Doctors Revision

Cardiovascular System

Acute Pulmonary Oedema

Acute accumulation of fluid in the interstitial spaces and alveoli of the lungs, typically due to rapidly increased pulmonary capillary pressure secondary to acute left ventricular failure (cardiogenic pulmonary oedema). Can also be non-cardiogenic (e.g., ARDS). A medical emergency.

Also known as: APO, Lung Congestion, Fluid in Lungs

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Referral and warning signs

When to refer

ALL cases of acute pulmonary oedema require immediate hospital admission (H/RR), often to a high dependency or intensive care setting, for urgent management and monitoring.

Red flags

  • Severe respiratory distress, accessory muscle use
  • SpO2 < 90% despite high flow oxygen
  • Pink, frothy sputum
  • Hypotension / Signs of shock
  • Altered mental status
  • Chest pain suggestive of ACS

Signs and symptoms

  • Severe dyspnoea (shortness of breath), often sudden onset.
  • Orthopnea (unable to lie flat).
  • Tachypnea (rapid breathing), use of accessory muscles.
  • Cough, often productive of pink, frothy sputum.
  • Wheezing ('cardiac asthma').
  • Tachycardia.
  • Pallor, sweating, cyanosis.
  • Anxiety, feeling of suffocation.
  • Widespread bilateral crepitations (crackles) on lung auscultation.
  • Raised JVP (if cardiogenic).
  • S3 gallop may be present.

Risk factors

  • Acute Myocardial Infarction
  • Acute decompensation of chronic heart failure
  • Severe hypertension / Hypertensive crisis
  • Acute severe valvular regurgitation (e.g., ruptured papillary muscle/chordae)
  • Arrhythmias (rapid AF, VT)
  • Fluid overload (iatrogenic or renal failure)
  • Non-cardiogenic causes: Acute Respiratory Distress Syndrome (ARDS) from sepsis, pneumonia, aspiration, trauma, pancreatitis; high altitude, neurogenic, drug reaction.

Diagnosis

Clinical assessment

Diagnosis is primarily clinical based on acute severe respiratory distress with characteristic signs (orthopnea, frothy sputum, bilateral crepitations). Identify potential triggers (MI, arrhythmia, non-adherence, infection). Differentiate cardiogenic from non-cardiogenic causes if possible (e.g., presence of raised JVP, S3 gallop suggests cardiogenic).

Investigations

  • Pulse Oximetry (SpO2): Usually low.
  • Arterial Blood Gas (ABG): Hypoxemia (low PaO2), PCO2 may be low initially (hyperventilation) then rise (fatigue). Respiratory acidosis.
  • Chest X-ray: Bilateral alveolar opacities ('bat wing' appearance), cardiomegaly, pleural effusions, Kerley B lines.
  • ECG: Identify underlying cause (MI, arrhythmia, LVH).
  • Echocardiogram (bedside if possible): Assess LV function, valve function.
  • Cardiac Enzymes (Troponin): If ACS suspected.
  • BNP/NT-proBNP: Usually markedly elevated in cardiogenic APO.
  • Blood tests: CBC, U&Es, Renal function.

Diagnostic criteria

Clinical presentation of acute respiratory distress with characteristic findings, supported by CXR, ABG, and potentially ECG/Echo/BNP.

Management

Non-pharmacological management

  • Positioning: Sit patient upright, legs dependent (reduces venous return).
  • Oxygen Therapy: High flow oxygen (e.g., via non-rebreather mask) aiming for SpO2 >94%.
  • Non-Invasive Ventilation (NIV): Continuous Positive Airway Pressure (CPAP) or Bi-level Positive Airway Pressure (BiPAP) can improve oxygenation and reduce work of breathing. Early consideration is key.
  • Mechanical Ventilation: If respiratory failure persists despite NIV, or patient obtunded/unable to protect airway.

Pharmacological treatment

  • Diuretics: Furosemide IV 40-80 mg (or higher, e.g., double patient's usual oral dose), repeat as needed based on response/urine output.
  • Vasodilators (Reduce preload and afterload):
  • - Nitrates: Glyceryl trinitrate (GTN) sublingual (500mcg) or spray initially. IV infusion if ongoing symptoms and BP adequate (SBP >100 mmHg).
  • Morphine: 2.5-5 mg slow IV (titrate). Reduces anxiety, causes venodilation (reduces preload). Use cautiously due to risk of respiratory depression, hypotension, nausea. (Less routinely used now compared to NIV/Nitrates).
  • Inotropes/Vasopressors (Specialist/ICU care): If cardiogenic shock present (e.g., Dobutamine, Norepinephrine).
  • Treat underlying cause: e.g., Reperfusion therapy for MI, rate/rhythm control for arrhythmia, manage hypertension.

Monitoring

  • Continuous monitoring: SpO2, respiratory rate/effort, heart rate, BP, ECG.
  • Frequent clinical reassessment.
  • Monitor urine output closely (catheterize if needed).
  • Monitor ABGs as indicated.

Complications

  • Respiratory failure / Arrest
  • Cardiogenic shock
  • Cardiac arrest
  • Myocardial injury
  • Renal failure
  • Death

Prevention

  • Optimal management of chronic heart failure.
  • Control of hypertension, diabetes, and other risk factors.
  • Adherence to medications and lifestyle advice.
  • Prompt treatment of ACS and arrhythmias.
  • Avoidance of fluid overload.

Patient education

  • (After stabilization) Explain the cause of the episode.
  • Reinforce importance of adherence to HF medications, diet, fluid restrictions.
  • Educate on early recognition of worsening symptoms and when to seek help.
  • Discuss management of underlying condition.

Uganda-specific notes

A frequent complication of uncontrolled hypertension and RHD. Access to NIV and ICU care is limited. Focus on positioning, oxygen, aggressive IV Furosemide, and nitrates (if BP allows). Morphine may be used more often due to lack of NIV. Early transfer if possible.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 4, Section 4.1.4

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