Circulatory shock
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The role of neutrophil oxidative burst activation (OBA) in the development of fulminant post-trauma adult respiratory distress syndrome (ARDS) was studied in 30 patients. Neutrophil (PMN) chemiluminescence (LE) was used as the index of OBA. Serially, for 8 days post-trauma, patient neutrophils (Pc) were studied in their own serum (Ps) normal serum (Ns), or Gey's solution (G). ⋯ These changes were all simultaneously significant (P less than 0.05 to P less than 0.0001) by Bonferroni t-statistic applied to ANOVA. The clinical importance of these physiologic and biochemical responses was emphasized by the significantly (P less than 0.005) increased mortality in the ARDS patients. These data suggest that PMN LE and simple measures of respiratory function are early biologic markers of the development of fulminant post-traumatic ARDS and can be used to predict ARDS severity.
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Although various hemodynamic changes occur during and following hemorrhagic shock, the progressive changes in microvascular blood flow (MBF) in various organs under those conditions have not been determined. To study this, non-heparinized rats were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% o the shed blood volume was returned in the form of Ringer's lactate (RL). The rats were then resuscitated with 2, 3, or 4 times (x) the volume of maximum bleedout with RL. ⋯ The results indicate that MBF was significantly decreased during hemorrhage and remained depressed 30-240 min post-resuscitation in all the measured organs. This was not due to the decreased hematocrit since acute hemodilution did not significantly depress MBF. These results indicate that 1) LDF is a useful technique for repeated assessment of MBF following hemorrhage and resuscitation; 2) resuscitation with 4x RL increased central venous pressure to more than twice the normal value but did not restore or maintain MBF, suggesting that pharmacological support may be needed under such conditions; 3) the lack of maintenance of MBF following hemorrhage and resuscitation may form the basis of multiple organ failure observed following severe and prolonged hemorrhagic shock.
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Previous studies of hypothermia and blood coagulation have focused on alterations in the levels of blood clotting elements using coagulation tests performed under normothermic conditions. However, because of the enzymatic nature of activated clotting factors, hypothermia should also be expected to affect clotting factor activities. Multiple determinations of activated partial thromboplastin times (APTT), prothrombin times (PT), and thrombin times (TT) were performed on commercially available normal human plasma at assay temperatures similar to those encountered clinically (25-37 degrees C). ⋯ Clotting time correlated significantly with assay temperature in a negative exponential fashion for all three tests (r = -0.97 for APTT, -0.93 for PT, -0.71 for TT, P less than 0.001 for all regressions). Clotting time prolongation appears proportional to the number of enzymatic steps involved. These data indicate that the coagulopathy observed during hypothermia is, in part, independent of clotting factor levels.
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The macro- and microcirculatory effect of small-volume resuscitation with hyperosmotic-hyperoncotic solutions was analyzed in 21 anesthetized beagles subjected to standardized traumatic-hemorrhagic hypotension (laparotomy and exteriorization of the intestine; MAP 40 mmHg for 75 min). Primary resuscitation consisted of bolus infusion of 10% of the blood loss (approx. 4 ml/kg) of either hyperosmotic (7.2%) saline -HSS-, hyperoncotic (10%) dextran 60 -HDS-, or hyperosomotic-hyperoncotic saline dextran (10% dextran 60 in 7.2% saline; HHS). Within 5 min CO was restored and systemic pressure significantly increased. ⋯ HHS). Despite the normalization of cardiac output by small volumes of hypertonic solutions, 7.2% saline alone failed to fully restore RBF after protracted traumatic hemorrhage. For the concept of small-volume resuscitation, the hyperosomotic-hyperoncotic solution of 10% dextran 60 in 7.2% saline appears to be most effective to improve organ perfusion during the prehospital period of trauma patients.
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Previous studies have shown that fluid resuscitation in septic shock improves oxygen consumption. Red cell transfusion during resuscitation from septic shock has also been shown to enhance oxygen consumption in patients with elevated lactate levels. This study investigates the effect of increasing oxygen delivery (DO2) through an isolated increase in arterial oxygen content following adequate fluid resuscitation from septic shock in humans. ⋯ Subset analysis revealed that a pretransfusion oxygen extraction ratio under 24% was associated with an increase in VO2, but the pretransfusion level of cardiac index, PAWP, lactate, or VO2 was not. An isolated increase in arterial oxygen content as a means of increasing DO2 does not improve VO2 in septic shock following adequate fluid resuscitation. Patients with a low oxygen extraction ratio (less than 24%) represent a subset of patients which did improve consumption with transfusion, and may represent a more severe microcirculatory disturbance not amenable to fluid loading.