The pathophysiology of shock.
This is a very brief, superficial and biased discussion of the pathophysiologic changes in shock. It was designed to provide some insight into the very complex changes that occur, with particular attention to a few examples of the impaired cell metabolism, including changes in ATP, cAMP, and calcium. Although inadequate tissue perfusion through nutrietn capillaries is the main etiologic factor in most types of shock, it is not the primary problem in many patients, particularly those with early or hyperdynamic sepsis. The importantance of oxygen consumption and the possible benefits of higher hemoglobin levels are discussed to some extent because of their possible clinical application.
D000137:Acid-Base Imbalance / Q000209:etiology; D002302:Cardiac Output; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D006801:Humans; D007668:Kidney / Q000098:blood supply; D008247:Lysosomes / Q000648:ultrastructure; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010974:Platelet Aggregation; D012119:Respiration; D012769:Shock / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D014661:Vasoconstriction
D010100:Oxygen