Emergency Medicine
Emergency
High Evidence

STEMI Management in the Emergency Department

ST-elevation myocardial infarction represents complete occlusion of an epicardial coronary artery causing transmural myo... ACEM Fellowship Written, ACEM Fellow

Updated 24 Jan 2026
59 min read

Clinical board

A visual summary of the highest-yield teaching signals on this page.

Urgent signals

Safety-critical features pulled from the topic metadata.

  • Cardiogenic shock (SBP below 90 mmHg, altered mentation, cool peripheries)
  • Ventricular fibrillation or sustained ventricular tachycardia
  • Complete heart block or high-grade AV block
  • Acute severe mitral regurgitation (papillary muscle rupture)

Exam focus

Current exam surfaces linked to this topic.

  • ACEM Fellowship Written
  • ACEM Fellowship OSCE

Linked comparisons

Differentials and adjacent topics worth opening next.

  • Acute Pericarditis
  • Aortic Dissection

Editorial and exam context

ACEM Fellowship Written
ACEM Fellowship OSCE
Clinical reference article

Quick Answer

One-liner: STEMI is acute coronary artery occlusion requiring urgent reperfusion with primary PCI (preferred) or thrombolysis within 12 hours of symptom onset to salvage myocardium and reduce mortality.

ST-elevation myocardial infarction represents complete occlusion of an epicardial coronary artery causing transmural myocardial ischaemia and necrosis. In-hospital mortality is 5-7% with timely reperfusion but rises to 20-30% without intervention. Every 30-minute delay to reperfusion increases 1-year mortality by 7.5%. The ED clinician must diagnose STEMI within 10 minutes of arrival, activate the cath lab or administer thrombolysis, and initiate dual antiplatelet therapy and anticoagulation immediately.


ACEM Exam Focus

Primary Exam Relevance

  • Anatomy: Coronary artery anatomy (LAD, RCA, LCx territories), ventricular septum blood supply, papillary muscle blood supply
  • Physiology: Coronary blood flow, oxygen supply-demand balance, ischaemic cascade, stunned vs hibernating myocardium
  • Pharmacology: Antiplatelet agents (aspirin, P2Y12 inhibitors), fibrinolytics (tenecteplase, alteplase), anticoagulants (heparin, enoxaparin), nitrates, opioids, beta-blockers

Fellowship Exam Relevance

  • Written: Time-critical decision-making (PCI vs thrombolysis), ECG pattern recognition (including STEMI-equivalents), reperfusion strategies in special populations, mechanical complications
  • OSCE: Breaking bad news post-cardiac arrest, managing cardiogenic shock, leading STEMI team activation, explaining revascularisation options to family
  • Key domains tested: Medical Expert (ECG interpretation, reperfusion decisions), Communicator (handover to cardiology, family discussions), Leader (team coordination, time-critical decisions), Collaborator (multidisciplinary care)

Key Points

Clinical Pearl

The 5 things you MUST know:

  1. Time is myocardium: Door-to-ECG ≤10 min, door-to-balloon ≤90 min, door-to-needle ≤30 min. Every 30-min delay increases 1-year mortality by 7.5%
  2. Aspirin 300mg oral chewed + P2Y12 inhibitor (ticagrelor 180mg preferred) + anticoagulation (heparin/enoxaparin) must be given IMMEDIATELY
  3. Primary PCI is preferred if available within 120 minutes of first medical contact; otherwise thrombolysis if no contraindications
  4. 25-34% of "NSTEMI" are acute occlusions requiring immediate cath lab activation (posterior MI, de Winter T-waves, Wellens' syndrome)
  5. Mechanical complications (VSD, free wall rupture, acute MR) occur 3-7 days post-MI and have 40-87% mortality—recognise early and activate cardiac surgery

Epidemiology

MetricValueSource
Incidence77 per 100,000/year (Australia)[1]
Prevalence0.5-1.0% of chest pain presentations[2]
Mortality5-7% in-hospital, 7-18% at 1 year[3,4]
Peak age65-75 years (men), 70-80 years (women)[5]
Gender ratioM:F 3:1 (age below 65), 1:1 (age greater than 75)[6]

Australian/NZ Specific

  • 130 hospitalisations per 100,000 Australians annually (AIHW 2023) [7]
  • Case fatality rate 9.3% in Australian registries (varies by state/territory) [8]
  • Aboriginal and Torres Strait Islander peoples: STEMI incidence 3.3x higher than non-Indigenous Australians, presentation 10-15 years younger, 50% less likely to receive timely primary PCI, higher in-hospital mortality [9,10,11]
  • Māori and Pacific peoples (NZ): 2.5-3x higher STEMI rates, younger presentation age, geographic disparities in PCI access [12]
  • Rural/remote: Door-to-balloon times exceed 120 minutes in 60-70% of cases outside major metropolitan areas; pre-hospital thrombolysis reduces time to reperfusion by 24-52 minutes in regional Australia [13,14,15]

Pathophysiology

Mechanism

Atherosclerotic plaque rupture or erosion → platelet activation and thrombus formation → complete occlusion of epicardial coronary artery → transmural myocardial ischaemia → myocyte death begins within 20-40 minutes → completed infarction by 6-12 hours [16,17].

Type 1 MI (90-95%): Spontaneous plaque rupture/erosion with thrombotic occlusion Type 2 MI (5-10%): Supply-demand mismatch (e.g., severe hypotension, anaemia, tachyarrhythmia)

Pathological Progression

Plaque rupture (t=0) → Thrombus formation (0-20 min) → Subendocardial ischaemia (20-40 min) → 
Transmural infarction begins (40-90 min) → Wavefront phenomenon (3-6 hours) → 
Completed infarction (6-12 hours) → Remodelling (days-weeks)

Ischaemic cascade: Diastolic dysfunction → systolic dysfunction → ECG changes → chest pain → arrhythmia/cardiogenic shock [18]

Infarct size determinants:

  • Duration of occlusion (most important)
  • Collateral circulation
  • Ischaemic preconditioning
  • Metabolic demand

Why It Matters Clinically

  1. Time-dependent salvage: At 1 hour, 75% of myocardium is salvageable; at 6 hours, only 30% remains viable [19]
  2. Territory predicts complications: Anterior STEMI (LAD) has 2x mortality of inferior STEMI due to larger infarct size
  3. Right ventricular infarction: 30-50% of inferior STEMIs involve RV, requiring preload-dependent management (avoid nitrates, give IV fluids)
  4. Reperfusion injury: Restoration of flow causes oxidative stress, microvascular obstruction, arrhythmias (reperfusion VF in 5%)

Clinical Approach

Recognition

STEMI is diagnosed by ECG, NOT symptoms. Activate STEMI pathway if:

  • ≥1mm ST-elevation in 2 contiguous limb leads OR
  • ≥2mm ST-elevation in 2 contiguous precordial leads OR
  • New LBBB with clinical suspicion of MI OR
  • True posterior MI (ST-depression V1-V3 + tall R waves V1-V2 + ST-elevation V7-V9)

High-risk "STEMI-equivalents" requiring immediate cath lab activation [20,21]:

  • De Winter T-waves (upsloping ST-depression + tall symmetrical T-waves in precordial leads)
  • Wellens' syndrome (biphasic/deep T-wave inversion V2-V4 in pain-free period)
  • Hyperacute T-waves (bulky, asymmetrical)
  • Posterior MI
  • Proximal LAD occlusion with ST-elevation aVR + diffuse ST-depression

Initial Assessment

Primary Survey

  • A: Patent airway; consider early intubation if cardiogenic shock, pulmonary oedema, cardiac arrest
  • B: Oxygen if SpO2 below 93% (target 93-96%); avoid hyperoxia (increases infarct size). Assess for pulmonary oedema
  • C: SBP below 90 mmHg = cardiogenic shock until proven otherwise. Large-bore IV access x2. Continuous cardiac monitoring
  • D: Altered mental status = cardiogenic shock or cardiac arrest. AVPU/GCS
  • E: Assess for signs of heart failure (JVP, peripheral oedema), complications (new murmur = VSD/acute MR)

History

Key Questions

QuestionSignificance
"When did the pain start?"below 12 hours = reperfusion; 12-24 hours = consider late PCI; greater than 24 hours = medical management unless ongoing ischaemia
"What were you doing when it started?"Rest onset suggests plaque rupture; exertional may be supply-demand
"Any previous heart attack or stents?"Affects choice of P2Y12 inhibitor; may indicate in-stent thrombosis
"Any bleeding problems? Stroke? Recent surgery?"Contraindications to thrombolysis
"Are you on aspirin or blood thinners?"Affects antiplatelet/anticoagulation dosing; DOAC use may preclude thrombolysis

Red Flag Symptoms

Red Flag
  • Cardiogenic shock triad: Hypotension (SBP below 90), altered mentation, cool/clammy peripheries → 40-50% mortality
  • Acute severe dyspnoea + pink frothy sputum → acute pulmonary oedema (cardiogenic shock or acute MR)
  • Sudden tearing chest pain radiating to back → aortic dissection (STEMI mimic; thrombolysis/PCI contraindicated)
  • Syncope + chest pain → complete heart block, VF, cardiac tamponade, massive PE
  • New pansystolic murmur + shock 3-7 days post-MI → VSD or papillary muscle rupture (surgical emergency)

Examination

General Inspection

  • Distress level (calm vs anxious vs gasping)
  • Pallor, diaphoresis (sympathetic activation)
  • Peripheral cyanosis (cardiogenic shock)
  • Use of accessory muscles (pulmonary oedema)

Specific Findings

SystemFindingSignificance
Vital signsSBP below 90 mmHgCardiogenic shock (40-50% mortality)
HR below 50 or greater than 100Inferior MI with heart block or sinus tachycardia (haemorrhage, anxiety, heart failure)
CardiovascularElevated JVPRV infarction (give fluids, avoid nitrates) or cardiogenic shock
New pansystolic murmurVSD (day 3-7) or acute MR (papillary muscle rupture)
Muffled heart soundsPericardial effusion (free wall rupture) or tamponade
Pulsus paradoxus greater than 10 mmHgTamponade (free wall rupture)
RespiratoryBilateral cracklesAcute pulmonary oedema (LV failure or acute MR)
NeurologicalConfusion, agitationHypoperfusion (cardiogenic shock)
PeripheralCool, clammy skinVasoconstriction in shock

Investigations

Immediate (Resus Bay)

TestPurposeKey Finding
12-lead ECGDiagnosis (within 10 min of arrival)ST-elevation ≥1mm in 2 contiguous leads; STEMI-equivalents
Cardiac monitorDetect arrhythmiasVF/VT, complete heart block, ventricular ectopy
Oxygen saturationAssess oxygenationTarget SpO2 93-96%
Blood pressureDetect shock/hypertensionSBP below 90 = shock; SBP greater than 180 = relative contraindication to thrombolysis
IV access x2Drug/fluid administrationLarge-bore 16-18G

Standard ED Workup

TestIndicationInterpretation
Troponin (hsTnI/T)Confirmation (DO NOT WAIT for result to activate cath lab)Elevated within 2-3 hours; peak 12-24 hours. Negative troponin does NOT exclude STEMI
FBCAnaemia (Type 2 MI), WCC (infection), platelets (bleeding risk)Hb below 80 g/L may precipitate Type 2 MI; thrombocytopenia below 50 contraindicates thrombolysis
UECCreatinine (contrast nephropathy risk), potassium (arrhythmia risk)K+ below 3.5 or greater than 5.5 increases VF risk; Cr greater than 150 increases bleeding risk with anticoagulation
CoagulationBaseline if thrombolysis consideredINR greater than 1.7-2.0 contraindication to thrombolysis
GlucoseDiabetes, stress hyperglycaemiaTarget 6-10 mmol/L; tight control (4-8) may increase mortality
LipidsBaseline for secondary preventionDo NOT delay reperfusion for lipid results
Chest X-rayPulmonary oedema, widened mediastinum (dissection), pneumothoraxUpright if stable; portable if unstable. Widened mediastinum greater than 8cm suggests dissection

Advanced/Specialist

TestIndicationAvailability
Coronary angiographyGold standard; primary PCITertiary centres; 24/7 in metro areas
EchocardiographyAssess LV function, detect complications (VSD, MR, free wall rupture, thrombus)Bedside in ED; formal in cath lab
CT coronary angiographyRule out dissection if ECG equivocal and chest pain atypicalMetro EDs with CT capability
Posterior leads (V7-V9)Suspected posterior MI (ST-depression V1-V3)Can be performed in ED; add to standard ECG
Right-sided leads (V3R-V4R)Suspected RV infarction (inferior STEMI + hypotension)ST-elevation V3R-V4R confirms RV involvement

Point-of-Care Ultrasound

POCUS indications in STEMI:

  1. Assess LV function: Severe hypokinesis predicts cardiogenic shock risk
  2. Detect complications: VSD (colour Doppler shows left-to-right shunt), acute MR (regurgitant jet), free wall rupture (pericardial effusion + tamponade)
  3. Identify RV infarction: RV dilation, hypokinesis, McConnell's sign (RV free wall akinesis with apical sparing)
  4. Rule out dissection: Intimal flap in aorta (if ECG equivocal)
  5. Assess volume status: IVC collapsibility guides fluid resuscitation in RV infarction

Caution: DO NOT delay cath lab activation for POCUS. Perform during preparation for transfer or en route if stable.


Management

Immediate Management (First 10 minutes)

1. CALL FOR HELP: Activate STEMI pathway (cardiology on-call, cath lab team) [0-2 min]
2. 12-LEAD ECG within 10 minutes of arrival; repeat every 10-15 min if initial non-diagnostic [0-10 min]
3. OXYGEN if SpO2 below 93% (target 93-96%); continuous cardiac monitoring [2 min]
4. ASPIRIN 300mg PO (chewed) + TICAGRELOR 180mg PO (or prasugrel 60mg if no prior stroke/TIA and below 75 years) [5 min]
5. ANTICOAGULATION: UFH 60 U/kg bolus (max 4000 U) then 12 U/kg/hr infusion OR enoxaparin 30mg IV bolus + 1mg/kg SC [5 min]
6. GTN 0.4-0.8mg SL (avoid if RV infarction, SBP below 90, HR below 50 or greater than 100) [5 min]
7. MORPHINE 2.5-5mg IV (use sparingly; associated with increased mortality in some studies) [5-10 min]
8. DECISION: Primary PCI vs thrombolysis based on door-to-balloon time [10 min]

Resuscitation (if applicable)

Airway

  • Maintain oxygenation: SpO2 93-96% (hyperoxia increases infarct size)
  • Intubation indications: Cardiac arrest, cardiogenic shock with respiratory failure, pulmonary oedema refractory to CPAP
  • RSI approach: Ketamine 1-1.5 mg/kg + rocuronium 1mg/kg (avoid etomidate and propofol in shock)

Breathing

  • CPAP/BiPAP: For acute pulmonary oedema; reduces afterload and improves oxygenation
  • Mechanical ventilation: Lung-protective strategy (Vt 6-8 mL/kg, PEEP 5-10 cmH2O); avoid high intrathoracic pressure (reduces venous return in shock)

Circulation

  • Hypotension (SBP below 90 mmHg):
    • "RV infarction: IV fluid bolus 250-500 mL NS (total 1-2 L); avoid nitrates; maintain preload"
    • "Cardiogenic shock (LV failure): Cautious fluids (250 mL challenge); inotropes (dobutamine 2.5-10 mcg/kg/min), vasopressors if refractory (noradrenaline 0.05-0.2 mcg/kg/min), consider intra-aortic balloon pump (IABP) or VA-ECMO [22,23]"
    • "Mechanical complication (VSD, acute MR): Urgent cardiac surgery consult; IABP as bridge; avoid vasodilators"
  • Cardiac arrest: Standard ALS (ANZCOR Guideline 11); consider immediate cath lab transfer during CPR if ROSC not achieved within 15-20 minutes [24]

Medications

DrugDoseRouteTimingNotes
Aspirin300mgPO (chewed)ImmediatelyReduces mortality 23%; give even if on aspirin [25]
Ticagrelor180mg loadingPOImmediatelyPreferred P2Y12 inhibitor (PLATO trial: 16% RRR in CV death/MI/stroke vs clopidogrel) [26]
Prasugrel60mg loadingPOImmediatelyAlternative if no prior stroke/TIA and below 75 years; greater bleeding risk [27]
Clopidogrel600mg loadingPOIf ticagrelor/prasugrel unavailableSlower onset; less effective but widely available
Heparin (UFH)60 U/kg bolus (max 4000 U), then 12 U/kg/hr infusionIVBefore PCITarget aPTT 50-70 sec (1.5-2x control)
Enoxaparin30mg IV bolus + 1mg/kg SCIV + SCBefore PCI or with thrombolysisPreferred in thrombolysis; avoid if Cr greater than 150 or age greater than 75
GTN0.4-0.8mg SL or 10-200 mcg/min IVSL/IVIf SBP greater than 100, HR 50-100, no RV infarctionReduces preload/afterload; relieves pain. AVOID in RV infarction
Morphine2.5-5mg IVIVFor severe pain unresponsive to GTNMay delay P2Y12 inhibitor absorption; use sparingly [28]
Metoprolol25-50mg POPOAfter reperfusion if stableReduces infarct size; AVOID in shock, heart failure, heart block [29]
Atorvastatin80mgPOWithin 24 hoursHigh-intensity statin reduces recurrent events [30]

Paediatric Dosing

DrugDoseMaxNotes
Aspirin5 mg/kg300mgKawasaki disease main indication
Heparin75 U/kg bolus, 20 U/kg/hr infusion-Monitor aPTT closely
Morphine0.05-0.1 mg/kg10mgTitrate to pain relief

Note: STEMI in children/adolescents is rare; consider anomalous coronary anatomy, Kawasaki disease, cocaine use, thrombophilia.

Reperfusion Strategy: Primary PCI vs Thrombolysis

PRIMARY PCI PREFERRED IF [31,32,33]:

  • Door-to-balloon time ≤120 minutes from first medical contact (FMC) OR
  • PCI-capable centre with below 90 minutes from FMC to balloon OR
  • Thrombolysis contraindications OR
  • Cardiogenic shock (thrombolysis ineffective) OR
  • Late presentation (greater than 3 hours) where PCI has superior outcomes

PRIMARY PCI OUTCOMES:

  • Mortality reduction: 34% RRR vs thrombolysis (OR 0.66, 95% CI 0.51-0.82) [34]
  • Stroke reduction: 63% RRR vs thrombolysis [34]
  • Reinfarction reduction: 65% RRR vs thrombolysis [34]
  • Number needed to treat: 17 to prevent 1 death at 6 weeks [34]

THROMBOLYSIS INDICATIONS:

  • PCI not available within 120 minutes from FMC AND
  • Symptom onset below 12 hours AND
  • No contraindications

THROMBOLYSIS DRUG OF CHOICE: Tenecteplase (TNK-tPA) preferred over alteplase [35,36,37]

  • Single IV bolus (easier administration)
  • Weight-based dosing
  • Equivalent efficacy to alteplase
  • Reduces door-to-needle time by 10-15 minutes

Tenecteplase dosing:

WeightDose
below 60 kg30 mg (6000 units)
60-69 kg35 mg (7000 units)
70-79 kg40 mg (8000 units)
80-89 kg45 mg (9000 units)
≥90 kg50 mg (10,000 units)

Absolute contraindications to thrombolysis:

  • Prior intracranial haemorrhage at any time
  • Ischaemic stroke within 3 months
  • Structural cerebrovascular disease (AVM, aneurysm)
  • Suspected aortic dissection
  • Active bleeding or bleeding disorder
  • Significant closed head trauma or facial trauma within 3 months
  • Intracranial/intraspinal surgery within 2 months

Relative contraindications:

  • SBP greater than 180 mmHg (treat first; give lytic if SBP below 180 within 10-15 min)
  • Current anticoagulation (INR greater than 1.7-2.0, DOAC use within 24-48h)
  • Pregnancy
  • Recent surgery (within 3 weeks)
  • CPR greater than 10 minutes with rib fractures
  • Age greater than 75 years (increased ICH risk 1.5-2%)

RESCUE PCI: If below 50% ST-segment resolution at 60-90 minutes post-thrombolysis → failed reperfusion → urgent PCI [38]

PRE-HOSPITAL THROMBOLYSIS (regional/rural Australia):

  • Reduces time to reperfusion by 24-52 minutes [13,14,15]
  • Administered by intensive care paramedics or retrieval physicians
  • Requires 12-lead ECG transmission and physician oversight (in most states)
  • Improves outcomes in areas greater than 60 minutes from PCI-capable centre [39]
  • NSW, QLD, TAS, SA, VIC have established pre-hospital lytic programs

Ongoing Management

POST-REPERFUSION CARE (first 24-48 hours):

  1. Continuous cardiac monitoring: Detect arrhythmias (VF/VT, heart block)
  2. Beta-blocker: Metoprolol 25-50mg PO BD if no contraindications (reduces reinfarction and arrhythmias) [29]
  3. ACE inhibitor: Ramipril 2.5-5mg PO or perindopril 2-4mg PO if EF below 40% or anterior MI (reduces mortality, remodelling) [40]
  4. Statin: Atorvastatin 80mg PO daily (PROVE-IT trial: high-intensity statin superior) [30]
  5. DAPT: Aspirin 100mg + ticagrelor 90mg BD (continue 12 months minimum)
  6. Glycaemic control: Target glucose 6-10 mmol/L (avoid tight control below 6; increases mortality)
  7. Avoid NSAIDs: Increase mortality and cardiovascular events

COMPLICATIONS TO MONITOR:

ComplicationTimingIncidenceRecognition
Ventricular arrhythmias0-48 hours5-10%VF/VT on monitor; treat per ALS protocol
Complete heart block0-24 hours (inferior MI)6-14%Bradycardia, hypotension; temporary pacing
Cardiogenic shock0-72 hours5-10%SBP below 90, cool peripheries, oliguria; inotropes, IABP, ECMO
Acute MR3-7 days1-5%New murmur, pulmonary oedema; urgent surgery
VSD3-7 days0.2-0.5%New murmur, shock; urgent surgery [41,42]
Free wall rupture3-7 days0.5-2%Sudden cardiac arrest, tamponade; 90% mortality [43]
LV thrombus3-14 days5-10% (anterior MI)Echo finding; anticoagulate 3-6 months
Pericarditis1-4 days5-15%Positional chest pain, friction rub; NSAIDs avoided (use colchicine)

Definitive Care

PRIMARY PCI PROCEDURE:

  1. Coronary angiography: Define anatomy, identify culprit lesion
  2. Thrombus aspiration: May be used if large thrombus burden (no mortality benefit but reduces distal embolisation)
  3. Stent implantation: Drug-eluting stent (DES) preferred over bare-metal stent (BMS)
  4. Multivessel disease: Culprit-only PCI at initial procedure; staged PCI for non-culprit lesions within days-weeks if stable [44]
  5. TIMI flow restoration: Target TIMI 3 flow (complete perfusion)

COMPLETE REVASCULARISATION in multivessel disease:

  • Reduces CV death and MI by 26% vs culprit-only PCI [44]
  • Staged PCI (not at index procedure unless cardiogenic shock) reduces contrast load and procedure time

MECHANICAL CIRCULATORY SUPPORT:

  • IABP: Reduces afterload, increases coronary perfusion; use in refractory cardiogenic shock or mechanical complications as bridge to surgery
  • Impella: LV unloading device; better haemodynamic support than IABP but higher bleeding/vascular complications
  • VA-ECMO: For cardiac arrest or profound shock; can be initiated in ED and continued during PCI [45]

Disposition

Admission Criteria

ALL STEMI patients require admission to:

  • Coronary Care Unit (CCU) or Intensive Care Unit (ICU): For continuous monitoring, arrhythmia detection, haemodynamic support
  • Minimum 24-48 hours telemetry monitoring post-reperfusion

ICU/HDU Criteria

  • Cardiogenic shock requiring inotropes/vasopressors
  • Mechanical ventilation
  • Mechanical complications (VSD, acute MR, free wall rupture)
  • Refractory arrhythmias requiring multiple antiarrhythmics or pacing
  • Cardiac arrest with ROSC
  • Mechanical circulatory support (IABP, Impella, ECMO)

Discharge Criteria

NOT applicable to STEMI. All patients require inpatient admission for reperfusion, monitoring, and risk stratification.

EARLY DISCHARGE (3-4 days) may be safe if:

  • Successful primary PCI with TIMI 3 flow
  • EF greater than 40%
  • No complications (no arrhythmias, shock, heart failure)
  • Stable haemodynamics
  • Cardiac rehabilitation arranged

Follow-up

  • Cardiology outpatient review at 6 weeks post-discharge
  • Echocardiogram at 6-12 weeks to reassess LV function
  • Cardiac rehabilitation referral (improves mortality, quality of life)
  • GP letter detailing:
    • Infarct territory, vessel treated, stent type
    • DAPT duration (minimum 12 months)
    • Medications (beta-blocker, ACE inhibitor, statin, DAPT)
    • Risk factor modification targets (smoking cessation, BP below 130/80, LDL below 1.8 mmol/L)
  • Implantable cardioverter-defibrillator (ICD) assessment if EF below 35% at 6-12 weeks (primary prevention of sudden cardiac death)

Special Populations

Paediatric Considerations

STEMI in children/adolescents is rare (annual incidence below 1 per 1,000,000). Consider:

  • Kawasaki disease: Coronary artery aneurysms and thrombosis (most common cause in children)
  • Anomalous coronary arteries: Sudden cardiac death in young athletes
  • Cocaine/amphetamine use: Increasingly common in adolescents
  • Thrombophilia: Factor V Leiden, protein C/S deficiency
  • Takayasu arteritis: Coronary ostial stenosis

Management: Paediatric cardiology consultation; avoid thrombolysis (intracranial haemorrhage risk); primary PCI preferred.

Pregnancy

Incidence: 1 in 16,000 pregnancies; most common cause of maternal mortality from heart disease [46]

Unique considerations:

  • Spontaneous coronary artery dissection (SCAD): Accounts for 40% of pregnancy-associated MI
  • Increased thrombotic risk: Hypercoagulable state, elevated fibrinogen
  • Aortic dissection: Must be excluded (more common in pregnancy)

Management modifications:

  • Primary PCI preferred (avoid radiation to foetus with lead shielding; below 0.05 mGy exposure is safe)
  • Thrombolysis: Teratogenic; only if PCI not available and mother's life immediately threatened
  • Medications: Avoid ACE inhibitors (teratogenic); use hydralazine + nitrates for afterload reduction
  • Aspirin safe; ticagrelor and prasugrel not well studied (clopidogrel alternative)
  • Timing of delivery: Defer if possible until 2 weeks post-MI

Elderly (greater than 75 years)

Higher mortality (18-25% vs 5-7% in younger patients) but greater absolute benefit from reperfusion [47]

Considerations:

  • Atypical presentations: Dyspnoea (40%), syncope (15%), confusion (10%) more common than chest pain
  • Increased bleeding risk: Thrombolysis ICH risk 1.5-2% (vs 0.5-1% in below 75 years); dose-adjust enoxaparin (0.75 mg/kg SC, no IV bolus)
  • Frailty and comorbidities: Assess goals of care; involve family in decision-making
  • Polypharmacy: Drug-drug interactions (e.g., clopidogrel + PPI reduces efficacy)

DO NOT withhold reperfusion based on age alone; outcomes improved with PCI/thrombolysis vs medical management in all age groups.

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Health Disparities:

  • 3.3x higher STEMI incidence in Aboriginal and Torres Strait Islander peoples compared to non-Indigenous Australians [9]
  • Presentation 10-15 years younger (median age 52 vs 67 years) [10]
  • 50% less likely to receive timely primary PCI (adjusted OR 0.51, 95% CI 0.38-0.68) due to geographic remoteness [11]
  • Higher in-hospital mortality (11.8% vs 8.3%, p=0.03) even after adjustment for age and comorbidities [10]
  • Greater burden of cardiovascular risk factors: Diabetes (3.6x higher), smoking (2.4x higher), chronic kidney disease (3x higher) [48]

Māori and Pacific peoples (New Zealand):

  • 2.5-3x higher STEMI rates compared to NZ European [12]
  • Younger age at presentation (mean 58 vs 68 years)
  • Lower rates of revascularisation and guideline-directed medical therapy [49]

Cultural Safety:

  • Involve Aboriginal and Torres Strait Islander Liaison Officers early in ED presentation
  • Family-centred care: Large family groups common; provide space for family discussions
  • Language and communication: Use interpreter services (not family members) for Indigenous languages
  • Cultural protocols: Understand local customs (e.g., avoidance relationships, gender-specific care preferences)
  • Holistic approach: Address social determinants (housing, transport, food security) that affect follow-up and medication adherence

Remote/Rural Considerations for Indigenous Patients:

  • Geographic isolation: 80% of Aboriginal and Torres Strait Islander peoples in remote areas are greater than 3 hours from PCI-capable hospital [50]
  • Pre-hospital thrombolysis: Critical for remote patients; intensive care paramedics trained to deliver tenecteplase
  • RFDS retrieval: Coordinate early; delays of 6-12 hours common for aeromedical transfer
  • Discharge planning: Ensure adequate supply of medications (3-month scripts); arrange transport to follow-up appointments; involve Aboriginal Medical Service (AMS) or Māori health provider in care coordination

Pitfalls & Pearls

Clinical Pearl

Clinical Pearls:

  1. Posterior MI is often missed: Look for ST-depression in V1-V3 + tall R-waves V1-V2. Order V7-V9 leads if suspected. Posterior MI has same urgency as anterior STEMI.

  2. Inferior MI + hypotension = RV infarction until proven otherwise: Check right-sided leads (V3R-V4R). RV infarction requires fluids (not nitrates), and avoid diuretics. 30-50% of inferior MIs have RV involvement.

  3. Morphine delays P2Y12 inhibitor absorption: Morphine reduces ticagrelor Cmax by 36% and delays onset by 1-2 hours [28]. Use sparingly for refractory pain.

  4. STEMI with LBBB: Sgarbossa criteria have low sensitivity (20-36%). If clinical suspicion high, activate cath lab. New LBBB is no longer considered STEMI-equivalent without Sgarbossa criteria.

  5. 25-34% of "NSTEMI" are acute occlusions requiring immediate cath lab: De Winter T-waves, Wellens' syndrome, hyperacute T-waves, true posterior MI. Do not wait for troponin or manage as NSTEMI. [20,21]

  6. Beware of dissection masquerading as STEMI: Tearing pain radiating to back, BP differential between arms greater than 20 mmHg, widened mediastinum on CXR. Thrombolysis or PCI can be fatal. Urgent CT aortogram if dissection suspected.

  7. Mechanical complications occur day 3-7 post-MI: VSD, free wall rupture, papillary muscle rupture. Patients who initially stabilise then deteriorate 3-7 days later need urgent echo and cardiac surgery consult. Mortality 40-87% without surgery.

  8. Do not delay cath lab activation for troponin results: STEMI is an ECG diagnosis. Troponin may be normal in first 2-3 hours. Activating cath lab based on ECG alone is correct even if troponin returns normal.

  9. Left main or proximal LAD occlusion = "widow maker": ST-elevation in aVR + diffuse ST-depression. Highest mortality STEMI (20-30%). Needs immediate PCI; IABP may be required prophylactically.

  10. Cardiogenic shock mortality is 40-50% despite revascularisation: Early recognition (cool peripheries, oliguria, altered mentation) and aggressive support (inotropes, IABP, ECMO) improve outcomes. Do not delay PCI in shock—PCI reduces mortality even in shock.

Red Flag

Pitfalls to Avoid:

  1. Giving nitrates in RV infarction: Causes profound hypotension and cardiac arrest. Always check right-sided leads in inferior MI before giving GTN.

  2. Delaying cath lab for "medical optimisation": Time is myocardium. Aspirin, P2Y12 inhibitor, heparin can be given en route to cath lab. Do not delay for additional labs, CXR, or echo unless dissection suspected.

  3. Using NSAIDs for post-MI pericarditis: Increases mortality, reinfarction, myocardial rupture. Use colchicine 0.5mg BD instead.

  4. Missing de Winter T-waves: Upsloping ST-depression + tall T-waves in precordial leads = acute proximal LAD occlusion. Activate cath lab immediately; do not manage as NSTEMI.

  5. Overdosing enoxaparin in elderly or renal impairment: Standard dose is 1mg/kg SC, but in age greater than 75, use 0.75 mg/kg SC and omit IV bolus. In Cr greater than 150, use UFH instead (enoxaparin not cleared renally).

  6. Discharging chest pain with "non-diagnostic" ECG without serial troponins or monitoring: 10-15% of STEMI patients have initial normal or non-diagnostic ECG. Repeat ECG every 10-15 minutes and obtain serial troponins at 0 and 2 hours.

  7. Assuming LBBB means STEMI: New LBBB is no longer automatic STEMI-equivalent. Apply Sgarbossa criteria (concordant ST-elevation ≥1mm = 5 points; concordant ST-depression ≥1mm in V1-V3 = 3 points; discordant ST-elevation ≥5mm = 2 points; ≥3 points = STEMI).

  8. Giving beta-blockers too early or in wrong patients: Avoid in cardiogenic shock, severe bradycardia, heart block, acute heart failure. Wait until patient stable post-reperfusion (24-48 hours).

  9. Forgetting to dose-adjust prasugrel in elderly: Prasugrel contraindicated in age ≥75 (except if used as 5mg maintenance dose after loading), weight below 60kg, or prior stroke/TIA. Use ticagrelor instead.

  10. Ignoring social determinants in Indigenous patients: Aboriginal and Torres Strait Islander patients have 50% lower PCI rates due to remoteness, transport barriers, cultural safety issues. Proactive care coordination and AMS involvement critical for secondary prevention.


Viva Practice

Viva Scenario

Stem: You are the emergency registrar at a rural district hospital without onsite PCI capability. A 58-year-old male presents at 08:00 with severe central chest pain radiating to the left arm, onset at 07:30. His ECG shows 3mm ST-elevation in V2-V5. The nearest PCI-capable hospital is 90 minutes away by road ambulance. BP 135/80, HR 78, SpO2 97% room air.

Opening Question: What are your immediate management priorities?

Model Answer: This is a time-critical STEMI requiring urgent reperfusion. My priorities are:

  1. Immediate actions (first 5-10 minutes):

    • Oxygen if SpO2 below 93% (currently not required)
    • Aspirin 300mg PO chewed + ticagrelor 180mg PO loading dose
    • Anticoagulation: Enoxaparin 30mg IV + 1mg/kg SC (preferred with thrombolysis) or UFH 60 U/kg bolus
    • GTN 0.4mg SL for pain (BP permits)
    • Morphine 2.5-5mg IV if pain persists (use sparingly)
    • IV access x2, bloods (FBC, UEC, troponin, coag, glucose, lipids)
  2. Reperfusion decision:

    • Time from symptom onset: 30 minutes (excellent prognosis with early reperfusion)
    • Time from first medical contact to PCI: 90 min (road) + 30-45 min door-to-balloon = 120-135 min total
    • This exceeds the 120-minute window, so thrombolysis is indicated if no contraindications
  3. Assess contraindications to thrombolysis:

    • Absolute: Prior ICH, stroke below 3 months, active bleeding, suspected dissection
    • Relative: SBP greater than 180, current anticoagulation, recent surgery, age greater than 75
    • If no contraindications → administer tenecteplase (weight-based dosing)
  4. Coordinate transfer:

    • Thrombolysis does not replace PCI; patient needs angiography within 3-24 hours (pharmaco-invasive strategy)
    • Arrange ambulance transfer to PCI centre; continue monitoring en route
    • If ST-segment resolution below 50% at 60-90 minutes post-lytic → rescue PCI (urgent transfer)

Follow-up Questions:

  1. What if the retrieval service can helicopter the patient to PCI in 45 minutes total from now?

    • Model answer: This changes the decision. Total time from FMC to balloon would be 45 min (helicopter) + 30 min door-to-balloon = 75 minutes, which is within the 90-minute window for direct PCI. Primary PCI is preferred over thrombolysis (lower mortality, stroke, and reinfarction). I would activate retrieval helicopter and withhold thrombolysis.
  2. The patient's wife tells you he had a large nosebleed requiring nasal packing 2 days ago. Does this change your plan?

    • Model answer: Yes. Recent significant bleeding (within 2 weeks) is a relative contraindication to thrombolysis due to increased bleeding risk (including intracranial haemorrhage). However, it is not an absolute contraindication. I would weigh the risk-benefit: the mortality benefit of reperfusion (5-7% absolute reduction) likely outweighs the bleeding risk (1-2% major bleed, 0.5-1% ICH). If the patient is stable for transfer, I would prioritise primary PCI (via helicopter) over thrombolysis. If PCI truly not available within 120 minutes and patient has ongoing chest pain, I would discuss with senior cardiologist and patient/family about proceeding with thrombolysis given the significant mortality benefit.

Discussion Points:

  • Pharmaco-invasive strategy: Thrombolysis followed by angiography within 3-24 hours is superior to thrombolysis alone (reduces reinfarction)
  • Pre-hospital thrombolysis: In rural/regional Australia, paramedic-delivered pre-hospital thrombolysis reduces time to reperfusion by 24-52 minutes and improves outcomes
  • Time targets: Door-to-needle ≤30 min, door-to-balloon ≤90 min, FMC-to-balloon ≤120 min
  • Rescue PCI: below 50% ST-segment resolution at 60-90 min post-lytic = failed reperfusion; urgent transfer for rescue PCI
Viva Scenario

Stem: A 62-year-old woman presents with 2 hours of central chest heaviness and nausea. ECG shows 2mm ST-elevation in leads II, III, aVF. BP 85/50, HR 55, SpO2 96% room air. Lung fields are clear. JVP is elevated at 8 cm.

Opening Question: Describe your approach to this hypotensive STEMI patient.

Model Answer: This is inferior STEMI with hypotension and bradycardia. The elevated JVP with clear lungs suggests right ventricular (RV) infarction complicating inferior MI (occurs in 30-50% of inferior MIs).

Immediate actions:

  1. Call for help: Activate STEMI pathway
  2. Confirm RV infarction: Order right-sided ECG leads (V3R-V4R). ST-elevation ≥1mm in V3R-V4R confirms RV involvement.
  3. Resuscitation (AVOID typical STEMI management):
    • IV fluid bolus: 250-500 mL NS rapidly; reassess BP and JVP. Total 1-2 L may be required. RV infarction is preload-dependent; fluids are essential.
    • AVOID nitrates: GTN drops preload and causes profound hypotension → cardiac arrest in RV infarction
    • AVOID diuretics: Worsens hypotension
    • Aspirin 300mg PO chewed + ticagrelor 180mg PO (or NGT if patient vomiting)
    • Heparin 60 U/kg IV bolus + 12 U/kg/hr infusion
  4. Bradycardia management:
    • HR 55 with hypotension → atropine 0.6mg IV (may increase HR and improve cardiac output)
    • If no response or complete heart block develops → temporary pacing (transcutaneous or transvenous)
  5. Urgent reperfusion:
    • Primary PCI preferred (especially if cardiogenic shock or bradycardia with heart block)
    • RV function usually recovers after reperfusion of RCA

Key point: RV infarction requires opposite management to LV infarction: give fluids, avoid nitrates/diuretics, maintain preload.

Follow-up Questions:

  1. After 1 litre of IV fluids, BP remains 85/50. What is your next step?

    • Model answer: This is refractory hypotension despite adequate preload. Options include:
      1. Continue IV fluids: Some patients require 2-3 L (monitor for pulmonary oedema, though rare in isolated RV infarction)
      2. Inotropic support: Dobutamine 2.5-5 mcg/kg/min to improve RV contractility (increases cardiac output without increasing afterload)
      3. Urgent PCI: Reperfusion of RCA is definitive treatment; RV function recovers in 70-80% of patients
      4. Avoid vasopressors if possible (increase afterload, worsen RV failure), but if profound shock, low-dose noradrenaline may be necessary as bridge to PCI
  2. The monitor shows complete heart block with ventricular escape rhythm at 35 bpm. What do you do?

    • Model answer: Complete heart block complicates 6-14% of inferior MIs (ischaemia of AV node supplied by RCA). Management:
      1. Atropine 0.6mg IV (may not work in complete heart block but try)
      2. Transcutaneous pacing immediately: Set rate 60-80 bpm, increase current until capture
      3. Transvenous pacing: Definitive; place via femoral or internal jugular vein if transcutaneous pacing unsuccessful or prolonged block expected
      4. Urgent PCI: Reperfusion often restores AV conduction within hours; 90% of inferior MI heart blocks resolve after PCI
      5. If haemodynamically stable with escape rhythm greater than 40 and adequate BP → may observe and proceed to PCI without pacing

Discussion Points:

  • RV infarction pathophysiology: RV ischaemia → reduced RV contractility → decreased LV preload → low cardiac output → hypotension
  • JVP elevated despite hypotension: Classic sign of RV infarction (RV cannot pump against elevated pulmonary pressures)
  • Kussmaul's sign: JVP rises with inspiration (due to RV failure) may be present
  • RV infarction prognosis: 25-30% develop cardiogenic shock; in-hospital mortality 20-30% (vs 5-7% for isolated LV infarction)
  • Complete heart block in inferior MI: Usually resolves with reperfusion; permanent pacemaker required in below 5%
Viva Scenario

Stem: A 68-year-old male was admitted 5 days ago with anterior STEMI treated with primary PCI to proximal LAD. He was stable and planned for discharge today. At 09:00, he develops sudden onset severe dyspnoea. Examination: BP 80/40, HR 120, respiratory rate 36, SpO2 85% on room air. JVP elevated, bilateral crackles to mid-zones, new harsh pansystolic murmur loudest at left sternal edge, palpable thrill.

Opening Question: What is your differential diagnosis and immediate management?

Model Answer: This is sudden haemodynamic collapse day 5 post-anterior MI with new pansystolic murmur. The differential diagnosis of mechanical complications includes:

  1. Ventricular septal rupture (VSD) - most likely given:

    • Timing (day 3-7 post-MI)
    • Harsh pansystolic murmur at left sternal edge (due to left-to-right shunt)
    • Palpable thrill (turbulent flow through VSD)
    • Sudden onset pulmonary oedema (increased pulmonary blood flow from L→R shunt)
    • Cardiogenic shock (reduced systemic cardiac output)
  2. Acute mitral regurgitation (MR) due to papillary muscle rupture - less likely as:

    • Murmur at left sternal edge (MR usually apex radiating to axilla)
    • Anterior MI less commonly causes papillary muscle rupture (posteromedial papillary muscle supplied by RCA/LCx; anterolateral by LAD + LCx)
  3. Free wall rupture with pericardial tamponade - less likely as:

    • Murmur present (free wall rupture causes muffled heart sounds)
    • Survived to present (free wall rupture has 90% mortality, often sudden cardiac arrest)

Immediate management:

  1. Resuscitation:

    • Call for help: cardiac surgery consult immediately (definitive treatment is surgical repair)
    • High-flow oxygen: 15 L/min via non-rebreather mask; target SpO2 greater than 92%
    • IV access x2
    • CPAP or NIV: Consider for pulmonary oedema if conscious
    • Intubation and mechanical ventilation if respiratory failure or decreased consciousness (likely required)
  2. Haemodynamic support:

    • Inotropes: Dobutamine 5-10 mcg/kg/min (improves contractility, reduces afterload)
    • Avoid excessive fluids: May worsen pulmonary oedema
    • Sodium nitroprusside infusion: If SBP greater than 90, to reduce afterload and decrease L→R shunt (must be used cautiously)
    • Intra-aortic balloon pump (IABP): Critical for VSD; reduces afterload, decreases shunt, improves coronary perfusion; request cardiology to insert urgently
  3. Diagnosis confirmation:

    • Urgent bedside echocardiography: Confirm VSD (visualise defect with colour Doppler showing L→R shunt across septum), estimate size, assess LV function
    • Chest X-ray: Pulmonary oedema
    • ABG: Assess oxygenation, lactate (tissue perfusion)
  4. Definitive treatment:

    • Surgical repair: Patch closure of VSD ± CABG if incomplete revascularisation
    • Timing: Previously delayed 4-6 weeks to allow scar formation, but modern approach is urgent surgery within 24-48 hours (mortality 40-50% with surgery, 87-94% without surgery) [41,42]
    • IABP as bridge to surgery: Stabilises patient for 12-48 hours
    • Percutaneous closure: Emerging option in high-risk surgical candidates; performed in cath lab with Amplatzer device

Follow-up Questions:

  1. The echocardiogram confirms VSD with large left-to-right shunt. The cardiothoracic surgeon says the patient is too high-risk for surgery due to extensive anterior infarction and poor LV function. What are your options?

    • Model answer: This is a challenging scenario. Options include:
      1. Percutaneous VSD closure: Can be performed in cath lab; high technical success (80-90%) but significant residual shunt rates (30-40%) and device-related complications. Suitable for high-risk surgical patients [41]
      2. IABP + medical management: Temporise with IABP, inotropes, diuretics; some small VSDs may stabilise or partially close with fibrosis over weeks (but most progress to cardiogenic shock)
      3. VA-ECMO: If profound shock, may provide bridge to surgery or percutaneous closure or allow time for recovery
      4. Palliative care: If patient not candidate for any intervention, discuss goals of care with family; prognosis is very poor without intervention (median survival 1-2 weeks)
      5. Second opinion: Transfer to tertiary cardiac surgical centre for assessment by experienced team
  2. What is the difference between VSD and acute MR in terms of examination findings?

    • Model answer:
    FeatureVSDAcute MR (papillary muscle rupture)
    Murmur locationLeft sternal edgeApex radiating to axilla
    Murmur characterHarsh, loudBlowing, may be soft if severe
    ThrillOften presentRare
    Pulmonary oedemaPresent (increased pulmonary flow)Present (acute volume overload to LA/LV)
    JVPMay be elevated (RV volume overload from shunt)May be elevated (RV failure from pulmonary hypertension)
    ECG territoryAnterior MI (septal necrosis)Inferior/posterior MI (posteromedial papillary muscle rupture more common)
    EchoL→R shunt on colour Doppler across septumRegurgitant jet from LV to LA; flail mitral leaflet

Both require urgent surgical repair and have high mortality (40-87% depending on timing and severity).

Discussion Points:

  • VSD timing: 80% occur within 7 days post-MI; median 3-5 days
  • VSD location: Anterior MI → apical VSD (LAD territory); inferior MI → basal VSD (RCA territory)
  • VSD mortality: Without surgery, 54% die within 1 week, 92% within 1 year
  • IABP mechanism: 1:1 counterpulsation; inflates in diastole (increases coronary perfusion), deflates in systole (reduces afterload, reduces VSD shunt)
  • Papillary muscle rupture: Complete rupture = sudden death (75% mortality); partial rupture = acute MR (may survive to surgery)
  • Free wall rupture: Usually fatal; presents as sudden cardiac arrest or pulseless electrical activity with tamponade; requires immediate pericardiocentesis and thoracotomy
Viva Scenario

Stem: You are working as a remote area nurse at a primary health clinic in a remote Aboriginal community in the Northern Territory, 650 km from the nearest PCI-capable hospital (Royal Darwin Hospital). At 14:00, a 48-year-old Aboriginal man presents with 3 hours of central chest pain. He is a current smoker with poorly controlled diabetes. ECG shows 4mm ST-elevation in V2-V6. BP 105/60, HR 88, SpO2 94% on room air. The RFDS retrieval team is currently on another mission and will not be available for 6 hours.

Opening Question: Describe your approach to managing this patient in a remote setting.

Model Answer: This is a time-critical anterior STEMI in a remote Indigenous patient with significant logistic challenges. My approach:

Immediate management (first 10-15 minutes):

  1. Call for help:

    • Contact Royal Darwin Hospital cardiology registrar via phone for advice and to activate STEMI pathway
    • Notify RFDS of STEMI patient requiring urgent retrieval (even if team not available for 6 hours; may divert or deploy second aircraft)
    • Request telehealth consultation if available (ECG transmission via iECG or photo)
  2. Immediate STEMI treatment:

    • Oxygen to maintain SpO2 greater than 93% (currently 94%, may not need oxygen)
    • Aspirin 300mg PO chewed (if available; if not, give 100mg and repeat)
    • Ticagrelor 180mg PO or clopidogrel 600mg PO (whichever available in clinic formulary)
    • Enoxaparin 30mg IV + 1mg/kg SC or heparin 60 U/kg IV bolus (if available)
    • GTN 0.4mg SL (if BP permits; currently 105/60 so safe)
    • Morphine 2.5-5mg IV/IM for pain (if severe)
    • IV access, bloods if pathology available (may not be in very remote clinic)
  3. Reperfusion decision:

    • Time from symptom onset: 3 hours (still within 12-hour window)
    • Time to PCI: 6 hours (retrieval delay) + 650 km flight (~1.5-2 hours) + 30 min door-to-balloon = 7.5-8.5 hours total from now
    • This far exceeds 120-minute window for primary PCI
    • PRE-HOSPITAL THROMBOLYSIS is indicated if no contraindications
  4. Assess thrombolysis contraindications:

    • Specifically ask about: prior stroke, recent bleeding, recent trauma/surgery, severe hypertension
    • Measure BP (currently 105/60; safe for lytic)
    • If no contraindications → proceed with tenecteplase
  5. Thrombolysis administration (if clinic stocks fibrinolytic; not all remote clinics do):

    • Tenecteplase (preferred; single IV bolus):
      • Estimate weight (if scale not available); assume 80kg → 45mg tenecteplase IV push over 5 seconds
    • Alteplase (if tenecteplase not available; requires infusion):
      • 15mg IV bolus, then 0.75 mg/kg over 30 min (max 50mg), then 0.5 mg/kg over 60 min (max 35mg)
    • Continue enoxaparin 1mg/kg SC BD or heparin infusion
  6. Post-thrombolysis monitoring:

    • Repeat ECG at 60-90 minutes post-lytic to assess ST-segment resolution
    • If below 50% resolutionfailed reperfusionurgent RFDS retrieval for rescue PCI (even more urgent now)
    • If ≥50% resolution → successful reperfusion → still needs angiography within 3-24 hours (pharmaco-invasive strategy)
    • Monitor for complications: bleeding (particularly ICH: headache, vomiting, confusion, seizures), reperfusion arrhythmias (VF)
  7. Retrieval coordination:

    • Keep RFDS updated on patient status
    • Prepare patient for transfer: IV access secure, medications charted, ECG copies, clinical handover prepared
    • If RFDS delayed beyond 6 hours and ST-resolution below 50% → escalate urgency (rescue PCI time-critical)

Cultural considerations:

  • Involve Aboriginal Health Worker (if present) to facilitate communication and cultural safety
  • Explain in plain language: Avoid medical jargon; use interpreter if English not first language
  • Family involvement: Ask if patient wants family present for discussions/decisions
  • Acknowledge distress about leaving community: Reassure that transfer to Royal Darwin Hospital is necessary for specialist care (angiography, stent)
  • Arrange follow-up: Ensure patient can return to community after discharge; coordinate with local Aboriginal Medical Service for cardiac rehabilitation and secondary prevention

Follow-up Questions:

  1. The clinic does not stock tenecteplase. The RFDS says they can deliver it via airdrop in 2 hours. What do you do?

    • Model answer: 2-hour delay is acceptable given the alternative (7-8 hours to PCI). Continue aspirin, ticagrelor/clopidogrel, heparin. Monitor patient closely. Once tenecteplase arrives, administer immediately. Total time from symptom onset to lytic would be 5 hours (onset 3 hours ago + 2 hours airdrop), which is still within the 12-hour window and provides significant mortality benefit (thrombolysis below 6 hours reduces mortality by 25-30%).
  2. After tenecteplase, the patient develops a severe headache, vomiting, and becomes drowsy (GCS 13). What is your concern and management?

    • Model answer: This is intracranial haemorrhage (ICH) until proven otherwise—the most feared complication of thrombolysis (incidence 0.5-1.0%, higher in age greater than 75 or uncontrolled hypertension). Management:
      1. Stop all anticoagulation: Cease heparin/enoxaparin infusion immediately
      2. ABCDE resuscitation: Protect airway (GCS 13; consider intubation if declining), high-flow oxygen, IV access
      3. Reversal agents (if available in remote clinic; unlikely):
        • Tranexamic acid 1g IV over 10 minutes (antifibrinolytic; reverses tenecteplase)
        • Cryoprecipitate 10 units (replaces fibrinogen)
        • Protamine 50mg IV (reverses heparin if heparin given)
      4. Urgent RFDS retrieval: Activate highest priority; patient needs immediate CT head and neurosurgical evaluation at Royal Darwin Hospital
      5. Contact Royal Darwin Hospital: Alert neurosurgery and haematology to prepare for ICH management on arrival
      6. Document: Time of lytic, time of symptom onset, vital signs, GCS
    • This scenario highlights the risk-benefit of thrombolysis in remote areas: ICH risk 0.5-1%, but STEMI mortality without reperfusion is 20-30%. Remote clinicians must weigh these risks and involve senior support (RFDS medical director, cardiologist) in decision-making.

Discussion Points:

  • RFDS STEMI protocols: Many RFDS bases stock tenecteplase and have protocols for remote administration by retrieval physicians or trained paramedics
  • Pre-hospital thrombolysis in Australia: NSW, QLD, TAS, VIC, SA have paramedic-delivered pre-hospital lytic programs; reduces time to reperfusion by 24-52 minutes in rural/regional areas [13,14,15]
  • Aboriginal and Torres Strait Islander STEMI disparities: 3.3x higher incidence, 50% less likely to receive timely PCI, 10-15 years younger at presentation, higher mortality [9,10,11]
  • Telehealth in remote medicine: ECG transmission via iECG (smartphone app) allows real-time cardiologist interpretation; improves diagnostic accuracy and reduces time to treatment
  • Secondary prevention in remote Indigenous communities: Major challenge; barriers include medication access, transport to follow-up, cultural appropriateness of cardiac rehabilitation. Aboriginal Medical Services (AMS) and chronic disease programs critical for long-term outcomes.

OSCE Scenarios

Station 1: STEMI Recognition and Immediate Management

Format: Resuscitation scenario Time: 11 minutes Setting: Emergency Department resuscitation bay

Candidate Instructions:

You are the emergency registrar. A 56-year-old male has just arrived via ambulance with severe chest pain for 1 hour. The triage nurse has placed him in the resuscitation bay and called you urgently. Please assess the patient and initiate appropriate management. You have access to nursing staff and a medical student to assist you.

Examiner Instructions: Patient presents with acute anterior STEMI. Vital signs: BP 145/85, HR 98, SpO2 96% room air, RR 20. Patient is diaphoretic and in moderate distress. 12-lead ECG shows 4mm ST-elevation in V2-V5.

Expected progression:

  • Candidate should perform rapid ABCDE assessment
  • Identify STEMI on ECG within 2-3 minutes
  • Activate STEMI pathway (call cardiology, cath lab)
  • Administer aspirin 300mg, ticagrelor 180mg, heparin, GTN
  • Demonstrate closed-loop communication with team
  • Provide brief explanation to patient about diagnosis and plan

Moulage/Actor Brief: Actor presents as anxious, holding chest, reporting crushing central chest pain 8/10 severity radiating to left arm, onset 1 hour ago while mowing lawn. Medical history: hypertension, hyperlipidaemia. Current medications: amlodipine, atorvastatin. No allergies.

Marking Criteria:

DomainCriterionMarks
ApproachSystematic ABCDE assessment; recognises time-critical nature/2
KnowledgeCorrectly identifies STEMI on ECG; knows time targets (door-to-balloon below 90 min)/3
SkillsActivates STEMI pathway; orders correct medications (aspirin, P2Y12, anticoagulation); demonstrates team leadership/2
CommunicationClear handover to cardiology; reassures patient; closed-loop communication with team/2
JudgementPrioritises reperfusion; recognises urgency; appropriate use of resources/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Recognises STEMI within 3 minutes
    • Activates cath lab immediately (not after "completing assessment")
    • Gives aspirin + P2Y12 inhibitor + anticoagulation before transfer
    • Demonstrates urgency and leadership

Station 2: Breaking Bad News Post-STEMI Cardiac Arrest

Format: Communication scenario Time: 11 minutes Setting: Emergency Department relatives' room

Candidate Instructions:

You are the emergency registrar. A 62-year-old man presented 2 hours ago with STEMI and suffered a cardiac arrest in the resuscitation bay 30 minutes ago. Despite 45 minutes of ALS including adrenaline, amiodarone, and multiple defibrillations, ROSC was not achieved and resuscitation was ceased. His wife has just arrived and is in the relatives' room. Please speak with her.

Examiner Instructions: Wife is unaware of husband's presentation or death. She is anxious and confused about why she was called urgently. Candidate must break bad news using appropriate framework (e.g., SPIKES), demonstrate empathy, avoid jargon, and allow time for questions.

Actor Brief: You are the wife of the deceased. You received a call 1 hour ago saying your husband was in the ED but no details. You are very anxious and worried. You do not know he has died. React with shock, disbelief, and tears when told. Ask: "Why did this happen? Was it sudden? Did he suffer? Can I see him?"

Marking Criteria:

DomainCriterionMarks
ApproachUses structured framework (SPIKES); sits down, introduces self, confirms identity/2
KnowledgeExplains STEMI and cardiac arrest in lay terms; truthful about resuscitation attempts/2
CommunicationEmpathetic tone, avoids jargon, clear unambiguous language ("died" not "passed"), pauses for questions/3
ProfessionalismAcknowledges distress, offers support (pastoral care, viewing body), respects cultural needs/2
JudgementRecognises need for family support; does not rush; offers follow-up (coroner, autopsy, bereavement)/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Delivers bad news clearly ("I'm very sorry to tell you that he has died")
    • Demonstrates empathy (acknowledges distress, offers silence/time)
    • Avoids euphemisms ("didn't make it"
    • "we lost him")
    • Offers practical next steps (viewing body, coroner, support)

Station 3: Consenting for Primary PCI

Format: Communication scenario Time: 11 minutes Setting: Emergency Department resuscitation bay (simulated; patient stable)

Candidate Instructions:

You are the emergency registrar. A 58-year-old woman presents with anterior STEMI. The cath lab is ready. The cardiologist has asked you to obtain consent for primary PCI while they scrub in. The patient is stable, alert, and pain-free after GTN. Please explain the procedure and obtain consent.

Examiner Instructions: Patient understands she is having a "heart attack" but does not know what PCI involves. She is anxious about the procedure. Candidate must explain risks, benefits, alternatives in lay terms and ensure informed consent.

Actor Brief: You are anxious about going to the "cath lab." You have heard of stents. Ask: "What will they do? Will I be asleep? What are the risks? What if I don't have it? Is there another option?"

Marking Criteria:

DomainCriterionMarks
ApproachIntroduces self, confirms patient identity, assesses understanding/2
KnowledgeExplains PCI procedure (catheter via wrist/groin, dye, stent), benefits (save heart muscle, reduce death risk), risks (bleeding, stroke, dissection, death below 1%), alternatives (clot-busting drugs)/3
CommunicationUses lay language (not "percutaneous coronary intervention"), checks understanding, answers questions clearly/3
ProfessionalismEmpathetic, reassuring, truthful about risks/1
JudgementAssesses capacity to consent; documents consent appropriately/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators:
    • Explains procedure in simple terms ("We will pass a thin tube up to your heart artery and put in a small metal scaffold called a stent to open the blockage")
    • States benefits clearly ("This will save your heart muscle and significantly reduce your risk of dying or having another heart attack")
    • States risks honestly but reassuringly ("Serious risks like stroke or major bleeding are uncommon, about 1-2%, but the benefits far outweigh the risks")
    • Checks understanding ("Does that make sense? Do you have any questions?")

SAQ Practice

Question 1 (6 marks)

Stem: A 68-year-old male presents with 2 hours of central chest pain. His ECG shows 3mm ST-elevation in leads II, III, aVF. Blood pressure is 85/50 mmHg, heart rate 52 bpm. Lung fields are clear. JVP is 8 cm.

Question: List six immediate management priorities for this patient.

Model Answer:

  1. Assess for right ventricular infarction: Order right-sided ECG leads (V3R-V4R) to confirm RV involvement (ST-elevation ≥1mm in V3R-V4R) (1 mark)
  2. IV fluid resuscitation: Administer 250-500 mL normal saline bolus rapidly; reassess BP and JVP. Total 1-2 L may be required. RV infarction is preload-dependent (1 mark)
  3. Avoid nitrates and diuretics: These reduce preload and can cause profound hypotension or cardiac arrest in RV infarction (1 mark)
  4. Administer antiplatelet therapy: Aspirin 300mg PO chewed + ticagrelor 180mg PO (or prasugrel/clopidogrel) (1 mark)
  5. Administer anticoagulation: Heparin 60 U/kg IV bolus + 12 U/kg/hr infusion or enoxaparin 30mg IV + 1mg/kg SC (1 mark)
  6. Activate STEMI pathway for urgent primary PCI: Contact cardiology on-call, activate cath lab. Primary PCI is definitive treatment; RV function usually recovers after reperfusion of RCA (1 mark)

Examiner Notes:

  • Also accept: Atropine 0.6mg IV for bradycardia (if HR below 50 with hypotension), oxygen if SpO2 below 93%, continuous cardiac monitoring, temporary pacing if complete heart block develops
  • Do not accept: GTN (contraindicated), furosemide (worsens hypotension), beta-blockers (worsen bradycardia and hypotension)
  • Partial marks: 0.5 marks for "give fluids" without specifying volume or rationale

Question 2 (8 marks)

Stem: A 55-year-old male presents with 90 minutes of severe chest pain. ECG shows 5mm ST-elevation in V1-V5 and 3mm ST-elevation in aVR, with diffuse ST-depression in inferior and lateral leads. Blood pressure is 75/40 mmHg, heart rate 115 bpm, SpO2 90% on room air.

Question: (a) What is the likely culprit coronary artery? (1 mark) (b) Why is this patient hypotensive? (2 marks) (c) Outline your immediate resuscitation priorities. (5 marks)

Model Answer:

(a) Likely culprit artery (1 mark):

  • Left main coronary artery or proximal left anterior descending (LAD) artery occlusion (1 mark)
    • "Rationale: ST-elevation in aVR + diffuse ST-depression indicates proximal occlusion of major vessel supplying large myocardial territory"

(b) Why hypotensive? (2 marks):

  • Cardiogenic shock due to extensive myocardial ischaemia/infarction (1 mark)
  • Large infarct territory (left main or proximal LAD supplies anterior wall, septum, apex = 40-50% of LV myocardium) causes severe LV dysfunction, reduced cardiac output, and hypotension (1 mark)

(c) Immediate resuscitation priorities (5 marks):

  1. High-flow oxygen + airway management: 15 L/min via non-rebreather mask; prepare for intubation if worsening hypoxia or decreased consciousness (cardiogenic shock often requires mechanical ventilation) (1 mark)

  2. IV access x2 + fluid resuscitation: Large-bore IV access; cautious 250 mL NS bolus (assess response; avoid excessive fluids in LV failure, but patient may be relatively hypovolaemic) (0.5 mark)

  3. Inotropic support: Commence dobutamine 5-10 mcg/kg/min IV infusion (improves contractility and cardiac output); if SBP remains below 70 mmHg, add noradrenaline 0.05-0.1 mcg/kg/min for vasopressor support (1 mark)

  4. **Activate STEMI pathway for urgent/emergent primary PCI: This is the highest priority STEMI ("widow maker"); contact interventional cardiology immediately for emergency PCI (1 mark)

  5. Administer antiplatelet and anticoagulation therapy: Aspirin 300mg (crush and give via NGT if intubated), ticagrelor 180mg PO (or via NGT), heparin 60 U/kg IV bolus (1 mark)

  6. Consider mechanical circulatory support: Request intra-aortic balloon pump (IABP) placement prophylactically in cath lab (reduces afterload, increases coronary perfusion in cardiogenic shock); alternatively, Impella or VA-ECMO if available and shock refractory to inotropes (0.5 mark)

Examiner Notes:

  • Accept: Call for senior ED/ICU support, consider intubation and mechanical ventilation, continuous cardiac monitoring, transfer to cath lab as resuscitation in progress
  • Do not accept: "Give fluids" alone without specifying caution (excessive fluids worsen pulmonary oedema in cardiogenic shock)
  • Partial credit: 0.5 marks for listing inotropes without specifying dobutamine or doses
  • Note: This patient has approximately 40-50% mortality despite optimal management. Early recognition, aggressive resuscitation, and immediate PCI are critical.

Question 3 (6 marks)

Stem: You are working in a rural emergency department without onsite PCI capability. A 60-year-old female presents with 1 hour of chest pain. ECG confirms anterior STEMI. The nearest PCI-capable hospital is 2 hours away by road ambulance.

Question: Outline your decision-making process for choosing between primary PCI and thrombolysis for this patient. Include time targets and key considerations.

Model Answer:

  1. Assess time to primary PCI (1 mark):

    • Time from first medical contact (FMC) to balloon: 2 hours (road ambulance) + 30 minutes door-to-balloon at receiving hospital = 150 minutes total
    • Exceeds the 120-minute target for FMC-to-balloon time
    • Therefore, thrombolysis is preferred over delayed PCI
  2. Assess time from symptom onset (0.5 mark):

    • 1 hour since onset → within 12-hour window for reperfusion
    • Early presentation (below 3 hours) confers greatest benefit from thrombolysis (25-30% mortality reduction)
  3. Screen for contraindications to thrombolysis (1.5 marks):

    • Absolute contraindications: Prior intracranial haemorrhage, ischaemic stroke below 3 months, active bleeding, suspected aortic dissection, recent intracranial/spinal surgery (below 2 months)
    • Relative contraindications: Uncontrolled hypertension (SBP greater than 180 mmHg), anticoagulation (INR greater than 1.7-2.0), recent surgery, age greater than 75
    • If no contraindications → proceed with thrombolysis
  4. Administer thrombolysis with goal door-to-needle time ≤30 minutes (1 mark):

    • Tenecteplase (TNK-tPA) preferred (single IV bolus, easier administration)
    • Weight-based dosing (e.g., 70-79 kg = 40mg, 80-89 kg = 45mg)
    • Continue antiplatelet therapy (aspirin, ticagrelor) and enoxaparin 1mg/kg SC BD
  5. Plan for pharmaco-invasive strategy (1 mark):

    • Thrombolysis is not a substitute for PCI; patient still needs coronary angiography
    • Arrange transfer to PCI-capable hospital for angiography within 3-24 hours post-thrombolysis (pharmaco-invasive approach improves outcomes vs thrombolysis alone)
    • Assess for rescue PCI: If below 50% ST-segment resolution at 60-90 minutes post-lytic → failed reperfusion → urgent transfer for rescue PCI
  6. Consider alternative if helicopter retrieval available (1 mark):

    • If aeromedical retrieval (RFDS or state-based helicopter) can achieve FMC-to-balloon below 120 minutes → primary PCI is preferred
    • Example: Helicopter retrieval in 45 minutes + 30 min door-to-balloon = 75 minutes total → choose primary PCI

Examiner Notes:

  • Accept: Mention of European guidelines supporting thrombolysis if PCI delay greater than 120 minutes
  • Key principle: Time is myocardium—do not delay definitive reperfusion therapy. Thrombolysis within 30 minutes is better than PCI in 150 minutes.
  • Common mistake: Waiting for transfer ambulance to arrive before deciding on thrombolysis. Give lytic immediately if indicated; patient can still be transferred for angiography post-lytic.

Question 4 (8 marks)

Stem: A 52-year-old man is admitted with anterior STEMI. He undergoes successful primary PCI to proximal LAD and is stable in CCU. On day 5 post-MI, he develops sudden severe dyspnoea. Examination reveals BP 80/50 mmHg, HR 120 bpm, bilateral crackles, and a harsh pansystolic murmur at the left sternal edge with a palpable thrill.

Question: (a) What is the most likely diagnosis? (1 mark) (b) Name two other mechanical complications that can occur post-MI. (2 marks) (c) Describe your immediate management. (5 marks)

Model Answer:

(a) Most likely diagnosis (1 mark):

  • Post-MI ventricular septal rupture (VSD) (1 mark)
    • "Rationale: Day 5 post-anterior MI, sudden dyspnoea + cardiogenic shock + harsh pansystolic murmur at left sternal edge + palpable thrill (turbulent flow through septal defect)"

(b) Two other mechanical complications (2 marks):

  1. Acute mitral regurgitation due to papillary muscle rupture (1 mark)
  2. Free wall rupture with pericardial tamponade (1 mark)
  • Also accept: LV aneurysm, LV pseudoaneurysm

(c) Immediate management (5 marks):

  1. Activate cardiac surgery immediately: Surgical repair is definitive treatment; call cardiothoracic surgery registrar/consultant urgently (1 mark)

  2. Resuscitation:

    • High-flow oxygen: 15 L/min non-rebreather; target SpO2 greater than 92%
    • Intubation and mechanical ventilation: Likely required given respiratory distress and shock
    • Inotropic support: Dobutamine 5-10 mcg/kg/min IV (improves contractility, reduces afterload)
    • Vasodilator therapy (if BP tolerates): Sodium nitroprusside infusion 0.5-5 mcg/kg/min to reduce afterload and decrease left-to-right shunt magnitude (use cautiously; requires arterial line monitoring) (1 mark for resuscitation measures)
  3. Intra-aortic balloon pump (IABP): Request cardiology to insert IABP urgently (via femoral artery); IABP reduces afterload, decreases VSD shunt, improves coronary perfusion, and stabilises patient as bridge to surgery (1 mark)

  4. Urgent echocardiography: Bedside transthoracic echo to confirm VSD (colour Doppler shows left-to-right shunt across interventricular septum), assess VSD size/location, estimate shunt fraction (Qp:Qs), and evaluate LV function. Transoesophageal echo in OR for surgical planning (1 mark)

  5. Prepare for urgent surgical repair:

    • Timing: Modern approach is surgery within 24-48 hours (historically delayed 4-6 weeks, but mortality too high with waiting)
    • Procedure: Patch closure of VSD ± CABG if incomplete revascularisation at initial PCI
    • Prognosis: Surgical mortality 40-50%, but medical management alone has 87-94% mortality
    • Alternative: Percutaneous VSD closure (Amplatzer device) if patient too high-risk for surgery (1 mark for definitive treatment planning)

Examiner Notes:

  • Accept: Consider VA-ECMO if refractory cardiogenic shock (as bridge to surgery or percutaneous closure)
  • Do not accept: "Medical management" alone (futile; patient will die without VSD repair)
  • Key discriminator: Recognises VSD based on clinical findings (murmur + thrill at left sternal edge, day 5 post-MI) and understands this is a surgical emergency requiring immediate cardiothoracic consultation

Australian Guidelines

ARC/ANZCOR

  • ANZCOR Guideline 11.3: Acute Coronary Syndromes (2023) [51]

    • Recommends aspirin 300mg + P2Y12 inhibitor (ticagrelor preferred) + anticoagulation immediately
    • Primary PCI preferred if FMC-to-balloon below 120 minutes
    • Thrombolysis if PCI unavailable within 120 minutes and below 12 hours from symptom onset
    • "Key difference from AHA: Australia/NZ emphasises pharmaco-invasive strategy (thrombolysis followed by routine PCI within 3-24 hours) in regional/rural settings"
  • ANZCOR Guideline 11: Adult Advanced Life Support (2023)

    • "Cardiac arrest during STEMI: Continue CPR and consider emergent PCI during resuscitation (eCPR protocol) if available"
    • "Adrenaline dosing in cardiac arrest: 1mg IV every 3-5 minutes"

Therapeutic Guidelines

  • Therapeutic Guidelines: Cardiovascular (2023) [52]
    • "Antiplatelet therapy: Aspirin 100mg daily + ticagrelor 90mg BD for 12 months minimum (DAPT)"
    • "Beta-blockers: Metoprolol or carvedilol recommended post-MI if no contraindications (reduce mortality and reinfarction)"
    • "ACE inhibitors: Start within 24 hours if EF below 40% or anterior MI; reduce mortality and prevent remodelling"
    • "High-intensity statin: Atorvastatin 80mg or rosuvastatin 40mg daily; LDL target below 1.8 mmol/L"

State-Specific

  • NSW Health STEMI Care Policy (PD2019_042) [53]:

    • Door-to-ECG ≤10 minutes
    • Door-to-balloon ≤90 minutes (PCI-capable hospitals), FMC-to-balloon ≤120 minutes
    • Pre-hospital 12-lead ECG and STEMI activation by paramedics (bypass protocol to PCI-capable hospital)
    • Pre-hospital thrombolysis in areas greater than 60 minutes from PCI centre
  • Victoria: Cardiac Clinical Network Guidelines [54]:

    • Statewide STEMI network coordinates care between rural hospitals and Melbourne PCI centres
    • Helicopter retrieval (ARV) for rural STEMI patients if appropriate
    • Pharmaco-invasive strategy (thrombolysis + routine PCI within 24 hours) for rural patients
  • Queensland: STEMI Guidelines [55]:

    • Pre-hospital thrombolysis by Queensland Ambulance Service intensive care paramedics
    • Retrieval via RFDS or LifeFlight for rural/remote patients

Remote/Rural Considerations

Pre-Hospital

  • Paramedic 12-lead ECG: Reduces door-to-balloon time by 15-30 minutes; enables pre-hospital STEMI diagnosis and cath lab activation en route [56]
  • Pre-hospital thrombolysis: Delivered by intensive care paramedics (ICP) or RFDS retrieval physicians in NSW, QLD, TAS, VIC, SA; reduces time to reperfusion by 24-52 minutes [13,14,15]
  • Bypass protocols: Paramedics transport directly to PCI-capable hospital (bypassing nearest non-PCI hospital) if within acceptable time frame

Resource-Limited Setting

When PCI is not available and thrombolysis contraindicated:

  1. Medical management: Aspirin, P2Y12 inhibitor, anticoagulation, beta-blocker, ACE inhibitor, statin (reduces mortality vs no treatment but inferior to reperfusion)
  2. Arrange urgent transfer: To PCI-capable centre for delayed PCI (benefit persists up to 12-24 hours post-symptom onset)
  3. Telemetry monitoring: Detect and treat arrhythmias (VF, VT, complete heart block)
  4. Treat complications aggressively: Heart failure, cardiogenic shock, arrhythmias

Limited resource formulary alternatives:

  • P2Y12 inhibitor: Clopidogrel 600mg loading if ticagrelor/prasugrel unavailable (less effective but widely available)
  • Anticoagulation: UFH instead of enoxaparin (easier to monitor with aPTT; can reverse with protamine)
  • Pain relief: Paracetamol + tramadol if morphine unavailable (less respiratory depression)

Retrieval

RFDS retrieval criteria for STEMI:

  1. All STEMI patients in remote areas (greater than 60 minutes from PCI centre) requiring coronary angiography
  2. Urgent retrieval (within 1-3 hours): Failed thrombolysis requiring rescue PCI, cardiogenic shock, refractory arrhythmias
  3. Routine retrieval (within 6-24 hours): Successful thrombolysis requiring pharmaco-invasive angiography

RFDS capabilities:

  • Pre-hospital thrombolysis: RFDS medical officers trained to administer tenecteplase
  • Mechanical ventilation: Portable ventilators for intubated patients
  • Blood products: Limited supply; type O-negative PRBC and FFP available
  • Inotropic support: Adrenaline, noradrenaline, dobutamine infusions
  • Limitations: No IABP, no ECMO (patient must be stabilised or transferred via road to tertiary centre if requires mechanical circulatory support)

Retrieval coordination:

  • Contact RFDS Coordination Centre (1800 XXX XXX varies by state) or state-based retrieval services (NSW: 1800 650 004; VIC ARV: 1300 368 661; QLD: 1300 799 127)
  • Provide clinical handover: STEMI territory, reperfusion strategy used, complications, current vital signs, inotrope doses
  • Prepare patient: Secure IV access, urinary catheter, ECG copies, medication chart, handover letter

Telemedicine

Remote ECG interpretation:

  • iECG transmission: Smartphone apps (e.g., AliveCor, iECG) allow paramedics or remote clinicians to transmit 12-lead ECG to cardiologist in real-time
  • Improves diagnostic accuracy and reduces time to cath lab activation by 10-20 minutes [57]

Remote consultation:

  • Video link with ED physician or cardiologist for guidance on reperfusion decision, troubleshooting complications
  • Particularly valuable in Indigenous communities with remote area nurses as primary clinicians

References

Guidelines

  1. Australian Institute of Health and Welfare (AIHW). Cardiovascular Disease Snapshot, 2023. Available from: https://www.aihw.gov.au/reports/heart-stroke-vascular-diseases/cardiovascular-health-compendium
  2. 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 Circ. 2016;25(9):895-951. PMID: 27476580
  3. Australian Resuscitation Council. ANZCOR Guideline 11.3: Acute Coronary Syndromes. 2023. Available from: https://resus.org.au

Key Evidence

  1. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361(9351):13-20. PMID: 12517460
  2. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379-1387. PMID: 23473396
  3. Li K, Zhang B, Zheng B, et al. Reperfusion Strategy of ST-Elevation Myocardial Infarction: A Meta-Analysis of Primary Percutaneous Coronary Intervention and Pharmaco-Invasive Therapy. Front Cardiovasc Med. 2022;9:813325. PMID: 35360047
  4. Claeys MJ, De Meester A, Convens C, et al. Contemporary mortality differences between primary percutaneous coronary intervention and thrombolysis in ST-segment elevation myocardial infarction. Arch Intern Med. 2011;171(6):544-549. PMID: 21098345
  5. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-2015. PMID: 17982182
  6. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes (PLATO trial). N Engl J Med. 2009;361(11):1045-1057. PMID: 19717846
  7. Scirica BM, Cannon CP, Emanuelsson H, et al. The incidence of bradyarrhythmias and clinical bradyarrhythmic events in patients with acute coronary syndromes treated with ticagrelor or clopidogrel in the PLATO trial. Eur Heart J. 2011;32(23):2979-2986. PMID: 21875856
  8. Morrow DA, Cannon CP, Jesse RL, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Circulation. 2007;115(13):e356-e375. PMID: 17384331
  9. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018;138(20):e618-e651. PMID: 30571511
  10. Khan AA, Chew DP, Maryam S, et al. Pre-hospital thrombolysis in ST-segment elevation myocardial infarction in regional Australia: long-term follow up. Intern Med J. 2020;50(6):711-715. PMID: 31237408
  11. Khan AA, Maryam S, Shah SF, et al. Pre-hospital thrombolysis in ST-segment elevation myocardial infarction: a regional Australian experience. Med J Aust. 2016;205(3):121-125. PMID: 27465767
  12. Johnston T, Oatley L, Eaves S, et al. Implementing prehospital thrombolysis in regional Tasmania: A retrospective cohort study. Int J Paramedicine. 2025;9(1):1-10.
  13. Jennings RB, Sommers HM, Smyth GA, et al. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch Pathol. 1960;70:68-78. PMID: 14407094
  14. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation. 1977;56(5):786-794. PMID: 912839
  15. Nesto RW, Kowalchuk GJ. The ischemic cascade: temporal sequence of hemodynamic, electrocardiographic and symptomatic expressions of ischemia. Am J Cardiol. 1987;59(7):23C-30C. PMID: 3825934
  16. Gersh BJ, Stone GW, White HD, Holmes DR Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA. 2005;293(8):979-986. PMID: 15728170
  17. Meyers HP, Bracey A, Lee D, et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. Int J Cardiol Heart Vasc. 2021;33:100767. PMID: 33912650
  18. Ricci F, Martini C, Scordo DM, et al. ECG Patterns of Occlusion Myocardial Infarction: A Narrative Review. Ann Emerg Med. 2025;85(4):330-340. PMID: 39147001
  19. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock (IABP-SHOCK II trial). N Engl J Med. 2012;367(14):1287-1296. PMID: 22920912
  20. Rao P, Khalpey Z, Smith R, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest. Circ Heart Fail. 2018;11(9):e004905. PMID: 30354401
  21. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94. PMID: 25281189
  22. Baigent C, Collins R, Appleby P, et al. ISIS-2: 10 year survival among patients with suspected acute myocardial infarction in randomised comparison of intravenous streptokinase, oral aspirin, both, or neither. BMJ. 1998;316(7141):1337-1343. PMID: 9563981
  23. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009;361(11):1045-1057. PMID: 19717846
  24. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-2015. PMID: 17982182
  25. Hobl EL, Stimpfl T, Ebner J, et al. Morphine decreases clopidogrel concentrations and effects: a randomized, double-blind, placebo-controlled trial. J Am Coll Cardiol. 2014;63(7):630-635. PMID: 24315907
  26. Freemantle N, Cleland J, Young P, et al. Beta blockade after myocardial infarction: systematic review and meta regression analysis. BMJ. 1999;318(7200):1730-1737. PMID: 10381708
  27. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes (PROVE IT-TIMI 22 trial). N Engl J Med. 2004;350(15):1495-1504. PMID: 15007110
  28. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol. 2013;61(4):e78-e140. PMID: 23256914
  29. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177. PMID: 28886621
  30. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation. 2025;151:e00-e00. PMID: 40014670
  31. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361(9351):13-20. PMID: 12517460
  32. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction (STREAM trial). N Engl J Med. 2013;368(15):1379-1387. PMID: 23473396
  33. Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-2) Investigators. Single-bolus tenecteplase compared with front-loaded alteplase in acute myocardial infarction: the ASSENT-2 double-blind randomised trial. Lancet. 1999;354(9180):716-722. PMID: 10475182
  34. Menon V, Harrington RA, Hochman JS, et al. Thrombolysis and adjunctive therapy in acute myocardial infarction: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 Suppl):549S-575S. PMID: 15383488
  35. Gershlick AH, Stephens-Lloyd A, Hughes S, et al. Rescue angioplasty after failed thrombolytic therapy for acute myocardial infarction (REACT trial). N Engl J Med. 2005;353(26):2758-2768. PMID: 16382062
  36. Steg PG, Bonnefoy E, Chabaud S, et al. Impact of time to treatment on mortality after prehospital fibrinolysis or primary angioplasty: data from the CAPTIM randomized clinical trial. Circulation. 2003;108(23):2851-2856. PMID: 14623806
  37. Pfeffer MA, Braunwald E, Moyé LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction (SAVE trial). N Engl J Med. 1992;327(10):669-677. PMID: 1386652
  38. Arnaoutakis GJ, Zhao Y, George TJ, et al. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg. 2012;94(2):436-444. PMID: 22543276
  39. Mantovani V, Mariscalco G, Leva C, et al. Mechanical complications of acute myocardial infarction: a multicenter study. Eur J Cardiothorac Surg. 2015;47(4):e132-e139. PMID: 25564213
  40. Becker RC, Gore JM, Lambrew C, et al. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol. 1996;27(6):1321-1326. PMID: 8626938
  41. Mehta SR, Wood DA, Storey RF, et al. Complete revascularization with multivessel PCI for myocardial infarction (COMPLETE trial). N Engl J Med. 2019;381(15):1411-1421. PMID: 31475795
  42. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94. PMID: 25281189
  43. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol. 2008;52(3):171-180. PMID: 18617065
  44. Bueno H, Betriu A, Heras M, et al. Primary angioplasty vs fibrinolysis in very old patients with acute myocardial infarction: TRIANA (TRatamiento del Infarto Agudo de miocardio eN Ancianos) randomized trial and pooled analysis with previous studies. Eur Heart J. 2011;32(1):51-60. PMID: 20870670
  45. Australian Institute of Health and Welfare (AIHW). Better Cardiac Care measures for Aboriginal and Torres Strait Islander people: sixth national report 2021. Cat. no. IHW 267. Canberra: AIHW; 2021.
  46. Kerr AJ, McLachlan A, Furness S, et al. The burden of modifiable cardiovascular risk factors in the coronary care unit by age, ethnicity, and socioeconomic status--PREDICT CVD-9. N Z Med J. 2008;121(1285):20-33. PMID: 19098945
  47. Taylor LK, Nelson MA, Gale M, et al. Cardiac procedures in ST-segment-elevation myocardial infarction - the influence of age, geography and Aboriginality. BMC Cardiovasc Disord. 2020;20(1):224. PMID: 32410569
  48. Dawson LP, Nehme Z, Barker G, et al. Chest pain epidemiology and care quality for Aboriginal and Torres Strait Islander peoples in Victoria, Australia: a population-based cohort study from 2015 to 2019. Lancet Reg Health West Pac. 2023;38:100839. PMID: 37484012
  49. Bradshaw PJ, Katzenellenbogen JM, Sanfilippo FM, et al. Validation study of GRACE risk scores in indigenous and non-indigenous patients hospitalized with acute coronary syndrome. BMC Cardiovasc Disord. 2015;15:151. PMID: 26577835
  50. Ilton MK, Walsh WF, Brown ADH, et al. A framework for overcoming disparities in management of acute coronary syndromes in the Australian Aboriginal and Torres Strait Islander population. A consensus statement from the National Heart Foundation of Australia. Med J Aust. 2014;200(11):639-643. PMID: 24938343

Systematic Reviews and Meta-Analyses

  1. Li K, Zhang B, Zheng B, et al. Reperfusion Strategy of ST-Elevation Myocardial Infarction: A Meta-Analysis of Primary Percutaneous Coronary Intervention and Pharmaco-Invasive Therapy. Front Cardiovasc Med. 2022;9:813325. PMID: 35360047
  2. Mehta RH, Starr AZ, Lopes RD, et al. Relationship of distance from PCI-capable hospital and treatment delay to outcomes in patients undergoing primary PCI for ST-elevation myocardial infarction. Eur Heart J Acute Cardiovasc Care. 2012;1(2):114-121. PMID: 24062898
  3. Terkelsen CJ, Sørensen JT, Maeng M, et al. System delay and mortality among patients with STEMI treated with primary percutaneous coronary intervention. JAMA. 2010;304(7):763-771. PMID: 20716739
  4. Diercks DB, Kontos MC, Chen AY, et al. Utilization and impact of pre-hospital electrocardiograms for patients with acute ST-segment elevation myocardial infarction: data from the NCDR (National Cardiovascular Data Registry) ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry. J Am Coll Cardiol. 2009;53(2):161-166. PMID: 19130984

Australian Context and Indigenous Health

  1. Agostino JW, Wong D, Paige E, et al. Cardiovascular disease risk assessment for Aboriginal and Torres Strait Islander adults aged under 35 years: a cohort study. Aust N Z J Public Health. 2020;44(3):225-231. PMID: 32172533
  2. Australian Institute of Health and Welfare. Review of cardiovascular health among Aboriginal and Torres Strait Islander people. Cat. no. IHW 203. Canberra: AIHW; 2019.
  3. NSW Health. Acute Coronary Syndrome (including STEMI) - Reperfusion Strategy. Policy Directive PD2019_042. Sydney: NSW Ministry of Health; 2019.
  4. Victorian Department of Health. Cardiac Clinical Network: STEMI Guidelines. Melbourne: State Government of Victoria; 2022.
  5. Queensland Health. Acute Coronary Syndrome Clinical Pathways. Brisbane: Queensland Government; 2023.

Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

Primary PCI or thrombolysis for STEMI?

Primary PCI preferred if door-to-balloon time below 120 min from first medical contact. Thrombolysis if PCI not available within 120 min and no contraindications.

When is rescue PCI indicated after thrombolysis?

If below 50% ST-segment resolution at 60-90 minutes post-thrombolysis, indicating failed reperfusion.

Which P2Y12 inhibitor in STEMI?

Ticagrelor 180mg loading dose preferred (PLATO trial). Prasugrel if no prior stroke/TIA and below 75 years.

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.