ECG CHANGES IN ACS

 ACS
 Coronary circulation
 Evolving changes
 Management
ACUTE CORONARY SYNDROME

 Clinical spectrum of ischaemic heart disease

includes:

-Unstable angina
-Non ST elevation myocardial infarction (NSTEMI)
-ST elevation myocardial infarction (STEMI)

Based on degree and acuteness of coronary occlusion.

PATHOGENESIS

 Coronary artery occlusion due to:

-Atherosclerotic plaque rupture, fissuring or
ulceration with

-Superimposed thrombosis and

-Coronary vasospasm.
-STEMI: Acute TOTAL occlusion of coronary artery

-NSTEMI: Acute SUB-TOTAL coronary artery

occlusion

-Unstable angina: Angina at rest without cardiac

biomarkers elevation.
CORONARY CIRCULATION
 RIGHT CORONARY ARTERY
(1)Ascending SA node  Right atrium
Branch
 Most of right ventricle
(2)Marginal branch  Part of left ventricle
(3)AV node branch
(diaphragmatic surface)
 Posterior 1/3 of IV
(4)Posterior interventricular septum
branch
 SA node (~60%)
*Dominance of coronary arterial  AV node (~80%)
system defined by which artery
gives rise to posterior
interventricular branch.
67%
LEFT CORONARY ARTERY

1)SA node branch  Left atrium

2)Anterior IV branch  Most of left ventricle

(Left ascending descending
–LAD)  Part of right ventricle

3)Circumflex branch  Anterior 2/3 IV septum,

including AV bundles (via
perforating IV septal
branches)

 SA node (40%)
 INFARCT SITE LEADS
Anterior
-Small V3-V4
-Extensive V1-V6

Anteroseptal V1-V3
Anterolateral I, avL, V4-V6
Lateral I, avL, V5-V6
Inferior II, III, avF
Posterior V1-V2 (Tall R, ST depression)
V7-V8 (ST elevation)
Right ventricular V4R, V5R
 Reciprocal Changes?

 During an acute STEMI, when ST segment

elevation is present in leads that face the
acute injury, ST segment depression will
often be present in leads that face the
“ischemic boundary”.
ECG
 Rate: Usually 25mm/s.
-One BIG square = 0.2s
-One small square = 0.04s

 PR: 0.12-0.20s. Start of P – start of QRS

 QRS: <0.12s

 QT: 0.38- 0.42s. QRS to end of T wave.

 ST segment: Isoelectric
-Planar elevation >1mm or depression >0.5mm implies
infarction/ischaemia

 T wave: Normally inverted in avR, V1 and occasionally V2.

Evolving Changes

 0-15 mins: Tall T

 15-60mins: ST elevation
 1-6H: Loss R (Poor R wave progression)
T inversion

 6-12H: Q wave, deep T wave

 12-24H: T inversion
 ST elevation: Active, ongoing, transmural
myocardial injury

 Q wave: Dead zone myocardium which

undergone irreversible damage and death.
(1) Clinical history ischaemic type chest pain

(2)ECG changes:
STEMI
-New onset ST elevation:

(a) > 0.1mV in 2 contiguous limb leads, or V4-V6

and / or
(b) > 0.2mV in 2 contiguous precordial leads V1-V3

-Presumed new LBBB

(3)Elevated cardiac markers

Inferior
Hyper K
PERICARDITIS
 Stage 1 – Widespread STE and PR depression with
reciprocal changes in Avr (1st 2 weeks)

 Stage 2 – Normalization of ST changes; generalized

T wave flattening (1 to 3 weeks)

 Stage 3– Flattened T waves become inverted (3 to

several weeks)

 Stage 4 – ECG returns to normal (several weeks

onwards)
 Steps to distinguish pericarditis from STEMI:
 Is there ST depression in a lead other than AVR or
V1? This is a STEMI
 Is there convex up or horizontal ST elevation? This is
a STEMI
 Is there ST elevation greater in III than II? This is a
STEMI
 Now look for PR depression in multiple leads… this
suggests pericarditis
MANAGEMENT

 Based on what is being encountered.

-STEMI  Thrombolysis / PCI

-NSTEMI, Unstable angina

CONTRAINDICATIONS

ABSOLUTE
(1)Intracranial hemorrhage risk
-Hx of intracranial hemorrhage
-Ischaemic stroke within 3 months
-Structural cerebral lesion (AV malforations), intracranial
neoplasm

(2)Bleeding risk
-Active bleeding/ bleeding diathesis (exclude menses)
-Head trauma within 3 months
-Suspected aortic dissection
RELATIVE
(1)Intracranial hemorrhage risk
-Uncontrolled HTN on presentation (>180/110)
-Ischaemic stroke > 3 months ago
-Hx of chronic, sever uncontrolled HTN

(2)Bleeding risk
-Current anticoagulation use in therapeutic dose (INR>2)
-Recent major surgery <3 weeks
-Traumatic/ prolonged CPR >10 mins
-Recent internal bleeding (GIT or urinary tract hemorrhage) within 4
weeks
-Non compressible vascular puncture
-Active peptic ulcer

(3)Others:
-Pregnancy
-Prior exposure of streptokinase (>5days within one year of 1st usage)
THROMBOLYTIC AGENT

(1)Streptokinase
-1.5 million Unit in 100mL NS/ D5% over 1 hour
-Antigenic Antibodies formation

(2)Alteplase
-Fibrin specific agent
-Achieves better reperfusion at 90 mins as compared to
streptokinase
-Higher rate of reocclusion. Heparin needs to be given for 48 hours

(3)Second generation fibrin specific agents: Tenecteplase,

Reteplase
GENERAL MEASURES

1)Complete bed rest

2)Avoid valsalva maneuvre
 Concomitant Therapy:

1)Oxygen

2)Antiplatelet agents
-Aspirin 300mg stat  75-150mg OD
-Clopidogrel 300mg stat  75mg OD
(Reduce odds of occluded infarct related artery, death or
reinfarction)

3)Analgesia
-Morphine 5-10mg IV with antiemetic
-SL GTN 0.5mg
-IV GTN if pain not relieved
4)B blocker : Improve survival post MI

5)ACE-inhibitor: Prevent remodeling

6)Statin: Start regardless of lipid level

7)Calcium channel blocker: Limited role in AMI. Routine

use not recommended.
-May be use as adjunct in hypertension and on-going
ischemia despite B blocker and nitrates used.
Percutaneous Coronary Intervention

Preferred reperfusion strategy if facilities available

1)Chest pain with objective ischaemia evidence that

persists for >24-48H after aggressive medical therapy.

2)Recurrent ischaemic episods despite optimal medical

therapy.

3)Hypotension or severe heart failure.

TIMI RISK SCORE
In NSTEMI/UA, used to categorize risk of death and ischaemic event .

HISTORY POINTS

Age >65 1

>3 CAD risk factors (FHx, HTN, 1

hypercholesterolemia, DM, active
smoker)
Known CAD (stenosis> 50%) 1

ASA used in past 1 week 1

PRESENTATION

Recent (<24H) severe angina 1

Increased cardiac markers 1

ST deviation >0.5mm 1

Total points (0-7)

Risk Score Death/ MI (%) Death, MI or Urgent
Revascularization
0/1 3 5

2 3 8

3 5 13

4 7 20

5 12 26

6/7 19 41
 KILLIP CLASSIFICATION
Severity of heart failure after AMI with mortality predictor.
CLASS DEFINITION APPROXIMATE
MORTALITY

I Absence of rales over lung fields 8%

and absent S3

II Rales over 50% or less of lung 30%

fields or presence of S3

III Rales more than 50% of lung 44%

fields (pulmonary oedema
frequently)
IV Shock 80-100%
REFERENCES

1) Murray, Ian B. Oxford Handbook of Clinical

Medicine; Oxford 8th Edition. 2010; 90-1.
2) Management of acute ST segment
elevation myocardial infarction. Clinical
Practice Guidelines Malaysia 2nd Edition.
2007; 1-3,11-18.
3) A. Maziar, Eric H. Myocardial Infarction.
Emedicine. 2012, Sep.