Basic ECG Reading

Japhet S. de Jesus, MD
 Information Gained from the ECG
the heart rate
the heart rhythm
whether there are conduction abnormalities
(abnormalities on how the electrical impulse spreads
across the heart)
whether there has been a prior heart attack
whether there may be coronary artery disease
whether the heart muscle has become abnormally
thickened
 Significant Features of the ECG
If the ECG indicates a heart attack or possible coronary
artery disease, further testing is often done to completely
define the nature of the problem and decide on the optimal
therapy. These tests often include a stress test and/or cardiac
catheterization.

If the heart muscle is thickened, an Echocardiogram is often

ordered to look for possible valvular heart disease or other
structural abnormalities.

Conduction abnormalities may be a clue to the diagnosis of

syncope (fainting), or may indicate underlying cardiac disease.
 The Limitations of the ECG
the ECG reveals the heart rate and rhythm only during the
time that the ECG is taken. (If intermittent cardiac rhythm
abnormalities are present, the ECG is likely to miss them.
Ambulatory monitoring is needed to record transient
arrhythmias.

The ECG can often be normal or nearly normal in patients

with undiagnosed coronary artery disease or other forms of
heart disease (false negative results.)

Many abnormalities that appear on the ECG turn out

to have no medical significance after a thorough
evaluation is done (false positive results).
The ECG consists of 12 views of the electrical impulse generated by the heart.
The 6 views on the left half of the ECG (I, II, III, aVR, aVl, and aVf) are generated
by the electrodes on the arms and legs; the 6 views on the right half (VI to V6) are
generated by the electrodes the chest. From these 12 views, various cardiac
abnormalities can be localized to specific areas of the heart.
 ECG lead placement
Limb Leads
RA Red Right arm
LA Yellow Left arm
LL Green Left leg
RL Black Right leg
Chest Leads
V1 Red 4th ICS RPSB
V2 Yellow 4th ICS LPSB
V3 Green Midway between V2 and V4
V4 Brown 5th ICS LMCL
V5 Black 5th ICS LAAL
V6 Violet 5th ICS LMAL
ECG PAPER
Conduction System
 Components of the ECG:

P wave - atrial systole

PR interval - delay in the AV
node
QRS complex - ventricular
systole
T wave - ventricular
repolarization
 ANALYZING A RHYTHM STRIP

P wave
PR Interval
QRS Complex
Q-T Interval
ST segment
T waves
 The recognition of the normal electrocardiogram
is made by excluding any recognized abnormality.

normal P waves
height <2.5 mm in lead II
width <0.11 s in lead II

* for abnormal P waves

right atrial hypertrophy,
left atrial hypertrophy,
atrial premature beat,
hyperkalemia
 The recognition of the normal electrocardiogram
is made by excluding any recognized abnormality.

normal PR interval
0.12 to 0.20 s ( 3-5 small squares)
* for short PR segment consider
Wolff-Parkinson-White syndrome
or Lown-Ganong-Levine syndrome

* for long PR interval = first degree heart block,

trifasicular block
 The recognition of the normal electrocardiogram
is made by excluding any recognized abnormality.

normal QRS complex

<0.12 s duration ( 3 small squares)
* for abnormally wide QRS consider
right or leftbundle branch block,
ventricular rhythm,
hyperkalaemia, etc.
no pathological Q waves
no evidence of left or right ventricular
hypertrophy
 normal QT interval
Normal = 0.42 s or less
Causes of long QT interval
* myocardial infarction, myocarditis, diffuse
myocardial disease
* hypocalcemia, hypothyroidism
* subarachnoid haemorrhage, intracerebral
haemorrhage
* drugs ( e.g., sotalol, amiodarone)
 normal ST segment
ST elevation or depression
* causes of elevation include acute MI,
left bundle branch block, normal variants
(e.g., athletic heart ), acute pericarditis
* causes of depression include myocardial
ischaemia, digoxin effect, ventricular
hypertrophy, acute posterior MI,
pulmonary embolus, left bundle branch
block
 normal T wave
* causes of tall T waves include hyperkalaemia,
hyperacute myocardial infaction, and
left bundle branch block
* causes of small, flattened or inverted T waves are
numerous and include ischaemia, age, race,
hyperventilation, anxiety, drinking iced water,
LVH, drugs (e.g., digoxin), pericarditis, PE,
intraventricular conduction delay (e.g., RBB)
and electrolyte disturbance.
 INTERVALS in ECG:

PR interval

QRS complex

QT wave
Basic Intervals : Normal Values

Normal
PR Interval .12-.20 msec
3-5 small sq.
QRS Complex 80-105 msec
1-1.5 small sq.
QT Interval < of R-R int.
5-10 small sq.
Measure the Intervals (lead II)

PR interval is 0.16 s
QRS interval (duration) is 0.08 s
QT interval is 0.40 s
 Basic ECG Reading
1. Calculating the RATE
2. Determining the RHYTHM
3. Knowing the AXIS
4. Identifying HYPERTROPHY and
CHAMBER ENLARGEMENT
5. Detecting ISCHEMIA, INJURY and
INFARCTION
6. Common CARDIAC ARRYTHMIAS
7. The BLOCKs A-V ; L&RBBB
Calculating
the
RATE
 Calculating the RATE
If rhythm is regular:
1500 divided by # of small squares (R-R
interval)
300 divided by # of big squares (R-R Interval)

If rhythm is irregular:
count number of beats in 6 seconds then
multiply by 10
Calculating the RATE (Regular Rhythm)

1500/Small squares (R-R Interval)

300/Big squares (R-R Interval)
 What is a Regular Rhythm?
measure the distance between 2 consecutive R-R
intervals and compare that distance with the other
R-R intervals.
For atrial rhythm, measure the distance between 2
consecutive P-P intervals.
Generally, a variation of up to 0.12 seconds (3
small boxes) is acceptable. The slower the heart
rate, the more acceptable the variation.
300/min ?

150/min ?

100/min ?

75/min ?

60/min ?

50/min ?
 What Is The Rate?

Atrial Fibrillation:QRS cmplx in 6-sec strip X 10

72/min
Calculating the RATE (Irregular Rhythm)

# of QRS cmplex in 6-sec strip X 10

90/min
 Calculating the RATE

Normal = 60 to 100 bpm

Bradycardia = less than 60 bpm
Tachycardia = more than 100 bpm
Determining
the
RHYTHM
 RHYTHM
Is there 1 P wave before each QRS?
Are P waves present and uniform in
appearance?
Is there a P wave before each QRS or are
there P waves that are not followed by
QRS complexes?
Is the atrial activity occurring so rapidly
that there are more atrial beats than QRS
complexes?
 RHYTHM

Is the PR interval within normal limits?

If the PR interval is less than 0.12 or more
than 0.20 second, conduction followed an
abnormal pathway or the impulse was
delayed in the area of the AV node.
Is the PR interval of conducted beats
constant or does it vary?
 RHYTHM

Is the QRS narrow or wide?

What is the duration of the QRS complex?
If it is 0.10 second or less (narrow), it is
presumed to be supraventricular in
origin.
If it is greater than 0.12 second (wide),
it is probably ventricular in origin.
Do the QRSs occur uniformly throughout
the strip?
 The recognition of the normal electrocardiogram
is made by excluding any recognized abnormality.

- normal sinus rhythm

each P wave is followed by a QRS
P waves normal for the subject
P wave rate 60-100 bpm with <10% variation
* rate <60 = sinus bradycardia
* rate >100 = sinus tachycardia
* variation >10% = sinus arrhythmia

- normal QRS axis

Knowing
the
AXIS
 Knowing the Axis

} 10 AVL

Lead I

} 10
AVR

AVF

AVF
 4 Basic QRS Axes
AXIS QRS (Lead I) QRS (AVF)

Normal Axis
+ +
Left Axis deviation
+ -
Right Axis Deviation
- +
Extreme Right Axis
Deviation - -
Interpret? Normal Axis
Interpret? Left Axis Deviation
 DIFFERENTIALS FOR LAD

Normal variant in short fat individuals

Left ventricular hypertrophy
Inferior wall infarction
Left bundle branch block
Left anterior fascicular block
WPW syndrome
ASD primum
Interpret? Right Axis Deviation
DIFFERENTIALS FOR RAD
Normal variant in tall thin individuals
Right ventricular hypertrophy
Lateral wall infarction
Pulmonary embolism
Left posterior fascicular block
WPW syndrome
ASD secundum
Interpret? Extreme Right Axis Deviation
 PRACTICE:
Rate /Rhythm/ Axis
Rate? , Rhythm?, Axis?
75/min sinus RAD
Rate? , Rhythm?, Axis?
30/min sinus Normal
Rate? , Rhythm?, Axis?
150/min sinus Normal
 Identifying
HYPERTROPHY
and
CHAMBER ENLARGEMENT
 Identifying hypertrophy or
chamber enlargement
Chambers that enlarge:
1. Right atrium
2. Left atrium
Chambers that hypertrophy:
3. Right ventricle
4. Left ventricle
 Identifying hypertrophy or
chamber enlargement
For Atrial enlargement, check
1. P wave in Lead II
2. P wave in Lead V1
For Ventricular hypertrophy, check
1. QRS in V1
2. QRS in V6
 Right Atrial Enlargement
Tall peaked P wave >2.5 mm and normal width in
lead II, III, or AVF
Increased in the initial positive P wave in V1
 Right Atrial Enlargement
Clinical implications:
Usually seen in patients with chronic
obstructive pulmonary disease
Patients with ECG change have more severe
pulmonary dysfunction, as well as
significantly reduced survival
Right Atrial Enlargement
 Left Atrial Enlargement
Features:
Width of the P wave >
0.12 sec in lead II
Notched P wave
P terminal force is >
0.04 sec & >1mm tall
Lead V1 shows large
biphasic P wave with
wide terminal
component
 Left Atrial Enlargement
Clinical implications:
Associated with more severe left ventricular
dysfunction in patients with ischemic heart
disease
More severe valve damage with mitral or
aortic valve disease
 Bi-atrial Enlargement
Features:
Tall and broad P wave in lead II, III or AVF
Large biphasic P wave in V1 with wide
terminal component
Bi-atrial Enlargement
 Atrial Abnormalities

Right atrial (RA) overload may cause tall, peaked P waves

Left atrial (LA) abnormality may cause broad, often notched P
waves in the limb leads and a biphasic P wave in lead V1 with a
prominent negative component representing delayed
depolarization of the LA
 Right Ventricular Hypertrophy
Sokolow-Lyon
R in V1 + S in V5-V6 >11 mm
R in V1 > 7mm
R:S ratio in V1 >1
RAD >+90 degrees
RVH
 DIFFERENTIALS FOR RVH

Tall R in V1
Normal in young adults and children
COPD
RBBB
True posterior infarction
WPW syndrome
 Left Ventricular Hypertrophy
Sokolow-Lyon
RV5 or RV6 + SV1 = 35 mm or greater
(Sokolow index) most widely used
R in aVL > 12 mm
R in aVF > 20 mm
R in I + S in III > 25 mm
S in V1 > 24 mm
Left Ventricular Hypertrophy
 DIFFERENTIALS FOR LVH

Hypertension
Aortic stenosis
Aortic insufficiency
Cardiomyopathy
Initial compensating mechanism in obesity,
smoking, dyslipidemia, obstructive sleep
apnea, DM
Left Ventricular Hypertrophy
 Detecting
ISCHEMIA, INJURY
and INFARCTION
 ECG Markers of
Coronary Artery Disease

1. T-wave inversion = ischemia

2. ST segment depression = ischemia
3. St segment elevation = acute injury pattern
4. Q wave = infarction
 Localizing the Lesion

1. V1, V2 = septal
2. V1 - V3 = anteroseptal
3. V1 - V4 = anterior
4. V1 V6= anterolateral
5. I, AVL, V5, V6 = lateral
6. I, AVL = high lateral
7. II, III, AVF = inferior
 Sensitivity & Specificity of ECG on
Ischemia & MI
INITIAL ECG
- diagnostic of acute MI in approximately 50%
- abnormal but not diagnostic in approx. 40%
- normal in about 10%.
- ***Serial tracings increase the sensitivity to near
95%
 ISCHEMIA
Findings vary: 4 major factors
1.Duration of the ischemic process (acute vs
evolving)
2.Extent (transmural vs nontransmural)
3.Topography (ant., post., inf.)
4.Presence of other underlying abnormality
(LBBB, WPW, pacemaker patterns)
ST segment and T wave in Ischemia

Diagnosis requires comparison with previous

ECGs and correlation with the clinical
presentation and laboratory data

Ischemia produces a range of ischemic

changes in the ST segment and T wave
depending on severity of ischemia and timing
of ECG
 ST and T wave Changes in Infarction
Development of new Q
waves on areas
overlying the infarct
which
>0.04. secs
duration
>25% of the
height of
associated R wave
Rules regarding Q waves:

1. Q waves in AVR are not significant.

2. Q waves in V1 are ignored unless with
abnormalities in other precordial leads.
3. Q waves in III are ignored unless with
abnormalities in II & AVF.
4. Q waves associated with ST changes are
more reliable than those without.
Rules regarding Q waves:

5. Q waves in the presence of LBBB are not

significant if located in V1 - V3
6. Q waves located in V1 - V2 are always
significant in the presence of RBBB.
7. Pathologic Q waves should be >0.04 secs
duration and >25% of the R wave
amplitude.
 Myocardial Infarction
ECG patterns in
Infarction
Ischemic zone
ST segment
depression
Injury zone
ST segment elevation
Infarction zone
Large Q wave
Evolution of ST segment Changes
in Myocardial Infarction

Normal ST Normal ST Normal ST

elevation
T wave Q wave
Q wave inversion
Q wave
 Time Course of Myocardial and
ECG Changes during Infarction
Normal
 Time Course of Myocardial and
ECG Changes during Infarction
Onset and first several hours

Normal R wave
Peaked ST segment and T wave

Subendocardial injury and

myocardial ischemia, no
infarction yet
 Time Course of Myocardial and
ECG Changes during Infarction
First day
 Time Course of Myocardial and
ECG Changes during Infarction
First and second days
 Time Course of Myocardial and
ECG Changes during Infarction
After 2 or 3 days
 Time Course of Myocardial and
ECG Changes during Infarction
After several weeks or months
Ischemia (T-wave inversion),
lateral wall
Inferior wall MI (Q wave)
Acute MI (ST elevation)anterolateral
Acute MI (ST elevation), inferior wall
Common Cardiac
Arrhythmias
 Causes of Cardiac Arrhythmias
Disturbances in automaticity

Disturbances in conduction

Combinations of altered automaticity and

conduction
 SINUS TACHYCARDIA
Normal looking QRS
rate >100 bpm
regular rhythm
P waves upright in I, II, AVF
SINUS TACHYCARDIA
 SINUS BRADYCARDIA
Normal looking QRS
rate <60 bpm
regular rhythm
P waves upright in I, II, AVF
SINUS BRADYCARDIA
SUPRAVENTRICULAR TACHYCARDIA
(Narrow Complex Tachycardia)
Atrial Fibrillation
Atrial Flutter
Paroxysmal SVT (PSVT)
Non paroxysmal atrial tachycardia
Multifocal atrial tachycardia (MAT)
Junctional tachycardia
 ATRIAL FIBRILLATION
Results from multiple areas of re-entry with in
the atria from multiple ectopic foci
AR = 400 - 700/min
VR is irregularly irregular
there are fibrillation waves
no organized atrial activity
no P waves
ATRIAL FIBRILLATION
Atrial Fibrillation with slow
ventricular response
Atrial Fibrillation with rapid
ventricular response
 ATRIAL FLUTTER

Atrial rate 220-350/min

ventricular rhythm may be regular
P waves: flutter waves resemble SAWTOOTH
or PICKET FENCE
ATRIAL FLUTTER
ATRIAL FLUTTER
PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA

Regular narrow-complex tachycardia

without discernible p waves
sudden onset or cessation
PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA
Supraventricular Tachycardia (SVT)
Ventricular Tachycardia
(Wide Complex Tachycardia)
 VENTRICULAR TACHYCARDIA
3 or more beats of ventricular origin in
successive at a rate > 100 BPM
May be well tolerated or may be life-threatening
May be pulseless or not
 VENTRICULAR TACHYCARDIA
No normal looking QRS complex
> 100 bpm; usually < 220 bpm
rhythm is regular but may be irregular
QRS > 0.12
QRS morphology often bizarre with notching
VENTRICULAR TACHYCARDIA
Torsades de Pointes
 VENTRICULAR TACHYCARDIA
Treatment:
lidocaine
procainamide
amiodarone
sotalol
if unstable:
electrical cardioversion or defibrillation
for torsades de pointes:
Magnesium Sulfate
overdrive pacing
Ventricular Tachycardia (VT)
Ventricular Tachycardia (VT)
 Premature Ventricular Complex

A depolarization arising in either ventricle

before the next expected sinus beat.
May be isolated or occur repetitively
Wide, bizarre looking complexes
PVC (unifocal)
PVCs in Salvo/ Non-sustained VT
Premature Ventricular Complex
 VENTRICULAR FIBRILLATION

single most important rhythm for an ACLS

provider to recognize
no organized ventricular depolarization
no EFFECTIVE cardiac output
may be coarse or fine
 VENTRICULAR FIBRILLATION

no normal looking QRS complex

rate is very rapid
rhythm is irregular waveform vary in size and
shape
no QRS, ST segment
no P or T waves
COARSE VENTRICULAR
FIBRILLATION
 VENTRICULAR FIBRILLATION

Management:

Only DEFIBRILLATION provides definitive

therapy.
 ASYSTOLE

absence of ventricular electrical activity

sometimes p waves or ventricular
escape beats (agonal beats) may occur
ASYSTOLE
 ASYSTOLE
Treatment:
epinephrine
atropine
search for reversible cause
CPR
ATRIOVERTRICULAR
BLOCKS
(A-V Blocks)
 Atrioventricular Block
First Degree AV Block
delay in passage of impulse from atria to
ventricles
treatment unnecessary when there are no
symptoms
normal QRS
regular rhythm
PR interval prolonged >0.20 sec.
First Degree A-V Block
First Degree A-V Block
 Second Degree AV Block
Some impulses are conducted
Some are blocked
MOBITZ Type I (Wenckebach)
progressive prolongation of PR
interval until an impulse is completely blocked
MOBITZ Type II
Occurrence of sudden dropped beat
Type I Second Degree AV Block
Type I Second Degree AV Block
Type II Second Degree AV Block
- No lengthening of PR interval before a
dropped beat
Type II Second Degree AV Block
 THIRD Degree AV Block

Complete Heart block , denotes complete

obstruction of impulse conduction from atria to
ventricle
Atria (P wave) beats independently of the
ventricles(QRS complexes).
Atria betas faster than ventricles
More P waves than QRS complexes.
THIRD Degree AV Block
LBBB and RBBB
 LBBB
Remember WILLAM
S wave in V1 and RSR in lead V5, V6.
New onset of LBBB is needs to be treated as
AMI
LBBB
 RBBB

Remember MARROW.
RSR in lead V1 and S wave in V5,
V6.
RBBB