ECG BASICS

By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
drbashir123@gmail.com
 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
 From RT to Lt
 Professor Dr Datuk
rajagopal N
 Dr Bashir associate
professor medicine
 Dr Urala HOD
gynae
 Dr Nagi reddy
tamma HOD-
opthomology
 Dr Setharamarao
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
Horizontal plane - the six
chest leads

LA
RA LV
V1 V2 RV V6
V3
V4 V5 V6
V5

V4
V1 V2 V3

6.5
Colour codes given by AHA
ECG Paper: Dimensions
5 mm

1 mm
Voltage
~Mass
0.1 mV

0.04 sec
0.2 sec

Speed = rate
 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
1 Small square = 0.04 second 1 Large square = 0.2 second 5 Large squares = 1 second

Time
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 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.
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.
Normal ECG

Slide 13
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 Abnormalities
 up in all leads except 1. Inverted P-wave
AVR.  Junctional rhythm.
 Duration. 2. Wide P-wave (P- mitrale)
< 2.5 mm.  LAE
 Amplitude. 3. Peaked P-wave (P-pulmonale)
 RAE
< 2.5 mm.
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.
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 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
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 don’t 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

 PRinterval time 0.12 seconds to 0.2

seconds.

 Thatis three small squares to five small

squares.
 PR interval
Definition: the time Abnormalities
interval between 1. Short PR interval
beginning of P-wave  WPW syndrome
to beginning of QRS
complex. 2. Long PR interval
 First degree heart
Normal PR interval
block
3-5mm or 3-5 small
squares on ECG graph
(0.12-0.2 sec)
 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.
 That’s 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 2. Tall R in V1

 Duration: < 2.5 mm.  RVH.
 Morphology: progression  RBBB.
from Short R and deep S  Posterior MI.
(r/s) in V1 to tall R and  WPW syndrome.
short S in V6 with small Q
3. abnormal Q wave
in V5-6.
[ > 25% of R wave]
Abnormalities:  MI.
1. Wide QRS complex  Hypertrophic
 Bundle branch block.
cardiomyopathy.
 Ventricular rhythm.  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
V6
V5
V4
V3
V2
V1

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.
 ST
Q

J point
 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
 Chroniclung 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
 Rightventricular 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
 Otherfindings 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
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)
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).

 Ityou 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
 Ifabnormal 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
 isdiagnosed 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
 isdiagnosed 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
 Itthen 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: ST depression:
More than one small More than one small
square square
 Acute MI.  Ischemia.
 Prinzmetal angina.  Ventricular strain.
 Acute pericarditis.  BBB.
 Early repolarization  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: 2. T- inversion:

< 10mm in the chest leads.

 Ischemia.
Abnormalities:  Myocardial infarction.
 Myocarditis
1. Peaked T-wave:  Ventricular strain
 Hyper-acute MI.  BBB.
 Hyperkalemia.  Hypokalemia.
 Normal variant  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:
 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
- 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 -
65 - 90 bpm R R

QT interval
 QT Interval
- Should be < 1/2 preceding R to
R interval -
65 - 90 bpm R R

QT interval

Normal QTc = 0.46 sec

Atrioventricular (AV) Heart
Block
 Classification of AV Heart
Blocks
Degree AV Conduction Pattern

Uniformly prolonged PR
1 Degree Block
St
interval
Progressive PR interval
2nd Degree, Mobitz Type I
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
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
 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

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)
• 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”

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

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

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.
2. 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): LASF

• QRS is normal width unless BBB is present 2.
• If LPHB occurs in the setting of an acute MI,
it is almost always accompanied by RBBB Lead III
and carries a mortality rate of 71%

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
 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
 Recognizing and Naming Beats & Rhythms

QRS is slightly different but still narrow,

Atrial Escape Beat 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
 Recognizing and Naming Beats & Rhythms

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
 Recognizing and Naming Beats & Rhythms

QRS is wide and much different ("bizarre") looking

than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
Ventricular
consequently, conduction through the ventricles did
Escape Beat
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 Conduction Path
Slow Recovery 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
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Premature Beat Impulse

Cardiac
Repolarizing Tissue Conduction
(long refractory period) Tissue
Fast Conduction Path Slow Conduction Path
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
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

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

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
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
 Recognizing and Naming Beats & Rhythms

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 C o m p e n s a to ry p a u s e
P V C 's a fte r th e o c c u ra n c e o f a P V C
 Recognizing and Naming Beats & Rhythms
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
 Recognizing and Naming Beats & Rhythms
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 The sooner defibrillation takes place,
• Ventricular Fibrillation the increased likelihood of survival

“R on T phenomenon”

time

Unconverted V-tach r V-fib

sinus beats V-tach
 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- Capture beat - note that

wave in front of PVC and the complex is narrow
the PVC is narrower than enough to suggest normal
the other PVC’s – this ventricular conduction.
indicates the beat is a This indicates that an
product of both the sinus atrial impulse has made it
node and an ectopic through and conduction
ventricular focus through the ventricles is
relatively normal.
 Recognizing and Naming Beats & Rhythms
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

Non conducted PAC Non conducted PAC

PAC
distorting a T-wave
 Recognizing and Naming Beats & Rhythms

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

Note different P-wave Note IRREGULAR

morphologies when the rhythm in the tachycardia
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

Rhythm usually begins in the tachycardia
with PAC
Sinus arrest or exit block
PAC
 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 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

OR
 Take6 sec strip (30 large boxes)
 Count the P/R waves X 10
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 PVC’s?
 Identifying AV Blocks:
Name Conduction PR-Int R-R Rhythm

1°: P=R > .20 Regular

2°:Mobitz P > R Progressive Irregular

I
2°:Mobitz P > R Constant Regular
II
3°: P>R Grossly Regular
Irregular (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

Anterior /
Inferior Septal
II, III, aVF 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
 PVC’s

 Uniformed/Multiformed

 Couplets/Salvos/Runs

 Bigeminy/Trigeminy/Quadrageminy
Uniformed PVC’s
R on T Phenomena
Multiformed PVC’s
PVC Couplets
PVC Salvos and Runs
Bigeminy PVC’s
Trigeminy PVC’s
Quadrageminy PVC’s
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
 TheECG 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.

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.
 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 person’s MI involves both the anterior wall (V2-
V4) 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

R • Occurs in the early stages

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

• Only diagnostic change of

R
myocardial infarction
ST
• At least 0.04 seconds in
P duration
T • Depth of more than 25% of
Q ensuing R wave
 T wave changes

• Late change
R
• Occurs as ST elevation
ST
P is returning to normal
• Apparent in many leads
T
Q
 Bundle branch block
Anterior wall MI Left 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
 Sequence of changes in
R
evolving AMI
R R
ST ST
T
P P P

T
QS Q
Q

1 minute after onset 1 hour or so after onset A few hours after onset

ST T
P P ST
P

T T
Q Q Q

A day or so after onset Later changes A few months after AMI

 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
 RIGHT LEFT

Inferior Antero-Septal
II, III, AVF V1,V2, V3,V4

Lateral
Posterior I, AVL, V5,
V1, V6
V2, V3
 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
 Changesoccurring 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
+ + + + +
+ _ _ _ _ _
+ __ _ Resting
+
_ _ _ _ +
+
+ + + + +
+
_ _ _ _ _ Na
_ _ ++
+ + + + + Ca in(slow)
_ + + _ Depolarised +
_ + + + + + _ Na in
_ _ _ _ _ +
+ ++ K out
K _ _ _ _ _ Ca
_ _
_ + + + + + _ Plateau
+ +
_ + + + + + _
_ _ _ _ _
+
K + + + + + +
+ _ _ _ _ _
_ _ +
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.

 Examples of T wave
abnormalities

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

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
Where’s the MI?
Where’s the MI?
Where’s the MI?
Final one…
 Which one is more
tachycardic during this
exercise test?
Any Questions?
I hope you have found this
session useful.