Physiological and metabolic correlations in human sepsis. Invited commentary.
The septic response in man appears to be a disease in which the infecting agent induces a state of disordered metabolic control in the host. The abnormal regulation of metabolic pathways causes a diversion of substrate utilization toward gluconeogenesis and ketone body formation and a reduction in oxidative energy-producing metabolism. This state of metabolic insufficiency is reflected in the pattern of cardiorespiratory, vascular, and physiological compensation. The precise magnitude of the resultant physiological compensation and its rate and direction of change can be quantified by the use of physiological state trajectories which also reflect the magnitude of underlying metabolic derrangements. The prognostic and therapeutic implications of these changes are discussed.
D000596:Amino Acids / Q000378:metabolism; D001794:Blood Pressure; D050260:Carbohydrate Metabolism; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008659:Metabolic Diseases / Q000209:etiology*; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood; D011379:Prognosis; D012044:Regression Analysis; D012119:Respiration; D012770:Shock, Cardiogenic / Q000378:metabolism / Q000503:physiopathology; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*; D013318:Stroke Volume; D013530:Surgical Wound Infection / Q000378:metabolism / Q000503:physiopathology*; D014655:Vascular Resistance; D014692:Ventilation-Perfusion Ratio; D014947:Wounds and Injuries / Q000378:metabolism / Q000503:physiopathology
D000596:Amino Acids; D002245:Carbon Dioxide; D010100:Oxygen