Download P wave

Basic EKG
By
Ragab Abdelsalam (MD)
Prof. of Cardiology
How to Read an
EKG Strip
* EKG paper is a grid where
time is measured along the
horizontal axis .
• Each small square is 1 mm in
length and represents 0.04
seconds .
• Each larger square is 5 mm in
length and represents 0.2
seconds .
•Voltage is
measured along the
vertical axis.
•10 mm is equal to
1mV in voltage.
A)When the rhythm is regular,
the heart rate is 300 divided by
the number of large squares
between the QRS complexes.
For example, if there are 4 large
squares between regular QRS
complexes, the heart rate is 75
(300/4=75).
B) The second method can
be used with an irregular rhythm
to estimate the rate.
Count the number of R waves
in a 6 second strip and multiply
by 10.
For example, if there are 7 R
waves in a 6 second strip, the
heart rate is 70 (7x10=70).
*Example:
Normal
Components of the
EKG Waveform
**Interestingly, the letters P,
Q, R, S, and T are not
abbreviations for any actual
words but were chosen
many years ago for their
position in the middle of the
alphabet .
>> P wave represents atrial
depolarization, >> P wave is
assessed for evidence of atrial
enlargement.
>> Similarly, QRS complex
is assessed to determine
ventricular enlargement.
THE NORMAL P- WAVE
> It represents the sum of
the depolarizations of the R &
L atria.
> Because the SAN
is
located in the RA , RA
depolarization begins slightly
before LA depolarization.
> Therefore, the initial
portion of the P wave primarily
reflects RA depolarization, and
the terminal portion of the P
wave reflects LA depolarization.
P wave usually has a smooth or
blunted apex.
• The normal time interval for
complete atrial depolarization
(duration of the P wave) is less than
0.12 seconds.
• Whether the P wave is +ve or –ve
&, it should not exceed 2.5 mm in
amplitude.
• P waves are best seen in II & V1.
• P wave morphology in
lead V1 is often biphasic.
• The P wave in V1
normally has an initial
positive deflection that reflects
RA depolarization and is
usually less than 1.5 mm in
amplitude.
• The terminal portion of the P
wave in lead V1 has a negative
deflection that reflects LA
depolarization and normally does
not exceed 1 mm in depth .
** P wave usually has the
largest upright deflection in lead II.
* Changes in P wave
morphology may result from :
> chamber enlargement,
> rhythm disturbances
> abnormalities in atrial conduction.
*** Therefore, it has been suggested
that the term atrial abnormality be used..
** P-mitrale is a term used
to describe a wide and
abnormally notched P wave
commonly seen in patients
who have mitral stenosis and
possible LA enlargement.
>> a broad, notched
P wave in leads I & II,
>> slurring of the
terminal portion of the
P wave.
.
Q- wave
> small, narrow Q in I, aVL, aVF, and V4-6 is
normal
> Less than one small square in width &
depth .
> In lead III it may be large & physiologic , if it
is only in this leads .
> It is size is affected with respiration,
especially in inferior leads
• The Normal QRS Complex
The QRS complex reflects ventricular
depolarization and is inscribed on the ECG
after ventricular activation.
• The initial vector is depolarization of
the IVS, which occurs from left to right.
This is followed by depolarization of the
ventricles.
• The impulse is delivered to the
subendocardium of both ventricles at
about the same time, resulting in an
almost simultaneous depolarization.
>The normal QRS duration is 0.06
to 0.10 seconds.
The amplitude of a QRS
is influenced by the thickness of the
muscle mass involved.
 The net wave of ventricular
depolarization, known as
the mean QRS vector, is directed
inferiorly and to the left .
> The QRS will be
predominantly upright in leads I, II,
III, aVL, aVF, V4, V5, and V6.
> Normally, a progressive
increment in the amplitude of the
R wave occurs from leads V1
through V6 while small q waves
begin to appear from leads V4
through V6.
• The R wave begins as a small
(<7 mm) upright waveform in lead V1
and becomes progressively taller
across the left precordia leads.
• In addition, the S wave is deep in
lead V1 and becomes progressively
smaller across the left
precordial leads
• Leads I, aVL, or V6 will show a
small initial q wave, representing
the mean septal vector traveling
away from the +ve electrode of
these leads.
• This q wave is followed by a
relatively tall R wave, which
represents the mean QRS vector
traveling through the LV toward the
+ve electrodes.
• > In V1 and V2, the mean septal vector
is directed towards these +ve
electrodes, inscribing a small r wave.
• > This is followed by a relatively deep
S wave, which results from the mean
QRS vector traveling through the LV
away from the positive electrodes
> The intrinsicoid deflection is a term
used to represent ventricular activation
time or the time required for peak
voltage to develop.
5. Frontal Plane QRS Axis
* Normal: -30 degrees to +90 degrees
* Abnormalities in the QRS Axis:
> Left Axis Deviation (LAD): > -30o (i.e., lead II
is mostly 'negative')
> Left Anterior Fascicular Block (LAFB): rS
complex in leads II, III, aVF, small q in leads I
and/or aVL, and axis -45o to -90o
> Some cases of inferior MI with Qr complex in
lead II (making lead II 'negative')
> Inferior MI + LAFB in same patient (QS or
qrS complex in lead II)
> Some cases of LVH
> Some cases of LBBB
> Ostium primum ASD and other endocardial
cushion defects
> Some cases of WPW syndrome (large
negative delta wave in lead II)
* Right Axis Deviation (RAD): > +90o
(i.e., lead I is mostly 'negative')
> Left Posterior Fascicular Block
(LPFB): rS complex in lead I, qR in
leads II, III, aVF (however, must first
exclude, on clinical basis, causes of
right heart overload; these will also give
same ECG picture of LPFB)
> Many causes of right heart overload
and pulmonary hypertension
> High lateral wall MI with Qr or QS
complex in leads I and aVL
> Some cases of RBBB
> Some cases of WPW syndrome
> Children, teenagers, and some young
adults
*Bizarre QRS axis:( Odd axis)
( +150o to -90o (i.e., lead I and lead II are
both negative)
> Consider limb lead error (usually right
and left arm reversal)
> Dextrocardia
> Some cases of complex congenital
heart disease (e.g., transposition)
> Some cases of ventricular tachycardia
• ST Segment and T wave
- More often the ST-T wave is a smooth,
continuous waveform beginning with the J-point
(end of QRS), slowly rising to the peak of the T and
followed by a rapid descent to the isoelectric
baseline or the onset of the U wave.
- This gives rise to an asymmetrical T wave.
- In some normal individuals, particularly women,
the T wave is symmetrical and a distinct, horizontal
ST segment is present .
* Normal ST segment elevation:
- This occurs in leads with large S waves
(e.g., V1-3),
- The normal configuration is concave
upward.
- ST segment elevation with concave upward
appearance may also be seen in other leads;
this is often called early repolarization,
although it's a term with little physiologic
meaning
> Convex or straight upward ST
segment elevation (e.g., leads II, III,
aVF) is abnormal and suggests
transmural injury or infarction:
ST segment depression is always an
abnormal finding, although often
nonspecific
 ST segment depression is often
characterized as "upsloping",
"horizontal", or "downsloping".
The normal U Wave:
* the most neglected of the ECG
waveforms.
- U wave amplitude is usually < 1/3
T wave amplitude in same lead
- U wave direction is the same as T
wave direction in that lead
- U waves are more prominent at
slow heart rates and usually best
seen in the right precordial leads .
- Origin of the U wave is thought
to be related to
afterdepolarizations which
interrupt or follow repolarization .
*
Intervals
A-PR interval: normals vary
with age and heart rate (0.12-0.20
sec.)
B. QRS duration: varies with age
C. QT interval
1. varies with heart rate
2. Bazett's formula
QTc= (QT measured) / (square
root of RR interval)
3. normal QTc
is less than or equal to 440 msec
• PR Interval
• measured from beginning of P to beginning
of QRS in the frontal plane
• Normal: 0.12 - 0.20s
* Short PR: < 0.12s
• Preexcitation syndromes :
- WPW (Wolff-Parkinson-White) Syndrome .
- LGL.
AV Junctional Rhythms with
retrograde atrial activation
(inverted P waves in II, III,
aVF).
• Ectopic atrial rhythms
originating near the AV node
• Normal variant
•
* Prolonged PR: >0.20s
- First degree AV block (PR interval usually
constant
- Intra-atrial conduction delay (uncommon (
- Slowed conduction in AV node (most common
site)
- Slowed conduction in His bundle (rare (
-Slowed conduction in bundle branch (when
contralateral bundle is blocked (
• Second degree AV block (PR interval
may be normal or prolonged; some P
waves do not conduct
- Type I (Wenckebach): Increasing PR
until nonconducted P wave occurs
-Type II (Mobitz): Fixed PR intervals plus
nonconducted P waves
• AV dissociation: Some PR's may
appear prolonged, but the P waves and
QRS complexes are dissociated.
3. QRS Duration
(duration of QRS complex in frontal plane):
Normal: 0.06 - 0.10s
*Prolonged QRS Duration (>0.10s):
- QRS duration 0.10 - 0.12s
> Incomplete right or left bundle branch
block
> Nonspecific intraventricular conduction
delay (IVCD)
> Some cases of left anterior or posterior
fascicular block
> Complete RBBB or LBBB
> Nonspecific IVCD
> Ectopic rhythms originating in the
ventricles (e.g., ventricular tachycardia,
pacemaker rhythm)
4. QT Interval
* It measured from beginning of QRS to end
of T wave in the frontal plane.
• Normal: heart rate dependent (corrected
QT = QTc = measured QT ¸ sq-root RR in
seconds; upper limit for QTc = 0.44 sec)
• Long QT Syndrome - "LQTS" (based on
upper limits for heart rate; QTc > 0.47 sec
for males and > 0.48 sec in females is
diagnostic for hereditary LQTS in absence
of other causes of increased QT)
Normal variation versus Abnormal ECG
1. Sinus Arrhythmias:
R-R is reduced during inspiration
If it is marked: DD. Atrial arrhythmias
Difi: (P-QRS-T)  Normal, only R-R interval is
varied.
2.
Dominant R in V1
May be observed in normal population However they
may be the only criteria for true posterior infarction
or RVH.
3. RSR pattern in V1
Also may be a normal variety especially in
children.
In some adult also but duration < 11 soc.
4. Absolute height of R or absolute depth of S in
precordial leads.
R in V5 or V6 or S in V2 may exceed 28 mm in
NORMAL fit and thin young person.
5. Q wave:
Normally may be observed in inferior lead
(II,III) & V5, V6  But should < 2 mm deep & <
1 mm in width.
In lead III a deep Q wave may be observed &
it seems to be pathological  but on deep
inspiration  it decreases significantly or
disappears
6.
ST segment Elevation (Important) BER.
7.
ST-depression: may be observed in normal
propel, especially pregnant women But it should be
less than 2 mm.
8.
T-wave inversion in V1-V3 : my be a sign of
RVH, but it usually observed in normal
especially black people.
Benign Early Repolarization
9. T-wave is the most changeable port of ECG
between individual, and in the same person
under variable conditions e.g it may be inverted
in some leads simply by hyperventilation.
10. Special group.
1. Athletes:
Variation in Rhythm
Most common is sinus Brdycardia.
Marked sinus arrhythmia.
Junctional Rhythm.
Variation in ECG pattern
Tall P waves.
Tall R & deep S.
Prominent septal Q.
Slight ST .
Tall symmetric T wave.
Biphasic T.
Prominent V wave.
2. Children especially < 10 Y:
Sinus tachycardia.
RAD.
Prominent R or rsR in V1.
Prominent S or V5, V6.
Sometimes invented T. wave in V1-V4.
Flattening T-wave and STdepression
Observed in hypokalemia, scamia.
Mainly in mid-precordial leads.
Same polarity of T.
 PR, then wide QRS, then flat T
then extreme wide QRS  VF
There is an inverse relation
between calcium and QT interval
Arrythmias
*PAC
Rate
normal or accelerated
usually have a different
morphology than sinus P waves
P wave
because they originate from an
ectopic pacemaker
QRS
normal
Conduct normal, however the ectopic beats
ion
may have a different P-R interval.
PAC's occur early in the cycle and
Rhythm they usually do not have a
Wandering Atrial Pacemaker
Wandering pacemaker
Rate
variable depending on
the site of the
pacemaker; usually 45100/ bpm.
P wave
also variable in
morphology
QRS
normal
Conduction
P-R interval varies
depending on the site of
the pacemaker
Rhythm
irregular
Sinus tachycardia
Rate
101-160/min
P wave
sinus
QRS
normal
Conduction
normal
Rhythm
regular or
slightly irregular
Rate
45-100/bpm
P wave
sinus
QRS
normal
Conduction
normal
regularly
irregular
Rhythm
Respiratory S Arrythmia
Rate
45-100/bpm
P wave
sinus
QRS
normal
Conduction
normal
Rhythm
regularly
irregular
*MAT
Rate
100-250/bpm
P wave
two or more ectopic P
waves with different
morphologies
QRS
normal
Conduction
P-R intervals vary
Rhythm
irregular
Atrial Flutter
-The atria can also produce a flutter pattern,
which is characterized by multiple sawtooth
edged p-waves before each QRS, called flutterwaves.
-In atrial flutter, there are many ectopic
pacemakers, in a more extreme
form of MAT.
*Atrial Flutter
Rate
atrial 250-350/min; ventricular
conduction depends on the
capability of the AV junction
(usually rate of 150-175 bpm).
P wave
not present; usually a "saw
tooth" pattern is present.
QRS
normal
Conduction
2:1 atrial to ventricular most
common.
Rhythm
usually regular, but can be
irregular if the AV block
varies.
*Atrial Fibrillation
Rate
P wave
QRS
Conduction
Rhythm
atrial rate usually between
400-650/bpm.
not present; wavy baseline
is seen instead.
normal
variable AV conduction; if
untreated the ventricular
response is usually rapid.
irregularly irregular. (This is
the hallmark of this
. )dysrhythmia
PJC
Rate
P wave
QRS
Conductio
n
Rhythm
normal or accelerated.
as with junctional rhythm.
normal
P-R interval < .12 secs if P
waves are present.
PJC's occur early in the
cycle of the baseline
rhythm. A full compensatory
pause may occur.
Junctional tachycardia
Rate
P wave
QRS
Conduction
Rhythm
faster than 60/bpm
as with junctional rhythm.
normal or widened with
aberrant ventricular
conduction.
P-R interval usually < .12
seconds if present
usually regular
*Junctional escape
Rate
40-60/bpm
P wave
inverted in leads where they
are normally upright; this
happens
normal
Conductio P-R interval < .12 seconds if
n
present.
irregular as a result of the
Rhythm
escape beats
QRS
PVC patterns
• Isolated: PVCs occur very
infrequently; there is no repeating or
identifiable pattern
• Bigeminy: a repeating pattern of a
normal beat followed by a PVC
• Trigeminy: repeating pattern of two
normal beats followed by a PVC
0 Couplet: two PVCs in a row
• R-on-T: a PVC that occurs so early in
the cardiac cycle that it falls on the T
wave of the preceding beat.
• Especially in persons experiencing
an acute myocardial infarction (AMI) or
hypokalemia, an R-on-T premature
ventricular contraction carries the risk of
causing the heart to go into ventricular
fibrillation
Type of Vent Extrasystoles
1. Interpolated: the extra systole lies
between 2 normal with correctly spaced
beats.
2. Displacing the normal complex after
extra systoles occurs only after a time
equal nearly to that separating 2 normals.
3. Commonest type: Extra systole with full
compensatory pause the interval between
the 2 normal before and after extra systole
is equal to twice the interval between 2
normal complexes (B+C = 2a)
PVC=Bigeminy
Rate variable
usually obscured by the QRS, PST or T wave
P wave
of the PVC
wide > 0.12 seconds; morphology is bizarre
with the ST segment and the T wave opposite
QRS
in polarity. May be multifocal and exhibit
different morphologies.
the impulse originates below the branching
Conductio
portion of the Bundle of His; full
n
compensatory pause is characteristic.
irregular. PVC's may occur in singles,
Rhythm
couplets or triplets; or in bigeminy, trigeminy
or quadrigeminy.
• Parasystole
Rarely, the ectopic focus is protected from
other influences, and does its own merry
thing.
This is termed `parasystole', and is
detected by noting the unvarying coupling
between extrasystoles, and the lack of
coupling between the extrasystole and
sinus beats!.
• Note the fusion beats as the
normal rhythm and parasystolic
rhythm transiently coincide...
Ventricular Arrythmias:
> Ventricular Tachycardia: occarrance
of three or more consecutive VPCs.,
at a rate greater than 100 b.p.m.
> Accelerated idioventricular rhythm
(is slow ventricular tachycordia) i.e.
rate 60-120 b.p.m.
> Ventricular flutter:
Vent.Tachycardia
Rate
usually between 100 to 220/bpm, but
can be as rapid as 250/bpm
P wave
obscured if present and are unrelated
to the QRS complexes.
QRS
wide and bizarre morphology
Conduction
PVCs as with
Rhythm
three or more ventricular beats in a
row; may be regular or irregular.
> Ventricular fibrillation :
It represents chaotic electrical
activity in the ventricles with
completely irregular electrical
activity with disorganized
mechanical action.
It is of two types:
1- Primary:
Occurs due to acute cardiac disease.
It shows rapid amplitude waves.
2- Secondary:
Occurs in prolonged anoxic and
depressed myocardium.
It shows slow and low amplitude &
more chaotic wave forms
*V.Fibrillation
Rate
P wave
QRS
Conduction
Rhythm
unattainable
may be present, but
obscured by
ventricular waves
not apparent
chaotic electrical
activity
chaotic electrical
activity
Identification of criteria of
ventricula tachycardia:
- Rate: > 100 b.p.m & < 250.
- Pattern: usually regular, rarely slight
irregularity.
- P – waves are usually not reorganized,
but rarely in slow V.T.
- QRS width: > 0.12 sec.
- P / QRS Relationship No (AVdissociation).
* Torades de pointes: is an
unusual form of VT, in which QRS
amplitude fluctuates in a sinusoidal
pattern.
*torsade de pointes
Rate
usually between 150 to
220/bpm,
P wave
obscured if present
QRS
wide and bizarre morphology
Conduction
as with PVCs
Rhythm
Irregular
*Ventricular
A systole:
- Rate: These is no rate.
- Pattern: There is a flat line.
- P – wave: May occasionally
occur spontaneously.
- No QRS is present.
* Pulseless Electrical Activity
Electromechanical Dissociation (PEA) or
(EMD)
- Rate: is profoundly bardycardiac to
tachycardia.
- Pattern: regular or irregular.
- P-wave: may or may not be present.
- QRS width: usually profoundly widened.
- P / QRS relationship: variable depending on
rhythm origin.
*Criteria
of Ventricular
Fibrillation :
- Rate: is greater than 300 b.p.m but too
disorganized to count.
- Pattern: may be :
Coarse: higher amplitude & lower frequency.
Fine: diminished amplitude & higher frequency.
- Sometimes wave forms of available width
& regularity with no identifiable P or QRS
complexes.
*Asystole
Rate
none
P wave
may be seen, but there is
no ventricular response
QRS
none
Conduction
none
Rhythm
none
*Idioventricular rhythm
Rate
P wave
QRS
Conduction
Rhythm
20 to 40 beats per
minute
Absent
Widened
Failure of primary
pacemaker
Regular
Bradyarrythmias
*Sinus bradycardia
Rate
P wave
40-59 bpm
sinus
QRS
normal (.06-.12)
P-R normal or slightly
prolonged at slower
rates
Conduction
Rhythm
regular or slightly
irregular
* Sinus Node disease:
–
–
–
–
Degenerative as in elderly.
Ischemic HD.
Viral infection.
Lupus disease.
• May be : - SA – block
- SA – arrest.
*Sinus ARREST
Rate
normal
P wave
those that are present are normal
QRS
normal
Conduction
normal
Rhythm
The basic rhythm is regular. The
length of the pause is not a
multiple of the sinus interval.
*Sinoatrial block
Rate
P wave
QRS
Conduction
Rhythm
normal or bradycardia
those present are
normal
normal
normal
basic rhythm is
regular*.
* Atrioventricular
node disease
and conduction defect:
– Ischemic heart disease.
– Autoimmune disease: Lupus,
Rieter’s.
– Sarcoidosis.
– Destruction by infection (Aortic
rest abscess).
– Prosthetic valves.
• First degree AV. block.
• It is the prolongation of
PR> 0.2 sec.
• Each P is followed by
QRS.
• Second degree AV block.
• Mobitz type I = Wenckebach:
• * ECG :
• - P  sinus.
• - PR: shows progressive
lengthening till dropped beat.
• - Rhythm : group beating.
• - R – R : Shorter.
Mobitz-type I
Rate
P wave
QRS
variable
normal morphology with constant P-P
interval
normal
Conduction
the P-R interval is progressively longer
until one P wave is blocked; the cycle
begins again following the blocked P wave.
Rhythm
irregular
• Mobitz type II:
* ECG:
- P >> Sinus.
- PR: normal or slightly prolonged & is the
same before & after dropped beat.
- QRS: usually normal >> Intermittent but
regular failure of P waves to conduct
through the AV ( Fixed P to QRS
relationship 1:2 ; 1:3 ; 1:4 ; ….) with
consequence bradycardia.
- Ventricular rate : 1/2, 1/3, 1/4.
*Mobitz type II
Rate
variable
P wave
normal with constant P-P intervals
QRS
usually widened because this is usually associated
with a bundle branch block.
Conduction
P-R interval may be normal or prolonged, but it is
constant until one P wave is not conducted to the
ventricles.
Rhythm
usually regular when AV conduction ratios are
constant
• Complete heart block:
* ECG :
- P wave >> sinus.
- P / QRS relationship >> non= AV
dissociation.
- QRS >>may be narrow
(Suprabifurcational); or wide if
infrabifurcational
Ventricular rate slow.
Third degree HB
Rate
atrial rate is usually normal; ventricular rate is usually
less than 70/bpm. The atrial rate is always faster than
the ventricular rate.
P wave
normal with constant P-P intervals, but not "married"
to the QRS complexes.
QRS
may be normal or widened depending on where the
escape pacemaker is located in the conduction system
Conduction
atrial and ventricular activities are unrelated due to the
complete blocking of the atrial impulses to the
ventricles.
Rhythm
irregular
*RBBB
Rate
variable
P wave
normal if the underlying rhythm is
sinus
QRS
wide; > 0.12 seconds
Conduction
This block occurs in the right or left
bundle branches or in both. The
ventricle that is supplied by the
blocked bundle is depolarized
abnormally.
Rhythm
regular or irregular depending on the
underlying rhythm.
'Trifasicular' block
1. . Right Bundle Branch Block
2.Left Anterior Hemiblock
3.Long PR interval
ATRIAL
ENLARGEMENT
A ) Left Atrial Enlargement
The ECG patterns for LA
enlargement may evolve from
conditions such as
> LA hypertension,
> LA hypertrophy,
> or impaired interatrial
conduction.
** P-mitrale is a term used
to describe a wide and
abnormally notched P wave
commonly seen in patients
who have mitral stenosis and
possible LA enlargement.
>> a broad, notched
P wave in leads I & II,
>> slurring of the
terminal portion of the
P wave.
>> The distance between
the two peaks of the notched P
wave is usually longer than
0.04 s.
>> P duration is > 0.12 s.
>> The amplitude is
slightly increased.
The term P terminal force:
A measurement of the
negative-terminal component of
the P wave in lead V1 and is used
to help detect enlargement of the
left atrium.
It is calculated by multiplying
the depth (in millimeters) of the
terminal P wave deflection by its
duration (in seconds).
The value is stated in
millimeters per second. A P terminal
force greater than 0.03 mm/sec is a
sign of left atrial enlargement.
* RA enlargement :
A) P-pulmonale ; ( P in III > P in II )
as in COLD .
B) P-congenitale: P- in II > P in III )
as in congenital HD >>> PS ,…
C) P-tricuspidale : ( P- wave is tall &
notched, with the first peak taller
than the second. As in TVD.
D) P-Ebstein: the tallest P-wave you
can see ( usually > ORS in II )
• Summary of ECG criteria
for RA enlargement
> Normal P wave duration
> Tall, peaked P waves with an
amplitude greater than 2.5 mm in leads
II, III, aVF
> Positive deflection of the P wave in
lead V1 or V2 is greater than 1.5 mm
> P wave axis in the frontal plane leads is
+75° or greater
Increased sympathetic tone can
increase the amplitude of the P
wave.
Moreover, the ECG of healthy
persons who have a tall, slim build
may reveal tall, peaked P waves
related to the more vertical position
of the heart
• A pseudo P-pulmonale pattern may
be seen in patients with LA
enlargement due to MV disease
• In a pseudo P-pulmonale pattern, as
seen in LA enlargement, analyzing lead
V1 for the presence of a negative P
terminal force may help in the
differential diagnosis of true vs pseudo
P-pulmonale.
Ventricular Enlargment
Left ventricular
Hypertrophy
Diagnostic ECG criteria of LV
enlargement
> Precordial leads
• The R wave amplitude in lead V5 or V6 plus the S
wave amplitude in lead V1 or V2 is greater than 35
mm
• The R wave amplitude in lead V5 is greater than 26
mm
• The R wave amplitude in lead V6 is greater than 18
mm
• The R wave amplitude in lead V6 is greater than the R
wave amplitude in lead V5
Limb leads
> The R wave in lead aVL is > 13 mm
> The R wave in lead aVF is > 21 mm
> The R wave in lead I is > 14 mm
>The R wave in lead I plus the S
wave amplitude in lead III is > 25
mm
Scott,s Criteria
Limb leads:
* R in 1+S in 3:
* R in aVL :
* R in aVF;
* S in aVR:
> 25 mm
> 7.5 mm
> 20mm
> 14 mm
Chest leads :
S in V1,or 2 + R in
V5,or 6: >35 mm
* R in V5 or V6 :
> 26 mm
* R + S in any V lead:
> 45 mm
*
Estes, Scoring system for LVH
1-R or S in limb lead:
20 mm or more
S in V1,2 or 3
25 mm or more
R in V4 ,5, 0r 6
25 mm or mor e
---------------------------------------------------------2-Any St-segment shift: > with digitalis
> without digitalis
---------------------------------------------------------3 – LAD -15 degree or more
---------------------------------------------------------4 – I.D in V5, 6 0.04 or more
3
----------3
1
----------2
--------1
5- QRS duration : 0.09 sec or more
1
6- P-terminal force in V1 > 0.04
3
-------------------------------------------------------- -------------
TOTAL
================================
5 or more= LVH
4 = probable
13
=======
*Cornell criteria:
- R wave in aVL + S wave in V3 >
24 mm
- Downsloping of ST-depression
& asymmetric T wave inversion
- Prominent U waves
Systolic Vs Diastolic
Overload
*In systolic overload
> the criteria of LV strain are
evident:
- St-segment depression
- T-wave inversion
- U-wave inversion in left precordial
leads.
* In diastolic Overload:
- R- wave is markedly
increased
- T-wave is upright , large &
pointed .
Clinical Mimics:
Age, body build, sex, and race can produce
ECG changes that mimic those of left ventricular
enlargement.

Adolescents and young adults may have
taller QRS complexes.

Men tend to have a greater QRS amplitude
than do women.
Blacks have a taller QRS voltage than their
white counterparts.
> Body build can either mimic
or mask left ventricular enlargement.
> In thin or emaciated persons, the QRS
amplitude tends to be greater, causing
LV enlargement to be overdiagnosed,
whereas in obese people, LV
enlargement can be underdiagnosed
because of decreased QRS voltage
from the insulating effects of fat.
> In addition, fever,
anemia, thyrotoxicosis, and other
high COP states can increase QRS
voltage without corresponding LV
enlargement.
Right Ventricular
Enlargement
> Normally, the left ventricle is anatomically and
electrophysiologically the dominant ventricle >
However, any condition
that causes an overload of the RV may lead to RV
enlargement.
> Examples include pulmonary
disease and congenital or acquired heart disease.
> Normally, the mean right ventricular vector
travels in an anterior and
rightward direction but is usually overshadowed by
the dominant left ventricle.
• Because of the anatomic differences
between the RV and LV, slight
enlargement of the RV usually does not
produce significant ECG
abnormalities.
• With increasing enlargement of the
RV , the RV mass may equal and may
eventually dominate theelectrical effects of
the LV
** ECG Characteristics
of RV Enlargement.
> The earliest manifestation of RV
enlargement is a progressive deviation of the
axis to the right.
> RAD seen in the limb leads is the
essential criterion in diagnosing RV enlargement.
> RAD that exceeds +100° is considered
significant for RV enlargement.
> In lead I, RAD is manifested by a QRS
complex that is more negative than positive
• A second ECG
manifestation is a
progressive decrease in the
depth of the S wave in V1.
•
Because lead V1 is
closer to the RV it is a more
sensitive lead to the
changes of RV enlargement.
• In cases of RV enlargement,
the S wave will be initially small
in lead V1 and become
progressively deeper toward
lead V6
•
Simultaneously, the
normal pattern of R wave
progression is interrupted
•
In patients with RV
enlargement, the R wave in lead V1 is
initially large (>7 mm) and becomes
progressively smaller toward lead V6.
• RV enlargement may also
result in a delayed intrinsicoid
deflection of more than 0.035
seconds in the right precordial leads
(V1 and V2)
• One of the most specific ECG signs in
patients with a severe degree of right
ventricular enlargement and hypertrophy is
a qR wave seen in lead V1.
• The reason for this qR wave is not fully
understood; however, it is believed to
result from the initial septal vectors being
altered because of the increased muscle
mass of the septum
• Additional criteria for RV
enlargement include ST-T wave
abnormalities representing ventricular
strain.
>> The ECG pattern for RV
ventricular strain includes
• ST depression
• T wave inversion in leads V1, V2, II,
III, and aVF.
*Summary of ECG
diagnostic criteria for RV
enlargement
1- RAD of 100° or more in the limb
leads ( essential criteria ).
2- R in lead V1 greater than S .
3- S in lead V6 greater than R .
4 - Delayed intrinsicoid
deflection in lead V1 greater than
0.035 seconds.
5 - Secondary ST-T wave
changes in leads V1, V2,, II, III,
aVF.
6 - RA enlargement.
7- qR in lead V1 (severe RV
enlargement).
Systolic Vs Diastolic •
Overload
RV-Systolic overload
-Markedly tall R in V!
- right precordial leads
strain
- rS pattern in lead V6
– Diastolic
Overload
* RV
- pattern of
incomplete or
complete RBBB.
NB.
1- S1,S2,S3 pattern is a reliable
index of RV Enlargement in
children
2- rS pattern all across the
precordial leads is an index of RV
enlargement in many cases of
emphysema.
> This pattern is termed (clockwise rotation ) or poor r-wave
progression.
3-The pattern of rSR’ in
V1 plus AF is an indication of
Mitral stenosis with PH
4-pattern of rSr’ plus left
axis deviatin in a patient with ASD
indicates Premium defect or
ASD+ MVP.
• Clinical Mimics.
A variety of other clinical conditions may produce
ECG findings suggestive of RV enlargement
when the condition does not exist.
> RAD may be due to left posterior fascicular
block.
>, ECG changes associated with inferior,
posterior, and high-lateral-wall myocardial
infarctions may mimic those of RV
enlargement.
> WPW syndrome, type A and right bundle
branch block may also produce a false-positive
result .
• The ECG manifestation of RV
enlargement may be a normal variant
in some adults, as persons who are
tall and slender tend to have:
> a vertical heart that can
produce findings false-positive for
RV enlargement.
Biventricular
Enlargement
** Diagnosis of biventricular
enlargement can be confusing.
> The increased electrical forces of
both ventricles may actually negate
each other, producing an ECG that
appears normal in amplitude.
>The ECG findings will be
influenced by the degree of
enlargement of each of the ventricles.
• ECG Manifestations of
Biventricular Enlargement.
> A variety of ECG clues are
suggestive of biventricular
enlargement; however, the best
criterion is the pattern of LA
enlargement (corresponding to LV
enlargement) along with evidence of
RV enlargement
* Katz-Watchel phenomenon
1- The transitional zone : V3, V4.
2- The deflections are biphasic &
equal .
3- R + S > 45 mm
 It is characteristically evident
in VSD
* Shallow “ S Syndrome
> Shallow S in V1
Plus Strikingly deeper
S in V2 .
Summary of ECG diagnostic
criteria for biventricular
enlargement:
1- Left artrial enlargement
2- S greater than or equal to R in lead V5 or
lead V6
3- S in lead V5 or lead V6 =7 mm or more
4- Right axis deviation of greaer than 100° in
the limb leads.
* The differential diagnosis of
prominent U waves includes all
the following except :
1- Hypokalemia .
2-Hyperkalemia.
3-Digitalis effect
4-Amiodarone.
5-Central nervous system disorders.
6-Left ventricular hypertrophy.
*Anatomical LVH is more likely
when Repolarization
abnormalities are added to
voltage criteria :
> False or
> True
Repolarization changes
associated with LVH:
1-ST segment & T wave deviation in
( same / opposite ) direction to
deflection of QRS.
2- ST segment ( elevation/
depression) in I , aVL ,III, aVF and
/ or V4-V6.
3- < 1-2 mm ST segment (
elevation /depression ) in
V1-V3.
4-Inverted ---- waves in leads I ,
aVL, V4-V6.
5- (Absent /
waves.
prominent ) U
* Factors reduce the sensitivity of
voltage criteria diagnostic of LVH
include all the following except:
1-Obesity
2- Thin body
habitus
3-Severe COPL
4-Pleural or peric.
eff.
5-CAD
6- Pneumothorax
7-Infiltrative HD
8-Severe RVH
9-LBBB
10-LA Fascicular
Block.
* Causes of RSR” complex
in V1 may include :
1-RVH.
2- Posterior MI.
3- WPW syndrome.
4-RBBB.
>> The associated ECG findings can
help in differential diagnosis
* Match each cause to associated
findings in the followings:
A. Right Axis Deviation.
B. Inferior MI.
C. RA abnormality.
D. Upright T waves in v1-v3,
E. T wave inversion in v1-v3.
F. ORS duration > 0.12 s.
G. Short PR interval.
• Making the accurate Field Diagnosis:
• There are elevations ( 1 mm )in two
contegous (connecting) leads:
Leads adjacent to eachother...
• There is at least one lead with reciprocal
changes..
• If the Q wave is more than 1/3 the size of
the R wave...
• Anterior Infarction
• ST elevation without abnormal Q wave
• Usually associated with occlusion of the
left anterior decending branch of the left
coronary artery (LCA)
• Lateral Infarction
• ST elevation with/without abnormal Q
wave
• May be a component of a mutiple-site
infarction
• Usually associated with abstruction of the
left circumflex artery
• Inferior Infarction
• ST elevation with/without abnormal Q
wave
• Usally associated with right coronary
artery (RCA) occlusion
• Right Ventricular Infarction
• Usually accompanies inferior MI due to proximal
acclusion of the RCA
• Best diagnosed by 1 - 2 mm ST elevation in lead V4R
• An important cause of hypotension in inferior MI
recognized by jugular venous distension with clear lung
fields
• Aggressive therapy is indicated, including: reprofussion,
adequate IV fluids for right heart filling, and pacingf to
maintain A-V synchrony if necessary
• Poterior Infarction
• Tall, broad (>0.04 sec) R wavr and ST
depression in V1 and V2 (reciprocal
changes)
• Frequestly associated with inferior MI
• Usually associated with obstruction of
RCA and or left circumflex coronary artery
• Pathological Q waves:
•
If the Q wave ( the first downward "negative"
deflected wave ) is more than 1/3 the size of the
R wave ( the first upward deflected "positive"
wave ) it is pathological and indicative of an
A.M.I.
If no R wave is recorded, then the infarct is
extreamly acute.
• There is no electrical activity of the ventricle
durring polarization and contraction.