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Titlebook: Critical Care Medicine Manual; Max Harry Weil,Protasio L. DaLuz Book 1978 Springer Science+Business Media New York 1978 Infusion.Notfallme

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楼主: Limbic-System
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Distributed Information Systemsties, pelvis, right atrial appendage, or a malignant organ. The venous disease and/or stasis as seen with congestive failure, infectious diseases, malignancies, blood dyscrasias, toxic agents, and convalescent periods for surgical procedures, childbirth, or fracture, may predispose to venous thrombi and potential pulmonary emboli.
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Weaning from Mechanical Ventilationa) vital capacity > 4–5 ml/kg, (b) inspiratory force > 10 cm H.O, . (d) positive end-expiratory pressure requirement < 10 cm H.O, (e) stable cardiovascular system, (f) chest-wall flailing not severe, and (g) close supervision by experienced physicians.
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Diagnosis and Treatment of Acute Pulmonary Thromboembolism and Fat Embolities, pelvis, right atrial appendage, or a malignant organ. The venous disease and/or stasis as seen with congestive failure, infectious diseases, malignancies, blood dyscrasias, toxic agents, and convalescent periods for surgical procedures, childbirth, or fracture, may predispose to venous thrombi and potential pulmonary emboli.
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Distributed Information Systemsly humidifies it (100% RH; 44 g H.O/m.). The oropharynx is less efficient in this regard. Bypassing the nose with a tracheal tube and inhaling dry gas brings movement of the carpet to a halt. Thus when the nasal air passages are bypassed, inhaled gas should be supplied with at least 100% RH at 37°C.
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,Die prozeßorientierte Organisation,ing Phase II. Phase II begins as the antigen reappears and immediately has a shattering interaction with the antibodies. This interaction triggers the release of at least three mediators: (a) histamine, (b) bradykinin, and (c) slow-reacting substance. The mediators have a profound systemic effect.
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Theorien als Strukturen: II. , Paradigmen,ndary (postresuscitative) cerebral changes that can be either ameliorated or prevented. With the use of titrated therapy aimed at restoring cerebral homeostasis, the chance for neuronal recovery may be enhanced [65]. The present chapter summarizes information on cerebral pathophysiology and some current therapeutic recommendations.
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