外科急诊创伤(英文)-休克及出血资料.ppt

Reduced perfusion of capillary beds Baroreceptors signal medulla Increased PVR Increased venous tone Increased HR Increased contractility BP returns to normal If blood loss is controlled no ill effects Cellular Ischemia Blood loss continues Venous constriction PVR increases maintaining SBP DBP also rises resulting in narrowing pulse pressure Pulse weakens Less blood directed to non-critical organs Skin- pale, cool, clammy Anaerobic metabolism ensues CO2 and lactic acid produced and accumulate Cellular hypoxialeads to cellular ischemia HR increases Blood becomes more acidotic Chemoreceptors increase RR/ depth Circulating catecholamines and acidosis results in AMS Arterioles hypoxic and fatigued Hemestasis occurs blood is drawn from interstitium 1L/hr Erythropoieten increases RBC production Recovery possible Sympathetic stimulation, reduced perfusion to kidneys, pancreas, liver cause hormone release Angiotensin II increases PVR reduces blood flow Lactic acid build up Hydrostatic pressure forces fluid into interstitium Compensatory mechanisms fail Interstitial edema decreases ability to provide O2 and remove CO2 Capillary cell membranes break down RBC’s clump, rouleax Build up of acids results in relaxation of post capillary sphincters Byproducts, K+ released by cells, agglutinated RBC’s released in venous circulation Results in profound metabolic acidosis and microscopic emboli CO= 0, PVR= 0, decrease BP, decrease cellular perfusion to critical organs irreversible Transcapillary Refill Following hypovolemia osmosis allows movement of fluid from intracellular and interstitial spaces into intravascular space 2L self limiting Hgb, Hct values inaccurate in actively bleeding patients Anemia present with hemodilution due to resuscitation, transcapillary refill Stages of Shock Compensated Shock Minimal Change Decompensated Shock System beginning to fail Irreversible Shock Ischemia and death imminent Decompensation Body’s compensatory mechanisms overwhelmed O2 delive