Acute Coronary Syndrome

and
Atypical ECGs

Presenter : Dr. Vikneshwaran

Supervisor : Dr. Thavan
 Definition
• ACS is a clinical spectrum of ischemic heart disease ranging from unstable angina, NSTEMI to STEMI depending
upon the degree and acuteness of coronary occlusion.
• MI is a clinical diagnosis based on the presence of
myocardial injury or necrosis as indicated by a rise and
fall of serum cardiac biomarkers. In addition, there
should be at least one of the following:
i. History consistent with chest pain of ischemic origin.
ii. ECG changes of ST elevation or presumed new LBBB.
iii. Imaging evidence of new loss of viable myocardium
or new regional wall motion abnormality.
iv. Identification of an intracoronary (IC) thrombus by
angiography or autopsy.
• ‘Reinfarction’ is used for MI that occurs within 28 days of
the incident event while recurrent MI occurs after 28 days.
STEMI
History
• Typical chest pain :
• located in the center of the chest
• radiate to the jaw or down the left arm
• occur at rest or with activity
• associated with sweating, nausea, vomiting and shortness of breath.

• Atypical presentation
• burning quality and localized to the epigastrium
• elderly, females and patients with diabetes
• unexplained fatigue, shortness of breath, dizziness, lightheadedness, unexplained sweating
and syncope
• Unlikely ACS
• Pleuritic chest pain
• Stabbing pain No Characteristic of
• Positional pain CP that can be
• Duration < 2mins safely discharge
• Pain can be localized with fingertip home without
further diagnostic
• Likely ACS testing
• Symptoms similar to previous angina attack
• Substernal, and unable to localize properly +/- radiation
• Brief, sudden unexplained dyspnea
• Worsened with exertion and improved by rest
• Diaphoresis, nausea, vomiting
• Other important points to note in the history are the presence of:
• Previous history of ischemic heart disease, PCI or CABG.
• Risk factors for atherosclerosis.
• Symptoms suggestive of previous transient ischemic attack (TIA) or other forms of vascular
disease.
ECG Dilemma ….
• Not all patient with ACS / AMI exhibit ECG changes
• Normal ECG does not rule out the diagnosis of ACS
• Poor Sensitivity (28%), good specificity (97%)

What is more specific SERIAL

and sensitive than the
initial ECG ?
ECG
Initial recognition
When the patient with suspected STEMI reaches the emergency
department, evaluation and initial management should be prompt
(FAST TRACK - RED ZONE) because the benefits of reperfusion therapy
are greater the earlier it is instituted.
• A quick targeted history should be taken and vital signs noted. The
diagnosis should be confirmed with an ECG, which should be done
and interpreted immediately within 10 minutes of first medical
contact (FMC).

TIME LOST IS MYOCARDIUM LOST

• ECG shows ST elevation (STE) in two contiguous leads with symptoms of ischaemia is
suggestive of STEMI. Cut-off points for new or presumed new STE (in absence of LVH and
LBBB) is:
• a) ≥ 0.1 mV (one box) STE in all leads except leads V2-V3.
• b) In V2-V3, a cut-off point of ≥ 0.25 mV (in males < 40 years), ≥ 0.2 mV (in
males ≥ 40 years) and ≥ 0.15 mV in females
• A new onset or presumed new LBBB with typical ischemic chest pain - treat as STEMI.
• In inferior STEMI – do right precordial lead (V4R) to see right ventricular (RV)
involvement.
• Those with ST depression in V1-V3, do ECG of the posterior chest wall (V7-V9) to identify
a true infero-basal (formerly known as infero-posterior) STEMI. The cut-off point for STE
in the posterior leads is ≥ 0.05 mV (≥ 0.1 mV in men < 40 years).
• ST elevation in lead AVR may be a predictor of left main/3 vessel CAD and carries an
adverse prognosis.
* In early stages of MI, initial ECG maybe normal or show hyperacute T-wave changes only.
If highly suspicion of STEMI, ECG should be repeated at least in 15 minutes to look for
progressive ST changes. Comparison with previous ECG’s may also be helpful.
Left Bundle Branch Block (LBBB)
• Normally the septum is activated from left to right, producing small Q waves in the lateral lead

• In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the
impulse spreads first to the RV via the right bundle branch and then to the LV via the septum

• This sequence of activation extends the QRS duration to > 120 ms and eliminates the normal
septal Q waves in the lateral leads

• The overall direction of depolarisation (from right to left) produces tall R waves in the lateral leads
(I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis
deviation

• As the ventricles are activated sequentially (right, then left) rather than simultaneously, this
produces a broad or notched (‘M’-shaped) R wave in the lateral leads.
Sgarbossa's criteria (1996)
Modified Sgarbossa's criteria (2012)
• Smith et al. presented a set of modified
Sgarbossa criteria which eliminated the third
criteria in the original model (Discordant STE
>5mm) and replaced it with a new rule that’s
a ratio rather than an absolute value (positive
if ST elevation/S-wave amplitude < -0.25).
• The point system of the original Sgarbossa
criteria was also eliminated, meaning that any
one of the three modified Sgarbossa criteria
is enough for a positive result.
• Modified Sgarbossa vs Original Weighted
Sgarbossa:
• Sensitivity: 80% vs 52%, Specificity: 99% vs 100%
• Modified Sgarbossa vs Unweighted Sgarbossa:
• Sensitivity: 80% vs 67%, Specificity: 99% vs 94%
Cardiac Markers
• history and ECG is of paramount importance in making the diagnosis
• rise and fall in the levels of serum cardiac biomarkers support the diagnosis of
STEMI
• One should not however, wait for the results of these biomarkers before
initiating reperfusion therapy
• If history and ECG suggestive of STEMI, preferred CE is CK-MB (troponin is not
necessary since there already ECG evidence of myocardial injury)
• If ECG and history not conclusive, then troponin is preferred
• troponins are not useful for the detection of reinfarction because it remains
elevated for 10-14 days and sometimes longer
• CK-MB measurements are useful for the diagnosis of reinfarction, patient with
recurrent chest pain following STEMI, a ≥ 20% increase in the value from the last
sample suggests reinfarction
Management
The following should be done immediately and
concomitantly in the emergency department:
• Assess and stabilize patient’s hemodynamics.
• Continuous ECG monitoring.
• GTN if chest pain persists (avoid if SBP < 90 mmHg).
• 300 mg of non-enteric coated aspirin chewed and swallowed if not given earlier.
• Clopidogrel at a dose of 300 mg should be given, if not given earlier.
• Venous access established and blood taken for cardiac biomarkers, FBC, RP, glucose and lipid profile. Preferably
two IV lines should be set up.
• Pain relief - morphine should be administered IV at 2-5 mg by slow bolus injection every 5-15 minutes as
necessary. Watch for adverse events – hypotension and respiratory depression.
• Anti-emetics (IV metoclopromide 10 mg or promethazine 25 mg) should be given with morphine and 8-hourly
as necessary.
• Intramuscular injections should be avoided.
• Oxygen by nasal prongs/facemask if SpO2 is less than 95%.
• Assessment for reperfusion strategy.
Antithrombotic therapy to
support primary PCI for STEMI
• IV unfractionated heparin
(UFH) with additional bolus to
maintain activated clotting
time (ACT) above 275.
• IV low molecular weight
heparin (LMWH) –
enoxaparin.
• IV fondaparinux is not
recommended because of the
risk of catheter thrombosis.
PCI Vs Fibrinolysis

Puan, kami mahu hantar puan

untuk ujian ‘angioplasti’ sebab…
 Starting January 2017
1st choice of Referral Hub
During Office hours ONLY
– Code MI
10 minutes DBT for hospital without PCI facility < 120 minutes.
Journey time ~ 40 minutes, Procedure ~ 40minutes

Notes:
• Stable patient that do not need resuscitation will
STAY in STEMI bay. Once Cardiologist Hospital
Serdang accepts the case, MECC HA will inform
MECC Hosp. Serdang and patient will be
transferred straight to ambulance. Resus MO will
inform Medical MO in case patient is sent back to
HA – for direct admission.
• Transfer Team: MO triage, SN/TL or MA PHC.

20 min
Bring MYSTEMI form and photocopy of ECG, no
need CXR or referral letter (optional). Please
familiarize yourself with the route to ICL as no
Hospital Serdang staff will accompany us. Patient
will be in ED for name tagging only.
• Passover case to ICL team and inform them if we
are going back. MUST bring back ONE copy of
MYSTEMI form. Remind ICL staff to call MECC HA
if they are transferring patient back to HA.
Door-in to door-out (DIDO) time of
• Retrieval Team: same team. MECC to inform
≤ 30 minutes decreases mortality! Resus MO and EP for direct admission to CCU.
*Every 3 minutes delay increases mortality by 1%.
 REMINDER
• No branula at right forearm
• Bilateral groin to be shaved prior to transfer
• Verbal consent should be obtained
• Contact number of patient and next to kin must be written in the
MySTEMI form

• Allergy history ??
• Last meal ??
 Fibrinolytics
STREPTOKINASE
 Most widely used agent.  It causes more rapid reperfusion of the
 It is not fibrin specific
 Despite having a lower risk of intracranial hemorrhage, the
reduction in mortality is less than with fibrin specific agents. 
 Streptokinase is antigenic and promotes the production of
antibodies. Thus the utilization of this agent for reinfarction
is less effective if given between 3 days and 1 or even 4 years 
after the first administration. PCI or fibrin specific agents
should then be considered
TENECTEPLASE (TNK-TPA)
occluded artery than streptokinase and is
given as a single bolus dose.
This is a weight based regimen and thus there
is a risk of bleeding if the weight has been
overestimated.
In patients over the age of 75, the dose should
be reduced by 50%.

TNK-tPA single IV bolus: 30 mg if < 60 kg

1.5 mega units in 100 ml NS or D5% over 1 hour. 35 mg if 60 to < 70 kg
40 mg if 70 to < 80 kg
45 mg if 80 to < 90 kg
50 mg if > 90 kg
Contraindications to fibrinolytic therapy
Absolute contraindications
• Risk of intracranial haemorrhage
o History of intracranial bleed.
o History of ischaemic stroke within 3 months.
o Known structural cerebral vascular lesion
(e.g.arteriovenous malformation).
o Known intracranial neoplasm.
• Risk of bleeding
o Active bleeding or bleeding diathesis (excluding
menses).
o Significant head trauma within 3 months.
o Suspected aortic dissection.
Others
o Pregnancy.
o Prior exposure (> 5 days and within 12 months of first
usage) to streptokinase (if planning to use same agent).
Relative contraindications
• Risk of intracranial haemorrhage
o Severe uncontrolled hypertension ( BP > 180/110
mmHg)
o Ischaemic stroke more than 3 months.
o History of chronic, severe uncontrolled hypertension.
• Risk of bleeding
o Current use of anticoagulation in therapeutic doses
(INR) > 2.
o Recent major surgery < 3 weeks.
o Traumatic or prolonged CPR > 10 minutes.
o Recent internal bleeding (e.g. gastrointestinal or
urinary tract haemorrhage) within 4 weeks.
o Non-compressible vascular puncture.
o Active peptic ulcer.
High-risk patients
High-risk patients include:
• Large infarcts.
• Anterior infarcts.
• Hypotension and cardiogenic shock.
• Significant arrhythmias.
• Elderly patients.
• Post-revascularisation (post-CABG and post-PCI).
• Post-infarct angina.
Those contraindicated for fibrinolysis
and in high risk patients, Primary PCI
is the preferred strategy.
The goals of time to reperfusion
therapy should be within:
• 30 minutes DNT
• 90 minutes DBT
- PCI delay time is < 60 minutes
Antithrombotic therapy
These agents are administered to those
who received fibrinolytic therapy and did
not undergo PCI.
1. UFH
• In patients > 75 years of age and with renal impairment (serum
creatinine (Scr) > 200 μ mol/L in women and > 250 μmol/L in men), UFH is preferable to LMWH.
2. LMWH - enoxaparin
3. Anti Xa inhibitor - fondaparinux
• May be given to those patients treated medically including those not receiving fibrinolytic therapy. In
STEMI patients not undergoing primary PCI and not receiving fibrinolytic therapy, fondaparinux was
shown to reduce mortality and reinfarction without increasing bleeding and stroke rates when compared
to UFH or placebo.
• It is associated with an increase in catheter-related thrombus and coronary angiographic complications.
Thus, fondaparinux is not recommended as the sole anticoagulant during PCI.
Successful reperfusion
There is no sensitive bedside clinical method to reliably detect successful
reperfusion. Some useful guides are:
• Resolution of chest pain (may be confounded by the use of narcotic
analgesics).
• Early return of ST segment elevation to isoelectric line or a decrease in the
height of the ST elevation by 50% (in the lead that records the highest ST
elevation) within 60-90 minutes of initiation of fibrinolytic therapy.
• Early peaking of CK and CK-MB levels.
• Restoration and/or maintenance of hemodynamic and/or electrical
stability.
Failed fibrinolysis
• Failure of fibrinolytic agents to open the occluded IRA is manifested as :
• continuing chest pain,
• Persistent hyper-acute ECG changes (< 50% resolution of ST
elevation in the lead showing the greatest degree of ST elevation
at presentation)
• haemodynamic instability.
• These patients are more likely to develop complications such as heart failure (HF) and
arrhythmias.
• The treatment of choice for these patients is RESCUE PCI.
They SHOULD NOT be given a second dose of a fibrinolytic agent.
This is because there has been no difference in event free survival demonstrated whether
these patients are given a repeat dose of a fibrinolytic agent or are treated conservatively.
Complications
1. Arrhythmias.
2. LV dysfunction and shock.
3. Mechanical complications.
4. RV infarction.
5. Others e.g. pericarditis.
NSTEMI
Diagnosis
Diagnosis is based on history + dynamic ECG (without persistent ST elevation), +
raised cardiac biomarkers.

ECG suggestive of UA/NSTEMI are: completely

normal ECG
• Dynamic ST/T changes
does not exclude
• ST depression > 0.5 mm in 2 or more contiguous leads the diagnosis

• T-wave inversion – deep symmetrical T-wave inversion

• Other ECG changes include new or presumed new onset bundle branch block
(BBB) and cardiac arrhythmias, especially sustained ventricular tachycardia.
Evidence of previous infarctions such as Q waves may be present.
Cardiac Biomarkers
• Cardiac troponins (troponin T or I)
are the recommended biomarkers
• Highly specific and sensitive for
myocardial injury and/or necrosis
(infarction)
• The troponin level may not be
elevated if the test is done early (<6
hours)
• To confidently exclude myocardial
necrosis (infarction), a repeat test
needs to be done 6–12 hours after
admission.
Unstable Angina
Diagnosis
Unstable angina may be classified as:
I. New onset of severe angina or
accelerated angina; no rest pain
II. Angina at rest within past month but not within preceding 48 hours (angina at
rest, subacute)
III. Angina at rest within 48 hours (angina at rest, acute)

It may be further classified according to clinical circumstances into either:

A) Secondary – develops in the presence of extracardiac disease
B) Primary – develops in the absence of extracardiac disease
C) Post-infarct – develops within 2 weeks of an acute MI
Management
If the history is suggestive of ACS :
• Give soluble aspirin 300 mg crushed stat
• Give sublingual GTN
• Do 12 lead ECG and cardiac biomarkers

If the ECG and cardiac biomarkers are suggestive of ACS

• Give clopidogrel 300 mg stat if available.
• Send the patient to the nearest healthcare facility where definitive treatment can be given.

If the ECG and cardiac biomarkers are inconclusive for ACS

• Low risk patients : they can be referred as outpatient for cardiac assessment.
• Intermediate / High Risk patients : should be admitted
Risk Scores
In clinical practice, 2 risk
scores that are
commonly used are:
• TIMI Risk Score
- it is less accurate in
predicting events, but is
simple and widely
accepted.
• GRACE risk scores
HEART Score
Atypical ECGs
 ST = MI
ELEVATION
DDx of ST Elevation
• Acute MI
• LBBB
• Brugada Syndrome
• Pericarditis
• Early Benign Repolarization
• Ventricular Hypertrophy
• Electrolyte Imbalance ELEVATION
• Aneurysm
• Osborne waves
• Non acclusive vasospasm
• Procedure
• Cardiac contusion
• Raised ICP
Brugada Syndrome
• ECG abnormalities with high incidence of sudden death in patient
with structurally normal heart
• Diagnosis depends on ECG & clinical criteria
• ST elevation is observed in > 1 precordial lead (V1-V3) in conjunction
with:
• Documented VT or VF
• family history of sudden cardiac death < 45 years old
• No structural heart disease
• Syncope of unknown origin
Brugada Type 1
Coved ST elevation >2mm in >1 of V1-3 followed by negative T-wave
Brugada Type 2
>2mm saddleback shaped ST elevation
Brugada Type 3
Can be morphology of type 1 or 2 but STE <2mm
• Only proven therapy is IMPLANTABLE CARDIOVERTER DEFIBRILLATOR
• Undiagnosed Brugada Syndrome have estimated mortality of 10% per
year
Pericarditis
• widespread concave (“saddleback”)
ST segment elevation with PR
segment depression in multiple
leads, typically involving I, II, III, aVF,
aVL, and V2-6.

• There is reciprocal ST depression and

PR elevation in leads aVR and V1

• Spodick’s sing - downward sloping TP

segment with specificity for acute
pericarditis
Benign Early Repolarisation (BER)
• mild concave ST elevation with peaked asymetrical T-waves mainly in the
precordial leads

• Does not follow anatomical distribution, no reciprocal changes

• notching of the J-point — the “fish-hook” pattern

• normal variant commonly seen in young, healthy patients

• prominent at slower heart rates and disappear in the presence of

tachycardia
Feature STEMI Pericarditis BER

ST segment distribution Follow anatomical Widespread Usually pre-cordial

distribution
Reciprocal changes Present Absent Absent

Shape of ST segment Usually convex, can be Concave Concave

cocave, horizontal
ST Elevation : T wave ratio NA > 0.25 < 0.25

Q waves Sometimes Usually absent Usually absent

PR Segment Isoelectric Depressed in leads with ST Isoelectric

Elevation, elevated in AVR
and V1
Notched J point Absent Absent Present

Evolving changes Yes Unlikely in ED Nil

Ventricular Hypertrophy (Left)
• In response to pressure overload
• S-wave in V1 + Tallest R in V5/6 > 35mm – Sokolov Lyon criteria
• Causes: HTN, aortic stenosis, aortic regurg, mitral regurg, coarcatation
of aorta
Aneurysm
• There is ST elevation with deep Q waves and inverted T waves in V1-3

• This pattern suggests the presence of a left ventricular aneurysm due

to a prior anteroseptal MI.

• paradoxical movement of the left ventricular wall during systole

J-Wave (Osborn Wave)
• Positive deflection at the J-point
• Seen in hypothermia, normal variant, hypercalcaemia
Non occlusive vasospasm (Prinzmetal’s angina)

• This causes a pattern of ST elevation that is very similar to acute

STEMI — i.e. localised ST elevation with reciprocal ST depression
occurring during episodes of chest pain.

• However, unlike acute STEMI the ECG changes are transient,

reversible with vasodilators and not usually associated with
myocardial necrosis.

• It may be impossible to differentiate these two conditions based on

the ECG alone.
Raised Intra-cranial Pressure
• ST elevation or depression that simulates myocardial ischaemia or
pericarditis

• more commonly, widespread, deep T-wave inversions (“cerebral T

waves”) with prolonged QT
DDx of ST Depression
• Miocardial Ischemia
• Reciprocal changes of STEMI
• Posterior MI
• Toxicity
• Electrolyte
• SVT
• BBB
• Venticular Hypertrophy
• Ventricular paced rythmn
• Encephalon haemorrhage
• Dilated cardiomyopathy
• Shock
Miocardial Ischemia
• upsloping, downsloping, or horizontal

• Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥

2 contiguous leads indicates myocardial ischaemia

• ST depression ≥ 1 mm is more specific and conveys a worse prognosis

• ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of

NSTEMI and predicts significant mortality (35% mortality at 30 days)

• Upsloping ST depression is non-specific for myocardial ischaemia.

Reciprocal Changes
• acute STEMI is associated with simultaneous ST depression in the
electrically opposite leads
• Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
• Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF
(± lead II).
• Reciprocal ST depression in V1-3 occurs with posterior infarction
Posterior Infarct
• ST depression in the anterior leads V1-3
• along with dominant R waves (“Q-wave equivalent”)
• upright T waves
• ST elevation in the posterior leads V7-9
De Winters T Waves
• up-sloping ST depression > 1mm with symmetrically peaked T waves
in the precordial leads
• No ST elevation in precordial leads
• ST segment elevation (0.5 – 1mm) in aVR
• highly specific for an acute occlusion of the left
anterior descending artery
• STEMI equivalent -> emergency reperfusion therapy
Drug
• Digoxin : ST depression with a “sagging” morphology, reminiscent of
Salvador Dali’s moustache.
Electrolyte
• Hypokalemia - widespread downsloping ST depression with T-wave
flattening/inversion, prominent U waves and a prolonged QU interval.
Supraventricular Tachycardia (SVT)
• widespread horizontal ST depression
• most prominent in the left precordial leads (V4-6)
• does not necessarily indicate the presence of myocardial ischaemia,
provided that it resolves with treatment
Right Bundle Branch Block
• left ventricle is activated normally, meaning that the early part of the QRS
complex is unchanged

• delayed right ventricular activation produces a secondary R wave (R’) in the

right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads

• Diagnosis criteria
• Broad QRS > 120 ms
• RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
• Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
Ventricular Hypertrophy (Right)
• Dominant R in V1, S in V5/6
• Usually present with right atrial enlargement (P-pulmonale) or right
ventricular strain pattern (ST depression/T-inversion V1-4)
• Causes – Pulm HTN, mitral stenosis, pulm embolism, chronic lung
disease, congenital heart disease (TOF)
Wellen’s Syndrome
• Deeply inverted or biphasic T waves in V2-3
• Presence of persistent R wave
• Can present in pain free state
• Highly specific for LAD critical stenosis
• High risk of extensive anterior MI in next few days to weeks
• Needs invasive therapy
• Type A & Type B
Type A Type B
Premature Ventricular Complexes
• Normal electrophysiological phenomenon
• Frequent PVCs may cause palpitation & skipped beat
• In patient with IHD, PVC may trigger tachyarryhtmia
• Unifocal or multifocal
• Premature beats arising from an ectopic focus within the ventricles
• Features of PVC
- Broad QRS
- Premature – occur earlier than expected impulse
- Discordant ST segment & T wave changes
- Bigeminy – every other beat is a pvc
- Trigemiy – every third beat is pvc
- Couplet – two consecutive pvc
- Triplet – three consecutive pvc
- Causes – myocardial ischaemia, hypokalaemia, hypoMg, b-agonist, digoxin
toxicity
PVC (Trigeminy)
PVC (Couplets)
Thank You