EKG PENYAKIT JANTUNG KORONER

Dr.Suhaemi,SpPD,Finasim
Anatomy
 EKG pada PJK
 Sarana diagnostik yang penting untuk
jantung koroner
 Yang ditangkap EKG ialah kelainan
miokard, yang disebabkan
terganggunya aliran koroner
Tingkat kerusakan miokard

 Iskemia → reversibel
 Injuri → reversibel

 Nekrosis → irreversibel , permanen

Gambaran EKG

 Iskemia dan injuri : kelainan pada

proses repolarisasi miokard→ segmen
ST dan gelombang T
 Nekrosis miokard : gangguan pada

proses depolarisasi → gelombang QRS

 Injuri miokard
a. Elevasi ST cembung ke atas,
spesifik untuk injuri (epikard)
b. Elevasi ST cekung ke atas, tidak
spesifik
c. Depresi ST yang dalam, menunjukkan
injuri subendokardial
PEMBULUH DARAH KORONER

RCA
LM
LAD LCx
Regions of the Myocardium:

Lateral
I, AVL,
V5-V6

Anterior /
Inferior Septal
II, III, aVF V1-V4
The Normal ECG
 Normal
ECG
 Standardization – 10 mm (2 boxes) = 1 mV
 Double and half standardization if required
 Sinus Rhythm – Each P followed by QRS, R-R constant
 P waves – always examine for in L2, V1, L1
 QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR
 QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm
 R wave progression from V1 to V6, QT interval < 0.4
 Axis normal – L1, L3, and aVF all will be positive
 ST Isoelectric, T waves ↑, Normal T↓ in aVR,V1, V2
GELOMBANG R DAN S DI LEAD PERIKORDIAL

V1 V2 V3 V4 V5 V6
R wave progression

 Normally…
 No q anteriorly
 R:S should increase
until V5
 R:S should be 1:2
by V3 and 1:1 by
V4
 Septal q laterally
Nomenklatur Kompleks QRS
ATHEROGENESIS
Plaque Rupture
 LCX
LMS

LAD
pangkal

ANGIOGRAFI KORONER (KATETERISASI)

Plak Stabil (stable plaque) Plak ruptur (ruptured plaque)
 Pathogenesis of ACS

Platelet
rupture

Platelet
Adhesion

Platelet
Sequence of events Activation
• Plaque Rupture Platelet
Aggregation
• Platelet Adhesion
• Platelet Activation
• Platelet Aggregation Thrombotic
Anti-platelet drugs Occlusion
• Thrombotic Occlusion
24
 Patofisiologi SKA
Erosi atau ruptur plak

Pembentukan trombus dan

embolisasi

Angina Pektoris tak Stabil (APTS) Infark Miokard dgnNon ST Infark Miokard
Elevasi dgn ST elevasi

Circulation 1998;98:2219-22
ER patient care

 Initial general treatment (memory aid: “MONA”

greets all patients
 Morphine, 2-4 mg repeated q 5-10 min
 Oxygen, 4 L/min; continue if S aO2 < 90%

 NTG, SL or spray, followed by IV for persistent or

recurrent discomfort
 Aspirin, 160 to 325 mg (chew and swallow)
 Myocardial Ischemia
 Myocardial ischemia results when the heart’s demand for oxygen exceeds its
supply from the coronary circulation. Ischemia can resolve by reducing the oxygen
needs of the heart or increasing blood flow by dilating the coronary arteries with
medication such as nitroglycerin.

 Myocardial ischemia delays repolarization. Characteristic EKG changes involve the

ST segment & the T wave. ST segment depression is suggestive of MI & is
considered significant when the ST segment is more than 1 mm below the baseline

 An inverted T wave will be present in the leads facing the affected area of the
ventricle if ischemia is present through the full thickness of the myocardium

 The T wave is usually upright if ischemia is present only in the subendocardial layer
Gelombang T
 Repolarisasi ventrikel
 Amplitudo normal :

- < 10 mm di sandapan
dada
- < 5 mm di sandapan
ekstremitas
- Min. 1 mm

Bentuk patologis Indikator

iskemik /infark
Gelombang T
Gelombang T
 Repolarisasi dimulai dari daerah yang
terdepolarisasi paling akhir
 Gelombang depolarisasi yang datang dan
repolarisasi yang menjauh menimbulkan gelombang
positif pada EKG
 T positif pada sandapan yang merekam defleksi
positif saat repolarisasi ventrikel (gelombang R
tinggi)
T Wave
Inversion
 Deep symmetric inverted T
waves
 In more than 2 precardial leads
 85% of the patients with such T
wave↓had > 75% stenosis of
the coronary artery
 T wave ↓are significantly
associated with MI or death
during follow up
 T wave
33 inversion
Myocardial Injury
 Myocardial injured cells do not function normally, affecting both
muscle contraction and the conduction of electrical impulses

 EKG changes include ST elevation, normally the ST segment is

isoelectric
 Elevation of the ST segment is consistent with injury
 ST segment elevation is earliest sign of AMI
 Significant if 1mm or greater in two contiguous leads
 ST segment will return to baseline over time, conditions
where it does not include: pericarditis & ventricular
aneurysm
Segmen ST

 Segmen ST menghubungkan kompleks QRS dan

gelombang T serta berdurasi 0,08-0,12 s (80-120
ms)
Segmen ST
 Menggambarkan waktu antara akhir depolarisasi
ventrikel dengan awal repolarisasi ventrikel
ST Segment
 Represents beginning of ventricular repolarization
 Measured immediately after QRS complex to the beginning of
the T wave
 Normally isoelectric
 Prolonged ST may indicate hypocalcemia
 Elevated ST may indicate pericarditis, infarction, aneurysms
 Depressed ST may indicate ischemia or digitalis toxicity or may
be nonspecific
 J-point is where the QRS complex and the ST segment meet
Reciprocal ST Depression

•ST depression often develop

at in leads “opposite” the
sight of infarction.

•Known as “reciprocal
depression.

•Can be helpful to confirm

STEMI.

•May represent “mirror

image” phenomenon.
Acute Inferior Infarct
Right Coronary Artery Distribution

Reciprocal depression

ST elevation
Acute Inferior Infarct
Right Coronary Artery Distribution

Reciprocal depression

ST elevation
Segmen ST
Diukur dari akhir QRS s/d awal gel T

Normal : Isoelektris

Kepentingan : Elevasi Pada injuri/infark akut

Depresi Pada iskemia

NON STEMI STEMI

ECG Changes

Ways the ECG can change include:

ST elevation &
depression

T-waves

peaked flattened inverted

Appearance of
pathologic Q-
waves
 ST Segment Changes: Identifying MI Mimics

 Objectives
 Evaluate common abnormalities that mimic
myocardial infarction.
 Identify the criteria for pericarditis and
evidence – based interventions.
 Differentiate between pulmonary embolus and
myocardial infarction using diagnostic criteria.
 ST Segment Changes: Identifying MI Mimics

▪ Acute Coronary Syndromes

– Unstable Angina
– Non ST segment Elevation MI
(NSTEMI)
– ST segment Elevation MI
(STEMI)
 ST Segment Changes: Identifying MI Mimics

▪ Acute Coronary Syndromes

– Clinical Symptoms
• typical
• atypical
 ST Segment Changes: Identifying MI Mimics

▪ Acute Coronary Syndromes

– Diagnostics
• Echocardiography
• Lab
–ABGs
–H & H
–enzymes
 ST Segment Changes: Identifying MI Mimics

▪ Acute Coronary Syndromes

– Diagnostics
• ECG (12 or 15 lead)
–T wave inversion
–ST segment elevation
–Q wave
–reciprocal ST segment
depression
ST Segment Changes: Identifying MI Mimics
 UNSTABLE STEMI
ANGINA/NSTEMI
 Ischemia and
55 Infarction

TRANSMURAL Injury ST
Elevation
 E

INFARCTION INJURY ISCHAEMIA

 Ischemia, Injury &
57 Infarction
1. Ischemia produces ST segment
Myocardial depression with or without T
inversion
Ischemia
2. Injury causes ST segment elevation
Myocardial Injury with or without loss of R wave
voltage
3. Infarction causes deep Q waves
with loss of R wave voltage.
Myocardial
Infarction
 ST Segment Changes: Identifying MI Mimics

SITE INDICATIVE RECIPROCAL

Septal V1, V2 None
Anterior V2, V3, V4 None
Anteroseptal V1, V2, V3, V4 None
Lateral I, aVL, V5, V6 II, III, aVF
Anterolateral I, aVL, V3, V4, V5, V6 II, III, aVF
Inferior II, III, aVF I, aVL, V2, V3
Posterior None V1, V2
 Septal

Lateral
Anterior

Lateral

Inferior
 Blood Supply of
60 Heart
RCA

LCX

LAD

RCA

LCA
 LEFT CIRCUMFLEX (LCX)
Supplies blood to
•Left atrium
•Left ventricle
•Lateral wall
•Posterior wall
•Inferior wall (if
dominant)
VI EDUCATION

Not to be copied or re-distributed

Source: data on file at Guidant
 Left Anterior Descending (LAD)
Supplies blood to the
left ventricle
•Anterior wall
•Lateral wall
•Apical wall
•Ventricular
septum

VI EDUCATION

Not to be copied or re-distributed

Source: data on file at Guidant
 Right Coronary Artery (RCA)

Supplies blood to
• Right atrium
• Right ventricle
• Posterior and inferior
walls of left ventricle
(if dominant)

VI EDUCATION

Not to be copied or re-distributed

Source: data on file at Guidant
 Blood Supply
of Heart
 Heart has four surfaces
 Anterior surface – LAD, Left Circumflex (LCx)
 Left lateral surface – LCx, partly LAD
 Inferior surface – RCA, LAD terminal portion
 Posterior surface – RCA, LCx branches
 Rt. and Lt. coronary arteries arise from aorta
 They are 2.5 mm at origin, 0.5 mm at the end
 Coronary arteries fill during diastole
 Flow - epicardium to endocardium –
poverty/plenty
 Blood Supply - MI
65 - Leads

ANTERIOR LATERAL INFERIOR POSTERIOR

LAD LAD or LCx RCA RCA + LCx
V1, V2, V3, V4 V5, V6, L1, aVL L2, L3, aVF V1, V2 Mirror
ST Segment Changes: Identifying MI Mimics
ST Segment Changes: Identifying MI Mimics

Variation to ST – Segment Elevation

ST Segment Changes: Identifying MI Mimics
 ST Segment Changes: Identifying MI Mimics

High acute risk factors for progression to

myocardial infarction or death
 recurrent chest pain at rest
 dynamic ST-segment changes: ST-segment
depression > 0.1 mV or transient (<30 min) ST-
segment elevation >0.1 mV
 elevated Troponin-I, Troponin-T, or CK-MB levels
ST Segment Changes: Identifying MI Mimics
ST Segment Changes: Identifying MI Mimics
ST Segment Changes: Identifying MI Mimics
ST Segment Changes: Identifying MI Mimics
ST Segment Changes: Identifying MI Mimics
29 y/o with chest pain
Diffuse ST elevation c/w pericarditis,
?PR segment depression
47 y/o male with chest pain
Acute inferior MI – culprit vessel RCA
41 y/o male with severe SOB
Extensive anterior/anterolateral MI
 Early
Repolarization

This ECG has all normal features

The ST-T (J) Junction point is
elevated. T waves are tall, May be inverted in LIII, The ST
segment initial portion is concave. This does not signify Ischemia
 What is in this ECG
79
 NSTE
MI
Non ST ↑ MI or NSTEMI, Non Q MI
 Or also called sub-endocardial Infarction
 Non transmural, restricted to the sub-endocardial
region - there will be no ST ↑ or Q waves
 ST depressions in anterio-lateral & inferior leads
 Prolonged chest pain, autonomic symptoms like
nausea, vomiting, diaphoresis
 Persistent ST-segment ↓even after resolution of pain
 Look at This ECG
81
 Very Striking
82
 What are these ECGs
83
 STEMI and
QWMI
STEMI and QWMI
 ST ↑ signifies severe transmural myocardial injury
– This is early stage before death of the muscle
tissue – the infarction
 Q waves signify muscle death – They appear late
in the sequence of MI and remain for a long time
 Presence of either is an indication for thrombolysis
 What is in this ECG ?
85
 What is striking ?
86

▪ Note the ST↑in V1, V2, V3

▪ T↓ in V1 to V5
▪ R wave voltages of all lateral
leads well preserved
▪ No ST ↑in the Lateral leads
 Guess How Old is this MI !
87
 Question 1

 What are the ECG abnormalities?

 What is the differential?
 Question 2

 What are the ECG abnormalities?

 What sort of ACS?
 What territory is affected?
 Question 3

 What are the ECG abnormalities

 What sort of ACS?
 What territory?
 Question 4

 What are the ECG abnormalities?

 Give 3 possible differentials
 Question 5

• What are the ECG abnormalities?

• What sort of ACS?
 What territory?
 ST Segment Changes: Identifying MI Mimics

• In Conclusion
– is the patient having a MI?
– a variety of conditions can mimic
infarction
▪ST segment changes
 ST Segment Changes: Identifying MI Mimics

• Prominent J with ST segment elevations

– hyperkalemia
– acute pulmonary embolism
– subarachnoid hemorrhage
– tricyclic antidepressant intoxication
95
ST Segment Depression

1. Upward sloping depression of ST segment is not indicative of

IHD
2. It is called J point depression or sagging ST seg
3. Downward slopping or Horizontal depression of ST segment
leading to T↓is significant of IHD
ST depression
 Lateral Wall
98 Ischemia
▪ Note the classical
ischemic ST depressions
▪ ST ↓ are seen in
V4,V5,V6 – lateral wall
▪ His ST segments retuned
to base line after
sublingual nitroglycerine
▪ His pain is precipitated by
effort
▪ Notice the tachycardia –
heart rate = 140
 Holter & TMT in
99 CAD
 Evolution of
100 Acute MI
A – Normal ST segment and T waves
B – ST mild ↑ and prominent T waves
C – Marked ST ↑ + merging upright T
D – ST elevation reduced, T↓,Q starts
E – Deep Q waves, ST segment returning to
baseline, T wave is inverted
F – ST became normal, T Upright, Only Q+
 Serial ECG
101 changes of MI
 Normal Q
102 waves

Notice the small

Normal Q in Lead I
 Pathological Q
103 wave

Notice the deep & wide

Infarction Q in Lead I
Old MIs
 Old STEMIs can leave permanent Q waves
 Territories are the same (anterior, inferior
lateral etc.)
 Poor R wave progression can also indicate an
old anterior STEMI
ER patient care

 Initial general treatment (memory aid: “MONA”

greets all patients
 Morphine, 2-4 mg repeated q 5-10 min
 Oxygen, 4 L/min; continue if S aO2 < 90%

 NTG, SL or spray, followed by IV for persistent or

recurrent discomfort
 Aspirin, 160 to 325 mg (chew and swallow)
STEMI
 Occluded coronary artery
 Emergency = myocardium is dying!
Antiplatelet
Obat Antikoagulan
NAMA OBAT KETERANGAN

HEPARIN (UFH) BOLUS 60-70 U/KG,

INFUS 1000 U/JAM,
APTT 1,5 – 2,5 KALI
KONTROL

ENOXAPARIN 1 MG/KG SETIAP 12 JAM

DALTEPARIN 120 U/KGBB SETIAP 12

JAM
 MEKANISME KERJA OBAT ANTI ANGINA

SIRKULASI SISTEMIK
AFTERLOAD

INOTROPIK NEGATIF

B-BLOCKER Ca ANTAGONIST
VERAPAMIL, DILTIAZEM
B-BLOCKER
NITRAT

NITRAT
DILATASI Ca ANTAGONIST ARTERIOL REST VESSEL

PRELOAD VENOUS CAP VESSEL

VENOUS RETURN

H.Opie 2001;34-35
 Which BP Drug to
114 Choose ?
1. HT + DM ACEi, ARB
2. HT + IHD ACEi, Perindopril + BB (Meto,
Carva)
3. HT + MRD ACEi + / or Methyl dopa (MD)
4. HT + CHF ARB, ACEi, Diuretics, No CCB
5. HT + Pregnancy MD or CCB (Amlo) No ACEi
6. HT + Asthma, COPD No beta blockers, Alpha blockers
OK
7. HT + Tachycardia No CCBs, Give BB
8. HT + Dyslipidemia No Diuretics- give ACEi, ARB, CCB
9. HT in elderly, ISH Indapamide, Diuretics, CCB
 THIS IS NOT THE
115
END
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ECG
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