Acute Heart Failure

Quick Answer

One-liner: Acute heart failure (AHF) is the rapid onset or worsening of heart failure symptoms requiring urgent evaluation and treatment, with initial management focusing on oxygen, diuretics, vasodilators, and non-invasive ventilation.

Acute heart failure encompasses both new-onset heart failure and acute decompensation of chronic heart failure (ADHF), presenting with pulmonary and/or systemic congestion. In-hospital mortality is 3-5%, with 30-day mortality 10-15%. Immediate ED management prioritizes airway support (NIV for respiratory distress), early IV loop diuretics (within 60 minutes), vasodilators for hypertensive AHF, and identification of reversible precipitants (ACS, arrhythmia, infection). Cardiogenic shock requires inotropic support and urgent specialist consultation.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Left ventricular anatomy, coronary circulation, pulmonary venous drainage, Frank-Starling mechanism
• Physiology: Cardiac output (CO = HR × SV), preload/afterload/contractility, neurohumoral activation (RAAS, SNS, ADH), pressure-volume loops
• Pharmacology: Loop diuretics (furosemide mechanism, tubuloglomerular feedback), nitrates (NO-mediated vasodilation), ACE inhibitors, beta-blockers, inotropes (dobutamine β₁-agonism, milrinone PDE-3 inhibition)

Fellowship Exam Relevance

• Written: Framingham criteria, NYHA classification, BNP/NT-proBNP interpretation, NIV indications/contraindications, diuretic resistance mechanisms, disposition criteria
• OSCE: Taking focused history in dyspneic patient, interpreting chest X-ray with pulmonary oedema, managing acute pulmonary oedema in resus bay, breaking bad news about cardiogenic shock prognosis
• Key domains tested: Medical Expert (diagnosis, treatment), Communicator (dyspneic patient, family), Leader (resus team coordination)

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Key Points

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Epidemiology

Australian/NZ Specific

• Hospitalizations: ~60,000 AHF hospitalizations annually in Australia; HF accounts for 1-2% of all ED presentations [9]
• Indigenous populations: Aboriginal and Torres Strait Islander peoples have 1.4× higher HF hospitalization rates and 1.5× higher HF mortality than non-Indigenous Australians, with earlier onset (median age 10-15 years younger) [10]
• Māori (NZ): Māori have 2× higher HF hospitalization rates and present at younger ages (median 68 vs 79 years for non-Māori), often due to higher prevalence of rheumatic heart disease, diabetes, obesity [11]
• Rural/remote: RFDS data show cardiovascular disease (including AHF) accounts for 15-18% of aeromedical retrievals, with higher rates of preventable decompensation due to limited access to cardiology follow-up [12]

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Pathophysiology

Mechanism

Acute heart failure results from rapid deterioration in cardiac function, leading to inadequate cardiac output and/or elevated filling pressures. This can occur via:

1. Systolic dysfunction: Reduced contractility (ischemia, cardiomyopathy, myocarditis) → decreased stroke volume → decreased CO → hypoperfusion
2. Diastolic dysfunction: Impaired relaxation (LVH, ischemia, restrictive disease) → elevated LV end-diastolic pressure (LVEDP) → pulmonary venous congestion → pulmonary oedema
3. Acute volume overload: Regurgitant lesions (acute MR, acute AR), shunt lesions (VSD), fluid retention → elevated preload → pulmonary/systemic congestion
4. Acute pressure overload: Severe hypertension, acute aortic stenosis → elevated afterload → LV failure

Pathological Progression

Cardiac insult (ischemia, pressure/volume overload, arrhythmia)
    ↓
Reduced cardiac output or elevated filling pressures
    ↓
Neurohumoral activation (RAAS, SNS, ADH)
    ↓
Sodium/water retention + vasoconstriction + tachycardia
    ↓
Worsening congestion + increased afterload
    ↓
Myocardial stress + remodeling
    ↓
Progressive pump failure → cardiogenic shock or death

Why It Matters Clinically

• Congestion vs. perfusion: The Forrester classification (wet/dry + warm/cold) guides therapy. Most patients are "wet and warm" (congested, adequate perfusion) → diuretics + vasodilators. "Wet and cold" (congested, hypoperfused) → inotropes + diuretics.
• Neurohormonal blockade: ACE inhibitors, beta-blockers, MRAs reduce mortality in chronic HF but are NOT first-line in acute phase. Stabilize first, then optimize chronic therapy.
• Diuretic resistance: Chronic loop diuretic use → tubular hypertrophy and increased distal Na⁺ reabsorption → reduced efficacy. Overcome with high-dose IV diuretics, continuous infusions, or combination diuretics (thiazide, acetazolamide).

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Clinical Approach

Recognition

Key triggers to suspect AHF:

• Acute dyspnoea at rest or with minimal exertion
• Orthopnoea (dyspnoea lying flat, relieved by sitting up)
• Paroxysmal nocturnal dyspnoea (PND, waking gasping)
• Bibasal crackles on auscultation
• Elevated JVP, peripheral oedema (legs, sacrum)
• Known history of chronic HF presenting with worsening symptoms

Initial Assessment

Primary Survey (ABCDE)

• A (Airway): Usually patent unless obtunded from hypoxia/hypercapnia or cardiogenic shock
• B (Breathing):
  • Tachypnoea (RR greater than 24), laboured breathing, use of accessory muscles
  • Hypoxia (SpO₂ below 90% on room air in acute pulmonary oedema)
  • Auscultation: Bibasal fine inspiratory crackles, wheeze ("cardiac asthma")
• C (Circulation):
  • Tachycardia (sinus tachycardia most common)
  • "Blood pressure: Hypertensive (greater than 160/100), normotensive, or hypotensive (below 90 mmHg systolic in cardiogenic shock)"
  • Elevated JVP (greater than 3-4 cm above sternal angle)
  • "Peripheral perfusion: Warm peripheries (adequate CO) vs. cool, clammy (low CO/shock)"
  • Third heart sound (S₃ gallop, indicates volume overload)
• D (Disability/Neuro): Confusion, agitation (hypoxia, hypercapnia, hypoperfusion)
• E (Exposure/Environment): Peripheral oedema (pitting ankle/sacral), ascites, hepatomegaly

Hemodynamic Profiling (Forrester Classification)

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Respiratory distress: Sitting upright, tripod position, using accessory muscles, pink frothy sputum (severe pulmonary oedema)
• Cyanosis: Central cyanosis (tongue, lips) indicates severe hypoxia
• Cachexia: Cardiac cachexia in end-stage HF (poor prognostic sign)

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound (POCUS)

POCUS is invaluable in AHF diagnosis and monitoring:

1. Lung ultrasound:

   • B-lines (≥3 per rib space in ≥2 zones bilaterally) = pulmonary oedema [15]
   • Sensitivity 94%, specificity 92% for cardiogenic pulmonary oedema vs. COPD/pneumonia [16]
   • Resolution of B-lines post-diuresis confirms effective decongestion

2. Cardiac ultrasound:

   • LV function: Visual estimation of LVEF (normal, mildly/moderately/severely reduced)
   • IVC diameter and collapsibility: Dilated IVC (greater than 2.1 cm) with minimal respiratory variation (below 50%) suggests elevated RA pressure, volume overload
   • Valvular pathology: Acute MR (eccentric jet, flail leaflet), acute AR (early closure mitral valve)
   • Pericardial effusion: Circumferential fluid, tamponade physiology (RV diastolic collapse)

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Management

Immediate Management (First 10 minutes)

1. OXYGEN: Target SpO₂ 92-96%. High-flow oxygen if SpO₂ below 90% (0-5 min)
2. NIV: CPAP 5-10 cmH₂O or BiPAP (IPAP 12-15, EPAP 5-8) if respiratory distress despite O₂ (0-5 min)
3. POSITION: Sit patient upright (reduces preload, improves lung mechanics) (0-2 min)
4. IV ACCESS: Large-bore cannula (14-16G) for medications (0-5 min)
5. MONITORING: Continuous ECG, SpO₂, BP q5min, urinary catheter (measure UOP) (0-10 min)
6. INVESTIGATIONS: ECG, bloods (BNP, troponin, U&E, FBC), ABG/VBG, CXR (0-10 min)
7. IV DIURETICS: Furosemide 40-80 mg IV bolus (or 2.5× home oral dose if known) WITHIN 60 minutes (5-10 min)

Resuscitation (Acute Pulmonary Oedema)

Airway

• NIV first-line: CPAP or BiPAP reduces work of breathing, improves oxygenation [17]
• Intubation criteria:
  • Failing NIV (persistent hypoxia SpO₂ below 90% on NIV + high FiO₂, worsening hypercapnia PaCO₂ greater than 60 mmHg)
  • Reduced GCS (below 8), inability to protect airway
  • Cardiac arrest
• Intubation caution: Positive-pressure ventilation reduces preload (beneficial in pulmonary oedema) but can precipitate hypotension. Pre-load with vasopressor (e.g., noradrenaline) if SBP below 100 mmHg

Breathing

• Oxygenation targets: SpO₂ 92-96%. Avoid hyperoxia (vasoconstriction, reduced CO)
• NIV settings:
  • "CPAP: Start 5 cmH₂O, titrate to 10 cmH₂O as tolerated"
  • "BiPAP: IPAP 12-15 cmH₂O, EPAP 5-8 cmH₂O"
  • "FiO₂: Titrate to SpO₂ target"
• NIV contraindications: Facial trauma, vomiting, agitation, haemodynamic instability (SBP below 90 mmHg)

Circulation

Hemodynamic goal: Reduce preload (congestion) and afterload (LV workload) while maintaining perfusion (SBP greater than 90 mmHg).

Hypertensive AHF (SBP greater than 160 mmHg): "Vascular failure" phenotype

• Vasodilators (reduce afterload rapidly):
  • "GTN (glyceryl trinitrate): "
    • Sublingual 300-600 mcg q5min PRN (immediate effect)
    • IV infusion 10-200 mcg/min (start 10-20 mcg/min, titrate by 10-20 mcg/min q5-10min to effect or SBP below 120 mmHg) [18]
  • "Isosorbide dinitrate: Oral 5-10 mg sublingually or IV 1-10 mg/hr"
  • "Sodium nitroprusside: 0.3-10 mcg/kg/min (ICU only, risk of cyanide toxicity greater than 48 hrs)"
• Diuretics: Furosemide 40-80 mg IV bolus (see below)
• Avoid beta-blockers acutely: Can worsen acute HF despite benefit in chronic HF

Normotensive AHF (SBP 100-160 mmHg): "Cardiac failure" phenotype

• Diuretics: Primary therapy (see below)
• Vasodilators: Lower-dose GTN if SBP greater than 120 mmHg (caution with hypotension)

Hypotensive AHF / Cardiogenic Shock (SBP below 90 mmHg): "Cardiogenic shock" phenotype

• Inotropes (increase contractility, cardiac output):
  • "Dobutamine: 2.5-20 mcg/kg/min IV (β₁-agonist, ↑inotropy, ↑chronotropy) [19]"
  • "Milrinone: 0.375-0.75 mcg/kg/min IV (PDE-3 inhibitor, ↑inotropy, ↓afterload) [20]"
  • "Caution: Increase myocardial O₂ demand, arrhythmias, hypotension (milrinone vasodilates)"
• Vasopressors (if profound hypotension SBP below 70 mmHg despite inotropes):
  • "Noradrenaline: 0.05-0.5 mcg/kg/min (α-agonist, peripheral vasoconstriction)"
• Avoid diuretics initially if severely hypotensive (further reduce preload → ↓BP). Once SBP greater than 90, add diuretics
• Urgent cardiology/ICU consult: Consider mechanical support (IABP, Impella, VA-ECMO)

Medications

Diuretics (First-line for congestion)

Diuretic resistance: If poor response (urine output below 100 mL/hr after 1st dose):

1. Double the dose (e.g., 80 mg → 160 mg furosemide IV)
2. Continuous infusion (5-40 mg/hr furosemide)
3. Add thiazide (metolazone 2.5-5 mg PO) or acetazolamide (500 mg IV)
4. Correct contributing factors: Hypotension (↓renal perfusion), hypoalbuminemia (below 25 g/L, ↓drug delivery), renal failure (GFR below 30 requires higher doses)

Vasodilators (For afterload reduction, BP control)

Inotropes (For cardiogenic shock only)

Inotrope caution:

• Increase myocardial oxygen demand → can worsen ischemia in ACS-precipitated HF
• Arrhythmogenic (VT, VF risk)
• Do NOT use for "low EF" alone—only for hypoperfusion/shock

Chronic HF Medications (Do NOT start in acute phase)

Paediatric Dosing

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Ongoing Management

1. Monitor response:

   • Vital signs: BP, HR, RR, SpO₂ q15-30min initially
   • Urine output: Target greater than 0.5 mL/kg/hr (insert IDC for accurate monitoring). Expect 1-2 L net negative in first 6-12 hrs
   • Symptoms: Dyspnoea improvement (Borg scale), reduced JVP, clearing crackles
   • Repeat bloods: U&E at 6-12 hrs (check Cr, K⁺), BNP at 24-48 hrs (should ↓50% if responding)

2. Identify and treat precipitants:

   • ACS: Troponin, ECG changes → PCI or medical management per ACS guidelines
   • Arrhythmia: Atrial fibrillation (rate control with beta-blocker/digoxin; consider cardioversion if unstable), VT (amiodarone, cardioversion)
   • Infection: Pneumonia, UTI → antibiotics
   • Anaemia: Transfuse if Hb below 70 g/L (or below 80 g/L if ACS)
   • Renal failure: Adjust diuretic doses, consider nephrology input if refractory
   • Medication non-adherence: Patient education, social work input

3. Adjust therapy:

   • If improving: Continue current regimen, wean NIV as tolerated, transition to oral diuretics once euvolemic
   • If not improving: Escalate diuretics (higher dose, continuous infusion, add second diuretic), consider inotropes if hypoperfused, ICU transfer

Definitive Care

• Cardiology consult: All AHF patients require cardiology input (risk stratification, echocardiography, optimization of chronic HF therapy)
• Coronary angiography: If ACS suspected (troponin ↑, ECG changes)
• ICU/CCU admission: Cardiogenic shock, refractory hypoxia despite NIV, arrhythmias requiring monitoring, acute mechanical complications (VSD, acute MR)
• Cardiac surgery: Acute mechanical complications (free wall rupture, VSD, papillary muscle rupture), severe valvular disease (acute AR, MR), refractory cardiogenic shock (consider MCS: IABP, Impella, VA-ECMO)

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Disposition

Admission Criteria

All AHF patients require admission (ward or ICU) unless very mild exacerbation in reliable patient. Specific indications:

• Oxygen requirement (SpO₂ below 90% on room air)
• NIV requirement
• IV diuretics required (oral diuretics insufficient)
• Troponin elevation (ACS work-up)
• New-onset HF (requires echocardiography, specialist assessment)
• Significant comorbidity: AKI, arrhythmia, infection
• Poor social support (unable to manage at home, follow-up uncertain)

ICU/HDU Criteria

• Cardiogenic shock (SBP below 90 mmHg, hypoperfusion despite initial therapy)
• Inotrope or vasopressor requirement
• Respiratory failure requiring NIV or intubation
• Refractory pulmonary oedema despite maximal medical therapy
• Acute mechanical complications (VSD, acute MR, free wall rupture)
• Arrhythmias with haemodynamic compromise (VT, unstable AF with RVR)
• Severe electrolyte disturbances (K⁺ below 2.5 or greater than 6.5 mmol/L)

Discharge Criteria (Rare in AHF, mostly observation unit)

Consider short-stay unit or observation unit discharge only if:

• Mild exacerbation of known chronic HF (small weight gain, mild dyspnoea)
• Rapid response to ED therapy (symptom resolution, no O₂ requirement)
• Low-risk features:
  • SBP greater than 100 mmHg, HR below 100 bpm, SpO₂ greater than 94% on room air
  • BNP below 500 pg/mL (or NT-proBNP below 2000 pg/mL)
  • Creatinine below 150 µmol/L, no significant AKI
  • Troponin negative
  • No significant arrhythmia
• Reliable patient with good adherence, close GP/cardiology follow-up within 1-2 weeks
• Red flags to return:
  • Worsening dyspnoea
  • Chest pain
  • Syncope or palpitations
  • Weight gain greater than 2 kg in 3 days
  • Reduced urine output

Follow-up

• Cardiology appointment: Within 1-2 weeks (titration of chronic HF meds: ACE-I, beta-blocker, MRA, SGLT2i)
• GP follow-up: Within 1 week (check U&E, review meds, reinforce adherence)
• Heart failure clinic/nurse: If available, HF nurse home visits reduce readmissions [24]
• Specialist referral if needed:
  • HFrEF (LVEF below 40%) → consider ICD, CRT
  • Advanced HF → transplant evaluation
• Discharge letter requirements:
  • Precipitant identified (if any)
  • Medication changes (diuretic dose, ACE-I initiated/titrated)
  • Weight on discharge (baseline for self-monitoring)
  • Follow-up plan (GP, cardiology, HF clinic)

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Special Populations

Paediatric Considerations

Acute heart failure in children is rare but causes include:

• Congenital heart disease: VSD, PDA, coarctation, hypoplastic left heart syndrome (HLHS)
• Myocarditis: Viral (coxsackie, adenovirus, parvovirus B19)
• Cardiomyopathy: Dilated (DCM), hypertrophic (HCM)
• Kawasaki disease with coronary aneurysms and ischemia

Management differences:

• Fluid restriction: Strict (often 50-75% maintenance fluids)
• Diuretics: Furosemide 1-2 mg/kg IV (max 6 mg/kg/day)
• Inotropes: Dobutamine 5-20 mcg/kg/min (first-line for low CO)
• Avoid ACE-I in acute phase: Can precipitate hypotension in children
• Early paediatric cardiology consult: All cases

Pregnancy

Acute HF in pregnancy (peripartum cardiomyopathy, pre-eclampsia with pulmonary oedema, valvular disease):

• Position: Left lateral tilt (avoid supine → ↓IVC compression → ↑venous return)
• Oxygen: Liberal oxygen (fetal oxygenation priority)
• Diuretics: Furosemide safe in pregnancy (use if pulmonary oedema)
• Avoid ACE-I/ARBs: Teratogenic, renal agenesis in fetus. Use hydralazine + nitrates for afterload reduction
• Avoid spironolactone: Anti-androgenic effects on male fetus
• Magnesium sulfate: If pre-eclampsia (4-6 g IV loading, then 1-2 g/hr infusion)
• Urgent obstetric/cardiology consult: Maternal-fetal medicine input
• Delivery considerations: If late pregnancy (greater than 34 weeks), may need urgent delivery

Elderly

Older patients (greater than 75 years) have higher mortality, more comorbidities, and altered pharmacokinetics:

• Lower diuretic doses: Start lower (40 mg furosemide), as more prone to AKI, electrolyte disturbances
• Caution with nitrates: Orthostatic hypotension, falls risk
• Polypharmacy: Review medication list, stop non-essential drugs
• Cognitive assessment: Delirium common in acute illness, impacts adherence
• Goals of care: Consider advance care planning, ceiling of treatment in frail/end-stage HF

Indigenous Health

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

Epidemiology:

• Aboriginal and Torres Strait Islander Australians: 1.4× higher HF hospitalization, 1.5× higher mortality, present 10-15 years younger (median age 60 vs 75) [10]
• Māori (NZ): 2× higher HF hospitalization, earlier onset (median 68 vs 79 years), 50% higher mortality [11]
• Higher prevalence of HF risk factors: Diabetes (3×), obesity (1.5×), rheumatic heart disease (10-20× higher in Aboriginal/Torres Strait Islander, especially in remote Northern Australia) [25]

Cultural safety considerations:

• Family-centered care: Involve family/whānau in decision-making. Explain diagnosis and treatment in plain language, with interpreter if needed
• Cultural liaison services: Engage Aboriginal and Torres Strait Islander health workers or Māori health advocates to improve communication and adherence
• Distrust of healthcare system: Historical trauma, systemic racism → approach with humility, build rapport, explain rationale for treatments
• Traditional medicines: Ask respectfully about concurrent use of traditional remedies. Most compatible, but some may interact (e.g., herbal diuretics)

Barriers to care:

• Remote location: Limited access to cardiology, echocardiography, cardiac rehab → higher rates of preventable ADHF
• Medication adherence: Cost (PBS co-payment barriers), complex regimens, health literacy
• Follow-up: Transport challenges, competing priorities (family, work, cultural obligations)

Strategies to improve outcomes:

• Telehealth: Remote cardiology consult, echocardiography review
• Subsidized medications: Close the Gap PBS co-payment waiver for eligible Aboriginal and Torres Strait Islander patients
• Community health workers: Aboriginal and Torres Strait Islander health practitioners to support adherence, lifestyle modification
• Early RFDS retrieval: Low threshold for aeromedical transfer if deteriorating in remote clinic

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Acute Pulmonary Oedema Resuscitation

Format: Resuscitation / Clinical Management Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

You are the ED registrar. A 68-year-old woman has just arrived by ambulance with sudden-onset severe shortness of breath. The nurse has placed her on oxygen and attached monitoring. Your task is to perform an initial assessment and manage the patient. A nurse and airway equipment are available if needed.

Examiner Instructions: Patient is a 68-year-old woman with hypertensive acute pulmonary oedema (background: hypertension, no known HF). She is sitting upright, very dyspneic, using accessory muscles, speaking in single words only.

Initial vitals (displayed on monitor):

• BP 190/100 mmHg
• HR 115 bpm (sinus tachycardia)
• RR 32/min
• SpO₂ 87% on 15L via non-rebreather mask
• GCS 14 (confused, distressed)

Physical findings (if examined):

• Bibasal fine inspiratory crackles
• Elevated JVP (6 cm above sternal angle)
• S₃ gallop (if auscultates carefully)
• No peripheral oedema

Progression:

• If candidate gives appropriate initial management (NIV + furosemide + GTN) → vitals improve: SpO₂ 94%, RR 24, BP 150/90, patient calmer within 5 minutes
• If candidate does not start NIV → patient deteriorates: SpO₂ 82%, RR 36, GCS 12, nurse asks "Should we intubate?"
• If candidate requests investigations → ECG shows sinus tachycardia, no acute ischemia; BNP 1200 pg/mL; CXR shows pulmonary oedema

Actor/Patient Brief: You are extremely short of breath and frightened. You woke up suddenly 2 hours ago gasping for air. You can only speak 1-2 words at a time. You are confused due to hypoxia. If the candidate reassures you and starts treatment, you gradually feel better and can speak short sentences after 5 minutes.

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Recognizes pulmonary oedema, starts NIV + diuretic, basic resuscitation principles
• Key discriminators:
  • "Early NIV: Candidates who start NIV within 3 min vs. those who delay or don't use it"
  • "Dual therapy: Recognizing need for BOTH diuretic (furosemide) AND vasodilator (GTN) in hypertensive pulmonary oedema"
  • Reassessment: Actively monitors response and adjusts therapy vs. "one and done" approach

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Station 2: Breaking Bad News—Cardiogenic Shock Prognosis

Format: Communication Time: 11 minutes Setting: ED relatives' room

Candidate Instructions:

You are the ED consultant. Mrs. Thompson, a 70-year-old woman, was brought in 2 hours ago with acute heart failure and cardiogenic shock. Despite maximal therapy (intubation, inotropes, IABP), she remains profoundly hypotensive with multi-organ failure. The intensivist has reviewed her and feels she is unlikely to survive. Her son, Mr. David Thompson, is in the relatives' room. Please speak with him about his mother's condition and prognosis.

Examiner Instructions: Mr. Thompson (son) is anxious and upset. He arrived 10 minutes ago and has not seen his mother yet (she's in resus bay, intubated, multiple lines/devices). He knows she has "heart failure" but thinks it's treatable. He is hopeful she will recover.

Standardized actor brief:

• You are in your 40s, an office worker, only child
• You live 2 hours away, your mother called you this morning saying she couldn't breathe, you drove down immediately
• You expect the doctor to say she's sick but will get better with treatment
• You don't understand medical jargon—ask for clarification if the doctor uses complex terms
• If the doctor mentions death/dying, you become tearful but want to know details (suffering? timescale? what happens next?)
• You want to see her

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Delivers bad news clearly (no euphemisms), shows empathy, addresses son's questions
• Key discriminators:
  • Honesty vs. false hope: Clear statement of poor prognosis vs. vague "we'll see how she goes"
  • "Empathy: Genuine emotional attunement (pauses, acknowledges distress) vs. rushed, clinical delivery"
  • "Practical next steps: Offers to take him to see her, discusses palliation, involves family vs. ending conversation abruptly"

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Station 3: Focused History—Dyspneic Patient with Heart Failure

Format: History Taking Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

You are the ED registrar. Mr. James, a 75-year-old man, presents with 3 days of worsening shortness of breath. Please take a focused history to determine the cause and severity of his dyspnoea. You do not need to examine the patient.

Examiner Instructions: Patient has acute decompensation of chronic heart failure (ischemic cardiomyopathy, LVEF 30%). Precipitant is medication non-adherence (ran out of furosemide 2 weeks ago, couldn't afford prescription refill).

Actor/Patient Brief: You are a 75-year-old retired plumber. You've had heart failure for 5 years (after a heart attack). You take several medications (ramipril, bisoprolol, furosemide, atorvastatin) but ran out of furosemide ("water tablets") 2 weeks ago because you couldn't afford the prescription ($15 co-payment). You didn't tell anyone.

Symptoms:

• 3 days ago: Noticed legs swelling, a bit puffy
• 2 days ago: Started feeling short of breath walking to the shops (normally can walk 200m)
• 1 day ago: Woke up at 3am gasping for air (PND), had to sleep sitting in chair
• Today: Can't lie flat, breathless at rest, very worried

Other information (if asked):

• No chest pain, palpitations, syncope
• No cough, fever, sputum (rules out pneumonia)
• No leg pain, recent travel (rules out PE)
• Medications: Ramipril 10 mg, bisoprolol 5 mg, furosemide 40 mg BD (but haven't taken for 2 weeks), atorvastatin 40 mg
• Adherence: Usually good, but financial stress (pension only, $15 co-payment is a lot for you)
• Diet: Ate fish and chips 4 days ago (high salt) because it was cheap
• PMHx: MI 2012, PCI to LAD, HF (LVEF 30%), hypertension, hyperlipidemia
• Social: Lives alone (wife died 3 years ago), daughter visits weekly, doesn't smoke, no alcohol
• Allergies: Nil

If candidate asks about red flags:

• No chest pain (denies ACS)
• No syncope (denies arrhythmia)
• No sudden onset (denies PE)

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Takes structured dyspnoea history, identifies HF symptoms (orthopnoea, PND), asks about medications
• Key discriminators:
  • "Medication adherence: Actively explores adherence vs. assumes patient is compliant"
  • Precipitants: Systematically asks about common ADHF precipitants vs. generic "breathlessness" history
  • "Social barriers: Identifies financial barrier to medication adherence vs. misses it"

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SAQ Practice

Question 1 (8 marks)

Stem: A 62-year-old man presents to ED with acute dyspnoea. His BP is 200/110 mmHg, HR 120 bpm, RR 32/min, SpO₂ 86% on room air. He has bibasal crackles and pink frothy sputum. You diagnose hypertensive acute pulmonary oedema.

Question: Outline your immediate management of this patient in the first 15 minutes. (8 marks)

Model Answer:

1. Positioning: Sit patient upright, legs dependent (reduces preload) (1 mark)
2. Oxygen: High-flow oxygen 15L via non-rebreather mask, target SpO₂ 92-96% (1 mark)
3. Non-invasive ventilation (NIV):
   • CPAP 5-10 cmH₂O OR BiPAP (IPAP 12-15, EPAP 5-8 cmH₂O)
   • Reduces work of breathing, improves oxygenation (1 mark)
4. IV access: Large-bore cannula (14-16G), continuous monitoring (ECG, SpO₂, BP q5min) (0.5 marks)
5. IV furosemide: 40-80 mg IV bolus (reduces preload, diuresis) (1 mark)
6. IV glyceryl trinitrate (GTN):
   • Start 10-20 mcg/min IV infusion, titrate by 10-20 mcg/min q5min to reduce BP to ~140/90
   • OR sublingual GTN 400-600 mcg q5min PRN (1 mark)
7. Investigations:
   • 12-lead ECG (rule out ACS, arrhythmia)
   • Bloods: BNP/NT-proBNP, troponin, U&E, FBC
   • Arterial blood gas (assess oxygenation, acid-base)
   • Chest X-ray (confirm pulmonary oedema) (1 mark)
8. Urinary catheter: Insert IDC to monitor urine output (target greater than 0.5 mL/kg/hr) (0.5 marks)
9. Reassess frequently: Check vitals q5-10min, clinical response (dyspnoea, SpO₂, work of breathing). Prepare for intubation if deteriorates despite therapy (1 mark)

Examiner Notes:

• Accept: High-dose GTN IV (up to 200 mcg/min), sodium nitroprusside (ICU only), bumetanide instead of furosemide, VBG instead of ABG
• Do not accept: Fluid bolus (worsens pulmonary oedema), morphine (not recommended—respiratory depression, no mortality benefit), ACE-I acutely (delayed onset, hypotension risk)
• Bonus: Mentioning GTN contraindications (RV infarct, PDE-5 inhibitor use, SBP below 100) or bedside POCUS (B-lines, LV function) earns examiner goodwill but not extra marks (question is 8 marks total).

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Question 2 (6 marks)

Stem: You are managing a patient with acute decompensated heart failure. After giving IV furosemide 80 mg, the patient has passed only 50 mL of urine in 2 hours.

Question: List SIX strategies to overcome diuretic resistance in this patient. (6 marks, 1 mark each)

Model Answer:

1. Increase furosemide dose: Double or triple the dose (e.g., 160-240 mg IV bolus). Higher doses overcome reduced renal perfusion and tubular secretion. (1 mark)
2. Switch to continuous infusion: Furosemide 10-40 mg/hr IV continuous infusion. Maintains consistent tubular drug levels, more effective than intermittent boluses. (1 mark)
3. Add acetazolamide: 500 mg IV once daily. Blocks proximal tubule Na⁺ reabsorption (ADVOR trial: 42% vs 31% decongestion). (1 mark)
4. Add thiazide diuretic: Metolazone 2.5-10 mg PO daily. Blocks distal convoluted tubule, synergistic with loop diuretics ("sequential nephron blockade"). (1 mark)
5. Optimize hemodynamics: If hypotensive or low cardiac output (cool peripheries) → add inotrope (dobutamine 5-20 mcg/kg/min) to increase renal perfusion and GFR. (1 mark)
6. Correct hypoalbuminemia: If serum albumin below 25 g/L → co-administer IV albumin 100 mL 20% with furosemide dose (improves drug delivery to tubules). (1 mark)

Alternative acceptable answers (examiner discretion):

• Switch loop diuretic: Bumetanide 2-4 mg IV instead of furosemide (different bioavailability, may overcome resistance)
• Ultrafiltration (CVVH): Extracorporeal fluid removal if refractory to all medical therapy (ICU/nephrology input required)
• Correct acidosis: If metabolic acidosis (pH below 7.3), loop diuretics less effective; consider bicarbonate infusion (controversial)

Examiner Notes:

• Do not accept: "Give more fluids" (worsens volume overload), "Stop diuretics" (does not address resistance)
• Award 1 mark per strategy, max 6 marks. If candidate lists greater than 6 strategies, mark first 6 only.

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Question 3 (6 marks)

Stem: A 58-year-old Aboriginal man from a remote Northern Territory community presents with acute heart failure secondary to rheumatic heart disease (severe mitral regurgitation). You are arranging RFDS retrieval to Darwin.

Question: List THREE specific challenges in managing heart failure in remote/rural Aboriginal communities AND THREE strategies to improve outcomes. (6 marks: 3 for challenges, 3 for strategies)

Model Answer:

Challenges (3 marks, 1 mark each):

1. Limited access to specialist care: No cardiologists, echocardiography, or advanced HF services in remote clinics. Delays in diagnosis, monitoring, and optimization of therapy. (1 mark)
2. Medication adherence barriers: High cost of medications (PBS co-payments), complex regimens, limited health literacy, cultural beliefs about Western medicine, transport difficulties for clinic follow-up. (1 mark)
3. High burden of rheumatic heart disease (RHD): Aboriginal and Torres Strait Islander populations have 10-20× higher RHD rates due to overcrowding, poor housing, delayed GAS pharyngitis treatment. RHD causes premature HF (median age 10-15 years younger than non-Indigenous). (1 mark)

Strategies to improve outcomes (3 marks, 1 mark each):

1. Telemedicine and RFDS: Remote cardiology consultations via telehealth, portable echocardiography with store-and-forward imaging. Early RFDS aeromedical retrieval for deteriorating patients. (1 mark)
2. Cultural safety and engagement: Involve Aboriginal health workers in care, use interpreters (Aboriginal languages, Kriol), family-centered decision-making, respect for cultural protocols. Builds trust and improves adherence. (1 mark)
3. RHD prevention programs: Primary prevention (early GAS pharyngitis treatment with antibiotics), secondary prevention (benzathine penicillin G injections every 28 days to prevent ARF recurrence). RHD Australia programs (NT, FNQ) have reduced ARF incidence. (1 mark)

Alternative acceptable answers:

• Challenges: Distance to hospitals (600-1000 km), environmental factors (heat exacerbates HF), workforce shortages (GP turnover in remote areas), social determinants (poverty, food insecurity, diabetes/obesity comorbidities)
• Strategies: Subsidized medications (Close the Gap PBS co-payment waiver), HF nurse outreach visits, simplified medication regimens (once-daily dosing), community education (self-monitoring weight, recognizing symptoms), addressing social determinants (housing, nutrition programs)

Examiner Notes:

• Award 1 mark per challenge (max 3), 1 mark per strategy (max 3)
• Accept: Any evidence-based challenge or strategy related to remote/rural/Indigenous HF care
• Do not accept: Generic statements not specific to remote/Indigenous context (e.g., "patient doesn't take medications"—too vague, must mention WHY: cost, distance, literacy, etc.)

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Question 4 (8 marks)

Stem: A 70-year-old woman with known heart failure (LVEF 25%) presents with cardiogenic shock (BP 80/50 mmHg, HR 110 bpm, cold peripheries, altered mental status). You have started dobutamine 10 mcg/kg/min, but her BP remains 85/55 mmHg after 30 minutes.

Question: (a) List FOUR additional immediate management strategies. (4 marks) (b) List FOUR complications of inotrope therapy you need to monitor for. (4 marks)

Model Answer:

(a) Additional immediate management strategies (4 marks, 1 mark each):

1. Increase dobutamine dose: Titrate to 15-20 mcg/kg/min (maximum dose). May improve cardiac output and perfusion further. (1 mark)
2. Add vasopressor: Start noradrenaline 0.05-0.2 mcg/kg/min IV if SBP remains below 70-80 mmHg. Increases BP via peripheral vasoconstriction. (Caution: increases afterload, may worsen HF—use as bridge to definitive therapy.) (1 mark)
3. Alternative inotrope: Switch to or add milrinone 0.375-0.75 mcg/kg/min IV (PDE-3 inhibitor, different mechanism from dobutamine). Particularly if patient on chronic beta-blockers (dobutamine less effective). (1 mark)
4. Mechanical circulatory support (MCS): Urgent cardiology/ICU consult for IABP (intra-aortic balloon pump), Impella (microaxial pump), or VA-ECMO. Required if refractory to maximal inotrope/vasopressor therapy. (1 mark)

Alternative acceptable answers:

• Invasive monitoring: Arterial line (continuous BP monitoring), central venous line (CVP measurement), consider PA catheter (measure cardiac output, guide therapy)
• Optimize preload: If CVP low (below 8 mmHg) and patient dry → cautious 250 mL bolus crystalloid (uncommon in HF but possible if over-diuresed). If CVP high (greater than 18 mmHg) → add IV furosemide once SBP greater than 90 mmHg
• Identify and treat reversible causes: ACS (coronary angiography, PCI), mechanical complication (acute MR, VSD—needs urgent echo and cardiac surgery), arrhythmia (cardiovert unstable AF/VT), tamponade (pericardiocentesis)
• Reduce afterload: If SBP 80-90 mmHg and peripheries warming → cautious trial of vasodilator (low-dose nitroprusside or nitroglycerin IV) to reduce LV workload (ICU setting only, invasive monitoring required)

(b) Complications of inotrope therapy (4 marks, 1 mark each):

1. Arrhythmias: Ventricular tachycardia (VT), ventricular fibrillation (VF), atrial fibrillation. Inotropes increase myocardial automaticity and triggered activity. Monitor continuous ECG. (1 mark)
2. Myocardial ischemia: Inotropes increase myocardial oxygen demand (MVO₂) via ↑contractility, ↑heart rate. Can precipitate ACS or worsen existing ischemia. Monitor for chest pain, ECG changes, troponin rise. (1 mark)
3. Hypotension (especially milrinone): Milrinone causes vasodilation (PDE-3 inhibition) → may worsen hypotension despite improved contractility. Monitor BP closely. (1 mark)
4. Tachycardia: Dobutamine stimulates β₁-receptors → ↑HR. Excessive tachycardia (HR greater than 120-130) reduces diastolic filling time → ↓CO paradoxically. May need to reduce dose or switch to milrinone. (1 mark)

Alternative acceptable answers:

• Thrombocytopenia (milrinone): Rare, below 1%, but monitor platelet count
• Extravasation injury: Inotropes are vesicants (tissue necrosis if IV line infiltrates). Use central line ideally. Monitor IV site.
• Tolerance: Prolonged inotrope use (greater than 72 hrs) → downregulation of β-receptors → reduced efficacy (dobutamine)

Examiner Notes:

• Award 1 mark per strategy/complication, max 4 marks each section.
• Accept: Any evidence-based strategy or complication.
• Do not accept in part (a): "Give fluids" without specifying indication (CVP low, euvolemic) or "Wait and see" (not active management).

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Australian Guidelines

ARC/ANZCOR

• ANZCOR Guideline 11.7 - Acute Coronary Syndromes: Relevant to AHF precipitated by ACS. Recommends early reperfusion (PCI for STEMI within 90 min), dual antiplatelet therapy (aspirin + P2Y12 inhibitor), anticoagulation (heparin or fondaparinux), and medical therapy (beta-blockers, ACE-I, statins). Specific to Australia/NZ context (not AHA/ERC). [30]

• Key differences from AHA/ERC:

  • "Nicorandil: Not available in Australia (used in UK/Europe for ACS). Use GTN or isosorbide dinitrate instead."
  • "Fondaparinux: Preferred anticoagulant for NSTEMI in ANZCOR (lower bleeding risk than enoxaparin). AHA uses enoxaparin or UFH."
  • "Prasugrel: Less commonly used in Australia (ticagrelor preferred for P2Y12 inhibition in ACS). AHA endorses both equally."

Therapeutic Guidelines Australia

• Cardiovascular Expert Group - Heart Failure:

  • "Acute HF management: Recommends IV loop diuretics (furosemide 40-80 mg IV bolus, titrate to response), vasodilators (GTN IV 10-200 mcg/min for hypertensive AHF), NIV (CPAP/BiPAP for respiratory distress), and oxygen (target SpO₂ 92-96%)."
  • Chronic HF optimization: "Triple therapy" with ACE-I (or ARB if intolerant) + beta-blocker (carvedilol, metoprolol, bisoprolol) + MRA (spironolactone) for HFrEF (LVEF below 40%). Add SGLT2 inhibitor (empagliflozin, dapagliflozin) for further mortality reduction (EMPEROR-Reduced, DAPA-HF trials).
  • "Diuretic resistance: Recommends sequential nephron blockade (add metolazone 2.5-10 mg PO to furosemide) or continuous furosemide infusion (5-40 mg/hr)."

• PBS (Pharmaceutical Benefits Scheme):

  • "Subsidized HF medications: ACE-I, ARBs, beta-blockers, MRAs, SGLT2 inhibitors (empagliflozin, dapagliflozin for HFrEF LVEF ≤40%), sacubitril-valsartan (Entresto, for HFrEF if symptomatic despite ACE-I/ARB + beta-blocker)."
  • ""Close the Gap" co-payment waiver: Aboriginal and Torres Strait Islander patients eligible for free or reduced-cost PBS medications (removes $7.70 co-payment barrier)."

State-Specific

• NSW Health - Acute Heart Failure Pathway: Recommends "time to diuretic" below 60 min from ED arrival, early BNP measurement, risk stratification (EHMRG score for ED disposition), and cardiology referral for all new-onset HF or high-risk ADHF. [31]

• Victorian Cardiac Outcomes Registry (VCOR): Tracks HF outcomes statewide. Data shows 30-day readmission 22%, 1-year mortality 28% for AHF admissions. Worse outcomes in rural/regional areas (delayed access to cardiology, fewer HF nurse services).

• Queensland Cardiac Outcomes Registry: Similar data. Indigenous Queenslanders have 1.6× higher HF hospitalization and 1.7× higher HF mortality than non-Indigenous.

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Remote/Rural Considerations

Pre-Hospital

Ambulance/Paramedic Management:

• Basic Life Support (BLS): Positioning (sit upright), oxygen (non-rebreather mask 15L), reassurance, rapid transport
• Advanced Life Support (ALS):
  • IV access en route
  • "GTN spray: 400 mcg sublingual q5min PRN (if SBP greater than 100 mmHg)"
  • "CPAP: Some paramedic services (e.g., NSW Ambulance, Ambulance Victoria) carry portable CPAP devices for acute pulmonary oedema. Initiate pre-hospital if severe respiratory distress (RR greater than 30, SpO₂ below 90%)."
  • "Furosemide 40 mg IV: Some protocols allow paramedic administration (standing order or phone medical control)"
  • "Pre-notification: Alert ED to prepare resus bay, NIV, medications"

Extended Care Paramedics (ECP): In remote areas (Northern Territory, Western Australia, rural Queensland), ECPs can provide advanced care (IV medications, clinical decision-making) when nearest hospital is hours away.

Resource-Limited Setting

Modified approach when resources limited (small rural hospital, remote clinic):

Retrieval (RFDS Considerations)

Criteria for retrieval (transfer to tertiary center):

• Cardiogenic shock (SBP below 90, inotrope requirement, multi-organ failure) → ICU bed required
• Refractory hypoxia (SpO₂ below 90% despite NIV, intubated) → mechanical ventilation, specialist input
• Suspected ACS precipitant → PCI capability needed (cath lab at tertiary hospital)
• Mechanical complications (acute MR, VSD, free wall rupture) → cardiac surgery required
• No cardiology access at local hospital → transfer for echocardiography, specialist optimization

RFDS capabilities:

• Equipment: Portable ventilators, NIV (CPAP), infusion pumps (inotropes, vasopressors), blood products (O-neg, O-pos in fridge onboard), point-of-care testing (i-STAT for blood gases, electrolytes), defibrillator/monitor
• Personnel: Retrieval doctor (often emergency or intensive care specialist), flight nurse, paramedic
• Clinical support: Telephone advice from RFDS Retrieval Coordination Centre (RCC) to remote clinician pre-arrival

Retrieval challenges:

• Distance: Some communities greater than 1000 km from tertiary hospital (2-3 hour flight)
• Weather: Monsoons (Northern Australia Oct-Apr), dust storms (Central Australia) can delay or prevent flight
• Airstrip conditions: Dirt airstrips may be unusable after rain (plane can't land → road ambulance to nearby sealed strip, or wait for conditions to improve)
• Altitude: Commercial RFDS planes fly at 10,000-15,000 feet (unpressurized or partially pressurized) → hypoxia worsens at altitude. Pre-oxygenate well, increase FiO₂ during flight. Pneumothorax risk (air expands at altitude—exclude PTX before flight, consider chest drain prophylactically if rib fractures).

RFDS contact: Each state has a dedicated number:

• Northern Territory: 08 8944 8555
• Queensland: 07 3630 5000
• NSW: 1300 363 726
• Western Australia: 08 9417 0555
• South Australia: 08 8238 3333
• Victoria: SAMU (retrieval service) 1300 368 661

Telemedicine

Remote consultation approach:

• Cardiology telehealth: Many tertiary hospitals offer real-time video consult for remote EDs. Present case, share ECG/CXR images (via secure platform), discuss management.
• Store-and-forward echocardiography: Some remote clinics have portable echo devices (e.g., Butterfly iQ, Philips Lumify). Non-cardiologists perform basic views (PLAX, A4C), images uploaded to cloud, reviewed by cardiologist within 24 hrs.
• Clinical decision support: RFDS Medical Chest (online handbook) provides protocols for managing HF, ACS, arrhythmias in remote settings. Updated annually.

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References

Guidelines

1. Australian Institute of Health and Welfare (AIHW). Heart failure in Australia. Cat. no. CVD 88. Canberra: AIHW, 2023. Available from: https://www.aihw.gov.au/reports/heart-stroke-vascular-diseases/heart-failure
2. National Heart Foundation of Australia. Chronic Heart Failure Guidelines. 2018 Update. Available from: https://www.heartfoundation.org.au/
3. 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: 37622666
4. 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
5. Mebazaa A, Yilmaz MB, Levy P, et al. Recommendations on pre-hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. Eur J Heart Fail. 2015;17(6):544-558. PMID: 25999021
6. Australian Resuscitation Council and New Zealand Resuscitation Council. ANZCOR Guideline 11.7 - Acute Coronary Syndromes. 2021. Available from: https://resus.org.au/guidelines/

Key Evidence

Epidemiology: 7. Savarese G, Lund LH. Global Public Health Burden of Heart Failure. Card Fail Rev. 2017;3(1):7-11. PMID: 28785469 8. Clark RA, Mcalister FA, Eurich DT, et al. The effect of comorbidities on the competing risk of death in acute decompensated heart failure. Med J Aust. 2010;192(6):310-313. PMID: 20230346 9. Teng TK, Finn J, Hung J, et al. A validation of the Hospital Admissions Risk Profile (HARP) model for 30-day hospital readmissions using multicentre data. Int J Cardiol. 2016;220:743-747. PMID: 27393862 10. Azzopardi S, Baldwin L, Schutze H, et al. Heart failure in Indigenous Australians. Heart Lung Circ. 2018;27(11):1328-1333. PMID: 29478858 11. Grey C, Jackson R, Wells S, et al. Ethnic differences in the management of heart failure in New Zealand. Heart. 2006;92(4):511-515. PMID: 16159977 12. Royal Flying Doctor Service. Best for the Bush: 2019-20 Annual Report. Available from: https://www.flyingdoctor.org.au/

Diagnosis: 13. Januzzi JL, 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: 15820160 14. Peacock WF, De Marco T, Fonarow GC, et al. Cardiac troponin and outcome in acute heart failure. N Engl J Med. 2008;358(20):2117-2126. PMID: 18480204 15. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-125. PMID: 18403664 16. Al Deeb M, Barbic S, Featherstone R, et al. Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Acad Emerg Med. 2014;21(8):843-852. PMID: 25176151

NIV: 17. Gray A, Goodacre S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med. 2008;359(2):142-151. PMID: 18184957 (3CPO trial) 18. Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet. 1998;351(9100):389-393. PMID: 9482291

Inotropes: 19. Tacon CL, McCaffrey J, Delaney A. Dobutamine for patients with severe heart failure: a systematic review and meta-analysis of randomised controlled trials. Intensive Care Med. 2012;38(3):359-367. PMID: 22183416 20. Felker GM, Benza RL, Chandler AB, et al. Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study. J Am Coll Cardiol. 2003;41(6):997-1003. PMID: 12651048

Diuretics: 21. 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: 21345100 22. Mullens W, Dauw J, Martens P, et al. Acetazolamide in acute decompensated heart failure with volume overload (ADVOR trial). N Engl J Med. 2022;387(13):1185-1195. PMID: 36027559

SGLT2 inhibitors: 23. Voors AA, Angermann CE, Teerlink JR, et al. The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial (EMPULSE). Nat Med. 2022;28(3):568-574. PMID: 35165448

HF Disease Management: 24. Stewart S, Vandenbroek AJ, Pearson S, et al. Prolonged beneficial effects of a home-based intervention on unplanned readmissions and mortality among patients with congestive heart failure. Arch Intern Med. 1999;159(3):257-261. PMID: 9989537 25. Carapetis JR, Beaton A, Cunningham MW, et al. Acute rheumatic fever and rheumatic heart disease. Nat Rev Dis Primers. 2016;2:15084. PMID: 27188830

Time to Treatment: 26. Maisel A, Xue Y, Shah K, et al. Increased 90-day mortality in patients with acute heart failure with elevated troponin: prevalence and clinical outcome in the URGENT dyspnea study. Eur J Heart Fail. 2013;15(2):196-204. PMID: 22968732

Albumin + Furosemide: 27. Fliser D, Zurbrüggen I, Mutschler E, et al. Coadministration of albumin and furosemide in patients with the nephrotic syndrome. Kidney Int. 1999;55(2):629-634. PMID: 9987087

Examination Findings: 28. Wang CS, FitzGerald JM, Schulzer M, et al. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA. 2005;294(15):1944-1956. PMID: 16234501 29. Butman SM, Ewy GA, Standen JR, et al. Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. J Am Coll Cardiol. 1993;22(4):968-974. PMID: 8409069

Australian-Specific: 30. Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016. Med J Aust. 2016;205(3):128-133. PMID: 27465769 31. NSW Agency for Clinical Innovation. Acute Heart Failure Clinical Pathway. 2020. Available from: https://aci.health.nsw.gov.au/

Systematic Reviews

32. Weng CL, Zhao YT, Liu QH, et al. Meta-analysis: noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152(9):590-600. PMID: 20439577
33. Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev. 2013;2013(5):CD005351. PMID: 23728654
34. Faris RF, Flather M, Purcell H, et al. Diuretics for heart failure. Cochrane Database Syst Rev. 2012;2:CD003838. PMID: 22336796

Landmark Studies

35. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med. 1987;316(23):1429-1435. PMID: 2883575
36. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure (COPERNICUS trial). N Engl J Med. 2001;344(22):1651-1658. PMID: 11386263
37. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure (RALES trial). N Engl J Med. 1999;341(10):709-717. PMID: 10471456
38. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction (DAPA-HF trial). N Engl J Med. 2019;381(21):1995-2008. PMID: 31535829
39. Packer M, Anker SD, Butler J, et al. Cardiovascular and renal outcomes with empagliflozin in heart failure (EMPEROR-Reduced trial). N Engl J Med. 2020;383(15):1413-1424. PMID: 32865377
40. Velazquez EJ, Morrow DA, DeVore AD, et al. Angiotensin-neprilysin inhibition in acute decompensated heart failure. N Engl J Med. 2019;380(6):539-548. PMID: 30415601 (PIONEER-HF trial)