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Lung and diaphragm-protective ventilation: setting new concepts in historical context.

DOI:10.1097/MCC.0000000000000689 From its inception, developments in mechanical ventilation have been propelled by new physiological insights. Modern mechanical ventilation was born in the midst of the Copenhagen poliomyelitis outbreak at Blegdams Hospital in 1952 [1]. Hundreds of patients with poliomyelitis were admitted and about 50% exhibited some measure of paralysis. A considerable number of patients with paralytic poliomyelitis exhibited bulbar involvement with respiratory failure, a devastating complication with a mortality rate close to 90% [2]. Patients that were dying suffered from shock with progressive acidemia, widely assumed to be attributable to sepsis and metabolic acidosis. Bjorn Ibsen’s famous gamble that the acidemia was actually attributable to hypoventilation and respiratory failure – at the time, clinical measurements of PaCO2 were not routinely available – proved correct when tracheostomy, airway suctioning, and positive pressure ventilation resuscitated a young woman in the throes of death [3]. This approach became standard and mortality fell precipitously to approximately 40% for the remainder of the epidemic [2]. The modern era of mechanical ventilation was born, brought about by a fundamental physiological insight about the mechanism of death. Two decades later, yet another physiological insight dramatically re-oriented thinking about the best approach to mechanical ventilation. Following Ibsen’s success, it became standard to use large pressures as needed to achieve a ‘normal’ minute volume and ‘normal’ arterial blood gas values. Indeed, some argued for supra-normal tidal volumes and hypocapnia to ensure patient comfort [4]. Webb and Tierney questioned this orthodoxy. In a classic experiment, they demonstrated that ventilation with injurious pressures could induce pulmonary edema in a previously uninjured lung, demonstrating that the same mechanical ventilation settings routinely employed in the care of patients with acute respiratory distress syndrome could actually cause a clinical and pathological picture that looked for all the world like acute respiratory distress syndrome [5]. Later it was demonstrated that the pulmonary inflammation provoked by ventilator-