PHYSIOLOGY Background: CARDIAC SYSTOLE & DIASTOLE

(Basic ECG – Dr. Polidario)

NOTE: This is only an outline of the topic. Some
of the notes in the presentation are not
indicated here specifically the flowcharts and
pictures. Please see the powerpoint for your
own convenience. Thank you & happy reading
guys! 

ELECTROCARDIOGRAM
 Valuable record of the heart’s electrical
activity
 Easy to understand
Tip: just recognize the waveforms

Indications for ordering an ECG :

1. To determine the cardiac rate
2. To accurately define cardiac rhythm
3. To diagnose old or new myocardial
infarction
4. To identify intracardiac conduction
disturbances
5. To aid in the diagnosis of ischemic heart
disease, pericarditis, myocarditis,
electrolyte abnormalities, and pacemaker
malfunction
ECG : Clinical Applications
Rhythm abnormalities
Chamber enlargement
Ischemia / Infarction
Arrhythmia Recognition
Important in any ACLS / CPR sequence
All algorithms start with identifying the rhythm
Cannot identify arrhythmia  cannot manage
correctly
Depolarization Contraction
Anatomy and Physiology of Cardiac
Conduction
 SINUS NODE (SA Node) - 60-100 BPM
at rest
-The Heart’s ‘Natural Pacemaker’
 ATRIOVENTRICULAR NODE (AV Node)
• Receives impulse from SA Node
• Delivers impulse to the His- Purkinje System
• 40-60 BPM if SA Node fails to deliver an
impulse
 BUNDLE OF HIS
• Begins conduction to the Ventricles
• AV Junctional Tissue: 40-60 BPM
 THE PURKINJE NETWORK
• Bundle Branches
• Purkinje Fibers
• Moves the impulse through the ventricles for
contraction
• Provides ‘Escape Rhythm’: 20-40 BPM
Impulse Formation In SA Node
Atrial Depolarization
Delay At AV Node
Conduction Through Bundle Branches
Conduction Through Purkinje Fibers
Ventricular Depolarization
Plateau Phase of Repolarization
Final Rapid (Phase 3) Repolarization
Normal ECG Activation
NORMAL SINUS RHYTHM
 Pacemaker impulses are initiated in the
SA node, traveling through atrial pathways, at
frequencies between 60-100 bpm.
 There is the presence of a P wave,
followed by a QRS complex at a regular rate.
Normal Sinus Rhythm
Look at the p waves:
• rate is 60-100/min
• cycle length do not vary by 10%
• PR interval is 0.12 - 0.20 sec.
• same contour in same lead?
• upright in I, II, aVF & left precordial
leads
• followed by QRST?
Normal ECG Activation  Normal Cardiac
Depolarization
 Any deviation from normal 
ARRHYTHMIA
 Limb Leads:
I, II, III, aVR, aVL, aVF explore the
electrical activity in the heart in a frontal
plane; i.e., the orientation of the heart
seen when looking directly at the anterior
chest.
 Standard Limb Leads:
 I, II, III; bipolar, form a set of axes 60°
apart
 Lead I:
 Composed of negative electrode on the
right arm and positive electrode on the
left arm.
 Lead II:
 Composed of negative electrode on the
right arm and positive electrode on the
left leg.
 Lead III:
 Composed of negative electrode on the
left arm and positive electrode on the left
leg.
Augmented Voltage Leads:
aVR, aVL aVF; unipolar ; form a set of axes 60°
apart but are rotated 30° from the axes of the
standard limb leads.
 aVR: Exploring electrode located at the right
shoulder.
 aVL: Exploring electrode located at the left
shoulder.
 aVF: Exploring electrode located at the left
foot.
 Reference Point for Augmented Leads:
The opposing standard limb lead; i.e., that
standard limb lead whose axis is perpendicular
to the particular augmented lead.
Position of chest leads :
 V1 4th ICS at the (R) sternal border
 V2 4th ICS at the (L) sternal border
 V3 halfway between V2 and V4
 V4 5th ICS at the (L) midclavicular
line
 V5 5th ICS at the (L) anterior axillary
line
 V6 5th ICS at the (L) mid-axillary line
 V3R halfway between V1 and V4R
  V4R 5th ICS at the (R) midclavicular line
P Wave Morphology
 The P wave in general should not be
more than 1 box wide or 1 box tall
 If it exceeds these, it generally means
that either or both atria is enlarged
(hypertrophied)
 The best lead to look at the P wave is V1
PR Interval
 The PR interval indicates AV conduction
time which is normally between 0.12 - 0.20
sec (3 - 5 boxes wide)
 If the PR interval is greater than 0.2 sec,
then an AV block is present.
QRS Morphology
The QRS complex can be quite difficult to
interpret.
 The things to consider are the following:
 Duration: should be 0.08 - 0.10 sec (2 - 2.5
boxes)
 If duration is prolonged, then the presence
of bundle branch blocks and WPW (if PR
interval is also abnormally shortened in
duration).
 Presence of Q waves:
 can indicate presence of infarct
if present in V1, V2, and V3.
 Q wave in III and aVR is normal.
 Q wave is significant if it is
greater than 1 box wide or greater than
1/3 the amplitude of the QRS complex.
ST Segment Morphology
 important because it can show whether
ischemia or infarct is present
 an ST segment depression indicates
ischemia while elevation generally indicates
infarction
 evaluate elevations or depressions 0.06
seconds after the J point (since the ST
segment can at times be sloping)
 The location of the ST elevations on the
ECG can help to identify a location of the
infarct
T Wave Morphology
 In general, T waves are in the same
direction as the largest deflection of the QRS
(normally the R wave)
U Wave Morphology
 The presence of U waves may indicate
hypokalemia
QTc Interval
 Represents the total time for both
ventricular depolarization and
repolarization
 measured from the beginning of the Q
wave to the end of the T wave
 Normal QT interval : 0.44 seconds
Steps in ECG Interpretation
 Rate
 Rhythm
 Axis
 Hypertrophy
 Ischemia and Infarction
 Miscellaneous findings (including
normal variants)
RegularityBeat to beat interval(R to R
intervals or P to P intervals) the same
Determination of Rate 2) if aVF is negative, check lead II.
Regular Rhythm  1500 / 23 = 65/min if lead II is positive, it is in the gray
zone.
FAST METHOD (ECG Interpretation)
if lead II is negative, there is left axis
REMEMBER….30015010075 60 50
deviation.
Determination of Rate
Irregular Rhythm Getting Axis Deviation :
 3 second strip Lead I Lead aVF
Rate/min = Number of complexes x  Normal Axis + +
20  Left Axis Deviation + -
 6 second strip:  Right Axis Deviation - +
Rate/min = Number of complexes x  Indeterminate Axis - -
10
Rhythm Analysis :
Know the Rate : 1. Identify the P wave
Rate interpretation has three possibilities : 2. Check the relation of P wave to QRS
1. Bradycardia (< 60 beats per minute) 3. Check PR interval
4. Check QRS duration
2. Normal rate (60 – 100 per minute)
5. Check the relation of R-R and P-P interval
3. Tachycardia (>100 beats per minute)
Sinus Bradycardia
Determination of Axis  Regularly occurring PQRST
 Axis: Defined as the mean vector of  Rate < 60 / min
ventricular
depolarization. Sinus Tachycardia
 Normal Axis: A mean vector between  Regularly occurring PQRST
+90 and
 Rate > 100 / min
0 degrees.
 "Gray Zone": A mean vector between 0
and -30 Sinus Arrhythmia
degrees. Equals normal.  Identical but irregularly occurring PQRST
 Right Axis Deviation: A mean vector of  longest PP or RR > the shortest by 0.16 sec
> +90 or more
degrees.
 Left Axis Deviation: A mean vector Premature Atrial Contraction
more  Prematurely occurring PQRST complex
negative than -30 degrees.  P wave different in configuration from the
sinus beat.
Determining the axis of the mean vector:  PR interval often long.
 Check lead aVF.  QRS narrow.
1) if aVF is positive, check lead I
 if lead I is positive, axis is normal. Premature Ventricular Contraction
 Prematurely occurring complex.  QRS rate constant except for the occasions
 Wide, bizarre looking QRS complex. when the sinus arrest occurs, then the QRS
 Usually no preceding P wave. rate transiently falls
 T wave opposite in deflection to the QRS
complex.
P wave - QRS relationships
 Complete compensatory pause following
every premature beat.  One P wave to each QRS complex
 P wave in front of the QRS
 P-R interval normal
 P-R interval constant
Wandering Atrial Pacemaker
 Variable P wave morphology
SINUS PAUSE
 Impulses originate from varying points in the
atrium Variable period of asystole
Sinus node
Sinus Bradycardia Junctional escape
 Regularly occurring PQRST Ventricular escape
 Rate < 60 / min AV Blocks
 Possible Sites for Conduction Block
SINUS PAUSE (SINUS ARREST)
Location Descriptive Term
 Case: If the SA Node does not fire
 Junction of sinus node Sino-atrial block
Do you have a P wave? None and atrial myocardium
Do you have a QRST? None
What is the interval between the previous beat  Within the atria Intra-atrial block
and the next beat following the pause? Less
than twice the normal interval Location Descriptive Term
 Atrio-ventricular Atrio-ventricular
CRITERIA FOR SINUS ARREST ( SINUS PAUSE)
junctional area block,
P waves (“heart block”)
 P waves present
 P waves of the same morphology, usual  Within the ventricles Intra-
 for the subject and the lead
ventricular block
 P waves axis normal
 P wave rate constant except for occasions
when sinus arrest occurs, then the P wave  Most important type of Heart Block is block
rate transiently falls in the Atrio-Ventricular Junctional Area.
 Rate less than 60 beats per minute
 FIRST DEGREE AV(Atrioventricular)
QRS complexes BLOCK
 QRS complexes present  PR interval > 0.20 sec
 QRS complex morphology usual for the  normal P wave
subject and the lead  normal QRS-T
 Abnormal PR segment  Progressive prolongation of the P-R
PR interval = Prolonged (> 0.20 sec) interval with each succeeding beat
until one P wave occurs without a QRS
Criteria for First Degree Heart Block (i.e. dropped beat)
 P waves present  Longest P-R interval is the one
 QRS complexes present immediately before the dropped beat.
 P waves morphology and axis usual for the  Shortest P-R interval is the one
subject associated with the first conducted beat
 QRS complexes morphology and axis usual for after the dropped beat.
the subject
 One P wave to each QRS complex SECOND DEGREE ATRIO-VENTRICULAR BLOCK
 P-R interval constant (MOBITZ I)
 P-R interval must be prolonged = ( i.e. > 0.20  Features
sec )  progressive prolongation of PR
interval
SECOND DEGREE ATRIOVENTRICULAR BLOCK  progressive shortening of the RR
 Type I - Mobitz type I or Wenckebach interval
 Type II - Mobitz type II  pause encompassing the blocked P
wave that is less than the sum of two
 SECOND DEGREE AV BLOCK P-P cycles
 site of delayed conduction can be
 normal P wave
predicted from the QRS complex:
 there is intermittent P waves not  QRS duration is normal- within
followed by QRS complex = dropped the AV node proximal to the His
beats bundle
Abnormal PR segment  QRS prolonged- within the AV
 Abnormal PR interval node, His-Purkinje system or
below the His bundle in the
bundle branches
2nd degree AV block Mobitz I
 Very long PR interval favor AV nodal
 Progressive lengthenin of PR interval w/ block
intermittent  small percentage of normal persons
dropped beats . during sleep and with some increased
frequency in trained athletes
CRITERIA FOR TYPE I SECOND DEGREE ATRIO-  asymptomatic individuals without
VENTRICULAR BLOCK (WENCKEBACH) structural heart disease excellent
prognosis and no therapy is required
 P waves present
 patients with structural heart
 QRS complexes present
disease course is determined by the
 P wave morphology and axis usual for
extent and severity of the structural
the subject
heart disease
 QRS complexes morphology and axis
 Permanent pacing is indicated for
usual for the subject
patients with type I second degree AV
 block with syncope, near syncope, or
bradycardia that exacerbates CHF or
angina
2nd degree AV block Mobitz II
Fixed PR interval w/ intermittent dropped
beats .
CRITERIA FOR TYPE II SECOND DEGREE ATRIO-
VENTRICULAR BLOCK (MOBITZ II)
 Within period of observation, one P wave is
not followed by a QRS complex.
 No change in P-R interval before the transient
failure of atrio-ventricular conduction.
 P-R interval constant for all conducted beats
 QRS complexes after the block have the same
morphology as those preceding it
2nd degree AV block Mobitz II
 Features
 constant P-P intervals and R-R
intervals
 constant PR intervals prior to the
unexpected failure of a P wave to
conduct to the ventricle
 a pause encompassing the blocked
P wave that equals two P-P cycles
 occurs almost exclusively in association with
a bundle branch block, and the anatomical
site of block is usually within or below the
His bundle
 In patients with normal QRS, it can be due
to a intra- Hisian AV block, but the block is
likely to be type I AV nodal block, which
exhibits small increments in AV conduction
time
 often progresses to complete AV block
producing syncopal attacks therefore
prophylactic ventricular or AV sequential
pacing is indicated in most patients, even
those who initially present without
symptoms
 2 : 1 AV BLOCK
 Can be a form of either a type I or type II AV
block
 very long PR interval supports type I block,
but if the PR interval of all the capture
complexes is constant despite a varying RP
interval, the type II AV block is likely
 A normal QRS duration supports a block
within the AV node (type I block) and a
prolonged QRS favors, but is not diagnostic
of block below the His bundle ( type II
block)
 treatment does not differ for those with
type I or II AV block
CRITERIA FOR HIGH-GRADE
ATRIO-VENTRICULAR BLOCK
 P waves present
 QRS complexes present
 Some P waves followed by QRS complexes
and some are not
 Atrio-ventricular conduction ratio is 3:1 or
higher
 P-R interval following a QRS is constant but
may be normal or prolonged
3rd degree AV block Complete  Heart Block
 Ventricular rate = 83 BPM
 Atrial rate = 100 BPM
 Complete atrioventricular block
 Impulses originate at both SA node and at
the subsidiary pacemaker below the block
 regularly occurring P waves and QRS
complexes
 atrial rate > ventricular rate
 P waves NOT related to the QRST
complexes
CRITERIA FOR THIRD DEGREE (“COMPLETE”)
ATRIO-VENTRICULAR BLOCK
 No recognizable consistent or meaningful
relationship between atrial and ventricular
activity
 ATRIO-VENTRICULAR DISSOCIATION
 QRS complexes often abnormal in
shape, duration and axis (occasionally
normal)
 QRS morphology constant
 QRS rate constant ( 15-60 beats/min )
 Any form of atrial activity seen (most
commonly sinus initiated)
THIRD DEGREE AV BLOCK
 Can result from block within the AV node
(usually congenital) or distal to the His
bundle (usually acquired)
 Acquired AV block most commonly can be
secondary to drug toxicity, ischemic heart
disease, or various degenerative processes;
other less common causes include infectious
etiologies, rheumatic diseases, infiltrative
processes, neuromyopathic disorders,
hypoxia, electrolyte disturbances, and
surgical trauma
ANATOMICAL SITES OF HEART BLOCK
His Bundle recordings:
 Proximal (delay or block in the AV node)
 Intra-Hisian (delay or block in the His
bundle)
 Infra-Hisian (delay or block in the distal
His bundle itself or the bundle branches
 Block within the AV node proximal to the
His bundle implies a favorable prognosis,
whereas block distal to the his bundle
implies a more serious prognosis
AV BLOCK (COMPLETE HEART BLOCK)
 At the level of the AV node
 result in a junctional escape rhythm
with a rate of 50 to 60 beats/min and
narrow QRS complex
 At the level below AV node (within His
Purkinje system: intraHis or infraHis)
 escape rhythm is approximately 40
beats/min, with a wide QRS complex
originating from the bundle branch and
Purkinje’s system
JUNCTIONAL RHYTHM
 Impulses from the AV node
 P wave inverted or buried w/in QRS or
follows the QRS
 Rate slow
 QRS narrow
IDIOVENTRICULAR RHYTHM
 Impulse ventricular in origin
 Absence of (N), upright P wave
associated with QRS complexes
 QRS > 0.10 sec
 T wave opposite in direction to QRS
 Rate < 40 / min
ACCELERATED IDIOVENTRICULAR RHYTHM
 Impulse ventricular in origin
 Absence of (N), upright P wave associated
with QRS complexes
 QRS > 0.10 sec
 T wave opposite in direction to QRS
 Rate = 40-120 / min
ACCELERATED JUNCTIONAL RHYTHM
 Impulses from the AV node
 P wave inverted or buried w/in QRS or
follows the QRS
 Rate 60-100 bpm
 QRS narrow
ASYSTOLE (VENTRICULAR STANDSTILL)
AGONAL RHYTHM
 Extreme sinus bradycardia with irregular,
idioventricular rhythm and occasional atrial
activity
 FAST RHYTHMS
a) SUPRAVENTRICULAR
 Narrow QRS Complex
Tachycardia
< 0.12 secs or < 120 msec
b) VENTRICULAR
 Wide QRS Complex Tachycardia
>0.12 secs or >120 msec
MULTIFOCAL ATRIAL TACHYCARDIA
 Impulses originate irregularly
and rapidly at different points
in the atrium
 Varying P wave, PR, PP and RR intervals
 Ventricular rate > 100/min
 3 different P wave morphologies
 Irregularly occurring QRS complexes
SUPRAVENTRICULAR TACHYCARDIA
• Characterized by tachycardia with a narrow
QRS complex
• sudden onset and termination
• 150-250 beats/min (180 to 200 bpm in
adults)
• regular rhythm
• QRS complex is normal in contour and
duration
• No P waves
 P waves are generally buried in the QRS
complex
 Often, P wave is seen just prior to or
just after the end of the QRS and causes a
subtle alteration in the QRS complex that
results in a pseudo-S or pseudo-r
ATRIAL FLUTTER
 Atrial rate = 220-300/min
( P as flutter waves )
 Variable degree of AV block
( irregular RR interval )
ATRIAL FIBRILLATION
 No discernible P waves
 Irregular RR interval
 TACHYCARDIA
a) SUPRAVENTRICULAR
 Narrow QRS Complex
Tachycardia
 < 0.12 secs or < 120 msec
b) VENTRICULAR
 Wide QRS Complex Tachycardia
 >0.12 secs or >120 msec
PREMATURE VENTRICULAR CONTRACTION
 Prematurely occurring complex.
 Wide, bizarre looking QRS complex.
 Usually no preceding P wave.
 T wave opposite in deflection to the QRS
complex.
 Complete compensatory pause following
every premature beat.
PREMATURE VENTRICULAR CONTRACTION
IN COUPLETS
 Two Premature ventricular contractions a) Nonsustained
occurring consecutively b) Sustained
c) Monomorphic
PREMATURE VENTRICULAR CONTRACTION IN d) Polymorphic
BIGEMINY
e) Torsades pointes
 Alternating normal sinus beat and a PVC
VENTRICULAR FIBRILLATION
PREMATURE VENTRICULAR CONTRACTION IN  Associated with coarse or fine chaotic
TRIGEMINY undulations of the ECG baseline
 PVC’s regularly occurring every third beat  No P wave
 No true QRS complexes
PREMATURE VENTRICULAR CONTRACTION  Indeterminate rate
IN QUADRIGEMINY 1. Coarse Fibrillation
 PVC’s regularly occurring every fourth 2. Fine Fibrillation
beat
WOLF PARKINSON WHITE SYNDROME
MULTIFOCAL PREMATURE VENTRICULAR  Supraventricular rhythm with wide
QRS complex because of pre-excitation
CONTRACTION
 Short or no PR segment followed by a
 PVC’s coming from different foci in the
delta wave (slurred upstroke of QRS)
ventricle
 PVC’s assuming different polarities in a single PACEMAKER RHYTHM
lead  No P wave (ventricular impulse origin)
 PVC’s of different morphology and coupling  Wide QRS complex (>0.10 sec)
interval  Pacemaker spike precede the wide
QRS complexes
PREMATURE VENTRICULAR CONTRACTION
 Don’t forget the steps
R ON T PHENOMENON
1. Regularity
 R or Q of the PVC occurring at the T wave of 2. Rate
the preceding sinus beat 3. Rhythm
 Most dangerous PVC 4. P-QRS-T
VENTRICULAR TACHYCARDIA 5. Intervals/Durations
6. Abnormal rhythms
 At least 3 consecutive PVC’s
 Rapid, bizarre, wide QRS complexes Important Points
(> 0.10 sec)  Review your arrhythmias
 No P wave (ventricular impulse origin)  Too fast
 Rate > 100 / min  Too slow
 Correlate clinically
 VENTRICULAR TACHYCARDIA  Treat the patient… not the monitor
  INFARCTION
Irreversible cell necrosis and death
Pathologic Q waves (may occur w/o Q
waves)

MYOCARDIAL ISCHEMIA /INFARCTION ELECTRICAL CHANGES ASSOCIATED WITH

Check for Ischemia and Infarction : ISCHEMIA
Ischemia and Infarction interpretation has 4  Injury
Possibilities: leakage of negative ions
1. WNL : no ischemia or infarction present negative displacement of the surface
ECG baseline (PR interval) in the
on ECG
leads facing the injured region
2. NSSTWC
ST segment relatively elevatedcompared
3. Myocardial ischemia changes to the ECG baseline
• Identify which myocardial area is  Q waves
ischemic Necrosis secondary to decreased blood
4. Myocardial infarction changes flow
• Identify which myocardial area is
infarcted CORRESPONDENCE OF SPECIFIC ECG LEADS
• Determine the timing of AND LEFT VENTRICULAR MYOCARDIAL AREA
infarction Leads Corresponding LV area
involved
II, III, AVF INFERIOR WALL
There are three main Stages of FIBRINOLYSIS
I, AVL HIGH LATERAL WALL
1. STAGE 1 =Moderate Atherosclerosis
V1, V2 SEPTAL WALL
ANGINA V3, V4 ANTERIOR WALL
2. STAGE 2 =Severe Atherosclerosis V5, V6 LATERAL WALL
CHRONIC ISCHAEMIA V1-V3 ANTEROSEPTAL WALL
3. STAGE 3 =Complete Occlusion V3-V6, I, AVL ANTEROLATERAL WALL
MYOCARDIAL INFARCT V5, V6, II, III, INFEROLATERAL WALL
AVF
ALMOST ALL DIFFUSE/GLOBAL/MASSIVE
STAGES OF ISCHEMIC STATES
LEADS
 ISCHEMIA
V3R, V4R RV WALL
deficient O2 delivery for given O2
demand  symmetrical T wave ECG Findings in Myocardial Ischemia :
inversion and ST depression Diagnostic Criteria :
 INJURY 1. At least 1 mm ST-segment depression
lack of critical blood supply 2. Symmetrically or deeply inverted T
 ST elevation in leads corresponding to waves
involved area 3. Abnormally tall T waves
 4. Normalization of abnormal T waves (1) occasional normal subjects
5. Prolongation of the QT interval in (2) pulmonary embolus
addition to above (3) coronary artery disease
6. Others: arrhythmias, bundle branch (4) ASD
blocks, AV blocks, or electrical alternans (5) active carditis
NOTE : Criteria 1 and 2 are more specific (6) RV diastolic overload

ECG Criteria for Myocardial Infarction : ECG criteria for RBBB

Diagnostic Criteria : (any of the ff.) 1. QRS duration exceeds 0.12 seconds
1. ST elevation ≥2 mm in 2 or more chest 2. RSR complex in V1
leads or ≥1 mm in 2 or more limb leads 3. Delayed S wave in Ι, V5, V6
2. Q waves ≥0.04 sec (1 small 4. ST/T must be opposite in direction to
the terminal QRS (is secondary to the
TIMING OF MYOCARDIAL INFARCTION block and does not predispose primary
Interpretatio Q ST T Approxim ST/T changes)
n wav elevati wave ate
e on Timing of Partial / Incomplete RBBB
MI
 diagnosed when the pattern of RBBB is
Hyperacute (-) (-/+) peake 0 – 6
present but the duration of the QRS does not
MI d hours
Acute MI (-/+) (++) (-/+) 6 – 24 exceed 0.1 seconds
hours
Recent MI (++) (++) invert 24 – 72 Left Bundle Branch Block
ed hours  Impulse passes to the left of the septum
Undetermine (++) (-) invert 72 hours – below the block (1a) at the same time as the
d age of MI ed 6 wks
paraseptal region. (1b)
 Activation of the RV follows (small
Old MI (++) (-) uprigh > 6 weeks
t magnitude). (2)
 Finally delayed activation of the LV which is
RIGHT BUNDLE BRANCH BLOCK slow due to conduction through normal
 The septum depolarises from left to right as myocardium. (3)
normal. (1)
 The left ventricle is depolarised as normal. (2) ECG criteria for LBBB
 Finally the right ventricle is depolarised late 1. Prolonged QRS complexes, greater than
(wide) in an anterior movement. (3) 0.12 seconds
 Resulting QRS is wide due to slow conduction 2. Wide, notched QRS (M shaped) Ι, AVL, V5,
through myocardial cells. V6
3. Wide, notched QS complexes are seen in V1
Significance of RBBB (due to spread of activation away from the
RBBB is seen in : electrode through septum + LV)
4. In V2, V3 small r wave is seen due to
activation of paraseptal region
Significance of LBBB
LBBB is seen in :
1. Always indicative of organic heart
disease
2. Found in ischaemic heart disease
3. Found in hypertension
Partial / Incomplete LBBB
 the pattern of LBBB is present but the
duration of the QRS does not exceed 0.1
seconds.
Check for Hypertrophy :
Hypertrophy Interpretation has Six possibilities
: 1. In lead V1 : wide terminal component of P
1. No hypertrophy
2. LVH
3. RVH
4. LAE
5. RAE
6. Combination of both
ATRIAL ENLARGEMENT
 To evaluate atrial enlargement, look at
the P waves in leads II and V1
 Lead II:
 P wave configuration to be a positive
deflection from the baseline that is
symmetric to its return to the baseline.
 Lead V1:
expect first a positive deflection and
then a negative deflection from the
baseline, resulting in a sinusoidal curve.
RIGHT ATRIAL ENLARGEMENT:
Generates an accentuated left-sided
portion of the P wave.
LEFT ATRIAL ENLARGEMENT:
Results in an accentuated right-sided
portion of the P wave.
RAE ECG Criteria :
 Any of the following :
1. In lead V1 : Tall initial component of
P wave w/c is ≥2 mm wide (0.08 sec) & ≥2
mm tall (p pulmonale)
2. In any lead : P wave ≥2.5 mm tall
LAE ECG criteria :
 Any of the following :
wave w/c is ≥1 mm wide (0.04 sec) & ≥1
mm deep (p mitrale)
2. In any lead : P wave wider than 0.12 sec (>3
small squares) or w/ a ≥1 mm notched in
the middle
BI-ATRIAL HYPERTROPHY
 ECG CRITERIA
 Diagnosis can be made whenever the
criteria for both right and left atrial
hypertrophy are fulfilled.
 Limb leads
1. p wave greater than 2.5 mm in height
2. p wave greater than 0.12 seconds in
duration
 V1
1. positive component greater than 2mm
in height
2. negative component greater than 1 mm
deep

VENTRICULAR HYPERTROPHY
 Right Ventricular Hypertrophy (RVH):
 When right ventricular muscle mass
become great enough, causing alterations
in the positivity of the right chest leads
 The diagnosis of RVH can be made when
right axial deviation is present and when
R > S in lead V1 or S > R in lead V6.
 Left Ventricular Hypertrophy (LVH):
 Hypertrophy of the left ventricle causes
an increase in the height and depth of the
QRS complexes
 LVH is present when the sum of the
S wave in V1 and the R wave in V5
or V6 (whichever is larger) > 35 mm.
 Accuracy in diagnosing LVH can be
improved by considering limb lead
criteria; i.e., if the sum of the R
wave in lead I and the S wave in
lead III > 25 mm
(2) QRS duration may be ↑ to above 0.12
seconds
(3) T wave ↓ may be present in the
precordial leads
(4) ECG criteria met for LVH with an axis of
+90° (RAD) is suggestive (not diagnostic)
of biventricular hypertrophy
(5) Occasionally RVH with LAD is seen
NOTE: This is only an outline of the topic. Some
of the notes in the powerpoint are not
indicated here especially the flowcharts and
pictures. Please see the powerpoint for your
own convenience. Thank you & happy reading!


RIGHT VENTRICULAR HYPERTROPHY

 ECG criteria
1. R wave ↑ in leads over right ventricles
V1, V2, V3. V4
2. The S wave in V6 becomes more
conspicuous
3. Right Axis Deviation
 moderate RVH – R wave dominance
V1, V2
 severe RVH – R wave dominance V1-
V4

BI-VENTRICULAR HYPERTROPHY
 ECG Criteria :
(1) It may exist without ECG changes