Acute Pulmonary Oedema

Overview – Acute Pulmonary Oedema

Acute cardiogenic pulmonary oedema is a medical emergency caused by decompensated left ventricular failure, leading to alveolar fluid overload and hypoxia. This guide outlines the key pathophysiological mechanisms, hallmark clinical signs, targeted investigations, and the LMNOP treatment protocol essential for urgent care.


Definition

  • Acute cardiogenic pulmonary oedema refers to the rapid accumulation of fluid in the alveolar spaces due to elevated pulmonary capillary pressures secondary to left ventricular failure.

Aetiology

  • Most commonly caused by severe decompensated left ventricular failure.
  • Often a complication of chronic congestive cardiac failure (CCF), myocardial infarction, arrhythmias, or hypertensive crisis.

Pathophysiology

  • Decreased LV function → elevated left atrial pressure
    → backflow into pulmonary veins → increased pulmonary capillary hydrostatic pressure
    fluid leaks into alveolar spaces
    impaired gas exchange and hypoxia
  • Can rapidly progress to acute respiratory failure.

Clinical Features

Symptoms

  • Sudden onset dyspnoea
  • Tachypnoea and tachycardia
  • Wet cough producing frothy, pink sputum
  • Diaphoresis (cold sweats)

Signs

  • Respiratory distress and hypoxia (↓SpO₂)
  • Bi-basal crackles on auscultation
  • Splitting of the second heart sound (S2)
  • Dullness to percussion (suggests effusions)
  • May also show signs of right-sided heart failure:
    • Raised JVP
    • Peripheral oedema
    • Ascites

Investigations

  • Chest X-Ray (CXR):
    • Pulmonary congestion
    • Diffuse alveolar infiltrates (“bat-wing” pattern)
    • Cardiomegaly
    • Pleural effusions
  • Electrocardiogram (ECG):
    • To assess for myocardial infarction or arrhythmias
  • Transthoracic echocardiogram (TTE):
    • Evaluates left ventricular function and ejection fraction
  • Blood tests:
    • FBC (anaemia/infection)
    • UEC (renal status)
    • LFTs (e.g. for alcohol-related liver disease)
    • TSH (thyroid dysfunction)
    • Lipids (cardiovascular risk)
    • BSL/HbA1c (diabetes control)

Management

Long-Term Heart Failure Regimen

  • ACE inhibitors (e.g. Perindopril) or ARBs (e.g. Candesartan)
  • Beta-blockers (e.g. Carvedilol)
  • Loop and potassium-sparing diuretics (e.g. Frusemide, Spironolactone)
  • Daily weight monitoring, fluid restriction, and low sodium diet

Emergency Management – “LMNOP” Protocol

  • L – Lasix:
    • Loop diuretic (Frusemide) → increases fluid excretion
  • M – Morphine:
    • Provides anxiolysis and reduces preload via vasodilation
  • N – Nitrates (GTN):
    • Reduces preload and improves myocardial oxygenation
  • O – Oxygen:
    • To maintain adequate oxygen saturation
  • P – Positive Pressure Ventilation (CPAP/BiPAP):
    • Improves oxygenation and reduces work of breathing

Summary – Acute Pulmonary Oedema

Acute cardiogenic pulmonary oedema results from sudden left ventricular decompensation and is marked by severe dyspnoea, frothy sputum, and respiratory failure. It requires rapid diagnosis and intervention with diuretics, oxygen, nitrates, and positive pressure ventilation. For patients already on heart failure therapy, decompensation often reflects underlying ischaemia or poor compliance. For more, visit our Cardiovascular Overview page.

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