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

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, Heparan sulfate

Lapisan Endotel
Lily LS. Pathophysiology of heart disease 1993

Ischemic Heart Disease (IHD)

Blood supply Ischemia Transient loss Infarction Persistent loss ST Segment Sub-endocardial Stable Angina NSTEMI ACS Depressed Transmural Variant Angina STEMI ACS Elevated

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Acute Coronary Syndromes

Minor Plaque Disruption NonOcclusive Thrombus Occlusive Thrombus

Non-Vulnerable Vulnerable Atherosclerotic Atheroscleroti Plaque c Plaque

Asymptomatic Unstable Angina or NonQ-MI

Myocardial Infarction or Sudden Cardiac Death Occlusive Thrombus

Major Plaque Disruption

ATHEROGENESIS

LCX LMS

LAD pangkal

ANGIOGRAFI KORONER (KATETERISASI)

Plak Stabil (stable plaque)

Plak ruptur (ruptured plaque)

Pathogenesis of ACS

Platelet rupture Platelet Adhesion Platelet Activation Platelet Aggregation

Sequence of events Plaque Rupture Platelet Adhesion Platelet Activation Platelet Aggregation Thrombotic Occlusion
19

Anti-platelet drugs

Thrombotic Occlusion

Patofisiologi SKA
Erosi atau ruptur plak
Pembentukan trombus dan embolisasi

Angina Pektoris tak Stabil (APTS)

Infark Miokard dgnNon ST Elevasi

Infark Miokard 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 hearts 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 wavehad > 75% stenosis of the coronary artery T wave are significantly associated with MI or death during follow up

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T wave 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

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P wave PR Interval QRS complex ST segment T Wave

ECG Complex

QT Interval
RR Interval

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Identify the ECG Complex

3

4 1 2

5 8

6
7

Putting it All Together

Segmen ST
Diukur dari akhir QRS s/d awal gel T
Normal : Isoelektris Kepentingan : Elevasi Depresi Pada injuri/infark akut Pada iskemia

NON STEMI

STEMI

ECG Changes
Ways the ECG can change include:
ST elevation & depression

T-waves peaked Appearance of pathologic Q-waves flattened inverted

ISKEMIA

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 ANGINA/NSTEMI

STEMI

50

Ischemia and Infarction

TRANSMURAL Injury ST Elevation

INFARCTION

INJURY

ISCHAEMIA

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Ischemia, Injury & Infarction

1.

Myocardial Ischemia
2.

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

Myocardial Injury Myocardial Infarction

3.

ST Segment Changes: Identifying MI Mimics

SITE

INDICATIVE

RECIPROCAL

Septal Anterior Anteroseptal

Lateral Anterolateral Inferior Posterior

V1, V2 V2, V3, V4 V1, V2, V3, V4

I, aVL, V5, V6 I, aVL, V3, V4, V5, V6 II, III, aVF None

None None None

II, III, aVF II, III, aVF I, aVL, V2, V3 V1, V2

Septal Lateral Anterior

Lateral

Inferior

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Blood Supply of 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

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Blood Supply MI - Leads

ANTERIOR LAD V1, V2, V3, V4

LATERAL LAD or LCx V5, V6, L1, aVL

INFERIOR RCA L2, L3, aVF

POSTERIOR RCA + LCx 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) STsegment 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 Repolarizati on

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

74

NST EMI
Non ST MI or NSTEMI, Non Q MI

Or also called sub-endocardial Infarction

Non transmural, restricted to the subendocardial 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

76

Very Striking
77

What are these ECGs

78

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

80

What is in this ECG ?

What is striking ?
81

Note the STin 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 !

82

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
90

Depression

1.

2. 3.

Upward sloping depression of ST segment is not indicative of IHD It is called J point depression or sagging ST seg Downward slopping or Horizontal depression of ST segment leading to Tis significant of IHD

ST depression

93

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

97

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

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!

104

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

105

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 Interferenc e

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

Antiplatelet

Obat Antikoagulan
NAMA OBAT
HEPARIN (UFH)

KETERANGAN
BOLUS 60-70 U/KG, INFUS 1000 U/JAM, APTT 1,5 2,5 KALI KONTROL 1 MG/KG SETIAP 12 JAM 120 U/KGBB SETIAP 12 JAM

ENOXAPARIN

DALTEPARIN

MEKANISME KERJA OBAT ANTI ANGINA

SIRKULASI SISTEMIK AFTERLOAD INOTROPIK NEGATIF B-BLOCKER VERAPAMIL, DILTIAZEM Ca ANTAGONIST B-BLOCKER NITRAT NITRAT Ca ANTAGONIST

DILATASI

ARTERIOL REST VESSEL VENOUS CAP VESSEL

PRELOAD VENOUS RETURN

H.Opie 2001;34-35

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1. 2.

3. 4. 5. 6.

7. 8. 9.

HT + DM HT + IHD Carva) HT + MRD HT + CHF HT + Pregnancy HT + Asthma, COPD OK HT + Tachycardia HT + Dyslipidemia HT in elderly, ISH

Which BP Drug to Choose ?

ACEi, ARB ACEi, Perindopril + BB (Meto, ACEi + / or Methyl dopa (MD) ARB, ACEi, Diuretics, No CCB MD or CCB (Amlo) No ACEi No beta blockers, Alpha blockers No CCBs, Give BB No Diuretics- give ACEi, ARB, CCB Indapamide, Diuretics, CCB

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