ECG
NORMAL ECG WAVE FORMS
BASIC INTERVALS
ABNORMAL WAVEFORMS
ST ELEVATION
ST DEPRESSION
• Myocardial ischaemia/
• Myocardial ischaemia/
•
•
•
•
infarction
Acute pericarditis,
myocarditis
LVH/LBBB
Brugada pattern (RBBB
with ST elevation in right
precordial leads )
Hyperkalemia
•
•
•
•
•
•
infarction
LVH (strain pattern )
LBBB,RBBB, WPW
Drugs ( digitalis )
Hypokalemia
Cardiomyopathies
Normal variant
TALL T WAVES
T WAVE INVERSION
• Hyperacute phase of AMI
• Myocardial
• Prinzmetal angina
ischaemia/infarction
• LVH/RVH
• LBBB/RBBB,WPW
• Hyperkalemia
• CVA
• LVH/LBBB
• Acute pericarditis
WIDE QRS
• Normal variant
• LBBB/RBBB, WPW,
VPC’s
• Hyperkalemia
QT PROLONGATION
• Electrolyte disturbances- hypokalemia, hypocalcemia,
•
•
•
•
hypomagnesemia
Drugs- classI and III antiarrhythmic agents,
phenothiazines, TCA, antibiotics (erythromycin,
pentamidine), terfinadine, cisapride
Myocardial ischaemia/ infarction
CVA
Congenital – Romano-Ward syndrome, Jervell and Lange
–Nielsen syndrome (AR with congenital deafness )
LOW VOLTAGE QRS
• Defines as QRS <5 mm in
all the limb leads and less
than 10 mm in all the chest
leads
• CAUSES
Normal variant
Obesity
Pleural/ pericardial effusion
COPD, Constrictive
pericarditis
Cardiomyopathies
CALCULATION OF RATE
If rate is regular
➢ No of large boxes (0.2 sec ) between 2 successive QRS
complexes (R-R interval ) and divide 300 by this number
Or
➢ 1500 divided by the number of small boxes (0.04 sec )
If rate is irregular
➢ Count the number of QRS complexes in 6 second interval
and multiply by 10
QRS AXIS
• Direction of ventricular
•
•
•
•
depolarisation
Normal axis is down and
to the left
Normal axis varies from
-30 ° to +110°
Axis > -30 ° or more
negative is LAD
Axis >+110° 0r more
positive is RAD
CAUSES OF AXIS
DEVIATION
RAD
• Spurious
• Normal variant
• Dextrocardia
• Right ventricular overload
( acute- pulmonary
embolism, severe asthma ;
chronic- COPD,
pulmonary stenosis,
pulmonary hypertension )
• Lateral wall MI
LAD
• Normal variant
• LVH
• LBBB
• Left anterior hemiblock
• Ostium primum ASD,
tricuspid atresia
ATRIAL ENLARGEMENT
• Normal P wave in every
lead is ≤ 2.5mm (0.25 mV)
in amplitude and less than
0.12 sec ( 3 small squares )
in width
• P wave exceeding any of
these dimensions in any
lead is abnormal
• Normal P wave is positive
in lead II and negative in
avR
RIGHT ATRIAL ENLARGEMENT
• Also known as P- pulmonale
• Abnormally tall P wave ( height >2.5mm )
• No effect on the total duration of atrial depolarisation , so
width remains normal
• Best seen in leads II,III, aVf and V1
LEFT ATRIAL ENLARGEMENT
• Also known as P-mitrale
• Because left atrium depolarises after the right atrium LAE
prolongs the total duration of atrial depolarisation so width
increases
• Classically, LAE produces a wide P wave ( > 0.12 sec ),
amplitude may be normal or increased
• Best seen in leads II and V1.
• In V1 a biphasic p wave may be seen, with a small initial
positive deflection followed by a wide negative deflection.
The negative component is longer than 0.04 sec in
CAUSES OF ATRIAL
ENLARGEMENT
RAE
• Pulmonary disease- BA,
pulmonary embolism,
emphysema, bronchitis
• Congenital heart diseasepulmonary stenosis, ASD,
tetralogy of Fallot,
Ebstein’s anomaly
LAE
• Valvular heart diseaseMS,MR,AS,AR
• Hypertensive heart disease
• CAD
• Cardiomyopathies
RIGHT VENTRICULAR
HYPERTROPHY
• R>S in V1
• Often associated with RAD
and T wave inversion in right
to mid precordial leads
• Affects both depolarisation
and repolarisation , so
inverted T waves in rightmid precordial leads (RV
strain )
• Causes- congenital heart
disease (PS, TOF, ASD,
eisenmenger’s syndrome),
LEFT VENTRICULAR
HYPERTROPHY
• Voltage of S in V1 + R in
V5 or V6 >35mm
• R wave in aVl ( 11to 13
mm )
• ST depression with
inverted T waves in leads
with tall R waves ( LV
strain )
• LAD or LAE, LV
conduction delay (wide
QRS ) may be seen
ATRIAL FIBRILLATION
• AF is one of the most common arryhthmias encountered in
clinical practice
• Classified into - paroxysmal (stops spontaneously within
7 days, usually within 48 hrs ), persistant (lasts for >7
days and usually requires cardioversion ) and permanent
(lasts indefinitely or fails to terminate or recurs even after
cardioversion )
• Causes- alcohol abuse ( holiday heart ), autonomic ,
congenital/coronary/hypertensive / valvular heart disease,
cardiomyopathy, cardiothoracic surgery, idiopathic,
thyrotoxicosis, pulmonary disease
ECG IN AF
• Irregular wavy baseline produced by rapid f waves
• An irregular ventricular rate
HEART BLOCK
Degree
AV conduction pattern
First degree block
Uniformly prolonged PR interval
2nd degree (intermittant conduction
failure )
Mobitz type I:
progressive PR
prolongation
3rd degree block
No AV conduction
Mobitz type II:
sudden conduction
failure
MOBITZ TYPE I
vs MOBITZ TYPE II
COMPLETE HEART BLOCK
• P waves are present with a regular atrial rate faster than
the ventricular rate
• QRS complexes are present with a slow (usually fixed )
ventricular rate
• The P waves have no relation with the QRS complexes
and PR intervals are completely variable because the
atria and the ventricles are completely disconnected
MYOCARDIAL INFARCTION
• Localisation of infarction
• Anterior – leads V3, V4 ( septal V1-V2)
Reciprocal changes- II, III, avf
• Lateral wall- I, aVl, V5, V6
Reciprocal changes – III, aVf, V1
• Inferior wall- II, III, aVf
Reciprocal changes- I, aVl
• Posterior wall - V1-V3 (depression) reciprocal changes
SEQUENCE OF CHANGES
• The ST segment elevations and the reciprocal changes can
be seen within minutes of the infarct . Tall positive T
waves ( hyperacute ) are also seen at this time and may
sometimes preceede the ST elevation . Sometimes new Q
waves may also appear( acute phase)
• After hours to days ST segments come back to baseline
and at the same time T waves become inverted in the leads
that showed ST elevation (evolving phase )
• Resolving plase- partial or complete regression of ST-T
changes and sometimes of Q waves
PATTERN OF ST ELEVATION
AND DEPRESSION
STEMI
NSTEMI
ECG IN SPECIAL SITUATIONS
HYPERKALEMIA
HYPOKALEMIA
• Tall and peaked T waves
• ST elevation
• Prolongation of PR, QRS and
• Appearance of U wave
• ST depression
QT
• Loss of P waves
• Sine-wave pattern and asystole
CARDIAC
DIGITALIS TOXICITY
NON CARDIAC
• Weakness
• Anorexia
• Nausea and vomiting
• Altered colour perception
• Mental status changes
Bradycardia
• Sinus bradycardia including
sinoatrial block
• Junctional (escape ) rhythm
• AV block including mobitz
type 1 and CHB
Tachycardia
• Accelerated / junctional
rhythm like
nonparoxysmal/junctional
tachycardia
• Atrial tachycardia with block
• Ventricular ectopy including
premature beats,