Pulmonary oedema and ARDS

After this note, you should be able to differentiate cardiogenic from non-cardiogenic pulmonary oedema, understand their pathophysiology, recognise clinical features, interpret investigations, and initiate emergency management. Always check drug doses and local protocols against the Kenya MoH guidelines and your hospital formulary.

Definition

Pulmonary oedema is the accumulation of excess fluid in the extravascular spaces of the lung (interstitium and alveoli), impairing gas exchange. It can be cardiogenic (due to elevated pulmonary capillary hydrostatic pressure from left heart failure) or non-cardiogenic (due to increased pulmonary capillary permeability, often termed Acute Respiratory Distress Syndrome - ARDS).

Anatomy and physiology you need

The lung's gas exchange unit consists of alveoli and surrounding capillaries. The alveolar-capillary membrane is extremely thin, facilitating efficient gas diffusion. Fluid balance across this membrane is governed by Starling forces: hydrostatic pressure (pushing fluid out of capillaries) and oncotic pressure (pulling fluid into capillaries). Lymphatic drainage in the lungs removes excess interstitial fluid.

• Alveoli: Air sacs where gas exchange occurs. Type I pneumocytes form the thin barrier, Type II pneumocytes produce surfactant.
• Pulmonary capillaries: Surround alveoli, carrying deoxygenated blood to be oxygenated.
• Interstitial space: Area between capillaries and alveoli.
• Lymphatics: Drain excess fluid from the interstitial space, preventing oedema.
• Pulmonary circulation: Low pressure, high flow system.

Causes and risk factors

Pathophysiology

Cardiogenic Pulmonary Oedema (CPO)

Left ventricular dysfunction (e.g., MI, heart failure) $\downarrow$ Increased left atrial pressure $\downarrow$ Increased pulmonary venous pressure $\downarrow$ Increased pulmonary capillary hydrostatic pressure $\downarrow$ Fluid transudation from capillaries into pulmonary interstitium $\downarrow$ Overwhelmed lymphatic drainage $\downarrow$ Fluid accumulation in interstitial space (interstitial oedema) $\downarrow$ Fluid spills into alveoli (alveolar oedema) $\downarrow$ Impaired gas exchange (V/Q mismatch, shunt) $\downarrow$ Hypoxemia

Non-Cardiogenic Pulmonary Oedema (NCPO) / ARDS

Direct or indirect lung injury (e.g., sepsis, pneumonia, aspiration) $\downarrow$ Systemic inflammatory response (release of cytokines, inflammatory mediators) $\downarrow$ Endothelial cell activation and injury in pulmonary capillaries $\downarrow$ Increased pulmonary capillary permeability ("leaky capillaries") $\downarrow$ Protein-rich fluid and inflammatory cells leak into interstitial space and alveoli $\downarrow$ Damage to Type I and Type II pneumocytes $\downarrow$ Surfactant dysfunction/loss $\downarrow$ Alveolar collapse (atelectasis) and impaired gas exchange $\downarrow$ Formation of hyaline membranes (fibrin, cellular debris) $\downarrow$ Severe V/Q mismatch and intrapulmonary shunt $\downarrow$ Refractory hypoxemia

Clinical features

History:

• Dyspnoea: Onset (acute/gradual), progression, severity (NYHA class if chronic), positional (orthopnoea, paroxysmal nocturnal dyspnoea - PND). Orthopnoea suggests redistribution of fluid from legs/abdomen to lungs in recumbency, increasing preload and pulmonary capillary pressure. PND is similar but occurs after several hours of sleep, often waking the patient.
• Cough: Character (dry/productive), sputum (frothy, pink-tinged - "pink frothy sputum" is classic for severe pulmonary oedema due to red blood cells extravasating into alveoli).
• Chest pain: Atypical chest discomfort may occur, but pleuritic pain is less common. Ischaemic chest pain suggests a cardiac cause.
• Palpitations: May indicate underlying arrhythmia or compensatory tachycardia.
• Fatigue/Weakness: Generalised symptoms, especially if cardiac output is compromised.
• Peripheral oedema: Swelling in lower limbs, sacrum, or abdomen (ascites) suggests fluid overload, often chronic.
• Past medical history: Previous cardiac disease (MI, heart failure, valvular disease), hypertension, renal disease, diabetes, liver disease, recent surgery, sepsis, trauma, transfusions, drug use (e.g., cocaine, NSAIDs, IV fluids).
• Medications: Adherence to diuretics, antihypertensives; new medications.
• Social history: Smoking, alcohol, illicit drug use.

Examination:

• General appearance: Anxious, distressed, tachypnoeic, using accessory muscles of respiration, orthopnoea (sitting upright). These indicate severe respiratory compromise.
• Vital signs:
  • Tachycardia: Compensatory mechanism for reduced cardiac output or due to underlying arrhythmia.
  • Tachypnoea: Increased respiratory rate to improve gas exchange and reduce CO2.
  • Hypertension/Hypotension: Hypertension often seen in acute cardiogenic pulmonary oedema due to sympathetic activation; hypotension suggests severe cardiac dysfunction or shock.
  • Hypoxia: Low SpO2 due to V/Q mismatch and shunt.
  • Fever: Suggests infection (e.g., pneumonia, sepsis leading to ARDS).
• Head and Neck:
  • Jugular Venous Pressure (JVP): Elevated JVP indicates increased right atrial pressure, common in cardiogenic pulmonary oedema.
  • Oral mucosa: Cyanosis (bluish discoloration) indicates severe hypoxemia.
• Respiratory System:
  • Inspection: Increased work of breathing, intercostal and subcostal recession, nasal flaring.
  • Palpation: Normal vocal fremitus (unless consolidation).
  • Percussion: Dullness at lung bases due to fluid accumulation.
  • Auscultation:
    • Fine inspiratory crackles (crepitations): Bilateral, basal, and often extending upwards. Occur due to opening of collapsed alveoli and small airways containing fluid.
    • Wheeze: "Cardiac asthma" due to bronchoconstriction from interstitial oedema.
    • Reduced breath sounds: If pleural effusion is significant.
• Cardiovascular System:
  • Palpation: Displaced apex beat (cardiomegaly), thrills (valvular disease).
  • Auscultation:
    • S3 gallop: Pathognomonic for left ventricular failure, due to rapid ventricular filling into a non-compliant ventricle.
    • Murmurs: Indicate valvular heart disease.
    • Pericardial rub: Suggests pericarditis.
• Abdomen:
  • Hepatomegaly: Tender, pulsatile liver suggests right heart failure.
  • Ascites: Fluid in the peritoneal cavity, indicating chronic fluid overload.
• Extremities:
  • Peripheral oedema: Pitting oedema in dependent areas (ankles, sacrum) indicates fluid overload.
  • Warm/cold peripheries: Warm suggests vasodilation (sepsis); cold suggests poor perfusion (cardiogenic shock).

Differential diagnosis

Investigations

Diagnosis and severity

Diagnosis of pulmonary oedema is primarily clinical, supported by investigations.

• Cardiogenic pulmonary oedema: Clinical features of heart failure (dyspnoea, orthopnoea, PND, elevated JVP, S3, peripheral oedema, crackles), elevated BNP, cardiomegaly/pulmonary venous congestion on CXR, and echocardiographic evidence of cardiac dysfunction.
• Non-cardiogenic pulmonary oedema (ARDS): Acute onset, severe hypoxemia (PaO2/FiO2 ratio <300 mmHg), bilateral infiltrates on CXR not fully explained by cardiac failure or fluid overload, and absence of elevated left atrial pressure (e.g., PCWP <18 mmHg if measured, or no clinical/echocardiographic evidence of cardiac failure).

Severity of ARDS (Berlin Definition):

• Mild ARDS: PaO2/FiO2 ratio 200-300 mmHg (with PEEP/CPAP ≥5 cmH2O)
• Moderate ARDS: PaO2/FiO2 ratio 100-200 mmHg (with PEEP/CPAP ≥5 cmH2O)
• Severe ARDS: PaO2/FiO2 ratio <100 mmHg (with PEEP/CPAP ≥5 cmH2O)

Management

Acute Pulmonary Oedema (Cardiogenic)

This is a medical emergency requiring rapid assessment and intervention.

1. Immediate Stabilisation:
   • Airway: Assess and secure. Intubation may be necessary if respiratory failure is severe or GCS is low.
   • Breathing: Administer high-flow oxygen (non-rebreather mask) to maintain SpO2 >90%. Consider non-invasive positive pressure ventilation (NIPPV) like CPAP or BiPAP early for moderate to severe respiratory distress, as it reduces work of breathing, improves oxygenation, and decreases preload.
   • Circulation: Establish IV access. Monitor blood pressure, heart rate, and rhythm.
   • Positioning: Sit the patient upright to reduce venous return to the heart and improve lung expansion.
   • Diuretics: Intravenous loop diuretics (e.g., furosemide) are cornerstone. Start with a bolus, then consider continuous infusion. Monitor urine output.
   • Vasodilators: Intravenous nitrates (e.g., glyceryl trinitrate) reduce preload and afterload, improving cardiac output and reducing pulmonary congestion. Use with caution in hypotensive patients.
   • Morphine: Can be used cautiously to reduce anxiety and dyspnoea, and has venodilatory effects. Avoid in hypotensive or hypercapnic patients.
   • Inotropes/Vasopressors: If cardiogenic shock is present (hypotension despite fluid optimisation), consider inotropes (e.g., dobutamine) or vasopressors (e.g., norepinephrine) guided by haemodynamic status.

1. Definitive Treatment: Address the underlying cause (e.g., treat acute coronary syndrome, manage arrhythmias, control hypertension).

1. Monitoring and Follow-up:
   • Continuous monitoring of vital signs, SpO2, ECG.
   • Regular assessment of respiratory status, urine output, and fluid balance.
   • Daily weights.
   • Electrolyte monitoring (especially potassium with diuretics).
   • Echocardiography to assess cardiac function and guide long-term management.

Acute Respiratory Distress Syndrome (ARDS)

Management is primarily supportive, focusing on lung-protective ventilation and treating the underlying cause.

1. Treat the Underlying Cause: Crucial for recovery (e.g., antibiotics for pneumonia, source control for sepsis).

1. Lung-Protective Ventilation: The cornerstone of ARDS management.
   • Low Tidal Volume (LTV): Target 4-8 mL/kg predicted body weight to avoid volutrauma.
   • Permissive Hypercapnia: Allow PaCO2 to rise if pH remains acceptable (e.g., >7.25) to facilitate LTV.
   • Positive End-Expiratory Pressure (PEEP): Apply PEEP to prevent alveolar collapse (atelectrauma) and improve oxygenation. Titrate PEEP based on oxygenation and plateau pressures.
   • Plateau Pressure Target: Keep plateau pressure <30 cmH2O to prevent barotrauma.
   • Driving Pressure: (Plateau pressure - PEEP) is a strong predictor of mortality; aim for <15 cmH2O.

1. Supportive Care:
   • Fluid Management: Conservative fluid strategy after initial resuscitation, aiming for euvolaemia, to minimise pulmonary oedema.
   • Prone Positioning: For severe ARDS (PaO2/FiO2 <150 mmHg), prone positioning improves oxygenation and reduces ventilator-induced lung injury by redistributing ventilation and perfusion.
   • Neuromuscular Blockade: Consider for severe ARDS to facilitate lung-protective ventilation and reduce oxygen consumption.
   • Sedation: Adequate sedation to ensure patient-ventilator synchrony and comfort.
   • Nutrition: Early enteral nutrition.
   • Prevention of Complications: DVT prophylaxis, stress ulcer prophylaxis.
   • Extracorporeal Membrane Oxygenation (ECMO): Consider for refractory severe ARDS in specialised centres.

Contraindications and Safety:

• Nitrates: Avoid in severe aortic stenosis or hypertrophic obstructive cardiomyopathy, and in patients with hypotension.
• Diuretics: Monitor for hypokalaemia, hypovolaemia, and renal impairment.
• NIPPV: Contraindicated in patients with impaired consciousness, haemodynamic instability, facial trauma, or inability to protect their airway.
• Lung-Protective Ventilation: Requires careful monitoring of ventilator parameters and patient response to avoid complications like pneumothorax.

Complications and Prognosis

Cardiogenic Pulmonary Oedema

• Acute: Respiratory failure, acute kidney injury, arrhythmias, cardiogenic shock, death.
• Chronic: Recurrent hospitalisations, worsening heart failure, renal dysfunction, poor quality of life.
• Prognosis: Depends on the underlying cardiac condition, severity of heart failure, and response to treatment.

ARDS

• Pulmonary: Barotrauma (pneumothorax, pneumomediastinum), ventilator-associated pneumonia (VAP), pulmonary fibrosis (long-term), persistent hypoxemia.
• Systemic: Multi-organ dysfunction syndrome (MODS), critical illness polyneuropathy/myopathy, deep vein thrombosis, sepsis, acute kidney injury, malnutrition.
• Prognosis: Mortality rates vary widely (25-45%) depending on severity and underlying cause. Survivors often have long-term physical, cognitive, and psychological impairments.

High-yield exam points

• Pulmonary Capillary Wedge Pressure (PCWP): Elevated PCWP (>18 mmHg) suggests cardiogenic pulmonary oedema. Normal PCWP (<18 mmHg) in the presence of bilateral infiltrates points towards non-cardiogenic pulmonary oedema (ARDS).
• Bilateral Infiltrates with Normal Heart Size: A classic CXR finding for ARDS, differentiating it from cardiogenic pulmonary oedema where cardiomegaly is often present.
• Fluid Management in ARDS: A conservative fluid strategy (after initial resuscitation) is preferred to minimise pulmonary oedema and improve outcomes, unlike cardiogenic pulmonary oedema where aggressive diuresis is key.
• Berlin Definition: Remember the four criteria for ARDS: acute onset, bilateral infiltrates not fully explained by effusions/collapse/nodules, respiratory failure not fully explained by cardiac failure/fluid overload (objective assessment needed if no risk factor), and PaO2/FiO2 ratio <300 mmHg with PEEP ≥5 cmH2O.
• Lung-Protective Ventilation: Key components are low tidal volume (4-8 mL/kg PBW), plateau pressure <30 cmH2O, and adequate PEEP.

Clinical case

A 68-year-old male with a history of hypertension and type 2 diabetes presents to the emergency department with sudden onset severe shortness of breath, orthopnoea, and a productive cough with pink frothy sputum. On examination, he is tachypnoeic (RR 32/min), tachycardic (HR 110 bpm), and hypertensive (BP 190/100 mmHg). SpO2 is 85% on room air. Auscultation reveals widespread bilateral inspiratory crackles and a third heart sound (S3). His JVP is elevated.

Question 1: What is the most likely diagnosis? Model Answer: Acute cardiogenic pulmonary oedema.

Question 2: Outline the immediate management steps for this patient. Model Answer: Administer high-flow oxygen, sit the patient upright, establish IV access, administer intravenous loop diuretics (e.g., furosemide), and consider intravenous nitrates (e.g., glyceryl trinitrate) given his hypertension. Consider NIPPV if respiratory distress persists.

Question 3: What investigation would be most helpful in confirming the diagnosis and assessing cardiac function? Model Answer: Echocardiography to assess left ventricular function, ejection fraction, and valvular abnormalities. BNP levels would also be supportive.

Practice questions

Question 1

A 55-year-old patient is admitted with severe dyspnoea and bilateral pulmonary infiltrates on chest X-ray. Initial ABG shows PaO2 60 mmHg on 100% FiO2. A pulmonary artery catheter is inserted, and the pulmonary capillary wedge pressure (PCWP) is measured at 12 mmHg. Which of the following is the most likely diagnosis?

A. Acute cardiogenic pulmonary oedema B. Acute Respiratory Distress Syndrome (ARDS) C. Severe asthma exacerbation D. Community-acquired pneumonia

Answer: B. Acute Respiratory Distress Syndrome (ARDS) Explanation: A normal PCWP (<18 mmHg) in the presence of bilateral infiltrates and severe hypoxemia points towards non-cardiogenic pulmonary oedema, characteristic of ARDS.

Question 2

Which of the following ventilator settings is a key component of lung-protective ventilation in ARDS?

A. High tidal volumes (10-12 mL/kg predicted body weight) B. Maintaining plateau pressure above 35 cmH2O C. Low tidal volumes (4-8 mL/kg predicted body weight) D. Avoiding positive end-expiratory pressure (PEEP)

Answer: C. Low tidal volumes (4-8 mL/kg predicted body weight) Explanation: Low tidal volumes are crucial to prevent volutrauma and ventilator-induced lung injury in ARDS.

Question 3

A patient presents with acute onset dyspnoea, orthopnoea, and pink frothy sputum. On examination, there are widespread bilateral crackles and an elevated JVP. Which medication class is a cornerstone of immediate management for this condition?

A. Bronchodilators B. Loop diuretics C. Corticosteroids D. Antibiotics

Answer: B. Loop diuretics Explanation: The presentation is classic for acute cardiogenic pulmonary oedema, where loop diuretics are essential to reduce fluid overload and pulmonary congestion.

Question 4

A 70-year-old male with a history of myocardial infarction develops acute pulmonary oedema. He is hypotensive (BP 80/50 mmHg) despite initial fluid resuscitation. Which of the following medications should be used with extreme caution or avoided in this patient?

A. Furosemide B. Oxygen C. Glyceryl trinitrate D. Dobutamine

Answer: C. Glyceryl trinitrate Explanation: Nitrates are vasodilators and can worsen hypotension, which is already present in this patient with cardiogenic shock.

Question 5

Which of the following is a common long-term complication in survivors of severe ARDS?

A. Complete resolution of lung function without sequelae B. Development of chronic obstructive pulmonary disease (COPD) C. Pulmonary fibrosis and persistent physical and cognitive impairments D. Increased risk of recurrent bacterial pneumonia only

Answer: C. Pulmonary fibrosis and persistent physical and cognitive impairments Explanation: Survivors of severe ARDS often experience long-term complications including pulmonary fibrosis, muscle weakness, and cognitive dysfunction.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.