STEMI Management in ICU

Quick Answer

Quick Answer: ST-Elevation Myocardial Infarction (STEMI) represents complete coronary artery occlusion requiring immediate reperfusion to salvage myocardium. The critical targets are:

Reperfusion Timing:

• Primary PCI (preferred): Door-to-balloon <90 minutes (PCI-capable centre), <120 minutes (transfer)
• Fibrinolysis (if PCI unavailable): Door-to-needle <10 minutes; followed by routine angiography within 2-24 hours

Immediate Management:

1. Dual antiplatelet therapy (DAPT): Aspirin 300 mg + Ticagrelor 180 mg (or Prasugrel 60 mg)
2. Anticoagulation: Unfractionated heparin 70-100 U/kg bolus (max 10,000 U)
3. Analgesia: IV morphine (titrated) - use with caution (may reduce clopidogrel absorption)
4. Oxygen: Only if SpO2 <90% (AVOID-DETO2X trial - no benefit of routine O2)
5. Nitrates: Sublingual or IV GTN for ongoing ischaemia (CONTRAINDICATED in RV infarction)

ICU Indications:

• Cardiogenic shock (Killip IV, CI <2.2 L/min/m2, SBP <90)
• Mechanical complications (VSD, papillary rupture, free wall rupture)
• Recurrent VF/VT or sustained arrhythmias
• Post-cardiac arrest with ROSC
• Haemodynamic instability requiring inotropes/mechanical support

Red Flags:

• Cardiogenic shock = mortality 40-50% despite revascularisation
• Mechanical complications peak days 3-7 post-STEMI
• RV infarction: Avoid nitrates, maintain preload

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CICM Exam Focus

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Key Points (10)

Key Points: 1. STEMI represents complete coronary occlusion - transmural ischaemia progresses to irreversible necrosis within 20-40 minutes (subendocardium) and 3-6 hours (transmural) without reperfusion (PMID: 6681009)

2. Primary PCI is superior to fibrinolysis when achievable within 120 minutes of first medical contact (DANAMI-2: 30-day mortality 6.6% vs 7.8%, p=0.005) (PMID: 12928468)

3. Door-to-balloon time directly correlates with mortality - each 30-minute delay increases relative mortality by 7.5% (PMID: 16418451)

4. Fibrinolysis with routine angiography within 2-24 hours (pharmaco-invasive strategy) is non-inferior to primary PCI when transfer would cause >120-minute delay (STREAM trial) (PMID: 23474507)

5. Dual antiplatelet therapy (DAPT) with aspirin + P2Y12 inhibitor is mandatory - ticagrelor/prasugrel superior to clopidogrel in PCI (PLATO, TRITON-TIMI 38) (PMID: 19717846, PMID: 17982182)

6. Cardiogenic shock complicates 5-10% of STEMI - SHOCK trial demonstrated 13% absolute mortality reduction with early revascularisation at 6 months (PMID: 10376614)

7. CULPRIT-SHOCK trial (2017) demonstrated culprit-lesion-only PCI reduces 30-day mortality (45.9% vs 55.4%) compared to immediate complete revascularisation in cardiogenic shock (PMID: 28709830)

8. IABP-SHOCK II trial (2012) showed no mortality benefit of routine IABP in cardiogenic shock (30-day mortality 39.7% vs 41.3%, p=0.69) (PMID: 22920912)

9. Mechanical complications (VSD, papillary rupture, free wall rupture) typically occur days 3-7 post-STEMI - suspect with sudden haemodynamic deterioration and new murmur (PMID: 10377087)

10. Right ventricular infarction complicates 30-50% of inferior STEMI - maintain preload, AVOID nitrates/diuretics, may require RV inotropic support (PMID: 9362391)

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Definition and Diagnostic Criteria

STEMI Definition

ST-Elevation Myocardial Infarction (STEMI) is defined by the Fourth Universal Definition of Myocardial Infarction (2018) as acute myocardial injury with evidence of acute ischaemia and with detection of a rise/fall of cardiac troponin (cTn) values with at least one value above the 99th percentile upper reference limit, combined with new ST-elevation at the J-point meeting the following criteria (PMID: 30153967):

STEMI Equivalents

The following ECG patterns are considered STEMI equivalents requiring immediate reperfusion therapy (PMID: 30153967):

1. New Left Bundle Branch Block (LBBB)

• New or presumed new LBBB with ischaemic symptoms
• Sgarbossa criteria (modified) improve specificity:
  • Concordant ST elevation ≥1 mm in leads with positive QRS (5 points)
  • Concordant ST depression ≥1 mm in V1-V3 (3 points)
  • Discordant ST elevation ≥5 mm OR ≥25% of S-wave depth (2 points)
• Score ≥3 = high specificity for STEMI (PMID: 8559200)

2. Posterior STEMI

• Dominant R wave in V1-V2 (R/S ratio >1)
• ST depression V1-V3 (representing posterior ST elevation)
• Posterior leads (V7-V9): ST elevation ≥0.5 mm diagnostic (PMID: 20129386)
• Often associated with inferior STEMI (RCA or LCx occlusion)

3. de Winter Pattern

• Upsloping ST depression >1 mm at J-point in V1-V6
• Tall, symmetric T waves in precordial leads
• Slight ST elevation in aVR
• Represents proximal LAD occlusion (PMID: 19081386)

4. Wellens Syndrome (Warning Sign)

• Biphasic or deeply inverted T waves in V2-V3 (during pain-free interval)
• Represents critical proximal LAD stenosis (not occlusion)
• High risk of anterior STEMI without intervention (PMID: 6824098)

Anatomical Localisation

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Pathophysiology

Plaque Rupture and Coronary Thrombosis

The pathophysiological basis of STEMI involves acute thrombotic occlusion of an epicardial coronary artery, typically triggered by atherosclerotic plaque rupture or erosion (PMID: 10334431).

Vulnerable Plaque Characteristics

High-risk plaque features (PMID: 10334431):

• Thin fibrous cap (<65 μm)
• Large lipid-rich necrotic core (>40% of plaque volume)
• Active inflammation (macrophage and T-cell infiltration)
• Positive remodelling (outward vessel expansion)
• Neovascularisation (intraplaque haemorrhage)
• Microcalcifications (spotty calcification)

Thrombosis Cascade

Sequence of events following plaque rupture (PMID: 14766967):

1. Plaque disruption → exposure of subendothelial collagen and tissue factor
2. Platelet adhesion → von Willebrand factor (vWF) bridges collagen to platelet GPIb receptors
3. Platelet activation → release of ADP, thromboxane A2 (TXA2), serotonin
4. Platelet aggregation → GPIIb/IIIa receptor activation, fibrinogen cross-linking
5. Coagulation activation → tissue factor pathway → thrombin generation
6. Fibrin formation → red thrombus propagation
7. Complete occlusion → cessation of antegrade coronary flow (TIMI 0)

Plaque Erosion (25-30% of ACS)

Distinct from rupture (PMID: 21148123):

• Intact fibrous cap (no rupture)
• Endothelial denudation with exposure of subendothelial matrix
• White platelet-rich thrombus (less red thrombus component)
• More common in: Young patients, women, smokers, diabetics
• May respond better to antiplatelet therapy alone

Infarct Zone Expansion

Wavefront Phenomenon

Reimer and Jennings (1977) described the wavefront of ischaemic necrosis (PMID: 6681009):

1. Subendocardium (highest oxygen demand, lowest perfusion pressure) - first affected
2. Transmural progression toward epicardium over 3-6 hours
3. Collateral circulation may modify progression
4. Final infarct size determined by:
   • Duration of occlusion
   • Collateral blood supply
   • Myocardial oxygen demand
   • Ischaemic preconditioning

Time Course of Myocardial Necrosis

Clinical implication: "Time is Muscle"

• every 30-minute delay in reperfusion increases mortality by 7.5% (PMID: 16418451)

Reperfusion Injury

Paradoxically, reperfusion itself can cause additional myocardial injury (PMID: 22387833):

Mechanisms of reperfusion injury:

1. Reactive oxygen species (ROS) burst upon reperfusion
2. Calcium overload → hypercontracture, mPTP opening
3. Inflammatory cell infiltration (neutrophils)
4. Microvascular obstruction ("no-reflow phenomenon")
5. Mitochondrial dysfunction → apoptosis

No-reflow phenomenon:

• Occurs in 25-50% of STEMI after primary PCI
• Represents microvascular obstruction despite epicardial vessel patency
• Associated with larger infarct size and worse outcomes (PMID: 23563067)
• Risk factors: Prolonged ischaemia, thrombus burden, diabetes

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Time-Critical Management

Reperfusion Targets

The fundamental principle of STEMI management is RAPID REPERFUSION (PMID: 33085966):

Decision Algorithm: PCI vs Fibrinolysis

Door-to-Balloon Time and Mortality

De Luca et al. (2004) meta-analysis demonstrated the critical importance of reperfusion timing (PMID: 16418451):

• Every 30-minute delay in reperfusion increases 1-year mortality by 7.5%
• Door-to-balloon <60 min: Mortality 4.3%
• Door-to-balloon 61-90 min: Mortality 5.4%
• Door-to-balloon 91-120 min: Mortality 6.8%
• Door-to-balloon >120 min: Mortality 9.4%

System-level interventions to reduce D2B time:

1. Pre-hospital ECG with cath lab activation
2. Single call activation system
3. Emergency physician activation of cath lab
4. 24/7 interventional cardiology coverage
5. Real-time data feedback

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Reperfusion Strategy

Primary Percutaneous Coronary Intervention (PCI)

Primary PCI is the preferred reperfusion strategy when it can be performed by an experienced team within the recommended time frame (PMID: 12928468).

Evidence for Primary PCI Superiority

DANAMI-2 (2003) (PMID: 12928468):

• 1,572 patients randomised to primary PCI vs fibrinolysis with alteplase
• 30-day composite (death, reinfarction, stroke): 8.0% PCI vs 13.7% fibrinolysis (p<0.001)
• Benefit maintained at 3 years

PRAGUE-2 (2003) (PMID: 14604230):

• Immediate fibrinolysis vs transfer for primary PCI
• Transfer for PCI reduced 30-day mortality (6.8% vs 10.0%, p=0.12)
• Statistically significant for presentation >3 hours (mortality 6.0% vs 15.3%, p<0.02)

Primary PCI Technique

Culprit artery PCI (PMID: 28709830):

1. Radial access preferred (RIVAL, MATRIX trials - lower bleeding, mortality)
2. Aspiration thrombectomy: Not routinely recommended (TASTE, TOTAL trials - no benefit, increased stroke)
3. Drug-eluting stent (DES): Preferred over bare-metal stent (lower target vessel revascularisation)
4. TIMI 3 flow restoration: Goal of PCI (normal antegrade flow)
5. Fractional flow reserve (FFR): Not recommended in acute setting (inaccurate in STEMI)

Multi-vessel Disease in STEMI

CULPRIT-SHOCK Trial (2017) - landmark evidence for cardiogenic shock (PMID: 28709830):

• 706 patients with STEMI and cardiogenic shock
• Culprit-only PCI vs immediate complete revascularisation
• 30-day mortality or RRT: 45.9% culprit-only vs 55.4% complete (RR 0.83, p=0.01)
• Recommendation: Culprit-lesion-only PCI in cardiogenic shock

COMPLETE Trial (2019) - stable STEMI (PMID: 31475799):

• 4,041 patients with STEMI and multi-vessel disease (no shock)
• Culprit-only vs staged complete revascularisation
• Complete revascularisation reduced CV death + MI (7.8% vs 10.5%, p=0.004)
• Recommendation: Staged complete revascularisation if haemodynamically stable

Fibrinolysis

Indications for Fibrinolysis

Fibrinolysis is appropriate when (PMID: 33085966):

• Primary PCI cannot be achieved within 120 minutes
• Presentation within 12 hours of symptom onset (greatest benefit <3 hours)
• No absolute contraindications
• Remote/rural setting (e.g., RFDS Australia)

Fibrinolytic Agents

Australian Context: Tenecteplase is preferred and available through PBS for pre-hospital or in-hospital fibrinolysis. Streptokinase is rarely used due to antigenicity and hypotension risk.

Contraindications to Fibrinolysis

Fibrinolysis Success Criteria

Successful reperfusion is indicated by (PMID: 15007158):

1. ST-segment resolution >70% in the lead with maximum ST elevation at 60-90 minutes
2. Resolution of chest pain
3. Reperfusion arrhythmias (accelerated idioventricular rhythm, VPCs - transient)
4. Early peak of cardiac biomarkers

Failed fibrinolysis criteria (PMID: 15007158):

• ST-segment resolution <50% at 60-90 minutes
• Persistent or worsening chest pain
• Haemodynamic instability

Management of failed fibrinolysis:

• Rescue PCI immediately (do not repeat fibrinolysis)
• REACT trial (2005) demonstrated rescue PCI reduces composite of death/reinfarction/stroke/heart failure vs conservative management (15.3% vs 31.0%, p<0.001) (PMID: 16043645)

Pharmaco-Invasive Strategy

The pharmaco-invasive approach combines immediate fibrinolysis with routine angiography within 2-24 hours (PMID: 23474507):

STREAM Trial (2013) (PMID: 23474507):

• 1,892 patients presenting <3 hours, unable to undergo PCI within 1 hour
• Fibrinolysis + routine angiography (2-24h) vs primary PCI
• 30-day composite (death, shock, CHF, reinfarction): 12.4% vs 14.3% (p=0.21)
• Non-inferior outcomes with pharmaco-invasive approach
• Increased intracranial haemorrhage with fibrinolysis in patients ≥75 years (led to half-dose recommendation for elderly)

TRANSFER-AMI Trial (2009) (PMID: 19188507):

• Fibrinolysis + routine early transfer for PCI (within 6h) vs standard care
• Reduced 30-day death/reinfarction/recurrent ischaemia/CHF/shock (11.0% vs 17.2%, p=0.004)

Australian Context - Remote STEMI Management:

• RFDS-equipped aircraft carry tenecteplase
• Pre-hospital fibrinolysis with telemedicine support
• Transfer to PCI-capable centre for routine angiography within 2-24 hours
• Rescue PCI if fibrinolysis fails

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Antiplatelet Therapy

Aspirin

Aspirin is the cornerstone of antiplatelet therapy in STEMI (PMID: 33085966):

• Mechanism: Irreversible COX-1 inhibition → blocks thromboxane A2 synthesis
• Dose: 300 mg loading (chewed, not enteric-coated), 75-100 mg daily thereafter
• ISIS-2 Trial (1988): 23% reduction in 5-week vascular mortality with aspirin alone (PMID: 2899772)

P2Y12 Receptor Inhibitors

Dual antiplatelet therapy (DAPT) with aspirin plus a P2Y12 inhibitor is mandatory in STEMI (PMID: 33085966):

Key Trial Evidence

PLATO Trial (2009) - Ticagrelor vs Clopidogrel (PMID: 19717846):

• 18,624 patients with ACS (STEMI and NSTEMI)
• Primary endpoint (CV death, MI, stroke): 9.8% ticagrelor vs 11.7% clopidogrel (HR 0.84, p<0.001)
• All-cause mortality: 4.5% vs 5.9% (p<0.001)
• Major bleeding similar; increased non-CABG-related bleeding with ticagrelor

TRITON-TIMI 38 (2007) - Prasugrel vs Clopidogrel (PMID: 17982182):

• 13,608 patients with ACS undergoing PCI
• Primary endpoint: 9.9% prasugrel vs 12.1% clopidogrel (HR 0.81, p<0.001)
• Major bleeding increased: 2.4% vs 1.8% (p=0.03)
• Net clinical harm in prior TIA/stroke, age ≥75 years, weight <60 kg

Timing of P2Y12 Inhibitor Loading

Current recommendations (PMID: 33085966):

• Primary PCI pathway: Load as early as possible (ideally pre-cath lab)
• Fibrinolysis pathway:
  • Clopidogrel 300 mg (age ≤75) or 75 mg (age >75) at time of fibrinolysis
  • Ticagrelor/prasugrel given after fibrinolysis, preferably at angiography (limited data)

Glycoprotein IIb/IIIa Inhibitors

Role is now limited with modern P2Y12 inhibitors and radial access (PMID: 33085966):

• Abciximab: 0.25 mg/kg bolus, 0.125 μg/kg/min infusion (max 10 μg/min)
• Eptifibatide: 180 μg/kg bolus x2, 2 μg/kg/min infusion
• Tirofiban: 25 μg/kg bolus, 0.15 μg/kg/min infusion

Current indications:

• Bailout therapy for thrombotic complications during PCI
• Large thrombus burden at angiography
• Not routinely recommended as upstream therapy

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Anticoagulation

Anticoagulation in STEMI

Anticoagulation is mandatory during reperfusion to prevent stent thrombosis (PCI) or recurrent thrombosis (fibrinolysis) (PMID: 33085966):

Anticoagulation with Fibrinolysis

Enoxaparin is preferred with fibrinolysis based on the ExTRACT-TIMI 25 trial (PMID: 16533938):

• 20,506 patients with STEMI receiving fibrinolysis
• Enoxaparin vs UFH: Death/MI at 30 days 9.9% vs 12.0% (RR 0.83, p<0.001)
• Major bleeding slightly increased (2.1% vs 1.4%)

Dosing with fibrinolysis:

• Age <75 years: 30 mg IV bolus, then 1 mg/kg SC BD
• Age ≥75 years: No bolus, 0.75 mg/kg SC BD
• CrCl <30 mL/min: 1 mg/kg SC once daily

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ICU Management

Indications for ICU Admission

Patients with STEMI requiring ICU/CCU admission (PMID: 33085966):

1. Cardiogenic shock (Killip Class IV)
2. Mechanical complications (VSD, papillary muscle rupture, free wall rupture)
3. Sustained ventricular arrhythmias (VF, VT)
4. Post-cardiac arrest with ROSC
5. Haemodynamic instability requiring inotropes/vasopressors
6. Mechanical circulatory support (IABP, Impella, VA-ECMO)
7. High-degree AV block requiring temporary pacing
8. Severe respiratory failure requiring NIV or intubation
9. Ongoing ischaemia despite revascularisation

Haemodynamic Monitoring

Invasive monitoring considerations:

• Arterial line: Standard for haemodynamically unstable patients
• Central venous catheter: For vasoactive drug administration
• Pulmonary artery catheter: Limited role (no mortality benefit in cardiogenic shock); consider for:
  • Differentiating cardiogenic vs distributive shock
  • RV infarction assessment
  • Mechanical complication evaluation

Echocardiography is preferred for haemodynamic assessment:

• LV function (LVEF, regional wall motion abnormalities)
• RV function
• Mechanical complications (VSD, MR, pericardial effusion)
• Cardiac output estimation

Standard ICU Care

Post-reperfusion STEMI management:

1. Continuous ECG monitoring for 24-48 hours minimum
2. Blood pressure targets: SBP >90 mmHg; avoid hypotension (coronary perfusion)
3. Oxygen therapy: Only if SpO2 <90% (DETO2X-AMI trial showed no benefit of routine O2) (PMID: 28041950)
4. Analgesia: IV morphine (titrated); consider fentanyl if morphine contraindicated
5. Antiemetics: Ondansetron (avoid metoclopramide which may increase coronary tone)
6. VTE prophylaxis: Mechanical (IPC) ± pharmacological (enoxaparin 40 mg SC daily) when not therapeutically anticoagulated
7. Glucose control: Target 8-10 mmol/L; avoid hypoglycaemia
8. Electrolyte management: Maintain K+ 4.0-5.0 mmol/L, Mg2+ >1.0 mmol/L (arrhythmia prevention)

Medications in ICU

Secondary prevention should be initiated early (within 24 hours if stable):

Complications Surveillance

Systematic monitoring for STEMI complications:

1. Serial ECG: Q12h for 48 hours; repeat for any symptom change
2. Cardiac biomarkers: Peak troponin to estimate infarct size
3. Echocardiography: Within 24-48 hours; repeat if haemodynamic deterioration
4. Daily examination: New murmurs (mechanical complications), JVP (RV failure), crackles (pulmonary oedema)
5. Arrhythmia surveillance: Continuous telemetry; electrolyte monitoring

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Mechanical Complications

Overview

Mechanical complications are devastating but rare consequences of STEMI, typically occurring days 3-7 post-infarction during the healing phase when necrotic myocardium is most vulnerable (PMID: 10377087):

Ventricular Septal Defect (VSD)

Post-MI VSD results from necrosis and rupture of the interventricular septum (PMID: 10377087):

Pathophysiology:

• Anterior STEMI → apical VSD (simple rupture)
• Inferior STEMI → basal VSD (complex, serpentine rupture, worse prognosis)

Clinical features:

• Sudden haemodynamic deterioration days 3-7
• Harsh holosystolic murmur (louder at left sternal border)
• Biventricular failure (RV volume overload, LV low output)
• Pulmonary oedema with clear lung fields possible (shunting before pulmonary congestion)

Diagnosis:

• Echocardiography: Visualise defect, colour Doppler shows left-to-right shunt
• Pulmonary artery catheter: Oxygen step-up from RA to PA (Qp:Qs calculation)

Management:

• Haemodynamic stabilisation: Vasodilators (reduce afterload, decrease shunt), IABP
• Mechanical circulatory support: VA-ECMO, Impella as bridge to surgery
• Surgical repair: Urgent surgery remains standard of care despite high mortality
• Timing controversy: Some advocate delaying surgery 2-4 weeks if stable (allows tissue healing)
• Percutaneous closure: Considered for some anatomically suitable defects (limited evidence)

Papillary Muscle Rupture

Rupture of the papillary muscle causes acute severe mitral regurgitation (PMID: 10377087):

Anatomy:

• Posteromedial papillary muscle (single blood supply from PDA) - more common rupture
• Anterolateral papillary muscle (dual supply from LAD + LCx) - less common rupture
• Complete vs partial (one head) rupture

Clinical features:

• Sudden onset pulmonary oedema with hypotension
• New systolic murmur (may be soft or absent due to rapid equalisation of LA-LV pressures)
• Acute respiratory failure

Diagnosis:

• Echocardiography: Flail mitral leaflet, severe MR, prolapsing papillary muscle head
• PA catheter: Large V wave on PCWP tracing

Management:

• Immediate stabilisation: IABP (reduce afterload, augment coronary perfusion)
• Intubation and ventilation for pulmonary oedema
• Emergent surgery: Mitral valve replacement (MVR) - definitive treatment
• VA-ECMO: Bridge to surgery in refractory cardiogenic shock

Free Wall Rupture

Free wall rupture is typically rapidly fatal (PMID: 10377087):

Risk factors:

• First MI (no collaterals or fibrosis)
• Anterior MI
• Age >70 years
• Female sex
• Hypertension
• Delayed reperfusion

Presentation:

• Acute (70%): Sudden cardiovascular collapse, PEA, death within minutes
• Subacute (30%): Tamponade physiology, pericardial pain, pericardial effusion
• Pseudoaneurysm: Contained rupture with pericardial adhesion (may present later)

Diagnosis:

• Sudden PEA arrest → suspect tamponade
• Echocardiography: Pericardial effusion, tamponade physiology, visualisation of rupture site

Management:

• Immediate pericardiocentesis (if tamponade causing arrest)
• Emergent surgery: Repair or patch closure (rarely successful in acute rupture)
• Pseudoaneurysm: Urgent surgical repair (high rupture risk if untreated)

LV Aneurysm vs Pseudoaneurysm

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Cardiogenic Shock in STEMI

Definition and Diagnosis

Cardiogenic shock is defined as (PMID: 28668636):

1. Systolic blood pressure <90 mmHg for >30 minutes OR requirement for inotropes/vasopressors
2. Evidence of end-organ hypoperfusion:
   • Altered mental status
   • Cold, clammy extremities
   • Oliguria (<0.5 mL/kg/hr)
   • Lactate >2 mmol/L
3. Cardiac index <2.2 L/min/m2 (if measured)
4. PCWP >15 mmHg (if measured)

Epidemiology and Prognosis

• Incidence: 5-10% of STEMI (PMID: 10376614)
• In-hospital mortality: 40-50% despite optimal care
• Timing: 75% present with shock at admission; 25% develop shock after admission

Killip Classification

Landmark Trials

SHOCK Trial (1999)

Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock? (PMID: 10376614)

• 302 patients with STEMI complicated by cardiogenic shock
• Emergency revascularisation (PCI or CABG) vs initial medical stabilisation
• 30-day mortality: 46.7% revascularisation vs 56.0% medical (p=0.11)
• 6-month mortality: 50.3% vs 63.1% (p=0.027)
• 12-month mortality: 46.7% vs 63.1% (p<0.01)

Conclusion: Early revascularisation improves survival at 6-12 months

IABP-SHOCK II Trial (2012)

Intra-Aortic Balloon Pump in Cardiogenic Shock II (PMID: 22920912):

• 600 patients with cardiogenic shock complicating STEMI planned for early revascularisation
• IABP vs no IABP (all received early PCI/CABG)
• 30-day mortality: 39.7% IABP vs 41.3% control (p=0.69)
• 12-month mortality: 52.0% vs 51.0% (p=0.91)
• No difference in secondary outcomes (lactate, renal function, APACHE II)

Conclusion: IABP does not reduce mortality in cardiogenic shock with early revascularisation

Current guideline status: IABP downgraded to Class III (no benefit) in ESC 2023 guidelines

CULPRIT-SHOCK Trial (2017)

Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock (PMID: 28709830):

• 706 patients with STEMI, cardiogenic shock, and multi-vessel disease
• Culprit-lesion-only PCI vs immediate complete revascularisation
• 30-day death or RRT: 45.9% culprit-only vs 55.4% complete (RR 0.83, p=0.01)
• 30-day mortality: 43.3% vs 51.5% (RR 0.84, p=0.03)

Conclusion: Culprit-lesion-only PCI should be the initial strategy in cardiogenic shock

Mechanical Circulatory Support

Intra-Aortic Balloon Pump (IABP)

Mechanism:

• Inflates in diastole → augments coronary and systemic perfusion
• Deflates in systole → reduces afterload
• Net effect: ↑ Cardiac output 0.5-1.0 L/min, ↑ MAP 10-20%

Haemodynamic effects:

• ↑ Diastolic pressure (coronary perfusion)
• ↓ Systolic pressure (afterload reduction)
• ↑ Cardiac output (modest, ~0.5 L/min)
• ↓ PCWP (preload reduction)

Current role: Second-line support; may be useful for:

• Bridge to definitive therapy
• Mechanical complications (MR, VSD)
• Refractory ischaemia
• NOT routine use in cardiogenic shock (IABP-SHOCK II)

Impella

Mechanism:

• Continuous axial flow pump placed across aortic valve
• Actively unloads LV, augments systemic perfusion

Device options:

• Impella CP: 3.7 L/min flow
• Impella 5.0/5.5: 5.0-5.5 L/min flow (requires surgical cutdown)

Evidence:

• IMPRESS Trial (2017) (PMID: 28967483): No mortality benefit over IABP in cardiogenic shock
• Observational data suggests possible benefit in carefully selected patients
• Currently used as escalation from IABP or bridge to ECMO/transplant

VA-ECMO

Mechanism:

• Full cardiopulmonary bypass via peripheral cannulation
• Femoral venous drainage, femoral arterial return

Considerations in STEMI:

• Provides complete circulatory support (up to 6 L/min)
• LV distension is a major concern (LV vent or Impella may be required)
• May reduce myocardial recovery
• Used as bridge to decision, bridge to transplant, or bridge to LVAD

Evidence:

• Limited RCT data; observational studies suggest benefit in refractory shock
• ECMO-CS Trial (ongoing): May provide definitive evidence

Management Algorithm for Cardiogenic Shock in STEMI

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Arrhythmias in STEMI

Overview

Arrhythmias are common in STEMI and range from benign to immediately life-threatening (PMID: 33085966):

• Ventricular fibrillation (VF): 5-10% of STEMI (80% within first 4 hours)
• Ventricular tachycardia (VT): 5-10%
• High-degree AV block: 5-10% (more common in inferior STEMI)
• Atrial fibrillation: 10-20%

Ventricular Fibrillation and Ventricular Tachycardia

Primary VF (Within 48 Hours)

Pathophysiology:

• Acute ischaemia creates electrical instability
• Re-entry circuits around infarct border zone
• Electrolyte imbalances (hypokalaemia, hypomagnesaemia)

Management:

• Immediate defibrillation (biphasic 150-200 J, or maximum monophasic)
• Correct electrolytes: K+ >4.0 mmol/L, Mg2+ >1.0 mmol/L
• IV amiodarone: 300 mg bolus for recurrent VF/VT
• IV lignocaine: Alternative if amiodarone contraindicated
• Beta-blockers: Reduce recurrence (IV metoprolol 5 mg x3)

Prognosis of primary VF:

• Increased in-hospital mortality
• No increased long-term mortality if revascularised (primary VF is marker of large infarct, not independent arrhythmic substrate)
• ICD NOT routinely indicated for primary VF (differs from late VF)

Late VF (>48 Hours)

Significance:

• Represents development of arrhythmogenic substrate (scar, re-entry)
• Higher long-term sudden death risk
• ICD indicated if LVEF ≤35% at 6-12 weeks post-MI (MADIT-II, SCD-HeFT) (PMID: 11907286, PMID: 15659722)

Bradyarrhythmias and AV Block

Inferior STEMI and AV Block

Pathophysiology:

• RCA supplies AV node in 90% of patients
• AV nodal ischaemia or increased vagal tone

Features:

• Narrow QRS escape rhythm (junctional)
• Often transient (resolves with reperfusion)
• Usually haemodynamically tolerated

Management:

• Atropine 0.5-1 mg IV (first-line for symptomatic bradycardia)
• Temporary pacing: If haemodynamically unstable or no response to atropine
• Permanent pacing rarely required (most resolve within 2-3 weeks)

Anterior STEMI and AV Block

Pathophysiology:

• Extensive septal necrosis involving His bundle and bundle branches
• Indicates large infarct size

Features:

• Wide QRS escape rhythm (ventricular)
• Often high-grade block (Mobitz II, complete heart block)
• Higher mortality (marker of extensive infarction)

Management:

• Temporary pacing: Usually required (unstable escape rhythm)
• Permanent pacing: May be required if persists >2-3 weeks
• Poor prognosis overall (reflects extensive myocardial damage)

Temporary Pacing Indications in STEMI

Class I indications (ACC/AHA):

• Asystole
• Symptomatic bradycardia unresponsive to atropine
• Bilateral bundle branch block (alternating BBB or RBBB + LAFB or LPFB)
• New bifascicular block with first-degree AV block
• Mobitz II second-degree AV block

Techniques:

• Transcutaneous pacing: Immediate bridge
• Transvenous pacing: Via internal jugular or femoral vein
• External pacing pads: Applied prophylactically if high-risk conduction disturbance

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Right Ventricular Infarction

Pathophysiology

Right ventricular infarction occurs in 30-50% of inferior STEMI (RCA occlusion proximal to RV branches) (PMID: 9362391):

Haemodynamic consequences:

• RV contractile dysfunction → reduced RV output
• Decreased LV preload (RV cannot deliver adequate blood to left heart)
• Interventricular septal shift (further impairs LV filling)
• Preload-dependent state: Cardiac output highly sensitive to filling pressures

Clinical Features

Classic triad (present in 25% of cases):

1. Hypotension
2. Elevated JVP (Kussmaul's sign may be present)
3. Clear lung fields

Other features:

• Right-sided heart failure signs (peripheral oedema, hepatomegaly)
• Severe hypotension with nitrate or diuretic administration
• High-degree AV block (common with proximal RCA occlusion)

Diagnosis

ECG:

• Inferior STEMI (II, III, aVF)
• Right-sided leads (V4R): ST elevation ≥1 mm (95% sensitive, 83% specific)
• ST elevation in III > II (suggests RCA rather than LCx)

Echocardiography:

• RV dilation
• RV free wall hypokinesis
• Paradoxical septal motion
• TAPSE <17 mm (RV longitudinal dysfunction)

Management

Prognosis:

• Higher in-hospital mortality (26% vs 13% inferior STEMI without RV involvement)
• RV function usually recovers with reperfusion (unlike LV)
• Mechanical support rarely required if reperfusion achieved

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Australian and New Zealand Context

CSANZ Guidelines

The Cardiac Society of Australia and New Zealand (CSANZ) Guidelines for Management of Acute Coronary Syndromes align with international guidelines with specific local considerations (CSANZ ACS Guidelines 2020):

1. Primary PCI is the preferred reperfusion strategy in centres with 24/7 capability
2. Pharmaco-invasive strategy is appropriate for remote/rural patients
3. State-based STEMI networks coordinate care (e.g., NSW STEMI Network, Victoria Cardiac Clinical Network)

Remote STEMI Management

Unique Australian challenges:

1. Vast geography: Patients may be >1,000 km from PCI-capable centre
2. Royal Flying Doctor Service (RFDS): Critical role in retrieval and pre-hospital care
3. Telemedicine: ECG transmission, cardiologist consultation
4. Pre-hospital fibrinolysis: Paramedic or nurse-administered tenecteplase with telemedicine support
5. Retrieval coordination: State retrieval services (e.g., Ambulance Victoria MICA, NSW Ambulance retrieval)

Pharmaco-invasive pathway in remote Australia:

1. Pre-hospital or ED fibrinolysis (tenecteplase)
2. Antiplatelet therapy (aspirin + clopidogrel)
3. Anticoagulation (enoxaparin or UFH)
4. RFDS or road retrieval to PCI-capable centre
5. Routine angiography within 2-24 hours
6. Rescue PCI if fibrinolysis fails (ST resolution <50%)

Indigenous Health Considerations

Aboriginal and Torres Strait Islander populations have significantly higher cardiovascular disease burden (PMID: 27899300):

Epidemiology:

• 2-3× higher IHD mortality rates
• Younger age at first MI (10-15 years earlier than non-Indigenous Australians)
• Higher rates of risk factors (diabetes, smoking, hypertension)

Barriers to care:

• Geographic remoteness
• Delayed presentation
• Cultural factors affecting healthcare engagement
• Lower rates of revascularisation procedures

Cultural considerations:

• Involve Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs)
• Extended family involvement in decision-making
• Sorry Business protocols (may affect family availability)
• Culturally safe communication
• Men's and women's business considerations
• Respect for Country and connection to land

Māori health considerations (New Zealand):

• Higher cardiovascular disease rates
• Whānau (extended family) involvement in care
• Tikanga (cultural protocols) respect
• Te Tiriti o Waitangi obligations
• Māori Health Workers involvement

State Retrieval Services

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SAQ Practice Questions

SAQ 1: STEMI Reperfusion and Complications (15 Marks)

SAQ: Question:

A 58-year-old man presents to a rural emergency department 90 minutes from the nearest PCI-capable hospital with 2 hours of crushing chest pain and diaphoresis. His ECG shows ST-elevation in leads II, III, aVF, and V4R.

a) Describe the immediate management priorities including reperfusion strategy decision-making. (5 marks)

b) On day 4 post-admission to ICU following successful fibrinolysis and angiography, the patient develops sudden hypotension (BP 70/50 mmHg), a new harsh holosystolic murmur, and pulmonary oedema. Discuss the differential diagnosis and immediate investigations. (5 marks)

c) The echocardiogram confirms a ventricular septal defect. Outline the management approach. (5 marks)

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Model Answer:

a) Immediate management priorities (5 marks):

ECG interpretation (1 mark):

• Inferior STEMI (ST elevation II, III, aVF)
• Right ventricular involvement (ST elevation V4R)
• Likely proximal RCA occlusion

Reperfusion decision (2 marks):

• 90 minutes transfer time = 180+ minutes door-to-balloon (unacceptable delay)
• Presentation <3 hours = maximum fibrinolysis benefit window
• Decision: Fibrinolysis with pharmaco-invasive approach
  • Tenecteplase 0.5 mg/kg single IV bolus (weight-based, max 50 mg)
  • Transfer for routine angiography within 2-24 hours
  • Rescue PCI if ST resolution <50% at 60-90 minutes

Adjunctive therapy (1 mark):

• Aspirin 300 mg
• Clopidogrel 300 mg (or 75 mg if >75 years) - use clopidogrel not ticagrelor with fibrinolysis
• Enoxaparin 30 mg IV bolus then 1 mg/kg SC BD

RV infarction considerations (1 mark):

• Avoid nitrates (preload-dependent state)
• Cautious fluid resuscitation if hypotensive
• Avoid diuretics

b) Day 4 deterioration differential and investigations (5 marks):

Differential diagnosis of acute deterioration day 3-7 (2 marks):

1. Mechanical complications:
   • Ventricular septal defect (VSD) - most likely given new murmur
   • Papillary muscle rupture with acute MR
   • Free wall rupture with tamponade
2. Reinfarction (stent thrombosis or other vessel)
3. Pulmonary embolism
4. Infection/sepsis

Immediate investigations (3 marks):

c) VSD management (5 marks):

Immediate stabilisation (2 marks):

• Vasodilator therapy (nitroprusside if tolerated) - reduces afterload, decreases shunt
• IABP insertion - reduces afterload, augments coronary perfusion
• Inotropic support (dobutamine/noradrenaline) for cardiogenic shock
• Diuretics for pulmonary oedema (cautiously)

Mechanical circulatory support (1 mark):

• VA-ECMO as bridge to surgery in refractory shock
• Impella less useful (does not address shunt)

Definitive management (2 marks):

• Surgical repair remains standard of care
• Urgent surgery recommended despite high operative mortality (40-50%)
• Controversy regarding timing: Some advocate delaying 2-4 weeks if patient stabilises (allows tissue healing, better surgical repair)
• Percutaneous closure: Considered for anatomically suitable defects but limited centres and expertise

Prognosis:

• Medical management mortality: 80-90%
• Surgical mortality: 40-50%
• Post-surgical survival improves with each passing day

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SAQ 2: Cardiogenic Shock Management (15 Marks)

SAQ: Question:

A 62-year-old woman presents with anterior STEMI (ST elevation V1-V6, I, aVL). After successful primary PCI to proximal LAD, she remains hypotensive (SBP 85 mmHg) on noradrenaline 0.3 μg/kg/min with lactate 4.5 mmol/L.

a) Define cardiogenic shock and describe the haemodynamic profile. (3 marks)

b) Outline the key evidence from landmark trials that should guide management decisions (SHOCK, IABP-SHOCK II, CULPRIT-SHOCK). (6 marks)

c) The patient deteriorates despite maximal medical therapy. Discuss mechanical circulatory support options and their evidence base. (6 marks)

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Model Answer:

a) Definition and haemodynamic profile (3 marks):

Definition (1 mark): Cardiogenic shock is a state of critical tissue hypoperfusion due to primary cardiac dysfunction, defined by:

• SBP <90 mmHg for >30 minutes OR vasopressor requirement
• Evidence of end-organ hypoperfusion (oliguria, altered mental status, cool extremities, lactate >2 mmol/L)

Haemodynamic profile (2 marks):

b) Landmark trial evidence (6 marks):

SHOCK Trial (1999) (2 marks):

• RCT of 302 patients with STEMI + cardiogenic shock
• Early revascularisation (PCI/CABG within 6h) vs initial medical stabilisation
• 30-day mortality: 46.7% vs 56.0% (NS)
• 6-month mortality: 50.3% vs 63.1% (p=0.027)
• Implication: Early revascularisation improves survival - foundational evidence

IABP-SHOCK II Trial (2012) (2 marks):

• RCT of 600 patients with cardiogenic shock and planned early revascularisation
• IABP vs no IABP (all received early PCI/CABG)
• 30-day mortality: 39.7% vs 41.3% (p=0.69) - NO DIFFERENCE
• 12-month mortality: No difference
• Implication: IABP provides no mortality benefit; downgraded in guidelines

CULPRIT-SHOCK Trial (2017) (2 marks):

• RCT of 706 patients with cardiogenic shock + multi-vessel disease
• Culprit-only PCI vs immediate complete revascularisation
• 30-day death or RRT: 45.9% vs 55.4% (p=0.01)
• 30-day mortality: 43.3% vs 51.5% (p=0.03)
• Implication: Culprit-lesion-only PCI should be initial strategy in cardiogenic shock

c) Mechanical circulatory support options (6 marks):

IABP (1 mark):

• Counterpulsation device: diastolic augmentation + systolic unloading
• Flow augmentation ~0.5 L/min (modest)
• Limited role given IABP-SHOCK II results
• May still consider for mechanical complications, refractory ischaemia

Impella (2 marks):

• Continuous axial flow pump across aortic valve
• Impella CP provides up to 3.7 L/min support
• Actively unloads LV (reduces LVEDP, wall stress, oxygen demand)
• Evidence:
  • "IMPRESS Trial (2017): No mortality benefit vs IABP in cardiogenic shock"
  • Observational data suggests possible benefit; active area of research
• Role: Escalation from IABP, bridge to ECMO/LVAD/transplant

VA-ECMO (2 marks):

• Full cardiopulmonary bypass via peripheral cannulation
• Provides complete circulatory support (up to 6 L/min)
• Concerns:
  • LV distension (may require venting with Impella or surgical vent)
  • Increased afterload may impair LV recovery
  • Anticoagulation requirements
• Role: Refractory shock, bridge to decision

Selection and escalation (1 mark):

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Hot Case Scenarios

Hot Case 1: Post-STEMI Day 4 with New Murmur

Case Study: Scenario:

You are called to assess a 67-year-old man on day 4 post-anterior STEMI treated with primary PCI. He has developed sudden hypotension (BP 75/50 mmHg), tachycardia (HR 120), and the nurse has noted a new loud murmur.

Examination Findings:

• Alert but pale, diaphoretic, peripherally cool
• JVP elevated to earlobes
• BP 75/50, HR 120, RR 30, SpO2 88% on 6L O2
• Harsh grade 4/6 holosystolic murmur at left lower sternal border with thrill
• Bilateral coarse crackles to mid-zones
• Noradrenaline 0.2 μg/kg/min running

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Examiner-Candidate Dialogue:

Examiner: This is day 4 of a 67-year-old man's ICU admission following anterior STEMI and primary PCI. The nurse has called you urgently because of sudden deterioration. Please examine the patient and talk me through your findings.

Candidate: [Approaches bedside, assesses safety] I can see the patient appears unwell - pale, diaphoretic, and in respiratory distress. Looking at the monitors, I note BP 75/50, HR 120 in sinus rhythm, RR 30, and SpO2 88% on 6 litres oxygen.

Candidate: [Examines patient systematically] On cardiovascular examination:

• JVP is elevated to the earlobes
• Apex beat is displaced laterally
• I can hear a harsh grade 4/6 holosystolic murmur loudest at the left lower sternal border with a palpable thrill
• There is bilateral pulmonary oedema with coarse crackles to the mid-zones
• Peripherally, the patient is cool with delayed capillary refill

Examiner: What is your differential diagnosis for this sudden deterioration?

Candidate: Given day 4 post-anterior STEMI with sudden haemodynamic collapse, new holosystolic murmur, and biventricular failure, my primary concern is a mechanical complication:

1. Ventricular septal defect (VSD) - most likely given harsh murmur at LLSB with thrill, biventricular failure
2. Papillary muscle rupture with acute severe MR - murmur may radiate to axilla
3. Free wall rupture with contained pseudoaneurysm - usually more dramatic presentation

Secondary considerations:

• Acute stent thrombosis with reinfarction
• New arrhythmia

Examiner: How would you confirm your diagnosis urgently?

Candidate: I would arrange urgent bedside echocardiography as the first-line investigation:

• Visualise the ventricular septum for defect
• Colour Doppler to identify left-to-right shunt
• Assess LV and RV function
• Exclude papillary muscle rupture and pericardial effusion

If PA catheter available, I would look for oxygen step-up from RA to PA (Qp:Qs >2 indicates significant shunt).

Examiner: The echo confirms a 1.5 cm VSD in the mid-septum with significant left-to-right shunt. How would you manage this patient?

Candidate: This is a surgical emergency. My management would include:

Immediate stabilisation:

1. Increase noradrenaline to maintain MAP >60 mmHg
2. Consider inotrope addition (dobutamine) for inotropy
3. Afterload reduction if BP permits - vasodilators reduce shunt fraction
4. Urgent IABP insertion - reduces afterload, augments coronary perfusion

Respiratory support:

• Increase oxygen delivery
• Consider NIV or intubation for respiratory failure

Escalation:

• If refractory shock: VA-ECMO as bridge to surgery

Definitive treatment:

• Urgent cardiothoracic surgery consultation
• Surgical VSD repair (patch closure)
• High operative mortality (40-50%) but far exceeds medical management (80-90% mortality)

Examiner: Would you delay surgery to allow tissue healing?

Candidate: This is controversial. While operating on friable, necrotic myocardium is technically challenging and associated with high failure rates, delaying surgery in unstable patients significantly increases mortality.

My approach would be:

• Unstable patient (like this case): Urgent surgery with mechanical support as bridge
• Stable patient on medical therapy: Some centres advocate waiting 2-4 weeks for tissue consolidation

Given this patient's cardiogenic shock, I would advocate for urgent surgical repair.

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Hot Case 2: RV Infarction with Hypotension

Case Study: Scenario:

A 54-year-old man is admitted to ICU following primary PCI for inferior STEMI. He is hypotensive (BP 80/55 mmHg) despite 2 litres of crystalloid resuscitation. Heart rate is 48 bpm with complete heart block on monitor.

Examination Findings:

• Drowsy but rousable
• JVP elevated to angle of jaw, Kussmaul's sign present
• BP 80/55, HR 48 (complete heart block), RR 22, SpO2 94% on 2L O2
• Heart sounds dual, no murmurs
• Lung fields clear
• Peripheral oedema to ankles

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Examiner-Candidate Dialogue:

Examiner: This is a 54-year-old man admitted following primary PCI for inferior STEMI. He remains hypotensive. Please assess and manage.

Candidate: [Systematic assessment] This patient has the classic triad of right ventricular infarction:

1. Hypotension (BP 80/55)
2. Elevated JVP with Kussmaul's sign (paradoxical rise with inspiration)
3. Clear lung fields

Additionally, he has complete heart block at 48 bpm - common with proximal RCA occlusion affecting the AV node.

Examiner: What is the pathophysiology of his hypotension?

Candidate: Right ventricular infarction creates a preload-dependent state:

1. RV contractile dysfunction reduces RV output
2. Reduced blood delivery to the left ventricle
3. LV underfilling despite elevated right-sided pressures
4. Reduced cardiac output and hypotension

The complete heart block further impairs cardiac output by:

• Loss of atrial contribution to ventricular filling (critical in stiff RV)
• Bradycardia reducing cardiac output (CO = SV × HR)

Examiner: How would you manage his haemodynamics?

Candidate: Key principles for RV infarction:

AVOID:

• Nitrates - will reduce preload and worsen hypotension
• Aggressive diuresis - reduces preload
• High PEEP if ventilated - reduces venous return

OPTIMISE:

1. Fluid resuscitation (cautious):

   • Further 250-500 mL crystalloid boluses
   • Monitor response - RV may reach plateau on Starling curve
   • Excessive fluid may worsen RV dilation and septal shift

2. Address bradycardia/heart block:

   • Atropine 0.5-1 mg IV (may not work in complete block)
   • Temporary pacing - ventricular or ideally AV sequential (preserve atrial kick)
   • Target HR 70-90

3. Inotropic support:

   • If no response to fluids and pacing
   • Dobutamine first-line (inotropy without excessive vasoconstriction)
   • Noradrenaline if significant hypotension persists

Examiner: He remains hypotensive despite fluids. Lactate is 3.5 mmol/L. What now?

Candidate: This represents cardiogenic shock from RV failure. I would:

1. Insert temporary pacing wire immediately for AV sequential pacing
2. Start dobutamine 2.5-5 μg/kg/min for inotropy
3. Add noradrenaline if MAP remains <65 mmHg
4. Review angiography - ensure complete revascularisation of RV branches
5. Consider inhaled pulmonary vasodilator (milrinone or nitric oxide) to reduce RV afterload

If refractory, mechanical support options for isolated RV failure:

• RVAD (right ventricular assist device)
• VA-ECMO (provides biventricular support)

Examiner: The cardiologist asks about prognosis for RV infarction.

Candidate: Compared to inferior STEMI without RV involvement:

• Higher in-hospital mortality (26% vs 13%)
• Higher rate of major complications

However, RV function typically recovers well with successful reperfusion:

• RV myocardium is more resistant to ischaemia (lower oxygen demand, collaterals)
• Most patients regain normal RV function
• Long-term prognosis good if they survive the acute phase

The complete heart block usually resolves within 2-3 weeks with RCA reperfusion. Permanent pacing is rarely required.

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Viva Scenarios

Viva 1: Reperfusion Strategy in STEMI

Viva: Scenario:

You are the ICU registrar consulted by ED regarding a 52-year-old man with 1 hour of chest pain and ST elevation in V1-V4. Your hospital does not have a 24/7 cath lab but can transfer to a PCI centre 90 minutes away.

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Examiner-Candidate Dialogue:

Examiner: Tell me about your approach to this patient.

Candidate: This is an anterior STEMI with presentation within 1 hour of symptom onset. My priorities are:

1. Confirm the diagnosis (ECG, brief history/examination)
2. Initiate antiplatelet and anticoagulation therapy
3. Decide on reperfusion strategy

Examiner: How do you decide between PCI and fibrinolysis?

Candidate: The key decision is based on expected time to reperfusion:

Primary PCI preferred if:

• Door-to-balloon time ≤90 minutes (PCI-capable centre)
• Or ≤120 minutes including transfer time

Fibrinolysis preferred if:

• Expected PCI delay >120 minutes
• Presentation <3 hours (maximum fibrinolysis benefit window)
• No absolute contraindications

For this patient:

• 90 minutes transfer + logistics = likely >120 minutes to balloon
• 1 hour symptom duration = within optimal fibrinolysis window
• I would recommend fibrinolysis with pharmaco-invasive strategy

Examiner: What does the pharmaco-invasive strategy involve?

Candidate: The pharmaco-invasive approach combines:

1. Immediate fibrinolysis in the ED
2. Routine transfer to PCI centre
3. Angiography within 2-24 hours (regardless of fibrinolysis success)
4. Rescue PCI immediately if fibrinolysis fails

Evidence from STREAM trial (2013) showed this approach is non-inferior to primary PCI when transfer delays exceed 120 minutes.

Examiner: What fibrinolytic agent would you use and what adjunctive therapy?

Candidate: Tenecteplase (TNK) is preferred:

• Single weight-based IV bolus (0.5 mg/kg, max 50 mg)
• Fibrin-specific with long half-life
• Simple to administer (single bolus vs infusion)

Adjunctive therapy:

• Aspirin 300 mg (chewed)
• Clopidogrel 300 mg (or 75 mg if >75 years) - NOT ticagrelor/prasugrel with fibrinolysis
• Enoxaparin: 30 mg IV bolus then 1 mg/kg SC BD (or UFH infusion)

Examiner: How do you assess whether fibrinolysis has worked?

Candidate: I assess ST-segment resolution at 60-90 minutes post-fibrinolysis:

Other signs of reperfusion:

• Resolution of chest pain
• Reperfusion arrhythmias (AIVR, VPCs)
• Early peak of troponin

The REACT trial showed rescue PCI significantly reduces death/reinfarction/stroke/heart failure compared to conservative management after failed fibrinolysis.

Examiner: What are the contraindications to fibrinolysis?

Candidate: Absolute contraindications:

• Prior intracranial haemorrhage
• Known structural cerebral vascular lesion or malignancy
• Ischaemic stroke within 3 months
• Suspected aortic dissection
• Active bleeding (excluding menses)
• Significant closed head trauma within 3 months

Relative contraindications:

• Uncontrolled hypertension (SBP >180, DBP >110)
• Prolonged CPR (>10 minutes)
• Recent internal bleeding (2-4 weeks)
• Pregnancy
• Current anticoagulation (INR >2)

For elderly patients (≥75 years), STREAM trial showed increased intracranial haemorrhage risk, so half-dose tenecteplase is now recommended.

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Viva 2: Mechanical Circulatory Support in Cardiogenic Shock

Viva: Scenario:

A 58-year-old woman is in cardiogenic shock post-anterior STEMI. Despite primary PCI restoring TIMI 3 flow and noradrenaline 0.4 μg/kg/min + dobutamine 10 μg/kg/min, she remains hypotensive with rising lactate.

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Examiner-Candidate Dialogue:

Examiner: She has refractory cardiogenic shock. What mechanical circulatory support options are available?

Candidate: The main options for mechanical circulatory support (MCS) in cardiogenic shock are:

1. Intra-Aortic Balloon Pump (IABP)
2. Impella (Impella CP, 5.0/5.5)
3. VA-ECMO (Veno-Arterial Extracorporeal Membrane Oxygenation)
4. TandemHeart (rarely used)

Examiner: What is the evidence for IABP in cardiogenic shock?

Candidate: The IABP-SHOCK II trial (2012) is the definitive evidence:

• 600 patients with cardiogenic shock and planned early revascularisation
• Randomised to IABP vs no IABP
• No difference in 30-day mortality (39.7% vs 41.3%, p=0.69)
• No difference at 12 months or in secondary outcomes

This led to IABP being downgraded to Class III (no benefit) in ESC 2023 guidelines for routine use in cardiogenic shock.

IABP may still have a role:

• Mechanical complications (VSD, acute MR)
• Refractory ischaemia
• As bridge in lower-resource settings

Examiner: What about Impella?

Candidate: Impella is an axial flow pump that actively unloads the left ventricle:

Advantages:

• Continuous flow (unlike IABP which is pulsatile)
• Actively unloads LV (reduces LVEDP, wall stress)
• Greater cardiac output augmentation (up to 5.5 L/min with Impella 5.0)

Evidence:

• IMPRESS trial (2017): 48 patients with cardiogenic shock + STEMI
• Impella CP vs IABP: No difference in 30-day mortality (46% vs 50%, p=0.92)
• Observational studies suggest possible benefit

Currently used for:

• Escalation after IABP failure
• Bridge to ECMO, LVAD, or transplant
• High-risk PCI (prophylactic)

Examiner: When would you consider VA-ECMO?

Candidate: VA-ECMO provides complete cardiopulmonary support and is indicated for:

1. Refractory cardiogenic shock not responding to inotropes + IABP/Impella
2. Cardiac arrest with potential for recovery (ECPR)
3. Bridge to decision - allows assessment of neurological status, recovery potential
4. Bridge to LVAD or transplant evaluation

Important considerations:

LV distension:

• VA-ECMO increases afterload on a failing LV
• Can cause LV distension and impair recovery
• May require LV venting with Impella or surgical vent

Technical aspects:

• Peripheral cannulation (femoral vein → femoral artery)
• Anticoagulation requirements
• Limb ischaemia risk (may need distal perfusion cannula)

Examiner: How do you decide which MCS device to use?

Candidate: My approach would be based on:

SCAI Shock Classification (Stages A-E):

• Stage C-D: Consider IABP → Impella escalation
• Stage D-E (deteriorating): VA-ECMO

Practical algorithm:

Examiner: What is the goal of MCS in this context?

Candidate: The goals are:

1. Restore end-organ perfusion - break the shock spiral
2. Unload the ventricle - reduce myocardial oxygen demand, allow recovery
3. Buy time - for myocardial recovery, assessment, or definitive therapy

Bridge options:

• Bridge to recovery (stunning resolves)
• Bridge to decision (assess prognosis, neurological status)
• Bridge to LVAD (long-term mechanical support)
• Bridge to transplant (definitive therapy)

For this patient in refractory shock despite maximal medical therapy, I would advocate for escalation to VA-ECMO with Impella for LV venting, with early discussion regarding transplant evaluation if recovery does not occur.

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Z guidelines, what is the preferred reperfusion strategy in remote Australia when PCI will be significantly delayed?

• Back: Pre-hospital or ED fibrinolysis (tenecteplase) with transfer for routine angiography within 2-24 hours (pharmaco-invasive strategy)

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References

Primary Guidelines

1. Lawton JS, Tamis-Holland JE, Bangalore S, et al. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the ACC/AHA Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(4):e18-e114. PMID: 34882435

2. Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the Management of Acute Coronary Syndromes. Eur Heart J. 2023;44(38):3720-3826. PMID: 37622654

3. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018;138(20):e618-e651. PMID: 30153967

Landmark Trials

4. Hochman JS, Sleeper LA, Webb JG, et al. Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock. SHOCK Investigators. N Engl J Med. 1999;341(9):625-634. PMID: 10376614

5. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock. N Engl J Med. 2012;367(14):1287-1296. PMID: 22920912

6. Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419-2432. PMID: 28709830

7. 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: 23474507

8. Andersen HR, Nielsen TT, Rasmussen K, et al. A Comparison of Coronary Angioplasty with Fibrinolytic Therapy in Acute Myocardial Infarction (DANAMI-2). N Engl J Med. 2003;349(8):733-742. PMID: 12928468

9. Cantor WJ, Fitchett D, Borgundvaag B, et al. Routine Early Angioplasty after Fibrinolysis for Acute Myocardial Infarction (TRANSFER-AMI). N Engl J Med. 2009;360(26):2705-2718. PMID: 19188507

10. Widimský P, Budesínský T, Vorác D, et al. Long Distance Transport for Primary Angioplasty vs Immediate Thrombolysis in Acute Myocardial Infarction (PRAGUE-2). Eur Heart J. 2003;24(1):94-104. PMID: 14604230

Antiplatelet and Anticoagulation

11. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes (PLATO). N Engl J Med. 2009;361(11):1045-1057. PMID: 19717846

12. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus Clopidogrel in Patients with Acute Coronary Syndromes (TRITON-TIMI 38). N Engl J Med. 2007;357(20):2001-2015. PMID: 17982182

13. Antman EM, Morrow DA, McCabe CH, et al. Enoxaparin versus Unfractionated Heparin with Fibrinolysis for ST-Elevation Myocardial Infarction (ExTRACT-TIMI 25). N Engl J Med. 2006;354(14):1477-1488. PMID: 16533938

14. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised Trial of Intravenous Streptokinase, Oral Aspirin, Both, or Neither Among 17,187 Cases of Suspected Acute Myocardial Infarction. Lancet. 1988;2(8607):349-360. PMID: 2899772

Reperfusion and Timing

15. De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time Delay to Treatment and Mortality in Primary Angioplasty for Acute Myocardial Infarction: Every Minute of Delay Counts. Circulation. 2004;109(10):1223-1225. PMID: 16418451

16. Gershlick AH, Stephens-Lloyd A, Hughes S, et al. Rescue Angioplasty after Failed Thrombolytic Therapy for Acute Myocardial Infarction (REACT). N Engl J Med. 2005;353(26):2758-2768. PMID: 16043645

17. Sutton AG, Campbell PG, Graham R, et al. A Randomized Trial of Rescue Angioplasty versus a Conservative Approach for Failed Fibrinolysis in ST-Segment Elevation Myocardial Infarction: The Middlesbrough Early Revascularization to Limit INfarction (MERLIN) Trial. J Am Coll Cardiol. 2004;44(2):287-296. PMID: 15007158

Mechanical Complications

18. Menon V, Webb JG, Hillis LD, et al. Outcome and Profile of Ventricular Septal Rupture with Cardiogenic Shock after Myocardial Infarction: A Report from the SHOCK Trial Registry. J Am Coll Cardiol. 2000;36(3 Suppl A):1110-1116. PMID: 10377087

19. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk Factors, Angiographic Patterns, and Outcomes in Patients with Ventricular Septal Defect Complicating Acute Myocardial Infarction. GUSTO-I Trial Investigators. Circulation. 2000;101(1):27-32. PMID: 10618300

Mechanical Circulatory Support

20. Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction (IMPRESS). J Am Coll Cardiol. 2017;69(3):278-287. PMID: 28668636

21. Thiele H, Sick P, Boudriot E, et al. Randomized Comparison of Intra-Aortic Balloon Support with a Percutaneous Left Ventricular Assist Device in Patients with Revascularized Acute Myocardial Infarction Complicated by Cardiogenic Shock. Eur Heart J. 2005;26(13):1276-1283. PMID: 15734770

Right Ventricular Infarction

22. Dell'Italia LJ. Reperfusion for Right Ventricular Infarction. N Engl J Med. 1998;338(14):978-980. PMID: 9521987

23. Ondrus T, Kanovsky J, Novotny T, et al. Right Ventricular Myocardial Infarction: From Pathophysiology to Prognosis. Exp Clin Cardiol. 2013;18(1):27-30. PMID: 24294033

24. Kinch JW, Ryan TJ. Right Ventricular Infarction. N Engl J Med. 1994;330(17):1211-1217. PMID: 9362391

STEMI Equivalents

25. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. GUSTO-1 Investigators. N Engl J Med. 1996;334(8):481-487. PMID: 8559200

26. de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA. A New ECG Sign of Proximal LAD Occlusion. N Engl J Med. 2008;359(19):2071-2073. PMID: 19081386

27. Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients with Acute Coronary Syndromes Presenting with Isolated Anterior ST-Segment Depression: A TRITON-TIMI 38 Substudy. JACC Cardiovasc Interv. 2010;3(8):806-811. PMID: 20723851

28. Wellens HJ, Gorgels A, Doevendans PA. The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk Stratification. Boston: Kluwer Academic Publishers; 2003.

Pathophysiology

29. Libby P. Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. N Engl J Med. 2013;368(21):2004-2013. PMID: 23697515

30. Davies MJ. The Pathophysiology of Acute Coronary Syndromes. Heart. 2000;83(3):361-366. PMID: 10677422

31. Falk E, Shah PK, Fuster V. Coronary Plaque Disruption. Circulation. 1995;92(3):657-671. PMID: 10334431

32. 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: 6681009

33. Hausenloy DJ, Yellon DM. Myocardial Ischemia-Reperfusion Injury: A Neglected Therapeutic Target. J Clin Invest. 2013;123(1):92-100. PMID: 23281415

34. Yellon DM, Hausenloy DJ. Myocardial Reperfusion Injury. N Engl J Med. 2007;357(11):1121-1135. PMID: 17855673

Arrhythmias

35. Mehta RH, Starr AZ, Lopes RD, et al. Incidence of and Outcomes Associated with Ventricular Tachycardia or Fibrillation in Patients Undergoing Primary Percutaneous Coronary Intervention. JAMA. 2009;301(17):1779-1789. PMID: 19417195

36. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic Implantation of a Defibrillator in Patients with Myocardial Infarction and Reduced Ejection Fraction (MADIT-II). N Engl J Med. 2002;346(12):877-883. PMID: 11907286

37. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an Implantable Cardioverter-Defibrillator for Congestive Heart Failure (SCD-HeFT). N Engl J Med. 2005;352(3):225-237. PMID: 15659722

Complete Revascularisation

38. Mehta SR, Wood DA, Storey RF, et al. Complete Revascularization with Multivessel PCI for Myocardial Infarction (COMPLETE). N Engl J Med. 2019;381(15):1411-1421. PMID: 31475799

Oxygen Therapy

39. Hofmann R, James SK, Jernberg T, et al. Oxygen Therapy in Suspected Acute Myocardial Infarction (DETO2X-AMI). N Engl J Med. 2017;377(13):1240-1249. PMID: 28041950

Australian/Indigenous Context

40. Brown A, O'Shea RL, Mott K, et al. A Strategy for Translating Evidence into Policy and Practice to Close the Gap—Developing National Recommendations for Cardiovascular Disease. Heart Lung Circ. 2015;24(2):119-125. PMID: 25453877

41. Cunningham J, O'Dea K, Dunbar T, et al. Socioeconomic Status and Diabetes Among Urban Indigenous Australians aged 15-64 Years in the DRUID Study. Ethn Health. 2008;13(1):23-37. PMID: 18066736

42. Bradshaw PJ, Alfonso HS, Finn J, et al. A Comparison of Coronary Heart Disease Event Rates Among Urban Australian Aboriginal People and a Matched Non-Aboriginal Population. J Epidemiol Community Health. 2011;65(4):315-319. PMID: 20682624

Biomarkers

43. Thygesen K, Mair J, Katus H, et al. Recommendations for the Use of Cardiac Troponin Measurement in Acute Cardiac Care. Eur Heart J. 2010;31(18):2197-2204. PMID: 20685679

Fibrinolysis

44. Van de Werf F, Bax J, Betriu A, et al. Management of Acute Myocardial Infarction in Patients Presenting with Persistent ST-Segment Elevation. Eur Heart J. 2008;29(23):2909-2945. PMID: 19004841

45. 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. Lancet. 1999;354(9180):716-722. PMID: 10475181

No-Reflow

46. Ndrepepa G, Tiroch K, Fusaro M, et al. 5-Year Prognostic Value of No-Reflow Phenomenon after Percutaneous Coronary Intervention in Patients with Acute Myocardial Infarction. J Am Coll Cardiol. 2010;55(21):2383-2389. PMID: 20488311

Posterior MI

47. Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST Segment Elevations in Posterior Chest Leads (V7 to V9) in Patients with Acute Inferior Myocardial Infarction: Application for Thrombolytic Therapy. J Am Coll Cardiol. 1998;31(3):506-511. PMID: 9502627

48. Wung SF, Drew BJ. New Electrocardiographic Criteria for Posterior Wall Acute Myocardial Ischemia Validated by a Percutaneous Transluminal Coronary Angioplasty Model of Acute Myocardial Infarction. Am J Cardiol. 2001;87(8):970-974. PMID: 11305989

Killip Classification

49. Khot UN, Jia G, Moliterno DJ, et al. Prognostic Importance of Physical Examination for Heart Failure in Non-ST-Elevation Acute Coronary Syndromes: The Enduring Value of Killip Classification. JAMA. 2003;290(16):2174-2181. PMID: 14570953

Cardiogenic Shock Definition

50. Baran DA, Grines CL, Bailey S, et al. SCAI Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock. Catheter Cardiovasc Interv. 2019;94(1):29-37. PMID: 30946527

Radial Access

51. Jolly SS, Yusuf S, Cairns J, et al. Radial versus Femoral Access for Coronary Angiography and Intervention in Patients with Acute Coronary Syndromes (RIVAL). Lancet. 2011;377(9775):1409-1420. PMID: 21470671

52. Valgimigli M, Gagnor A, Calabró P, et al. Radial versus Femoral Access in Patients with Acute Coronary Syndromes Undergoing Invasive Management (MATRIX). Lancet. 2015;385(9986):2465-2476. PMID: 25791214

Thrombectomy

53. Jolly SS, Cairns JA, Yusuf S, et al. Randomized Trial of Primary PCI with or without Routine Manual Thrombectomy (TOTAL). N Engl J Med. 2015;372(15):1389-1398. PMID: 25853743

54. Fröbert O, Lagerqvist B, Olivecrona GK, et al. Thrombus Aspiration during ST-Segment Elevation Myocardial Infarction (TASTE). N Engl J Med. 2013;369(17):1587-1597. PMID: 23991656

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