Abstract
Many physiologic and chemical mechanisms have been incriminated in the pathogenesis of respiratory failure or adult respiratory distress syndrome (ARDS) [1–11]. The relevance of these proposed mechanisms remains unclear because they have not been related to the natural history of this clinical disorder. Since it is tacitly assumed that patients develop ARDS from a baseline of normal hemodynamic and respiratory values, it follows that cardiorespiratory changes in ARDS should be compared with normal values. This conventional approach focuses on altered lung function and gas exchange after the symptom complex has become clinically manifest; it tends to ignore antecedent circulatory and peripheral oxygen transport changes that, having precipitated the disorder, probably have pathogenic relevance.
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Shoemaker, W.C. (1982). Therapy of adult respiratory failure after hemorrhage and trauma based on an analysis of antecedent physiologic determinants. In: Prakash, O. (eds) Applied Physiology in Clinical Respiratory Care. Developments in Critical Care Medicine and Anaesthesiology, vol 1. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-7567-5_6
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DOI: https://doi.org/10.1007/978-94-009-7567-5_6
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