BRITISH THORACIC AND TUBERCULOSIS ASSOCIATION 325

not appear to differentiate the patients who survived or died. The cost of the programme was insignificant when compared to the daily cost of a hospital bed, and the cost of physician care constituted less than 3 per cent of the total. The management was primarily carried out by para- medical personnel, and, where indicated, mechanical aids. This made unnecessary prolonged stays in the hospital and obviated otherwise necessary confinement in nursing homes or extended care institutions. The patient and family appear to appreciate the opportunity to remain in comfortable and familiar surroundings along with the remainder of the family during the late phases of the illness. The programme is an integral and essential component of the management of patients with chronic respiratory insufficiency.

Pulmonary Physiology in Relation to Asthma G. J. R. MCHARDY (Edinburgh)

The pathological changes in asthma cause airway obstruction, which alters the mechanical properties of the lungs, affects pulmonary gas exchange and causes changes in the arterial 0, and CO, pressures.

Ventilatory capacity (FEV, FVC and FEV%) is reduced. Improvement after adrenaline but not after atropine is a hint that the patient will respond to corticosteroids. Lung volumes are increased, giving increased elastic recoil and widening the airways at total lung capacity (TLC). The increased residual volume indicates early closure of the airways in expiration. Overinflation of the lungs increases the elastic work of breathing, and may cause inspiratory dyspnoea. Rapid changes in lung volume may occur in response to therapy, but the FEV may not immediately improve as TLC declines, because the airways have become narrower. The lungs of the patients with asthma are less compliant than normal. Bronchial muscle activity may be estimated by measuring bronchial endomural pressure, and can be shown to decrease in response to bronchodilators.

Arterial Pco, is normal or low in mild or moderate asthma. Elevation of Pco, is a sinister sign found in severe attacks or accompanying exhaustion, and is an indication to consider artificial ventilation.

Arterial PO, is lowered, approximately in proportion to the severity of the attack, and may fall to near-lethal levels. It may remain low for weeks after a severe attack and be abnormal even in symptom-free intervals. Arterial PO, may fall after bronchodilators (particularly adrenaline or isoprenaline) have been given, due to a worsening of the distribution of ventilation and perfusion in the lung, possibly because the drugs act as pulmonary vasodilators and increase blood-flow to poorly ventilated areas. The patient must therefore be given enough oxygen to overcome the effects of the disease and of therapy.

The Management of Acute Asthma with High Dosage Corticotrophin I. W. G~~~~(London)(with M. FRIEDMAN)

The effect of corticotrophin suspended in gelatin in doses varying from 40 i.u.-400 i.u. was studied in volunteer subjects to determine the optimum dose required to produce prolonged continuous adrenal cortical stimulation. Increasing the dose beyond 200 i.u. did not produce a greater intensity or prolongation of adreno-cortical function. This amount of corticotrophin could be suspended in 1 ml. gelatin for ease of administration. The duration of stimulation produced by this dose is approximately 36 hours.

The effect of a single large dose of corticotrophin in gelatin was investigated in 13 asthmatic subjects during an exacerbation. All except one patient responded satisfactorily, requiring two or more injections. Seven of these needed prolonged corticotrophin therapy in conventional doses after discharge from hospital to maintain adequate control of the asthma.

The advantages of using high dosage corticotrophin in this way as against exogenous adrenal steroids is the ease with which this therapy can be discontinued. The use of corticotrophin in the