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Acute Pulmonary Oedema

 

Definitions in pulmonary oedema

  • Acute pulmonary oedema: Accumulation of fluid in the lung parenchyma leading to impaired gas exchange between the air in the alveoli and pulmonary capillaries.
  • Cardiac failure: clinical syndrome where the heart is unable to function adequately as a pump to meet the demands of the body; characterised by:
    • Typical symptoms, including dyspnoea, orthopnoea, ankle swelling
    • Typical signs, including bibasal crepitations, raised jugular venous pressure (JVP)
    • Objective evidence of a structural or functional abnormality including cardiomegaly, third heart sound, abnormality on echocardiogram (echo)
  • Left ventricular failure (LVF): failure of the LV causing congestion of the pulmonary veins
  • Right ventricular failure (RVF): failure of the RV causing congestion of the systemic veins
  • Congestive cardiac failure (CCF): LVF and RVF co-exist, the latter usually secondary to the former
  • Cor pulmonale: RVF secondary to chronic lung pathology eg chronic obstructive pulmonary disease (COPD)
  • Low output cardiac failure: cardiac failure secondary to inadequate pumping and supply
  • High output cardiac failure: cardiac failure secondary to excessive demand
  • Acute pulmonary oedema: rapid accumulation of fluid in the alveoli and parenchyma of the lung
    • Cardiogenic pulmonary oedema: caused by elevated pulmonary capillary pressure due to decompensated LVF
    • Non-cardiogenic: caused by injury to the lung parenchyma or vasculature

 

Causes of acute pulmonary oedema

  • Cardiac
    • Acute coronary syndrome (ACS)
    • Cardiac arrhythmia e.g. atrial fibrillation (AF)
    • Valvular heart disease
    • Hypertension
    • Cardiomyopathy
    • Cardiac tamponade
  • Non-cardiac
    • Non-compliance with medication
    • Negatively inotropic medication
    • Fluid overload
    • High output cardiac failure
      • Anaemia
      • Thyrotoxicosis
      • Sepsis
    • Acute respiratory distress syndrome (ARDS)
    • Renal artery stenosis (RAS)

 

Pathophysiology of acute pulmonary oedema

  • Blood pressure (BP) = cardiac output (CO) x systemic vascular resistance (SVR)
  • CO = heart rate (HR) x stroke volume (SV)
  • SV depends on preload, myocardial contractility and afterload
  • As the heart begins to fail, compensatory mechanisms maintain CO & BP
  • Increased sympathetic tone increases SVR and stimulates renin secretion
  • The renin-angiotensin-aldosterone system (RAAS) increases salt and fluid retention, which initially increases preload, end diastolic volume (EDV), SV and therefore CO via the Frank-Starling mechanism, but over time leads to cardiac dilatation and a reduction in contractility and CO, together with congestion of the pulmonary and systemic veins with associated tissue oedema
  • As alveolar oedema increases, diffusion of oxygen into the pulmonary capillaries is impaired, which manifests as dyspnoea; venous return to the already congested heart and lungs increases when the patient lies flat, which manifests as orthopnoea and paroxysmal nocturnal dyspnoea (PND)
  • Acute pulmonary oedema can be precipitated by sudden increases in preload (volume overload or fluid retention), decreases in contractility (ischaemia, infarction, arrhythmia, valvular failure, cardiomyopathy, drugs), increases in afterload (systemic or pulmonary hypertension) or direct damage to the lungs themselves

 

History in acute pulmonary oedema

  • Fatigue
  • Worsening dyspnoea progressing from an exercise tolerance of dyspnoea on exertion to at rest
  • Orthopnoea
  • PND
  • Cough productive of pink, frothy sputum
  • Ankle swelling

 

Video explaining left vs right-sided heart failure

 

Examination in acute pulmonary oedema

  • LVF
    • Respiratory distress
    • Tachypnoea
    • Bibasal crepitations
    • Cardiac wheeze
    • Tachycardia
    • Displaced apex beat
    • Third heart sound
  • RVF
    • RV heave
    • Raised JVP
    • Hepatomegaly
    • Peripheral oedema
  • Patients with acute pulmonary oedema are likely to have features of LVF and RVF simultaneously

 

Initial investigation of acute pulmonary oedema

  • Arterial blood gas (ABG)
  • Full blood count
  • Urea & electrolytes
  • Magnesium
  • Calcium
  • Thyroid function tests
  • 12 lead ECG. Unlikely to be normal; may show:
    • Ischaemia
    • Infarction
    • Left ventricular hypertrophy (LVH)
    • Arrhythmia
  • Chest radiograph (CXR) – ABCDE mnemonic
    • Alveolar oedema
    • Bats wing hilar shadowing and Kerley B lines
    • Cardiomegaly
    • Diversion to the upper lobes (distension of upper pulmonary veins)
    • Effusions: blunting of the costophrenic angles

 

Further investigation of acute pulmonary oedema

  • Echocardiogram (echo)

 

Initial management of acute pulmonary oedema

  • Assess the patient from an ABCDE perspective
  • Sit patient upright and attach monitoring: pulse oximeter, BP cuff, three-lead cardiac monitoring
  • Maintain a patent airway
    • Use manoeuvres, adjuncts, supraglottic or definitive airways as indicated and suction any sputum or secretions
  • Give oxygen
    • Initally 15L through non-rebreather mask
    • Titrate to achieve oxygen saturations (SpO2) 94-98% or 88-92% if known to have COPD
  • Obtain intravenous (IV) access and take bloods
    • Consider troponin if concerned about cardiac event
  • Perform ABG
  • Furosemide 40 mg IV
    • To diurese
  • Morphine 2.5-10 mg IV
    • To dilate venous system, decreasing preload and also improve breathing symptomatically
  • Request 12 lead ECG and portable CXR
  • Glyceryl trinitrate (GTN) 1mg/ml IV infusion at 2 ml/hour if inadequate response to the above interventions
    • Titrate rate upwards maintaining SBP >90 mmHg
    • If there is any delay in gaining IV access, 2 puffs of GTN can initially be given sublingually
  • CPAP
    • If severe oedema or if inadequate response to medical therapy, start continuous positive airway pressure (CPAP)
    • Relevant contraindications to CPAP (and any non-invasive ventilation) in this setting include:
      • Vomiting (pre-empt by giving antiemetic)
      • Fixed airway obstruction
      • Undrained pneumothorax
      • Patient is unable to protect their own airway (e.g. moribund with low GCS or copious secretions)
      • Patient refusal
    • CPAP improves oxygenation by:
      • Delivering high flow oxygen; improving functional residual capacity (FRC)l; recruiting alveoli; splinting airways; reducing the work of breathing and drving pulmonary oedema back into the circulation
  • If evidence of cardiogenic shock is present, avoid/discontinue nitrates and give cautious fluid challenges of 250 ml; if this fails to correct hypotension, patients will require inotropic support

 

Further management of acute pulmonary oedema

  • Any patient requiring ongoing CPAP or inotropic support will need referral to high dependency unit (HDU) for:
    • Arterial line: facilitates continuous BP monitoring and frequent ABG sampling
    • Central line: facilitates central venous pressure (CVP) and central venous oxygen saturation (ScvO2) monitoring as well as delivery of inotropic agents
    • Cardiac monitoring
    • Urine output monitoring

 

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