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.