ECG Basics and Criteria

Made Super Easy

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 Heart Rate Calculation
• 300 / no of large boxes.
• 1500/ no.of small boxes
• If irregular rate, multiply the no.of QRS
complexes by 6 in a 10 sec strip. er

oo =
53b m
 Heart Rate Calculation
• 300 / no of large boxes.
• 1500/ no.of small boxes >Yaye
• If irregular rate, multiply the no.of QRS square

complexes by 6 in a 10 sec strip. Y

300
=

-
-
-

=>
75bpr

⑰= 60-100bpr
Tachycardia -> >100bprl
*
*

*
Bradycaldia -> <6obpr
 RHYTHM
• If there is a P=-
wave before every QRS
--

complex and it has a "sinus morphology",

----2x
then “normal sinus rhythm” or “NSR” is said
-

to be present.
• A sinus morphology is an upright P wave in
lead II and biphasic (up and down) in lead
V1.
• If the P wave has a different morphology
than the typical sinus morphology, then it is
termed "ectopic" simply meaning coming
x
from somewhere other than the sinus node.
from somewhere other than the sinus node.

123.1234+ 23y
--

72bpr
200
=
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520
↓
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187bom
Anxiety 1500
=>
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-> exercise
 - varies with Respiration

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ventricates,

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-> -> Irregulal Rhyth

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* D
Varying P wave morphology int
FFppustained
anything

↓ x < s

- > (type of suproventricula

p p sawapp tachycardia)

each PRS2p wave present

I Before
Not all waves generated in Atria
is
are to reach ventricles

F
Varying P wave morphology

w
-

-F 00 pre
=>

N
B

saw-toch
 -
Irregular rhyth

Varying P wave morphology

c ->
Rentry
x

-> noultiple small

wavelets
wandering
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FFF

=>Nooware
-

are
->
Multiple PRS wa
Varying P wave morphology

a
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->

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 - >
HR> 100 Apre

vi
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3
 -

(pSv7)
 ->- 30to
* + 900

RAD ->
> 900
900
Varying P wave morphology
30 to
LAD-
-
-

1800
EAD7-90° to

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#j. C avR
-

avF
-

-
avL
-

*
 Axis determination
• The fastest, non-specific method to determine
the QRS axis is to find the major direction of
the QRS complex (positive or negative) in
leads I and aVF.
 ~
-
O

↑-
Of
r
 It even in

L
0

Cleft Leaves)
 ·thes" and
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8
W

(Right reacher)
EAD
 +
↓
Both C
t Normal axis

&
is
 2
RASY
-

ight
*
reaches (Right axis deviatis)
causes
- (WiIAM)

Camphysema) O

j -

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 ->
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-
= >
=>

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Conduction Abnormalities
 ⑭D ⑭
- -
>

VI V6 VI VC

& a
Conduction Abnormalities
F - T
-

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 (wition)
Left Bundle Branch Block

M
A
• QRS duration of > 120 milliseconds.
• Absence of Q wave in leads I, V5, and V6.
• Monomorphic R wave in I, V5, and V6.
• ST and T wave displacement opposite to the
major deflection of the QRS complex.
• If the QRS complex is widened and
downwardly deflected in lead V1, a left bundle
branch block is present. If the QRS complex is
widened and upward deflected in lead V1, then
a right bundle branch block is present.
Right Bundle Branch Block
(Malow)

W
• QRS duration of > 120 milliseconds
• rsR' "bunny ear" pattern in the anterior
precordial leads (leads V1-V3)
• Slurred S waves in leads I, aVL and frequently
V5 and V6.
Right Bundle Branch Block
 -

(William LAFB/LAHB -> LAD

>

↓ * D

A
• Left axis deviation of at least -45
• The presence of a qR complex in lead I and a
rS complex in lead III.
• Usually a rS complex in lead II and III
(sometimes aVF as well).
 LPHB/LPFB MaRRoW
RAD

Right -> Reaches

1. Right axis deviation of 90 to 180 degrees
2. The presence of a qR complex in lead III and
a rS complex in lead I.
3. Absence of right atrial
enlargement and/or right ventricular
hypertrophy
First degree AV Block
PWave Precedes PRS
->
-> PR interval >0.2000
*A
 Second degree type -1 block
swenbebach)

-
Second Degree Type -2 Block

O
2:1 AV block
Third Degree AV block
 Tricuspid
* it is
ico
value

Chamber Enlargements
-> left Atrial r. mitvale
->

-> Right Atrial -> p. pulmonal e

 M

Notched
t
F
-

Chamber Enlargements
=

r
 Left Atrial Enlargement (Mitrale)
↓
Notched

M
 CP. Pulmonae)

↑ > 2.5MM
-
 Left Ventricular Hypertrophy
T
o

↑
 Criteria to diagnose LVH
• Cornell criteria- Add the R wave in aVL and the S
wave in V3. If the sum is > 28 mm in males or > 20
mm in females, then LVH is present.
• Modified Cornell criteria- R in avL > 12mm.
• Sokolow- Lyon criteria – S in v1 plus R in v5 /v6 >
35 mm.
Right Ventricular Hypertrophy

d
 Causes of tall R waves in V1
• RVH
• Posterior wall MI
• Duchenne muscular dystrophy( isolated post
wall hypertrophy )
• Right bundle branch Block
• Lead misplacement if v1 is placed too high.
• Wolff parkinson type A.
Poor R wave Progression

↑
 Causes of poor R wave progression
1. Old anterior myocardial infarction
2. Lead misplacement (frequently in obese
women)
3. Left bundle branch block or left anterior
fascicular block
4. Left ventricular hypertrophy
5. WPW syndrome
6. Dextrocardia · misplace

7. Tension pneumothorax with mediastinal

shift
Ischemic Heart Disease
Compiled by
Dr. Bhargav Shreeram. G
FOCAL ATRIAL TACHYCARDIA / PAROXYSMAL ATRIAL TACHYCARDIA
NARROW QRS COMPLEX TACHYCARDIA
REGULAR R-R INTERVAL
EVERY QRS COMPLEX PRECEEDED BY ABNORMAL MORPHOLOGY P WAVE
 MULTIFOCAL ATRIAL TACHYCARDIA
NARROW QRS COMPLEX TACHYCARDIA
IRREGULAR R-R INTERVAL
>=3 ABNORMAL MORPHOLOGY P WAVES
 JUNCTIONAL TACHYCARDIA
NARROW QRS COMPLEX TACHYCARDIA
REGULAR R-R INTERVAL
RETROGRADE P WAVE
 AV NODAL RE-ENTRANT TACHYCARDIA
NARROW QRS COMPLEX TACHYCARDIA
REGULAR R-R INTERVAL
R-P INTERVAL <80ms
P WAVE BURIED WITHIN QRS COMPLEX/ NOT SEEN (in 2/3rd patients)
P WAVE ON ASCENDING LIMB OF T WAVE / PSEUDO S-WAVE(in 1/3rd patients)
 ORTHODROMIC AV RE-ENTRANT TACHYCARDIA (CONCEALED WPW)
NARROW QRS COMPLEX TACHYCARDIA
REGULAR R-R INTERVAL
P WAVE LIES OUTSIDE QRS COMPLEX
R-P INTERVAL >80ms
ELECTRICAL ALTERNANS MAYBE SEEN

ANTIDROMIC AV RE-ENTRANT TACHYCARDIA (MANIFEST WPW)

WIDE QRS COMPLEX TACHYCARDIA
 SINUS TACHYCARDIA
REGULAR NARROW QRS COMPLEX TACHYCARDIA
EVERY QRS COMPLEX PRECEEDED BY P WAVE

J
PR INTERVAL - NORMAL
REGULAR R-R INTERVAL

--
>
 ATRIAL FLUTTER
NARROW QRS COMPLEX TACHYCARDIA (250-350/min)
REGULAR R-R INTERVAL
SAW TOOTH PATTERN - POINTED P & T WAVES

=-->
 ATRIAL FLUTTER WITH AV-BLOCK
IRREGULAR R-R INTERVAL
 ATRIAL FIBRILLATION
NARROW QRS COMPLEX TACHYCARDIA (300-400/min)
IRREGULAR R-R INTERVAL
P WAVE - ABSENT
 VENTRICULAR PREMATURE BEAT / EXTRA SYSTOLE
WIDE QRS COMPLEX, NOT PRECEEDED BY P WAVE
ALWAYS FOLLOWED BY COMPENSATORY PAUSE
CONSTANT COUPLING INTERVAL
SECONDARY ST-T CHANGES

VENTRICULAR BIGEMINY
ONE VENTRICULAR PREMATURE BEAT AFTER EACH NORMAL BEAT
 VENTRICULAR TRIGEMINY
ONE VENTRICULAR PREMATURE BEATS AFTER TWO NORMAL BEATS (or)
TWO VENTRICULAR PREMATURE BEATS AFTER EACH NORMAL BEAT

VENTRICULAR COUPLET
TWO VENTRICULAR PREMATURE BEATS TOGETHER
 VENTRICULAR TACHYCARDIA
WIDE QRS COMPLEX TACHYCARDIA - SPINDLE APPEARANCE
>=3 CONSECUTIVE PREMATURE VENTRICULAR BEATS @ 100/min
NORTHWEST AXIS (-120 DEGREES) WITH POSITIVE QRS COMPLEX IN aVR
FUSION BEATS (AV DISSOCIATION) & CAPTURE BEATS
JOSEPHSON'S SIGN - NOTCHING NEAR NADIR OF S-WAVE
BRUGADA SIGN - DISTANCE FROM ONSET OF QRS COMPLEX TO NADIR OF S-WAVE >100ms
 TORSADES DE POINTES CF wisting

POLYMORPHIC VENTRICULAR TACHYCARDIA Roads)

PROLONGED QT INTERVAL
EARLY AFTER REPOLARIZATION
 VENTRICULAR FLUTTER
MONOMORPHIC VENTRICULAR TACHYCARDIA (>250-300/min)
 VENTRICULAR FIBRILLATION
DISORDERED VENTRICULAR ACTIVATION (>500/min)
NO IDENTIFIABLE QRS COMPLEX
P WAVES ABSENT
 WOLF PARKINSON WHITE (WPW) SYNDROME
WIDE QRS COMPLEX TACHYCARDIA
SHORT P-R INTERVAL
P WAVE - NORMAL MORPHOLOGY
SECONDARY ST-T CHANGES
DELTA WAVES ON SLURRED UPSTROKE OF QRS COMPLEX
 DIGOXIN TOXICITY
ATRIAL TACHYCARDIA WITH 2:1 BLOCK (TWO P WAVES FOLLOWED BY ONE QRS COMPLEX)
DELAYED AFTER DEPOLARIZATION
SHORTENED QT INTERVAL
ST DEPRESSION / HOCKEY STICK SIGN
NOT SEEN IN DIGOXIN TOXICITY - ATRIAL FIBRILLATION, TYPE 2B HEART BLOCK
ACCELERATED IDIOVENTRICULAR RHYTHM
REPERFUSION ARRHYTHMIA
BROAD QRS COMPLEXES
 WELLEN SYNDROME
BIPHASIC T WAVE IN V1-V3 - MARKER OF REPERFUSION OF ABORTED ANTERIOR STEMI
 ARRHYTHMOGENIC RV DYSPLASIA
EPSILON WAVE
 LEFT BUNDLE BRANCH MORPHOLOGY
SLIGHTLY WIDE QRS COMPLEXES IN LEADS I, aVL, V5,V6

LEFT BUNDLE BRANCH PATTERN

M PATTERN/RSR' PATTERN IN V5 & V6
W PATTERN IN V1 & V2
DOMINANT S WAVE IN V1
ABSENCE OF Q WAVES IN V5,V6
SLURRING OF R WAVE PEAK IN V5-V6
 RIGHT BUNDLE BRANCH BLOCK
↳ (Mauow)
TALL T WAVE IN V1 & V2 WITH RSR' PATTERN/M PATTERN
W PATTERN IN V5 & V6

--

VI Vz(VG

W
 LEFT ANTERIOR FASCICULAR BLOCK
LEFT AXIS DEVIATION
qR COMPLEXES IN LEADS I, aVL
rS COMPLEXES IN LEADS II, III, aVF
PROLONGED R WAVE PEAK TIME IN aVL
 LEFT POSTERIOR FASCICULAR BLOCK
RIGHT AXIS DEVIATION
rS COMPLEXES IN LEADS I, aVL
qR COMPLEXES IN LEADS II, III, aVF
PROLONGED R WAVE PEAK TIME IN aVF
 BIFASCICULAR BLOCK
RBBB CHANGES
LEFT AXIS DEVIATION (LEFT ANTERIOR FASCICULAR BLOCK)
 TRIFASCICULAR BLOCK
RBBB CHANGES
LEFT AXIS DEVIATION (LEFT ANTERIOR FASCICULAR BLOCK)
PROLONGED P-R INTERVAL (3rd DEGREE HEART BLOCK)
 LEFT ATRIAL ENLARGEMENT
P MITRALE (WIDE & BIFID P WAVES)
*

↓otched

RIGHT ATRIAL ENLARGEMENT

P PULMONALE ( TALL & PEAKED P WAVES)
-

peahed
 LEFT VENTRICULAR HYPERTROPHY
(A) S-WAVE IN V1/V2 + R-WAVE IN V5/V6 >35mm or >7 Big Boxes
Or
(B) R-WAVE IN aVL >11mm
 RIGHT VENTRICULAR HYPERTROPHY
(A) TALL R-WAVE IN V1>7mm (or) [R/S] RATIO IN V1>1
or
(B) DOMINANT S-WAVE IN V5/V6 >7mm DEEP (or) [R/S] RATIO IN V5 or V6<1
 BRUGADA SYNDROME
ST ELEVATION IN V1-V3
RBBB CHANGES
NEGATIVE T WAVES IN V1-V3
 1ST DEGREE AV BLOCK
PR INTERVAL PROLONGED
P WAVE FOLLOWED BY QRS COMPLEX
 MOBITZ TYPE I / WENKEBACH BLOCK
PR INTERVAL LENGTHENS TILL ONE P WAVE IS NOT FOLLOWED BY QRS COMPLEX

MOBITZ TYPE II BLOCK

PR INTERVAL REMAINS CONSTANT
P WAVE NOT FOLLOWED BY QRS COMPLEX
 3RD DEGREE AV BLOCK / COMPLETE AV BLOCK
NO RELATIONSHIP BETWEEN P WAVE & QRS COMPLEX
P-P & R-R INTERVAL CONSTANT
 UNSTABLE ANGINA/ NSTEMI
NORMAL ST SEGMENTS & T WAVES
INVERTED U WAVES IN LATERAL LEADS
 ACUTE MYOCARDIAL INFARCTION
1) HYPERACUTE PEAKED T WAVES FOLLOWED BY T WAVE INVERSION
2) PATHOLOGICAL Q WAVES
3) ST-T CHANGES or LBBB CHANGES
 INFERIOR WALL MI
ST ELEVATION IN II,III,aVF
 LATERAL WALL MI
ST ELEVATION IN I,aVL,V5,V6

Vu,v6 'I AL
I

Cateral
 SEPTAL WALL MI
ST ELEVATION IN V1,V2
 ANTERIOR WALL MI
ST ELEVATION IN V2-V4
 ANTEROLATERAL WALL MI
ST ELEVATION IN I,aVL,V3-V6

EXTENSIVE ANTEROLATERAL WALL MI

ST ELEVATION IN I,aVL,V1-V6
 ANTEROSEPTAL WALL MI
ST ELEVATION IN V1-V4
 POSTERIOR WALL MI
ST DEPRESSION IN V1-V4, TALL R WAVES
 RIGHT VENTRICULAR MI
ST ELEVATION IN V3r-V6r, V1
ST DEPRESSION IN V2
 NSTEMI / SUBENDOCARDIAL INFARCTION
SYMMETRIC T WAVE INVERSIONS
 -
HYPOTHERMIA courgeon Josh)
*

OSBORN WAVES / J WAVES (50s H elevated t

I
si
-
->- segment
Elevated) ↑
=

sugeon temp
 cunder x
- >
-

↑
↑
-
T

-
c
+2 [5

LOW CaST
07
5TPFT
.

-
-5
 HYPERCALCEMIA
T
-
F
OSBORN WAVES / J WAVES
SHORTENED QT INTERVAL
DECREASED ST SEGMENT DURATION
 HYPOCALCEMIA
PROLONGED QT INTERVAL
LENGTHENING OF ST SEGMENT
 HYPERMAGNESEMIA
WIDE QRS COMPLEX
PROLONGED QT INTERVAL
PROLONGED PR INTERVAL
 HYPOMAGNESEMIA
WIDE QRS COMPLEX st
depression
·

PROLONGED QT INTERVAL
POLYMORPHIC VENTRICULAR TACHYCARDIA (TORSADES DE POINTES)
 HYPERKALEMIA
TALL/PEAKED T WAVES
WIDE QRS COMPLEX
PROLONGED PR INTERVAL
ST SEGMENT DEPRESSION
SMALL/ABSENT P WAVES
SINE WAVE PATTERN
SHORTENED QT INTERVAL
ATRIAL FIBRILLATION
 HYPOKALEMIA -

FLAT T WAVE
WIDE QRS COMPLEX
PROLONGED PR INTERVAL
ST SEGMENT DEPRESSION
SIGNIFICANT U-WAVE >2/3rd of T-WAVE - PSEUDO P PULMONALE
ROLLER COASTER PATTERN - INVERTED T WAVE
PROLONGED QT INTERVAL
 ACUTE PERICARDITIS
GLOBAL ST ELEVATION (CONCAVE UPWARDS)
PR SEGMENT DEPRESSION (EXCEPT in aVR - ELEVATED)
DIFFUSE T WAVE INVERSION
 CONSTRICTIVE PERICARDITIS
LOW VOLTAGE QRS COMPLEXES
DIFFUSE T WAVE FLATTENING
 CARDIAC TAMPONADE
ELECTRICAL ALTERNANS - R-R INTERVAL CONSTANT, BUT ALTERNATING HEIGHT OF R
WAVES (TALL & SHORT)
 MITRAL STENOSIS
P MITRALE (WIDE & BIFID P WAVES)
RIGHT AXIS DEVIATION
RVH CHANGES
 AORTIC STENOSIS
LVH CHANGES
 RESTRICTIVE CARDIOMYOPATHY
LOW VOLTAGE QRS COMPLEXES
 DILATED CARDIOMYOPATHY
NON SPECIFIC ST-T CHANGES
 HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY
LVH CHANGES
ST-T CHANGES
GIANT T WAVE INVERSIONS
 TAKOTSUBO CARDIOMYOPATHY
STEMI LIKE CHANGES IN V2-V6 - TOMBSTONE PATTERN
 LEFT SIDED PNEUMOTHORAX
REDUCED R WAVE AMPLITUDE
AMPLITUDE CHANGES IN QRS COMPLEX
T WAVE INVERSION IN PRECORDIAL LEADS
RIGHT AXIS DEVIATION
MASSIVE PULMONARY EMBOLISM / COR PULMONALE
TACHYCARDIA
S1Q3T3 PATTERN
DEEP S WAVE IN LEAD I
DEEP Q WAVES IN LEAD III
INVERTED T WAVES IN LEAD III
 PULMONARY ARTERIAL HYPERTENSION
[R/S] RATIO IN V1
RIGHT AXIS DEVIATION
RVH CHANGES
 DEXTROCARDIA
REVERSE R WAVE PROGRESSION
RIGHT AXIS DEVIATION RALPH DEO
GLOBAL NEGATIVITY IN LEAD I
I<
-

RAD
↓ arE

↓
 Line op
comment
Thank You.

Medzeimer