Acute Coronary Syndromes


  • Coronary artery disease accounts for > 30% of death in West and presents acutely as acute coronary syndromes
  • Acute coronary syndrome (ACS) is a catch all term that refers to ischemic symptoms resulting from acute coronary occlusion
  • All patients who present with a suspected acute coronary syndrome must be assessed in the ED on an urgent (category 2) basis and have an ECG performed within 10 minutes of first acute clinical contact
  • A clinician with ECG expertise should review the ECG
  • A “CODE STEMI” activation system should be in place in any hospital that has an acute percutaneous coronary intervention service


STEMI (S-T Segment Elevation Myocardial Infarction)

  • presentation with clinical symptoms consistent with an acute coronary syndrome together with S-T segment elevation on ECG
  • New LBBB may be included in this sub-heading as the treatment approach is similar to STEMI

NSTEACS (non S-T Segment elevation acute coronary syndrome)

  • NSTEACS refers to any acute coronary syndrome which does not show S-T segment elevation
  • The ECG may show S-T segment depression or transient S-T segment elevation, but often will be normal

Non-STEMI (Non S-T Segment Elevation Myocardial Infarction)

  • By definition this will be shown by an elevation of serum troponin levels in the absence of S-T segment elevation

Unstable Angina

  • A small but still significant proportion (< 4 %) of patients presenting with possible cardiac chest pain in whom biomarkers and ECGs are normal will have unstable angina due to underlying coronary artery disease
  • Note that “unstable angina” is measured against a patient’s usual pattern of “stable angina” which is most commonly classified according to the New York Heart Association’s Functional Classification of Angina
  • New onset angina should be considered unstable in the first instance


Risk factors (these are of little diagnostic use in the acute setting):

  • diabetes mellitus
  • hypertension
  • lipids
  • family history
  • male
  • obesity
  • previous MI
  • hormone replacement for menopause
  • inactivity


Type 1

  • Spontaneous MI
  • Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis.

Type 2

  • MI secondary to ischaemic imbalance
  • Myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anemia, respiratory failure, hypotension, and hypertension with or without LVH

Type 3

  • MI resulting in death when biomarker values are unavailable
  • Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in cases cardiac biomarkers were not collected

Type 4a

  • MI related to PCI (there are complex specific criteria)

Type 4b

  • MI related to stent thrombosis (there are complex specific criteria)

Type 5

  • MI related to CABG MI related to CABG (there are complex specific criteria)


Class 1

  • Patients with cardiac disease but without resulting limitation of physical activity.
  • Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.

Class II

  • Patients with cardiac disease resulting in slight limitation of physical activity.
  • They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.

Class III

  • Patients with cardiac disease resulting in marked limitation of physical activity.
  • They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.

Class IV

  • Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort.
  • Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.


Very High Risk

  • Haemodynamic instability:
    • Heart failure/ cardiogenic shock
    • Mechanical complications of myocardial infarction
  • Life-threatening arrhythmias or cardiac arrest
  • Recurrent or ongoing ischaemia (e.g. chest pain refractory to medical treatment) or recurrent dynamic ST segment and/or T wave changes, particularly with:
    • Intermittent ST segment elevation
    • de Winter T wave changes
    • Wellens syndrome (or LMCA syndrome)
    • Widespread ST elevation in two or more coronary territories

High Risk

  • Rise and/or fall in troponin level consistent with myocardial infarction
  • Dynamic episode of ST segment and/or T wave changes with or without symptoms
  • GRACE score >140

Intermediate Risk

  • Diabetes mellitus
  • Renal insufficiency (glomerular filtration rate < 60mL/min/1.73m2)
  • Left ventricular ejection fraction ≤ 40 %
  • Prior revascularization:
    • Percutaneous coronary intervention
    • Coronary artery bypass grafting
  • GRACE score >109 and <140

Low Risk

  • Patients with NSTEACS who have both of:
    • no recurrent symptoms
    • no risk criteria (as listed above)


An ECG should be performed as soon as possible in a patient with a presentation consistent with ACS

  • If a diagnosis of STEMI or new LBBB is made on ECG a brief and directed history and examination is needed to determine the best reperfusion strategy
  • If STEMI or new LBBB is ruled out and the patient has possible NSTEACS, risk stratification assessment into high, intermediate or low risk for an adverse event is performed.


  • History of the event
    • When did the pain commence?
    • Establish the nature of pain and its duration
    • ACS may present as a ‘chest pain’ surrogate (e.g. shortness of breath, lethargy); especially in elderly females
  • previous coronary interventions or investigations? (e.g. thrombolysis, stent or CABG)
  • comorbidities (especially contra-indications to thrombolysis)
  • medications
    • Warfarin, antiplatelet agents or NOACs
    • Has an aspirin or other anti-platelet agent already been taken?
    • sildenafil (GTN may have an excessive effect if used)
  • allergies (especially aspirin)


  • generally unhelpful in establishing the diagnosis of ACS
  • Assess any immediate ABC issues
  • Vital signs (blood pressure is especially important with respect to the decision to thrombolyse
  • Degree of patient anxiety/ distress
  • Look for any evidence of heart failure or (e.g. S3/S4, APO, edema, distended tender liver)
  • Look for any evidence of cardiogenic shock (altered mental state, poor skin perfusion +/- hypotension)

Clinical Risk Stratification for ACS in Patients Presenting with Chest Pain (i.e. possible not confirmed NSTEACS)

  • High Risk Patients
    • those presenting with clinical symptoms consistent with ACS and any of the following high risk features:
      • Persistent or dynamic S-T segment changes on ECG:
        • S-T segment depression ≥ 0.5 mm
        • New T wave inversion ≥ 2.0 mm in more than 2 contiguous leads
        • Transient S-T segment elevation ≥ 0.5 mm in more than 2 contiguous leads
        • ECG changes consistent with critical coronary artery stenosis, e.g. Wellens Syndrome or LMCA stenosis syndrome.
      • Hemodynamic compromise
        • Systolic blood pressure ≤ 90 mmHg
        • Signs of poor peripheral perfusion
        • Signs of cardiac failure or frank pulmonary edema, (ie Killip class > 1)
        • New onset of mitral regurgitation
        • Syncope
      • Ongoing pain, or recurrent episodes of pain despite initial treatment whilst in the ED
      • Arrhythmias requiring treatment such as sustained ventricular tachycardia
      • Diaphoresis
      • Elevated serum troponin
      • High risk co-morbidities:
        • Left ventricular systolic dysfunction (ejection fraction < 0.4)
        • Past PCI or CAGS
        • Past myocardial infarction
    • Intermediate Risk Patients
      • those presenting with clinical symptoms consistent with ACS but do not have high risk or low risk criteria
    • Low Risk Patients
      • Age < 40 years
      • Symptoms that are atypical for angina
      • Remain symptom free
      • Absence of known CAD
      • Normal troponin levels
      • Normal ECG (including no transient changes)

Assessment of bleeding risk

  • The routine use of a validated risk stratification tool, such as the CRUSADE Score, for bleeding events assists with individual patient clinical decision making
  • The CRUSADE Score is available on MDCALC [CRUSADE Score for Post-MI Bleeding Risk]
  • The CRUSADE score risk stratifies patients for bleeding complications according to 8 parameters:
    • Heart Rate
    • Systolic Blood Pressure
    • Hematocrit
    • Creatinine Clearance
    • Sex
    • Signs of CHF at Presentation
    • History of Vascular Disease
    • History of Diabetes Mellitus



  • FBC
  • UEC/ glucose (especially K)
  • Cardiac troponin I
    • Normal levels are considered vary according to the exact assay that is being used
    • In general terms a normal level is considered to be < 99th percentile for the assay
    • may persist for 5-14 days post infarction
    • Reinfarction can also be assessed via troponin levels (CK/CKMB is now obsolete and not required)
    • Rising versus falling levels
      • For the vast majority of patients being investigated for possible MI, a rising pattern is suggestive of the diagnosis of MI
      • In patients who present late following MI, troponin elevations may have already peaked and in this context, a falling troponin pattern is significant
      • Note that all troponin assays, regardless of their detection sensitivity do not rule out unstable angina or stable coronary ischemia
      • Clinical management decisions should not be based solely on troponin levels, but on thorough investigation and risk assessment that includes detailed clinical assessment, observation, repeated ECG tests, and where available functional testing
    • An initial troponin level should be done on all cases of suspected ACS with a second level done at 6 hours (sensitive assay) or 3 hours (highly sensitive assay) from the onset of the chest pain.
      • Note that some patients that fit specific low risk stratification criteria may be suitable for validated accelerated diagnostic pathways.


  • All patients who present with a suspected ACS must have an ECG within 10 minutes of first acute clinical contact
  • A clinician with ECG expertise should review the ECG
  • The immediate decision pathway then involves the ECG stratification of STEMI, from NSTEACS
  • STEMI minimum criteria:
    • STEMI is defined as presentation with clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
      • ≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
      • ≥ 1.5 mm ST elevation in V2-3 in women
      • ≥ 1 mm ST elevation in other leads
      • New LBBB (LBBB should be considered new unless there is evidence otherwise)
  • Findings in ACS
    • may be normal
    • classic changes in acute myocardial infarction
      • peaked T waves with ST elevation
      • gradual loss of R wave
      • development of pathological Q wave and TWI
    • anatomical localisation of ST elevation
      • Anteroseptal = LAD
      • Anterolateral = Cx
      • Inferior = RCA
      • Posterior = Cx or PDA (off RCA)
  • Minimal S-T changes can be difficult to interpret, especially in those with pre-existing CAD or other significant CVS disease. In such cases:
    • Comparison with old ECGs will be useful
    • Smith-Modified Sgarbossa Criteria can help if LBBB or paced:
      • ≥ 1 lead with ≥1 mm of concordant ST elevation
      • ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression
      • ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave.
    • In cases of LBBB urgent echocardiography may be useful, if readily available, to detect wall motion abnormalities (suggesting myocardial ischaemia) and hence assist in decision making


  • This should not be allowed to delay any treatment measures, especially reperfusion therapies.
  • If an x-ray is done this should be in the Resus bay, except for stable low risk patients who may be suitable to leave the department for their x-ray, this will need to be judged on a case by case basis.
  • Look for cardiomegaly, cardiac failure and differentials of chest pain (e.g. PE, pneumonia, pneumothorax, esophageal rupture, aortic dissection)

Echocardiography (not a routine test in ACS, but may be considered on an urgent basis in selected cases)

  • Confirmation of wall motion abnormalities when the diagnosis of ACS is unclear (pericarditis or myocarditis is being considered for example or in cases of LBBB)
  • Cardiogenic shock
  • Inferior infarction where evidence of right ventricular infarction is being sort
  • If secondary complications are suspected, such as cardiac tamponade or valvular disruption

Coronary Angiography

  • This is the definitive investigation for any patient with a STEMI who is to undergo a PCI
  • Patients with high or very high risk NSTEACS should be referred to cardiology urgently for consideration of a urgent coronary angiogram.



  • cardiac failure
  • post-infarction ischaemia
  • ventricular free wall rupture
    • therapy: pericardiocentesis and repair
  • ventricular septal rupture
    • therapy: IABP, inotropes, surgery
  • acute mitral regurgitation
    • therapy: afterload reduction, IABP, inotropes, surgery ASAP
  • right ventricular infarction
    • therapy: IV fluids, inotropes, AV synchrony, IABP, reperfusion
  • arrhythmias
    • therapy: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)
  • cardiogenic shock
    • therapy: must get revascularisation (PCI or CABG) within 24 hours
  • thromboembolism
    • therapy: mural thrombus -> anticoagulate
  • pericarditis and Dressler’s syndrome
  • complications of therapy, e.g. haemorrhage, coronary artery dissection, stent thrombosis, surgical complications


Journal articles

  • Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016. The Medical journal of Australia. 205(3):128-33. 2016
  • Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand: Australian Clinical Guidelines for the Management of Acute Coronary Syndromes 2016. Heart, lung & circulation. 25(9):895-951. 2016. [pubmed] [free full text]
  • Delewi R, Zijlstra F, Piek JJ. Left ventricular thrombus formation after acute myocardial infarction. Heart. 2012 Dec;98(23):1743-9. doi: 10.1136/heartjnl-2012-301962. Review. PubMed PMID: 23151669; PubMed Central PMCID: PMC3505867.
  • Thygesen K, Alpert JS, Jaffe AS. Third universal definition of myocardial infarction. Circulation. 126(16):2020-35. 2012. [pubmed]

FOAM and web resources

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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