Thirteen baboons were bled into shock and maintained at 60 mm Hg and 40 mm Hg for 2 hours, respectively, followed by resuscitation with shed blood and Ringer's lactate. In eight animals restoration of baseline left atrial pressure (LAP) was considered complete resuscitation and was maintained at baseline values with infusion of Ringer's for 18 hours. Five animals were resuscitated to baseline mean arterial pressure (MAP) and maintained with Ringer's. Complete hemodynamic parameters were recorded preshock, during shock, and hourly post-resuscitation for 18 hours. Organ blood flow was measured from radioactive microsphere injections at baseline, during shock, and 2 and 18 hours post-resuscitation. Blood volume was determined (Evans' blue) at baseline and 18 hours.
Characteristic hemodynamic changes were noted with shock which returned to normal for the 18 hours post-resuscitation. Animals resuscitated to baseline MAP remained stable with additional small volumes of Ringer's whereas, using LAP as the parameter for resuscitation, increasing fluid requirements to maintain LAP, began at 3 to 4 hours and was paralleled by a corresponding increase in urine output. At 18 hours intake was 450 cc/hour and output nearly 350 cc/hour (both [asymptotically equal to] 4 times baseline). Organ blood flow altered as expected during shock and at 18 hours persistent, significant (p < 0.05) reduction in organ blood flow was noted in the splanchnic circulation (gut and spleen) in both groups. Blood volume was significantly below baseline (< 90%) at 18 hours.
The data suggest a persistence of a teleologically important mechanism to protect the organism during shock which is not shut off by effective resuscitation as judged by hemodynamic criteria. Furthermore, the excessive fluid intake and output necessary to maintain baseline LAP suggest resetting of normal mechanisms for regulation of blood volume, and LAP may then not be a reliable parameter of resuscitation from hemorrhagic shock. These observations describe a prolonged abnormality in blood volume and flow distribution which may contribute to the syndrome of multiple organ failure following resuscitation from shock.
(C) Williams & Wilkins 1983. All Rights Reserved.