Approach to Acute

Coronary Syndrome

Presented by: Dr.Noor Alqiq & Dr.Dina Darwish

Supervised By: Dr.Rasheed Ibdah
Ischemic Heart Disease Classification :
• Chronic ischemic heart disease ( stable Angina)
Fixed atherosclerotic lesions that narrow the major coronary arteries (>=70%)
Ischemia happens due to imbalance b/w blood supply and O2 demand leading to
inadequate perfusion
Predictably and reproducibly > usually with exertion and remits with rest or NTG
• Acute Coronary Syndrome (ACS)
Caused by atherosclerotic plaque rupture with superimposed intracoronary
thrombosis that leads to subtotal or total occlusion of coronary arteries
Can be divided into : ST-elevation MI and Non-ST Elevation-ACS
> Same clinical presentation and pathophysiology but differ in ECG and cardiac
enzymes
• NSTE-ACS:
• Unstable Angina:
Subtotal occlusion > Subendocardial Ischemia ( Normal cardiac enzymes ±
ST depressions and/or T wave inversions on ECG )
• NSTEMI:
Subtotal occlusion > Subendocardial Infarction ( elevated cardiac enzymes
± ST depressions and/or T wave inversions on ECG )

• STEMI:
Total occlusion > transmural infarction
( elevated cardiac enzymes +ST elevations on ECG )
 fourth universal definition of type 1 MI:
The criteria includes detection of a rise and/or fall of cardiac troponins
with at least one value above the 99th percentile of URL + at least one of
the following :
1- new ischemic ECG changes
2- development of pathologic Q waves
3- symptoms of acute myocardial ischemia
4- imaging evidence of new regional wall
motion abnormality or loss of viable myocardium
in a pattern consistent with an ischemic etiology
5- identification of coronary thrombus by angiography
Clinical features :
Presentation :
1- Acute chest pain : The classic and m.c symptom of ACS.
Usulally :
Site : retrosternal
onset : sudden
Charecterstic: more discomfort than pain and it may be difficult
for patient to describe and localize ( Visceral pain) ,
terms frequently used by patients include : heaviness , tightness
, squeezing , burning
Radiation: shoulders , epigastrium , arms , neck and lower jaw
Duration: variable but generally >= 30 min up to 12 hours
(depend on collaterals)
Exacerbating or relieving factor : not affected by position or
respiration , not relieved by rest or NTG
2- Nausea and Vomiting ( usually once )
3- Diaphoresis
4- SOB ( acute heart failure )
5- palpitations ( arrhythmias )
6- dizziness or L.O.C
7-general fatigue and weakness
8-Sudden cardiac death (more than one quarter of MI patients die,
presumably from ventricular fibrillation, m.c.c of death
prehospital)

• P.S : this classic presentation is not seen always , Female gender, patients
with diabetes, and older age are all presenting with vague symptoms or even
can be asymptomatic . A high degree of suspicion is warranted in such cases.
Complications of Acute MI:
• Congestive Heart failure
• Cardiogenic Shock (m.c.c of death in-hospital)
• Arrhythmias ( V.fib is m.c.c of death pre-hospital)
• Mechanical complications
- Free wall rupture ( cardiac tamponade )
-Rupture of interventricular septum (VSD)
-Papillary muscle rupture (acute MR )
 Risk Factors :
Non modifiable :
- Older Age (males > 45 , females > 55)
- Gender (male)
- Family hx of premature CAD or sudden death in first degree relative ( males < 55 , females<65)
- Previous history of ACS or PAD
Modifiable :
- Hyperlipidemia ( elevated LDL)
- HTN ( m.c risk factor )
- DM (worst risk factor)
- Smoking
- Obesity
- Sedentary life style
Physical Examination:
• The examination should include assessment of hemodynamic status and a screening neurologic
examination , esp if thrombolysis is a potential therapy
• General distress and diaphoresis are often seen
• Examination Usually unremarkable (no classic signs of ACS ) , unless co-pathologies are present
• Patients may present with signs of complications of MI:
• CHF
Jugular venous distention
Pulmonary crackles
S3 gallop
LLE
• Cardiogenic shock
Hypotension , tachycardia , impaired cognition , cool pale skin
• acute MR
new MR murmur , pulmonary crackles and hypoxia
• Rt vent infarction:
Hypotension , bradycardia or AV block , elevated JVP , hepatomegaly and clear lung
 ECG findings:
• Peaked T waves (hyperacute T wave ): occur very early and may be missed
(in 2 or more anatomically contiguous leads)
• ST-segment elevation: indicates transmural infarction (diagnostic)
J-point elevation above baseline of at least 1 mm in two or more
anatomically contiguous leads , other than V2-V3 , where the following
diagnostic thresholds apply
J-point (where the QRS complex joins the ST segment)
-The right-sided leads V4R, V5R, and V6R : should be obtained if there is evidence of inferior wall ischemia demonstrated
by ST elevation in leads II, III, and aVF.
-The posterior leads V7, V8, and V9 : may also be helpful if there is evidence of posterior wall ischemia as suggested by
prominent R waves and ST depressions in leads V1 and V2
• Reciprocal ST segment depression : represent coexisting ischemia
with the infarction (manifestation of infarct extension)
is defined as horizontal or down sloping STD (>=1mm )in leads that
are separate and distinct from leads manifesting STE.
• Q waves : Evidence of necrosis , usually seen late and can last for along time
the presence of new pathological Q waves indicates acute myocardial infarction but the mere presence of Q
waves does not necessarily mean that a new myocardial infarction is taking place. ( sign of previous
myocardial infarction.)
Physiological Q waves : <1 small sq width , < 2 small sq height , leads: I, aVL, V5, and V6
Pathological Q waves : abnormal shape , abnormal sites , at least in 2 contiguous leads in
same anatomical wall
• LBBB :
- ECG diagnostic criteria : Wide QRS (>2.5 small sq) , dominant S wave in V1,
broad monophasic R wave in lateral leads (I, AvL ,V5, V6) , absence of Q waves
in lateral leads

If New LBBB : considered an ST-segment elevation equivalent in patients presenting

with chest pain .

If old LBBB with symptoms of Ischemia :

Traditional Ischemic ECG changes are not diagnostic in the presence of LBBB
Bcz > LBBB may have ST elevations or depressions and abnormal T waves ,
without ischemia
- Smith-Modified Sgarbossa criteria :
• Concordant ST elevation ≥ 1 mm in ≥ 1 lead
• Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
• Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1
mm STE, as defined by ≥ 25% of the depth of the preceding S-wave
• ST-segment depression and/or T wave inversion :
- indicates subendocardial ischemia or infarction
- according to j-point ( horizontal or down sloping J-point depression
>=0.5 mm in tow or more anatomically contiguous leads )
- T wave inversion >=1mm in 2 or more contiguous leads

P.S : The leads which display these changes Not necessarily reflect the
exact ischemic area ( this contrasts against ST- elevation that is
indicative of infarct area)
 How to Approach (in ER)?
• Clinicians should consider possibility of ACS in any adult who presents to ED
complaining of acute chest pain or discomfort .( ACS until proving otherwise)
• Keep In Mind Serious DDX of Acute chest Pain:
1- Aortic Dissection ( which can cause ST-segment elevation if the dissection
involves the left or right coronary artery due to transmural myocardial ischemia.)
2- Pulmonary Embolism
3-Tension Pneumothorax
4- pericardial Tamponade
5- Mediastinitis ( esophageal rupture)
• Patients should be rapidly evaluated to determine
if their symptoms are suggestive of ACS or other DDx
• If ACS is the leading Diagnosis , initial assessment and interventions must be
performed rapidly ( Goal : within 10 minutes)

1- assess and stabilize Airway , Breathing and Circulation (ABC) and check Vital
signs
2- focused and rapid history and physical exam
3- 12-lead ECG
- if the initial ECG is not diagnostic but the patient still has chest pain and highly
suspicious for ACS > repeated at least every 15-30 min)
3- Attach cardiac and oxygen saturation monitors
-supplemental oxygen given only if patient is hypoxic (<94%)
-Administration of oxygen to normoxic patients , have direct vasoconstrictor effect
on coronary arteries
4- Resuscitation equipment brought to bed side (Defibrillator > if cardiac arrest /
airway equipments )
5- Establish IV access and blood work obtained :
• Serial Cardiac enzymes tests > first reading of –ve cardiac enzymes not exclude MI
1-Troponins (I and T) : most important enzyme test and highest sensitivity (Greater sensitivity and specificity than CK-MB for
myocardial injury)
Increases within 3-5 h and peaks within 24-48 h then returns to normal in 5-14days
Consider positive if : detection of a rise and/or fall of cTn levels (dynamic changes) with at least one value above the 99th
percentile of upper reference limit
2- CK: not very specific (can go up in many other conditions)
3-CK-MB :isoenzyme of CK , found primarily in heart muscle cells
Increases within 4-8h and peaks in 24h then returns to Normal in 48-72 h
helpful in detecting recurrent infarction ( quicker return to baseline than troponin)
• CBC ( HB , Platelets ) (anemia exacerbates myocardial ischemia , and patients with low HB may require blood transfusion)
Electrolytes ( to replace deficient electrolytes , esp. k+ and mg+2 to lower arrythmia risk)
KFT ( baseline , Contrast-induced nephropathy)
PT / PTT / INR (risk of bleeding)
Lipid profile (assess risk factors )
HBA1c / RBS (assess RF)
TFT (to rule out thyrotoxicosis , risk of thyroid storm )
Chest Xray (pulmonary edema )
Echo (EF% , assess wall motion and abnormalities (hypokinesia and akinesia)> may indicate ischemia)
6- Aspirin 162 to 325 mg to be chewed (get into the bloodstream faster )
- All patients with suspected ACS should be given aspirin unless contraindicated (if AD is considered ,
aspirin allergy )
- if oral administration is not feasible , give as rectal suppository

7- 3 sublingual NG tablets (0.4mg) , 1 tablet at a time , spaced 5 min apart , or NG spray under tongue every
5 minutes for 3 doses
- symptomatic relief > coronary vasodilation
- decrease preload > systemic venodilation
- if patient has persistent chest discomfort , hypertension or signs of heart failure > may add IV NG
- Contraindicated if:
i. signs of hemodynamic compromise (SBP <90 and bradycardia) ( eg. Right ventricular infarction
(preload dependent)
ii. use of PED5 inhibitors (within 24-48h)

8- Morphine sulphate(2-4mg slow IV push every 5-15min)

-controversial >although provides good pain relief but may mask worsening symptoms and cause
hypotension
- Used if chest pain refractory to nitrate and other anti- anginal therapies
- Avoid in inferior MI (cause hypotension)
Initial Triage of emergency department patients with acute coronary syndrome:

• IF STEMI > admission to CCU+ initiate medical therapy + activate cath

team or rapid transfer PCI-capable center (goal: urgent PCI within 90min
of ED arrival)
If Non PCI- capable center and no C/I of thrombolysis > go to thrombolytic
therapy ( goal : within 30 min)

Successful thrombolytic therapy CRITERIA :

CLINICALLY: significant relief of pain >or =50% (a 5-point reduction
on a 1 to 10 subjective scale)
ELECTRICALLY: > or =50% reduction of ST segment elevation or
ventricular reperfusion arrhythmia (accelerated idioventricular rhythm )
BIOLOGICALLY: early peaking of cardiac enzymes levels
• IF NSTE-ACS (NSTEMI /UA) :
- should undergo early risk stratification (TIMI risk score or Grace risk score )
- TIMI risk score : The score predicts risk of acute MI , coronary
revascularization or death at 14-days
- GRACE risk score : incorporates physical examination findings, clinical
features, ECG findings, and biomarker variables (creatinine levels,
elevated cardiac enzymes) to predict mortality and MI risk in-hospital
and to six months.
Low risk (TlMl 0-2 or GRACE 1-108) > D/C on optimal medical therapy & OPC appointment ( for
reassessment)
Intermediate risk (TlMl 3-4 or GRACE 109-140) > admission to floor + initiate medical therapy +
delayed PCI (within 24-72h)
High risk (TlMl 5-7 or GRACE 141-372) > admission to CCU + initiate medical therapy + early PCI
(within 24h)

Indications of urgent PCI:

- Cardiogenic shock (hemodynamic unstable)
- Overt heart failure
- Persistent or recurrent chest pain despite medical therapy
- Sky high cardiac enzymes (trending up)
- Previous CABG and last remaining artery