ECG BASICS

By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
[email protected]
From Right to Left
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prof gynae
Dr Bashir associate
professor Medicine
Dr Udaman
neurologist
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ortho
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From RT to Lt
Professor Dr Datuk
rajagopal N
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professor medicine
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gynae
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opthomology
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Prof ortho


ELECTROGRAPHY MADE
EASY


ULTIMATE AIM TO HELP PATIENTS

ECG machine
Limb and chest leads
When an ECG is taken we put 4 limb leads
or electrodes with different colour codes on
upper and lower limbs one each at wrists
and ankles by applying some jelly for close
contact.
We also put six chest leads at specific areas
over the chest
So in reality we see only 10 chest leads.
Position of limb and chest leads

Four limb leads


Six chest leads
V1- 4th intercostal space to the right of sternum
V2- 4th intercostal space to the left of sternum
V3- halfway between V2 and V4
V4- 5th intercostal space in the left mid-clavicular line
V5- 5th intercostal space in the left anterior axillary line
V6- 5th intercostal space in the left mid axillary line

V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
Horizontal plane - the six
chest leads
V6
V6
RA
LA
LV
RV
6.5
Colour codes given by AHA
ECG Paper: Dimensions
5 mm
1 mm
0.1 mV
0.04 sec
0.2 sec
Speed = rate
Voltage
~Mass
ECG paper and timing
ECG paper speed = 25mm/sec
Voltage calibration 1 mV = 1cm

ECG paper - standard calibrations
each small square = 1mm
each large square = 5mm

Timings
1 small square = 0.04sec
1 large square = 0.2sec
25 small squares = 1sec
5 large squares = 1sec

After applying these leads on different
positions then these leads are connected to a
connector and then to ECG machine.
The speed of machine kept usually
25mm/second.calibration or standardization
done while machine is switched on.
ECG paper
5 Large squares = 1 second
Time
1 Large square = 0.2 second 1 Small square = 0.04 second
2 Large squares = 1 cm
6.1
The first step while reading ECG is to look
for standardization is properly done.
Look for this mark and see that this mark
exactly covers two big squares on graph.
STANDARDISATION ECG
amplitude scale
Normal amplitude
10 mm/mV
Half amplitude
5 mm/mV
Double amplitude
20 mm/mV
ECG WAVES
You will see then base line or isoelectric
line that is in line with P-Q interval and
beginning of S-T segment.
From this line first positive deflection will
arise as P wave then other waves as shown
in next slide.
Small negative deflections Q wave and S
wave also arise from this line.
ECG WAVES
The Normal ECG
Normal Intervals:
PR 0.12-0.20s
QRS duration <0.12s
QTc 0.33-0.43s
Simplified normal Position of
leads on ECG graph
Lead 1# upward PQRS
Lead 2# upward PQRS
Lead 3# upward PQRS
Lead AVR#downward or negative PQRS
Lead AVL# upward PQRS
Lead AVF# upwards PQRS

Simplified normal Position of
leads on ECG graph
Chest lead V1# negative or downward
PQRS
Chest leads V2-V3-V4-V5-V6 all are
upright from base line .The R wave slowly
increasing in height from V1 to V6.
So in normal ECG you see only AVR and
V1 as negative or downward defelections as
shown in next slide.
Slide 13
Normal ECG
NSR
P-wave
Normal P wave length from beginning of P
wave to end of P wave is 2 and a half small
square.
Height of P wave from base line or
isoelectric line is also 2 and a half small
square.
P-wave
Normal values
1. up in all leads except
AVR.
2. Duration.
< 2.5 mm.
3. Amplitude.
< 2.5 mm.


Abnormalities
1. Inverted P-wave
Junctional rhythm.
2. Wide P-wave (P- mitrale)
LAE
3. Peaked P-wave (P-pulmonale)
RAE
4. Saw-tooth appearance
Atrial flutter
5. Absent normal P wave
Atrial fibrillation
Slide 9
P wave height 2 and half small
squares ,width also 2 and half
small square
Shape of P wave
The upward limb and downward limbs of P
wave are equal.
Summit or apex of P wave is slightly
rounded.

P pulmonale & P mitrale
P pulmonale-Summit or apex of P wave
becomes arrow like pointed or pyramid
shape,the height also becomes more than
two small squares from base line.
P waves best seen in lead 2 and V1.

P pulmonale & P mitrale
P mitrale- the apex or summit of p wave
may become notched .the notch should be at
least more than one small square.
Duration of P becomes more than two and a
half small squares.
Slide 14
Slide 16
Left Atrial Enlargement
Criteria

P wave duration in II >than 2
and half small squares with
notched p wave
or
Negative component of
biphasic P wave in V
1
1
small box in area
Right Atrial Enlargement
Criteria


P wave height in II >2 and
half small squares and are
also tall and peaked.
or

Positive component of
biphasic P wave in V
1
> 1
small box in area
Slide 15
Atrial fibrillation
P waves thrown into number of small
abnormal P waves before each QRS
complex
The duration of R-R interval varies
The amplitude of R-R varies
Abnormal P waves dont resemble one
another.
Slide 41
Atrial flutter
The P waves thrown into number of
abnormal P waves before each QRS
complex.
But these abnormal P waves almost
resemble one another and are more
prominent like saw tooth appearance.
Slide 40
Junctional rhythm
In Junctional rhythm the P waves may be
absent or inverted.in next slide u can see
these inverted P waves.
Slide 43
Paroxysmal atrial tachycardia
The P and T waves you cant make out
separately
The P and T waves are merged in one
The R-R intervals do not vary but remain
constant and same.
The heart rate being very high around 150
and higher.
Slide 39
NORMAL P-R INTERVAL

PR interval time 0.12 seconds to 0.2
seconds.

That is three small squares to five small
squares.

PR interval
Definition: the time
interval between
beginning of P-wave
to beginning of QRS
complex.
Normal PR interval
3-5mm or 3-5 small
squares on ECG graph
(0.12-0.2 sec)
Abnormalities
1. Short PR interval
WPW syndrome
2. Long PR interval
First degree heart
block

Short P-R interval
Short P-R interval seen in WPW syndrome or pre-
excitation syndrome or LG syndrome
P-R interval is less than three small squares.
The beginning of R wave slopes gradually up and
is slightly widened called Delta wave.
There may be S-T changes also like ST depression
and T wave inversion.

Slide 17
Lengthening of P-R interval
Occurs in first degree heart block.
The P-R interval is more than 5 small
squares or > than 0.2 seconds.
This you will see in all leads and is same
fixed lengthening .
Slide 44
Q WAVES
Q waves <0.04 second.
Thats is less than one small square
duration.
Height <25% or <
1
/
4
of R wave height.

Normal Q wave
Abnormal Q waves
The duration or width of Q waves becomes
more than one small square on ECG graph.
The depth of Q wave becomes more than
25% of R wave.
The above changes comprise pathological Q
wave and happens commonly in myocardial
infarction and septal hypertrophy.
Q wave in MI
Q wave in septal hypertrophy


QRS COMPLEX
QRS duration <0.11 s
That is less than almost three small squares
Some books write 2 and a half small
squares.
Height of R wave is (V1-V6) >8 mm some
say >10 mm chest leads (in at least one of
chest leads).
QRS complex
Normal values
Duration: < 2.5 mm.
Morphology: progression
from Short R and deep S
(r/s) in V1 to tall R and
short S in V6 with small Q
in V5-6.
Abnormalities:
1. Wide QRS complex
Bundle branch block.
Ventricular rhythm.

2. Tall R in V1
RVH.
RBBB.
Posterior MI.
WPW syndrome.
3. abnormal Q wave
[ > 25% of R wave]
MI.
Hypertrophic
cardiomyopathy.
Normal variant.


Small voltage QRS
Defined as < 5 mm peak-to-peak in all limb
leads or <10 mm in precordial chest leads.
causes pulmonary disease,
hypothyroidism, obesity, cardiomyopathy.
Acute causes pleural and/or pericardial
effusions
Normal upward progression of
R wave from V1 to V6
V
1

V
2

V
3

V
4

V
5

V
6

The R wave in the precordial leads must grow from V1 to at
least V4
J point
The term J point means Junctional point at
the end of S wave between S wave and
beginning of S-T segment.
J point
Q
S
ST
L V H-Voltage Criteria
In adult with normal chest wall
SV1+RV5 >35 mm
or
SV1 >20 mm
or
RV6 >20 mm

Left ventricular
hypertrophy-Voltage
Criteria

Count small squares of downward R wave
in V1 plus small squares of R wave in V5 .
If it comes to more than 35 small squares
then it is suggestive of LVH.
LEFT VENTRICULAR
HYPERTROPHY
Right ventricular hypertrophy
Normally you see R wave is downward
deflection in V1.but if you see upward R
wave in V1 then it is suggestive of RVH
etc.
Dominant or upward R wave
in V1

Causes
RBBB
Chronic lung disease, PE
Posterior MI
WPW Type A
Dextrocardia
Duchenne muscular dystrophy
Right Ventricular Hypertrophy
WILL SHOW AS
Right axis deviation (RAD)
Precordial leads
In V1, R wave > S wave
In V6, S wave > R wave
Usual manifestation is pulmonary disease or
congenital heart disease


Right Ventricular Hypertrophy

Right ventricular hypertrophy
Right ventricular hypertrophy (RVH)
increases the height of the R wave in V1.
And R wave in V1 greater than 7 boxes in
height, or larger than the S wave, is
suspicious for RVH. Other findings are
necessary to confirm the ECG diagnosis.
Right Ventricular Hypertrophy
Other findings in RVH include right axis
deviation, taller R waves in the right
precordial leads (V1-V3), and deeper S
waves in the left precordial (V4-V6). The T
wave is inverted in V1 (and often in V2).

Right Ventricular Hypertrophy
True posterior infarction may also cause a
tall R wave in V1, but the T wave is usually
upright, and there is usually some evidence
of inferior infarction (ST-T changes or Qs
in II, III, and F).

Right Ventricular Hypertrophy
A large R wave in V1, when not
accompanied by evidence of infarction, nor
by evidence of RVH (right axis, inverted T
wave in V1), may be benign counter-
clockwise rotation of the heart. This can be
seen with abnormal chest shape.
Right Ventricular Hypertrophy
Tall R wave in V
1

Right axis deviation
Right atrial enlargement
Down sloping ST depressions in V
1
-V
3
( RV strain
pattern)

Although there is no widely accepted criteria for
detecting the presence of RVH, any combination of
the following EKG features is suggestive of its
presence:
Right Ventricular Hypertrophy
Left Ventricular Hypertrophy
Left Ventricular Hypertrophy
ECG criteria for RBBB

(1) QRS duration exceeds 0.12 seconds or
2 and half small squares roughly in V1 and
may also see it in V2.
(2) RSR complex in V1 may extend to V2.

ECG criteria for RBBB
ST/T must be opposite in direction to the terminal
QRS(is secondary to the block and does not mean
primary ST/T changes).

It you meet all above criteria it is then complete
right bundle branch block.
In incomplete bundle branch block the duration of
QRS will be within normal limits.

RBBB & MI
If abnormal Q waves are present they will
not be masked by the RBBB pattern.
This is because there is no alteration of the
initial part of the complex RS (in V1) and
abnormal Q waves can still be seen.
Significance of RBBB
RBBB is seen in :-
(1) occasional normal subjects
(2) pulmonary embolus
(3) coronary artery disease
(4) ASD
(5) active Carditis
(6) RV diastolic overload
Partial / Incomplete RBBB
is diagnosed when the pattern of RBBB is
present but the duration of the QRS does
not exceed 0.12 seconds or roughly 2 and a
half small squares.
In next slide you will see
ECG characteristics of a typical RBBB
showing wide QRS complexes with a
terminal R wave in lead V1 and slurred S
wave in lead V6.
Also you see R wave has become upright in
V1.QRS duration has also increased making
it complete RBBB.


ECG criteria for LBBB
(1)Prolonged QRS complexes, greater than 0.12
seconds or roughly 2 and half small squares in all
leads almost.
(2)Wide, notched QRS (M shaped) V5, V6
(3)Wide, notched QS complexes are seen in V1
(due to spread of activation away from the
electrode through septum + LV)
(4)In V2, V3 small r wave may be seen due to
activation of para septal region
ECG criteria for LBBB
So look in all leads for QRS duration to
make it complete LBBB or incomplete
LBBB as u did in RBBB.
Look in V5 and V6 for M shaped pattern at
summit or apex of R wave.
Look for any changes as S-T depression and
T wave in inversion if any.
Significance of LBBB
LBBB is seen in :-
(1) Always indicative of organic heart disease
(2) Found in ischemic heart disease
(3) Found in hypertension.
MI should not be diagnosed in the presence of
LBBB Q waves are masked by LBBB pattern
Cannot diagnose the presence of MI with LBBB
Partial / Incomplete LBBB
is diagnosed when the pattern of LBBB is
present but the duration of the QRS does
not exceed 0.12 seconds or roughly 2 and
half small squares.


NORMAL ST- SEGMENT

it's isoelectric.
[i.e. at same level of PR
or PQ segment at least
in the beginning]

NORMAL CONCAVITY OF S-T
SEGMENT
It then gradually slopes upwards making
concavity upwards and not going more
than one small square upwards from
isoelectric line or one small square below
isoelectric line.
In MI this concavity may get lost and
become convex upwards called coving of
S-T segment.

Abnormalities
1. ST elevation:
More than one small
square
Acute MI.
Prinzmetal angina.
Acute pericarditis.
Early repolarization
ST depression:
More than one small
square
Ischemia.
Ventricular strain.
BBB.
Hypokalemia.
Digoxin effect.

Slide 11
Slide 12
Stress test ECG note the ST Depression

Note the arrows pointing ST
depression
ST depression & Troponin T
positive is NON STEMI
Coving of S-T segment
Concavity lost and convexity appear facing
upwards.
Diagnostic criteria for AMI
Q wave duration of more than
0.04 seconds
Q wave depth of more than 25%
of ensuing r wave
ST elevation in leads facing
infarct (or depression in opposite
leads)
Deep T wave inversion overlying
and adjacent to infarct
Cardiac arrhythmias


Abnormalities of ST- segment
Q waves in myocardial
infarction


T-wave
Normal values.
1.amplitude:

< 10mm in the chest leads.

Abnormalities:

1. Peaked T-wave:
Hyper-acute MI.
Hyperkalemia.
Normal variant
.
2. T- inversion:


Ischemia.
Myocardial infarction.
Myocarditis
Ventricular strain
BBB.
Hypokalemia.
Digoxin effect.
QT- interval

Definition: Time interval between beginning of
QRS complex to the end of T wave.
Normally: At normal HR: QT 11mm (0.44 sec)

Abnormalities:
1. Prolonged QT interval: hypocalcemia and
congenital long QT syndrome.
2. Short QT interval: hypercalcemia.
QT Interval
- Should be < 1/2 preceding R to
R interval -
QT Interval
- Should be < 1/2 preceding R to
R interval -
QT interval
QT Interval
- Should be < 1/2 preceding R to
R interval -
QT interval
QT Interval
- Should be < 1/2 preceding R to
R interval -
R R
QT interval
QT Interval
- Should be < 1/2 preceding R to
R interval -
R R
QT interval
QT Interval
- Should be < 1/2 preceding R to
R interval -
R R
QT interval
QT Interval
- Should be < 1/2 preceding R to
R interval -
R R
QT interval
65 - 90 bpm
QT Interval
- Should be < 1/2 preceding R to
R interval -
R R
QT interval
65 - 90 bpm
Normal QT
c
= 0.46 sec
Atrioventricular (AV) Heart
Block

Classification of AV Heart
Blocks
Degree AV Conduction Pattern
1
St
Degree Block
Uniformly prolonged PR
interval
2
nd
Degree, Mobitz Type I
Progressive PR interval
prolongation
2
nd
Degree, Mobitz Type II Sudden conduction failure
3
rd
Degree Block No AV conduction
AV Blocks
First Degree
Prolonged AV conduction time
PR interval > 0.20 seconds




1
st
Degree AV Block
Prolongation of the PR interval, which is constant
All P waves are conducted
1st degree AV Block:

Regular Rhythm
PRI > .20 seconds or 5 small squares and is CONSTANT
Usually does not require treatment
PRI > .20 seconds
First Degree Block
prolonged PR interval

Analyze the Rhythm
AV Blocks
Second Degree
Definition
More Ps than QRSs
Every QRS caused by a P


Second-Degree AV Block

There is intermittent failure of the supraventricular
impulse to be conducted to the ventricles

Some of the P waves are not followed by a QRS
complex.The conduction ratio (P/QRS ratio) may
be set at 2:1,3:1,3:2,4:3,and so forth


Second Degree

Types
Type I
Wenckebach phenomenon

Type II
Fixed or Classical

Type I Second-Degree AV
Block: Wenckebach
Phenomenon

ECG findings
1.Progressive lengthening of the PR
interval until a P wave is blocked

Pattern Repeats.
PRI = .24 sec PRI = .36 sec PRI = .40 sec
QRS is
dropped

Irregular Rhythm
PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse)
PRI is NOT CONSTANT

Pause
4:3 Wenckebach (conduction ratio may not be constant)
2nd degree AV Block (Mobitz I also called Wenckebach):
Type II Second-Degree AV
Block:
Mobitz Type II
ECG findings

1.Intermittent or unexpected blocked P waves
you dont know when QRS drops
2.P-R intervals may be normal or prolonged,but
they remain constant
4. A long rhythm strip may help
Second Degree AV Block
Mobitz type I or Winckebach
Mobitz type II

Type 1
(Wenckebach)
Progressive prolongation of the PR interval until a P
wave is not conducted.

Constant PR interval with unexpected intermittent failure to conduct
Type 2
Mobitz Type I
MOBITZ TYPE 1
2nd degree AV Block (Mobitz II):
Irregular Rhythm
QRS complexes may be somewhat wide (greater than .12 seconds)
Non-conducted sinus impulses appear at unexpected irregular intervals
PRI may be normal or prolonged but is CONSTANT and fixed
Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart
block (3rd degree block)
Its appearance in the setting of an acute MI identifies a high risk patient
Cause: anterioseptal MI,
Treatment: may require pacemaker in the case of fibrotic conduction system
Non-conducted
sinus impulses
2:1 block 3:1 block
PRI is CONSTANT
Analyze the Rhythm
Second Degree Mobitz

Characteristics
Atrial rate > Ventricular rate
QRS usually longer than 0.12 sec
Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)
Analyze the Rhythm
Mobitz II
Definition: Mobitz II is characterized by 2-4 P
waves before each QRS. The PR pf the
conducted P wave will be constant for each QRS
. EKG Characteristics:Atrial and ventricular rate
is irregular. P Wave: Present in two, three or four
to one conduction with the QRS. PR Interval
constant for each P wave prior to the QRS. QRS
may or may not be within normal limits.
Mobitz Type II
Mobitz Type II
Sudden appearance of a single, non-
conducted sinus P wave...
Advanced Second-Degree
AV Block
Two or more consecutive nonconducted sinus P
waves
Complete AV Block

Characteristics
Atrioventricular dissociation
Regular P-P and R-R but without association
between the two
Atrial rate > Ventricular rate
QRS > 0.12 sec

3
rd
Degree (Complete) AV Block
EKG Characteristics: No relationship between P waves and QRS complexes
Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes
Complete heart block
P waves are not conducted to the ventricles
because of block at the AV node. The P
waves are indicated below and show no
relation to the QRS complexes. They 'probe'
every part of the ventricular cycle but are
never conducted.

3rd degree AV Block (Complete Heart Block):
Irregular Rhythm
QRS complexes may be narrow or broad depending on the level of the block
Atria and ventricles beat independent of one another (AV dissociation)
QRSs have their own rhythm, P-waves have their own rhythm
May be caused by inferior MI and its presence worsens the prognosis
Treatment: usually requires pacemaker
QRS intervals
P-wave intervals note how the P-waves sometimes distort QRS
complexes or T-waves
Third-Degree (Complete) AV
Block
Third-Degree (Complete) AV
Block

The P wave bears no relation to the
QRS complexes, and the PR intervals
are completely variable


30 AV Block
AV dissociation
atria and ventricles beating on their own
no relation between Ps & QRSs
Atrial rate is different from ventricular
ventricular rate: 30-60 bpm
Rhythm is regular for both
QRS can be narrow or wide
depends on site of pacemaker!

Key points
Wenckebach
look for group beating & changing PR
Mobitz II
look for reg. atrial rhythm & consistent PR
3o block
atrial & ventricular rhythm regular
rate is different!!!
no consistent PR

Left Anterior Fascicular Block
Left axis deviation , usually -45 to -90 degrees

QRS duration usually <0.12s unless coexisting RBBB

Poor R wave progression in leads V1-V3 and deeper S
waves in leads V5 and V6

There is RS pattern with R wave in lead II > lead III
S wave in lead III > lead II

QR pattern in lead I and AVL,with small Q wave
No other causes of left axis deviation

Left Anterior Hemiblock (LAHB):
1. Left axis deviation (> -30 degrees) will be noted
and there will be a prominent S-wave in Leads
II, and III
LPIF
LASF
LBB
1.
2.
Lead III
Lead I
Lead AVF
Left Posterior Fascicular Block

Right axis deviation
QR pattern in inferior leads (II,III,AVF)
small q wave
RS patter in lead lead I and AVL(small R
with deep S)

Left Posterior Hemiblock (LPHB):
1. Right axis deviation and there will be a prominent
S-wave in Leads I. Q-waves may be noted in III
and AVF.
Notes on (LPHB):
QRS is normal width unless BBB is present
If LPHB occurs in the setting of an acute MI,
it is almost always accompanied by RBBB
and carries a mortality rate of 71%
LPIF
LASF
LBB
1.
2.
Lead III
Lead I
Lead AVF
Bifascicular Bundle Branch
Block
RBBB with either left anterior or left posterior
fascicular block
Diagnostic criteria
1.Prolongation of the QRS duration to 0.12 second
or longer
2.RSR pattern in lead V1,with the R being broad
and slurred
3.Wide,slurred S wave in leads I,V5 and V6
4.Left axis or right axis deviation

Trifascicular Block

The combination of RBBB, LAFB and long
PR interval

Implies that conduction is delayed in the
third fascicle
Indications For Implantation of
Permanent Pacing in Acquired AV
Blocks

1.Third-degree AV block, Bradycardia with symptoms
Asystole
e.Neuromuscular diseases with AV block (Myotonic
muscular dystrophy)
2.Second-degree AV block with symptomatic bradycardia
Cardiac Pacemakers
Definition
Delivers artificial stimulus to heart
Causes depolarization and contraction
Uses
Bradyarrhythmias
Asystole
Tachyarrhythmias (overdrive pacing)
Cardiac Pacemakers
Types
Fixed
Fires at constant rate
Can discharge on T-wave
Very rare
Demand
Senses patients rhythm
Fires only if no activity sensed after preset interval (escape
interval)
Transcutaneous vs Transvenous vs Implanted
Cardiac Pacemakers
Cardiac Pacemakers
Demand Pacemaker Types
Ventricular
Fires ventricles
Atrial
Fires atria
Atria fire ventricles
Requires intact AV conduction
Cardiac Pacemakers
Demand Pacemaker Types
Atrial Synchronous
Senses atria
Fires ventricles
AV Sequential
Two electrodes
Fires atria/ventricles in sequence

Cardiac Pacemakers
Problems
Failure to capture
No response to pacemaker artifact
Bradycardia may result
Cause: high threshold
Management
Increase amps on temporary pacemaker
Treat as symptomatic bradycardia

Cardiac Pacemakers
Problems
Failure to sense
Spike follows QRS within escape interval
May cause R-on-T phenomenon
Management
Increase sensitivity
Attempt to override permanent pacer with temporary
Be prepared to manage VF
Implanted Defibrillators
AICD
Automated
Implanted Cardio-
Defibrillator
Uses
Tachyarrhythmias
Malignant
arrhythmias
VT
VF
Implanted Defibrillators
Programmed at insertion to deliver predetermined
therapies with a set order and number of therapies
including:
pacing
overdrive pacing
cardioversion with increasing energies
defibrillation with increasing energies
standby mode
Effect of standby mode on Paramedic treatments
Implanted Defibrillators
Potential Complications
Fails to deliver therapies as intended
worst complication
requires Paramedic intervention
Delivers therapies when NOT appropriate
broken or malfunctioning lead
parameters for delivery are not specific enough
Continues to deliver shocks
parameters for delivery are not specific enough and device
senses a reset
may be shut off (not standby mode) with donut-magnet
Sinus Exit Block
Due to abnormal function of SA node
MI, drugs, hypoxia, vagal tone
Impulse blocked from leaving SA node
usually transient
Produces 1 missed cycle
can confuse with sinus pause or arrest
Sinus block
ARRTHYMIAS AND
ECTOPIC BEATS

normal ("sinus") beats
sinus node doesn't fire leading
to a period of asystole (sick
sinus syndrome)
p-wave has different shape
indicating it did not originate in
the sinus node, but somewhere
in the atria. It is therefore called
an "atrial" beat
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
Atrial Escape Beat
Recognizing and Naming Beats & Rhythms
there is no p wave, indicating that it did
not originate anywhere in the atria, but
since the QRS complex is still thin and
normal looking, we can conclude that the
beat originated somewhere near the AV
junction. The beat is therefore called a
"junctional" or a nodal beat
Junctional Escape Beat
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
Recognizing and Naming Beats & Rhythms
actually a "retrograde p-wave may sometimes be
seen on the right hand side of beats that
originate in the ventricles, indicating that
depolarization has spread back up through the
atria from the ventricles
QRS is wide and much different ("bizarre") looking
than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
consequently, conduction through the ventricles did
not take place through normal pathways. It is
therefore called a ventricular beat
Ventricular
Escape Beat
there is no p wave, indicating that the beat
did not originate anywhere in the atria
Recognizing and Naming Beats & Rhythms
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
The Re-Entry Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
Tissues with these type of circuits may exist:
in microscopic size in the SA node, AV node, or any type of heart tissue
in a macroscopic structure such as an accessory pathway in WPW
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
1. An arrhythmia is triggered by a premature beat
2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway
only
Repolarizing Tissue
(long refractory period)
The Re-Entry Mechanism of Ectopic Beats & Rhythms
3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
The Re-Entry Mechanism of Ectopic Beats & Rhythms
4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation re-enters the pathway and continues in a
circular movement. This creates the re-entry circuit

Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
The Re-Entry Mechanism of Ectopic Beats & Rhythms
Recognizing and Naming Beats & Rhythms
Premature Ventricular Contractions (PVCs, VPBs, extrasystoles):
A ventricular ectopic focus discharges causing an early beat
Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre"
QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
PVCs are sometimes described by lay people as skipped heart beats
Multifocal
PVC's
Compensatory pause
after the occurance of a PVC
R on T
phenomemon
Recognizing and Naming Beats & Rhythms
Characteristics of PVC's
PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave)
T-waves for PVCs are usually large and opposite in polarity to terminal QRS
Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle
Every other beat being a PVC (bigeminy) may indicate coronary artery disease
Some PVCs come between 2 normal sinus beats and are called interpolated PVCs
Interpolated PVC note the sinus
rhythm is undisturbed
The classic PVC note the
compensatory pause
PVC's are Dangerous When:
They are frequent (> 30% of complexes) or are increasing in frequency
The come close to or on top of a preceding T-wave (R on T)
Three or more PVC's in a row (run of V-tach)
Any PVC in the setting of an acute MI
PVC's come from different foci ("multifocal" or "multiformed")

These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:
Ventricular Tachycardia
Ventricular Fibrillation
Recognizing and Naming Beats & Rhythms
sinus beats
Unconverted V-tach r V-fib
V-tach
R on T phenomenon
time
The sooner defibrillation takes place,
the increased likelihood of survival
Recognizing and Naming Beats & Rhythms
Notes on V-tach:
Causes of V-tach
Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
Typical V-tach patient
MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
V-tach complexes are likely to be similar and the rhythm regular
Irregular V-Tach rhythms may be due to to:
breakthrough of atrial conduction
atria may capture the entire beat beat
an atrial beat may merge with an ectopic ventricular beat (fusion beat)
Fusion beat - note p-
wave in front of PVC and
the PVC is narrower than
the other PVCs this
indicates the beat is a
product of both the sinus
node and an ectopic
ventricular focus
Capture beat - note that
the complex is narrow
enough to suggest normal
ventricular conduction.
This indicates that an
atrial impulse has made it
through and conduction
through the ventricles is
relatively normal.
Recognizing and Naming Beats & Rhythms
Premature Atrial Contractions (PACs):
An ectopic focus in the atria discharges causing an early beat
The P-wave of the PAC will not look like a normal sinus P-wave (different morphology)
QRS is narrow and normal looking because ventricular depolarization is normal
PACs may not activate the myocardium if it is still refractory (non-conducted PACs)
PACs may be benign: caused by stress, alcohol, caffeine, and tobacco
PACs may also be caused by ischemia, acute MIs, d electrolytes, atrial hypertrophy
PACs may also precede PSVT
PAC
Non conducted PAC Non conducted PAC
distorting a T-wave
Premature Junctional Contractions (PJCs):
An ectopic focus in or around the AV junction discharges causing an early beat
The beat has no P-wave
QRS is narrow and normal looking because ventricular depolarization is normal
PJCs are usually benign and require not treatment unless they initiate a more serious rhythm

Recognizing and Naming Beats & Rhythms
PJC
Recognizing and Naming Beats & Rhythms
Multifocal Atrial Tachycardia (MAT):
Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles
QRS complexes are almost identical to the sinus beats
Rate is usually between 100 and 200 beats per minute
The rhythm is always IRREGULAR
P-waves of different morphologies (shapes) may be seen if the rhythm is slow
If the rate < 100 bpm, the rhythm may be referred to as wandering pacemaker
Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF
Treatments: Ca
++
channel blockers, b blockers, potassium, magnesium, supportive therapy for
underlying causes mentioned above (antiarrhythmic drugs are often ineffective)
Note IRREGULAR
rhythm in the tachycardia
Note different P-wave
morphologies when the
tachycardia begins
Recognizing and Naming Beats & Rhythms
Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT):
A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted
normally to the ventricles (usually initiated by a PAC)
QRS complexes are almost identical to the sinus beats
Rate is usually between 150 and 250 beats per minute
The rhythm is always REGULAR
Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q)
Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter
May be terminated by carotid massage
u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction
Treatment: ablation of focus, Adenosine (d AV conduction), Ca
++
Channel blockers
Note REGULAR rhythm
in the tachycardia
Rhythm usually begins
with PAC
Sinus arrest or exit block
PAC
J unctional Premature Beat
single ectopic beat that originates in the AV node
or
Bundle of His area of the condunction system
Retrograde P waves immediately preceding the
QRS

Retrograde P waves immediately following the
QRS
Absent P waves (buried in the QRS)
Junctional Escape Beat
Junctional Rhythm
Rate: 40 to 60 beats/minute (atrial and ventricular)
Rhythm: regular atrial and ventricular rhythm
P wave: usually inverted, may be upright; may
precede,
follow or be hidden in the QRS complex; may
be absent
PR interval: not measurable or less than .20 sec.
Junctional Rhythm
MaligMalignant PVC
patterns
Frequent PVCs
Multiform PVCs
Runs of consecutive PVCs
R on T phenomenon PVC that falls on a T
wave
PVC during acute MI
Types of PVCs
Uniform
Multiform
PVC rhythm patterns
Bigeminy PVC occurs every other
complex
Couplets 2 PVCs in a row
Trigeminy Two PVCs for every three
complexes
Junctional Escape Rhythm
Ventricular tachycardia
(VTach)

3 or more PVCs in a row at a rate of 120 to
200 bts/min-1
Ventricular fibrillation (VFib)
No visible P or QRS complexes. Waves
appear as fibrillating waves
Torsades de Pointes
Type of VT known as twisting of the
points.
Usually seen in those with prolonged QT
intervals caused by

Why 1500 / X?
Paper Speed: 25 mm/ sec
60 seconds / minute
60 X 25 = 1500 mm / minute

Take 6 sec strip (30 large boxes)
Count the P/R waves X 10


OR
Atrial Fibrillation:
Regular Irregular
Premature Beats: PVC
Widened QRS, not associated with
preceding P wave
Usually does not disrupt P-wave
regularity
T wave is inverted after PVC
Followed by compensatory
ventricular pause
Notice a Pattern in the PVCs?
Identifying AV Blocks:
1: P = R > .20
Regular
2:Mobitz
I
P > R
Progressive Irregular
2:Mobitz
II
P > R
Constant Regular
3: P > R
Grossly
Irregular
Regular
(20-40 bpm)
Name Conduction PR-Int R-R Rhythm
Most Important Questions
of Arrhythmias
What is the mechanism?
Problems in impulse formation?
(automaticity or ectopic foci)
Problems in impulse
conductivity? (block or re-entry)
Where is the origin?
Atria, Junction, Ventricles?
QRS Axis
Check Leads:


1 and AVF
Interpreting Axis
Deviation:
Normal Electrical Axis:
(Lead I + / aVF +)
Left Axis Deviation:
Lead I + / aVF
Pregnancy, LV hypertrophy etc
Right Axis Deviation:
Lead I - / aVF +
Emphysema, RV hypertrophy etc.


NW Axis (No Mans Land)
Both I and aVF are
Check to see if leads are
transposed (- vs +)
Indicates:
Emphysema
Hyperkalemia
VTach
Determining Regions of
CAD: ST-changes in leads
RCA: Inferior myocardium
II, III, aVF
LCA: Lateral myocardium
I, aVL, V5, V6
LAD: Anterior/Septal
myocardium
V1-V4
Regions of the
Myocardium:
Inferior
II, III, aVF
Lateral
I, AVL,
V5-V6
Anterior /
Septal
V1-V4
Sinus Arrhythmia
Sinus Arrest/Pause
Sinoatrial Exit Block
Premature Atrial Complexes
(PACs)
Wandering Atrial Pacemaker
(WAP)
Supraventricular Tachycardia
(SVT)
Wolff-Parkinson-White
Syndrome (WPW)
Atrial Flutter
Atrial Fibrillation
(A-fib)
Premature Junctional
Complexes (PJC)
Junctional Rhythm
Junctional Rhythm
Accelerated Junctional Rhythm
Junctional Tachycardia
Premature Ventricular
Complexes (PVC's)
Note Complexes not
Contractions
PVCs

Uniformed/Multiformed

Couplets/Salvos/Runs

Bigeminy/Trigeminy/Quadrageminy
Uniformed PVCs
R on T Phenomena
Multiformed PVCs
PVC Couplets
PVC Salvos and Runs
Bigeminy PVCs
Trigeminy PVCs
Quadrageminy PVCs
Ventricular Escape Beats
Idioventricular Rhythm
Ventricular Tachycardia (VT)
Rate: 101-250 beats/min
Rhythm: regular
P waves: absent
PR interval: none
QRS duration: > 0.12 sec. often difficult to
differentiate between QRS and T wave
Note: Monomorphic - same shape
and amplitude
Ventricular Tachycardia (VT)
V Tach
Torsades de Pointes (TdeP)
Rate: 150-300 beats/min
Rhythm: regular or irregular
P waves: none
PR interval: none
QRS duration: > 0.12 sec. gradual alteration
in amplitude and direction of the QRS
complexes
Torsades de Pointes (TdeP)
Ventricular Fibrillation (VF)
Rate: CNO as no discernible complexes
Rhythm: rapid and chaotic
P waves: none
PR interval: none
QRS duration: none
Note: Fine vs. coarse?
Ventricular Fibrillation (VF)
Ventricular Fibrillation (VF)
Asystole
(Cardiac Standstill)
Rate: none
Rhythm: none
P waves: none
PR interval: not measurable
QRS duration: absent
Asystole
(Cardiac Standstill)
Asystole
The Mother of all Bradycardias
Atrial Pacemaker
(Single Chamber)
pacemaker
Capture?
Ventricular Pacemaker
(Single Chamber)
pacemaker
Dual Paced Rhythm
pacemaker
Pulseless Electrical Activity
(PEA)
The absence of a detectable pulse and blood
pressure

Presence of electrical activity of the heart as
evidenced by ECG rhythm, but not VF or VT

= 0/0 mmHg
+
ventricular bigeminy
The ECG trace below shows
ventricular bigeminy, in which
every other beat is a ventricular
ectopic beat. These beats are
premature, wider, and larger than
the sinus beats.


ventricular bigeminy

ventricular trigeminy;
The occurrence of more than one
type of ventricular ectopic impulse
morphology is evidence of
multifocal ventricular ectopics. In
this example, the ventricular
ectopic beats are both wide and
premature, but differ considerably
in shape

ventricular trigeminy

ventricular trigeminy

MYOCARDIAL
INFARACTION

Diagnosing a MI
To diagnose a myocardial infarction you need
to go beyond looking at a rhythm strip and
obtain a 12-Lead ECG.
Rhythm
Strip
12-Lead
ECG
ST Elevation
One way to
diagnose an
acute MI is to
look for
elevation of the
ST segment.

ST Elevation (cont)
Elevation of the ST
segment (greater
than 1 small box)
in 2 leads is
consistent with a
myocardial
infarction.

Anterior Myocardial Infarction
If you see changes in leads V
1
- V
4
that
are consistent with a myocardial
infarction, you can conclude that it is an
anterior wall myocardial infarction.
Putting it all Together
Do you think this person is having a myocardial
infarction. If so, where?
Interpretation
Yes, this person is having an acute anterior wall
myocardial infarction.
Putting it all Together
Now, where do you think this person is having
a myocardial infarction?
Inferior Wall MI
This is an inferior MI. Note the ST elevation in
leads II, III and aVF.
Putting it all Together
How about now?
Anterolateral MI
This persons MI involves both the anterior wall (V
2
-
V
4
) and the lateral wall (V
5
-V
6
, I, and aVL)!
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
The ST segment should start isoelectric except in V1
and V2 where it may be elevated
Characteristic changes in AMI
ST segment elevation over area of damage
ST depression in leads opposite infarction
Pathological Q waves
Reduced R waves
Inverted T waves
ST elevation hyperacute
phase
R
P
Q
ST
Occurs in the early stages
Occurs in the leads facing
the infarction
Slight ST elevation may be
normal in V
1
or V
2

Deep Q wave
R
P
Q
T
ST
Only diagnostic change of
myocardial infarction
At least 0.04 seconds in
duration
Depth of more than 25% of
ensuing R wave
T wave changes
R
P
Q
T
ST
Late change
Occurs as ST elevation
is returning to normal
Apparent in many leads
Bundle branch block
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Anterior wall MI
Left bundle branch block
Sequence of changes in
evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI



Q
R
P
Q
T
ST
R
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
T
ST
R
P
Q
T
Anterior infarction
Anterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left
coronary
artery
Inferior infarction
Inferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right
coronary
artery

Lateral infarction
Lateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left
circumflex
coronary
artery
Diagnostic criteria for AMI
Q wave duration of more than
0.04 seconds
Q wave depth of more than 25%
of ensuing r wave
ST elevation in leads facing
infarct (or depression in opposite
leads)
Deep T wave inversion overlying
and adjacent to infarct
Cardiac arrhythmias


Surfaces of the Left Ventricle
Inferior - underneath

Anterior - front

Lateral - left side

Posterior - back
Inferior Surface
Leads II, III and avF look UP from below to the inferior
surface of the left ventricle
Mostly perfused by the Right Coronary Artery
Inferior Leads

II
III
aVF
Anterior Surface
The front of the heart viewing the left ventricle and the
septum
Leads V2, V3 and V4 look towards this surface
Mostly fed by the Left Anterior Descending branch of the
Left artery
Anterior Leads

V2
V3
V4
Lateral Surface
The left sided wall of the left ventricle
Leads V5 and V6, I and avL look at this surface
Mostly fed by the Circumflex branch of the left artery
Lateral Leads

V5, V6, I, aVL
Posterior Surface
Posterior wall infarcts are rare
Posterior diagnoses can be made by looking at the anterior
leads as a mirror image. Normally there are inferior
ischaemic changes
Blood supply predominantly from the Right Coronary
Artery
Inferior
II, III, AVF
Antero-Septal
V1,V2, V3,V4
Lateral
I, AVL, V5,
V6
Posterior
V1, V2, V3
RIGHT
LEFT
ST Segment Elevation

The ST segment lies above the isoelectric line:

Represents myocardial injury
It is the hallmark of Myocardial Infarction
The injured myocardium is slow to repolarise and
remains more positively charged than the
surrounding areas
Other causes to be ruled out include pericarditis
and ventricular aneurysm
ST-Segment Elevation
T wave inversion in an
evolving MI
The ECG in ST Elevation MI
The Hyper-acute Phase
Less than 12 hours
ST segment elevation is the hallmark ECG abnormality
of acute myocardial infarction (Quinn, 1996)
The ECG changes are evidence that the ischaemic
myocardium cannot completely depolarize or repolarize as
normal
Usually occurs within a few hours of infarction
May vary in severity from 1mm to tombstone elevation
The Fully Evolved Phase
24 - 48 hours from the onset of a myocardial infarction
ST segment elevation is less (coming back to baseline).
T waves are inverting.
Pathological Q waves are developing (>2mm)
The Chronic Stabilised Phase
Isoelectric ST segments
T waves upright.
Pathological Q waves.
May take months or weeks.
Reciprocal Changes
Changes occurring on the opposite side of
the myocardium that is infarcting


Reciprocal Changes ie S-T
depression in some leads in
MI
Non ST Elevation MI
Commonly ST depression and deep T wave
inversion
History of chest pain typical of MI
Other autonomic nervous symptoms present
Biochemistry results required to diagnose
MI
Q-waves may or may not form on the ECG

Changes in NSTEMI
Action potentials and
electrophysiology
Ca in(slow)
++
K out
+
Na in
+
Resting
Depolarised
Repolarised
Plateau
+ + + + +
+ + + + +
+ + + + +
+ + + + +
+ + + + +
+ + + + +
+ + + + +
+ + + + +
+ +
+
+
+
+
+
+
+
+
+
+
+
+
+ +
Ca
++
K
+
K
+
Na
+
_ _ _ _ _
_ _ _ _ _
_ _ _ _ _
_ _ _ _ _
_ _ _ _ _
_
_
_
_ _ _ _ _
_
_
_
_ _ _ _ _
_
_
_
_ _ _ _ _
_
_
_
_ _
_ _
3.2
LVH and strain pattern
Ventricular Strain
Strain is often associated with ventricular hypertrophy
Characterized by moderate depression of the ST segment.
Copyright 2002 BMJ Publishing Group Ltd.
Channer, K. et al. BMJ 2002;324:1023-1026
Non-ischaemic ST segment changes: in patient taking digoxin (top)
and in patient with left ventricular hypertrophy (bottom)
Copyright 2002 BMJ Publishing Group Ltd.
Channer, K. et al. BMJ 2002;324:1023-1026
Examples of T wave
abnormalities
Sick Sinus Syndrome
Sinoatrial block (note the pause
is twice the P-P interval)
Sinus arrest with pause of 4.4 s
before generation and conduction
of a junctional escape beat
Severe sinus bradycardia
Bundle Branch Block
Left Bundle Branch Block
Widened QRS (> 0.12 sec, or 3 small
squares)
Two R waves appear R and R in V5 and
V6, and sometimes Lead I, AVL.
Have predominately negative QRS in V1,
V2, V3 (reciprocal changes).
Right Bundle Branch Block
Wheres the MI?
Wheres the MI?
Wheres the MI?
Final one

Which one is more
tachycardic during this
exercise test?
Any Questions?
Thanks for paying attention.

I hope you have found this
session useful.