Basic and Clinical Practice

of Electrocardiography
Andi Wahjono Adi,MD,FIHA
Department of Cardiology and Vascular Medicine
University of Muhammadiyah Malang Hospital
Depolarization-Repolarization

Goldberger,2013
Cardiac Conduction Pathway

Leonard S Lily, 2011

 Three basic laws of electrocardiography

A, A positive complex is seen in any lead if the wave of depolarization spreads toward the positive pole of that
lead.B, A negative complex is seen if the depolarization wave spreads toward the negative pole (away from the
positive pole) of the lead. C, A biphasic (partly positive, partly negative) complex is seen if the mean direction of
the wave is at right angles (perpendicular) to the lead. These three basic laws apply to both the P wave (atrial
depolarization) and the QRS complex (ventricular depolarization).
Goldberger,2013
 Spatial relationships of the six chest leads,
which record electrical voltages transmitted
onto the horizontal plane.

Spatial relationships of the six limb leads,

which record electrical voltages transmitted
onto the frontal plane of the body.
ECG Paper

Goldberger,2013
Calibration

Before taking an ECG, the operator must check to see that the machine is properly
calibrated, so that the 1-mV standardization mark is 10 mm tall. A,
Electrocardiograph set at normal standardization. B, One-half standardization. C,
Two times normal
Goldberger,2013
How to Calculate Heart Rate..?

Heart rate (beats per minute) can be measured by counting the number of large
(0.2-sec) time boxes between two successive QRS complexes and dividing 300 by
this number (300 ÷ 4 = 75 beats/min)
or the number of small (0.04-sec) time boxes between successive QRS complexes
can be counted (about 20 beats) and divided into 1500
Goldberger,2013
1 Minute ECG Record

Goldberger,2013
Limb Lead Placement

Shirley A. Jones,2005
Precordial Lead Placement

Lead Positive Electrode Placement View of Heart

V1 4th Intercostal space to right of sternum Septum

V2 4th Intercostal space to left of sternum Septum
V3 Directly between V2 and V4 Anterior
V4 5th Intercostal space at left midclavicular line Anterior
V5 Level with V4 at left anterior axillary line Lateral
V6 Level with V5 at left midaxillary line Lateral

Shirley A. Jones,2005
Right Ventricle Lead Placement

Chest lead Position

V1R 4th Intercostal space to left of sternum

V2R 4th Intercostal space to right of sternum
V3R Directly between V2R and V4R
V4R 5th Intercostal space at right midclavicular line
V5R Level with V4R at right anterior axillary line
V6R Level with V5R at right midaxillary line

Shirley A. Jones,2005
Posterior Lead Placement

Chest lead Position Heart views

V4R 5th Intercostal space in right anterior Right ventricle
midclavicular line
V8 Posterior 5th intercostal space in left Posterior wall of LV
midscapular line
Shirley A. Jones,2005
V9 Directly between V8 and spinal Posterior wall of LV
column at posterior 5th intercostal space
Emergency Lead Placement

Shirley A. Jones,2005
Artifacts

Goldberger,2013
Sinus rhythm
Sinus Bradycardia- sinus tachycardia
Sinus Aritmia

Heart rate normally increases on inspiration and slows down with expiration as a result of changes
in vagal tone associated with or induced by the different phases of respiration (increase with
inspiration; decrease with expiration). This finding, a key aspect of heart rate variability, is
physiologic and is especially noticeable in children, young adults, and athletes.
Artifacts

Goldberger,2013
Reverse Lead

As a general rule, when lead I shows a negative P wave and a negative QRS,
reversal of the left and right arm electrodes should be suspected
Goldberger,2013
Axis Deviation
Frontal axis

Leonard S Lily, 2011

Left Axis Deviation(LAD) RAD Superior/Extreme

Goldberger,2013
Horizontal Axis

Clockwise

Counter Clockwise

R waves in the chest leads normally become relatively taller from lead V1 to the left chest leads. A, Notice the
transition in lead V3. B, Somewhat delayed R wave progression, with the transition in lead V5. C, Early
transition in lead V2.
Goldberger,2013
Chamber Enlargement
Right and left atrium atrium enlargement
Overload of the right atrium (RA) may cause tall, peaked P waves in the extremity chest
leads. An abnormality of the left atrium (LA) may cause broad, often notched P waves in
the extremity leads and a biphasic P wave in lead V1 with a prominent negative
component representing delayed depolarization of the left atrium

Goldberger,2013
Right atrial enlargement

P Pulmonal

George J Taylor,2006
Left atrial enlargement

P Terminal Force
P Mitral

George J Taylor,2006
Left Ventricular Hypertrophy

Goldberger,2013
LVH Criteria
Sokolow-Lyon voltages SV1 + R V5 > 3.5 mV (35 mm), or
RaVL > 1.1 mV (11 mm)
Romhilt-Estes point Any limb lead R wave or S wave >2.0 mV(3 points)
score system* or S V1 or S V2 ≥3.0 mV (3 points)
or R V5 to R V6 ≥3.0 mV (3 points)
ST-T wave abnormality, no digitalistherapy (3 points)
ST-T wave abnormality, digitalis therapy(1 point)
Left atrial abnormality (3 points)
Left axis deviation ≥ −30°(2 points)
QRS duration ≥ 90 msec (1 point)
Intrinsicoid deflection in V5 or V6≥50 msec (1 point)
Cornell voltage criteria SV3 + R aVL ≥2.8 mV (for men)
SV3 + R aVL >2.0 mV (for women)
Goldberger,2013
Right Ventricular Hypertrophy

Goldberger,2013
RVH Criteria
R in V1 ≥ 0.7 mV
QR in V1
R/S in V1> 1 with R >0.5 mV
R/S in V5 or V6 <1
S in V5 or V6 >0.7 mV
R in V5 or V6 ≥0.4 mV with S in V1 ≤0.2 mV
Right axis deviation (>90°)
S1Q3 pattern
S1S2S3 pattern
P pulmonale

Goldberger,2013
Ischemia,Injury,Necrosis
Ischemia,Injury,Necrosis
Wellen sign
Evolution of an Acute Myocardial Infarction
Localization of Infarction
Lead Localization Artery
V1-V2 Septal LAD-septal perforator branch
V3-V4 Anterior LAD-Diagonal branch
V5-V6 Lateral LCx-anterolateral marginal branch,LAD diagonal-branch
V1-V4 Anteroseptal LAD septal perforator,diagonal branch
V3-V6 Anterolateral LCx-anterolateral marginal branch,LAD diagonal-branch
V1-V6 Anterior Extensive LAD,LCx
I,AVL High Lateral LCx
II,III,AVF Inferior RCA or LCx
V7-V9 Posterior RCA or LCx
V4R-6R Right Ventricle RCA
Infarct Related Artery
Infarct Related Artery
Premature Complexes
Atrial extrasystole /Premature atrial contraction
Ventricular extrasystole/Premature ventricular contraction
Single PVC

Bigemini

Couplet Salvo

Khawaja,2006
Trigemini
Compensatory Pause
Ventricular Atrial
Atrial
Compensatory Pause

Complete vs incomplete

Ventricular Atrial
Lown Criteria

Malignant

ventricular extrasystoles contributed significant additional risk for cardiac death even in the three
highest Lown grades, 4A, 4B, and 5. The Lown grading system assumes that, of the four
complex features used, R on T ventricular extrasystoles have the greatest risk for subsequent
cardiac death.
J Thomas Bigger et al,1981
Escape Rhythm
Junctional rhythm
Accelerated junctional escape rhythm
Idioventricular rhythm
Accelerated Idioventricular Rhythm (AIVR)
Bradyarrhythmias &
Heart Block
 Sino Atrial Block
First degree Abnormal prolongation of the sinoatrial
conduction time, usually with a delay at a fixed
interval
Second-degree type 1 Intermittent failure of the sinus impulse to exit
the sinus node with Wenckebach periodicity of
the P wave
Second-degree type 2 Abrupt absence of one or more P waves because
of failure of the impulse to exit the sinus node,
without previous progressive prolongation of
sinoatrial conduction time (without progressive
shortening of the P-P intervals)
Third degree or sinus Absence of P waves owing to failure of the sinus
arrest impulse to conduct to the atrium
Cannot be detected on surface EC G.
Progressively decreasing P-P intervals before a
pause caused by an absent “dropped” P wave.
The pauses associated with this type of
sinoatrial exit block are less than twice the
shortest sinus cycle
The sinus pause should be an exact multiple (2
: 1, 3 : 1, 4 : 1) of the immediately preceding P-
P interval
Long pauses resulting in lower pacemaker
escape rhythm. It cannot be differentiated
from sinus arrest on a 12-lead
ECG.
Sinus pause and Sinus(SA) exit block

The monitor lead shows sinus bradycardia with a long pause (about 2.4 sec).

Pause due to 2:1 sinus (SA) exit block. Note the sudden pause which is almost exactly twice the
baseline P-P interval. This distinctive finding is consistent with intermittent “exit block” of SA node
depolarization, such that a P wave, which denotes atrial depolarization, does not occur even though
the sinus pacemaker is firing appropriately. The reason for this “missing” P-QRS-T signal is that the
sinus impulse is blocked intermittently from exiting the sinus node.
Sinus Arrest

Sinus arrest following abrupt cessation of paroxysmal atrial fibrillation (AF). The mechanism is due to
“overdrive suppression” of the SA node during the rapid stimulation of the atria during the AF. Such
extended pauses may cause lightheadedness or syncope. This combination is an example of the
brady-tachy syndrome. Resumption of sinus rhythm starts to occur after the prolonged sinus arrest.
Brady-Tachy Syndrome ( Sick Sinus Syndrome)
Atrioventricular Block
1st Degree AV Block
2nd Degree AV Block-Wenkebach
2nd AV Block-Mobitz Type 2
3rd Degree AV Block(Total AV Block)
Bundle Branch Block
Left Bundle Branch Block

LBBB may be the first clue to four previously undiagnosed but clinically important
abnormalities: Advanced coronary artery disease, Valvular heart disease, Hypertensive
heart disease, Cardiomyopathy
Right Bundle Block
Fascicular Block
LAHB LPHB

• LAFB is a very common, nonspecific abnormality and may be seen with hypertension, aortic valve
disease, coronary disease, and aging and sometimes without identifiable cause
• LPFB is rare and can be considered only after other, more common causes of RAD have been
exclude.These factors include RVH, normal variant, emphysema, lateral wall infarction, and acute
pulmonary embolism (or other causes of acute right ventricular overload).
• Complete BBB, unlike fascicular blocks (hemiblocks), do not cause a
characteristic shift in the mean QRS axis.
• LAFB shifts the QRS axis to the left by delaying activation of the more
superior and leftward portions of the left ventricle.
• LPFB shifts it inferiorly and to the right by delaying activation of the
more inferior and rightward portions of the left ventricle. In both cases
the QRS axis therefore is shifted toward the direction of delayed
activation.
Bifasicular Block ( RBBB+LPHB)
Bifasicular Block(RBBB+LAHB)
 Intraventricular conduction defect

With a nonspecific intraventricular conduction delay (ICVD), the QRS complex is abnormally wide (0.12 sec).
However, such a pattern is not typical of left or right bundle branch block. In this patient the pattern was caused
by an anterolateral wall Q wave myocardial infarction
Tachyarrhythmia
Wandering atrial pacemaker
Multifokal atrial tachycardia
Atrial Fibrilation
Atrial Flutter
Atrial tachycardia
Supraventricular Tachycardia (SVT)
Ventricular Tachycardia (VT)
Torsades de pointes

Spindle
Ventricular Fibrilation (VF)
Asystole
Pre Excitation Syndrome
Wolf Parkinson White Syndrome
Miscelaneous
Long QT syndrome
Hyperkalemia

The earliest change with hyperkalemia is peaking (“tenting”) of the T waves. With progressive
increases in the serum potassium concentration, the QRS complexes widen, the P waves decrease in
amplitude and may disappear, and finally a sine wave pattern leads to asystole unless emergency
therapy is given
Severe Hyperkalemia
Hypokalemia

ECG leads from a patient with a markedly low serum potassium concentration of 2.2 mEq/L. Notice the
prominent U waves, with flattened T waves.
Pulmonary Embolism
 MEMBACA IRAMA EKG

QRS Complex ? -Asistol

-V F
(-)
(+)

-Takikardia/
Cepat/Lambat?
-Bradikardia

-Lebar? (Ventrikular? )
QRS complex lebar / sempit

-Sempit? (Supraventrikular)
 QRS regular /irregular ?

Gelombang P ? Normal / abnormal ?

-1 P diikuti 1 QRS
Ada hubungan antara gel.P dan QRS complex
-Jarak tepat antara gelombang P
? dan QRS complex