ECG

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 INTRODUCTION
● ECG is the graphic display of the electrical
forces generated by the heart. Its history dates
back to 1887 when AUGUSTUS D WALLER
recorded the electrical activities of the heart,
but felt it would be of less help in clinical
practice. In 1902, WILLEM EINTHOVEN
recorded an electric current from human heart
using an instrument called string galvanometer.
In 1911, 1st ECG machine was made by the
CAMBRIDGE SCIENTIFIC INSTRUMENT
SOCIETY & was delivered to Sir THOMAS
LEWIS in London.

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 CONT……………………
• It is composed of 12 leads. It is used to
diagnose chamber enlargement,
conduction abnormalities, dysrhythmias,
MCI, drug effects, electrolyte alterations.
Application of more advanced ECG
technology includes exercise stress test
to detect CAD, HOLTER/ TELEMETRY
monitoring & electrophysiological testing
to diagnose & treat dysrhythmias &
increased use of pace maker technology.
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 LEADS
• There are 12 leads which gives electrical activity of the
heart of the heart in 12 different directions.
• LIMB LEADS- electrodes placed on or adjacent to 4
limbs.
• SIX in number--- I, I I, I I I, aVR, aVL, aVF.
•
CHEST LEADS—precordial leads placed on specific
areas of chest.
• V1, V2, V3, V4, V5, V6 .
• Limb electrodes are placed on right arm (RA), left arm
(LA), left leg (LL).
• Right leg (RL) electrode is a ground electrode.
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 COLOUR CODE
• RA – white

• LA - black

• RL – green

• LL - red

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 standard six chest electrode sites
• V1 4th intercostals space,rt sternal border
• V2 4th intercostals space, lt sternal border
• V3 5th intercostal space, midway b’n V2
& V4
• V4 5th intercostals space midclavicular
line
• V5 5th intercostals space ant. Axillary line
• V6 5th intercostals space mid axillary line
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 ECG Electrode Placement
Exercise Configuration
The right & left arm
electrodes are transferred
Standard Configuration to the upper torso while Standard Configuration
Right Arm (white) the leg electrodes are Right Leg (green - ground)
transferred to the lower
Left Arm (black) torso Left Leg (red)

Precordial
Leads

V1 red V3 green V5 orange

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V2 yellow V4 blue V6 violet
 bipolar leads
• LEAD I--- Left arm (+), right arm (-)

• LEAD II—Left leg (+), right arm (-)

• LEAD III--- Left leg (+), left arm(-)

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Bipolar Leads

• 1 positive and 1 negative

electrode
– RA always negative
– LL always positive
• Traditional limb leads are
examples of these
– Lead I
– Lead II
– Lead III
• View from a vertical plane

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 unipolar limb leads
• The same limb electrodes are used to
form 3 unipolar limb leads aVR, aVL, aVF.
a =augmented, V=unipolar. They use only
one electrode at a time to record the
electrical forces generated from the heart.
• aVR = Rt arm electrode.
• aVL = Lt arm electrode
• aVF = Lt leg electrode
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Unipolar Leads

• 1 positive electrode & 1

negative “reference
point”
– calculated by using
summation of 2 negative
leads
• Augmented Limb Leads
– aVR, aVF, aVL
– view from a vertical plane
• Precordial or Chest
Leads
– V1-V6
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– view from a horizontal
• ECG records only the electrical event that is the
stimulus for mechanical contraction. This electrical
process is called action potential. It has 5 phases,
recorded in the form of P- QRS- T wave forms.
• P wave—phase 0 of action potential correlates with P
wave in the muscle cells of atria.
• QRS wave--- In the muscle cell of ventricles, phase 0 of
action potential corelates with QRS complex.
• Phase 1,2,3---repolarisation phenomenon.
• ST—phase 2
• T wave- phase 3.

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[Link] 13
P- WAVE

• It preceeds QRS [Link] is

positive in leads I,II,aVF & V4
through V6. It is negative in
leads aVR, & biphasic in aVL, &
V1 through V3. It is gently
rounded, not peaked or notched.
Its height is normally less than
3mm, & width less than .11
seconds.
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QRS- COMPLEX
□ Represents depolarization of ventricular
muscle cells. It follows each P wave. It is
predominantly +ve in leads that look at
the heart from the heart from the lt side (I,
aVL, V5, V6 ) & in leads that look at the
inferior undersurface of the heart (I I, I I I,
aVF ). It is –ve in leads that look at the
heart from the rt side(aVR, V1, V2). It is
biphasic in leads V3, V4 & sometimes I I I.
Normal QRS complex is less than 25mm
high & less than .10 sec in duration.
□
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ST SEGMENT

▪ Interval of time b’n the end of QRS

complex ( a junction called the J point )
& the beginning of T wave. ST segment
represents the beginning of ventricular
repolarisation. It is normally isoelectric.
Greater degrees of ST segment
displacements may indicate ischaemia,
injury, strain, drug or metabolic effects.
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 T WAVE

■ T represents the end of repolarisation of

the ventricles & always follows the QRS
complex. It is normally oriented in the
same direction as the QRS complex. It is
slightly rounded & asymmetrical & usually
exhibits a smooth take off from the end
of ST segment.

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 U WAVE
■ Its significance is unknown, but may
represent further repolarisation of
ventricles. It is observed in chest leads.
It may be upright in patients with
hypokalemia or inverted in patients
with ischaemia or it ventricular
hypertrophy.

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[Link] 19
 PR SEGMENT

• Distance from the end of P wave to the

beginning of QRS complex. It represents
the total amount of time required for
depolarisation of atria.

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 PR INTERVAL
• Measures from the beginning of P wave
to the beginning of QRS complex. It
represents the total amount of time
required for depolarization of atria ( p
wave) as well as the time required for the
impulse to travel slowly through the AV
junction, through the bundle branches, &
just upto the point of QRS.

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 QRS INTERVAL
■ Measured from the beginning of QRS
complex to its end point, called the J
point. It represents the time required for
repolarisation of both ventricles. The
normal QRS interval is less than .1 sec
mostly .08 sec.

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 Waveform Components:
J-Point

Junction between end of QRS

and beginning of ST segment;
Where QRS stops & makes a
sudden sharp change of
direction

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QT INTERVAL

● The QT interval represents the total time

required for both depolarization &
repolarisation of the ventricles to occur. It
is measured from the beginning of QRS
complex to the end of T wave. The
normal QT interval ranges from .35 to .45
seconds. The length of QT interval
normally varies according to age, gender,
& heart rate. As the heart rate increases
the QT interval decreases & vice versa.
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 Specifics of R wave progression
● The initial portion of the QRS complex represents
depolarization of the septum. The remainder of the QRS
complex represents depolarization of the rt & lt
ventricles. Sincee the lt ventricle is much larger than the
rt , most of the QRS complex reflects depolarization
forces recorded from the larger lt ventricle. In lead V1,
septal depolarization is represented by small r wave, the
rest of QRS is –ve because depolarization forces are
moving away from the recording electrode. In lead V6,
septal depolarization is represented by small q wave,
the rest of QRS is +ve.

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 NORMAL PACE MAKER RATES
• Automatic pace maker cells in the SA
node generate impulses at a rate of b’n
60 to 100 beats/minute. If the SA node
fails to generate an impulse, then the
lower escape pacemaker site takes over.
It has a slower intrinsic rate of discharge.
The AV junction has an intrinsic rate of 40
to 60 bpm. If the AV junction takes over at
a rate of 40 to 60 bpm, when SA node
fails it is called junctional escape rhythm.
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• Ventricular pacemaker cells
have an intrinsic rate of
discharge of 15 to 40 bpm. If
impulses above the ventricles,
fails to reach ventricles,
ventricles beat at a rate of 15
to 40 bpm. This is called
ventricular escape rhythm.
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ECG basics – Paper Speed & Heart
Rate
.1
mv
pape
Voltage
r

.5
mv
.04 Time .20
seconds seconds
Paper speed = 25mm /
second
Heart Rate = number of R-waves in a 6 second strip divided by
10 = 1500 divided by the number of small boxes
between
consecutive R-waves
= large square estimation counts
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( 300 - 150 - 100 - 75 - 60 - 50 - 43 ) 28
 ECG GRAPH PAPER
• Composed of horizontal & vertical lines with light lines
and dark lines that intersect to form small & large
squares. Horizontal measurements reflects units of time,
vertical measurement reflects measurement of voltage.
• Each small square= 1 mm =.04 sec in width, .1mv in
height.
• Each large square= 5 mm =.20 sec in width, .5mV in
height. It consists of 25 small squares.
• The standard speed for recording the ECG is 25mm/sec.

• At this speed 5 large squares are present.

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 ECG STANDARDISATION
• Standardisation is adjusted to increase or
decrease the size of QRS in order to
make ECG interpretation easier. At STD
1 (normal standardization) a box of 1 mV
in height is recorded. (equals to 2 large
squares or 10mm) . At ½ standardization,
a box .5mV in height is recorded (equals
1 large square or 5mm)

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[Link] 31
CALCULATION OF HEART RATE
• 1500 method
• This method is used only if the rhythm is regular. Count
the no. of small squares b’n 2 consecutive QRS
[Link] are 1500 small squares in a minute
(.04 sec /square. Divide the no. of small squares by
1500. This result equals heart rate/minute.
• 2] Count the no. of large boxes b’n 2 succesive QRS
complex & divide a constant by this.(300)
• 3] If the heart rate is irregular counting the no. of cardiac
cycle every 6 seconds & multiply this by 10. A cardiac
cycle is the interval b’n 2 successive R waves. (top of
ECG paper is scored with vertical marks every 3
seconds.)

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 LEAD AXIS

The QRS axis represents the major direction of

depolarization in the ventricles. It is determined
by analyzing the shape of QRS complex in each
lead. The deflection of QRS complex may be
predominantly +ve, -ve, or biphasic. Each lead
records a QRS complex with a particular shape
because each lead looks at the heart from a
different direction. The direction of ventricular
depolarization in each lead is called lead axis.

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 Axis Quadrants
Quadrants
• Left axis -90
+120
-30 to -90 ° ° -60
°
• Normal axis aVR ° aV
-150 No
-30 to 90° LAD L
° Man’s
• Right axis -30°
Land
90 to 180°
+180 0° I
• Extreme Right axis
° Norma
or “No Man’s Land
RAD l
-90 to 180° +30°
+150
°
+120 +60
° +90° °
III aVF II
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[Link] 35
 NORMAL SINUS RHYTHM
• In NSR pacemaker impulses are initiated
in the SA node, travel through the atrial
pathways, and are delayed at the AV
node. The P wave is usually upright in
lead I I, I I I, aVF & V1. P-P & R-R
intervals are equal & regular. Atrial &
ventricular rates are identical & range b’n
60-100 bpm.

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SINUS TACHYCARDIA

⚪ Sinus rhyrhm at a rate equal to or

greater than 100bpm.

⚪ SINUS BRADYCARDIA

⚪ Sinus rate with rate less than 60

bpm.

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■ Causes
■ Vagal stimulation, physiologic causes(in
well trained athletes), sleep.
■ Hypothyroidism, hypothermia, electrolyte
imbalance (hyperkalemia)
■ Inf. Wall myocardial ischaemia
■ sick sinus syndrome.

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 SINUS ARRHYTHMIA (sinus dysrhythmia )

• Here there is a sinus rhythm with a rate that

varies with respiration. It is usually a benign
rhythm disturbance characterized by alternate
speeding up & slowing down of the heart rate.
Respiratory sinus arrhythmia is a normal finding
in children & young adults.
• Non respiratory sinus arrhythmia may be
observed in persons with cardiac diseases, MCI,
esp. in association with sinus bradycardia,
digoxin therapy or enhanced vagal tone.
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• The characteristics of sinus arrhythmia
are the same as those of NSR but the R-
R interval varies.
• In resp. SA the rate increases with
inspiration & decreases with expiration.
• In non resp. SA there is irregularity of the
rhythm.

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ATRIAL FIBRILLATION
Supra ventricular dysrhythmia,
characterised by multiple ectopic
atrial foci, uncoordinated atrial
contraction & a classically irregular
ventricular rate.
Etiology
Heart failure, IHD, valvular
heart disease, cardiomyopathy, CHD,
WPW Syndrome, Sick sinus syndrome.

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● Characteristics
● No P wave instead fibrillatory wave,
represents abnormal impulses that arise
within the atria. ‘f’ waves are small, poorly
defined, distorts the base line , fine or coarse
in appearance.
● R-R interval is irregular b’coz conduction
through AV node is variable.
● QRS complex usually narrow unless
conduction in ventricles are [Link]
waves are best diagnosed in leads I I, I I I,
aVF, V1 & V2.
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[Link] 43
 ATRIAL FLUTTER
• It is supraventricular dysrhythmia
characterized by the appearance of saw
toothed shaped flutter waves at a rate b’n
250 to 350/minute.
• ETIOLOGY
• Hyperthyroidism
• Valvular diseases
• IHD, MCI
• Pericardial diseases.
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• P wave absent. Flutter wave represents
abnormal depolarization of atria. They
assume a saw toothed or picket fence
shape mostly seen in leads I I, III, aVF &
V1.
• Ventricular rate slower than atrial rate
b’coz AV nodes trigger impulses.
• The conduction rate of F waves to QRS
complex is an even multiple. (2:1, 4:1,
6:1)
• R-R ratio is regular if the conduction
ratio is even.
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[Link] 46
 VENTRICULAR DYSRHYTHMIA
• Ventricular premature complex is a premature
ectopic impulse that originates some where in
the ventricles below the Bundle of His. Also
called Ventricular premature complex.
• Etiology
• 1. Stress, exercise, alcohol, caffeine, electrolyte
imbalance
• [Link], MCI, cardiomyopathy, CHD, hypoxemia,
reperfusion after thrombolytic therapy ,
Heart surgery or contact of endocardium with
catheters.

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Charecteristics

■ Ectopic QRS complex is earlier than expected.

■ R_R interval irregular, ectopic QRS complex is
wider than normal QRS complex and its
morphology is different than the normal beat.
■ The ST segment and T wave slope in opposite
direction form ectopic QRS complex. B’coz
depolarization is abnormal repolarisation is
also abnormal.

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 VENTRICULAR FLUTTER
• Is ventricular rhythm that looks like a very
rapid ventricular tachycardia.
• Characteristics
• Rate b’n 250- 300 /minute
• Discrete QRS complex as well as ST
segment & T wave deflections are
difficult to visualize. Large amplitude wave
form appear continuously.
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 TORSADE DE POINTES
• Is a unique variant of ventricular tachycardia in which
QRS complex appears to twist around the baseline,
frequently found with abnormal prolongation of the QT
interval.
• Etiology
• Electrolyte abnormalities(hypomagnesemia,
hypokalemia, hypocalcemia)
• Psycotropic drugs
• Acute MCI
• Here the amplitude of QRS complex waxes & [Link]
was originally described by DESSERTENNE as ‘twisting
of the points’. Ventricular rate is extremely rapid.
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VENTRICULAR ASYSTOLE
□ Complete absence of electric activity of the
heart (cardiac standstill). Represents the
terminal cardiac event in a variety of
diseases.
□ Etiology
□ Failure of normal intrinsic cardiac
pacemakers(due to drugs, MCI).
Protracted episodes of ventricular failure.
□ Characteristics
□ No ECG wave form identifiable. Baseline
flat.

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ATRIOVENTRICULAR
BLOCK
• First Degree
• Here consistently prolonged conduction b’n
atria & the ventricles. It is characterized by a
partial block within the AV node resulting in
prolongation of PR interval & preservation of
underlying rhythm.
• Etiology
• Drugs, increased vagal tone, hyperkalemia, MCI,
Myocarditis.
• Characteristics
• P-R interval greater than .2 sec
• Length of prolonged P-R interval constant.

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 Second degree – MOBITZ TYPE
1 or WENCHEBACH
• Intermittant conduction b’n atria & ventricles. Location of
block within AV node.
• Etiology
• Digitalis, excessive vagal tone, Inf. Wall MCI, IHD, Myocarditis
• Characteristics
• Progressive lengthening of P-R interval until a QRS complex is
dropped.
• P wave appears on time , but no QRS follows.
• P-P interval constant, as the P-R interval gets longer, R-R interval
gets shorter.
• R-R interval is irregular owing to dropped beats, causing QRS
complexes to appear clustered together.

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Second degree AV block—TYPE II-
MOBITZ TYPE II
Reflects intermittent & sudden loss of conduction
b’n the atria and the ventricles. It is dangerous &
can proceed to complete heart block.
Etiology
Ant. Wall MCI, drugs
Characteristics
P-P interval & P-R interval regular. R_R interval
irregular b’coz of intermittent & sudden
appearance of dropped beats. QRS wider than
normal b’coz of associated conduction block in
ventricles.
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 THIRD DEGREE AV BLOCK
• Complete heart block represents complete absence of
conduction b’n atria & ventricles. An escape pace maker
below the level of the block may take over at a slower
rate. There is independent beating b’n atria & ventricles.
P wave appears at one rate where as QRS complex
appears at slower rate.
• Etiology
• Drug toxicity, excessive vagal tone , acute MCI,
myocarditis, endocarditis.
• Characteristics
• P-P interval & R-R interval constant. Atria & ventricles
rate different.

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 RIGHT BUNDLE BRANCH
BLOCK
• Results from conduction delay or block within the Right bundle
branch.
• Etiology
• Rt ventricular hypertrophy, rt ventricular strain, ASD, CAD,
Myocarditis.
• Charecteristics
• QRS complex is .12sec or more in width. (If greater than or equal to
.12sec, block is complete RBBB, if b’n .10 .12sec, block is
incomplete RBBB.
• QRS complex is predominantly positive and often assumes an rSR’
[rabbit ear] morphology in right precordial leads V1 & V2.
• A wide or deep S wave in lt sided leads I, aVL, V5 & V6 represents
delayed activation of rt ventricle.
• A downsloping ST segment & inverted T wave in leads V1 & V2
represents secondary repolarising changes.

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 RBBB
• RBBB in V1
– no change in initial
impulse travel
• small r wave
– impulse depolarizes
LV by itself since
RBBB
– RV depolarized by
impulse thru muscle
• it now contributes to
complex R-S-
– travels toward + R´
electrode creating
positive deflection
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– rSR’ pattern in V1 & V2

R S R’

J
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poin
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LEFT BUNDLE BRANCH BLOCK

• Left bundle branch block results from a conduction delay or block

within the left bundle branch.
• Etiology
• Lt ventricular hypertrophy, cardiomyopathy, H.T, CAD, myocarditis
• Charecteristics
• The QRS complex is .12 seconds or more in width.
• The Qrs complex is predominantly _ve in rt chest leads V1 & V2. A
wide, deep S wave makes up the majority of the QRS complex &
represents delayed activation of the lt ventricle.
• The QRS complex often assmes a +ve rSR’ morphology in leads I,
aVL, V5, V6.
• The ST segment & T wave are oriented in the opposite direction to
the main QRS. They are called secondary ST changes and are
normally found in LBBB.

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 LBBB
• LBBB in V1
– initial deflection altered
since travels right to left
now
• Q wave or small q wave
– RV depolarizes
unopposed
• may produce small r
wave
– travels across septum
to depolarize LV
• deep S wave
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DIFFERENCE B’N BUNDLE
BRANCH BLOCKS
RBBB LBBB
▪ QRS wide & ▪ QRS wide &
predominantly +ve in predominantly _ve in
V1 V1
▪ RSR’ in V1 ▪ RSR’ in V6
▪ Deep S in V6 ▪ Wide Deep S in lead
V1

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MYOCARDIAL INFARCTION
□ The diagnosis of MCI is based on patient’s clinical
history, serum cardiac enzymes, & ECG. For an
accurate diagnosis and evaluation of MCI, injury &
infarction, serial ECG’s must be obtained.
□ ECG changes of ISCHAEMIA, INJURY, INFARCTION
□ Myocardial ischaemia denotes a temporary
reversible reduction of blood supply to heart muscles
and is the earliest manifestation of reduced coronary
blood flow. Ischaemia is represented by T wave
changes on the ECG. The normally upright,
asymmetrical T wave becomes deeply inverted &
symmetrical.T wave inversion is seen during episodes
of acute ischaemia but may not show up for hours or
days after the initial event.

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• MYOCARDIAL INJURY results from an acute prolonged
reduction in blood supply to the myocardium. Injury is
represented by ST segment changes. ST segment elevation
occurs during subepicardial injury, often appearing within
minutes to hours after the acute event. The ST segment is
displaced upwards from the baseline and its shape is coved or
convex. The J point (at the beginning of ST SEGMENT) is also
elevated. This injury pattern represents reduced blood supply
through a major epicardial coronary artery supplying oxygen to
a large portion of heart’s outer surface.
• 2 imp. Causes for this is atherosclerosis with sudden clot
formation & coronary artery spasm.
• ST SEGMENT depression occurs during sub endocarial injury
where subendocardium is injured when blood supply is
compromised.
• ST segment depression is a clinical indicator of CAD during
stress test. The morphology of ST segment depression during
exercise and the duration of ST segment depression after
exercise are important criteria in assessing the severity of CAD.
[Link] 64
 INFARCTION
◆ MCI denotes irreversible death of heart
muscles due to prolonged artery
occlusion. The classic ECG clue to
infarction is the appearance of significant
Q waves in leads representing the area of
damage.
◆ Abnormal Q waves represents electrically
silent areas of infracted heart muscle.
The appearance of significant Q waves
may be immediate or may lag behind
other changes of acute MI by hours to
days.
[Link] 65
[Link] 66
 Key points
Accurate evaluation of MCI, injury and infarction require examination of
serial ECG.
Ischaemia denotes temporary reversible reduction of blood supply to the
heart muscle. It is reflected by T wave inversion on the ECG.
Acute ischaemia may cause normalization of T wave in patients with
preexisting T wave inversion.
Injury denotes prolonged, but reversible reduction of blood supply to the
heart muscles. It is reflected by either elevation or depression of ST
segment on ECG.
ST segment elevation is associated with sub epicardial injury, whereas ST
segment depression is associated with subendocardial injury.
Infarction denotes irreversible death of heart muscle. It may produce
significant Qwaves on ECG.
The time when the classic ECG changes of infarction appear is highly
variable. Acute ST segment elevation is the first indicator, followed by T
inversion and development of significant Q waves.
Thrombolytics administered as soon as possible after the onset of acute MI
may prevent tissue death by restoring blood flow through a coronary vessel.

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ECG CLUES TO RIGHT ATRIAL
ENLARGEMENT

• Tall peaked P wave greater than 2.5mm

in height) in inf. Leads II, III, & aVF
• Tall initial upstroke of the P wave in lead
V1 with a small terminal negative
deflection. P wave width remains normal.

RAH IS ALSO CALLED P pulmonale.

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[Link] 69
 P MITRALE
● Notched or m shaped P waves in leads I,
II, aVL (also called P mitrale).
● Small initial upstoke of the P wave in lead
V1 with a deep terminal –ve deflection.
● P wave width wider than normal(greater
than .11 sec)
● Left atrial enlargement is called P mitrale.

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[Link] 71
 WOLFF PARKINSON WHITE
SYNDROME
• The Wolff-Parkinson-White(wpw) syndrome
represents a form of ventricular preexitation in
which the ventricles are depolarized using both
a congenital accessory bypass tracts and
normal AV conduction.
• ECG CHANGES IN WPW include
• Shorter PR interval (.12 sec)
• Slurring of the initial QRS deflection.(delta wave)
• Wide QRS

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HYPOTHERMIA

• Osborne wave in the terminal QRS

complex [j wave ] when core body
temperature falls to 30degree c

[Link] 73
 HYPOKALEMIA
• Serum potassium level less than 3.5 mEq/ ltre

• Etiology
• [Link]
• 2. Renal tubular acidosis
• 3. Insulin effect
• 4. Hyperaldosteronism
• 5. Diuretics
• 6. Vomiting
• 7. Diarrhoea
• 8. Excessive diaphoresis
• 9. Burns
• 10. Hypomagnesemia

• Decreased amplitude of T wave.(low voltage T waves)

• PROMINENT u waves.
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 HYPERKALEMIA
• SERUM K+ >5.1 mEq/litre
• Etiology
• Renal failure
• Adrenal insufficiency
• Acidosis
• Trauma or ischaemia
• Potassium replacement therapy
• Potassium sparing drugs
• Tall peaked T waves.

[Link] 75
 HYPOMAGNESEMIA
• SERUM Mg <1.5mEq/litre
• Etiology
• Diuretics
• Gastrointestinal loses.
• Inadequate dietary intake
• Liver diseases.
• ECG changes similar to those observed
with hypokalemia.

[Link] 76
ECG CLUES TO LEFT ATRIAL
ENLARGEMENT
• Notched or m shaped P waves in leads I,
II, aVL (also called P mitrale).
• Small initial upstoke of the P wave in lead
V1 with a deep terminal –ve deflection.
• P wave width wider than normal(greater
than .11 sec)
• Left atrial enlargement is called P mitrale.

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VENTRICULAR ANEURYSM

• PERSISTANT ST SEGMENT
ELEVATION.

[Link] 78
[Link] 79