ACUTE CARDIOGENIC PULMONARY OEDEMA

    DEFINITION

    Acute cardiogenic pulmonary oedema is a sudden rise in pulmonary
    capillary pressure causing engorgement of pulmonary vessels (blood
    and lymphatic), and exudation into the interstitial and
    intraalveolar spaces, manifested by varying degrees of respiratory
    distress.

    TOXIC CAUSES

    Arises as a secondary complication of those intoxications causing:

         Arrhythmias (bradycardias, supraventricular tachycardia,
           ventricular tachycardia)
         Myocardial depression (shock)
         Myocardial ischaemia
         Severe hypertension.  

    NON-TOXIC CAUSES

    Acute hypervolaemia
    Cardiac dysrhythmias
    Cardiac depressant drugs 
    Hypertension
    Left side valvular disease 
    Myocardial infarction
    Myocarditis
    Severe myocardial ischaemia

    CLINICAL FEATURES

    Dyspnea, tachypnea, air hunger, coughing, expectoration of
    frothing, sometimes blood-stained sputum and a feeling of impending
    death.

    Tachycardia, hypertension or hypotension, gallop rhythm, basal or
    generalized crackles and wheezing.

    DIFFERENTIAL DIAGNOSIS

    Adult respiratory distress syndrome (ARDS) 
    Aspiration pneumonitis
    Asthma 
    Bronchial hypersecretion.
    Chronic obstructive pulmonary disease 
    Noncardiogenic pulmonary oedema
    Pneumonic bronchopneumonia

    RELEVANT INVESTIGATIONS

    Arterial blood gases
    Chest x-ray 
    Echocardiogram 
    Electrocardiograph
    Serum electrolytes and creatinine, blood urea 

    TREATMENT

    Acute cardiogenic pulmonary oedema is a medical emergency, and
    treatment should not be postponed.  The treatment includes:

         Seated or semi-recumbent position,
          Oxygen in high concentration,
          Nitroglycerin may be given as sublingual spray (two puffs or
         0.8mg) or one sublingual tablet. Repeat if necessary.
          Furosemide:  give 60 to 80 mg intravenous bolus in adults,
         or 1 mg/kg in children.  May be repeated after one hour.

    If the patient does not respond to the above measures, then
    institute:

         Intravenous  Nitroglycerin:  give by continuous drip,
         initially at 10 to 20 µg/min;
         if necessary increase by increments of 10 µg/min at 5 to 10
         minute intervals, up to 80 µg/min.

         Continuous Positive Airway Pressure (CPAP) - may be delivered
         by mask.

         Intermittent Positive Pressure Ventilation (IPPV) delivered by
         mechanical ventilator.  IPPV should be instituted at once if
         the patient presents with signs of cerebral hypoxia, shock,
         PaO2 < 60 mmHg (Fi02 > 0.5), severe metabolic acidosis,
         or PaCO2 > 60 mmHg. 

    CLINICAL COURSE AND MONITORING

    Close monitoring is indicated until the condition resolves and may
    include:

         Pulse rate and blood pressure
         Cardiac rhythm
         Urine output
         Pulse oximetry
         Serial ECGs and arterial blood gases
         Pulmonary artery wedge pressure
         Capnography

    Proper investigation and management of any underlying condition
    must be considered.

    LONG TERM COMPLICATIONS

    Potential long term complications depend on the duration and
    severity of hypoxia and hypotension, and on the diagnostic and
    therapeutic measures undertaken.  Post-hypoxic cerebral and renal
    damage are of particular concern.

    AUTHOR(S)/PEER REVIEW

    Author:        J. Szajewski, Director, Warsaw Poison Control
                   Centre, Warsaw. Poland.
    Peer Review:   Berlin, October 1995: A. Jaeger, R. Dowsett, J.
                   Szajewski, V. Danel, A. Wong.