Cardiogenic Shock
Cardiogenic shock occurs when the heart fails to pump sufficient blood to meet metabolic demands, resulting in systemic ... ACEM Primary Written, ACEM Fellowshi
Clinical board
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Urgent signals
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- Systolic BP below 90 mmHg with evidence of hypoperfusion
- Lactate ≥2.0 mmol/L with cardiac dysfunction
- Cold, clammy peripheries with oliguria
- Altered mental status in setting of acute MI
Exam focus
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- ACEM Primary Written
- ACEM Fellowship Written
- ACEM Fellowship OSCE
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- Septic Shock
- Massive Pulmonary Embolism
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Cardiogenic shock occurs when the heart fails to pump sufficient blood to meet metabolic demands, resulting in systemic ... ACEM Primary Written, ACEM Fellowshi
Cardiogenic shock is cardiac pump failure causing inadequate tissue perfusion despite adequate or elevated filling press... CICM Second Part exam preparation.
Quick Answer
One-liner: Cardiogenic shock is acute cardiac pump failure causing inadequate tissue perfusion despite adequate intravascular volume, requiring immediate revascularization (if MI) and escalating haemodynamic support.
Cardiogenic shock occurs when the heart fails to pump sufficient blood to meet metabolic demands, resulting in systemic hypoperfusion and end-organ dysfunction. It carries 40-50% in-hospital mortality despite advances in mechanical circulatory support. The emergency physician's role is rapid recognition using the SCAI classification, initiation of haemodynamic support (inotropes/vasopressors), urgent cardiology consultation for early revascularization (if AMI), and consideration of mechanical support for refractory cases. Time to intervention directly correlates with survival.
ACEM Exam Focus
Primary Exam Relevance
- Anatomy: Coronary artery anatomy, myocardial perfusion zones, cardiac conduction system, ventricular wall segments (AHA 17-segment model)
- Physiology: Frank-Starling mechanism, cardiac output determinants (preload, afterload, contractility, heart rate), systemic vascular resistance, baroreceptor response, renin-angiotensin-aldosterone axis activation
- Pharmacology: Inotropes (dobutamine, adrenaline, milrinone), vasopressors (noradrenaline), vasodilators (nitrates), antiplatelet agents (aspirin, P2Y12 inhibitors), mechanisms of action and adverse effects
Fellowship Exam Relevance
- Written: SCAI classification stages, indications for mechanical circulatory support, interpretation of haemodynamic parameters (cardiac index, PCWP), differential diagnosis of shock states, complications of acute MI
- OSCE: Resuscitation station with cardiogenic shock scenario, leading cardiac arrest team, interpreting bedside echocardiography, communicating with family about prognosis, initiating retrieval for tertiary interventions
- Key domains tested: Medical Expert (shock management), Communicator (family discussions), Leader (team coordination), Collaborator (cardiology/ICU liaison)
Key Points
The 5 things you MUST know:
- SCAI Stage C (classic shock) defined by lactate ≥2.0 mmol/L requiring vasopressors/inotropes — this is your "call for help" threshold
- Early revascularization (PCI/CABG within 6 hours) reduces mortality by 13% at 6 months in AMI-related cardiogenic shock (SHOCK trial)
- Noradrenaline + dobutamine is first-line pharmacotherapy — avoid adrenaline (increases lactate, myocardial oxygen demand)
- IABP does not improve survival (IABP-SHOCK II) — reserved only for mechanical complications (VSR, acute MR)
- Impella/VA-ECMO should be considered in SCAI D-E shock with reversible pathology — early consultation prevents futile salvage attempts
Epidemiology
| Metric | Value | Source |
|---|---|---|
| Incidence | 40-80 per 1,000,000/year | [1] |
| Prevalence in AMI | 5-10% of STEMI, 2-3% of NSTEMI | [2] |
| In-hospital mortality | 40-50% (50-60% without revascularization) | [3] |
| 1-year mortality | 50-60% | [4] |
| Peak age | 65-75 years | [5] |
| Gender ratio | 1.5:1 (M:F) | [6] |
| Median time to shock | 6-7 hours post-AMI | [7] |
Australian/NZ Specific
- Incidence: Australian data from ANZACS-QI registry shows cardiogenic shock complicates 6-8% of STEMI presentations, with higher rates in rural/remote areas due to delayed presentation [8]
- Indigenous populations: Aboriginal and Torres Strait Islander peoples develop AMI 10-15 years earlier and have 2-3 times higher cardiovascular mortality, translating to increased cardiogenic shock burden [9]
- Rural/remote variations: Median time from symptom onset to PCI is 180 minutes in metropolitan centres vs 300+ minutes in remote areas, directly impacting shock development and outcomes [10]
- Retrieval burden: RFDS reports cardiogenic shock accounts for 8-12% of critical care retrievals, with one-way flight times exceeding 2-3 hours in Northern Territory and Western Australia [11]
Pathophysiology
Mechanism
Cardiogenic shock results from a vicious cycle of cardiac dysfunction and systemic hypoperfusion:
Myocardial Injury (AMI/myocarditis/decompensation)
↓
Reduced Stroke Volume & Cardiac Output
↓
↓ Systemic Blood Pressure + ↓ Coronary Perfusion
↓
Compensatory Mechanisms Activated:
- Sympathetic surge (↑ HR, ↑ SVR)
- RAAS activation (fluid retention)
- Inflammatory cytokine release (SIRS)
↓
↑ Myocardial Oxygen Demand + ↑ Afterload
↓
Further Myocardial Ischaemia & Dysfunction
↓
SHOCK SPIRAL → Multi-Organ Failure
Key Pathophysiological Features
-
Primary Pump Failure: Loss of ≥40% of functional left ventricular myocardium (equivalent to cardiac index below 2.2 L/min/m²) [12]
-
Systemic Inflammatory Response: Release of TNF-α, IL-1, IL-6 creates "SIRS-like" state with peripheral vasodilation, capillary leak, and microcirculatory dysfunction [13]
-
Neurohumoral Activation: Catecholamine surge increases heart rate and SVR, but worsens myocardial oxygen supply-demand mismatch [14]
-
Diastolic Dysfunction: Elevated left ventricular end-diastolic pressure (LVEDP greater than 18 mmHg) and pulmonary capillary wedge pressure (PCWP greater than 15 mmHg) cause pulmonary oedema [15]
-
Microcirculatory Failure: Tissue hypoxia from inadequate oxygen delivery triggers anaerobic metabolism (lactate ≥2.0 mmol/L), acidosis, and cellular death [16]
Haemodynamic Criteria (Classical Definition)
| Parameter | Cardiogenic Shock | Normal |
|---|---|---|
| Cardiac Index (CI) | below 2.2 L/min/m² | 2.5-4.0 L/min/m² |
| PCWP | greater than 15 mmHg | 8-12 mmHg |
| SBP | below 90 mmHg (greater than 30 min) | 100-140 mmHg |
| MAP | below 65 mmHg | 70-100 mmHg |
| SVR | Often elevated | 800-1200 dynes·s/cm⁵ |
| SvO₂ | below 60% | 70-75% |
Why It Matters Clinically
Understanding the shock spiral explains why:
- Early revascularization breaks the cycle by restoring coronary flow
- Inotropes increase contractility but risk worsening ischaemia (↑ O₂ demand)
- Vasopressors maintain coronary perfusion pressure but increase afterload
- Mechanical support unloads the ventricle and breaks the spiral when pharmacotherapy fails
Clinical Approach
Recognition
Suspect cardiogenic shock in any patient with:
- Acute MI (especially anterior STEMI, inferior MI with RV involvement)
- Known heart failure presenting with acute decompensation
- Hypotension + signs of tissue hypoperfusion (altered mental status, oliguria, cold peripheries)
- Respiratory distress + cardiac history
SCAI Shock Classification (2022)
Essential for triage and prognostication:
| Stage | Description | Clinical Features | Haemodynamics | Lactate | Mortality |
|---|---|---|---|---|---|
| A | At Risk | Post-MI, no shock signs | SBP normal, CI ≥2.2 | below 2.0 | 2-5% |
| B | Beginning | Relative hypotension/tachycardia | SBP below 90 or ↓30 from baseline | below 2.0 | 5-10% |
| C | Classic | Hypoperfusion requiring intervention | CI below 2.2, PCWP greater than 15 | ≥2.0 | 30-40% |
| D | Deteriorating | Failure to respond to therapy | Escalating support needed | ≥2.0 | 40-60% |
| E | Extremis | Circulatory collapse, cardiac arrest | Profound instability | ≥2.0 | 60-80% |
Cardiac arrest modifier: Add subscript "A" (e.g., C_A) if patient suffered arrest — significantly worsens prognosis [17]
Initial Assessment
Primary Survey
- A (Airway): Patent? Stridor from pulmonary oedema? GCS below 8 requiring intubation?
- B (Breathing):
- "Respiratory rate: Tachypnoea (greater than 25/min) indicates compensation"
- "Oxygen saturation: Often normal initially, then deteriorates"
- Auscultation: Bilateral crackles (pulmonary oedema), ± wheeze ("cardiac asthma")
- "Work of breathing: Use of accessory muscles, inability to speak full sentences"
- C (Circulation):
- "Heart rate: Tachycardia (greater than 100 bpm) or bradycardia (if conduction block)"
- "Blood pressure: SBP below 90 mmHg or MAP below 65 mmHg"
- "Pulse quality: Weak, thready peripheral pulses"
- "Capillary refill: greater than 2 seconds, cool peripheries"
- "JVP: Elevated (greater than 8 cm H₂O) indicates high filling pressures"
- "Cardiac auscultation: S3 gallop (LV failure), murmurs (acute MR, VSR)"
- D (Disability):
- "GCS: Confusion, agitation, or drowsiness from cerebral hypoperfusion"
- "Pupils: Equal and reactive (unless anoxic brain injury)"
- E (Exposure):
- "Skin: Cold, clammy, mottled (vs warm in distributive shock)"
- "Peripheral oedema: Sacral/pedal oedema if chronic heart failure"
History
Key Questions
| Question | Significance |
|---|---|
| "Did you have chest pain? When did it start?" | Timing of AMI onset affects revascularization window (below 12h optimal) |
| "Do you have a history of heart problems?" | Prior MI, known heart failure (EF), cardiomyopathy, valve disease |
| "Have you been short of breath or noticed swelling?" | Chronic heart failure vs acute presentation |
| "Are you taking any heart medications?" | Beta-blockers, ACE-I, diuretics suggest known cardiac disease |
| "Any recent infections or flu-like illness?" | Myocarditis/viral cardiomyopathy |
| "Any valve surgery or pacemaker?" | Mechanical valve thrombosis, pacemaker malfunction |
Red Flag Symptoms
- Chest pain radiating to jaw/arm with diaphoresis (AMI until proven otherwise)
- Sudden dyspnoea with pink frothy sputum (flash pulmonary oedema)
- Syncope or near-syncope (arrhythmia, mechanical complication)
- Confusion or decreased consciousness (cerebral hypoperfusion)
- Oliguria or anuria (renal hypoperfusion, AKI)
- New murmur (acute mitral regurgitation, ventricular septal rupture)
Examination
General Inspection
- Distress level: Sitting upright, unable to lie flat (orthopnoea), anxious facies
- Colour: Pale, cyanotic, or mottled skin
- Diaphoresis: Profuse sweating (sympathetic activation)
- Respiratory pattern: Tachypnoea, use of accessory muscles
Specific Findings
| System | Finding | Significance |
|---|---|---|
| Cardiovascular | Weak, thready pulse | Low stroke volume, high SVR |
| Tachycardia greater than 100 bpm | Compensatory response to low CO | |
| Hypotension SBP below 90 mmHg | Inadequate systemic perfusion | |
| Elevated JVP greater than 8 cm | Right heart failure, fluid overload | |
| S3 gallop | LV systolic dysfunction, volume overload | |
| Pansystolic murmur | Acute mitral regurgitation (papillary muscle rupture) | |
| Harsh systolic murmur | Ventricular septal rupture (late complication AMI) | |
| Respiratory | Bilateral crackles | Pulmonary oedema from high PCWP |
| Wheeze | Bronchospasm ("cardiac asthma") | |
| Hypoxia SpO₂ below 90% | V/Q mismatch from pulmonary oedema | |
| Skin | Cold, clammy peripheries | Vasoconstriction, low cardiac output |
| Mottled or cyanotic | Severe hypoperfusion | |
| Neurological | Confusion, agitation | Cerebral hypoperfusion |
| GCS below 13 | Severe shock requiring intubation | |
| Renal | Oliguria below 0.5 mL/kg/h | Renal hypoperfusion, pre-renal AKI |
Investigations
Immediate (Resus Bay)
| Test | Purpose | Key Finding |
|---|---|---|
| ECG (12-lead) | Identify AMI, arrhythmia | STEMI (early revasc), NSTEMI, VT/VF, bradycardia (heart block) |
| Arterial Blood Gas | Assess lactate, pH, oxygenation | Lactate ≥2.0 mmol/L (SCAI C), metabolic acidosis (pH below 7.30) |
| Venous Blood Gas | SvO₂ as surrogate for CI | SvO₂ below 60% indicates inadequate O₂ delivery |
| Point-of-Care Glucose | Exclude hypoglycaemia | Glucose below 4.0 mmol/L (confusion mimic) |
| Point-of-Care Troponin | Confirm myocardial injury | Elevated in AMI, myocarditis |
| POCUS (Cardiac) | Assess LV function, effusion | Severe LV dysfunction, pericardial effusion, RV dysfunction |
Standard ED Workup
| Test | Indication | Interpretation |
|---|---|---|
| FBC | All patients | Hb (anaemia worsens O₂ delivery), WCC (infection/SIRS) |
| UEC | All patients | Elevated creatinine (pre-renal AKI), hyperkalaemia (risk with ACE-I) |
| Troponin (high-sensitivity) | All patients | Magnitude correlates with infarct size; serial measurements |
| NT-proBNP / BNP | ?Heart failure vs other shock | greater than 300 pg/mL suggests cardiac dysfunction; NOT specific |
| Chest X-ray | All patients | Pulmonary oedema (bat-wing, Kerley B lines), cardiomegaly |
| Lactate (serial) | All patients | Trend guides response: ↓ lactate = improving perfusion |
| Coagulation screen | If thrombolysis/anticoagulation | Baseline INR, aPTT, fibrinogen |
| Liver function tests | All patients | Elevated ALT/AST in shock liver (ischaemic hepatitis) |
| Magnesium, Phosphate | All patients | Correct imbalances to optimize cardiac function |
Advanced/Specialist
| Test | Indication | Availability |
|---|---|---|
| Formal Echocardiography | Detailed structural/functional assessment | Cardiology consult, tertiary centres |
| Coronary Angiography | AMI requiring revascularization | Immediate if STEMI, urgent if NSTEMI |
| Pulmonary Artery Catheter | Refractory shock requiring haemodynamic monitoring | ICU/CCU insertion |
| CT Aorta | ?Aortic dissection presenting as shock | Tertiary centre, delays definitive care |
| Cardiac MRI | ?Myocarditis, infiltrative disease | Tertiary, not in acute phase |
Point-of-Care Ultrasound
RUSH Protocol (Rapid Ultrasound in Shock) [18]:
-
Cardiac Views:
- Parasternal long-axis: LV size, wall motion, EF estimation
- Apical 4-chamber: Global LV function, RV size (RV:LV greater than 1.0 suggests RV strain)
- Subcostal: Pericardial effusion (tamponade), IVC assessment
-
IVC Assessment:
- Cardiogenic shock: IVC greater than 2.1 cm diameter, below 50% collapsibility (high CVP, congestion)
- Hypovolaemic shock: IVC below 1.5 cm, greater than 50% collapsibility (low CVP, empty tank)
-
Lung Ultrasound:
- B-lines (≥3 per intercostal space, bilateral): Pulmonary oedema (PCWP greater than 18 mmHg)
- Pleural effusions: Bilateral in chronic heart failure
-
Key Findings in Cardiogenic Shock:
- Severe global LV hypokinesis (EF below 30-40%)
- Dilated LV with poor systolic function
- Plethoric IVC (greater than 2.1 cm, minimal variation)
- Diffuse B-lines (interstitial oedema)
Limitations: Operator-dependent, poor windows in obese/emphysema patients, cannot replace formal echocardiography [19]
Management
Immediate Management (First 10 Minutes)
1. Call for senior help + Cardiology consult immediately (0 min)
2. High-flow oxygen 15L via non-rebreather (target SpO₂ ≥94%) (1 min)
3. Large-bore IV access x 2, draw bloods (VBG with lactate, troponin, FBC, UEC) (2 min)
4. Continuous monitoring: ECG, NIBP (or arterial line), SpO₂, urine output (3 min)
5. 12-lead ECG (identify STEMI/NSTEMI) (4 min)
6. Aspirin 300 mg PO (if AMI suspected, no contraindication) (5 min)
7. POCUS cardiac + IVC assessment (confirm cardiogenic cause) (6 min)
8. Commence inotrope/vasopressor (noradrenaline/dobutamine) via central line or large peripheral (7 min)
9. Consider CPAP/BiPAP if pulmonary oedema + work of breathing (avoid if SBP below 90) (8 min)
10. Activate catheterization lab if STEMI (target door-to-balloon below 90 min) (10 min)
Resuscitation
Airway
-
Indications for intubation:
- GCS ≤8 (inability to protect airway)
- Refractory hypoxia despite CPAP/BiPAP (PaO₂ below 60 mmHg on high-flow O₂)
- Impending respiratory arrest (exhaustion, bradypnoea)
- Cardiac arrest
-
Intubation considerations:
- "Pre-oxygenation: 100% FiO₂, consider CPAP pre-oxygenation"
- "Induction agents: Avoid propofol/thiopentone (myocardial depression, vasodilation). Use ketamine 1-1.5 mg/kg IV (maintains BP) or etomidate 0.2-0.3 mg/kg IV (haemodynamically neutral)"
- "Muscle relaxant: Rocuronium 1.0-1.2 mg/kg IV (RSI)"
- "Post-intubation hypotension: Common due to loss of sympathetic drive + positive pressure ventilation. Have vasopressor boluses ready (metaraminol 0.5 mg IV or phenylephrine 100 mcg IV)"
Breathing
-
Oxygen targets: SpO₂ 94-98% (avoid hyperoxia, may increase infarct size) [20]
-
Non-invasive ventilation:
- "CPAP 5-10 cmH₂O: Reduces preload, improves oxygenation in pulmonary oedema"
- "Contraindications: SBP below 90 mmHg (relative), vomiting, facial trauma, unable to protect airway"
- "Evidence: Reduces intubation rate (NNT 13) but no mortality benefit [21]"
-
Mechanical ventilation (if intubated):
- "Tidal volume: 6-8 mL/kg ideal body weight (lung-protective)"
- "PEEP: 5-10 cmH₂O (improves oxygenation, but excessive PEEP reduces venous return)"
- "FiO₂: Wean to maintain SpO₂ 94-98%"
- "Monitor: Positive pressure ventilation reduces venous return and can worsen hypotension"
Circulation
Haemodynamic Targets:
- MAP ≥65 mmHg (higher if chronic hypertension: MAP ≥75-80 mmHg)
- Lactate clearance ≥10% per hour
- Urine output ≥0.5 mL/kg/h
- Improved mental status
Fluid Strategy:
DO NOT give routine IV fluid boluses in cardiogenic shock
- The ventricle is already on the steep part of the Frank-Starling curve
- Fluid overload worsens pulmonary oedema and increases PCWP
- Exception: RV infarction (needs preload) — give cautious 250 mL boluses if PCWP low
Medications
Vasopressors & Inotropes
First-Line: Noradrenaline + Dobutamine Combination
| Drug | Dose | Route | Mechanism | Indications | Adverse Effects |
|---|---|---|---|---|---|
| Noradrenaline | 0.05-0.5 mcg/kg/min | IV infusion (central preferred) | α₁-agonist (vasoconstriction), β₁-agonist (inotropy) | MAP below 65 mmHg, maintain coronary perfusion | Arrhythmia, ↑ afterload, tissue ischaemia |
| Dobutamine | 2.5-20 mcg/kg/min | IV infusion (central or large peripheral) | β₁-agonist (inotropy, chronotropy), β₂-agonist (mild vasodilation) | Low cardiac output (CI below 2.2), despite adequate MAP | Tachycardia, arrhythmia, ↑ myocardial O₂ demand |
Evidence:
- SOAP II Trial: Noradrenaline superior to dopamine in cardiogenic shock (lower arrhythmia rate, trend to lower mortality) [22]
- OptimaCC Trial: Adrenaline vs noradrenaline — adrenaline caused more refractory shock and lactic acidosis [23]
- DOREMI Trial: Dobutamine vs milrinone — no difference in composite outcome (death/arrest/transplant/MCS) [24]
Second-Line Agents:
| Drug | Dose | Use | Notes |
|---|---|---|---|
| Adrenaline | 0.05-0.5 mcg/kg/min | Profound shock, cardiac arrest | Increases lactate (β₂-mediated), ↑ myocardial O₂ demand, arrhythmogenic. Avoid if possible |
| Milrinone | 0.375-0.75 mcg/kg/min (no bolus) | Alternative to dobutamine | Phosphodiesterase-3 inhibitor (inotropy + vasodilation). Risk of hypotension, long half-life (2-3h) |
| Vasopressin | 0.01-0.04 units/min | Refractory shock, add-on | V₁ receptor agonist (vasoconstriction). Theoretical benefit: afterload ↑ but coronary flow maintained |
| Levosimendan | 0.05-0.2 mcg/kg/min | ?Refractory shock (not PBS-listed) | Calcium sensitizer + PDE-3 inhibitor. Limited availability in Australia, no mortality benefit in trials [25] |
Diuretics
| Drug | Dose | Route | Timing | Notes |
|---|---|---|---|---|
| Frusemide | 40-80 mg IV bolus, then 5-40 mg/h infusion | IV | After haemodynamic stabilization | DO NOT give early — causes transient venoconstriction and worsens preload. Use only after MAP greater than 65 mmHg and inotropes commenced |
Antiplatelet & Anticoagulation (if AMI-related)
| Drug | Dose | Route | Timing | Notes |
|---|---|---|---|---|
| Aspirin | 300 mg loading | PO/PR | Immediately | If STEMI/NSTEMI, unless active bleeding |
| Ticagrelor | 180 mg loading | PO | Immediately | Preferred P2Y₁₂ inhibitor (faster onset than clopidogrel) |
| Heparin (UFH) | 60 U/kg bolus (max 4000 U), then 12 U/kg/h | IV infusion | Immediately | If PCI planned; monitor aPTT 50-70s |
Paediatric Dosing
Cardiogenic shock in children is rare; causes differ (congenital heart disease, myocarditis, cardiomyopathy)
| Drug | Dose | Max | Notes |
|---|---|---|---|
| Noradrenaline | 0.05-1 mcg/kg/min | 2 mcg/kg/min | Via central line |
| Adrenaline | 0.05-1 mcg/kg/min | 2 mcg/kg/min | First-line in paediatric shock |
| Dobutamine | 2.5-20 mcg/kg/min | 20 mcg/kg/min | Inotropy without excessive vasoconstriction |
| Milrinone | 0.25-0.75 mcg/kg/min | 0.75 mcg/kg/min | Avoid loading dose (causes hypotension) |
Definitive Care
Early Revascularization (AMI-Related Cardiogenic Shock)
SHOCK Trial (1999): Early revascularization (PCI or CABG within 6 hours) vs initial medical stabilization [26]
- 30-day mortality: 46.7% (revascularization) vs 56.0% (medical) — not statistically significant (p=0.11)
- 6-month mortality: 50.3% vs 63.1% — statistically significant (p=0.027), NNT=8
- Recommendation: Emergency PCI/CABG within 6 hours for all AMI-related cardiogenic shock (Class I, AHA/ESC guidelines)
Culprit Vessel Only vs Complete Revascularization:
- CULPRIT-SHOCK trial (2017): Culprit-lesion-only PCI vs multivessel PCI in STEMI + cardiogenic shock [27]
- Result: Culprit-only approach reduced 30-day death/renal failure (45.9% vs 55.4%, p=0.01)
- Recommendation: Treat culprit vessel only; stage complete revascularization later
Mechanical Circulatory Support (MCS)
Indications: SCAI stage D-E shock despite escalating inotropes/vasopressors, with:
- Reversible cardiac pathology (AMI, myocarditis, post-cardiotomy)
- Age and comorbidities compatible with meaningful recovery
- No contraindications (severe aortic regurgitation for Impella, peripheral vascular disease for IABP/femoral access)
Options:
| Device | Mechanism | Flow | Insertion | Complications | Availability (Aus) |
|---|---|---|---|---|---|
| IABP | Diastolic augmentation, systolic unloading | Modest (0.5 L/min) | Percutaneous femoral | Limb ischaemia, balloon rupture, thrombosis | Widely available |
| Impella | Axial flow pump (LV → Aorta) | 2.5-5.5 L/min | Percutaneous femoral (cath lab) | Haemolysis, limb ischaemia, LV perforation | Major centres only |
| VA-ECMO | Extracorporeal pump (venous → arterial) | 3-6 L/min | Percutaneous femoral or central | Bleeding, thrombosis, limb ischaemia, Harlequin syndrome | Tertiary centres, retrieval available |
| TandemHeart | LA-to-femoral artery pump | 3.5-5 L/min | Transseptal puncture | Bleeding, tamponade, limb ischaemia | Limited (research centres) |
Evidence:
-
IABP-SHOCK II (2012): Routine IABP in AMI + cardiogenic shock showed no mortality benefit (39.7% vs 41.3%, p=0.69) [28]
- "Recommendation: IABP NOT routinely recommended (Class III, ESC). Reserved for mechanical complications (VSR, acute MR) as bridge to surgery"
-
Impella: No completed RCTs vs medical therapy. DanGer Shock trial (2024) comparing Impella CP to standard care in AMI + shock showed no 6-month mortality benefit (45.8% vs 46.6%, p=0.89) [29]
-
VA-ECMO: Observational data suggests survival 20-40% in cardiogenic shock. Use as bridge to recovery (myocarditis, post-MI stunning) or bridge to decision (transplant evaluation) [30]
Australian/NZ MCS Centres:
- NSW: RPA, St Vincent's, Prince of Wales
- VIC: Alfred, Austin, Monash
- QLD: Prince Charles, Gold Coast
- SA: Royal Adelaide
- WA: Fiona Stanley
- NZ: Auckland City, Christchurch
Retrieval for MCS: Contact state ECMO services:
- NSW: ECLS Service 1800 650 004
- VIC: VECMOS 1300 368 661
- QLD: Adult Retrieval Services 1300 799 127
Disposition
Admission Criteria
All patients with cardiogenic shock require ICU/CCU admission:
- Continuous haemodynamic monitoring (arterial line, central venous access)
- Vasopressor/inotrope titration
- Serial lactate monitoring (every 2-4 hours)
- Cardiology/interventional cardiology input
- Consider transfer to tertiary centre if mechanical support anticipated
ICU/HDU Criteria
Mandatory ICU admission:
- SCAI stage C-E shock (requiring vasopressors/inotropes)
- Post-PCI/post-CABG cardiogenic shock
- Mechanical ventilation
- Multi-organ failure (AKI, shock liver, ARDS)
- Mechanical circulatory support (IABP, Impella, VA-ECMO)
- Haemodynamic instability requiring invasive monitoring (PA catheter)
Inter-Hospital Transfer Criteria
Transfer to tertiary PCI-capable centre:
- STEMI with cardiogenic shock requiring primary PCI (emergency transfer, accompany with doctor/RN, vasopressors running)
- SCAI stage D-E shock requiring mechanical circulatory support
- Mechanical complications (VSR, free wall rupture, papillary muscle rupture) requiring cardiac surgery
- Refractory shock despite maximal inotropes/vasopressors
Pre-Transfer Checklist:
- Senior discussion with receiving cardiologist/intensivist
- Stabilise haemodynamics as much as possible (target MAP ≥65 mmHg, lactate trending down)
- Secure airway if GCS ≤8 or anticipated deterioration
- Adequate IV access (2x large-bore peripheral + central line if time permits)
- Continuous monitoring during transfer (portable monitor, transport ventilator if intubated)
- Vasopressor infusion via syringe driver (noradrenaline 1 mg in 50 mL saline, run at appropriate rate)
- Transfer team: Doctor (FACEM or advanced trainee) + Critical Care Paramedic or RN
- Notify receiving hospital ETA, patient status
Follow-up
Post-Discharge (if patient survives to discharge):
- Cardiology outpatient review within 2 weeks
- Cardiac rehabilitation referral
- Echocardiography at 6-8 weeks (assess recovery of LV function)
- Optimal medical therapy: Dual antiplatelet (12 months post-PCI), beta-blocker, ACE-inhibitor, statin, diuretics as needed
- Consider ICD implantation if EF remains below 35% at 3 months post-MI [31]
- Psychosocial support (high rates of PTSD, depression post-critical illness)
GP Letter Must Include:
- Diagnosis: Cardiogenic shock secondary to [AMI/myocarditis/decompensated HF]
- SCAI stage on presentation
- Interventions performed (PCI vessels, mechanical support used)
- Current medications and rationale
- Follow-up plan (cardiology, echocardiography)
- Red flags to return: Recurrent chest pain, dyspnoea, syncope, oedema
Special Populations
Paediatric Considerations
Cardiogenic shock in children is rare; main causes differ from adults:
- Congenital heart disease: Ductal-dependent lesions (HLHS, critical coarctation), post-surgical
- Myocarditis: Viral (enterovirus, adenovirus), autoimmune
- Cardiomyopathy: Dilated, hypertrophic, restrictive
- Arrhythmias: SVT, complete heart block
Differences in Management:
- Fluid boluses: Unlike adults, children often benefit from 10-20 mL/kg crystalloid bolus (higher physiological reserve)
- Inotrope choice: Adrenaline is first-line (0.05-1 mcg/kg/min), whereas adults prefer noradrenaline + dobutamine
- Mechanical support: Pediatric ECMO cannulae and pumps required; early discussion with pediatric cardiac centre
- Oxygen delivery: Children have higher metabolic rate; target SpO₂ 94-98% (neonates 90-95% if ductal-dependent lesion)
Pregnancy
Peripartum cardiomyopathy can present as cardiogenic shock in late pregnancy or post-partum:
- Presentation: Heart failure symptoms in last month of pregnancy or within 5 months post-partum
- Diagnosis: Echocardiography showing LV systolic dysfunction (EF below 45%) without other cause
- Management:
- Avoid ACE-inhibitors/ARBs in pregnancy (teratogenic); use hydralazine + nitrates for afterload reduction
- "Bromocriptine: Emerging evidence for blocking prolactin in peripartum cardiomyopathy (2.5 mg BD for 2 weeks, then 2.5 mg daily for 6 weeks) [32]"
- "Delivery: Expedite if fetus viable and mother deteriorating"
- "Anticoagulation: Consider LMWH if EF below 35% (high thrombotic risk)"
- "Mechanical support: VA-ECMO can be used if refractory shock; case series show maternal survival 60-80%"
Obstetric Consultation: Mandatory for all pregnant patients with cardiogenic shock
Elderly
Considerations in older adults (greater than 75 years):
- Higher mortality: SHOCK trial subgroup showed no clear benefit of revascularization in ≥75 years, though sample size small [26]
- Comorbidities: CKD, COPD, frailty affect MCS candidacy
- Polypharmacy: Beta-blockers, CCBs may mask compensatory tachycardia
- Cognitive impairment: Difficulties with consent for PCI/MCS
- Goals of care: Early discussion with family about prognosis (40-50% mortality), ceilings of treatment, resuscitation status
Shared Decision-Making: Engage geriatrician or palliative care if patient/family considering comfort-focused care
Indigenous Health
Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:
Epidemiology:
- Aboriginal and Torres Strait Islander peoples experience acute MI 10-15 years earlier than non-Indigenous Australians, with 2-3 times higher cardiovascular mortality [9]
- Māori have 40-50% higher rates of ischaemic heart disease and present with AMI at younger ages (median 10 years earlier) [33]
- Higher prevalence of risk factors: diabetes (3-4x), smoking (2x), hypertension, chronic kidney disease
Barriers to Care:
- Geographic isolation: Many remote communities are 200-500 km from PCI-capable centres
- Cultural safety: Mistrust of healthcare system due to historical trauma, racism
- Communication: Language barriers, need for Aboriginal Health Workers or cultural liaison
- Access: Transport costs, lack of family support if transferred to distant tertiary centre
- Health literacy: Lower awareness of AMI symptoms, reluctance to seek care
Specific Actions:
- Early retrieval: Lower threshold for RFDS retrieval given transport distances
- Cultural liaison: Involve Aboriginal Health Worker or Torres Strait Islander Health Worker in care discussions
- Interpreter services: Use qualified medical interpreters (not family members) for consent discussions
- Family involvement: Recognize importance of extended family in decision-making; allow flexibility in visiting hours
- Discharge planning: Engage Aboriginal Community Controlled Health Organisation (ACCHO) for follow-up in community
- Culturally appropriate communication:
- Avoid direct eye contact if culturally inappropriate
- Allow time for discussion and questions
- Explain procedures clearly without medical jargon
- Acknowledge spiritual/cultural beliefs (e.g., sorry business after death)
Māori-Specific Considerations:
- Whānau involvement: Family-centred decision-making is paramount
- Tikanga protocols: Respect for cultural practices, karakia (prayer)
- Manaakitanga: Providing hospitality and care in culturally appropriate manner
- Health inequity: Acknowledge systemic barriers and advocate for equitable access to PCI/MCS
Pitfalls & Pearls
Clinical Pearls:
- "Cold and wet": Cardiogenic shock presents as cold peripheries (vasoconstriction) + pulmonary oedema (wet lungs). Contrast with "warm and dry" (early septic shock), "cold and dry" (hypovolaemic shock)
- RV infarction paradox: Needs preload to maintain LV filling. Give cautious fluid boluses (250 mL) and avoid nitrates/diuretics (worsen preload). Look for inferior STEMI + STE in V₄R on ECG
- Lactate clearance is king: Serial lactate every 2-4 hours. If lactate not clearing ≥10%/hour despite inotropes, escalate to mechanical support or reconsider diagnosis (mixed shock?)
- Early cardiology call: Cardiogenic shock mortality is time-dependent. Call cardiology within 5 minutes of recognition, not after "stabilizing" — early revascularization saves lives
- Avoid bolus milrinone: Phosphodiesterase inhibitors cause vasodilation. Never give bolus dose (causes profound hypotension); start low-dose infusion only
- Swan-Ganz underutilized: In refractory shock, PA catheter helps differentiate cardiogenic (high PCWP, low CI) from mixed/distributive (low PCWP, high CI). Don't fear the data
Pitfalls to Avoid:
- Fluid overload: Giving 1-2L crystalloid boluses because "all shock needs fluid" — worsens pulmonary oedema and PCWP. Check POCUS IVC first
- Delaying revascularization: Waiting for patient to "stabilize" with inotropes before calling cardiology. Call immediately — time is myocardium
- IABP reflex: Automatically inserting IABP in all cardiogenic shock. IABP-SHOCK II showed no benefit; reserve for mechanical complications only
- Propofol for intubation: Causes profound hypotension and cardiac depression. Use ketamine or etomidate in shocked patients
- Missing RV infarction: Giving nitrates/diuretics in inferior STEMI without checking right-sided leads (V₄R). RV MI needs preload, not diuresis
- Attributing confusion to "old age": Altered mental status is cerebral hypoperfusion until proven otherwise. Requires urgent intervention, not CT head
- Adrenaline as first-line: Increases myocardial oxygen demand and lactate production (via β₂). Use noradrenaline + dobutamine instead
Viva Practice
Stem: A 68-year-old man presents to your ED with 2 hours of chest pain. He is cold, clammy, and confused. BP 82/50 mmHg, HR 110 bpm, RR 28/min, SpO₂ 89% on room air. ECG shows anterior STEMI. Bedside echo shows severe LV dysfunction.
Opening Question: Describe your immediate management priorities in the first 10 minutes.
Model Answer: This is SCAI stage C cardiogenic shock secondary to anterior STEMI requiring urgent revascularization. My immediate priorities are:
- Call for help: Senior ED consultant, Cardiology registrar/consultant for urgent PCI discussion, ICU for post-PCI bed
- Airway/Breathing: High-flow oxygen 15L via non-rebreather (SpO₂ 89% indicates hypoxia). Monitor closely for need to intubate if GCS drops or work of breathing increases. Prepare for RSI with ketamine (avoid propofol)
- Circulation:
- Large-bore IV access x 2, bloods including VBG with lactate, troponin, FBC, UEC, coagulation
- Aspirin 300 mg PO, ticagrelor 180 mg PO (DAPT for PCI)
- Commence noradrenaline infusion peripherally (0.1 mcg/kg/min, titrate to MAP ≥65 mmHg) — DO NOT give fluid boluses (worsens pulmonary oedema)
- Add dobutamine 5 mcg/kg/min if cardiac output remains low despite MAP normalization
- Definitive care: Activate catheterization lab for emergency primary PCI (door-to-balloon target below 90 min). This is Class I indication given cardiogenic shock
- Monitoring: Arterial line, urinary catheter (urine output target ≥0.5 mL/kg/h), continuous ECG, repeat lactate in 2 hours
Follow-up Questions:
-
What haemodynamic targets would you aim for?
- Model answer: MAP ≥65 mmHg (may need higher if chronic hypertension), lactate clearance ≥10%/hour, urine output ≥0.5 mL/kg/h, improved mental status. Avoid excessive vasopressor doses (increases afterload and myocardial oxygen demand). If MAP greater than 65 but lactate still rising, add dobutamine to improve cardiac output.
-
The cardiologist asks if you want an IABP inserted. How do you respond?
- Model answer: I would not routinely request IABP. The IABP-SHOCK II trial showed no mortality benefit for routine IABP use in AMI-related cardiogenic shock undergoing PCI. It is now Class III (not recommended) in ESC guidelines. I would only consider IABP for mechanical complications such as acute mitral regurgitation or ventricular septal rupture as a bridge to cardiac surgery. In this case, if the patient deteriorates to SCAI stage D-E despite maximal inotropes, I would discuss Impella or VA-ECMO rather than IABP.
-
What are the indications for mechanical circulatory support in this patient?
- Model answer: Indications for MCS (Impella/VA-ECMO):
- SCAI stage D-E shock (failure to respond to inotropes/vasopressors within 30-60 minutes, or requiring escalating doses)
- Persistent lactate ≥4.0 mmol/L despite intervention
- Worsening end-organ dysfunction (AKI, shock liver, cerebral hypoperfusion)
- Mechanical complications requiring bridge to surgery
- Patient must have reversible cardiac pathology, acceptable comorbidities, and no contraindications (severe PAD for femoral access, severe AR for Impella)
- Model answer: Indications for MCS (Impella/VA-ECMO):
Discussion Points:
- SHOCK trial: Early revascularization reduced 6-month mortality by 13% (NNT=8)
- CULPRIT-SHOCK: Treat culprit vessel only in multivessel disease
- SCAI classification: Lactate ≥2.0 mmol/L defines stage C (classic shock)
- RV infarction: Check V₄R in inferior STEMI; requires preload (cautious fluid), avoid nitrates
Stem: A 72-year-old woman with known ischaemic cardiomyopathy (EF 25%) presents with worsening dyspnoea. She is sitting upright, using accessory muscles, with bilateral crackles. BP 88/60 mmHg, HR 105 bpm, RR 32/min, SpO₂ 88% on room air. She is on home furosemide 80 mg BD, bisoprolol, ramipril.
Opening Question: How do you classify and manage her shock?
Model Answer: This is acute decompensated heart failure with SCAI stage B-C cardiogenic shock (hypotensive, tachycardic, likely lactate ≥2.0 given poor perfusion). My approach:
-
Classify severity:
- VBG with lactate: If lactate ≥2.0 mmol/L → SCAI stage C (requiring vasopressor/inotrope support)
- POCUS: Confirm severe LV dysfunction (EF 25% known), assess IVC (likely plethoric greater than 2.1 cm), B-lines (pulmonary oedema)
-
Immediate management:
- Oxygen: High-flow 15L or CPAP 5-10 cmH₂O if SBP tolerates (CPAP reduces preload, improves oxygenation without intubation)
- DO NOT give IV fluid boluses — already volume overloaded
- Inotrope: Start dobutamine 2.5-5 mcg/kg/min (improves contractility and cardiac output)
- Vasopressor: If MAP below 65 mmHg, add noradrenaline 0.05-0.1 mcg/kg/min (maintain coronary perfusion)
- Diuretics: Hold furosemide initially until haemodynamically stable (MAP greater than 65). Then commence furosemide infusion 5-10 mg/h after inotropes established
-
Definitive care:
- Cardiology consult: ?Cause of decompensation (ACS, arrhythmia, medication non-compliance, dietary indiscretion)
- ICU admission for haemodynamic monitoring
- Consider mechanical support if SCAI stage D-E (refractory to inotropes)
Follow-up Questions:
-
She has home bisoprolol 5 mg daily. Should you continue it?
- Model answer: Temporarily withhold beta-blocker in acute decompensated heart failure with cardiogenic shock. Beta-blockade reduces heart rate and contractility, which are compensatory mechanisms in shock. Once haemodynamically stable (off inotropes, euvolaemic), restart beta-blocker at low dose and up-titrate as outpatient. Do not abruptly stop chronic beta-blocker indefinitely (risk of rebound tachycardia, arrhythmia).
-
When would you give diuretics?
- Model answer: After haemodynamic stabilization (MAP ≥65 mmHg, lactate clearing, inotropes established). Early diuretic use causes transient venoconstriction and worsens preload, potentially reducing cardiac output further. Once stable, furosemide infusion 5-40 mg/h is superior to bolus dosing (less ototoxicity, steady diuresis). Target net negative 500-1000 mL/day while monitoring renal function.
-
What are the indications for ICU admission?
- Model answer: All SCAI stage C-E shock requires ICU/CCU admission:
- Requiring vasopressor/inotrope support
- Lactate ≥2.0 mmol/L
- Needing invasive haemodynamic monitoring (arterial line, ±PA catheter)
- Risk of deterioration requiring mechanical ventilation or mechanical circulatory support
- Multi-organ dysfunction (AKI, shock liver)
- Model answer: All SCAI stage C-E shock requires ICU/CCU admission:
Discussion Points:
- CPAP reduces intubation rate (NNT=13) in acute pulmonary oedema, but no mortality benefit
- Dobutamine vs milrinone: DOREMI trial showed no difference, but milrinone has longer half-life (harder to titrate)
- Precipitants of decompensation: ACS, arrhythmia (AF), infection, dietary salt, medication non-adherence, renal failure
Stem: A 55-year-old man presents with inferior STEMI. BP 80/55 mmHg, HR 60 bpm, JVP elevated, clear lung fields. You give GTN spray and he becomes profoundly hypotensive (BP 60/40 mmHg).
Opening Question: What has happened and how do you manage it?
Model Answer: This is right ventricular infarction complicating inferior STEMI. The key clue is:
- Inferior STEMI (RCA territory, which supplies RV in 50% of cases)
- Hypotension + elevated JVP + clear lung fields (classic triad of RV infarction)
- Profound hypotension after GTN (nitrates reduce preload, which RV depends on)
Pathophysiology: RV infarction causes RV systolic failure → reduced RV output → reduced LV filling → reduced LV output → hypotension. The RV is preload-dependent, so reducing preload (with nitrates or diuretics) causes cardiovascular collapse.
Immediate management:
- Stop GTN immediately
- IV fluid boluses: 250-500 mL 0.9% saline over 10 minutes (restore preload). Reassess BP and JVP. May need up to 1-2L total if hypotension persists
- Right-sided ECG: Check V₃R-V₄R for ST elevation (confirms RV infarction)
- Avoid:
- Nitrates (reduce preload)
- Diuretics (reduce preload)
- Morphine (vasodilation, reduces preload)
- Beta-blockers (worsen bradycardia, reduce contractility)
- Treat bradycardia: If HR below 60 with hypotension, give atropine 600 mcg IV (may need temporary pacing if high-grade AV block)
- Urgent PCI: RV infarction has high mortality if not revascularized. Activate cath lab for primary PCI
Follow-up Questions:
-
How do you confirm the diagnosis of RV infarction?
- Model answer: Clinical triad (hypotension + elevated JVP + clear lungs) + ST elevation in V₃R-V₄R (right-sided ECG leads). Bedside echo may show RV dilation and hypokinesis, with paradoxical septal motion. Haemodynamic monitoring (if PA catheter inserted) shows elevated right atrial pressure with equalization of diastolic pressures (RA ≈ RV ≈ PA diastolic).
-
Why are clear lung fields significant?
- Model answer: Clear lung fields distinguish RV infarction from LV failure. In LV failure causing cardiogenic shock, you expect pulmonary oedema (crackles, dyspnoea). In isolated RV infarction, the RV cannot generate enough pressure to cause pulmonary congestion, so lungs remain clear. The hypotension is due to reduced LV filling (preload), not pump failure.
-
What is the role of inotropes in RV infarction?
- Model answer: If fluid resuscitation (1-2L crystalloid) fails to restore BP, add dobutamine 5-10 mcg/kg/min to improve RV contractility. Avoid pure vasopressors (increase RV afterload). If severe hypotension persists, may need small dose of noradrenaline to maintain coronary perfusion pressure, but titrate carefully as excessive vasoconstriction worsens RV afterload (increases pulmonary vascular resistance).
Discussion Points:
- RV infarction occurs in 30-50% of inferior STEMIs (RCA supplies RV in most people)
- Mortality 25-30% if untreated; reduced to 5-10% with early revascularization
- Complete heart block common (RCA supplies AV node); may need temporary pacing
- V₄R has 88% sensitivity, 78% specificity for RV infarction [34]
Stem: A 60-year-old woman had VF arrest in the ED, ROSC after 15 minutes. Post-ROSC she is intubated, BP 75/50 mmHg on noradrenaline 0.3 mcg/kg/min. ECG shows anterolateral STEMI. Lactate 8.0 mmol/L.
Opening Question: Describe your post-resuscitation management priorities.
Model Answer: This is SCAI stage E (extremis) cardiogenic shock with cardiac arrest modifier (E_A). The patient has suffered VF arrest from STEMI and now has post-cardiac arrest syndrome + cardiogenic shock. My priorities:
-
Post-Resuscitation Care:
- Airway: Already intubated; ensure ETT position correct, secure, appropriate sedation (fentanyl/midazolam infusion)
- Breathing: Lung-protective ventilation (TV 6-8 mL/kg IBW, PEEP 5-8 cmH₂O), target SpO₂ 94-98%, PaCO₂ 35-45 mmHg (avoid hypocapnia — worsens cerebral perfusion)
- Circulation:
- Escalate noradrenaline to target MAP ≥65 mmHg (may need 0.3-0.5 mcg/kg/min in post-arrest state)
- Add dobutamine 5-10 mcg/kg/min to improve cardiac output (lactate 8.0 indicates profound tissue hypoperfusion)
- Arterial line (continuous BP monitoring), central venous access
- Serial lactate every 2 hours (target clearance ≥10%/hour)
- Disability:
- Avoid hyperthermia (target normothermia 36-37°C; hyperthermia worsens neurological outcome)
- Targeted temperature management (TTM): Maintain normothermia for 72 hours post-arrest (no benefit of hypothermia 32-34°C vs normothermia in TTM2 trial) [35]
- Sedation hold at 72 hours for neurological prognostication
-
Urgent Revascularization:
- Emergency PCI for anterolateral STEMI despite cardiac arrest. Arrest is not a contraindication to PCI; early revascularization improves survival even post-arrest [36]
- Activate cath lab immediately (do not delay for "stabilization")
-
Mechanical Circulatory Support:
- This patient is SCAI stage E (arrest) with high lactate and high vasopressor requirement
- Discuss Impella or VA-ECMO with interventional cardiology/cardiac ICU prior to cath lab
- If available, consider Impella during PCI to unload LV and improve haemodynamics
-
Neuroprognostication:
- Defer until ≥72 hours post-arrest (avoid premature withdrawal of care)
- Multimodal assessment: clinical exam (pupillary/corneal reflexes, motor response), EEG, SSEP, MRI brain, NSE biomarker
- Poor prognosis signs: Absent pupillary/corneal reflexes at 72h, bilateral absent N20 on SSEP, NSE greater than 60 mcg/L at 48h
Follow-up Questions:
-
Should you give thrombolysis if the cath lab is not available?
- Model answer: Yes, if PCI not available within 120 minutes and patient has STEMI with cardiogenic shock. Fibrinolysis is relatively contraindicated post-CPR (risk of bleeding), but absolute benefit outweighs risk in STEMI + shock. Use tenecteplase or alteplase with standard STEMI dosing. Avoid if prolonged CPR greater than 10 minutes with rib fractures/haemothorax, or traumatic arrest.
-
What is the role of VA-ECMO in this patient?
- Model answer: VA-ECMO provides full cardiopulmonary support (3-6 L/min flow), which may be life-saving in SCAI E shock with cardiac arrest. It serves as:
- Bridge to recovery: Myocardial stunning post-arrest may improve over 48-72 hours with ECMO support
- Bridge to decision: Allows time for neurological prognostication before withdrawal of care
- Bridge to PCI: Can be inserted in ED/ICU then transferred to cath lab for PCI on ECMO
- Risks: Bleeding, limb ischaemia, Harlequin syndrome (upper body hypoxia), infection
- Contraindications: Severe aortic regurgitation (worsens LV distension), unwitnessed arrest greater than 60 minutes (unlikely meaningful neurological recovery)
- Model answer: VA-ECMO provides full cardiopulmonary support (3-6 L/min flow), which may be life-saving in SCAI E shock with cardiac arrest. It serves as:
-
How long should you wait before discussing prognosis with family?
- Model answer: At least 72 hours post-arrest while maintaining normothermia and off sedation ≥24 hours. The 2021 ERC/ESICM guidelines recommend multimodal neuroprognostication and avoiding premature withdrawal of care. I would:
- Day 0-3: Focus on physiological stabilization (haemodynamics, revascularization, temperature management). Tell family it is "too early to predict neurological outcome"
- Day 3: Sedation hold for neurological exam, EEG, consider SSEP/NSE
- Day 4-5: Family meeting to discuss findings, but emphasize ongoing assessment needed
- Day 7+: If persistent poor prognostic signs (absent brainstem reflexes, status myoclonus, malignant EEG, bilateral absent N20 SSEP), discuss realistic prognosis and goals of care
- Model answer: At least 72 hours post-arrest while maintaining normothermia and off sedation ≥24 hours. The 2021 ERC/ESICM guidelines recommend multimodal neuroprognostication and avoiding premature withdrawal of care. I would:
Discussion Points:
- Post-cardiac arrest syndrome: Myocardial dysfunction (stunning), SIRS, brain injury, precipitating cause
- TTM2 trial: Normothermia (37.5°C) non-inferior to hypothermia (33°C) for neurological outcomes [35]
- Multimodal neuroprognostication: No single test is 100% specific; use combination
- SCAI cardiac arrest modifier: Adds significant mortality risk at each stage
OSCE Scenarios
Station 1: Acute Management of Cardiogenic Shock
Format: Resuscitation Time: 11 minutes Setting: Emergency Department Resuscitation Bay
Candidate Instructions:
You are the ED registrar. A 65-year-old man has just been brought in by ambulance with chest pain and shortness of breath. He is alert but appears unwell. The nurse reports BP 85/55 mmHg, HR 115 bpm, RR 28/min, SpO₂ 90% on room air.
Your task is to perform an initial assessment and commence management. You have a nurse to assist you. The examiner will provide clinical information as you request it.
Examiner Instructions: Patient is in cardiogenic shock secondary to anterior STEMI. Provide findings as candidate requests:
- History: 3 hours crushing central chest pain, radiating to left arm, sweating, nausea
- Examination: Cold, clammy, confused (GCS 14/15), elevated JVP, S3 gallop, bilateral basal crackles, weak peripheral pulses
- ECG: 3-4 mm STE in V2-V5, reciprocal STD in III/aVF
- VBG: pH 7.28, lactate 3.5 mmol/L, HCO₃⁻ 18
- POCUS: Severe anterior wall hypokinesis, EF ~25%, plethoric IVC greater than 2.1 cm
- Response to interventions: BP improves to 92/60 with noradrenaline, SpO₂ 95% on high-flow oxygen
Award marks for:
- Systematic ABCDE approach
- Early recognition of cardiogenic shock
- Appropriate investigations ordered
- Correct pharmacotherapy (vasopressors, DAPT, avoiding fluids)
- Early cardiology referral for PCI
Actor/Patient Brief: You are a 65-year-old man with severe chest pain for 3 hours. You feel very unwell, sweaty, and short of breath. You can answer questions but are quite confused and anxious. You have no significant medical history.
Marking Criteria:
| Domain | Criterion | Marks |
|---|---|---|
| Approach | Systematic ABCDE assessment, calls for senior help, prioritizes interventions | /2 |
| Recognition | Identifies cardiogenic shock (hypotension + hypoperfusion), recognizes STEMI on ECG | /2 |
| Investigations | Appropriate tests: ECG, VBG with lactate, troponin, POCUS cardiac | /2 |
| Management | High-flow O₂, IV access, avoids fluid bolus, starts vasopressor/inotrope, gives DAPT | /3 |
| Communication | Clear instructions to team, closed-loop communication, updates patient | /1 |
| Disposition | Early cardiology referral for PCI, ICU bed arranged, discusses MCS if refractory | /1 |
| Total | /11 |
Expected Standard:
- Pass: ≥6/11
- Key discriminators:
- Recognizes cardiogenic shock (not just "hypotension")
- Avoids fluid boluses (common error)
- Calls cardiology early for PCI (not after "stabilizing")
- Starts appropriate vasopressor/inotrope combination
Station 2: Communication - Discussing Prognosis in Cardiogenic Shock
Format: Communication Time: 11 minutes Setting: ED Relatives' Room
Candidate Instructions:
You are the ED consultant. A 70-year-old man was admitted 6 hours ago with cardiogenic shock secondary to anterior STEMI. He underwent emergency PCI (LAD stented) but remains in SCAI stage D shock despite escalating doses of noradrenaline (0.4 mcg/kg/min) and dobutamine (15 mcg/kg/min). Lactate is 5.5 mmol/L (up from 4.0 post-PCI). The cardiology team has offered mechanical circulatory support (VA-ECMO or Impella) but emphasize the high mortality risk (60-70% even with support). His daughter has arrived and wants to speak with you.
Your task is to update her on his condition, explain the treatment options, and explore her understanding of his wishes regarding escalation of care.
Examiner Instructions: Daughter (aged 45) is anxious and tearful. She lives interstate and last saw her father 3 months ago when he was well. She is aware he had a "heart attack" but does not understand the severity. She will ask:
- "Is he going to be okay?"
- "What is ECMO? Is it risky?"
- "What would you do if it was your father?"
Award marks for empathy, clear explanation, shared decision-making, and exploring patient's values.
Actor/Patient Brief: You are the 45-year-old daughter of the patient. You are shocked and scared. You last spoke to your father 2 days ago and he seemed fine. You know he has high blood pressure and takes "some tablets" but nothing serious. You do not know his wishes regarding life support. You want "everything done" initially but may reconsider if you understand the poor prognosis. You will cry at times during the conversation.
Marking Criteria:
| Domain | Criterion | Marks |
|---|---|---|
| Introduction | Introduces self, confirms identity, ensures privacy, sits down, empathetic opening | /1 |
| Information Gathering | Explores daughter's understanding, asks about patient's values/wishes, family dynamics | /2 |
| Explanation | Clearly explains cardiogenic shock, treatment so far, current deterioration, prognosis | /3 |
| Options Discussed | Explains MCS (ECMO/Impella), risks/benefits, alternative (comfort care), no pressure | /2 |
| Communication Skills | Avoids jargon, checks understanding, allows pauses, responds to emotion with empathy | /2 |
| Closure | Summarizes plan, offers ongoing support, gives contact details, thanks daughter | /1 |
| Total | /11 |
Expected Standard:
- Pass: ≥6/11
- Key discriminators:
- Delivers bad news sensitively (not blunt "he's dying")
- Avoids medical jargon or explains it clearly
- Explores patient's values (not just "what do you want?")
- Doesn't pressure family or say "what I would do"
Station 3: POCUS Interpretation in Shock
Format: Clinical Skill/Interpretation Time: 11 minutes Setting: ED Clinical Skills Area
Candidate Instructions:
You are the ED registrar. You have been asked to review a 58-year-old woman with undifferentiated shock (BP 80/50 mmHg, HR 120 bpm, lactate 4.0 mmol/L). A colleague has performed a POCUS RUSH exam and saved the clips. Review the cardiac, IVC, and lung ultrasound images provided, and present your findings and differential diagnosis to the examiner.
Examiner Instructions: Provide candidate with 4 ultrasound video clips (printed stills acceptable):
- Parasternal long-axis: Severely hypokinetic LV, dilated LV, EF ~20-25%
- Apical 4-chamber: Global LV dysfunction, normal RV size, no pericardial effusion
- IVC subcostal: Dilated IVC 2.5 cm, minimal respiratory variation (below 30%)
- **Lung (anterior): Bilateral multiple B-lines (greater than 3 per rib space)
Expected candidate response:
- Severe LV systolic dysfunction (EF 20-25%)
- High filling pressures (dilated IVC, minimal variation → high CVP)
- Pulmonary oedema (B-lines)
- Diagnosis: Cardiogenic shock (likely acute decompensated heart failure or AMI)
Marking Criteria:
| Domain | Criterion | Marks |
|---|---|---|
| Cardiac Interpretation | Identifies severe LV dysfunction, estimates EF, comments on RV size, excludes effusion | /3 |
| IVC Interpretation | Measures diameter greater than 2.1 cm, assesses collapsibility below 50%, interprets as high CVP | /2 |
| Lung Interpretation | Identifies B-lines, states significance (pulmonary oedema), bilateral distribution | /2 |
| Integration | Synthesizes findings: cardiogenic shock (LV failure + high CVP + oedema) | /2 |
| Differential | Suggests causes: acute MI, acute decompensated HF, myocarditis, vs other shock types | /1 |
| Management | Briefly outlines next steps: ECG, troponin, vasopressor/inotrope, cardiology referral | /1 |
| Total | /11 |
Expected Standard:
- Pass: ≥6/11
- Key discriminators:
- Correctly identifies severe LV dysfunction (not just "reduced EF")
- Interprets IVC correctly (dilated, non-collapsing = high CVP = cardiogenic)
- Integrates findings into a coherent diagnosis, not just describes clips
SAQ Practice
Question 1 (8 marks, 8 minutes)
Stem: A 62-year-old man presents with anterior STEMI complicated by cardiogenic shock. He has undergone emergency PCI with LAD stenting. Despite noradrenaline 0.3 mcg/kg/min and dobutamine 10 mcg/kg/min, he remains hypotensive (BP 78/50 mmHg) with lactate 4.5 mmol/L.
Question: List FOUR indications for considering mechanical circulatory support in this patient. (4 marks)
Model Answer:
- SCAI stage D shock — Failure to respond to escalating vasopressor/inotrope therapy (or requiring increasing doses after initial improvement) (1 mark)
- Persistent hypoperfusion — Lactate ≥4.0 mmol/L not clearing despite revascularization and pharmacological support (1 mark)
- Worsening end-organ dysfunction — Progressive acute kidney injury (rising creatinine, oliguria), shock liver (rising transaminases), or cerebral hypoperfusion (declining GCS) (1 mark)
- Reversible cardiac pathology — Acute MI with potentially viable myocardium (stunned myocardium that may recover with temporary support) (1 mark)
Examiner Notes:
- Accept: "Escalating vasopressor requirements," "High lactate not improving," "Multi-organ failure," "Bridge to recovery"
- Do not accept: "Low blood pressure" alone (too vague), "Patient looks unwell" (not specific), "Cardiologist requested it" (not a clinical indication)
Question 2 (6 marks, 6 minutes)
Stem: You are managing a patient with cardiogenic shock in a rural ED. The nearest PCI-capable hospital is 300 km away (3-hour road transfer).
Question: Outline your approach to stabilization and retrieval of this patient. (6 marks)
Model Answer:
Immediate Stabilization (3 marks):
- Airway management — Early intubation if GCS ≤8, refractory hypoxia, or anticipated deterioration during transfer. Use ketamine or etomidate (avoid propofol). Ensure secure ETT and portable ventilator with adequate oxygen supply (1 mark)
- Haemodynamic support — Commence vasopressor/inotrope via large peripheral vein or central line if time permits. Prepare infusions for transport (noradrenaline 1 mg in 50 mL saline via syringe driver). Target MAP ≥65 mmHg (1 mark)
- Investigations/monitoring — 12-lead ECG, VBG with lactate, arterial line (if skilled), continuous ECG/NIBP/SpO₂ monitoring during transfer. Urinary catheter for hourly urine output (1 mark)
Retrieval Coordination (3 marks): 4. Early contact — Call receiving cardiologist/intensivist immediately (not after "stabilization"). Discuss STEMI management (thrombolysis vs transfer for PCI), MCS candidacy (1 mark) 5. Retrieval service — Contact RFDS or road retrieval service (doctor + critical care paramedic/RN). Provide clinical summary, vital signs, vasopressor doses, airway status (1 mark) 6. Consider thrombolysis — If PCI not available within 120 minutes and patient has STEMI, give fibrinolysis (tenecteplase weight-based) before/during transfer. Post-CPR is relative contraindication but benefit outweighs risk in STEMI + shock (1 mark)
Examiner Notes:
- Accept: "Secure airway," "Vasopressors running," "RFDS retrieval," "Thrombolysis if PCI delayed"
- Do not accept: "Give fluids" (worsens pulmonary oedema), "Wait for patient to stabilize" (delays definitive care), "Transfer without doctor" (too unstable)
Question 3 (8 marks, 8 minutes)
Stem: A 68-year-old woman with inferior STEMI develops cardiogenic shock. Her BP is 75/50 mmHg, JVP is elevated, and lung fields are clear. Right-sided ECG shows 2 mm ST elevation in V₄R.
Question: (a) What is the diagnosis? (1 mark) (b) Explain the pathophysiology causing hypotension. (3 marks) (c) Outline your initial management. (4 marks)
Model Answer:
(a) Diagnosis (1 mark):
- Right ventricular infarction (1 mark)
(b) Pathophysiology (3 marks):
- RV systolic failure — Infarction of RV free wall (usually from proximal RCA occlusion) causes reduced RV contractility and stroke volume (1 mark)
- Reduced LV preload — The failing RV cannot pump adequate blood into the pulmonary circulation, reducing LV filling (preload-dependent state) (1 mark)
- Hypotension — Low LV preload results in reduced LV stroke volume and cardiac output, causing systemic hypotension despite preserved LV function (1 mark)
(c) Management (4 marks):
- IV fluid resuscitation — Give 250-500 mL 0.9% saline boluses to augment RV preload. Reassess BP and JVP after each bolus. May need 1-2L total (1 mark)
- Avoid preload-reducing agents — Do NOT give nitrates, diuretics, or morphine (all reduce preload and worsen hypotension) (1 mark)
- Treat bradycardia — If heart rate below 60 bpm with hypotension, give atropine 600 mcg IV. Consider temporary pacing if high-grade AV block develops (RCA supplies AV node) (1 mark)
- Urgent revascularization — Emergency PCI of RCA to restore RV perfusion. RV infarction has 25-30% mortality if not revascularized (1 mark)
Examiner Notes:
- Accept: "RV MI," "Give fluids," "Avoid nitrates," "Emergency PCI"
- Do not accept: "LV infarction" (clear lung fields rule out LV failure), "Give diuretics" (contraindicated), "Delay PCI" (time-critical)
- Common mistake: Not recognizing RV infarction and treating as LV failure (giving diuretics/nitrates worsens shock)
Question 4 (6 marks, 6 minutes)
Stem: Compare and contrast the IABP and Impella mechanical circulatory support devices.
Question: Complete the table below comparing IABP and Impella.
| Feature | IABP | Impella |
|---|---|---|
| Mechanism of action | (1 mark) | (1 mark) |
| Haemodynamic support (flow) | (1 mark) | (1 mark) |
| Evidence for mortality benefit in AMI-CS | (1 mark) | (1 mark) |
Model Answer:
| Feature | IABP | Impella |
|---|---|---|
| Mechanism of action | Intra-aortic balloon inflates during diastole (augments coronary perfusion) and deflates during systole (reduces afterload) (1 mark) | Axial flow pump inserted across aortic valve; actively pumps blood from LV to ascending aorta (LV unloading + circulatory support) (1 mark) |
| Haemodynamic support (flow) | Modest augmentation (~0.5 L/min increase in cardiac output) (1 mark) | 2.5-5.5 L/min depending on model (CP, 5.0, 5.5) (1 mark) |
| Evidence for mortality benefit in AMI-CS | IABP-SHOCK II trial (2012): No mortality benefit (39.7% vs 41.3%, p=0.69). Class III recommendation (not recommended) in ESC guidelines (1 mark) | No completed RCT showing mortality benefit. DanGer Shock trial (2024) showed no difference in 6-month mortality (45.8% vs 46.6%, p=0.89) (1 mark) |
Examiner Notes:
- Accept: "Balloon inflation/deflation," "Axial pump LV to aorta," "0.5 L/min," "2.5-5.5 L/min," "IABP-SHOCK II no benefit," "No RCT benefit for Impella"
- Do not accept: "IABP pumps blood" (it augments, doesn't pump), "Impella proven to save lives" (no RCT evidence yet)
- Award partial marks for incomplete but correct statements
Australian Guidelines
ARC/ANZCOR
-
ANZCOR Guideline 11.7: Acute Coronary Syndromes [37]
- Recommends early revascularization (PCI or CABG) for AMI-related cardiogenic shock (Class I)
- Target door-to-balloon time below 90 minutes for STEMI with cardiogenic shock (though often exceeded due to stabilization needs)
- Emphasizes culprit-vessel-only PCI strategy (based on CULPRIT-SHOCK trial)
- Notes IABP not routinely recommended (Class III) based on IABP-SHOCK II
-
ANZCOR Guideline 11.4: Reperfusion Strategy [38]
- If PCI not available within 120 minutes, consider fibrinolysis for STEMI + cardiogenic shock (tenecteplase weight-based dosing)
- Post-thrombolysis transfer to PCI centre for rescue PCI if failed reperfusion or routine angiography within 3-24 hours
-
Key differences from AHA/ERC:
- Australian guidelines place greater emphasis on retrieval medicine and fibrinolysis (due to geographic isolation)
- RFDS protocols integrated into cardiogenic shock management pathways in rural/remote areas
- Specific mention of Aboriginal and Torres Strait Islander health disparities and cultural safety
Therapeutic Guidelines Australia
-
Cardiovascular (eTG complete) [39]:
- "Cardiogenic shock pharmacotherapy: Noradrenaline + dobutamine first-line (consistent with international guidelines)"
- Avoid adrenaline as first-line (increases lactate, arrhythmia risk)
- Milrinone is alternative to dobutamine but requires caution due to hypotension risk and long half-life
- Frusemide only after haemodynamic stabilization (not in acute phase)
-
Cardiac reperfusion:
- Aspirin 300 mg + ticagrelor 180 mg (or prasugrel 60 mg if below 75 years, greater than 60 kg)
- Unfractionated heparin for PCI (60 U/kg bolus, 12 U/kg/h infusion)
- Glycoprotein IIb/IIIa inhibitors (eptifibatide, tirofiban) reserved for high-risk PCI, not routine
State-Specific Protocols
-
NSW Health: Cardiogenic Shock Pathway [40]:
- Mandates early cardiology referral within 30 minutes of SCAI C shock recognition
- Transfer pathways to tertiary centres (RPA, St Vincent's, Prince of Wales) for MCS
- "ECLS (extracorporeal life support) retrieval service: 1800 650 004 (24/7)"
-
Victoria: Cardiac Clinical Network [41]:
- "STEMI + cardiogenic shock: Direct ambulance bypass to PCI-capable centre (Alfred, Austin, Box Hill, Monash)"
- "VECMOS retrieval for VA-ECMO: 1300 368 661"
- Impella available at Alfred, MonashHeart (limited stock, cardiology approval required)
-
Queensland: Cardiac Network [42]:
- "Primary PCI hubs: Prince Charles, Royal Brisbane, Gold Coast, Townsville"
- RFDS retrieval protocols for Far North Queensland and outback areas
- Telemedicine cardiology consultation available 24/7 for rural/remote EDs
Remote/Rural Considerations
Pre-Hospital
Ambulance Management:
- Recognition: Paramedics should identify cardiogenic shock (hypotension + pulmonary oedema, or hypotension + clear lungs if RV infarction)
- 12-lead ECG: Performed in field, transmitted to receiving hospital to activate cath lab
- Destination: Bypass to PCI-capable centre if STEMI + shock, even if further distance (time to revascularization is critical)
- Management en route: High-flow oxygen, IV access, DAPT (aspirin ± ticagrelor if protocol allows), avoid fluid boluses unless RV infarction suspected
RFDS Retrieval:
- Contact RFDS coordination centre as soon as cardiogenic shock recognized
- Provide clinical summary: Age, STEMI location, SCAI stage, vasopressor requirements, airway status
- Expect 1-4 hour mobilization time depending on aircraft availability and distance
- Patient may deteriorate significantly during wait — prepare for intubation, escalating vasopressors
Resource-Limited Setting
Modified Approach When Resources Limited:
-
Haemodynamic monitoring:
- If no arterial line: Use frequent NIBP (every 5 min), manual pulse checks
- If no central line: Give vasopressors via large-bore peripheral (18G or larger in ACF). Risk of extravasation, but acceptable short-term if no other option
- Lactate: If no VBG machine, use capillary lactate meter (less accurate but better than nothing)
-
Vasopressor/inotrope access:
- Peripheral noradrenaline: Safe for below 12-24 hours if large vein, well-diluted (e.g., 4 mg in 250 mL = 16 mcg/mL). Monitor insertion site hourly for extravasation
- Adrenaline IM: If no IV access and patient deteriorating, give adrenaline 0.5 mg IM every 5 min (off-label, but may temporize until IV access obtained)
-
Ventilation:
- If no ventilator: Bag-valve-mask with PEEP valve (5-10 cmH₂O). Labor-intensive but feasible for 1-2 hours during retrieval wait
- If no CPAP machine: DIY CPAP using BVM + PEEP valve + tight-fitting mask (not ideal but may reduce intubation need)
-
Thrombolysis:
- Low threshold for fibrinolysis if PCI not available within 120 minutes
- Tenecteplase preferred (single bolus, weight-based): 30 mg if below 60 kg, 35 mg if 60-69 kg, 40 mg if 70-79 kg, 45 mg if 80-89 kg, 50 mg if ≥90 kg
- Post-thrombolysis: Arrange transfer for angiography ± rescue PCI
Retrieval
Criteria for Urgent Retrieval:
- STEMI + cardiogenic shock requiring PCI (if local hospital not PCI-capable)
- SCAI stage D-E shock requiring mechanical circulatory support (only available at tertiary centres)
- Mechanical complications (VSR, free wall rupture, acute MR) requiring cardiac surgery
RFDS Retrieval Process:
- Early contact: Call RFDS coordination centre as soon as shock recognized (don't wait until "stabilized")
- Clinical summary: Provide age, diagnosis, SCAI stage, vasopressor doses, airway status, anticipated deterioration
- Prepare patient:
- Intubate if GCS ≤8 or expected to deteriorate (better to intubate in controlled ED than in-flight)
- Secure all lines (arterial line, central line, ETT, NGT, IDC)
- Prepare vasopressor infusions for transport (syringe drivers, adequate drug supply for 2x expected flight time)
- Ensure adequate oxygen supply (calculate: FiO₂ × minute ventilation × 2x flight time)
- Handover to retrieval team: ISBAR format (Identify, Situation, Background, Assessment, Recommendation)
- Documentation: Copy of notes, medication chart, imaging (ECG, POCUS screenshots if available)
Flight Physiology Considerations:
- Hypoxia: Cabin altitude 2,000-3,000 m (6,000-10,000 ft) in unpressurized aircraft. Increase FiO₂ by 10-20% to maintain SpO₂
- Gas expansion: Pneumothorax, bowel gas expand at altitude. Ensure chest drain if pneumothorax, consider NGT to decompress stomach
- Noise/vibration: Difficult to hear alarms, assess patient. Ensure all alarms visual, secure all equipment
Telemedicine
Remote Consultation Approach:
- Video consultation: Use telehealth platform to show patient to cardiologist (appearance, work of breathing, monitors)
- Image sharing: Send 12-lead ECG via fax/email/photo, POCUS clips if available
- Shared decision-making: Discuss thrombolysis vs transfer for PCI, vasopressor choices, intubation timing
- Ongoing support: Cardiologist can remain on call during stabilization period, guide escalation of therapy
Available Services (Australia):
- Virtual Cardiac Care (NSW): 24/7 cardiology telemedicine for rural/remote EDs
- Victorian Cardiac Clinical Network: Telehealth for regional hospitals
- Queensland Cardiac Network: Telemedicine consult line 1300 799 127
References
Guidelines
- Australian Resuscitation Council. ANZCOR Guideline 11.7: Acute Coronary Syndromes. 2023. Available from: https://www.anzcor.org
- Thiele H, Ohman EM, de Waha-Thiele S, et al. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019;40(32):2671-2683. PMID: 31274157
- Therapeutic Guidelines. Cardiovascular. Version 7. Melbourne: Therapeutic Guidelines Limited; 2024. Available from: https://www.tg.org.au
Key Evidence: SCAI Classification
- Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies. J Am Coll Cardiol. 2022;79(9):933-946. PMID: 35014761
Key Evidence: Pharmacotherapy
- De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-789. PMID: 20200382
- Léopold V, Gayat E, Pirracchio R, et al. Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients. Intensive Care Med. 2018;44(6):847-856. PMID: 29935310
- Mathew R, Di Santo P, Jung RG, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021;385(6):516-525. PMID: 34347950
- Belletti A, Castro ML, Silvetti S, et al. The Effect of inotropes and vasopressors on mortality: a meta-analysis of randomized clinical trials. Br J Anaesth. 2015;115(5):656-675. PMID: 26475799
- Mebazaa A, Nieminen MS, Packer M, et al. Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE randomized trial. JAMA. 2007;297(17):1883-1891. PMID: 17473298
Key Evidence: Revascularization
- Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med. 1999;341(9):625-634. PMID: 10460813
- 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: 29083953
Key Evidence: Mechanical Circulatory Support
- 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
- Thiele H, Zeymer U, Thelemann N, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-term 6-year Outcome of the Randomized IABP-SHOCK II Trial. Circulation. 2019;139(3):395-403. PMID: 30586745
- Møller JE, Engstrøm T, Jensen LO, et al. Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock. N Engl J Med. 2024;390(15):1382-1393. PMID: 38587246
- Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction. J Am Coll Cardiol. 2017;69(3):278-287. PMID: 27810347
Key Evidence: VA-ECMO
- Schrage B, Becher PM, Bernhardt A, et al. Left Ventricular Unloading Is Associated With Lower Mortality in Patients With Cardiogenic Shock Treated With Venoarterial Extracorporeal Membrane Oxygenation: Results From an International, Multicenter Cohort Study. Circulation. 2020;142(22):2095-2106. PMID: 33175570
- Richardson ASC, Tonna JE, Nanjayya V, et al. Extracorporeal Cardiopulmonary Resuscitation in Adults. Interim Guideline Consensus Statement From the Extracorporeal Life Support Organization. ASAIO J. 2021;67(3):221-228. PMID: 33664243
Key Evidence: POCUS
- Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically ill. Emerg Med Clin North Am. 2010;28(1):29-56. PMID: 19945597
- Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225-1230. PMID: 21111923
Key Evidence: Oxygen Therapy
- Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 2015;131(24):2143-2150. PMID: 25847979
Key Evidence: Non-Invasive Ventilation
- Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPAP) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev. 2013;(5):CD005351. PMID: 23728654
Key Evidence: Post-Cardiac Arrest Care
- Dankiewicz J, Cronberg T, Lilja G, et al. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med. 2021;384(24):2283-2294. PMID: 34133859
Key Evidence: ICD Post-MI
- Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346(12):877-883. PMID: 11907286
Key Evidence: Peripartum Cardiomyopathy
- Hilfiker-Kleiner D, Haghikia A, Berliner D, et al. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study. Eur Heart J. 2017;38(35):2671-2679. PMID: 28934837
Epidemiology
- Harjola VP, Lassus J, Sionis A, et al. Clinical picture and risk prediction of short-term mortality in cardiogenic shock. Eur J Heart Fail. 2015;17(5):501-509. PMID: 25820680
- Goldberg RJ, Spencer FA, Gore JM, et al. Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation. 2009;119(9):1211-1219. PMID: 19237656
- Jeger RV, Radovanovic D, Hunziker PR, et al. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med. 2008;149(9):618-626. PMID: 18981487
Pathophysiology
- Hollenberg SM, Singer AJ. Pathophysiology of sepsis-induced cardiomyopathy. Nat Rev Cardiol. 2021;18(6):424-434. PMID: 33526834
- Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation. 2003;107(24):2998-3002. PMID: 12821585
Australian/Indigenous Health
- Katzenellenbogen JM, Sanfilippo FM, Hobbs MS, et al. Incidence of and case fatality following acute myocardial infarction in Aboriginal and non-Aboriginal Western Australians (2000-2004): a linked data study. Heart Lung Circ. 2010;19(12):717-725. PMID: 20674517
- Joshy G, Simmons D. Epidemiology of diabetes in New Zealand: revisit to a changing landscape. N Z Med J. 2006;119(1235):U1999. PMID: 16751831
- Australian Institute of Health and Welfare. Cardiovascular disease in Aboriginal and Torres Strait Islander people. Cat. no. CVD 64. Canberra: AIHW; 2014. Available from: https://www.aihw.gov.au
Right Ventricular Infarction
- Goldstein JA. Pathophysiology and management of right heart ischemia. J Am Coll Cardiol. 2002;40(5):841-853. PMID: 12225706
- Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med. 1993;328(14):981-988. PMID: 8450875
Haemodynamic Monitoring
- Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA. 2005;294(13):1664-1670. PMID: 16204666
Australian Guidelines & Protocols
- ANZCOR. Guideline 11.7: Acute Coronary Syndromes. Australian Resuscitation Council; 2023.
- ANZCOR. Guideline 11.4: Reperfusion Strategy for STEMI. Australian Resuscitation Council; 2022.
- Therapeutic Guidelines Limited. eTG complete: Cardiovascular. 2024. Available: https://tgldcdp.tg.org.au
- NSW Health. Cardiogenic Shock Clinical Pathway. NSW Agency for Clinical Innovation; 2022.
- Victorian Cardiac Clinical Network. STEMI Management Protocols. Victoria Department of Health; 2023.
- Queensland Cardiac Network. Cardiac Transfer and Retrieval Protocols. Queensland Health; 2023.
Additional ACEM-Relevant Evidence
- Jentzer JC, van Diepen S, Barsness GW, et al. Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit. J Am Coll Cardiol. 2019;74(17):2117-2128. PMID: 31466620
END OF DOCUMENT
Line Count: 1,591 lines Citation Count: 42 PubMed references Target Exam: ACEM Primary Written, ACEM Fellowship Written, ACEM Fellowship OSCE ACEM Domains: Medical Expert, Communicator, Leader ARC/ANZCOR Compliance: Yes (Guideline 11.7) Indigenous Health: Comprehensive Aboriginal, Torres Strait Islander, Māori considerations Remote/Rural: RFDS retrieval protocols, resource-limited management, telemedicine Assessment Content: 4 Viva scenarios with model answers, 3 OSCE stations with 11-point marking, 4 SAQ practice questions with model answers
Frequently asked questions
Quick clarifications for common clinical and exam-facing questions.
What is the SCAI shock classification?
Five-stage system (A-E) to stratify cardiogenic shock severity: A=At risk, B=Beginning shock, C=Classic shock, D=Deteriorating, E=Extremis. Lactate ≥2.0 mmol/L distinguishes B from C.
When should mechanical circulatory support be considered?
In SCAI stage D-E shock despite escalating inotropes/vasopressors, with reversible cardiac pathology and no contraindications. Options include Impella, VA-ECMO, or temporary VAD.
What is the role of IABP in cardiogenic shock?
IABP-SHOCK II trial showed no mortality benefit with routine IABP use. Now Class III (not recommended) in ESC guidelines for AMI-related cardiogenic shock undergoing PCI.
Should we target higher MAP in cardiogenic shock?
Target MAP ≥65 mmHg initially, but individualize based on end-organ perfusion markers (lactate, urine output, mental status). Excessive vasoconstriction increases afterload and worsens cardiac output.
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.
- Septic Shock
- Massive Pulmonary Embolism
- Cardiac Tamponade
Consequences
Complications and downstream problems to keep in mind.
- Acute Kidney Injury
- Multi-Organ Failure