title: Endpoints of resuscitation.
abstract: Despite the multiple causes of the shock state, all causes possess the common abnormality of oxygen supply not meeting tissue metabolic demands. Compensatory mechanisms may mask the severity of hypoxemia and hypoperfusion, since catecholamines and extracellular fluid shifts initially compensate for the physiologic derangements associated with patients in shock. Despite the achievement of normal physiologic parameters after resuscitation, significant metabolic acidosis may continue to be present in the tissues, as evidenced by increased lactate levels and metabolic acidosis. This review discusses the major endpoints of resuscitation in clinical use.
authors: Division of Trauma and Emergency Surgery, Department of Surgery, UT Health Science Center San Antonio, 7703 Floyd Curl Drive, Mail Code 7740, San Antonio, TX 78229-3900, USA. Electronic address: cestero@uthscsa.edu.
authors: Ramon F
authors: RF
authors: Cestero
authors: Division of Trauma and Emergency Surgery, Department of Surgery, UT Health Science Center San Antonio, 7703 Floyd Curl Drive, Mail Code 7740, San Antonio, TX 78229-3900, USA.
authors: Daniel L
authors: DL
authors: Dent
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001784:Blood Gas Analysis; D001794:Blood Pressure; D004452:Echocardiography; D006801:Humans; D008365:Manometry; D011674:Pulse; D012151:Resuscitation; D012769:Shock / Q000175:diagnosis* / Q000209:etiology / Q000628:therapy*; D019265:Spectroscopy, Near-Infrared; D013318:Stroke Volume
chemical_list: D015415:Biomarkers
keywords: Hypoperfusion; Oxygen demand; Resuscitation; Shock