ECG INTERPRETATION AND COMMON ECG

FINDINGS

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014
NUR LIYANA HANAPI

THIS IS FOR INTERNAL USE ONLY AND NOT INTENDED FOR PUBLICATION
 MBBS 220 UITM 7th BATCH 2009/2014

To my study group
I always felt that learning ECG was tedious and cumbersome. It took me 3 years
to actually understand it, or so that I believe to understand (hopefully I’m
understanding the right thing). These are my notes (based on my
understanding) and a compilation of various references. I tried to simplify
matters as simple as possible. Hopefully it would be of a help. At least, to help
to give a rough idea or as a quick reference of what to learn. I didn’t cover
100% of the ECG books only those commonly asked and a MUST know. Please
don’t take my notes wholly (I’m no specialist, I can make mistakes too)
DO OPEN YOUR TEXTBOOKS!

Last Say..
No matter what year you are
GOOD LUCK FOR PROFESSIONAL EXAMS!
BECAUSE IT’S CLOSER THAN YOU THINK AHAKS =)

YANAHANAPI Page 2
 MBBS 220 UITM 7th BATCH 2009/2014

CONTENT

Page

CHAPTER 1 BASIC KNOWLEDGE ON ECG 4

CHAPTER 2 CONDUCTION PROBLEMS 12

CHAPTER 3 RHYTHM AND RATE PROBLEMS 17

CHAPTER 4 P, QRS AND T WAVE MORPHOLOGY 28

CHAPTER 5 ISCHEMIC AND INFARCTIVE PATTERN CHANGES 33

OTHER ECG 41

APPENDIX AND REFERENCE

YANAHANAPI Page 3
 MBBS 220 UITM 7th BATCH 2009/2014

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014

CHAPTER 1: BASIC KNOWLEDGE ON ECG

Where to start?

The ECG graph paper

The smallest square is measured 1mm per box
The largerst square is made up of 5 small boxes = 5mm
The speed of the graph paper tracing is around 25mm/sec

1 small box = 1mm = 0.04 seconds

1 large box (5 small boxes) = 5 mm = 0.2 seconds
Amplitude 1mm = 1 mV

YANAHANAPI Page 4
 MBBS 220 UITM 7th BATCH 2009/2014

What is ECG
An electrocardiogram (ECG or EKG) records the electrical voltages/impulse (potentials) produced in the heart. It does this by means of
metal electrodes (connected to an electrocardiograph) placed on the patient's chest wall and extremities.

The 12 lead ECG is made up of

- three standard limb leads (I, II and III)

- the augmented limb leads (aVR, aVL and aVF)
- six precordial leads (V1, V2, V3, V4, V5 and V6).

The leads act as ‘window’ to view various surface of the heart – in combination that is!

Heart surface Leads

Lateral surface of the heart I, II, and AVL
Inferior surface of the heart II, III and AVF
Right atrium AVR
Right ventricle V1 to V2
Septal and anterior wall of the left ventricle (antrerolateral) V3 to V4
Lateral wall left ventricle V5 to V6

YANAHANAPI Page 5
 MBBS 220 UITM 7th BATCH 2009/2014

Basic physiology in ECG

Pacemaker cell (SA nodes – location at the RA opening superior vena cava )
↓
Stimulus spread downwards and to the left (atria)
Atria depolarization
↓
Reaches AV nodes (location at the top of the interventricular septum )
There is an AV delay (why? – allow both atrium to contract completely)
↓
Goes to AV junction
To the bundle of his (left and right purkinje fibres)
↓
Ventricular depolarization

Normal circumstances, when the sinus node is pacing the heart = sinus rhythm
AV junction can also act as an independent pacemaker of the heart in the case where the sinus node fails to function properly, the AV
junction can act as an escape pacemaker.

** Pace of conduction is fattest : at the purkinje fibres

Pace of conduction is slowest: at the AV nodes

YANAHANAPI Page 6
 MBBS 220 UITM 7th BATCH 2009/2014

Basic ECG waves

Depolarization cardiac electrical stimulation or activation

Repolarization return of heart muscle cells to their resting state after stimulation
(depolarization)
Polarize (resting) Not in the state of repolarization/depolarization

The spread of stimuli through the atria and ventricles followed by the return of stimulated atrial and ventricular muscle to the resting
state produces the electrical currents recorded on the ECG.

For better understanding of the vector please refer to APPENDIC

Waves and Complexes

Wave Signify Normal time taken (sec) Normal amplitude

P wave atrial depolarization (stimulation) 0.08-0.12 sec ( ~2-3 small 2.3 mm
boxes)
QRS complex ventricular depolarization (stimulation) <0.1 sec (2 ½ small boxes) Variable
T wave ventricular repolarization (recovery) 0.04-0.08 sec (~1-2 small box) < 5mm in limb leads
<10 mm in Precordial leads

** any excitation/impulse moving towards the leads would cause an upward deflection and those that moves away from it would result in
a negative deflection
** in an normal heart the left ventricle exerts more than the right ventricle (this is due to in the left has a larger muscle mass)

YANAHANAPI Page 7
 MBBS 220 UITM 7th BATCH 2009/2014

** septal depolarization would occur from left  right

Intervals and segments

Intervals and Signify Normal time taken

segments (sec)

PR intervals From the start of the P wave to the Amount of time taken for the excitation to spread 0.12- 0.2 sec
start of the QRS complex from the SA node till the bundle of his (including (3 -5 small boxes)
your AV node delay)
Indicator for heart block (prolong)

PR segment From the end of the P wave to the flat, usually isoelectric segment
start of the QRS complex abnormal if depressed/elevated ie acute -
pericarditis/atrial ischemia

J point The junction between the QRS Elevation or depression of the J point is seen with -
complex and the ST segment the various causes of ST segment abnormality.

QT interval From the start of the QRS complex Time taken for the ventricular depolarization Male: < 0.4 sec
to the end of the T wave (stimulation) and repolarize Female: <0.44 sec
(~10 small boxes)
ST segment From the end of the QRS complex (J flat, isoelectric section of the ECG
point) to the start of the T wave represents the interval between ventricular -
depolarisation and repolarisation

YANAHANAPI Page 8
 MBBS 220 UITM 7th BATCH 2009/2014

Determining the normal cardiac axis

Normal cardiac axis is determined by looking at lead I, II and III

Normal propagation of a normal cardiac axis

In a RIGHT cardiac axis deviation In a LEFT cardiac axis deviation

There would be a negative deflecture (s wave) in lead II and III

There would be a negative deflecture (s wave) in lead I
Reason being that:
And a positive deflecture in lead II and III
Reason being that: 1. Increased mass on the left ventricle causing a much more
prominent impulse as it moves away. (depolarization of
1. Increased mass on the right ventricle causing a much
the ventricle is of left  right)
more prominent impulse as it moves towards it
2. Conduction problem (most common)
(depolarization of the ventricle is of left  right) causing
an upward deflection.
2. Any stress that come from the pulmonary Causes left axis deviation:

Causes right axis deviation: - Left ventricular hypertrophy

- Right ventricular hypertrophy

- Cor pulmonale
- Congenital heart disorder
- Pulmonary Embolism

YANAHANAPI Page 9
 MBBS 220 UITM 7th BATCH 2009/2014

Interpretating a normal ECG

1. Look at the rhythm – sinus rhythm or not?

2. What is the rate? – determine by looking at lead II
3. How is the axis?
4. Any abnormalities in the leads (check according to group)
5. Come to a conclusion

Calculating the heart rate

Heart Rate

Atrial rate = between 2 P waves

Ventricular rate = between 2 QRS waves

Calculation

Regular rhythm
300/large boxes (from R-R)= heart rate
Thus using formula of Rate: 300/R-R interval
: 300/3.5
: 86 beat per minute
Irregular rhythm
Count number of QRS complexes within 10 sec x 6 = heart rate
Interval range: (shortest RR) between(longest RR) beats per minute

YANAHANAPI Page 10
 MBBS 220 UITM 7th BATCH 2009/2014

COMMON ECG FINDING PROBLEMS

1st degree

conduction heart block 2nd degree

norrow complex
3rd degree
(atrial origin)
arrythmias
wide complex
(ventricular
origin)
common
problems
STEMI

ACS

Non STEMI
ischemic heart
change

abnormal P,
QRS,T waves and drugs toxicity
PR/ST segement

electrolyte
derangement
pulmonary

others

pericarditis

YANAHANAPI Page 11
 MBBS 220 UITM 7th BATCH 2009/2014

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014

CHAPTER 2: CONDUCTION PROBLEMS

Conduction
Problems

Distal Part of
AV nodes and Right and Left
Left Bundle
Bundle of His Bundle Branch
Branch

Right bundle
1st degree
branch Block

Left Bundle
2nd degree
Branch Block

3rd degree
(complete
Block)

The most common thing that you should know off is

1. AV nodes and Bundle of His Block

2. Right and Left Bundle Branch Block

YANAHANAPI Page 12
 MBBS 220 UITM 7th BATCH 2009/2014

AV NODES AND BUNDLE OF HIS BLOCK

It could be divided into 3:

Degree of Heart Block Description

1st degree Heart Block Prolonged PR interval > 0.2 sec

Delay along the conduction pathway

2nd degree Heart Block 2 types of variant

1. Mobitz Type I (Wenckebach Phenomenon): progressive prolonging of PR interval (with
each beat) then followed by failure of atrial depolarization (P wave). Then restart with the shortest
PR interval and keeps prolonging until there’s another drop in the P wave. The cycle continues
The constant PR interval + presence of atrial contraction (P wave) without a subsequent
ventricular contraction (QRS complex)
2. Mobitz type II phenomenon: Alternate conducted and non conducted beats (P waves: QRS
complex) ie 2:1 or 3: 1

3rd degree Heart Block Complete disassociation between atril (P wave) contraction and ventricular (QRS complexes) contraction

1ST DEGREE HEAR BLOCK

** Note although the PR interval is prolonged (0.2 sec) the PR interval is constant with every beat/cycle

YANAHANAPI Page 13
 MBBS 220 UITM 7th BATCH 2009/2014

2ND DEGREE HEART BLOCK

1. Mobitz Type I (Wenckenbach Phenomenon)

** Note that there is a prolonging of PR interval with every cycle/beats then there is a missed beat. Afterwards the same cycle
continues. (classical presentation )

2. Mobitz Type II

3rd DEGREE HEART BLOCK

YANAHANAPI Page 14
 MBBS 220 UITM 7th BATCH 2009/2014

RIGHT BUNDLE BRANCH BLOCK AND LEFT BUNDLE BRANCH BLOCK

Principle to remember:

1. Septal depolariaes from left  right

2. Left side exerts more influence on ECG as the muscle
mass is more
3. Excitation that moves towards a lead would cause
upward (positive) deflection

RBBB and LBBB

Delay in depolarization of the ventricles due to the problem in conduction in the bundle branch
Causing widening of the QRS complex
More than 4 small boxes = >0.12 sec

Right Bundle Branch Block Left bundle Branch Block

[Impulse is not conducted in the right ventricle ] [Impulse is not conducted in the left ventricle ]

1.Septal depolarized from left to right: 1.Septal depolarized from right to left:
- R wave formed in R ventricle in lead V1 - Q wave formed in L ventricle in lead V6
- Small S wave in L ventricle in lead V6 - R wave in R ventricle in lead V1

2.Excitation goes to the left side: 2.Excitation goes to the right side first, despite left having a larger
- R wave form in L ventricle lead V6 muscle mass, it’s enough to form an R wave :
- S wave in the R ventricle lead V1 - R wave form in L ventricle lead V1
- S wave in the R ventricle lead V6
3. Right ventricle depolarize much later than the left as they is a
problem in the conduction pathway: 3.After that the left ventricle depolarize
- Causing a R wave (additional) to be formed in lead V1 - R wave form in L ventricle lead V6
- Deep S wave in lead V6 - S wave in the R ventricle lead V1

YANAHANAPI Page 15
 MBBS 220 UITM 7th BATCH 2009/2014

This gives ris to the RSR pattern (W) in lead V 1 This gives ris to the RSR pattern (W) in lead V 1
The width of the QRS complex is NORMAL (< 0.12 sec)
It is a normal variant sometimes (not much of significance)

Best seen at lead V1 Best seen at lead V6

V1 – M wave V1- W wave
V6 – would have a Q wave fisrt = W wave V6 – M wave
Coupled with : T inversion at lead I, V2, V5-V6

YANAHANAPI Page 16
 MBBS 220 UITM 7th BATCH 2009/2014

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014

CHAPTER 3: RHYTHM AND RATE PROBLEMS

Tachycardia

Sinus rhythm

Bradycardia
Rhythm
problems
narrow (atrial
origin)
Non sinus rhythm QRS complex
broad complex
(ventricular
origin)

SINUS ARRHYTHMIAS

What is a sinus rhythm?

Rhythm that is generated by the SA node. It is a P wave followed by a normal QRS complex and T wave.
1 P wave generates 1 QRS complex

The rate of the SA node is controlled by vagus innervations

YANAHANAPI Page 17
 MBBS 220 UITM 7th BATCH 2009/2014

Abnormal sinus rhythm occurs when there is a problem with the rate

1. Tachycardia: > 100 beats per minute

2. Bradycardia: < 60 beats per minute

RECAP

If the rhythm is regular, the RR interval should be constant throughout the ECG. By marking on a piece of paper the distance between two
R waves, and comparing this distance between pairs of QRS complexes on the ECG

In this example:

R-R interval: 3 ½ small boxes

Thus using formula of Rate: 300/R-R interval

: 300/3.5
: 86 beat per minute

Next, check to see if a P wave is present before each of the QRS complexes.

Causes of sinus tachycardia Causes of sinus bradycardia

Exercise Athletic training

Fear Fainting attacks
Thyrotoxicosis Hypothermia
Heamorhage Myxoedema
Right after an myocardial infarction

YANAHANAPI Page 18
 MBBS 220 UITM 7th BATCH 2009/2014

Abnormal Rhythm

3 places where abnormal rhythms could initially occur

1. Atrial
2. Junctional (AV nodes)
3. Ventricular

To make it more easily to understand, the abnormal rhythm (source) could be divided:

1. Supraventricular
2. Ventricular

Supraventricular rhythms Ventricular rhythms

Constitutes of: Consist of:

1. Sinus rhythms 1. Ventricular rhythms
2. Arterial rhythms
3. Junctional rhythms

In supraventricular rhythm the excitation spreads to the ventricles As the impulse originates from the ventricles, the conduction is
normaly via bundle of his and purkinje fibres. Therefore regardless much more slower (sbb x pkai conventional way- bundle of His)
where the impulse arise (in this case supraventricularly) the QRS is therefore you would have a broad QRS complex.
normal

Exception : in supraventricular arrhythmias with LBBB

QRS narrow (normal) QRS broad base

YANAHANAPI Page 19
 MBBS 220 UITM 7th BATCH 2009/2014

Atrial tachycardia 1. Ventricular tachycardia

1. Atrial flutter 2. Ventricle fibrillation
2. Atrial fibrillation 3. Wolf Parkinson White Syndrome
3. Supraventricular tachycardia

ATRIAL TACHYCARDIA

- Atrial tachycardias occur when there is an atrial discharge rate of more than 150 beats/min
- The AV node could only relay the discharge of less than 200 beats/min and not more than that – as aprotective mechanism, so
not all excitation are relayed to ventricular contraction causing AV block picture – which could cause insufficient contraction
– affect cardiac output (mampuih ventricle kne kerja kalau mcm tu- limit rate ialah 150 beats/minute)
- If there is a discharge rate of more that 200 beats/min there would be an AV block where P waves would not be followed by a
QRS complex.

ATRIAL FLUTTER

YANAHANAPI Page 20
 MBBS 220 UITM 7th BATCH 2009/2014

Atrial Rate 250- 350 beats per minute

Characteristic “Saw-tooth”appearance best seen at lead II and AVR
P waves Still present (identifiable)
Would exhibits AV block if rate is >200 beats/min ie 2: 1, 3:1 block
QRS complex Narrow complex (relatively normal)
Ventricular rate 150 beats per minute
T waves Normal
Condition - acute ischemic heart disease
- pulmonary embolism
- organic heart disease

ATRIAL FIBRILATION

Atrial Rate Undefined (absent P waves)

Characteristic P waves are replaced with rapidly quivering small deflection of variable amplitude
Irregular baseline
P waves Absent of normal P wave
QRS complex Narrow complex
Ventricular rate established between 100 - 160 beats per minute
T waves Normal
Condition - rheumatic heart disease
- pulmonary emboli,
- cardiomyopathy
- pericarditis,
- ischemic heart disease
- thyrotoxicosis

YANAHANAPI Page 21
 MBBS 220 UITM 7th BATCH 2009/2014

SUPRAVENTRICULAR TACHYCARDIA

There are 2 variants (good to know)

AV NODAL RE-ENTRY (common) AV RE- ENTRY

Establish the re-entry solely within the AV node accessory pathway is used to return electrical conduction back to
the atria

P waves are absent P waves are always present outside of the QRS complex
As usually P waves are buried within the QRS compelx

Pathophysiology of re-entry phenomenon

A. Wave enters the recurrent nodule

B. Current moves through the myocardium thus
enter the reentrant focus nodule (the reentrant
focus nodule is insukated from the surrounding)
C. The rest of the myocardium depolarized-
repolarized first, much faster rate than the
reentrant focus nodule (impulse moves through
it slowly)
D. When the current exits from the reentrant
nodule the surrounding myocardium already
becomes vulnerable to excitation, thus charges
that flow out the reentry focus acts as another
impulse (ectopic) causing excitation
E. The impulse than travels through the fibres back
into the reentrant focus. Cycle starts all over

YANAHANAPI Page 22
 MBBS 220 UITM 7th BATCH 2009/2014

Atrial Rate Undefined (absent P waves)

Characteristic P waves are buried within the QRS compelx
P waves Absent of normal P wave
QRS complex Narrow complex
Ventricular rate 180 beats per minute
T waves Normal
Condition - usually benign and is easily converted to sinus rhythm by vagal
maneuvers/carotid massage/adenosine

VENTRICULAR TACHYCARDIA

YANAHANAPI Page 23
 MBBS 220 UITM 7th BATCH 2009/2014

Atrial Rate Undefined (absent P waves)

Characteristic Regular road QRS complexes, P waves buried in the broad complexes
P waves Absent P wave
QRS complex Broad complexes >0.24 sec
Ventricular rate 200 beats per minute
T waves None

Condition chronic sustained VT is most commonly associated with

- coronary artery disease
- dilated cardiomyopathy
- prior myocardial infarction
- severe heart disease
-

VENTRICLE FIBRILLATION

IMPORTANT TO RECOGNIZED A VENTRICULAR FIBRILLATION AS THE CONDITION IS FATAL AS THE VENTRICLE CANNOIT PRODUCE SUFFICIENT
CARDIAC OUTPUT

Atrial Rate None

Characteristic Chaotic irregular deflections of varying amplitude
P waves Absent P wave
QRS complex None identifiable
Ventricular rate 150-500 beats per minute
T waves None
Condition Preceeded by Torcedes de Pointes: management of torcedes is by shortnening the QT
interval (as it caused by prolonged QT interval)

YANAHANAPI Page 24
 MBBS 220 UITM 7th BATCH 2009/2014

Torsedes de Pointes versus Ventricular Fibrillation

Both seem somewhat very (VERY) similar to each other on ECG but it’s is different

Torsedes de Pointes Ventricular Fibrillation

- Torsades de Point means twisting of the - Total chaotic irregular electrical impulse
points.(If looking at the tracing makes you - There is no pattern what so ever
think of the words "spindle," "twisting,"
or "ribbon," it's torsades)
- Torsades is a polymorphinc ventricular
tachycardia
- It’s definitely more organized than a V
fibrillation

Comparison of Torsedes de Pointes (1st pic) and Ventricular Fibrillation (2nd pic)

TdP Above (oscillatory pattern)

V-Fib Irregular (sharp) chaotic electrical impulses

YANAHANAPI Page 25
 MBBS 220 UITM 7th BATCH 2009/2014

WOLF PARKINSON WHITE

Another variant of reentrant tachyarrythmias

Pathophysiology

- Due to a possible accessory pathway between the atrial and the ventricle. Normally there should be none
- The accessory pathway/bundle connects directly the atria and the heart ( this causes excitation without impulse not having to
go through the AV node delay)
- Excitation occurs early – resulting shortening of the PR interval  leading to an upstroke wave: delta wave
- The pre excitation that catches up with the normal excitation (those which go through the Bundle of His) to form normal QRS
complexes
- T wave would be abnormal because of the abnormal repolarization

YANAHANAPI Page 26
 MBBS 220 UITM 7th BATCH 2009/2014

Atrial Rate -
Characteristic Accelerated ventricular impulse formation lead to the development of delta waves
As a result, the PR interval is shortened to less than 0.12 seconds
Dominant R wave in lead V1
P waves P wave present
QRS complex Broad complexes + >0.10 sec
Ventricular rate -
T waves Abnormal (abnormal repolarization)

Condition The important condition that is related to this condition is when the reentry circuit
is established  this results in sustained tachycardia

YANAHANAPI Page 27
 MBBS 220 UITM 7th BATCH 2009/2014

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014

CHAPTER 4: P, QRS AND T WAVE MORPHOLOGY

Abnormalities in the P wave

Normal variant P wave: 1 mm x 1mm

Normal amplitude must be <2.5 mm

Abnormality that can occur in a P wave

1. Tall P wave (peaked): Right atrial hypertrophy

2. Broad Bifid P wave: Left atrial hypertrophy

Example of Tall Peaked P wave

Characteristic: amplitude of the P wave is > 2.5 mm (best seen at lead II) and also present in other leads

YANAHANAPI Page 28
 MBBS 220 UITM 7th BATCH 2009/2014

Example of broad Bifid P Wave

Characteristic: P wave duration ≥ 0.12s

: Notched P wave in limb leads with the inter-peak duration ≥ 0.04s

QRS Abnormalities

A normal QRS complex would be:

1. QRS interval : should not exceede 3 small boxes

2. S wave is always more prominent than R wave in lead V1
3. R in V5-V6 should be less than 25 mm (5 large boxes)
4. Left leads Q wave (presence due to septal depolarization) normally should be 1mm across and 2 mm deep

Abnormalities

1. Increased in width
a. Bundle branch block
b. Ventricular ectopics
c. Ventricular extrasystole
d. Ventricular tachycardia
2. Increased in height
a. Left ventricle hypertrophy
b. Right ventricle hypertrophy

YANAHANAPI Page 29
 MBBS 220 UITM 7th BATCH 2009/2014

Left ventricular hypertrophy

1. Deep S wave (more than 25 mm) in V1, V2

2. Tall R wave in (more than 25 mm) in V5, V6
3. Inverted T wave in V5 V6
4. Left axis deviation (downward deflection in lead III) – refer back to earlier parts of notes

Good to know
Few criteria to diagnose left ventricular hypertrophy

1. ESTES criteria for LVH

2. Limb-lead voltage criteria
3. Chest-lead voltage criteria

Right ventricular hypertrophy

1. Note that the R wave is more prominent than the S wave

2. Presence of S wave in lead V6
3. Right axis deviation (prominent upward deflection in lead III)

YANAHANAPI Page 30
 MBBS 220 UITM 7th BATCH 2009/2014

The Q waves

Is actually depolarization of the septal (frm left --> right)

Any Q wave that is >1mm across and/or >2mm deep = pathological wave
Presence: signify infarction (according to the group leads)

Look

Heart surface Leads

Lateral surface of the heart I, II, and AVL
Inferior surface of the heart II, III and AVF
Right atrium AVR
Right ventricle V1 to V2
Septal and anterior wall of the left ventricle (antrerolateral) V3 to V4
Lateral wall left ventricle V5 to V6

YANAHANAPI Page 31
 MBBS 220 UITM 7th BATCH 2009/2014

ST segment

ST depression or elevation (in reference to the isoelectric lines)

1. elevation suggestive of ACUTE infarction - looking on a group of leads

2. depression suggestive of ischemia
3. if there is ST elevation in major of leads to consider pericarditis

T wave

Inversion is normal:
1. AVR
2. V1, V2 and sometimes V3

Pathological T wave is when

1. Indication of ischemia
2. Ventricle hypertrophy - at the leads looking at the left and right depending on which side
3. Bundle brach block
4. Digoxin treatment

***Q wave, ST segment and T inversion would be discussed more in ischemic changes of the heart

YANAHANAPI Page 32
 MBBS 220 UITM 7th BATCH 2009/2014

MBBS 220 UITM

MEDICINE 5TH YEAR 2013/2014
7th BATCH 2009/2014

CHAPTER 5: ISCHEMIC AND INFARCTIVE PATTERN CHANGES

Ischemia and Infarction involve 1 major artery at a time

To have them (all arteries) to be involve simultaneously is a rare coincidence

In such event occurance would effect the following part of the heart

1. Anterior wall
2. Lateral wall
3. Inferior wall

Table of Region of the Heart Involvement and the Barnches that supplies Them

Region Branches Artery Lead

Anterior wall Anterior descending Artery Precordial leads (V1-V4)
Lateral wall Circumflex Artery Lead I, AVL and (V4-V6)
Inferior wall Right coronary Artery Lead II, III, AVF

YANAHANAPI Page 33
 MBBS 220 UITM 7th BATCH 2009/2014

If the large vessels may involve a more extensive area;

1. Occlusion of the large right coronary artery : inferolateral involvement

2. Occlusion of the large anterior descending artery: anterolateaal involvement

If there is a global changes (involving al leads) = suspicious for pericarditis

ST Segment

Isoelectric: no voltage activity recorded on ECG

Reason being

1. There is no electrical activity at all

2. The positive and the negative impulses are equal and cancel out each other

Therefore to determine the baseline: is to look at the segment prior to the P wave

ST segment depression (depressed well below the baseline ischemia is present

Usually occurs in subendochardial involvement
Where the coronary artery is stenossed but not totally occluded

Ischemia: lack of perfusion a result of mismatch in perfusion and cell demand

YANAHANAPI Page 34
 MBBS 220 UITM 7th BATCH 2009/2014

Addition for check mark/hockey stick appearance

**With the ST segment dowmn slopping/horizontal (typical for ischemia)

J point – depressed (below base line) but then ST segment moves upwards ( not specific for ischemia)

Differential diagnosis for ST depression

1. LVH
2. Digitalis
3. Hypokalemia

**Should accompanied with suggestive clinical history. Even with with finding of T wave flattening and inversion does not change the
fact that is non specific.

There are non specific ST-T wave changes – clinical significance

YANAHANAPI Page 35
 MBBS 220 UITM 7th BATCH 2009/2014

T wave Inversion

Observed during acute ischemia (patient is currently having chest pain)

Usually associated with ST segment changes (depression/elevation) – resolved after pain subside
T wave inversion maybe permanent even after the pain subside

Indicate diagnosis of:

1. Non STEMI infarction (subendocardial infarction and NOT transmural infarction)

Other differential diagnosis

1. Pericarditis (global –all leads)

2. Myocarditis (global –all leads)
3. Juvenile Pattern – children and young adults with no cardiac disease
4. Intracranial bleed (sape2 tanye prof sazli eikh?)

YANAHANAPI Page 36
 MBBS 220 UITM 7th BATCH 2009/2014

ST segment Elevation

Common cause would be of transmural MI (STEMI)

Total occlusion of the coronary vessels
It would resolve in 24-48 hours with exception of anterior MI (chronic)
Also occurs in vasopastic and prinzmental angina

Non ischemic causes of ST elevation includes

1. Acute pericarditis
2. Early repolarization

ST elevation in lead II, II, AVF and the lateral leads suggestive of Inferolateral MI

Significant Q wave
Are wide and broad: 1mm deep and 1mm wide
Normal finding in

- Lead III
- Lead V1

other than that the Q wave is deemed pathological

signifying transmural MI (post)

YANAHANAPI Page 37
 MBBS 220 UITM 7th BATCH 2009/2014

Evolution of a Myocardial Infarction

Evolving Changes in an Episode of Acute Myocardial Infarction

1. Within the early minutes of onset of pain, there would be hyperacute tall T waves (peaked T waves) – the initiation of ST
elevation
2. Within an hour the ST segment would be noticeably elevated, indicating the onset on myocardial necrosis
3. If thrombolysis is administered, we would be looking for specific changes on the ECG. A 50% reduction in ST segment elevation
is a good indicator of success. In this picture, the ST elevation has reduced by more than 50% from picture 2. We would expect
to see these changes within 90 minutes of administering thrombolysis. You can also see the T wave invertion is much
deeper. This is a good sign of reperfusion. (blood flow returning to the damaged area.)
4. 24 hours later, the ST segment may have returned to the iso-electric line. In this picture you can see the ST segment is back on
the iso-electric line but the T wave remains inverted. It may stay inverted for days, weeks or months.
5. After a few months the ECG looks relatively normal. Compare picture 6 with picture 1. They look much the same but for the
deep Q wave in picture.
6. A deep Q wave is an indicator of myocardial tissue death and will remain on the ECG. A "pathological" Q wave
is not "time-specific". It may be there from a previous heart attack and therefore is not part of the criteria for evaluating an
Acute Myocardial Infarction.

Source from : http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/acs/changes.php

YANAHANAPI Page 38
 MBBS 220 UITM 7th BATCH 2009/2014

Example:

ACUTE ANTEROLATERAL ST ELAVATION MYOCARDIAL INFARCTION (STEMI)

Lead II shows sinus rhythm, with ventricular rate of 75 beats per minute, noted that there is ST elevation in lead I,II, AVL V 2- V5 with
presence of pathological Q wave in the precordial leads
Suggestive of anterolateral STEMI which correspond to the occlusion of the Left descending Artery

**ACUTE INFERIOR+POSTERIOR ST ELAVATION MYOCARDIAL INFARCTION (STEMI)

Lead II shows sinus rhythm, with ventricular rate of 86 beats per minute, noted that there is ST elevation in lead II,III and AVF with ST
depression in lead V1-V2 suggestive of posterior infarction also
Suggestive of posterior inferior STEMI which correspond to the occlusion of the Right Coronary Artery

YANAHANAPI Page 39
 MBBS 220 UITM 7th BATCH 2009/2014

ACUTE SEPTAL MYOCARDIAL INFARCTION (STEMI)

Lead II shows sinus rhythm, with ventricular rate of 86 beats per minute, noted that there is ST elevation in lead V2-V3 with T inversion in
the involved lead
Suggestive of septaS STEMI

PULMONARY EMBOLISM

- Deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic” finding (but rare)
- Sinus tachycardia (most common presentation)

**Extra:

Endocardial surface of the posterior wall faces the precordial leads, changes resulting from the
infarction will be reversed on the ECG.

Therefore, ST segments in leads overlying the posterior region of the heart (V1 and V2) are initially
horizontally depressed.

As the infarction evolves, lead V1 demonstrates an R wave (which in fact represents a Q wave in
reverse).

YANAHANAPI Page 40
 MBBS 220 UITM 7th BATCH 2009/2014

OTHER FORM OF ECG

YANAHANAPI Page 41
 MBBS 220 UITM 7th BATCH 2009/2014

HYPERKALEMIA

Mild hyperkalemia (serum levels less than 6.5 mEq/l):

- leads II, V2 and V4 demonstrate tall, tented, symmetrical T waves with a narrow base. The P wave remains normal, as does the
QRS complex

Moderate hyperkalemia (6.5 mEq/l - 8.0 mEq/l):

- QRS complex broadens and the S wave is widened in leads V3 - V6.

- S wave become continuous with the tented T waves and eventually the ST segment disappears
- Duration of the P wave is increased, while the amplitude is decreased

Severe Hyperkalemia greater than 8.0 mEq/l :

- P wave duration and PR interval duration both increase, until the P wave eventually disappears entirely.
- QRS complex is diffusely broadened and continuous with the tall, tented T wave in all leads

YANAHANAPI Page 42
 MBBS 220 UITM 7th BATCH 2009/2014

HYPOKALEMIA

- Associated with progressive ST depression, progressive flattening or inversion of the T waves

- development of U waves
- increased amplitude and duration of the P wave
- increase amplitude of QRS complexes
- slight increase in the duration of the PR interval
- hypokalemia affects automaticity of the pacemaker cells and leads to multiple arrhythmias such as sinus bradycardia,
atrioventricular block, atrial flutter and Torsades de Pointes

DIGOXIN EFFECT

ST sagging and shortening, best seen in leads V4, V5 and V6

YANAHANAPI Page 43
 MBBS 220 UITM 7th BATCH 2009/2014

ACUTE PERICARDITIS

- Acute pericarditis demonstrate diffuse ST segment elevation in all leads except aVR and V1
- ST changes are sometimes associated with concurrent PR segment depression in the same leads and an increased sinus heart
rate
- 2-5 days after the acute presentation, the ST segments return to baseline. Following this return to baseline, the T waves in all
leads except aVR become inverted.

PACEMAKERS

- electrical impulses are seen as "pacemaker spikes" identified by their abrupt vertical spike (arrows below), preceding the
atrial or ventricular complex

YANAHANAPI Page 44
 MBBS 220 UITM 7th BATCH 2009/2014

APPENDIX
&
REFFERENCE

YANAHANAPI Page 45
 MBBS 220 UITM 7th BATCH 2009/2014

VECTORS OF ECG

The positive signs is your LEADS ( x kesah la limb or precordial leads)

- a positive (upward) deflection if the impulse propagates straight towards your lead
- a negative (downward) deflection if the impulse propagates away from your lead

YANAHANAPI Page 46
 MBBS 220 UITM 7th BATCH 2009/2014

YANAHANAPI Page 47
 MBBS 220 UITM 7th BATCH 2009/2014

POSITION OF THE LIMB LEADS AND THE PERICARDIAL LEADS

YANAHANAPI Page 48
 MBBS 220 UITM 7th BATCH 2009/2014

REFERENCE

150 PRACTICE ECG: INTERPRETATION AND REVIEW (3RD EDITION)

ECG MADE EASY. John R Hampton
THE ECG IN PRACTICE (5TH EDITION)
THE ECG WORKBOOK (2ND EDITION)
THE COMPLETE GUIDE TO ECGS (3RD EDITION)

YANAHANAPI Page 49