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EKG Penyakit Jantung Koroner

Dr.Suhaemi,SpPD,Finasim
PEMBULUH DARAH KORONER

RCA
LM
LAD LCx
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
Nomenklatur Kompleks QRS
NORMAL
Tunika media
Tunika Intima

Barrier

EDRF, NO, PDGF


Zat antitrombotik:
Prostaccyclin,
Lapisan Endotel Heparan sulfate

Lily LS. Pathophysiology of heart disease 1993


Ischemic Heart Disease (IHD)

Blood supply Sub-endocardial Transmural

Ischemia Stable Variant


Transient loss Angina Angina

Infarction NSTEMI STEMI


Persistent loss ACS ACS

ST Segment Depressed Elevated


Acute Coronary Syndromes

Minor
Plaque Non- Occlusive
Disruption Occlusive Thrombus
Thrombus

Non-Vulnerable Vulnerable
Atherosclerotic Atherosclerotic
Plaque Plaque Myocardial
Infarction or
Asymptomatic Sudden
Unstable Cardiac
Angina or Non- Death
Q-MI
Major Occlusive
Plaque Thrombus
Disruption

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ATHEROGENESIS
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
• Platelet Adhesion Aggregation
• Platelet Activation
• Platelet Aggregation Thrombotic
• Thrombotic Occlusion Anti-platelet drugs Occlusion

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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 SaO2 < 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 inversion

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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
ECG Complex
P wave
PR Interval
QRS complex
ST segment
T Wave
QT Interval
RR Interval

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Identify the ECG Complex

4
5
1
8
2

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Putting it All Together
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
ISKEMIA
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 Infarction

TRANSMURAL Injury ST
Elevation

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Ischemia, Injury & Infarction

1. Ischemia produces ST segment


Myocardial depression with or without T
inversion
Ischemia
2. Injury causes ST segment
elevation with or without loss of
Myocardial Injury R wave voltage
3. Infarction causes deep Q waves
with loss of R wave voltage.
Myocardial
Infarction

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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 V 1, V 2
Septal

Lateral
Anterior

Lateral

Inferior
Blood Supply of Heart
RCA

LCX

LAD

RCA

LCA
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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 - 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
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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
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

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NSTEMI

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

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Very Striking

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What are these ECGs

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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 ?

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What is
striking ?

 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

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Guess How Old is this MI !

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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
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

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ST depression
Lateral Wall 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

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Holter & TMT in CAD

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Evolution of 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+

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Serial ECG changes of MI

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Normal Q waves

Notice the small


Normal Q in Lead I
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Pathological Q wave

Notice the deep & wide


Infarction Q in Lead I
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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 SaO2 < 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!
Wandering base line

 In non co-operative child


 Excessive movements of limbs
 Movement disorders of CNS
 Not properly earthed machine
 Additional wet ground earth
helps

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Muscle Tremor

 Limb movements cause baseline fluctuations


 Tense muscles cause tremor of baseline
 Hairy chest interferes with proper contact of chest
leads – better to shave the area if needed.
 Reassurance, starting recording a few minutes after
the leads are placed – reduce muscle tension
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AC Interference

 Any electrical gadgets in the same line may interfere


 Like Mixie, Motor, Musical tube lights etc
 Proper earthing is essential
 Dedicated direct line for ECG power point
 Use battery mode, Artifacts are quite misleading
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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 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 + DyslipidemiaNo Diuretics- give ACEi, ARB, CCB
9. HT in elderly, ISH Indapamide, Diuretics, CCB

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THIS IS NOT THE END

 This only a beginning and certainly not the end


 We look forward for more learning
experiences
 Please write to us what you felt about this
ECG
 Contact address and phone are in the
beginning

Thank YOU

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