Dear Editor,

We read with interest the review by Donn and Sinha (1) on minimising ventilator induced lung injury (VILI) in preterm infants. As they say fundamental to achieving this is the avoidance of repetitive alveolar recruitment/derecruitment and overdistension (1). Lung protective strategies must focus on avoiding these mechanical causes of VILI and aim to maximise compliance, pulmonary mechanics and gas exchange. The authors state this can be achieved by applying ventilation on the mid-point of the inflation limb of the pressure-volume (PV) relationship, as demonstrated in their Figure 5 (1). We suggest that the region of optimal ventilation occurs on the deflation limb of the PV relationship just above its point of maximal curvature, also known as the closing pressure. This is supported by mathematical modelling and animal studies showing that, compared to the inflation limb, better lung compliance (2), gas exchange (3) and less VILI (3) can be achieved by applying ventilation on the deflation limb. We have recently shown that targeting this region is practicable in ventilated neonates, and results in better gas exchange at a lower applied pressure, confirming earlier animal and adult studies (4). Targeting the deflation limb will also avoid atelectotrauma. In the diseased human lung, alveolar recruitment continues through the full extent of inflation to total lung capacity (5), meaning that ventilation anywhere on the inflation limb will involve repetitive alveolar recruitment/derecruitment. By contrast, alveoli are more uniformly recruited and remain stable throughout tidal breathing when ventilation is applied on the deflation limb (6).

In conclusion, we agree that reducing VILI is a complex and multifactorial process but suggest that until the ‘right questions’ include how best to recruit the lung and identify the point of optimal ventilation, the ‘right answers’ will continue to elude clinicians, irrespective of the mode of ventilation.

References:

1. Donn SM, Sinha SK. Minimising ventilator induced lung injury in preterm infants. Arch Dis Child Fetal Neonatal Ed. 2006; 91: F226-F230

2. Hickling KG. Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open- lung positive end-expiratory pressure: a mathematical model of acute respiratory distress syndrome lungs. Am J Respir Crit Care Med 2001;163:69 -78.

3. van Kaam AH, de Jaegere A, Haitsma JJ, van Aalderen Wm, Kok Jh, Lachmann B. Positive pressure ventilation with the open lung concept optimizes gas exchange and reduces ventilator-induced lung injury in newborn piglets. Pediatr Res 2003; 53: 245 – 253.

4. Tingay DG, Mills JF, Morley CJ, Pellicano A, Dargaville PA. The Deflation Limb of the Pressure-Volume Relationship in Infants during High- Frequency Ventilation. Am J Respir Crit Care Med 2006; 173: 414-420.

5. Crotti S, Mascheroni D, Caironi P, Pelosi P, Ronzoni G, Mondino M, Marini JJ, Gattinoni L. Recruitment and derecruitment during acute respiratory failure: a clinical study. Am J Respir Crit Care Med 2001; 164: 131-140.

6. Schiller HJ, Steinberg J, Halter J, McCann U, DaSilva M, Gatto LA, Carney D, Nieman G. Alveolar inflation during generation of a quasi-static pressure/volume curve in the acutely injured lung. Crit Care Med 2003; 31: 1126 – 1133.