Structure determines function

نویسنده

  • Mark J. Heulitt
چکیده

In this special issue of the Journal of Pediatric Intensive Care, we have compiled a series of articles relating to mechanical ventilation. We have chosen to select articles that do not address the usual reviews on mechanical ventilation but rather topics that our readers may find unique and interesting. The title of my editorial, “Structure determines function”, relates to that first lecture in physiology when it was discussed that changes in the shape of a protein, cell or organ will usually result in a change of function of that structure. This is never so true as in a discussion of the physiology of positive pressure mechanical ventilation in pediatric patients. Over the past 20 years, there has been a growing body of literature that served as the basis of a “protective lung strategy” in patients with acute lung injury and acute respiratory distress syndrome [1,2]. I published the first review on this topic in pediatric patients in Respiratory Care in 1995 [3,4]. Since then, pediatric intensivists have modified their practice in an attempt to limit iatrogenic lung injury. These strategies, though still debated, usually include a low tidal volume strategy, limited levels of plateau pressure and inspired oxygen with adequate level of positive end expiratory pressure. The basis of the iatrogenic lung injury caused by positive pressure mechanical ventilation is a distortion of normal lung architecture (change in structure) with a subsequent change in pulmonary function of gas exchange (change in function). Therefore, all strategies are based in a desire to preserve the normal lung structure, thus function. Adjusting mechanical ventilator strategies as describe above can minimize ventilator induced lung injury and thus decrease mortality [1,2]. Recent reviews have demonstrated reduced mortality rates of 18–35% in pediatric patients [5,6]. The exact lower limit of the amount of tidal volume that causes structural damage, especially in pediatric patients, is still not known. We know the strategies of the 1980’s and early 1990’s of tidal volumes in excess of 10 mL per kg are deleterious, but the ideal tidal volume in children is still unknown. Due to the lack of this knowledge, strategies have developed to limit the tidal volume (8 mL per kg or less) along with inspired oxygen and plateau pressure. Further complicating this discussion is the inexact nature of our ability to accurately measure tidal volume in mechanically ventilated pediatric patients. I must remind the reader that we never measure tidal volume during mechanical ventilation, but measure flow and then integrate the flow changes to determine volume. Of course, this technique will not be accurate if not all flow is measured by the pneumotachograph (flow measuring device) such as when the flow is retained in the ventilator circuit (loss due to compression volume), or if there is an airway leak. It has been proposed that due to the above difficulties that in small pediatric patients, accurate tidal volume can only be guaranteed if tidal volume *Address for correspondence: Mark J. Heulitt, Physiology and Biophysics, College of Medicine, University of Arkansas for Medical Sciences, Applied Respiratory Physiology Laboratory Arkansas Children’s Hospital Research Institute, Little Rock, AR 722023591, USA. Tel.: +1 501 364 1858; Fax: +1 501 364 3188; E-mail: [email protected]. Journal of Pediatric Intensive Care 2 (2013) 1–3 DOI 10.3233/PIC-13041 IOS Press 1

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تاریخ انتشار 2013