The pathophysiology of shock.
Trauma often includes considerable losses of blood and plasma that may lead to hypovolemia and shock. The initial response of the body to trauma and hemorrhage is characterized by a neuroendocrine-mediated general defence reaction for the maintenance of circulatory homeostasis and substrate availability for vital organ function. Endogenous fluid is mobilized from intracellular and interstitial sources into the vascular compartment. This transcapillary refill is achieved by activation of glucose osmotic and neurogenic adaptive vascular mechanisms. The metabolic consequences of insufficient tissue perfusion are anaerobic glycolysis with increased production of lactate and hydrogen ions, acidosis, impaired mitochondrial energy production, disturbed ionic homeostasis across cell membranes, and reduced functional capacity of tissue cells. The shock- and trauma-induced alterations in tissue perfusion and metabolism vary, depending on the autoregulatory capacity of an organ, its basal metabolic requirements, its high energy phosphagen reserves, and its ongoing functional activity. Metabolic alterations impairing organ function occur early in the kidney and the liver and late in the heart and the brain. The ischemic tolerance of the skeletal muscle cell is considerable but vast amounts of lactic acid are produced, which at reperfusion will reach central blood and disturb vital organ function. Tissue factors released from mechanically traumatized or hypoxic cells will activate cascade systems and may induce alterations in remote organs, i.e. result in the development of multiorgan failure.
Haljamäe
H
H
Department of Anaesthesiology, University of Göteborg, Sweden.
D015687:Cell Hypoxia / Q000502:physiology; D006801:Humans; D012769:Shock / Q000378:metabolism / Q000503:physiopathology*