TextbookCardiologyAcute Heart Failure

Acute Heart Failure

Rapid onset or worsening of heart failure symptoms requiring urgent medical intervention. May present as de novo acute HF or acute decompensation of chronic HF.

Key Facts

Presentation: acute dyspnoea, orthopnoea, pink frothy sputum, bilateral crepitations, elevated JVP Immediate management: sit upright, IV furosemide 40-80mg, oxygen if SpO₂ <94%, GTN infusion if SBP >90 mmHg Do NOT give morphine routinely (NICE NG106) — associated with increased mortality in acute HF NT-proBNP: aids diagnosis; >300 pg/mL supportive (with clinical context) CPAP/NIV: consider if respiratory distress persists despite initial treatment (3CPO trial) Cardiogenic shock: inotropes (dobutamine 2.5-10mcg/kg/min), consider IABP/Impella In-hospital mortality: ~5-10%; 1-year mortality post-discharge: ~25-30% Before discharge: ensure optimisation of HF medications; arrange follow-up within 2 weeks

Overview

Key Facts

Acute heart failure (AHF) is the rapid onset or worsening of signs and symptoms of heart failure. It may present as a first episode (de novo) or more commonly as an acute decompensation of chronic heart failure (ADCHF). It is a medical emergency requiring urgent assessment and treatment.

Epidemiology

  • ~80,000 admissions per year in England
  • Accounts for ~5% of all emergency medical admissions
  • Mean age at presentation: ~75 years
  • In-hospital mortality: ~5-10%
  • 30-day readmission rate: ~25%
  • 1-year mortality post-discharge: ~25-30%

Aetiology

Precipitants of acute decompensation:

  • Acute coronary syndrome
  • Arrhythmia (especially new-onset AF with rapid ventricular rate)
  • Medication non-adherence or dietary indiscretion
  • Infection/sepsis
  • Uncontrolled hypertension
  • Acute valvular dysfunction (MR, AR)
  • Pulmonary embolism
  • Renal failure
  • Anaemia
  • Thyrotoxicosis

Pathophysiology

  • Acute increase in LV filling pressures → pulmonary congestion → pulmonary oedema
  • Neurohormonal activation (RAAS, SNS) causes vasoconstriction and fluid retention
  • Forward failure: reduced cardiac output → hypoperfusion
  • Backward failure: elevated filling pressures → congestion
  • Acute pulmonary oedema: fluid transudation into alveoli impairs gas exchange

Clinical Presentation

Acute Pulmonary Oedema

  • Severe dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
  • Pink frothy sputum
  • Bilateral fine crepitations
  • Tachypnoea, tachycardia
  • Elevated JVP
  • Third heart sound (S3)
  • Hypoxia

Cardiogenic Shock

  • Hypotension (SBP <90 mmHg)
  • Cold, clammy peripheries
  • Oliguria (<0.5 mL/kg/h)
  • Confusion, altered consciousness
  • Elevated lactate

Right Heart Failure Predominant

  • Peripheral oedema
  • Elevated JVP
  • Hepatomegaly, ascites
  • Right-sided pleural effusion

Red Flags

  • SBP <90 mmHg (cardiogenic shock)
  • SpO₂ <90% despite high-flow oxygen
  • Respiratory rate >25/min
  • Altered consciousness
  • Concurrent acute MI

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Acute exacerbation of COPDSmoking history, wheeze, hyperinflationSpirometry, CXR, ABG
PneumoniaFever, productive cough, consolidation on CXRCXR, blood cultures, CRP
Pulmonary embolismPleuritic pain, DVT risk factors, acute RV strainCTPA, D-dimer
ARDSBilateral infiltrates, risk factor (sepsis, trauma), PaO₂/FiO₂ <300Berlin criteria
Acute asthmaWheeze, atopy history, PEFR reducedPEFR, CXR
Cardiac tamponadeBeck triad (hypotension, muffled HS, elevated JVP), pulsus paradoxusEcho
Nephrotic syndromeHeavy proteinuria, hypoalbuminaemiaACR, albumin

Diagnosis / Investigation

Bedside

  • ECG: ischaemia, arrhythmia, LVH
  • Observations: HR, BP, SpO₂, RR, urine output
  • ABG: hypoxia, type 1 respiratory failure, metabolic acidosis (if shock)

Bloods

  • NT-proBNP (or BNP): >300 pg/mL supportive; also prognostic
  • Troponin: exclude ACS as precipitant
  • U&Es: renal function, electrolytes
  • FBC: anaemia, infection
  • LFTs: hepatic congestion
  • CRP: infection screen
  • Lactate: tissue perfusion
  • TFTs: thyroid dysfunction

Imaging

  • Chest X-ray: upper lobe venous distension, bilateral alveolar shadowing, Kerley B lines, cardiomegaly, pleural effusions
  • Echocardiography: urgent — assess LV/RV function, valvular abnormalities, pericardial effusion
  • Lung ultrasound: B-lines (interstitial oedema) — increasingly used at bedside

Special Tests

  • Coronary angiography: if ACS precipitant
  • Pulmonary artery catheterisation: in refractory shock (rarely needed)

Management

Non-pharmacological

  • Sit patient upright (reduces venous return and work of breathing)
  • High-flow oxygen if SpO₂ <94%
  • Continuous monitoring: ECG, SpO₂, BP, urine output
  • Fluid restriction: 1.5L/day
  • Daily weights

Pharmacological

Acute management (wet and warm — congested, adequate perfusion):

  • IV furosemide 40-80mg bolus (or double usual oral dose if already on furosemide); repeat/increase as needed
  • If poor response: furosemide infusion 5-40mg/hour or add metolazone 2.5-10mg OD (sequential nephron blockade)
  • GTN infusion 1-10mg/hour: if SBP >90 mmHg (reduces preload and afterload)
  • Do NOT routinely give morphine (NICE NG106 — increased ICU admission and mortality)
  • CPAP/BiPAP: if persistent respiratory distress despite initial treatment (improves oxygenation and work of breathing)

Cardiogenic shock (wet and cold):

  • Dobutamine 2.5-10 mcg/kg/min (inotrope)
  • Noradrenaline if significant hypotension (vasopressor)
  • Milrinone: phosphodiesterase inhibitor (inodilator)
  • Levosimendan: calcium sensitiser (limited UK availability)
  • Consider mechanical circulatory support: IABP, Impella, VA-ECMO

Before discharge:

  • Initiate/optimise HFrEF quadruple therapy before discharge where possible
  • SGLT2 inhibitor can be started in hospital (EMPULSE trial)
  • Arrange specialist heart failure follow-up within 2 weeks of discharge
  • Cardiac rehabilitation referral
  • Medication reconciliation and patient education

Surgical/Interventional

  • PCI/CABG if ACS precipitant
  • Valve surgery/intervention if acute valvular cause
  • Mechanical circulatory support for refractory cardiogenic shock
  • Ultrafiltration for diuretic-resistant fluid overload

Referral Criteria

  • All patients: specialist heart failure team review during admission
  • Cardiogenic shock: intensive care and/or advanced HF centre
  • Refractory to medical therapy: consider transplant assessment

Prognosis

  • In-hospital mortality: ~5-10%
  • 30-day mortality: ~10-15%
  • 1-year mortality post-discharge: ~25-30%
  • 30-day readmission rate: ~25%
  • Prognosis worse with: cardiogenic shock, ACS trigger, low SBP at admission, high BNP, renal dysfunction
  • De novo AHF generally has better prognosis than ADCHF
  • Each hospitalisation for HF is associated with progressive decline and worsened outcomes

Other Relevant Information

Clinical Profiles in Acute Heart Failure

ProfileCongestionPerfusionManagement
Warm and wetYesAdequateDiuretics ± vasodilators
Cold and wetYesPoorInotropes + diuretics
Cold and dryNoPoorFluids cautiously ± inotropes
Warm and dryNoAdequateAdjust oral therapy

CXR Signs of Heart Failure (ABCDE)

LetterFeature
AAlveolar oedema (bat-wing shadowing)
BKerley B lines (interstitial oedema)
CCardiomegaly (CTR >50%)
DDiversion of blood to upper lobes
EEffusion (pleural)