ECG Basics Part 1

Dr Honey
 Learning objectives
Anatomy of blood supply of heart
Physiology of conducting system of
heart
Interpreting normal ECG- Rate,
rhythm, axis ,wave morphology,
interval & segments
Clinical application : rhythm
abnormalities, conduction
abnormalities, chamber enlargement,
myocardial ischemia
Fundamentals of ECG basics
 Cont.
AVR, AVL and AVF make up an equilateral
triangle, known as Einthovens Triangle.
Information is gathered between these leads
to create three more vectors:
Lead I information between AVR and AVL
Lead II information between AVR and AVF
Lead III information between AVL and AVF
The limb leads I, II and III are called bipolar
leads because they have two associated
electrodes.
Blood supply of heart
View from chest lead
Cont.
 Electrical Conduction System of
the Heart

Different structures depolarises at different speed

 Blood supply of conduction
system
The conducting system provides the heart its automatic rhythmic beat.
Consists of cardiac muscle cells and conducting fibers that are
specialized for initiating impulses and conducting them rapidly through
the heart

Sinoatrial (SA) node is located at the junction of the anteromedial

aspect of the superior vena cava (SVC) and the right atrium (RA)..

In 55-60% of the hearts, artery supplying the sinus node branches from
the right coronary artery

In another 40-45%, the left circumflex artery supplies the SA node.

There are 3 intra-atrial pathways: (1) anterior internodal pathway, (2)

middle internodal tract, and (3) posterior internodal tract
 Cont.
The atrioventricular (AV) node is a superficial structure located just
beneath the RA endocardium, anterior to the ostium of the coronary sinus,
and directly above the insertion of the septal leaflet of the tricuspid valve.

In 85-90% of human hearts, the arterial supply to the AV node is a branch

from the right coronary
In the remaining 10-15% of the hearts, a branch of the left circumflex
coronary artery provides the AV nodal artery.

The bundle of His is a structure that connects with the distal part of the AV
node,

Branches from the anterior and posterior descending coronary arteries

supply the upper muscular interventricular septum with blood, which
makes the conduction system at this site more impervious to the
ischaemic damage, unless the ischemia is extensive.
 P wave : depolarisation of atria
QRS complex : depolarisation of
ventricles
T wave : ventricular repolarisation

Q: first negative deflection after the p-wave

R: positive deflection
S: negative deflection after the R-wave
Small print letters (q, r, s) are used to describe
deflections of small amplitude. For example: qRS =
small q, tall R, deep S.
LETS START THE JOURNEY
 1.Rate
Normal ?
Bradycardia?
Tachycardia?

Usual paper speed = 25mm/sec

1 mm (small square) = 0.04 sec
5 mm (big square) = 0.2 sec
Regular rhythm: 300/ no of large boxes between two R
waves

Irregular rhythm - count number of QRS complexes in 6

seconds, multiply by 10 to obtain rate in BPM
 2.Rhythm
In normal heart, depolarisation begins in SA
node= sinus rhythm

Sinus rhythm(SR) : every P wave is followed

by a QRS, RR interval regular

Atria or AV node depolarisation = atrial or

junctional rhythm

Ventricular depolarisation= ventricular rhythm

 Criteria for sinus rhythm
Rate- 60-99 bpm
Rhythm- regular
P wave 1 per QRS , all same shape
in same lead
PR interval- normal
QRS complex- <0.12 sec,all same
shape
 Regular rhythm
Supraventricular rhythm
- originates above the ventricles: SA, atrial muscle or
AV node
- Depolarisation spreads normally into ventricles, hence
QRS compex is the same: narrow and normally shaped
- Repolarisation is normal so T wave is normal shape

Ventricular rhythm:
- QRS complex is wide and abnormal as depolarisation
spreads slowly
- Repolarisation abnormal, hence inverted T wave
 Irregular rhythm
(supraventricular arrhythmia)
1. Premature atrial complexes
2. Premature junctional complexes
3. Atrial fibrillation
4. Atrial flutter
5. Ectopic atrial tachycardia and rhythm
6. Multifocal atrial tachycardia
7. Paroxysmal supraventricular tachycardia
8. Junctional rhythms and tachycardias
 1.Premature atrial rhythm
Rate- Any
Rhythm- irregular
P wave different shape in same lead
QRS complex- <0.12 sec,all same shape ( if conducted PAC)
2.Premature junctional
rhythm
 3.Atrial fibrillation
Rate- ventricular any rate
Rhythm- irregularly irregular
P wave wavy baseline, not visible
PR interval- unmeasurable
QRS complex- <0.12 sec,all same shape
 4.Atrial flutter
Rate- 250-350 bpm
P wave all same shape in same lead( saw-tooth appearance)
PR interval- unmearsurable
QRS complex- <0.12 sec,all same shape
 6.Multifocal atrial
Rate- >100bpm tachycardia
Rhythm- irregularly irregular
P wave different shape in same lead
PR interval- normal
QRS complex- <0.12 sec,all same shape
7.Supraventricular tachycardia(AVNRT)
Rate- >150bpm
Rhythm- regular rhythm( if paroxysmal SVT- irregular rhythm)
P wave absent
QRS complex- <0.12 sec,all same shape
 8.Junctional escape rhythm
Rate- 40-60 bpm
P wave absent or retrograde p wave
QRS complex- <0.12 sec,all same
shape
 Ventricular arrhythmia
Premature ventricular complexes (PV
Cs)
Aberrancy vs. ventricular ectopy
Ventricular tachycardia
Differential diagnosis of wide QRS
tachycardias
Accelerated ventricular rhythms
Idioventricular rhythm
Ventricular Parasystole
Premature ventricular
rhythm
Accelerated idioventricular
rhythm
Ventricular
tachycardia
Exercise: Rate & Rhythm
3.Axis
 P wave
Are P-waves present?
Do they occur regularly?
Does each QRS have P wave?
Do P-waves size & shape look normal?
( smooth,rounded, bifid, upright, biphasic,
inverted,tall tented,flutter, fibrillation)
Normal P wave morphology: upright,short
& rounded in all leads except aVR,
biphasic in III, aVL, V1, V2
 PR interval
PR interval represents conduction
through AV node and his bundle,
measures time taken for depolarisation
wave to spread from atria to IVS
Normal 0.12-0.2 sec
Shortened ? abnormal connection
between atria and ventricles pre-
excitation
Prolong ? conduction block
 Conduction defects
1st degree block- PR interval>0.2 sec

2nd degree block- atrial depolarisation intermittently fails to induce

ventricular depolarisation.
- Mobitz Type I: Wenckebach= progressive prolongation of PR till
dropped beat, and shortened PR interval following the dropped beat.
Failure of conduction at AV node
- Mobitz type II = intermittent non conducted P waves without
progressive prolongation of PR interval. Failure of conduction at His-
Purkinje system

3rd degree block/complete heart block- results from either his

bundle disease or from bilateral bundle branch block
- complete AV dissociation
first degree block
Mobitz type 1
Mobitz type 2
complete heart block
 Q wave
Small Q normally seen in I, aVL, V4-
V6 due to initial septal depolarisation
, <0.03secs, <3mm deep
Pathologic Q waves >0.03s, in leads
V1- V3
 QRS complex
Represents time for ventricular
depolarisation
Normal 0.12 sec( 3small square)
Longer than 0.12sec wide QRS
complex
Shorter than 0.12sec? narrow QRS
complex
Left Bundle Branch Block (LBBB) QRS ends negatively
in V1
Right Bundle Branch Block (RBBB) RsR pattern in V1
Pulmonary embolism
 features suggestive other features:
of PE:
sinus tachycardia
RBBB
dominant R wave
extreme right axis
in V1
deviation

S1 Q3 T3
P pulmonale

T inversion in V1- nonspecific ST and

V4 and lead III (RV T changes,
strain pattern) including STE
 ST segment
ST segment represents the interval
between the end of ventricular
depolarisation (QRS complex) and
the beginning of repolarisation (T
wave)
Normal ST segment- isoelectric,
same level as the ECG trace between
T wave to the next P wave
Causes of ST elevation

(ELEVATION)
Early repolarisation
LBBB
Electrolyte imbalance
Ventricular hypertrophy
Aneurysm(ventricular)
Treatment(pericardiocente
sis)
Injury( AMI, contusion)
Osborne
wave(hypothermia)
Non-occlusive vasospasm
 Causes of ST depression

Ischemia
strain
Digoxin toxicity
Hypokalemia
hypomagnesemia
 T wave
Causes of T wave Causes of Peak T
inversion wave
Inverted in aVR, V1 and sometimes V2

Ischemia
Ventricular Normal
hypertrophy
Hyperkalemia
BBB
Hyperacute MI
Drug induced
Ventricular origin of
depolarisattion
Increased ICP
 QT interval
Normal less than half RR interval

Bazetts formula: QT = QT / RR
C

QTc is prolonged if >440ms in men

or >460ms in women

QTc is abnormally short if <350ms

 Causes of Prolong QT
interval
Hypokalemia
Hypocalcemia
Hypomagnesemia
Hypothermia
Myocardial ischemia
Increased ICP
Drug induced- Congenital long QT
syndrome
Hypokalemia causing
Torsades de Pointes
Short QT d/t
hypercalcemia
ECG changes in( useful in
MCQ)
Hyperkalemia hypokalemia

Tall tented T
T wave flattening and
Prolong PR interval inversion
Flat P wave ST depression
Widened QRS U wave
prolonged QT (or QU)
Bradycardia
interval
High degree AV block
Sine wave
Hyperkalemia
Clinical application
 Atrial enlargement
Left atrial enlargement

produces broad, bifid P wave in

lead II (P mitrale)

In lead II, bifid P with >40ms

between the two peaks; total P
duration >110ms

In lead V1, biphasic P with terminal

negative portion >40ms and/or
>1mm deep

classically seen in mitral stenosis

when a/w LV hypertrophy, can be

seen in systemic hypertension,
aortic stenosis, MR, hypertrophic
cardiomyopathy
 Right atrial enlargement

produces peak P wave (P

pulmonale) with
amplitude >2.5mm in
inferior leads or >1.5mm
V1 & V2

seen in pulmonary
hypertension
 Ventricular hypertrophy
LVH - increased R wave
amplitude in the left-sided ECG
leads (I, aVL and V4-6) and
increased S wave depth in the RVH
right-sided leads (III, aVR, V1-3)

Sokolov-Lyon criteria Rt axis deviation

S wave depth V1 + tallest R
wave height V5/6 >35mm
LV strain pattern ST
depression and T inversion at
left-sided leads
Dominant R wave in V1,
dominant S wave in V5-6
RV strain pattern ST
depression/T inversion in
right precordial (V1-3) and
inferior leads
Myocardial ischemia
 ECG Criteria for diagnosing
STEMI
New ST elevation at the J point in at
least 2 contiguous leads of 2 mm
(0.2 mV) in men
or 1.5 mm (0.15 mV) in women in
leads V2V3
and/or of 1 mm (0.1mV) in other
contiguous chest leads or the limb
leads.
Anteroseptal STEMI
Inferior-lateral-posterior
STEMI
 Post MI
Posterior extension suggested by:
Horizontal ST depression in V1-3
Tall R waves in V2-3
Dominant R wave (R/S ratio >1) in V2
Upright T wave in V2-3
 RV infarct
RV involvement is suggested by:

ST elevation in V1 (the only standard lead that looks

directly at RV)

ST elevation in lead III > lead II

Other features:

magnitude of STE in V1 > V2

ST in V1 is isoelectric but ST in V2 is markedly

depressed

STE in V1 and ST depression in V2

Inferior STEMI + RV
infarct
Pericarditis
 Case 1
54 year-old man, presents with two hours of crushing
central chest pain with dyspnoea.
PMH: Type II DM, HPT
Social Hx: Smoker, lorry driver
 Case 2:
23 year-old female with 2 hours history
of sudden onset of palpitations
No significant past medical history
 Case 3:
76 year old female with three months
history of palpitations
PMH: Hypertension,TIA
 Case 4:
81 year-old lady with 3 weeks history of
syncope and giddiness
PMH: Hypertension
 Case 6:
24 year-old man with no known medical
illness.
Medical check up for employment
 Case 7:
52 year-old male presents with 3 days history
of pleuritic chest pain and breathlessness.
PMH: Hypertension
History of right femur fracture
 Case 8
70 year-old lady, presents with fever and
productive cough of one week
Case 9 :This 45-year-old Indian man has decreased effort
tolerance 3/12

1.What is the diagnosis?

2.List three causes of this ECG finding.

 Take home massage
1.Rate Tachycardia or bradycardia?

2. Pattern of QRS complexes Regular or irregular?

If irregular is it regularly irregular or irregularly irregular?

3. QRS morphology
Narrow complex sinus, atrial or junctional origin.
Wide complex ventricular origin, or supraventricular with aberrant conduction.

4. P waves
Absent sinus arrest, atrial fibrillation
Present morphology and PR interval may suggest sinus, atrial, junctional or even
retrograde from the ventricles.

5. Relationship between P waves and QRS complexes

AV association (may be difficult to distinguish from isorhythmic dissociation)
AV dissociation
complete atrial and ventricular activity is always independent.
incomplete intermittent capture.