Resuscitation
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In a region with a population of 250,000 people, all emergency calls for cardiac arrest were prospectively registered during a period of 6 years. Timing of events were carefully registered as were treatment and the participation of 3 ambulances equipped with defibrillators. When time until initial treatment of cardiac arrest was below 5 min, 12% could be resuscitated and discharged alive. ⋯ S. A. In those cases where treatment could be initiated within 5 min, results were comparable.
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A previously established model in awake rats of hemorrhagic shock (HS) with 25% spontaneous survival rate (without resuscitation) was used to evaluate the effects of 4 novel life-supporting first aid (LSFA) measures on survival time and rate. After shed blood volume (SBV) of 3.25 ml/100 g, withdrawn over 20 min, hemodynamic and respiratory responses were recorded to 3 h and survival to 24 h. ⋯ Compared with group I, median survival times during HS 0-3 h were longer in groups II and III; and self-resuscitation attempts were longer in groups II, III and IV. We conclude that in untreated severe hemorrhagic shock, chances of survival to delayed arrival of advanced life support with i.v. fluid resuscitation might be increased with O2 inhalation and/or moderate external cooling.
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We previously determined that in awake, unmonitored Sprague-Dawley rats, bleeding of 2.5 ml/100 g over 20 min resulted in hemorrhagic shock (HS) with about a 75% survival rate over 24 h, and bleeding of 3.0 ml/100 g in about 25% survival to 24 h. In the present study, we monitored systolic and mean arterial pressure (MAP), central venous pressure (CVP), breathing movements, electroencephalogram (EEG), and arterial blood gases to 3 h in order to study dying patterns. After cannulation under light anesthesia and awakening for 2 h, the rats were bled over 20 min. ⋯ EEG depression began with hypotension to MAP less than or equal to 50 mmHg. During HS, PaO2 increased, and PaCO2, pHa, and Hct all decreased. The results suggest that this model with SBV of 3.25 ml/100 g would give a low, but not zero 3 h survival, and therefore would be suitable for the study of responses to field resuscitation potentials.
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A simple rat model was developed for the study of spontaneous survival after volume-controlled hemorrhage. The objective was to determine in awake, unrestrained rats the shed blood volume (SBV) in ml/100 g body weight that without fluid resuscitation, would result in either a high or a low percentage of survivors within 24 h. About 24 h after cannulation under light anesthesia, the awake rats were insulted with arterial blood withdrawal at a constant rate over 20 min, while mean arterial pressure (MAP) was monitored (N = 78). ⋯ SBV of 2.50 ml/100 g should be suitable for testing additional insults. SBV of 3.00 ml/100 g should be suitable for testing resuscitative therapies. The model should be modified to allow monitoring of key variables after hemorrhage.
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The immediate organ damage seen after multiple trauma and in shock is a typical example of non-bacterial inflammation triggered by activation of various mediators of both the humoral and cellular systems. Anaphylatoxins and the low-flow syndrome during the shock phase account for increased PMN* margination, which in turn causes pulmonary leukostasis and may provoke massive mediator release by PMN (oxygen radicals, proteinases, eicosanoids, PAF etc). This probably leads to severe endothelial cell damage, especially in the lung. ⋯ TNF is secreted by monocytes/macrophages (MO/MA) in response to LPS. Via macrophage derived cytokines and by LPS there is activation of endothelial cells, with increased adhesiveness for PMN. Both due to this increased adhesiveness and the presence of LPS and cytokines, PMN undergo massive activation, which causes mediator release and tissue damage.(ABSTRACT TRUNCATED AT 400 WORDS)