It seems surprising now, but the concept of respiratory failure is quite a recent development in respiratory medicine. Up until the middle of the 20th century, when chest physicians were dealing primarily with tuberculosis, it was virtually overlooked.1 The principles of the biochemical control of respiration had only recently been demonstrated, arterial blood analysis was difficult and time-consuming, and the understanding of acid-base metabolism was primitive by modern standards. The work of Moran Campbell and his colleagues,2 however, clarified the physiological basis of the clinical presentations of respiratory failure. The “blue bloater” who hypoventilated and developed right heart failure was contrasted with the “pink puffer” who suffered breathlessness but maintained a normal carbon dioxide tension and near normal oxygen tension. The adverse effect of supplemental oxygen of removing the hypoxic drive and exacerbating respiratory failure was recognised and controlled oxygen therapy using Venturi masks became established.

At the same time as these ideas about respiratory failure due to chronic obstructive pulmonary disease (COPD) were developing, a separate line of thought was evolving. Poliomyelitis—which until the early 1900s had caused only sporadic infections—began to appear in epidemics in the USA and many northern European countries and left thousands of children and some adults paralysed. These epidemics reached their peak in the 1950s until the advent of the Salk and Sabin immunisations. Acute hypercapnic respiratory failure due to respiratory muscle weakness was often fatal.

The first effective treatment was the tank ventilator or iron lung which was developed in 1928 by Drinker, an engineer with the Consolidated Gas Company of New York …