Why Acute Heart Failure Is Examined
Acute heart failure (AHF) is one of the most common causes of acute medical admission in the UK, with over 100,000 admissions annually. It is examined in OSCEs as an acute deterioration station (patient on the ward with increasing breathlessness and oxygen requirements), prescribing station (write the management plan), and clinical reasoning. Examiners test recognition, correct fluid management, and escalation decisions.
Recognising Acute Decompensated Heart Failure
Symptoms
- Acute breathlessness (orthopnoea, PND, dyspnoea at rest)
- Pink frothy sputum (pulmonary oedema)
- Ankle swelling (worsening over days to weeks)
- Fatigue, reduced exercise tolerance
Signs — RAISED JVP + Lung Crepitations
| System | Signs |
|---|---|
| Cardiovascular | Raised JVP, S3 gallop (most specific for LVF), displaced apex (cardiomegaly), tachycardia, pulsus alternans |
| Respiratory | Bibasal crackles (pulmonary oedema), pleural effusions (stony dull), wheeze ("cardiac asthma") |
| Peripheral | Pitting oedema (ankles, sacrum in bedbound), cool peripheries (low output) |
| General | Tachypnoea, SpO2 reduced, hypertension or hypotension (cardiogenic shock) |
🧠 Mnemonic
Signs of raised filling pressure — OEDEMA:
- O rthopnoea (lying flat causes dyspnoea)
- E levated JVP
- D ependent oedema (pitting)
- E xternal signs: displaced apex, gallop rhythm
- M oist crackles (bibasal)
- A scites (in severe, chronic cases)
Investigations
| Investigation | Expected findings in AHF |
|---|---|
| CXR | Cardiomegaly (CTR above 0.5), upper lobe diversion, Kerley B lines, bat-wing (perihilar) shadowing, pleural effusions |
| ECG | Identify precipitant: AF (most common), LBBB, ischaemia, LVH |
| BNP / NT-proBNP | Raised (BNP above 100 pg/mL or NT-proBNP above 300 pg/mL) — useful rule-out for HF in breathless patient; very high levels indicate worse prognosis |
| Troponin | Raised if ACS is precipitant or from demand ischaemia |
| U&E / creatinine | Baseline before diuretics; AKI may follow aggressive diuresis |
| Echo | Confirms diagnosis, differentiates HFrEF (EF below 40%) from HFpEF (EF above 50%), identifies valvular cause |
| ABG | Type 1 respiratory failure (low pO2, normal/low CO2) in pulmonary oedema |
Common Precipitants — FAILURES
🧠 Mnemonic
FAILURES — precipitants of acute decompensated heart failure:
- F orgot medications (non-compliance — most common)
- A rrhythmia (AF, VT — commonest arrhythmic trigger)
- I schaemia / infarction (new MI)
- L ife stressors (physical — infection, surgery, PE, anaemia)
- U pload (excessive fluid or salt intake)
- R enal failure (fluid retention)
- E ndocrine (thyrotoxicosis, pregnancy)
- S tepdown (medications reduced — diuretics stopped)
Immediate Management
1. Positioning
- Sit the patient upright — reduces venous return (preload) and improves diaphragm excursion
2. Oxygen
- Target SpO2 94-98%
- High-flow if SpO2 below 94%
- Avoid high-flow oxygen in COPD + HF — titrate to SpO2 88-92%
3. IV Furosemide
| Presentation | Dose |
|---|---|
| Not on regular furosemide | 40-80 mg IV bolus |
| On regular oral furosemide | IV dose = at least oral daily dose (e.g., oral 80 mg/day → IV 80 mg) |
| Severe/refractory pulmonary oedema | 80-160 mg IV; consider furosemide infusion |
Monitor: urine output (catheterise), U&E after 4-6 hours, blood pressure.
⚠️ Red Flag
Furosemide can cause AKI in patients who are euvolaemic or volume-depleted. Always assess whether the patient is genuinely fluid overloaded (raised JVP, bibasal crackles, CXR evidence) before giving large doses. If SBP below 90 or cardiogenic shock — do not give furosemide; seek urgent specialist review.
4. GTN (Glyceryl Trinitrate)
- Vasodilator — reduces preload and afterload, relieves pulmonary oedema rapidly
- IV GTN infusion: 10-200 micrograms/min, titrated to symptom relief and SBP (target above 100 mmHg)
- Contraindicated if: SBP below 90 mmHg, RV infarction, phosphodiesterase inhibitor use (sildenafil — severe hypotension)
5. Morphine
- No longer routinely recommended in AHF (2016 ESC guidelines)
- Associated with increased mortality, higher ITU admission rate, and more mechanical ventilation in observational data
- May be considered for palliation of severe distress in end-stage HF
Non-Invasive Ventilation (NIV)
CPAP (Continuous Positive Airway Pressure)
- Indicated for acute cardiogenic pulmonary oedema with SpO2 below 90% despite high-flow oxygen
- Improves oxygenation by splinting open alveoli and reducing venous return (reducing preload)
- Reduces need for intubation and improves short-term survival (CPAP trial)
- Starting settings: 5-10 cmH2O, titrate to SpO2 and clinical response
- Not suitable for: GCS below 12 (aspiration risk), facial trauma, active vomiting, pneumothorax
BiPAP
- Use in AHF + COPD (hypercapnic respiratory failure)
- Provides inspiratory pressure support as well as CPAP
Killip Classification (Severity in Context of MI)
| Class | Features | Mortality |
|---|---|---|
| I | No HF | 6% |
| II | S3 gallop or bibasal crackles | 17% |
| III | Frank pulmonary oedema | 38% |
| IV | Cardiogenic shock (SBP below 90) | 81% |
Frequently Asked Questions
"What is the difference between HFrEF and HFpEF?"
HFrEF (heart failure with reduced ejection fraction) has LVEF below 40% — the ventricle is dilated, weak, and cannot contract effectively. Causes: ischaemic cardiomyopathy (most common), dilated cardiomyopathy, alcohol. HFpEF (heart failure with preserved ejection fraction) has LVEF above 50% — the ventricle is stiff and cannot relax and fill properly (diastolic dysfunction). Causes: hypertension, diabetes, obesity, AF. HFpEF has the same mortality as HFrEF but fewer disease-modifying treatments.
"Why is BNP raised in heart failure and what other conditions raise it?"
BNP (B-type natriuretic peptide) is released from cardiomyocytes in response to wall stress from elevated filling pressures. It acts as a vasodilator and natriuretic agent. NT-proBNP is the inactive cleavage product, with a longer half-life. Both are raised in HF proportional to severity. Other causes of raised BNP: PE (RV strain), acute MI, renal failure (reduced clearance), COPD (cor pulmonale), AF, sepsis. A very low BNP (below 100 pg/mL) effectively excludes heart failure as the cause of breathlessness.
"When do you escalate to ITU in acute heart failure?"
Escalate urgently when: SBP below 90 mmHg (cardiogenic shock), SpO2 not improving with maximum medical therapy and CPAP, respiratory rate above 35/min with exhaustion, GCS falling, or development of arrhythmia causing haemodynamic compromise. Cardiogenic shock has 50% in-hospital mortality — consider inotropes (dobutamine), intra-aortic balloon pump, and mechanical circulatory support devices. Early escalation improves outcomes.
"How do you manage acute heart failure in a patient with severe renal impairment?"
Diuresis may worsen renal function — this is an acceptable and expected trade-off when the patient is profoundly volume-overloaded. Aim for net negative fluid balance while monitoring U&E and creatinine closely (4-6 hourly initially). If diuresis is insufficient, consider furosemide infusion, metolazone (add-on thiazide for diuretic resistance), or ultrafiltration. Involve nephrology early if creatinine is rising significantly. Do not withhold diuretics purely because of pre-existing CKD if the patient is in pulmonary oedema.
"What long-term medications reduce mortality in HFrEF?"
The four pillars of HFrEF treatment (the "fantastic four"): ACE inhibitor or ARB or sacubitril-valsartan (ARNI), beta-blocker (bisoprolol, carvedilol), mineralocorticoid receptor antagonist (spironolactone or eplerenone), and SGLT-2 inhibitor (empagliflozin or dapagliflozin — recently added, reduce hospitalisation and mortality independently). All four have additive mortality benefit. Loop diuretics (furosemide) improve symptoms and quality of life but do not reduce mortality.
Related Posts
- Heart Failure History OSCE — systematic history for the patient with known or suspected heart failure
- Chest X-Ray Interpretation OSCE — identifying pulmonary oedema, cardiomegaly, and pleural effusions
- Acute Kidney Injury OSCE — managing AKI as a complication of aggressive diuresis in heart failure