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Yasuki Fujita, Yuji Fujino, Akinori Uchiyama, Takashi Mashimo, Masaji Nishimura
Med Sci Monit 2007; 13(6): LE6-7
Dear Editor, We thank Dr. Schultz for the comments and appreciate the opportunity to reply. As Dr. Schultz pointed out, the mean airway pressure (mPaw) differed between the groups . While the difference was about 2 cm H2O, it was higher when Paw during inspiratory phase was concerned. We agree with Dr. Schultz that mPaw might have been partly responsible for the injury. Flow pattern also differed between the groups. We know that flow pattern in spontaneous breathing is decelerating, and it is close to that of pressure-regulated volume control (PRVC). However, peak inspiratory flow in ARDS patients is much higher than that of healthy persons, because respiratory center in ARDS is stimulated . In ARDS, the decelerating flow pattern is superior to a square waveform from the view point of work of breathing . However, physiological rational is not always best in critically ill patients. In ARDS fairly amount of the lung was collapsed, and it is considered to increase shear stress between open and collapsed alveoli [4-6]. We speculated that higher the inspiratory flow, larger the shearing stress. While it could be possible to ventilate the animals in PRVC with a high peak flow in square flow pattern, when the setting peak flow is very high, inspiratory time is really short. We do not think very high peak flow in VC could have led the different results. We know that tidal volume (VT) used in our study (20 ml/kg) was high comparing to a standard of ventilatory management in ICU. We totally agree with Dr. Schultz on the point, and this is the most important issue in our study. However, in animal studies, we do not necessarily follow ventilatory management for patients. We have learned a lot from ventilator-induced lung injury with high PIP up to 40 cm H2O . If we could ventilate the animals with lower VT for longer period like 3 days or longer, we could have had the results as Dr. Schultz commented. However, it was impossible in our laboratory. Nevertheless, we totally agree with Dr. Schultz comment on the point. Sincerely, Yasuki Fujita, Yuji Fujino, Akinori Uchiyama References: 1. Fujita Y, Fujino Y, Uchiyama A et al: High peak inspiratory flow can aggravate ventilator-induced lung injury in rabbits. Med Sci Monit, 2007; 13(4): BR95-100 2. Hering R, Zinserling J, Wrigge H et al: Effects of spontaneous breathing during airway pressure release ventilation on respiratory work and muscle blood flow in experimental lung injury. Chest, 2005; 128: 2991-98 3. Kallet RH, Campbell AR, Alonso JA et al: The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome. Respir Care, 2000; 45: 1085-1096 4. Puybasset L, Cluzel P, Chao N et al. and the CT scan ARDS study group. A computed tomography scan assessment of regional lung volume in acute lung injury. Am J Respir Crit Care Med, 1998; 158: 1644-55 5. Muscedere JG, Mullen JBM, Gan K, Slutsky AS: Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med, 1994; 149: 1327-34 6. Gattinoni L, Pelosi P, Crotti S, Valenza F: Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med, 1995; 151: 1807-14 7. Dreyfuss D, Basset G, Soler P, Saumon G: Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Respir Dis, 1985; 132: 880-84.