Cardiovascular and metabolic changes in shock and sepsis. Review fo changing concepts.
The commonly accepted sequence of low blood flow, tissue hypoxia, lacticacidosis and death does not apply to all patients dying from shock. The hyperdynamic circulation characteristic of severe sepsis is not likely due to peripheral arteriovenous shunts, since in skeletal muscle at least, capillary blood flow is increased and varies directly with cardiac index. A hyperdynamic circulatory state is seen in many patients with sepsis and may be related to metabolic changes rather than changes in oxygen transport. Skeletal muscle capillary blood flow is increased in fasting normal subjects and septic postoperative patients, both of whom are catabolic. Therefore, elevated blood flow, which is characteristic of severe sepsis, may be a response to or necessary for the catabolism of body protein required for energy production. Profound metabolic abnormalities resulting in rapid catabolism may be responsible for the demise of the septic patient. If this concept of sepsis is accepted, it follows that treatment which heretofore has been aimed at increasing blood flow and blood pressure should be redirected to therapy which provides energy substrates and alters hormonal patterns to favor anabolism.
D000138:Acidosis; D002302:Cardiac Output; D002395:Catecholamines / Q000378:metabolism; D005934:Glucagon / Q000378:metabolism; D006801:Humans; D000860:Hypoxia; D007773:Lactates / Q000097:blood; D009132:Muscles / Q000098:blood supply*; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*
D002395:Catecholamines; D007773:Lactates; D005934:Glucagon