PEEP improved PaO 2 linearly, and the putative mechanism was the prevention of alveolar end-expiratory collapse and/or airway closure. first tested the effect of increasing PEEP from 0 to 15 cmH 2O in ten patients with ARDS. To investigate its mechanism Falke et al. To improve PaO 2 the key maneuver, after the report by Ashbaugh et al. The most common side effects were pneumothorax and pulmonary hyperinflation, collectively termed barotrauma. Actually the recommended standard care was V T between 12 and 15 ml/kg. Maintaining normal PCO 2 was not considered a problem, as it was common to use high pressure and volume ventilation, with tidal volume (V T) even exceeding 20 ml/kg. To understand the progress of research in this period it is important to realize that the ultimate, undisputed target in ARDS patients was to maintain normal arterial PCO 2 and PO 2. Often, as new knowledge progresses, old knowledge is abandoned or forgotten. Some of the “new” concepts are nothing more than rediscoveries. How does the “baby lung” fit into this framework? The concept was introduced in the middle 1980s, but before discussing its place a brief history of the ARDS physiopathology and treatment is necessary. Interestingly, PEEP was described as a “buying time maneuver,” preventing alveolar collapse at end-expiration. At autopsy the lungs were heavy (average 2110 g), and microscopic examination revealed areas of alveolar atelectasis, interstitial and alveolar hemorrhage and edema, dilated and congested capillaries. Respiratory system compliance ranged from 5 to 16 ml/cmH 2O, all patients were hypoxemic, and PCO 2 ranged from 22 to 69 mmHg. Positive end-expiratory pressure (PEEP) was applied in five of them (three survived) and zero end-expiratory pressure (ZEEP) in the remaining seven (two survived). The 12 patients described there had ARDS of pulmonary and extrapulmonary origin, some with fluid overload and shock. It is worth rereading the original paper as it clearly outlines the basic physiopathology and management problems which continue to be a matter of scientific debate. The practical message is straightforward: the smaller the “baby lung,” the greater is the potential for unsafe mechanical ventilation.Īdult respiratory distress syndrome (ARDS) was first described in 1967. In this context, what appears dangerous is not the V T/kg ratio but instead the V T/”baby lung” ratio. Conclusionsįrom a physiological perspective the “baby lung” helps to understand ventilator-induced lung injury. This provides a rational for “gentle lung treatment” and a background to explain concepts such as baro- and volutrauma. However, the density redistribution in prone position shows that the “baby lung” is a functional and not an anatomical concept. Initially we taught that the “baby lung” is a distinct anatomical structure, in the nondependent lung regions. The respiratory system compliance is linearly related to the “baby lung” dimensions, suggesting that the acute respiratory distress syndrome lung is not “stiff” but instead small, with nearly normal intrinsic elasticity. The “baby lung” concept originated as an offspring of computed tomography examinations which showed in most patients with acute lung injury/acute respiratory distress syndrome that the normally aerated tissue has the dimensions of the lung of a 5- to 6-year-old child (300–500 g aerated tissue).

Barotrauma lungs