By A. F. Junod (auth.), Dr. J. L. Vincent (eds.)
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Extra info for 6th International Symposium on Intensive Care and Emergency Medicine: Brussels, Belgium, April 15–18, 1986
Traber DL, Schlag G, Redl H, Strohmeier W, Traber LD (1985) Pulmonary microvascular changes during hyperdynamic sepsis. Am J Physiol, (in press) 12. Nuytinck HKS, Goris RJA, Redl H, Schlag G, van Munster P (1985) Posttraumatic complications and inflammatory mediators. Arch Surg, (in press) 13. Goris RJA, Draaisma J (1982) Causes of death after blunt trauma. J Trauma 22: 141-146 14. Goris RJA, te Boekhorst TPA, Nuytinck KS, Gimbrere JSF (1985) Multiple-organ failure. Generalized autodestructive inflammation?
Depending on volume status, the central venous pressure, or right atrial pressure, will either stay the same or will also increase. If the central nervous system is intact, there will be marked efforts to breathe against the occluded airway, and fluctuations of pleural pressure will be reflected in the hemodynamic tracing. Thermodilution cardiac output measurements, due to the change in the mixed venous oxygen saturation, drop significantly during asphyxia to 50% of the preasphyxia level. If near-drowning occurs and aspiration does ensue, several factors are important .
This damage can be caused by several mediators and toxic products. 3. Incipient interstitial perivascular edema originating around the microvasculature marks the beginning of the process. It becomes more severe after several hours and leads to the posttraumatic ARDS. 4. Depending on the severity of the multiple fractures and soft tissue trauma isolated fat emboli may be present. Fat globules and granulocytes aggregates may occupy a capillary causing mechanical obstruction of the lung's microcirculation.
6th International Symposium on Intensive Care and Emergency Medicine: Brussels, Belgium, April 15–18, 1986 by A. F. Junod (auth.), Dr. J. L. Vincent (eds.)