bypassed

is

tachycardia

bypassed

bundie

delay

back

( LGL )

is

node

James

node

delay

QRS

part

forms

transmit

to

second

circuit

without

QRS

This

have

people

some

bundle
accessory

ventricle

node

the

paroxysmal

His

Ganong

The

The

short

is

cause

can

entry

AV

no

however

Importance

bundle
re

atrium

is

Kent

bundle

His

PR

there

of

bundle

the

is

connection

the

bundles

occurs

syndrome

'

the

connection between

these

( WPW

White

Parkinson

Complex
Depolarisation

the

of

shape

Complex

depolarisation

of

wave

QRS

the

heart

the

through

spreads

spreading

through

the

lead

VR 4

look

11

of

spread

axis

1,11

upward

QRS

lead

the

predominantly
Complex

QRS

Depolarisation
,

from

moving away

at

right
generating

angles
equal

waves

Axis

Cardiac

leads

towards

causing

downward

RGS

cardiac

the

causes

lead

to

of

but

which

moving

Depolarisation

The

complex
the

ventricles

predominantly

once

in

Depolarisation
the

at

direction

average

directions

many

the

shows

is

in

the
.

The

111
.

at

heart

the

depolarisation
axis

can

be

from

leads
through
opposite

directions

wave

derived

most

easily

the

The

average

ventricles

from

the

QRS

is

direction
the

called

complex

in

f)

Axis

Normal

'

b.)
_~~

spreading
therefore

a.

Yahn

"

towards

leads

associated

with

leads

these

all

Axis

left

'

"

ventricle

right

hypertrophied
The

The

is

conditions

Right

left

presence
ventricular

lead

towards

that

axis
should

left

The

QRS

depolarisation

strain

pulmonary

deviation
alert

hypertrophy

you
.

to

look

lead

are

for

towards

predominantly
111

deviation
QRS

is

due

other

to

to

is

conduction

lead

11

of

influence
but

normally

detects

significant
signs of right

seldom

also

in

excess

ventricle

significant

not

deflection

enlarged

due

themselves

in

in

be

can
an

heart

the

swings

predominantly negative

it

mainly

axis

the

becomes

the

until

becomes

ventricle

axis

Left

becomes

111

because

with

the

negative

away

positive
associated

becomes

left

hypertrophied

swings

in

the

When

depolarisation

deflection

spreading

axis

lead

in

because

spreading

more

right

deflection

is

becomes
the

then

the

negative

in

than

"

Deviation

"

in

Him
or
#
it
,*

towards

is

deflection

Yionrb
;

"

the

deflection

lead

in

111

the

greater

Deviation

'

If

1,11 {

predominantly upward

"n

Axis

Right

mean
:7i'
atiiia
:p
:ia!iiHY"
in
is
:":

However

left

the

The

oil
i.
-90

left

axis

deviation

,Yy
,

-30

if

...

...

axis

+r

'

Normal

LEAD

"

+60

+90

ve

ve

SA

range

lower

Left

upper

AXIS

Normal
LAD

lower

RAD

Right upper

ve

Left

Right

tve

ve

"

'

tve

tue
-

QUADRANT

VF

Conduction

the

in

Method

IEADAVF

tve

axis

+120

is

Quadrant

cardiac

deviation

+90

to

The

Right

axis

cardiac

normal

'

Extreme

Problems

it 's

node

AV

node

bundle

HIS

da

t.F.F.yg.fr
v

The

AV

node

{ is

muscle

His

bundle

from

squares

not

the

First

Degree

The

interval

PR

but

( AV )

be

may

Heart

is

called

This

is

not

sign of

Intermittent

of

His

AV )

220ms

heart

( six

small

block

important

itself

in

disease

carditis

disturbances

calcium

blockers

channel

blockers )

beta

Block

Heart

of

failure

ventricular

toxicity

electrolyte
drugs

sec

rheumatic

digoxiw
-

0.20

artery

acute

Degree (

beyond

coronary

Second

of

spread

the

than

this

with

the

Block

prolonged

is

to

node

greater

branches

for

taken

SA

normally

interference

time

the

is

depolarisation

Bundle

interval

PR

excitation

to

pass

through

the

AV

node

or

the

bundle

AV node

There
1
.

variations

are

Type

Mobitz
-

Progressive
{
beat

then
,

usually

ckebach

Wenckebach

lengthening

failure

of

followed

benign

by
.

AV

of

conduction

of
beat

conducted

node

blocked

interval

PR

the

atrial

an

cycle )

Eng
ti%e
Mobitz

RBB

LBB

Second
2a

Mobitz

Type

beats

Most

Block

Heart

Degree

conducted

are

there

occasionally

subsequent
Zb

to

Two

One

followed

3 :L

complexes

Block

Occurs

when

atrial

by

times

non

conducted

beats

as

many

as

beats

one

or

waves

),
QRS

be

is

contraction
ventricles
'

block

due

by

to

the

beats

no

the

occurs

from

are

ventricles

depolarising

are

focus

phenomenon

caused

this

mechanism
muscle

but

normal

when

escape

usually

heart

( Complete)

acute

an

also

May

four

ventricular

chronic

or

blocked

's

fiber

atrial

three

or

complete

by

slow

the

be

May

two

then
or

the

to

conducted

within

followed

Heart

excited

nonconducted

dg

three

or

Degree

block

Commonly

Third

heart

complete

beat

twice

without

Purkinje

but

atrial

giving

interval

depolarisation

depolarisation
by

PR

constant

atrial

conducted

conducted

3.

Alternative

is

ventricular

Commonly

with

in

ml

fibrosis

block

( it

oatients

the

around

both

of

it

is

transient

bundle

of

branches

bundle

9%9%9
'*

)
His

OR

Block

in

Junction

al

leaves

node

upper

foci

to

escape

Block

'

in

bundle

HIS

only

Bundle

is

the

QRS

bundle

of

Right
Indicates
QRS

His

paths

foci

HIS

the

blocked

are

focus

ventricular

bundle

911
so

escapes

Bundle

complex

of

of

>

120

or

depolarisation

the

in

right

the

left

of

of

part

ms

branches

both

complete

causes

Branch

delay

either

depolarisation

if

seen

Block

problems

through

complex

QRS

also

is

itself

muscle

of

be

will

muscle

widening

wide

leaves

ventricular

conduction
there

ventricular

abnormal

branches

bundle

Below

or

Block

Branch

there

If

entirenode

of

avocado

begins
has

block

heart

the

within
same

ventricular

the

effect

as

block

of

the

Block
in

the

normal

right

side

duration

of

the
are

heart

quite

but
,

common

RBBB

patterns
in

with

healthy

people

In

RBBB

conduction

no

depolarised
Q

in

wave

Vo

The

RSR

'

be

left

Always
is

The

right

muscle

V6

small

causing

an

the

to

excitation

after

the

the

reach

conducting

normal

of

complex

pathway

Left

width

normal

right

resulting

in

It

120ms )

than

( less

block !

branch

bundle

heart

right

disease

be

can

to

left

causing

small

left
of

the

usually

Va

an

is

It

ventricle

Vi

causes

associated

also

left

the

lead

in

wave

left

the
.

before

depolarised

is

there

lead

RBBB

is

best

is

considered

to

ventricle

lead

in

wave

The

Vi

septum
R

an

an

an

despite

so

wave

with

wave

is

an

RSR

smaller

lead

in

in

wave

the
Va

Vi

lead

inversion

in

Subsequent

another

the

lateral

lead

in

seen

there

where

pattern

leads

V,

lead

in

wave

right

of

is

of

in

Block

ventricle
mass

wave

depolarisation
R

in

wave

is

from

lead

of

QRS

indication

in

Va

partial

Branch

depolarised

wave

'

vavieut

an

an

for

depolarises

lead

with

ventricle

heart

normal

failure

in

left

the

therefore

called

Bundle

causing

septum

the

the

of

pattern
normal

in

than

complex

sometimes

Va

lead

ventricle

QRS

'

in

because

wide

usual

as

to

spreads

wave

right

side

but

branch

right

the

longer

ventricle

left

then

an

takes

the

excitation

{
It

from

down

occurs

Vi
s

LBBB

is

best

Distal

seen

with

complex

Parts

in

of

lead

notched

't
A

RBB

where

top

is

there

pattern )

broad

QRS

V6

LBB
Anterior

" 313

V6

The

fasicle

right

but

the

posterior

-1

therefore
'

bundle

left

'

fascicles

spreads

'

has

branch

bundle

no

has

branch

main
two

into

ventricles

the

anterior

depolarisation

The

divisions

wave
.

by

three

Fntehialiinaxisaepenasonnntnenuae

U
-

.ae?eau9eiYnteion
;

depolarisation
ventricle

of

posterior

fas

.de

left

right

it

has

more

of

the

contains

influence

more

on

muscle

than

the

cardiac

the

axis

the

If

ventricle

to

has

axis

rotates

bundle
the

bloc

's

left

axis

left

or

the

through
hemi

blocked

block

The

block

so

the

left

cardiac

the

left

anterior

fascicle
if

but

{
to

posterior

hemi

posterior

left

due

therefore

is

conduct

to

fascicle

posterior

deviation

anterior

fails

branch

bundle

left

the

depolarised

right

shows

ECG

of

rarely

only

is

of

this

left

the

does

occur

deviatio

axis

m.
there

when

is

there

be

upwards

fascicular

fasicle

anterior

is

RBBB

depolarisation

normal

the

RBBB

left

axis

deviation

left

the

fascicle

widespread

damage

blocked

are

large

its

the

system

muscle

shows

ECG

conducting

the

to

because

normal

with

ventricle

block

bifasciculav

of

remains

usually

anterior

left

the

axis

cardiac

the

RBBB

Actions
First

often

Second

in

seen

acute

Block

Degree

Ml

2 :L

type

3 :L

Third

Always

for

need

need

specific

pacing

treatment
if

especially

slow

is

indicates

Consider

tissue

conducting

disease

more

often

fibrosis

pacing

Atrial

defect

No

treatment

septal
specific

Aortic

If

severe

Axis

Left

LVH

left

Axis

stenosis

isohqemiu

asymptomatic

It

not

do

LBBB
-

MI

often

RBBB
-

indicate

may

block

Wenckebach

dg

rate

ischemic

disease

Block

Degree

block

4 :L

ventricular

heart

indicates

Mobitz

Block

Degree

people

fever

rheumatic

usually

normal

chest

action

no

pain

Deviation

disease

needed

indicate

may

intervention

mit

causes

Deviation

RBBB

conducting

Indicates

severe

Pacemaker

required

intermittent

if

complete

the

disease

tissue

has

patient

heart

block

symptoms

suggestive

of

than

ABNORMALITY

PWAVE

QRIRATIO

QRS

QRSSHAPE

REGULARITY

Occasional
ie

extra

Normal

Sypravehtriculdr

Ventricular

Abnormal

systoles
Sustained

RHYTHM

RATE

Present

:L

Normal

Regular

Sinus

Normal

Rhythm

Atrial

sl50/m

Tachycardia
Irregular
More
waves

Normal

Regular

Normal

Sinus

Rhythm

Slow

Atrial

Escape

Fast

Atrial

Normal

Tachycardia

to

Block

with

QRS

Slow

2nd

Degree

Block
.

Abnormal

Slow

Complete
Block

Heart

Absent

nla

Regular

Normal

Junction

Fast

al

Tachycardia
Junctional

Slow

Escape
Abnormal

Junction

Fast

al

Tachycardia
with

BBB

or

Ventricular

Tachycardia
Irregular

Normal

Atrial

Fibrillation
Abnormal

Atrial

Fibrillation
with

BBB

QRS

Ventricular

absent

Fibrillation
or

standstill
zoos

g-

Abnormalities

wave

atrium

hypertrophy

Peaked

Broad

Abnormalities

tricuspid

e.g.

bifid

of

the

QRS

mitral

e.g.

stenosis

stenosis

Complex

'

Normal

branch

Bundle

block

Muscle

In

abnormal

indicates

In

Height
9

in

muscle

ventricle
4

electrical

in

Right

Best

in

seen

){

is

Deep

Tall

of

Va

by
,

by

in

Vi

left

Vl

,V5 {
axis

wolves
V6

deviation

in

leads

these

but

show

may

are

than

less

Embolism

or

3
4

cares

wave

axis

1)

lead

in

waves

deviation

in

waves

lead

RBBB

Inverted

Vi
Vz
6

tachycardia

Peaked

Right

RVH

many

sinus

Tall

with

in

present

normal

or

wave

wave

septal

to

presents

(S

Inverted
I

deep

only

Vz
-

2mm

Pulmonary

is

25mm

leads

across

although

Hypertrophy
Is

1mm

ECG

wave

wave

than

the

25mm

due

waves

( Vs

abnormal

deviation

Ventricular

ett

depth

accompanied

peaked

in

axis

right

height of

mostly

wave

Usually

exceeds

wave

wave

upright

becomes

than

depolarisation

hypertrophy
complex

)
,

lead

of

height

the

ventricular

activity

ventricular

Left

Vi

than

ventricle

left

less

is

either

in

mass

greater

is

lead

wave

Va

ventricle

wave

the

slow

depolarisation
-

120ms

squares

right

than

greater

no

small

the

syndrome

(3
2

WPW

Duration

ventricle

in

Complex

QRS

depolarisation

Focal

hypertension )

pulmonary

or

'

wave

Width
-

valve

wave

hypertrophy

atrial

the

Right
Left

of

in

waves

lead

spreading

V}

equals

wave

to

less

of

segment

ST

the

in
limb { sl
Elevation
slmm
Abnormalities
acute
myocardial injury

5mm

chest

in

usually

due

infarction

recent

to

or

Depression

ischaemiq

Down

Mll

V,

Vz

or

normally

MH

inferior

an

In

wave

posterior

treatment

digoxin

large

Sloping

ward

note

80ms

indicates

complicating

Anterior

lateral

AVR

vi

Septal

V4

11

Interior

all

Vz

Septal

Vs

Lateral

111

Inferior

AVF

Va

lateral

Abnormalities

of

the

Inferior

Anterior

Vs

wave

pevicaiditis
Inversion

Causes

normality

ischaemig

leads

hypertrophy

BBB

Ml

biphasic

show

treatment

Digoxih

'

waves

initially

upright

then

Infarction

Myocardial
After

sometimes

adjacent

inverted

ventricular

Ml
^

4.
-

If

waves

appear

waves

become

ST

an

returns

is

wave

Ventricular

baseline
not

hr

so

thickness

full
inversion

but

no

does
Waves

not
.

non

cause
.

an

causes

inverted

RVH

causes

inverted

Twqves

Branch

Block

Abnormal

path

repolarisation

of

in

waves

in

left

right

depolarisation

is

ventricle
ventricle

normally

leads
leads

( 1,11

electrical

window

STEMI

Hypertrophy

LVH

Bundle
-

be

24.48

inverted

to

infarction
will

there

elevation

ST

1.

VL

,Vs,V6 )

( Vs )

associated

with

abnormal

path of

Abnormalities

Other

Electrolyte

Abnormalities

Mgt

Mgt
Catt

Chest

of

disappearance

wave

segment

ST

wide

QRS

wave

QT

interval

QT

interval

prolongation
shortens

Pericardia

Non

specific

Coronary

of

the

infarctions

artery

is

triad

this

area

of

cause

can

the

total

the

left

exposed

core

of

partial

or

involve
usually
be
depolarised

cannot
ml

forms

of

surface

the

On

atheromatous

of

rupture

the

by

caused

artery

thrombus

of

conditions

coronary

plaque

occlusion

pain

clinical

within

plaque

Intermittent

Syndromes

spectrum

the

back

in

pain

Muscular

area

radiates

pain

pain

Oesophageal

the

inspiration

on

Acute

for

Angina

worse

dissection

disease

pleuritic

other

had

's

Aortic

Acute

Pneumothorax

wave

:PE
.

Pain

Causes

flattening

wave

Peaked

YCQH

Peaked

kt

flattening
Kt
{

Twave

an

the

as

ischaemia

cells

injury

wall

the

necrotic

are

necrosis

of

but

ventricle

This

of

any

these

may

occur

alone

lschaemiq

Inverted

ischaehnia

in

Vi

V6

alone

is

indicates

the

elevation

of

Pevicarditis

wave

infarct

the

of

persistent

normal

be

inversion

wave

from

inversion

any

Vz

in

Vs

stenosis

coronary

infarct

an

aneurysm
to

of

periphery

can

marked

segment

return

not

descending

ventricular

the

pathological

acuteness

cause

at

inversion

Syndrome

ST

is

angina

cause
wave

anterior

in

considered
's

characteristic

can

leads

Wellen

Injury

supply

wave

limb

the
.

blood

reduced

outward
elevation

ST

baliooning
in

most

of

chest

wall

the

leads

can

does

baseline

produces

ST

elevation

that

may

also

elevate

the

Necrosis

indicates

significant

waves

analysing

when

tissue

dead

0.04

sec

always

waves

AVR

ignore

Posterior

large

or

in

Vz

VG

in

coronary

Vi

.jo#j$ia+eraroinhAn
Inferior
Qin

11,111

AVF

Right

Circumflex

a.

coronary

Anterior

Qin

Vi

Vy

descending
Anterior
branch
blocks

Hemi

often

blocks

Hemi

to

supply
supplies

one

the

both

the

can

result

divisions

posterior
in

while

block

an

diminished
branch

anterior

the

divisions

associated

bundle

left

the

posterior

hemi

of

division

anterior

The

ml

an

coronary

branch

descending

therefore

blood

supplies

either

in

artery

Infarction

Myocardial

diagnosis

two

or

infarction

with

occur

based

made

biochemical

markers

clinical

on

troponin

presentation

ECG

changes

Unstable
-

Angina
depression

ST

normal

to

return

Causes

STEMI
-

ST

limb

leads

If

anterior

NSTEMI
T

wave

may

inversion

at

contiguous

least

elevation

troponinl

pericardia

acute
acute

severe

or

's

heart

failure

myocardial

prevent

formation

aneurysm

presented

in

plasma
PE

acute

leads )

wave

ST

least

at

J2mm

or

ventricular

in

slmm

contiguous pre cordial

treatment
Prompt
damage

elevation

of

persists
should

be

left

sepsis

and

or

renal

failure

false

positive

shock

a.

Pacemakers
Produce

small

bypasses

blocked
of

activation

for

D
2

letter

First

letter

Cardiac

paced

( A

both

SA

node

or

intrinsic

right

the

sense

pace

may

the

atrium

ventricle

right

the

is

used

when

to

A ,V

sensed

rate

the

sensed

response

inhibition
R

chambers

the

or

D)
( A

event

is

modulation

pacing

for

,VorD

I
,

programmable

Arrest

Classified

Shock

is

able

Rhythms

ventricular

non

or

fibrillation

VF

CPR

able

shock

thump

both

In

( VT

synchronised

2
3

200J

unsuccessful

If

unsuccessful

Defribrillate

10

min

If

VF

For

Shock

CPR

or

pulse

1mg

pulse

iv.

360J

PT

less

persists
adrenaline

with
VF

give

amiodarone

give
1mg

Rhythms

Causes

activity

( PEA

iv.

of

bolus

iv.

2g

non

'

shock

able

rhythms

Hypoxia

electrical

300mg

iv

sulphate

magnesium

systole
less

not

360J

adrenaline

shocks

refractory
able

at

of

Further

veto

12

defribrillate
give

7.2

compressions

chest

If

( after

at

Resume

part

thump

shock

One

first

the

does

VF

ensure

Precordial

'

Actions
I

cases

synchronised

tachycardia

ventricular

less

pulse

cordial

pre

able

shock

either

as

treatment

Non

replaces

pacemakers
G

chamber

the

describes

pacemaker

Fourth

ventricles

describes

letter

For

Most

either

letter

Third

atria

describes

duel

Second

bundle

His

the

that

discharge

electrical

Hypovolqemia
Hyperkalaemia

Hypokalaemia
Hypocalcaemia

Hypoglycaemia
Tamponade

Tension

.Toxic
.

Thrombo

pneumothorax
substances
embolism

eg

PE

of

Three

Syndromes
in
relatively
Brugada Syndrome

Key

Easily

asymptomatic

detected

1.

RBBB

with

ST

Susceptible

to

Implantation
2

Wellen

3.

inversion

wave

Ant

in

deadly
with

Vi

,Vz,V3

arrhythmia

ICT

's

neccessavy

Syndrome

elevation

patients

in

Vz

stenosis
descending coronary a.
with
Angioplasty
stenting required
QT
Syndrome
long
QT
interval
longer than 42 of cardiac cycle
ventricular
Predisposed to
arrhythmia 's
.

COPD
Minimises

all

With

so

COPD
there

is

large
ST

right
usually RVHG
the

wave

depression

large

wave

particularly

ventricle

therefore

the

QRS

works

RAD

complexes

against

Embolism

Pulmonary

waves

wave

inversion

in

in

in

lead

11

111

Vi

V4

tendency

towards

RAD

considerable

resistance

For

look

To

What

Rhythm {

1
.

Wave
rhythm

sinus

Abnormalities
Conduction
-

peaked

QRS

predominantly

down

wide

tall

lead

in

deviation

axis

114111

leads

in

deviation

axis

in

ml

Vo

pericarditis

ischemia

in

BBB

WPW

RVH

in

waves

depressed

V,

in

waves

raised

LVH

digoxin

Waves

peaked

flat

hyperkalaemia

in

prolonged

inverted

tall

segment

ST

hypertrophy

origin

ventricular

height
-

hypertrophy

atrial

down

width

predominantly

broad

atrial

QRS

5.

Complex

QRS

Axis

Cardiac
-

tall

notched

BBB

(0.12-0.20)

block

heart

of

evidence

of

evidence

in

in

hypokalaemia

ischaemiq

infarction

LVH

RVH

PE

BBB

Waves
-

hypokalqemiq
Method

nick

Rhythm

1
.

sinus

no

1.

Rate

3.

Axis

PR

5.51

rhythm
waves

Interval

Segment

stable

present )

wave

interval

( AF )