Habibie Arifianto

PPDS Kardiologi & KV FK UNS

Heart Anatomy
Heart Anatomy - Valves
Heart Anatomy - Vascularization
Conduction System of the Heart
Depolarization & Repolarization
The heart cell specialties

Property Ability
Automaticity Generates electrical impulses without involving the
nervous system

Excitability Responds to electrical stimulaton

Conductivity Passes or propagates electrical impulses from cell to
cell

Contractility Shortnens in response to electrical stimulation

Conduction System
Sinoatrial Node (SA Node)
Rhythmic rate : 60 100 bpm
Internodal Pathway
Anterior, middle, posterior pathways
Atrioventricular Node (AV Node)
Regions : atrionodal (AN), nodal (N),
nodal-His (NH)
Delays the impulse
Conduction System

Bundle of His
Rate : 40 60 bpm
Bundle Branches
LBB & RBB
LBB : anterior, posterior, septal fascicles

Purkinje Fibers
Rate : 20 40 bpm
How its all begun?

Wilhelm Einthoven
Semarang , Oost Indische
1860
Development of the machine!
Standard EKG Leads
Extremity Leads Placement
Bipolar Limb Leads
(Einthoven Leads)
Augmented Unipolar Limb Leads
(Wilson Leads)
Standard Precordial Leads
Precordial Leads Placement
Standard Precordial Leads Placement

Lead V1 : 4th ICS right sternal border

th
Lead V2 : 4 ICS left sternal border

Lead V3 : between V2-V4

Lead V4 : 5th ICS left mid clavicular

Lead V5 : 5th ICS left anterior axillaries line

Lead V6 : 5th ICS left mid axillaries line

Additional Precordial Leads

Lead V7 : 5th ICS left posterior axillaries line

Lead V8 : 5th ICS left posterior scapular line
Lead V9 : 5th ICS left posterior vertebral line
Lead V3R-V5R : Right side chest, equal position with
standard V3, V4, V5

Performed when theres an acute myocardial

infarction on inferior leads
Reverse Precordial Leads
Posterior Precordial Leads
EKG paper
EKG wave form nomenclature
Normal EKG wave
P wave
No more than 2.5 mm in

height
No more than 0.11 sec in

duration
Positive : I,II,aVF,V2-6

May be positive, negative, or

biphasic : III,aVL,V1
Normal EKG wave
PR interval
0.12 0.20 sec in adult,

may be shorter in children

and longer in elders
Normal EKG wave
QRS Complex
0.06 0.10 sec

Q : 1st negative deflection after P

R : 1st positive deflection after P

S : negative deflection

after R
Normal EKG wave
ST Segment
Isoelectric (flat)
Normal EKG wave
T wave
Limb leads : no more than 5 mm (height)

Precordial leads : no more than 10 mm (height)

R wave progression
Progression of R waves on precordial
leads
Poor R-wave progression :
Infarction (anteroseptal)
LBBB

LVH

Dilated Cardiomyopathy

Severe COPD (emphysema)

Territorial EKG

Leads View of Heart

I, aVL High Lateral
II, III, aVF Inferior
V1, V2 Septal
V3, V4 Localized Anterior
V5, V6 Lateral
V7, V8, V9 Posterior
V3R, V4R, V5R Right Ventricel
V1-V4 Anteroseptal
V3-V6 Anterolateral
V1-V6 Anterior
I, aVL, V1-V6 Extensive anterior
How to read an EKG?
1. Heart Rate
2. Rhythm
3. Axis
4. Enlargement/ hypertrophy
5. Injury (ischemic/ infarct)
Heart Rate
Large Boxes 300/R-R interval
Small Boxes 1500/R-R interval

Six-Second Strip Method count how many

complete QRS complexes in 6 sec strip x 10
Try to count this one..
Try to count this EKG rate
How about this?
How about the arrhythmia
Heart Rate
Triplets methods
Help count the rate!
Now, try for this one
Rhythm
Rhythm
 Axis

Axis Lead I Lead aVF

Normo Axis + +
Left Axis Deviation + -
Right Axis - +
Deviation
Extreme Right Axis - -
Deviation
Axis
Extreme Right Axis Deviation (no mans
land)
emphysematous
hyperkalemia
Leads transposition
artificial cardiac pacing
Ventricular Tachycardia
Axis
Right Axis Deviation
Normal on children and skinny adults
Right Ventricular Hypertrophy
Chronic lung disease
Anterolateral MCI
Left posterior hemiblock
Pulmonary Embolism
Wolff-Parkinson-White syndrome
Left sided accessory pathway
Atria septal defect
Axis
Left Axis Deviation
Left anterior hemiblock
Inferior MCI
Artificial cardiac pacing
Emphysema
Hiperkalemia
Wolff-Parkinson-White syndrome - right sided accessory
pathway
Tricuspid atresia
Ostium primum ASD
Left Ventricular Hypertrophy
Axis
Try to guess the axis..
Axis
How about this?
Axis
One more
Enlargement
Right Atrial Enlargement
Left Atrial Enlargement

Right Ventricular Hypertrophy

Left Ventricular Hypertrophy
Enlargement (Atrial)
Right Atrial Enlargement
Etiology:
Tricuspid valve regurgitation

Tricuspid valve stenosis

Pulmonal regurgitation

Pulmonal stenosis

Pulmonary hypertension

Chronic lung disease

Left ventricular hypertrophy

Atrial septal defect

Enlargement (Atrial)
Tall and peaked P wave (p pulmonal)
Best seen at lead II, III, aVF
Early dominant biphasic p wave on V1
Enlargement (Atrial)
Enlargement (Atrial)
Left Atrial Enlargement
Etiology:
Mitral valve stenosis

Mitral valve regurgitation

Aortic valve stenosis

Aortic valve regurgitation

Left Ventricular Hypertrophy

Enlargement (Atrial)
Wide and notched p wave (p mitral)
Negative dominant biphasic p wave on V1(p terminal
force)
Enlargement (Atrial)
Enlargement (Atrial)
How the p wave was formed
Enlargement (Atrial)
Just look at V1
Enlargement (Ventricular)
Right Ventricular Hypertrophy
Etiology:
Chronic lung disease

Ventricular Septal Defect

Tetralogy of Fallot
Enlargement (Ventricular)
Criteria:
Enlargement (Ventricular)
Enlargement (Ventricular)
Left Ventricular Hypertrophy
Etiology
Hipertensive Heart Disease

Dilated Cardiomyopathy

Aortic Stenosis

Aortic Regurgitation
Enlargement (Ventricular)
Criteria
Enlargement (Ventricular)
Enlargement
A 67 years old men with long standing
hypertension
Enlargement
A 71 years old man with COPD.
Help the ER doctor!
A 45 years old man with history of alcoholic abuse, and now
suffered with severe dilated cardiomyopathy
Enlargement
A 26 years old girl with ventricular
septal defect
Injury
Ischaemic
Acute Myocardial Infarction
Old Myocardial Infarction
Injury

EKG
Yes

No Lab
Yes

No
Injury
Injury
Injury
Injury
Q wave duration of more
than 0.04 seconds
Q wave depth of more than
25% of ensuing r wave
ST elevation in leads facing
infarct (or depression in
opposite leads)
Deep T wave inversion
overlying and adjacent to
infarct
Cardiac arrhythmias
Injury
Characteristic changes in AMI
ST segment elevation over area of damage
ST depression in leads opposite infarction
Pathological Q waves
Reduced R waves
Inverted T waves
Injury
ST segment elevation
Occurs in the early
R
stages
ST
Occurs in the leads
facing the infarction
P
Slight ST elevation may
be normal in V1 or V2
Two small box for
Q
precordial leads, one
small boxes for limb
leads
Convex shaped
Injury

Q wave
R Only diagnostic
ST change of myocardial
infarction
P
At least 0.04 seconds
in duration
T
Depth of more than
Q 25% of ensuing R
wave
Injury

R
Inverted T wave
ST
P Late change

Occurs as ST elevation is
returning to normal
Apparent in many leads
T

Q
Injury
Evolution on EKG

1 minute after onset A few minutes or A few hours or

so after onset So after onset

A day or so after onset Latter changes Old myocardial infarction

Injury
Injury
Injury
Injury
Injury
Injury
83 years old lady with sudden shortness
of breath and cold extremities
Injury
58 years old male with severe acute
chest pain..
Injury
56 years old uncontrolled diabetic male
feel sudden chest discomfort 5 hours ago
Arrhythmias
Disturbances of automaticity
Narrow complex QRS
SA node
Atrial
Junctional
Wide complex QRS
Disturbance of conductivity
Block
SA Block
AV block
Interventricular block
Preexitation syndrome
Arrhythmias
Disturbance of conductivity
AV block
1 AV block
2 AV Block
Mobitz I (Wenkebach)
Mobitz II
3 AV Block / Total AV block
1 st AV Block
1st AV block
Rhythm : Regular
Rate : Usually normal
P wave : Sinus P wave present; one P wave to each QRS
PR : Prolonged ( greater than 0.20 seconds )
QRS : Normal
1 st AV Block
 nd
2 AV Block
2nd AV block, Mobitz I
Rhythm : Irregular
Rate : Usually slow but can be normal
P wave : Sinus P wave present;
some not followed by QRS complexes
PR : Progressively lengthens
QRS : Normal
 nd
2 AV Block
Key points:
Progressive lengthening of PR interval
A P wave then fails to be conducted (drop beats)

PR interval resets and cycle repeats

 nd
2 AV Block
2nd AV block, Mobitz II
Rhythm : Regular usually; can be irregular if conduction ratios vary
Rate : Usually slow
P wave : Two, three, or four P waves before each QRS
PR : PR interval of beat with QRS is constant; PR interval may
be normal or prolonged
QRS : Normal if block in His bundle; wide if block involves bundle
branches
 nd
2 AV Block
Key points:
PR intervals normal and constant
An occasion p waves fails to be conducted
3 rd AV block
3 AV Block
Rhythm : Regular
Rate : 40 60 if block in His bundle; 30 40 if block
involves bundle branches
P wave : Sinus P wave present; bear no relationship to QRS;
can be found hidden in QRS complexes and T waves
PR : Varies greatly
QRS : Normal if block in His bundle; wide if block involves
bundle branches
3 rd AV block
Key point:
No relationship between P and QRS
Interventricular Block
Interventricular Block
Arrhythmias
Arrhythmias
Arrhythmias
Disturbances of automaticity
Narrow complex QRS
SA node
Atrial
Junctional

Wide complex QRS

Arrhythmias
SA node
Arrhythmias
SA node
Arrhythmias
SA node
Arrhythmias
SA node
Arrhythmias
Atrial
Arrhythmias
Atrial
Arrhythmias
Atrial
Arrhythmias
Atrial
Arrhythmias
Atrial
Atrial Fibrillation
Atrial Fibrillation
Types (onset)
Paroxismal - less 48 hrs
Persistent - less 2 weeks
Permanent AF as basic rhythm

Types (Ventricular Response)

Rapid VR (HR>100 bpm)
Controlled / normo VR (HR 60-100 bpm)
Slow VR (HR<60 bpm)
Atrial Fibrillation
Cause:
Cardiac
Accute myocardial infarction
LAE

Extra cardiac
Hyperthyroid
Electrolytes imbalance
Toxic
Atrial Fibrillation
Physical Examination
Pulsus deficit
Irregularly irregular heart beat

Therapy
Rhythm control
Rate control
Arrhythmias
Junctional
Arrhythmias
Ventricular
Arrhythmias
Ventricular
Arrhythmias
Ventricular
Arrhythmias
Ventricular
Arrhythmias
Ventricular
Arrhythmias
 How to identify arrhythmias ?

Treat the patient, not the monitor