Acute Heart Failure in ICU

Quick Answer

Acute heart failure (AHF) is the rapid onset or worsening of heart failure symptoms requiring urgent evaluation and treatment. Use the Nohria-Stevenson classification to categorize patients: wet/warm (congested, adequate perfusion - most common, 67%) vs wet/cold (congested, hypoperfused - cardiogenic shock, 28%). Immediate management follows CHAMPIT trigger identification (Coronary syndrome, Hypertension, Arrhythmia, Mechanical cause, Pulmonary embolism, Infection, Tamponade). For congestion: IV diuretics at 2-2.5x oral daily dose (DOSE trial, PMID: 21352018). For hypoperfusion: noradrenaline first-line vasopressor (SOAP II, PMID: 20802220), dobutamine for low cardiac output. Cardiogenic shock (SBP less than 90, lactate greater than 2, end-organ dysfunction) requires early revascularization for ACS (SHOCK trial, PMID: 10460813) and consideration of mechanical support (Impella - DanGer Shock, PMID: 38587239; VA-ECMO - ECLS-SHOCK, PMID: 37634145). IABP NOT recommended routinely for MI-related cardiogenic shock (IABP-SHOCK II, PMID: 22972210).

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CICM Exam Focus

Second Part Written Exam

SAQ themes (high-yield):

• Initial assessment and classification of AHF using Nohria-Stevenson
• Diuretic strategies: dosing, bolus vs infusion, resistance management
• Inotrope and vasopressor selection in cardiogenic shock
• Indications and evidence for mechanical circulatory support (IABP, Impella, ECMO)
• Management of acute-on-chronic heart failure with preserved vs reduced ejection fraction
• NIV in acute pulmonary oedema
• Cardiogenic shock definition and management escalation
• Acute mechanical complications requiring surgical intervention

Expected SAQ stems:

• "A 68-year-old man presents with acute pulmonary oedema following STEMI. Describe your initial management and indications for escalation."
• "Outline the evidence for and against mechanical circulatory support in cardiogenic shock."
• "A patient on IV furosemide has inadequate urine output despite dose escalation. Describe diuretic resistance and management strategies."

Second Part Hot Case

Common presentations:

• Ventilated patient post-MI with cardiogenic shock on multiple inotropes
• Patient on VA-ECMO following refractory cardiac arrest
• Chronic heart failure patient with acute decompensation and renal impairment
• Post-cardiac surgery patient with low cardiac output syndrome
• Rheumatic valve disease with acute decompensation (Indigenous patient)

Examiner expectations:

• Systematic one-minute summary including haemodynamic status
• Integration of clinical findings with echocardiographic data
• Rational inotrope/vasopressor selection with dose ranges
• Understanding of mechanical support indications and contraindications
• Prognosis discussion with family communication approach

Second Part Viva

Core topics:

• Pathophysiology of acute heart failure and cardiogenic shock
• Frank-Starling mechanism and its failure
• Neurohormonal activation and its consequences
• Comparison of inotropes: dobutamine vs milrinone vs levosimendan
• IABP physiology: augmented diastolic pressure, reduced afterload
• VA-ECMO configuration and complications
• Evidence interpretation: DOSE, IABP-SHOCK II, ECLS-SHOCK, DanGer Shock

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Key Points

1. Nohria-Stevenson classification divides AHF into four profiles based on congestion (wet/dry) and perfusion (warm/cold); wet/warm is commonest (67%), wet/cold represents cardiogenic shock (28%) with mortality 50-60% (PMID: 12544220)

2. CHAMPIT identifies reversible triggers: Coronary syndrome, Hypertension, Arrhythmia, Mechanical cause, Pulmonary embolism, Infection, Tamponade - must be excluded/treated immediately

3. IV loop diuretics are first-line for congestion; start at 2-2.5x oral daily dose (ESC Guidelines, PMID: 34447992); DOSE trial showed no difference between bolus and continuous infusion (PMID: 21352018)

4. NIV (CPAP/BiPAP) reduces intubation rates and mortality in acute pulmonary oedema; start CPAP 5-10 cmH2O or BiPAP 10/5 cmH2O (3CPO trial, PMID: 18621006)

5. Noradrenaline is preferred first-line vasopressor over dopamine (SOAP II trial - reduced arrhythmias, PMID: 20802220); add dobutamine if persistent low cardiac output

6. Cardiogenic shock definition: SBP less than 90 mmHg (or vasopressor requirement), clinical signs of hypoperfusion, lactate greater than 2 mmol/L; SCAI stages classify severity A-E

7. Early revascularization is mandated in MI-related cardiogenic shock - 6-month and 1-year mortality benefit (SHOCK trial, PMID: 10460813); do not delay for stabilization

8. IABP is NOT recommended routinely for MI-related cardiogenic shock (IABP-SHOCK II: no mortality benefit, PMID: 22972210); consider only for mechanical complications

9. Impella shows 180-day mortality benefit in AMI-related cardiogenic shock (DanGer Shock 2024, PMID: 38587239); VA-ECMO routine use showed no benefit (ECLS-SHOCK, PMID: 37634145)

10. Indigenous Australians have high rates of rheumatic heart disease (RHD) causing acute valve failure; require culturally appropriate care with Aboriginal Health Worker/Liaison Officer involvement (PMID: 24204364)

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Definition

Acute Heart Failure (AHF)

Definition (ESC 2021, PMID: 34447992):

Acute heart failure is defined as the rapid onset or worsening of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment.

AHF is a clinical syndrome rather than a single diagnosis. It encompasses:

1. De novo AHF: First presentation of heart failure (typically acute and dramatic)
2. Acutely decompensated chronic heart failure (ADHF): Worsening of established heart failure
3. Cardiogenic shock: Severe form with end-organ hypoperfusion

Classification by Ejection Fraction

ICU relevance: HFrEF and HFmrEF may respond to inotropes; HFpEF management focuses on rate control, preload optimization, and treating underlying causes.

Cardiogenic Shock Definition

ESC/EACTS Definition (PMID: 34447992):

• SBP less than 90 mmHg (or vasopressor requirement to maintain SBP ≥90)
• Clinical signs of hypoperfusion: cold extremities, oliguria, altered mental status
• Biochemical markers: lactate greater than 2 mmol/L, end-organ dysfunction

SCAI Classification (2019, PMID: 30711358):

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Classification: Nohria-Stevenson

The Nohria-Stevenson classification (PMID: 12544220) is the cornerstone of AHF clinical assessment, guiding initial therapy based on two clinical parameters:

Assessment Parameters

Congestion (Wet vs Dry):

• Signs of congestion (WET): Orthopnoea, elevated JVP, pulmonary crackles, peripheral oedema, hepatomegaly, hepatojugular reflux, S3 gallop
• No congestion (DRY): Absence of above signs, normal JVP

Perfusion (Warm vs Cold):

• Adequate perfusion (WARM): Warm extremities, normal capillary refill (less than 3 seconds), adequate urine output, normal mentation
• Poor perfusion (COLD): Cool extremities, prolonged capillary refill (greater than 3 seconds), oliguria, confusion, narrow pulse pressure, hypotension

Four Clinical Profiles

Clinical Pearl: Profile B is the most common presentation (67%); Profile C represents cardiogenic shock with highest mortality.

Bedside Assessment Accuracy

The Nohria-Stevenson classification correlates with invasive haemodynamic measurements:

• Congestion correlates with PCWP greater than 22 mmHg
• Hypoperfusion correlates with cardiac index less than 2.2 L/min/m²

Prognostic value (PMID: 12544220):

• Profile A: 6-month mortality 5%
• Profile B: 6-month mortality 20%
• Profile C: 6-month mortality 35%
• Profile L: 6-month mortality 15%

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Pathophysiology

Normal Cardiac Function

Frank-Starling Mechanism: The heart's ability to increase stroke volume in response to increased preload (venous return). Within physiological limits, increased sarcomere stretch leads to increased contractile force.

Determinants of Cardiac Output:

• CO = HR × SV
• SV depends on: Preload (venous return), Afterload (vascular resistance), Contractility (inotropy)

Pathophysiology of Acute Heart Failure

1. Reduced Contractility (Systolic Dysfunction)

Primary mechanisms:

• Myocardial ischaemia/infarction → cardiomyocyte necrosis → reduced contractile mass
• Myocarditis → inflammatory infiltration → contractile dysfunction
• Dilated cardiomyopathy → sarcomere disarray → ineffective contraction

Consequences:

• Reduced stroke volume → decreased cardiac output
• Increased end-diastolic volume → elevated filling pressures
• Pulmonary venous congestion → pulmonary oedema
• Systemic venous congestion → peripheral oedema, hepatic congestion

2. Impaired Relaxation (Diastolic Dysfunction)

Primary mechanisms:

• Hypertensive heart disease → concentric hypertrophy → impaired relaxation
• Ischaemia → impaired lusitropy (active relaxation is energy-dependent)
• Restrictive cardiomyopathy → stiff myocardium → impaired filling

Consequences:

• Elevated filling pressures despite normal/near-normal EF
• Pulmonary congestion with relatively preserved systolic function
• Sensitivity to preload and heart rate changes

3. Neurohormonal Activation

The failing heart triggers compensatory mechanisms that are initially adaptive but become maladaptive:

Sympathetic Nervous System Activation:

• Increased catecholamines → tachycardia, vasoconstriction
• Short-term: maintains blood pressure
• Long-term: myocardial toxicity, arrhythmias, increased afterload

Renin-Angiotensin-Aldosterone System (RAAS):

• Decreased renal perfusion → renin release → angiotensin II → aldosterone
• Effects: vasoconstriction, sodium/water retention, myocardial fibrosis
• Contributes to volume overload and ventricular remodelling

Natriuretic Peptides:

• ANP (atria) and BNP (ventricles) released in response to wall stretch
• Effects: natriuresis, diuresis, vasodilation
• Overwhelmed in severe heart failure → diagnostic utility (PMID: 15869614)

Vasopressin (ADH):

• Non-osmotic release in heart failure
• Contributes to fluid retention and hyponatraemia

4. Cardiogenic Shock Cascade

Shock Spiral (PMID: 10460813):

1. Severe myocardial dysfunction → reduced CO
2. Hypotension → reduced coronary perfusion pressure
3. Myocardial ischaemia worsens → further dysfunction
4. SIRS activation → vasodilation, capillary leak
5. Multi-organ failure → death

Key insight: This positive feedback loop explains why cardiogenic shock has 40-60% mortality despite optimal therapy.

Pulmonary Oedema Physiology

Starling Equation Applied:

• Jv = Kf [(Pc - Pi) - σ(πc - πi)]
• Increased pulmonary capillary pressure (Pc greater than 25 mmHg) → transudation
• Acutely: interstitial oedema → alveolar flooding → V/Q mismatch → hypoxaemia
• Lymphatic drainage capacity exceeded (normally 20 mL/hour)

Flash Pulmonary Oedema:

• Sudden onset, often with preserved EF
• Causes: severe hypertension, acute MR, renal artery stenosis
• Mechanism: acute afterload increase → LV decompensation → rapid Pc rise

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Aetiology

CHAMPIT - Acute Triggers (ESC 2021)

Must identify and treat immediately:

Underlying Causes of Heart Failure

Ischaemic Heart Disease (50-70%):

• Acute MI with LV dysfunction
• Chronic ischaemic cardiomyopathy
• Hibernating myocardium

Valvular Heart Disease:

• Aortic stenosis (afterload increase)
• Mitral regurgitation (volume overload)
• Rheumatic heart disease (significant in Indigenous populations, PMID: 24204364)

Cardiomyopathies:

• Dilated cardiomyopathy (idiopathic, familial, toxic - alcohol, chemotherapy)
• Hypertrophic cardiomyopathy (outflow obstruction)
• Takotsubo cardiomyopathy (stress-induced, apical ballooning)
• Peripartum cardiomyopathy

Hypertensive Heart Disease:

• Long-standing hypertension → LVH → diastolic dysfunction → HFpEF
• Hypertensive emergency → flash pulmonary oedema

Arrhythmias:

• Tachycardia-induced cardiomyopathy (persistent rapid AF)
• Bradycardia (complete heart block, sick sinus)

High-Output States:

• Severe anaemia
• Thyrotoxicosis
• Arteriovenous fistula

Precipitants of Decompensation

• Non-adherence to medications or fluid/salt restriction
• Ischaemia (silent or symptomatic)
• Arrhythmia (new AF common)
• Infection (pneumonia, UTI, sepsis)
• Drugs: NSAIDs, negative inotropes, calcium channel blockers
• Renal deterioration (cardiorenal syndrome)
• Anaemia (undiagnosed or blood loss)
• Thyroid dysfunction
• Pregnancy (peripartum cardiomyopathy or unmasking underlying disease)

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Clinical Assessment

History

Symptoms of Congestion:

• Dyspnoea (exertional → rest → orthopnoea → PND)
• Peripheral oedema (ankle → sacral in bedridden)
• Abdominal distension (ascites, hepatomegaly)
• Anorexia, nausea (gut oedema)

Symptoms of Hypoperfusion:

• Fatigue, weakness
• Confusion, altered mentation
• Reduced urine output

Temporal Pattern:

• Acute (hours): ACS, arrhythmia, mechanical complication
• Subacute (days-weeks): Infection, non-adherence, progression

Functional Class (NYHA):

• Class I: No limitation
• Class II: Slight limitation
• Class III: Marked limitation
• Class IV: Symptoms at rest

Physical Examination

Vital Signs:

• Blood pressure: Hypotension (SBP less than 90) = shock; severe hypertension = consider flash oedema
• Heart rate: Tachycardia (compensatory); bradycardia (drugs, conduction disease)
• Respiratory rate: Tachypnoea indicates pulmonary congestion
• SpO2: Hypoxaemia with pulmonary oedema

Signs of Congestion (ELEVATED FILLING PRESSURES):

Signs of Hypoperfusion (LOW CARDIAC OUTPUT):

Cardiac Examination:

• Displaced apex (LV dilatation)
• Murmurs (MR, AS may be causative)
• Pericardial rub (pericarditis, post-MI)

Application of Nohria-Stevenson at Bedside

Step 1: Assess Congestion

• Elevated JVP, crackles, oedema, orthopnoea = WET
• No congestion signs = DRY

Step 2: Assess Perfusion

• Warm peripheries, normal CRT, normal mentation = WARM
• Cold peripheries, prolonged CRT, confusion, oliguria = COLD

Step 3: Classify

• WARM + WET = Profile B → Diuretics ± vasodilators
• COLD + WET = Profile C → Inotropes ± vasopressors ± MCS
• WARM + DRY = Profile A → Optimise therapy
• COLD + DRY = Profile L → Careful volume trial, inotropes

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Investigations

Immediate Investigations (Within 15-30 Minutes)

ECG (12-lead):

• STEMI/NSTEMI → urgent revascularization
• Arrhythmia (AF, VT, heart block) → specific management
• LVH (voltage criteria) → hypertensive heart disease
• Low voltage, electrical alternans → pericardial effusion/tamponade

Blood Tests:

Chest X-ray:

• Cardiomegaly: CTR greater than 0.5
• Pulmonary oedema: Kerley B lines, upper lobe diversion, perihilar haze ("bat-wing")
• Pleural effusions: Blunted costophrenic angles
• Normal CXR does NOT exclude AHF

Echocardiography (Within 24-48 Hours, Urgent if Shock)

Essential Assessment:

In Cardiogenic Shock (URGENT echo):

• Mechanical complications: VSD, papillary muscle rupture, free wall rupture
• Severe valve dysfunction
• Tamponade
• RV infarct

Haemodynamic Monitoring

Non-Invasive:

• Serial clinical assessment (warm/cold, wet/dry)
• Urine output monitoring
• Lactate clearance

Invasive (Consider in Shock):

Arterial Line:

• Continuous BP monitoring
• ABG sampling
• Pulse pressure variation (PPV) for fluid responsiveness

Central Venous Catheter:

• CVP measurement (limited utility but trends useful)
• Central venous oxygen saturation (ScvO2 less than 65% suggests inadequate delivery)

Pulmonary Artery Catheter (Swan-Ganz):

• Not routinely recommended (ESCAPE trial, PMID: 16183740)
• Consider in: diagnostic uncertainty, refractory shock, complex management
• Measurements: PCWP, CO, SVR, PA pressures

Typical Haemodynamic Profiles:

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Initial Stabilization

Immediate Priorities (First 30-60 Minutes)

Airway and Breathing:

• Supplemental oxygen if SpO2 less than 90% (target 94-98%)
• NIV (CPAP/BiPAP) for respiratory distress with pulmonary oedema
  • CPAP 5-10 cmH2O or BiPAP 10/5 cmH2O
  • "Reduces intubation and mortality (3CPO trial, PMID: 18621006)"
  • "Mechanism: decreases preload (increased intrathoracic pressure), reduces work of breathing"
• Intubation if: GCS less than 8, respiratory failure despite NIV, airway protection needed

Circulation:

• IV access (preferably two large-bore)
• Continuous monitoring (ECG, SpO2, BP)
• Urinary catheter for urine output monitoring (target greater than 0.5 mL/kg/hr)

Classify Haemodynamic Profile:

• Congested → Diuretics, vasodilators
• Hypoperfused → Inotropes, vasopressors
• Both → Combined approach

Position

• Upright position (sitting, legs dependent) reduces preload
• Supine position worsens pulmonary oedema
• Exception: Cardiogenic shock with hypotension may tolerate head-of-bed elevation only 30°

NIV in Acute Pulmonary Oedema

Evidence (3CPO Trial, PMID: 18621006):

• Randomized 1,069 patients to standard oxygen, CPAP, or NIPPV
• NIV reduced dyspnoea, respiratory rate, acidosis
• 7-day mortality trend: NIV 9.8% vs O2 11.7% (not significant)
• Reduced intubation: Combined NIV groups

Settings:

• CPAP: 5-10 cmH2O
• BiPAP: IPAP 10-15 cmH2O, EPAP 5-8 cmH2O
• Titrate to comfort and oxygenation

Contraindications:

• Immediate intubation required
• GCS less than 8
• Vomiting, aspiration risk
• Facial trauma/surgery
• Cardiogenic shock with severe hypotension (relative - can trial with close monitoring)

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Diuretic Therapy

Initial Diuretic Strategy (ESC 2021)

First-Line: IV Loop Diuretics

Dosing (PMID: 34447992):

• Diuretic-naive: Furosemide 20-40 mg IV
• On oral diuretics: Give 2-2.5 times the oral daily dose as IV
• Example: Patient on oral furosemide 80 mg daily → 160-200 mg IV

Monitoring:

• Urine output target: greater than 100 mL/hour for first 6 hours
• If inadequate response at 2 hours, double the dose (max single dose 200-400 mg)
• Weigh daily, aim for 0.5-1 kg/day weight loss

DOSE Trial (2011, PMID: 21352018)

Design:

• 2 x 2 factorial: High-dose (2.5x oral) vs Low-dose (1x oral); Bolus vs Continuous infusion
• 308 patients with ADHF

Key Findings:

• No significant difference in patient-assessed symptoms at 72 hours
• No difference in renal function change
• High-dose group: trend toward better decongestion (greater weight loss, fluid loss)
• No difference between bolus and continuous infusion

Clinical Implication:

• Start at 2-2.5x oral dose (safe and potentially more effective for decongestion)
• No advantage of continuous infusion over bolus

Diuretic Resistance

Definition: Failure to achieve adequate diuresis despite escalating loop diuretic doses.

Mechanisms:

1. Reduced renal perfusion: Low cardiac output, hypovolaemia
2. Neurohormonal activation: RAAS activation causes sodium reabsorption
3. Post-diuretic sodium retention: Compensatory reabsorption between doses
4. Braking phenomenon: Chronic diuretic use → distal tubule hypertrophy
5. Hypoalbuminaemia: Reduced diuretic delivery (protein-bound)
6. NSAIDs: Reduce prostaglandin-mediated vasodilation

Strategies for Diuretic Resistance:

CARRESS-HF Trial (2012, PMID: 23126250)

Design:

• 188 patients with ADHF, worsening renal function
• Ultrafiltration vs stepped pharmacological therapy

Key Findings:

• No difference in weight loss at 96 hours
• Higher creatinine rise with ultrafiltration
• More adverse events (bleeding, catheter-related) with UF

Clinical Implication:

• Ultrafiltration is NOT superior to aggressive diuretic therapy
• Reserve for refractory cases or volume overload in ESKD

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Vasodilator Therapy

Indications

Vasodilators are appropriate for:

• Profile B (warm + wet) with SBP greater than 90 mmHg
• Hypertensive crisis with pulmonary oedema
• Severe mitral or aortic regurgitation (afterload reduction)

Contraindications:

• SBP less than 90 mmHg (hypotension, cardiogenic shock)
• Severe aortic stenosis (fixed obstruction)
• Right ventricular infarction (RV preload-dependent)

Glyceryl Trinitrate (GTN)

Mechanism:

• NO donor → venodilation (reduces preload) at low doses
• Arterial vasodilation (reduces afterload) at higher doses
• Coronary vasodilation

Dosing:

• Start 10-20 mcg/min IV
• Titrate by 10-20 mcg/min every 5-10 minutes
• Target: symptom relief, SBP 100-110 mmHg, reduction in filling pressures
• Maximum typically 200-400 mcg/min

Monitoring:

• Continuous BP (arterial line if on high doses)
• Headache common (nitrate-induced)
• Tachyphylaxis develops after 24-48 hours continuous use

Sodium Nitroprusside

Mechanism:

• NO donor → balanced arterial and venous vasodilation
• Rapid onset, rapid offset (half-life 2 minutes)
• Potent afterload reduction

Indications:

• Hypertensive emergency with pulmonary oedema
• Severe MR or AR (afterload reduction)
• AHF refractory to GTN

Dosing:

• Start 0.3 mcg/kg/min
• Titrate by 0.5 mcg/kg/min every 5 minutes
• Maximum 5 mcg/kg/min (risk of cyanide toxicity above this)

Cautions:

• Cyanide toxicity: Risk with high doses (greater than 4 mcg/kg/min) or prolonged use (greater than 48 hours), hepatic/renal impairment
• Monitor thiocyanate levels if prolonged use
• Avoid in severe hepatic/renal impairment

Nesiritide

Mechanism: Recombinant BNP, causes vasodilation and natriuresis

Evidence (ASCEND-HF, PMID: 21631327):

• No mortality benefit, no significant symptom improvement
• NOT recommended in current guidelines

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Inotropic Support

Indications for Inotropes

ESC 2021 Indications:

• Cardiogenic shock (Profile C - cold and wet)
• Severe hypotension with signs of hypoperfusion
• End-organ dysfunction despite adequate filling pressures
• Bridge to definitive therapy (revascularization, MCS, transplant)

Goals:

• Improve cardiac output
• Maintain end-organ perfusion
• Stabilize haemodynamics pending definitive management

Dobutamine

Mechanism:

• Synthetic catecholamine
• Predominant β1-agonist (positive inotrope, mild chronotrope)
• Some β2 effect (vasodilation)
• Net effect: increased CO, mild reduction in SVR

Dosing:

• Start 2.5 mcg/kg/min
• Titrate by 2.5 mcg/kg/min every 10-15 minutes
• Usual range 2.5-20 mcg/kg/min
• Higher doses increase tachycardia, arrhythmia risk

Advantages:

• Widely available, familiar
• Effective for increasing CO

Disadvantages:

• Tachycardia (increases myocardial O2 demand)
• Arrhythmogenic
• Hypotension possible (β2-mediated vasodilation)
• Tolerance develops after 72 hours (β-receptor downregulation)

Milrinone

Mechanism:

• Phosphodiesterase-3 (PDE3) inhibitor
• Increases intracellular cAMP (bypasses β-receptors)
• Positive inotrope + vasodilator ("inodilator")
• Pulmonary vasodilation (useful in RV failure, pulmonary hypertension)

Dosing:

• Loading dose: 50 mcg/kg over 10 minutes (often omitted due to hypotension risk)
• Maintenance: 0.375-0.75 mcg/kg/min
• Reduce dose in renal impairment (renally eliminated)

Advantages:

• Less tachycardia than dobutamine
• No β-receptor downregulation (works in β-blocker patients)
• Pulmonary vasodilation

Disadvantages:

• Significant vasodilation → may cause hypotension
• Pro-arrhythmic
• Accumulates in renal impairment
• OPTIME-CHF (PMID: 12124420): No benefit, increased harm in ischaemic cardiomyopathy

Levosimendan

Mechanism:

• Calcium sensitizer: Increases troponin C sensitivity to calcium
• ATP-sensitive K+ channel opener → vasodilation
• Increases contractility WITHOUT increasing intracellular calcium or O2 demand

Dosing:

• Loading dose: 6-12 mcg/kg over 10 minutes (often omitted)
• Maintenance: 0.05-0.2 mcg/kg/min
• Duration: 24 hours (active metabolite has 80-hour half-life)

Evidence:

LIDO Trial (2002, PMID: 11983158):

• Levosimendan vs dobutamine in severe low-output HF
• Levosimendan: better haemodynamics, reduced 180-day mortality (26% vs 38%)

SURVIVE Trial (2007, PMID: 17473298):

• Larger trial (1,327 patients), levosimendan vs dobutamine
• No difference in 180-day mortality (primary endpoint)
• Levosimendan: greater BNP reduction, trend toward early benefit

Advantages:

• No increase in myocardial O2 demand
• Prolonged effect (active metabolite)
• Potential benefit in β-blocked patients

Disadvantages:

• Hypotension (vasodilation)
• Expensive, not universally available
• Neutral mortality evidence in large trial

Noradrenaline (Norepinephrine)

Mechanism:

• Endogenous catecholamine
• Potent α1-agonist (vasoconstriction)
• Moderate β1-agonist (inotropy)
• Increases SVR and MAP

Indications:

• Cardiogenic shock with hypotension (MAP less than 65 mmHg)
• First-line vasopressor (SOAP II, PMID: 20802220)

Dosing:

• Start 0.05-0.1 mcg/kg/min
• Titrate to MAP ≥65 mmHg
• Usual range 0.1-1 mcg/kg/min

SOAP II Trial (2010, PMID: 20802220):

• Noradrenaline vs dopamine in shock (cardiogenic subgroup)
• Noradrenaline: fewer arrhythmias, trend toward lower mortality in cardiogenic shock subgroup

Clinical Pearl: In cardiogenic shock, typically start noradrenaline for MAP, add dobutamine if CO remains low.

Adrenaline (Epinephrine)

Mechanism:

• Potent α and β agonist
• High doses: predominantly α (vasoconstriction)
• Low doses: more β effect (inotropy, chronotropy)

Indications:

• Refractory shock
• Post-cardiac arrest
• Anaphylaxis

Concerns in Cardiogenic Shock:

• Tachycardia, increased O2 demand
• Arrhythmogenic
• May worsen ischaemia
• Generally NOT preferred in cardiogenic shock vs noradrenaline + dobutamine

Dopamine

NOT recommended as first-line in cardiogenic shock (SOAP II, PMID: 20802220):

• Higher rate of arrhythmias vs noradrenaline
• No mortality benefit

May still have role in:

• Bradycardia-related hypotension
• Low-dose (2-5 mcg/kg/min) for "renal dose"
• NOT effective (ROSE-AHF, PMID: 24557235)

Inotrope/Vasopressor Combination Strategies

Cardiogenic Shock Approach:

1. If MAP less than 65 mmHg with cold peripheries:

   • Start noradrenaline 0.05-0.1 mcg/kg/min, titrate to MAP ≥65

2. If MAP adequate but signs of low CO persist:

   • Add dobutamine 2.5-5 mcg/kg/min
   • Alternative: milrinone (if RV failure, pulmonary hypertension, β-blocked)

3. If refractory:

   • Escalate doses
   • Add adrenaline
   • Consider mechanical support early

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Mechanical Circulatory Support

Indications for MCS

ESC 2021 Indications:

• Cardiogenic shock refractory to inotropes/vasopressors
• Bridge to recovery (BTR)
• Bridge to decision (BTD)
• Bridge to transplant (BTT)
• Bridge to durable LVAD

Selection Factors:

• Aetiology (reversible vs irreversible)
• RV function (isolated LV vs biventricular failure)
• Comorbidities
• Age and candidacy for advanced therapies
• Local expertise and availability

Intra-Aortic Balloon Pump (IABP)

Mechanism:

• Helium-filled balloon in descending aorta
• Inflation in diastole: Augments coronary perfusion pressure
• Deflation in systole: Reduces afterload, decreases myocardial O2 demand

Haemodynamic Effects:

• Increases diastolic pressure (coronary perfusion)
• Decreases systolic pressure (afterload)
• Modest CO increase (0.5-1 L/min)
• Reduces PCWP

IABP-SHOCK II Trial (2012, PMID: 22972210):

Design:

• 600 patients with AMI-related cardiogenic shock undergoing revascularization
• IABP vs no mechanical support

Key Findings:

• No difference in 30-day mortality (39.7% IABP vs 41.3% control)
• No difference in secondary outcomes
• No significant harm

Clinical Implication:

• IABP NOT routinely recommended for AMI-cardiogenic shock (ESC Class III, PMID: 34447992)
• May still consider for mechanical complications (acute MR, VSD) as bridge to surgery

Contraindications:

• Severe aortic regurgitation
• Aortic dissection
• Severe peripheral vascular disease
• Tachyarrhythmias (poor timing)

Impella

Device Types:

Mechanism:

• Microaxial flow pump across aortic valve
• Aspirates blood from LV, expels into ascending aorta
• Active LV unloading (differentiates from IABP)
• Reduces LVEDP, wall stress, O2 demand

Evidence:

ISAR-SHOCK (2008, PMID: 18556114):

• Impella 2.5 vs IABP in 26 patients
• Impella: better haemodynamic support, higher cardiac index
• No mortality difference (small study)

IMPRESS-in-Severe SHOCK (2017, PMID: 27810774):

• Impella CP vs IABP in 48 patients with severe cardiogenic shock
• No difference in 30-day mortality (46% vs 50%)
• Higher complication rate with Impella

DanGer Shock Trial (2024, PMID: 38587239):

• Landmark trial: 355 patients, STEMI-related cardiogenic shock
• Impella CP (before PCI) vs standard care
• 180-day mortality: 45.8% Impella vs 58.5% control (HR 0.74, p=0.04)
• NNT = 8
• Higher rate of limb complications, bleeding, haemolysis with Impella

Clinical Implication:

• First positive MCS trial in AMI-cardiogenic shock
• Consider Impella in STEMI-related cardiogenic shock (especially SCAI C/D)
• Weigh benefit against complications (limb ischaemia, bleeding)

VA-ECMO (Venoarterial Extracorporeal Membrane Oxygenation)

Configuration:

• Drainage: large venous cannula (femoral vein → RA)
• Return: arterial cannula (femoral artery → aorta)
• Provides both circulatory support (up to 6-7 L/min) and gas exchange

Indications:

• Refractory cardiogenic shock
• Cardiac arrest (ECPR - extracorporeal CPR)
• Bridge to decision/recovery/transplant/LVAD
• Biventricular failure

ECLS-SHOCK Trial (2023, PMID: 37634145):

Design:

• 420 patients, AMI-related cardiogenic shock
• Early routine VA-ECMO vs standard care (optional rescue ECMO allowed)

Key Findings:

• No difference in 30-day mortality (47.8% ECMO vs 49.0% control)
• Higher complications with ECMO: bleeding, limb ischaemia, stroke

Clinical Implication:

• Routine early VA-ECMO NOT recommended for AMI-cardiogenic shock
• May still consider for:
  • Refractory shock failing other therapies
  • Cardiac arrest (ECPR)
  • Biventricular failure
  • Bridge to LVAD/transplant

Complications:

• Limb ischaemia (distal perfusion cannula mandatory)
• Bleeding (anticoagulation)
• LV distension ("Harlequin syndrome" if differential hypoxia)
• Stroke
• Infection
• Haemolysis

LV Unloading with ECMO: VA-ECMO increases LV afterload → LV distension possible → may require:

• IABP (controversial)
• Impella ("ECPELLA" configuration)
• Septostomy
• LV vent

MCS Device Selection

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Cardiogenic Shock

Definition and Recognition

ESC Definition:

• SBP less than 90 mmHg for greater than 30 minutes (or vasopressors required to maintain SBP ≥90)
• Clinical signs of hypoperfusion (cold extremities, oliguria, confusion)
• Elevated lactate (greater than 2 mmol/L)
• Evidence of cardiac dysfunction on imaging

Incidence:

• Complicates 5-10% of acute MI
• Hospital mortality 40-60% despite optimal therapy

SCAI Shock Stages (2019, PMID: 30711358)

Management Escalation

Step 1: Initial Resuscitation

• IV access, monitoring
• Address CHAMPIT triggers
• Noradrenaline for MAP ≥65 mmHg
• Echocardiography (urgent - mechanical complication?)

Step 2: Revascularization (if ACS)

• Emergency coronary angiography
• PCI or CABG as indicated
• Do NOT delay for stabilization (SHOCK trial, PMID: 10460813)

Step 3: Inotropic Support

• Add dobutamine if CO remains low
• Consider milrinone if RV failure or β-blocked
• Monitor lactate clearance

Step 4: Mechanical Support

• Consider Impella if STEMI-related shock (DanGer Shock)
• Consider VA-ECMO if:
  • Biventricular failure
  • Cardiac arrest (ECPR)
  • Refractory to inotropes
  • Bridge to LVAD/transplant

Step 5: Advanced Therapies

• LVAD (bridge or destination)
• Heart transplantation
• Palliative care discussion if not candidate

SHOCK Trial (1999, PMID: 10460813)

Design:

• 302 patients with AMI-related cardiogenic shock
• Emergency revascularization (PCI/CABG) vs initial medical stabilization

Key Findings:

• 30-day mortality: 46.7% revascularization vs 56.0% medical (not significant)
• 6-month mortality: 50.3% vs 63.1% (p=0.027) - SIGNIFICANT
• 1-year mortality: 53% vs 66% - benefit maintained

Clinical Implication:

• Emergency revascularization is mandated in AMI-related cardiogenic shock
• Survival benefit emerges at 6 months, persists long-term
• Do not delay for "stabilization"
• proceed immediately to cath lab

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Special Populations

Indigenous Australian and NZ Populations

Rheumatic Heart Disease (PMID: 24204364, 32675031):

• Aboriginal and Torres Strait Islander Australians have world's highest rates of RHD
• Prevalence in endemic areas: 2-3% (compared to effectively zero in general Australian population)
• Predominantly affects young people (median age of valve surgery 26 years)
• Multi-valve involvement common (MR, AR, MS)

Clinical Implications:

• AHF in Indigenous patients may be due to RHD - check for valve disease
• Younger patients presenting with HF - consider RHD
• May require valve surgery rather than medical management alone

Cultural Considerations:

• Involve Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs)
• Family/community involvement in decision-making
• Language interpretation services
• Cultural safety - acknowledge historical trauma affecting healthcare engagement
• Whānau involvement for Māori patients (New Zealand)
• Consider impact of geographic remoteness on follow-up and access to surgery

Benzathine Penicillin Prophylaxis:

• Secondary prophylaxis is critical to prevent recurrent ARF and progressive valve damage
• Poor compliance linked to progression to HF
• Address barriers to regular IM injections

Peripartum Cardiomyopathy

Definition: HFrEF presenting in last month of pregnancy or within 5 months postpartum, without other cause

Risk Factors:

• Older maternal age
• Multiparity
• Pre-eclampsia/eclampsia
• African descent
• Prolonged tocolytic therapy

Management:

• Standard HF therapy (some modifications in pregnancy)
• ACEi/ARB contraindicated in pregnancy; use after delivery
• Anticoagulation if LVEF less than 35%
• Bromocriptine may improve recovery (experimental)

Prognosis:

• 50% recover LVEF to normal within 6-12 months
• Recurrence risk in subsequent pregnancies if LVEF remains reduced

Right Ventricular Failure

Causes:

• RV infarction (inferior MI)
• Massive PE
• Pulmonary hypertension
• LV failure with biventricular dysfunction
• Post-cardiac surgery

Unique Management:

• Avoid excessive volume loading (RV preload-dependent to a point, but overloading worsens)
• Maintain systemic perfusion (noradrenaline for MAP)
• Milrinone preferred inotrope (pulmonary vasodilation)
• Inhaled nitric oxide or prostacyclin for pulmonary vasodilation
• Consider RV support (Impella RP, VA-ECMO)

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Prognosis and Outcomes

Mortality

In-Hospital Mortality (PMID: 34447992):

• AHF without shock: 5-10%
• Cardiogenic shock: 40-60%

Predictors of Poor Outcome:

• Hypotension (SBP less than 90)
• Elevated lactate
• Low serum sodium (less than 130 mmol/L)
• Elevated creatinine/declining renal function
• Low cardiac index
• High BNP/NT-proBNP
• SCAI stage D/E

Long-Term Outcomes

Post-Discharge:

• 30-day readmission: 20-25%
• 1-year mortality: 25-30%
• 5-year mortality: 50-75% (depending on EF, comorbidities)

Factors Improving Prognosis:

• GDMT optimization (ACEi/ARB/ARNI, β-blocker, MRA, SGLT2i)
• CRT if indicated
• ICD for SCD prevention
• Heart failure clinic follow-up
• Exercise rehabilitation

---

Australian/NZ Context

Healthcare System Considerations

Retrieval and Transfer:

• Consider early discussion with tertiary cardiac centre for cardiogenic shock
• VA-ECMO and Impella availability limited to major centres
• RFDS/state retrieval services for remote presentations
• Telemedicine consultation for management guidance

Transplant Services:

• Limited transplant centres in Australia (Sydney, Melbourne, Brisbane, Perth, Adelaide)
• New Zealand transplant at Auckland City Hospital
• Long waiting lists - bridge strategies essential

PBS Considerations:

• Levosimendan is PBS-listed for short-term treatment of acute decompensated heart failure
• SGLT2 inhibitors PBS-listed for HFrEF (dapagliflozin, empagliflozin)
• Sacubitril-valsartan (Entresto) PBS-listed for HFrEF

Indigenous Health

Key Points:

• Rheumatic heart disease is a leading cause of HF in Indigenous Australians
• Earlier presentation of HF (younger age)
• Higher mortality rates
• Geographic barriers to accessing tertiary cardiac care
• Cultural considerations in consent and family involvement

Recommendations:

• Screen for RHD in Indigenous patients presenting with HF
• Involve AHW/ALO early
• Consider family involvement in goals of care discussions
• Arrange culturally appropriate follow-up
• Address secondary prevention of ARF

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SAQ Practice Questions

SAQ 1: Acute Pulmonary Oedema Management (15 Marks)

Stem: A 72-year-old woman presents to the emergency department with sudden-onset severe dyspnoea. She has a history of hypertension and type 2 diabetes. On arrival: GCS 14, RR 36/min, SpO2 82% on room air, BP 210/130 mmHg, HR 115/min. On examination: diaphoretic, unable to speak in full sentences, diffuse bilateral crackles to mid-zones, JVP elevated to ear lobes.

Questions:

(a) What is the most likely diagnosis and what Nohria-Stevenson profile does this represent? (2 marks)

(b) Outline your immediate management priorities in the first 30 minutes. (5 marks)

(c) What diuretic strategy would you employ, and what is the evidence for your approach? (4 marks)

(d) After initial treatment, her BP is 145/90 mmHg, SpO2 92% on CPAP, and she remains tachypnoeic with ongoing crackles. What is the role of vasodilator therapy and what agents would you consider? (4 marks)

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Model Answer:

(a) Most likely diagnosis and Nohria-Stevenson profile (2 marks)

• Diagnosis: Acute pulmonary oedema / Flash pulmonary oedema secondary to hypertensive emergency (1 mark)
• Profile B (Warm and Wet) - evidence of severe congestion (elevated JVP, bilateral crackles, severe dyspnoea) with adequate perfusion (warm, hypertensive, conscious) (1 mark)

(b) Immediate management priorities (5 marks) - 1 mark each for 5 of:

1. Positioning: Sit upright with legs dependent to reduce preload
2. Oxygen: High-flow oxygen via face mask, target SpO2 94-98%
3. Non-invasive ventilation: CPAP 5-10 cmH2O immediately (reduces preload via increased intrathoracic pressure, reduces work of breathing, improves oxygenation) - 3CPO trial showed reduced intubation
4. Vascular access: Large-bore IV, bloods (troponin, BNP, UECs, FBC, lactate)
5. IV diuretic: Furosemide 40-80 mg IV bolus (if diuretic-naive) or 2-2.5x oral dose
6. Monitoring: Continuous ECG, SpO2, urinary catheter, arterial line for BP monitoring
7. GTN infusion: Start 10-20 mcg/min given severe hypertension and pulmonary oedema
8. Investigations: ECG (exclude STEMI), CXR, urgent echocardiography
9. Prepare for intubation if NIV fails or GCS deteriorates

(c) Diuretic strategy (4 marks)

• Initial dose: 2-2.5 times oral daily dose IV, or 40-80 mg IV furosemide if diuretic-naive (1 mark)
• Evidence - DOSE trial (PMID: 21352018): Compared high-dose (2.5x oral) vs low-dose (1x oral) and bolus vs continuous infusion in 308 patients with ADHF (1 mark)
• Key findings: No significant difference in symptoms or renal function; trend toward better decongestion with high-dose; no difference between bolus and continuous infusion (1 mark)
• Monitoring and escalation: Target urine output >100 mL/hour; if inadequate response at 2 hours, double the dose; consider adding thiazide (metolazone) if resistant (1 mark)

(d) Vasodilator therapy (4 marks)

• Role: Indicated in Profile B with SBP >90 mmHg for afterload reduction and symptom relief (1 mark)
• GTN infusion: First-line vasodilator; start 10-20 mcg/min, titrate by 10-20 mcg/min every 5-10 minutes to symptom relief and BP reduction (target SBP 100-120 mmHg); mechanism is venodilation (reduces preload) at low doses, arterial vasodilation at higher doses (1.5 marks)
• Sodium nitroprusside: Alternative if GTN insufficient; start 0.3 mcg/kg/min; more potent balanced vasodilator; caution with prolonged use (>48h) or renal impairment due to cyanide toxicity risk (1 mark)
• Monitoring: Arterial line essential for continuous BP monitoring; watch for excessive hypotension (0.5 marks)

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SAQ 2: Cardiogenic Shock Management (15 Marks)

Stem:

Questions:

(a) Define cardiogenic shock and classify this patient's SCAI stage. (3 marks)

(b) Outline your immediate pharmacological management, including specific agents and doses. (4 marks)

(c) The patient remains in shock despite noradrenaline 0.4 mcg/kg/min and dobutamine 10 mcg/kg/min. Lactate is now 6.8 mmol/L. Discuss the role and evidence for mechanical circulatory support in this patient. (6 marks)

(d) What factors would influence your decision regarding escalation to advanced therapies (LVAD, transplantation)? (2 marks)

---

Model Answer:

(a) Definition and SCAI stage (3 marks)

• Cardiogenic shock definition (ESC): SBP <90 mmHg for >30 min OR vasopressor requirement to maintain SBP ≥90 mmHg; PLUS clinical signs of hypoperfusion (cold extremities, oliguria, altered mental status); PLUS elevated lactate >2 mmol/L (1.5 marks)
• SCAI Stage C-D (1.5 marks):
  • "Stage C (Classic shock): Hypotension + hypoperfusion + elevated lactate = present"
  • Progressing toward Stage D (Deteriorating) given failure to improve post-PCI with ongoing hypoperfusion
  • Not yet Stage E (no arrest, not refractory to initial therapy yet)

(b) Pharmacological management (4 marks)

• Noradrenaline (first-line vasopressor): Start 0.05-0.1 mcg/kg/min, titrate to MAP ≥65 mmHg; preferred over dopamine (SOAP II trial - fewer arrhythmias); via central line (1.5 marks)
• Dobutamine (inotrope): Add once MAP stable; start 2.5-5 mcg/kg/min, titrate to 10-20 mcg/kg/min; increases cardiac output via β1-stimulation (1 mark)
• Alternative inotrope - Milrinone: 0.375-0.75 mcg/kg/min if inadequate response to dobutamine or β-blocked; avoid loading dose due to hypotension risk; reduce dose in renal impairment (0.5 marks)
• Monitoring: Arterial lactate every 2-4 hours (target clearance), urine output, ScvO2 if central line available (target >65%), serial echocardiography (0.5 marks)
• Avoid excessive fluids: This patient is likely not fluid-responsive and has LV failure; cautious volume assessment only (0.5 marks)

(c) Mechanical circulatory support (6 marks)

Current evidence for MCS in AMI-related cardiogenic shock:

IABP (1 mark):

• IABP-SHOCK II (PMID: 22972210): 600 patients, IABP vs no MCS; no mortality benefit (39.7% vs 41.3%)
• NOT recommended routinely (ESC Class III recommendation)
• May consider for mechanical complications (VSD, acute MR) as bridge to surgery

Impella (2 marks):

• DanGer Shock Trial (2024, PMID: 38587239): 355 patients, STEMI-related cardiogenic shock
• Impella CP (inserted before PCI) vs standard care
• 180-day mortality: 45.8% vs 58.5% (HR 0.74, p=0.04), NNT = 8
• First positive MCS trial in AMI-shock
• Higher complication rate: limb ischaemia, bleeding, haemolysis
• Would be appropriate to consider in this patient given refractory shock post-PCI

VA-ECMO (2 marks):

• ECLS-SHOCK (2023, PMID: 37634145): 420 patients, early VA-ECMO vs standard care
• No mortality difference (47.8% vs 49.0%)
• Higher complications with ECMO
• Not recommended routinely; may consider if cardiac arrest, biventricular failure, or bridge to LVAD/transplant
• ECMO does not unload LV (may worsen); may need "ECPELLA" or LV venting

Recommendation for this patient (1 mark):

• Impella CP would be the preferred MCS option based on DanGer Shock evidence
• Discuss with cardiac surgical team regarding insertion and eligibility for advanced therapies
• Continue medical therapy while arranging MCS

(d) Factors for advanced therapy escalation (2 marks) - 0.5 marks each:

• Age and biological fitness (typically <65-70 for transplant)
• Comorbidities (diabetes, renal function, peripheral vascular disease)
• Neurological status (prognosis post-anoxic injury if prolonged shock)
• Psychosocial factors (compliance, social support)
• Reversibility of shock (if recovery expected, bridge to recovery; if not, bridge to durable therapy)
• Access to LVAD/transplant program (availability, waiting times)
• Patient/family wishes regarding aggressive therapy

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Hot Case Scenarios

Hot Case 1: Post-MI Cardiogenic Shock on MCS

Scenario: You are asked to review a 52-year-old man on Day 2 post-anterior STEMI complicated by cardiogenic shock. He has an Impella CP in situ, noradrenaline at 0.15 mcg/kg/min, and dobutamine at 7.5 mcg/kg/min. He is intubated and ventilated on minimal settings.

---

Examiner-Candidate Dialogue:

Examiner: "Please examine this patient and provide a one-minute summary."

Candidate: (After systematic examination)

"This is a 52-year-old man, Day 2 following anterior STEMI complicated by cardiogenic shock, currently supported with Impella CP mechanical circulatory support.

• MAP is 72 mmHg on noradrenaline 0.15 mcg/kg/min and dobutamine 7.5 mcg/kg/min

• Heart rate 94/min, sinus rhythm

• Peripheries are warm, capillary refill under 3 seconds

• Most recent lactate is 2.4 mmol/L and trending down from 5.8 mmol/L yesterday

• Urine output improved to 40 mL/hour

• Intubated, on SIMV/PS with FiO2 0.35, PEEP 8

• P/F ratio approximately 280, no evidence of pulmonary oedema on most recent CXR

Other:

• Impella is at P8, with adequate positioning on fluoroscopy
• Anticoagulation is with heparin infusion, APTT 55 seconds
• Renal function stable, creatinine 142
• No signs of limb ischaemia on examination of right groin and distal limb

Impression: This patient is improving with MCS support. The key questions are: (1) trajectory for weaning Impella, (2) neurological prognosis if there was any peri-arrest period, and (3) longer-term recovery of ventricular function and need for advanced therapies."

---

Examiner: "The echocardiogram today shows LVEF 25%, up from 15% yesterday. The Impella is weaning appropriately. What is your plan?"

Candidate: "This is encouraging and suggests myocardial recovery. My approach would be:

Impella Weaning:

• Gradual reduction of Impella support (P-level) with monitoring of haemodynamic response
• Target: maintain MAP >65, lactate stability, adequate urine output
• Serial echocardiography during weaning to assess LV function
• When at P2 for 4-6 hours with stable haemodynamics, consider removal

Inotrope Weaning:

• As Impella is weaned, reassess inotrope requirements
• Aim to wean dobutamine first if haemodynamically stable
• Wean noradrenaline as perfusion indicators improve

Neuroprognostication:

• If there was peri-arrest period, formal neurological assessment once sedation cleared
• Multimodal approach if concerns: clinical examination, EEG, imaging (MRI DWI)

Longer-term Planning:

• Initiate guideline-directed medical therapy (GDMT) as tolerated: ACEi/ARB, β-blocker (titrate carefully), MRA, SGLT2i
• ICD assessment in 3-6 months if EF remains ≤35%
• Cardiac rehabilitation referral
• Secondary prevention: statin, antiplatelet therapy, glycaemic control"

---

Examiner: "His wife asks about his long-term prognosis. How would you approach this conversation?"

Candidate: "I would arrange to speak with his wife in a quiet, private space, ideally with a nurse or social worker present.

I would:

1. Assess understanding: 'What have you been told so far about his condition?'
2. Acknowledge the severity: 'He has been very unwell with damage to the heart muscle after the heart attack. He needed a mechanical pump to support his heart.'
3. Provide cautious optimism: 'The good news is that his heart function is showing signs of improvement, and we are starting to reduce the support.'
4. Be honest about uncertainty: 'It is still early, and we cannot be certain about long-term outcome. Some people recover good heart function; others may need ongoing treatment or devices.'
5. Address specific concerns: Ask what worries her most and address those directly.
6. Outline next steps: Weaning support, rehabilitation, follow-up.
7. Offer support: Social worker, pastoral care, family meetings.

I would document the conversation and plan for regular updates."

---

Hot Case 2: Rheumatic Heart Disease with Acute Decompensation

Scenario: You are asked to review a 34-year-old Aboriginal woman from a remote Northern Territory community who has been transferred with acute heart failure. She has known rheumatic heart disease with severe mitral regurgitation. She is on BiPAP, furosemide infusion, and milrinone.

---

Examiner-Candidate Dialogue:

Examiner: "Please examine this patient and provide a summary."

Candidate: (After examination)

"This is a 34-year-old Aboriginal woman with known rheumatic heart disease (severe MR) presenting with acute decompensated heart failure.

Current Status:

• On BiPAP with FiO2 0.5, achieving SpO2 92%
• BP 95/58 mmHg, HR 105/min in atrial fibrillation
• Elevated JVP to angle of jaw, bilateral pulmonary crackles to mid-zones
• Pansystolic murmur at apex radiating to axilla, consistent with severe MR
• Mild peripheral oedema

Support:

• Furosemide infusion at 10 mg/hour
• Milrinone at 0.5 mcg/kg/min (appropriate for afterload reduction in MR)
• No vasopressors currently

Impression: Acute-on-chronic heart failure in the setting of rheumatic MR, likely precipitated by atrial fibrillation with rapid ventricular response. She is wet and borderline warm/cold (Profile B-C). Key priorities are: (1) rate control, (2) optimising decongestion, (3) urgent cardiothoracic surgical review for valve intervention."

---

Examiner: "What are your management priorities?"

Candidate:

"Immediate Priorities:

1. Rate control for AF: Target HR 80-100 to allow diastolic filling

   • Digoxin loading preferred (renally cleared, adjust for renal function): 500 mcg IV over 2 hours, then maintenance 125-250 mcg daily
   • Avoid β-blockers and calcium channel blockers in acute decompensation (negative inotropy)
   • Amiodarone if above fails: 300 mg IV over 1 hour, then 900 mg over 24 hours

2. Optimise preload reduction:

   • Continue furosemide infusion, monitor urine output
   • Daily weights, aim for net negative fluid balance 1-2 L/day
   • Consider adding thiazide if diuretic resistance

3. Afterload reduction for MR:

   • Milrinone is appropriate (inodilator, reduces SVR)
   • Add GTN infusion if BP tolerates, to reduce regurgitant volume

4. Cardiothoracic surgical consultation:

   • This patient likely needs mitral valve surgery (repair or replacement)
   • Urgent transfer to tertiary cardiac surgery centre
   • May need to stabilise and optimise before surgery

5. Anticoagulation for AF:

   • Start heparin infusion for AF (will need therapeutic anticoagulation)
   • Transition to warfarin if valve replacement anticipated (mechanical valve)

Indigenous Health Considerations:

1. Involve Aboriginal Health Worker (AHW) and Aboriginal Liaison Officer (ALO) early
2. Family/community involvement: She may have travelled far from home; ensure family can visit or participate in discussions via phone
3. Communication: Use clear, simple language; ensure she understands her condition and treatment options
4. Cultural considerations: Ask about any cultural needs or concerns; ensure culturally appropriate care
5. Secondary prevention: Benzathine penicillin prophylaxis is critical post-valve surgery to prevent recurrence"

---

Examiner: "She is stabilising. What discussion would you have with the cardiac surgery team?"

Candidate: "I would present a structured handover:

Summary: 'This is a 34-year-old Aboriginal woman with rheumatic heart disease and severe symptomatic MR, now presenting with acute decompensated heart failure with new AF.'

Current Status: 'She is stabilised on BiPAP, milrinone, and furosemide infusion. Rate-controlled with digoxin.'

Key Questions:

1. 'Is she a candidate for mitral valve surgery, and if so, what is the urgency?'
2. 'Repair vs replacement - what is your assessment?'
3. 'If surgery is planned, what optimisation do you recommend prior (timing of surgery, anticoagulation bridging, etc.)?'
4. 'Does she need TOE to assess valve morphology and LA thrombus?'

Logistical Issues:

• Transfer arrangements to tertiary centre
• Family needs to be notified and supported
• Cultural liaison arrangements at receiving hospital"

---

Viva Scenarios

Viva 1: Pathophysiology and Initial Management

Opening Stem: A 68-year-old man presents to the emergency department with acute dyspnoea. He has a history of ischaemic cardiomyopathy with LVEF 25%. He is diaphoretic, with BP 85/60 mmHg and SpO2 88% on room air.

---

Examiner: "Describe the pathophysiology of acute heart failure in this patient."

Candidate: "This patient has acute decompensation of chronic systolic heart failure. The pathophysiology involves:

1. Primary Insult - Reduced Contractility:

• His ischaemic cardiomyopathy has caused loss of functional myocardium
• LVEF 25% indicates severely reduced contractile reserve
• Reduced stroke volume leads to inadequate cardiac output

2. Frank-Starling Failure:

• Normally, increased preload leads to increased contractile force
• In the failing heart, this mechanism is exhausted
• Further volume loading does not increase stroke volume

3. Neurohormonal Activation:

• Reduced cardiac output triggers compensatory mechanisms:
  • "Sympathetic activation: Tachycardia, vasoconstriction (increases afterload)"
  • "RAAS activation: Sodium and water retention, further vasoconstriction"
  • "ADH release: Water retention, hyponatraemia"
• These are initially compensatory but become maladaptive

4. Pulmonary Congestion:

• Elevated left ventricular end-diastolic pressure
• Backs up into pulmonary veins and capillaries
• When pulmonary capillary pressure exceeds 25 mmHg, transudation into interstitium and alveoli
• V/Q mismatch causes hypoxaemia

5. Hypoperfusion:

• Reduced cardiac output causes tissue hypoperfusion
• Organ dysfunction: renal (oliguria), hepatic (congestion), cerebral (confusion)
• Anaerobic metabolism leads to elevated lactate"

---

Examiner: "How would you classify this patient using the Nohria-Stevenson system?"

Candidate: "Based on the clinical features:

Congestion Assessment (Wet vs Dry):

• He has acute dyspnoea, SpO2 88%, diaphoresis
• These suggest pulmonary congestion = WET

Perfusion Assessment (Warm vs Cold):

• BP 85/60 mmHg = hypotension
• Diaphoresis suggests sympathetic activation
• I would examine for cool peripheries, prolonged capillary refill, oliguria, confusion
• These features suggest hypoperfusion = COLD

Classification: Profile C (Cold and Wet) - This represents cardiogenic shock.

This is the highest-risk profile with mortality 40-60%. He requires urgent intervention including vasopressors, inotropes, and consideration of mechanical support."

---

Examiner: "What are your initial management priorities?"

Candidate: "This is a time-critical emergency. My priorities are:

1. Resuscitation (first 15 minutes):

• High-flow oxygen, target SpO2 94-98%
• IV access, continuous monitoring
• 12-lead ECG to exclude STEMI as trigger
• Urgent bloods: troponin, BNP, lactate, UECs, FBC

2. Haemodynamic Support:

• Start noradrenaline 0.05-0.1 mcg/kg/min via central line (or large peripheral while central access obtained)
• Target MAP ≥65 mmHg
• Once MAP adequate, add dobutamine 2.5-5 mcg/kg/min to augment cardiac output

3. Ventilatory Support:

• NIV (CPAP/BiPAP) if patient can protect airway and tolerate mask
• Caution: positive pressure reduces preload - may worsen hypotension in shock
• Intubation if severe hypoxaemia or reduced consciousness

4. CHAMPIT Screen:

• Exclude acute coronary syndrome (ECG, troponin) - if STEMI, urgent PCI
• Exclude arrhythmia - if VT or bradycardia, treat specifically
• Urgent echo to exclude mechanical complication (MR, VSD), tamponade, RV failure

5. Diuretics:

• Hold initial diuretics if severely hypotensive
• Once MAP >65 mmHg, cautious IV furosemide to relieve congestion

6. Escalation Planning:

• Early discussion with cardiology and cardiac surgery
• Consider MCS if refractory (Impella preferred for ischaemic cardiogenic shock)"

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Viva 2: Evidence for Mechanical Circulatory Support

Opening Stem: You are asked to discuss the evidence for mechanical circulatory support in cardiogenic shock at a departmental journal club.

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Examiner: "Start by discussing the IABP evidence."

Candidate: "The key trial for IABP is IABP-SHOCK II, published in 2012.

IABP-SHOCK II (PMID: 22972210):

• Design: Randomised, open-label trial in Germany and Switzerland
• Population: 600 patients with AMI-related cardiogenic shock undergoing early revascularization
• Intervention: IABP plus PCI vs PCI alone

Results:

• 30-day mortality: 39.7% IABP vs 41.3% control (p=0.69)
• No difference in secondary outcomes including renal function, lactate, APACHE II

Conclusion:

• IABP does NOT improve survival in AMI-related cardiogenic shock
• ESC guidelines now give IABP a Class III (no benefit) recommendation for routine use

Limitations:

• Control group could receive IABP as rescue therapy (10% crossover)
• IABP is a modest support device (0.5-1 L/min CO augmentation)

Current Role:

• May still consider for mechanical complications (acute MR, VSD) as bridge to surgery
• Not for routine AMI-cardiogenic shock"

---

Examiner: "What about the more recent Impella evidence?"

Candidate: "The landmark trial is DanGer Shock, published in 2024.

DanGer Shock (PMID: 38587239):

• Design: Randomised, open-label trial across Denmark and Germany
• Population: 355 patients with STEMI-related cardiogenic shock (SCAI Stage C/D)
• Intervention: Impella CP (inserted BEFORE PCI) vs standard care (which could include IABP or VA-ECMO)

Key Inclusion Criteria:

• STEMI with cardiogenic shock
• SCAI Stage C or D
• Planned for PCI
• Lactate ≥2.5 mmol/L

Results:

• 180-day all-cause mortality: 45.8% Impella vs 58.5% control (HR 0.74, p=0.04)
• Number needed to treat: 8

Complications:

• Higher rates with Impella: severe bleeding (21.8% vs 11.9%), limb ischaemia, haemolysis, device malfunction

Significance:

• First positive MCS trial in AMI-cardiogenic shock
• Changes practice: Impella should be considered in STEMI-shock
• Emphasises early insertion (before PCI) for LV unloading

Comparison to Prior Impella Trials:

• ISAR-SHOCK (small, showed better haemodynamics)
• IMPRESS-in-Severe SHOCK (no mortality benefit, but higher complication rate)"

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Examiner: "What about VA-ECMO? Discuss ECLS-SHOCK."

Candidate: "ECLS-SHOCK was published in 2023 and addressed VA-ECMO in AMI-related shock.

ECLS-SHOCK (PMID: 37634145):

• Design: Randomised, open-label trial in Germany
• Population: 420 patients with AMI-related cardiogenic shock undergoing early revascularization
• Intervention: Early VA-ECMO initiation vs standard care (could include rescue ECMO)

Results:

• 30-day mortality: 47.8% ECMO vs 49.0% control (p=0.81)
• No difference in any secondary outcomes

Complications with ECMO:

• Moderate-to-severe bleeding: 23.4% vs 9.6%
• Limb ischaemia: 10.8% vs 3.8%
• Stroke: 3.9% vs 2.9%

Conclusions:

• Routine early VA-ECMO does NOT improve survival in AMI-cardiogenic shock
• Significant harm from complications
• Likely due to:
  • ECMO does not unload LV (increases afterload)
  • Complications outweigh potential benefit in this population

Current Role of VA-ECMO:

• Not for routine AMI-shock
• Consider for:
  • Biventricular failure
  • Cardiac arrest (ECPR)
  • Refractory shock as bridge to LVAD or transplant
  • Respiratory failure in addition to circulatory failure"

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Examiner: "Based on this evidence, how would you approach MCS selection?"

Candidate: "Based on current evidence, my approach would be:

AMI-Related Cardiogenic Shock (SCAI C/D):

1. First-line: Inotropes and vasopressors
2. If refractory: Impella CP (based on DanGer Shock)
   • Ideally inserted before PCI
   • Discuss with interventional cardiology
3. IABP: Only for mechanical complications (VSD, acute MR)
4. VA-ECMO: Not routine; reserve for cardiac arrest (ECPR), biventricular failure, or bridge to advanced therapies

Non-AMI Cardiogenic Shock:

• Less evidence; individualised decision
• VA-ECMO may have greater role (can support both ventricles, oxygenation)
• Impella if predominantly LV failure

General Principles:

• Early shock team activation
• Multi-disciplinary decision (intensivist, cardiologist, cardiac surgeon)
• Consider trajectory - is this patient a candidate for LVAD or transplant?
• Weigh benefits against complication rates"

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References

Primary Guidelines

1. McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42(36):3599-3726. PMID: 34447992

2. McDonagh TA, Metra M, Adamo M, et al. 2023 Focused Update of the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2023;44(37):3627-3639. PMID: 37622657

3. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145(18):e895-e1032. PMID: 35363499

Landmark Trials - Diuretics

4. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure (DOSE trial). N Engl J Med. 2011;364(9):797-805. PMID: 21352018

5. Bart BA, Goldsmith SR, Lee KL, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome (CARRESS-HF). N Engl J Med. 2012;367(24):2296-2304. PMID: 23126250

6. Chen HH, Anstrom KJ, Givertz MM, et al. Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: the ROSE acute heart failure randomized trial. JAMA. 2013;310(23):2533-2543. PMID: 24557235

Landmark Trials - Inotropes and Vasopressors

7. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock (SOAP II). N Engl J Med. 2010;362(9):779-789. PMID: 20802220

8. Follath F, Cleland JG, Just H, et al. Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (LIDO study). Lancet. 2002;360(9328):196-202. PMID: 11983158

9. 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

10. Cuffe MS, Califf RM, Adams KF Jr, et al. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial (OPTIME-CHF). JAMA. 2002;287(12):1541-1547. PMID: 12124420

Landmark Trials - Mechanical Circulatory Support

11. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock (IABP-SHOCK II). N Engl J Med. 2012;367(14):1287-1296. PMID: 22972210

12. 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 IABP-SHOCK II trial. Circulation. 2019;139(3):395-403. PMID: 30586715

13. Møller JE, Engstrøm T, Jensen LO, et al. Microaxial flow pump or standard care in infarct-related cardiogenic shock (DanGer Shock). N Engl J Med. 2024;390(15):1382-1393. PMID: 38587239

14. Thiele H, Zeymer U, Akin I, et al. Extracorporeal life support in infarct-related cardiogenic shock (ECLS-SHOCK). N Engl J Med. 2023;389(14):1286-1297. PMID: 37634145

15. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping (ISAR-SHOCK). J Am Coll Cardiol. 2008;52(19):1584-1588. PMID: 18556114

16. 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-in-Severe SHOCK). J Am Coll Cardiol. 2017;69(3):278-287. PMID: 27810774

Cardiogenic Shock - Revascularization

17. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock (SHOCK trial). N Engl J Med. 1999;341(9):625-634. PMID: 10460813

18. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA. 2006;295(21):2511-2515. PMID: 16757723

Classification and Prognostication

19. Nohria A, Tsang SW, Fang JC, et al. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. J Am Coll Cardiol. 2003;41(10):1797-1804. PMID: 12544220

20. 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: 30711358

21. Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study. Am J Cardiol. 2005;95(8):948-954. PMID: 15869614

22. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167. PMID: 12124404

NIV in Acute Pulmonary Oedema

23. Gray A, Goodacre S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema (3CPO trial). N Engl J Med. 2008;359(2):142-151. PMID: 18621006

24. Masip J, Roque M, Sánchez B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA. 2005;294(24):3124-3130. PMID: 16380593

Vasodilators

25. O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure (ASCEND-HF). N Engl J Med. 2011;365(1):32-43. PMID: 21631327

PA Catheter

26. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness (ESCAPE trial). JAMA. 2005;294(13):1625-1633. PMID: 16193740

Indigenous Health and Rheumatic Heart Disease

27. Wyber R, Zühlke L, Carapetis J. The case for global investment in rheumatic heart disease control. Bull World Health Organ. 2014;92(10):768-770. PMID: 24204364

28. Remenyi B, Carapetis J, Wyber R, et al. Position statement of the World Heart Federation on the prevention and control of rheumatic heart disease. Nat Rev Cardiol. 2013;10(5):284-292. PMID: 23546444

29. Marijon E, Mirabel M, Celermajer DS, Jouven X. Rheumatic heart disease. Lancet. 2012;379(9819):953-964. PMID: 22405798

30. Carapetis JR, Beaton A, Cunningham MW, et al. Acute rheumatic fever and rheumatic heart disease. Nat Rev Dis Primers. 2016;2:15084. PMID: 27188830

31. Zühlke L, Karthikeyan G, Engel ME, et al. Clinical outcomes in 3343 children and adults with rheumatic heart disease from 14 low- and middle-income countries: 2-year follow-up of the Global Rheumatic Heart Disease Registry (REMEDY study). Circulation. 2016;134(19):1456-1466. PMID: 27702773

32. Ralph AP, Carapetis JR. Group A streptococcal diseases and their global burden. Curr Top Microbiol Immunol. 2013;368:1-27. PMID: 23242849

Australian Context

33. Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Guidelines for the Prevention, Detection, and Management of Heart Failure in Australia 2018. Heart Lung Circ. 2018;27(10):1123-1208. PMID: 30077227

Additional Key References

34. Mentz RJ, O'Connor CM. Pathophysiology and clinical evaluation of acute heart failure. Nat Rev Cardiol. 2016;13(1):28-35. PMID: 26370473

35. Mebazaa A, Yilmaz MB, Levy P, et al. Recommendations on pre-hospital and early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2015;17(6):544-558. PMID: 25999021

36. Harjola VP, Mebazaa A, Čelutkienė J, et al. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J Heart Fail. 2016;18(3):226-241. PMID: 26995592

37. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136(16):e52-e68. PMID: 28874387

38. 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

39. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2016;37(27):2129-2200. PMID: 27206819

40. Mebazaa A, Tolppanen H, Mueller C, et al. Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med. 2016;42(2):147-163. PMID: 26370688

41. Levy B, Bastien O, Karim B, et al. Experts' recommendations for the management of adult patients with cardiogenic shock. Ann Intensive Care. 2015;5(1):17. PMID: 26152849

42. Werdan K, Gielen S, Ebelt H, Hochman JS. Mechanical circulatory support in cardiogenic shock. Eur Heart J. 2014;35(3):156-167. PMID: 24014387

43. Stretch R, Sauer CM, Yuh DD, Bonde P. National trends in the utilization of short-term mechanical circulatory support: incidence, outcomes, and cost analysis. J Am Coll Cardiol. 2014;64(14):1407-1415. PMID: 25277608

44. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll Cardiol. 2019;73(13):1659-1669. PMID: 30947919

45. Basir MB, Kapur NK, Patel K, et al. Improved outcomes associated with the use of shock protocols: updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):1173-1183. PMID: 30913342

46. Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/STS Clinical expert consensus statement on the use of percutaneous mechanical circulatory support devices in cardiovascular care. J Am Coll Cardiol. 2015;65(19):e7-e26. PMID: 25861963

47. Abrams D, Garan AR, Abdelbary A, et al. Position paper for the organization of ECMO programs for cardiac failure in adults. Intensive Care Med. 2018;44(6):717-729. PMID: 29450594

48. Combes A, Brodie D, Chen YS, et al. The ICM research agenda on extracorporeal life support. Intensive Care Med. 2017;43(9):1306-1318. PMID: 28676869

49. Lorusso R, Shekar K, MacLaren G, et al. ELSO interim guidelines for venoarterial extracorporeal membrane oxygenation in adult cardiac patients. ASAIO J. 2021;67(8):827-844. PMID: 34165170

50. Thiele H, Jobs A, Ouweneel DM, et al. Percutaneous short-term active mechanical support devices in cardiogenic shock: a systematic review and collaborative meta-analysis of randomized trials. Eur Heart J. 2017;38(47):3523-3531. PMID: 29020341

51. Kolte D, Khera S, Aronow WS, et al. Trends in incidence, management, and outcomes of cardiogenic shock complicating ST-elevation myocardial infarction in the United States. J Am Heart Assoc. 2014;3(1):e000590. PMID: 24419737

52. Wayangankar SA, Bangalore S, McCoy LA, et al. Temporal trends and outcomes of patients undergoing percutaneous coronary interventions for cardiogenic shock in the setting of acute myocardial infarction. JACC Cardiovasc Interv. 2016;9(4):341-351. PMID: 26803417

53. Samsky MD, Morrow DA, Proudfoot AG, et al. Cardiogenic shock after acute myocardial infarction: a review. JAMA. 2021;326(18):1840-1850. PMID: 34751704

54. 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: 31548097

55. Ceglarek U, Schellong P, Engel C, et al. Utility of lactate and mortality prediction in cardiogenic shock. Crit Care. 2022;26(1):232. PMID: 35915454

56. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support. J Am Coll Cardiol. 2015;66(23):2664-2674. PMID: 26670067

57. Kapur NK, Davila CD, Chweich H, et al. Protecting the vulnerable left ventricle: the art of unloading with VA-ECMO. Circ Heart Fail. 2019;12(4):e006581. PMID: 31002533

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Related Topics

• Cardiogenic Shock
• Acute Coronary Syndromes
• Cardiac Arrhythmias
• Pulmonary Embolism
• VA-ECMO
• Inotropes and Vasopressors
• Non-Invasive Ventilation