ECG

ECG BASICS
By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
drbashir123@gmail.com

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From Right to Left
Dr.Smitha associate
prof gynae
Dr Bashir associate
professor Medicine
Dr Udaman
neurologist
Dr Patnaik HOD
ortho
Dr Tin swe aye paeds

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From RT to Lt
Professor Dr Datuk
rajagopal N
Dr Bashir associate
professor medicine
Dr Urala HOD
gynae
Dr Nagi reddy
tamma HODopthomology
Dr Setharamarao
Prof ortho

ELECTROGRAPHY MADE
EASY

 ULTIMATE

AIM TO HELP PATIENTS

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

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Horizontal plane - the six
chest leads
LA
RA
V1

V2

LV
RV

V6

V3
V4 V5 V6
V5
V4
V1

V2

V3

6.5

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
Voltage calibration 1 mV

= 25mm/sec
= 1cm



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



Timings
– 1 small square
– 1 large square
– 25 small squares
– 5 large squares

=
=
=
=

0.04sec
0.2sec
1sec
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
1 Small square = 0.04 second

2 Large squares = 1 cm

1 Large square = 0.2 second

5 Large squares = 1 second

Time

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

Half amplitude

Double amplitude

10 mm/mV

5 mm/mV

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.

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.

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

P wave height 2 and half small
squares ,width also 2 and half
small square

Slide 9

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.

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 V1 ≥ 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 V1 > 1
“small box” in area

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 don’t resemble one
another.

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.

Junctional rhythm
 In

Junctional rhythm the P waves may be
absent or inverted.in next slide u can see
these inverted P waves.

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.

NORMAL P-R INTERVAL
 PR

interval
seconds.

 That

time 0.12 seconds to 0.2

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 preexcitation 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.

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 .

Q WAVES
Q

waves
<0.04 second.
 That’s is less than one small square
duration.
 Height <25% or < 1/4 of R wave height.

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.

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
V1

V2

V3

V4

V5

V6

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.

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.

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 (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.

 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).

 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).

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 “counterclockwise rotation of the heart.” This can be
seen with abnormal chest shape.


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:
 Tall

R wave in V1

 Right

axis deviation
 Right atrial enlargement
 Down sloping ST depressions in V1-V3 ( RV strain
pattern)

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
ST elevation:
More than one small
square
1.






Acute MI.
Prinzmetal angina.
Acute pericarditis.
Early repolarization

ST depression:
More than one small
square






Ischemia.
Ventricular strain.
BBB.
Hypokalemia.
Digoxin effect.

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

upwards.

lost and convexity appear facing

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

Q waves in myocardial
infarction

T-wave
Normal values.
1.amplitude:
< 10mm in the chest leads.

.
2. T- inversion:



Abnormalities:



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








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.
2.

Prolonged QT interval: hypocalcemia and
congenital long QT syndrome.
Short QT interval: hypercalcemia.

QT Interval
- Should be < 1/2 preceding R to
R interval -

QT Interval
R interval -

QT interval

QT Interval
R interval R

QT interval

R

QT Interval
R interval 65 - 90 bpm

R

QT interval

R

QT Interval
R interval 65 - 90 bpm

R

QT interval

Normal QTc = 0.46 sec

R

Atrioventricular (AV) Heart
Block

Classification of AV Heart
Blocks
Degree

AV Conduction Pattern

1St Degree Block

Uniformly prolonged PR
interval

2nd Degree, Mobitz Type I

Progressive PR interval
prolongation

2nd Degree, Mobitz Type II

Sudden conduction failure

3rd Degree Block

No AV conduction

AV Blocks
 First

Degree

– Prolonged AV conduction time
– PR interval > 0.20 seconds

1st 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

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

2nd degree AV Block (“Mobitz I” also called “Wenckebach”):

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

PRI = .24 sec

PRI = .36 sec

PRI = .40 sec

QRS is
“dropped”

Pause
4:3 Wenckebach (conduction ratio may not be constant)

Pattern Repeats………….

Type II Second-Degree AV
Block:
Mobitz Type II


ECG findings

1.Intermittent or unexpected blocked P waves
you don’t 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.

Type 2

Constant PR interval with unexpected intermittent failure to conduct

2nd degree AV Block (“Mobitz II”):
• 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)
• It’s 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

PRI is CONSTANT

Non-conducted
sinus impulses

“2:1 block”

“3:1 block”

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)

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

Sudden appearance of a single, nonconducted 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

3rd 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”) :
• QRS complexes may be narrow or broad depending on the level of the block
• Atria and ventricles beat independent of one another (AV dissociation)
• QRS’s have their own rhythm, P-waves have their own rhythm
• May be caused by inferior MI and it’s 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 P’s & QRS’s
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

LBB
LPIF

Lead I

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

1.

LASF

2.

Lead III

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)

Lead I

LBB
LPIF

Left Posterior Hemiblock (LPHB):
1.

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%

LASF
2.
Lead III

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 patient’s rhythm
Fires only if no activity sensed after preset interval (escape
interval)

– Transcutaneous vs Transvenous vs Implanted

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 CardioDefibrillator



Uses
– Tachyarrhythmias
– Malignant

arrhythmias



VT
VF

 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

 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

Recognizing and Naming Beats & Rhythms
Atrial Escape Beat

QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal

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


Junctional Escape Beat

QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal

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


Ventricular
Escape Beat

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

there is no p wave, indicating that the beat
did not originate anywhere in the atria
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

The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery

Slow Conduction Path
Fast Recovery

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

Premature Beat Impulse
Cardiac
Repolarizing Tissue
Conduction
(long refractory period)
Tissue
Slow Recovery

Fast Recovery

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

Cardiac
Conduction
Tissue
Slow Recovery

Fast Recovery

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

Cardiac
Conduction
Tissue
Slow Recovery

Fast Recovery

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

Premature Ventricular Contractions (PVC’s, VPB’s, 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
• PVC’s are sometimes described by lay people as “skipped heart beats”

R on T
phenom em on

M u lt if o c a l
P V C 's

C o m p e n s a to ry p a u s e
a fte r th e o c c u r a n c e o f a P V C

Characteristics of PVC's
• PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
• Every other beat being a PVC (bigeminy) may indicate coronary artery disease
• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s

The classic PVC – note the
compensatory pause

Interpolated PVC – note the sinus
rhythm is undisturbed

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

The sooner defibrillation takes place,
the increased likelihood of survival

“R on T phenomenon”
time

sinus beats

V-tach

Unconverted V-tach r V-fib

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 pwave in front of PVC and
the PVC is narrower than
the other PVC’s – 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.

Premature Atrial Contractions (PAC’s):
• 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
• PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)
• PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco
• PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy
• PAC’s may also precede PSVT

PAC

Non conducted PAC

Non conducted PAC
distorting a T-wave

Premature Junctional Contractions (PJC’s):
• 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
• PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm

PJC

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,  blockers, potassium, magnesium, supportive therapy for
underlying causes mentioned above (antiarrhythmic drugs are often ineffective)

Note different P-wave
morphologies when the
tachycardia begins

Note IRREGULAR
rhythm in the tachycardia

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

Rhythm usually begins
with PAC

Note REGULAR rhythm
in the tachycardia

Junctional 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 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.

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


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

OR
 Take

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

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 PVC’s?

Identifying AV Blocks:
Name

1°:

Conduction

P=R

PR-Int

> .20

R-R Rhythm

Regular

2°:Mobitz P > R
I

Progressive Irregular

2°:Mobitz P > R
II

Constant

Regular

3°:

Grossly
Irregular

Regular

P>R

(20-40 bpm)

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 Man’s 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:
Lateral
I, AVL,
V5-V6
Inferior
II, III, aVF

Anterior /
Septal
V1-V4

Premature Atrial Complexes
(PACs)

Wandering Atrial Pacemaker
(WAP)

Supraventricular Tachycardia
(SVT)

Wolff-Parkinson-White
Syndrome (WPW)

Premature Junctional
Complexes (PJC)

Premature Ventricular
Complexes (PVC's)

Note – Complexes not
Contractions

PVC’s
 Uniformed/Multiformed
 Couplets/Salvos/Runs
 Bigeminy/Trigeminy/Quadrageminy

Ventricular Tachycardia (VT)
 Rate:

101-250 beats/min

 Rhythm:
P

regular

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

Torsades de Pointes (TdeP)
 Rate:

150-300 beats/min

 Rhythm:
P

regular or irregular

waves: none

 PR

interval: none

 QRS

duration: > 0.12 sec. gradual alteration
in amplitude and direction of the QRS
complexes

Ventricular Fibrillation (VF)
 Rate:

CNO as no discernible complexes

 Rhythm:
P

rapid and chaotic

waves: none

 PR

interval: none

 QRS

duration: none
Note: Fine vs. coarse?

Asystole
(Cardiac Standstill)
 Rate:

none

 Rhythm:
P

none

waves: none

 PR

interval: not measurable

 QRS

duration: absent

Asystole
The Mother of all Bradycardias

Atrial Pacemaker
(Single Chamber)

pacemaker

•Capture?

Ventricular Pacemaker
(Single Chamber)

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 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

Diagnosing a MI
To diagnose a myocardial infarction you need
to go beyond looking at a rhythm strip and
obtain a 12-Lead ECG.
12-Lead
ECG

Rhythm
Strip

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 V1 - V4 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.

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.

How about now?

Anterolateral MI
This person’s MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, 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
• Occurs in the early stages

R
ST
P

Q

• Occurs in the leads facing
the infarction
• Slight ST elevation may be
normal in V1 or V2

Deep Q wave
• Only diagnostic change of
myocardial infarction

R
ST

• At least 0.04 seconds in
duration

P
T
Q

• Depth of more than 25% of
ensuing R wave

T wave changes
• Late change
R

• Occurs as ST elevation
is returning to normal

ST

P

• Apparent in many leads
T
Q

Bundle branch block
Anterior wall MI
I II III

aVR aVL aVF

V1 V2 V3

Left bundle branch block
V4 V5 V6

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Sequence of changes in
evolving AMI
R

R
T

R

ST

ST

P

P

P

QS

T

Q

1 minute after onset

Q

1 hour or so after onset

A few hours after onset

R
ST

P

P
T

Q

A day or so after onset

ST

T

P
T

Q

Later changes

Q

A few months after AMI

Anterior infarction
Anterior infarction

I II III

Left
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Inferior infarction
Inferior infarction

I II III

Right
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Lateral infarction
Lateral infarction

I II III

Left
circumflex
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

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

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

RIGHT

Inferior
II, III, AVF

Posterior
V1,
V2, V3

LEFT

Antero-Septal
V1,V2, V3,V4

Lateral
I, AVL, V5,
V6

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

T wave inversion in an
evolving 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

+ + + +
_ _ _ _
_
_ _ _ _
+ + + +

+
+
+

+
+ _
+ __
+
+

Action potentials and
electrophysiology
+

Na

_ _ _ _ _

_
_
+ + + + +
_ +
+ _
_ + + + + + _
_ _ _ _ _
+

_
_
_ + + + + + _
+
+
_ + + + + + _
_ _ _ _ _

+

K

_ _ _ _ _

+
+ _
_
+
_
+
+

+ + + +
_ _ _ _
_
_ _ _ _
+ + + +

+
+
+

K

Resting

Depolarised

Ca
+

Na

++
in(slow)

in

K

++

Ca

+
out

Plateau

Repolarised

3.2

LVH and strain pattern
Ventricular Strain
Strain is often associated with ventricular hypertrophy
Characterized by moderate depression of the ST segment.

Non-ischaemic ST segment changes: in patient taking digoxin (top)
and in patient with left ventricular hypertrophy (bottom)

Channer, K. et al. BMJ 2002;324:1023-1026
Copyright ©2002 BMJ Publishing Group Ltd.

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

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).

Which one is more
tachycardic during this
exercise test?

I hope you have found this
session useful.

ECG

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