RESPIRATORY FAILURE

    DEFINITION

    Failure to fully arterialize the blood passing through through the
    lungs, giving rise to hypoxia (paO2 less than 8 kPa or 60 mmHg)
    and/or hypercapnia (paCO2 greater than 6 kPa or 45 mmHg).

    TOXIC CAUSES

    Secondary to ventilatory failure from

         (i)  Central nervous system depression of toxic origin

         (ii) Weakness of ventilatory muscles
              Botulism
              Carbamate pesticides
              Muscle relaxants 
              Organophosphorus pesticides and warfare agents
              Snakebite
              Strychnine

    Secondary to pulmonary pathology
         ARDS 
         Cardiogenic pulmonary oedema
         Chlorine and other irritant gases 
         Non-cardiogenic pulmonary oedema 
         Paraquat 
         Pulmonary aspiration and pneumonitis
              Activated charcoal 
              Gastric contents
              Hydrocarbons
         Smoke inhalation

    NON-TOXIC CAUSES

    Bronchial asthma
    Bronchiectasis
    Cardiogenic pulmonary oedema
    Chronic obstructive airways disease
    Depressed level of consciousness of non-toxic aetiology
    Muscle weakness of non-toxic aetiology e.g myasthenia gravis
    Thoracic trauma
    Pneumonia
    Pulmonary thromboembolism
    Upper airways obstruction

    CLINICAL FEATURES

    The clinical features are predominantly those of the underlying
    intoxication.

    Where respiratory failure is from CNS depression, the patient will
    have a decreased level of consciousness and decreased respiratory rate
    (less than 10 breaths/minute) and/or respiratory volume.

    Where respiratory failure is secondary to respiratory muscle
    paralysis, there will be generalised muscle weakness and it is
    predominantly respiratory volume that is decreased.

    Where respiratory failure is secondary to lung pathology, respiratory
    rate and volume may both be increased.

    The clinical features of hypercarbia and hypoxia in non-comatose
    patients are restlessness, agitation, dyspnoea and cyanosis.  The
    depth of cyanosis is not an accurate reflection of the severity of
    ventilatory insufficiency. 

    Hypercarbia produces cerebral vasodilation and can lead to raised
    intracranial pressure and cerebral oedema.  Clinically, this is
    manifested by headache and drowsiness progressing to coma. 
    Peripherally, the acidosis associated with hypercarbia produces
    vasodilation resulting in warm limbs and bounding pulses.

    RELEVANT INVESTIGATIONS

    Arterial blood gas analysis

         Reveals a respiratory acidosis (pH < 7.35 and pCO2 > 45 mm Hg)
    which may be partially compensated for by a rise in HCO3-
    concentration.  The pO2 is reduced if supplemental oxygen has not
    been administered. The degree of elevation of the pCO2 is the best
    measure of the severity of ventilatory failure. 
    Chest x-ray
    ECG

    TREATMENT

    Treatment is supportive.  All patients should receive supplemental
    oxygen. Comatose patients should be intubated and the upper airways
    cleared from obstructions and mucous by suction.  Mechanical
    ventilation is indicated in all patients with symptomatic or worsening
    hypercarbia or in whom oxygenation cannot be maintained with
    supplemental oxygen via a facemask.   Positive End Expiratory Pressure
    (PEEP) is sometimes useful to increase lung volume further and improve
    oxygenation by opening previously collapsed alveoli.

    CLINICAL COURSE AND MONITORING

    A dramatic clinical improvement is usually observed once adequate
    ventilation and oxygenation is assured.  The duration and degree of
    ventilatory support required depends on the agent and mechanism
    responsible for the development of respiratory failure.

    Careful monitoring of vital signs, oxygenation (pulse oximetry),
    arterial blood gases, fluid and electrolyte balance, is required until
    recovery of respiratory function.  This usually requires admission to
    an intensive care facility.  

    LONG-TERM COMPLICATIONS

    Hypoxic brain injury.

    AUTHOR(S)/REVIEWERS

    Authors:       Dr. A.N.P. van Heijst, Baarnseweg 42 A, NL-3735 MJ
                   Bosch en Duin, The Netherlands.  
                   Dr. J. Szajewski, Warsaw Poisons Control Centre,
                   Szpital Praski, Pl. Weteranow 4, 03-701 Warszawa,
                   Poland.

    Reviewers:     Birmingham 3/99:  T. Meredith, L. Murray, A. Nantel,
                   J. Szajewski.