Circulatory shock
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The present study examines the effects of resuscitation fluid composition on myocardial function, myocardial high-energy phosphate content, and survival following third-degree anesthetic burn to 35-40% body surface area in the guinea pig. Treatment regimens used were 1) no resuscitation, 2) isotonic saline, 3) Ringer's lactate and 4) Ringer's acetate. Fluids were administered at the rate of 0.334 ml/kg/hr/% burn for 4 hr following injury, at which time myocardial function was assessed. ⋯ However, by 48 hr, only acetate-treated animals survived. These data indicate that important differences exist in the effectiveness of different resuscitation fluids and that Ringer's lactate, the fluid most often utilized clinically, may not provide optimum benefit. In light of these results, serious consideration should be given to the substitution of acetate for lactate during the resuscitation of burn shock patients.
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Gram-negative septic shock remains a major clinical problem. One frequently encountered complication of sepsis is disseminated intravascular coagulation (DIC). The present study was to determine in an Escherichia coli endotoxemia awake rat model the efficacy of antithrombin-III (AT-III) prophylaxis and to explore the role of DIC in the pathogenesis of endotoxemia. ⋯ Results of this study suggest that AT-III prophylaxis is very protective above a threshold dosage in an endotoxemic rat model and that protection is in part due to ameliorating DIC. Our data also suggest that DIC occurs very early during endotoxemia and may in part be responsible for the pathogenesis of endotoxemia in the rat. We conclude that AT-III prophylaxis may be efficacious in conditions of impending DIC, such as gram-negative septicemia/endotoxemia.
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We prospectively studied 18 patients with septic shock prior to and during volume infusion in order to evaluate their hemodynamic response to fluid repletion. Fluid challenge increased left heart filling pressure from 7.7 +/- 0.5 to 15.4 +/- 0.6 mm Hg (P less than .01). The increases in left ventricular filling were associated with significant increases in stroke volume index from 25.4 +/- 2.5 to 35.7 +/- 2.5 ml/min/M2 and cardiac index from 2.49 +/- 0.19 to 3.32 +/- 0.16 L/min/M2. ⋯ Over the next 24 hours of maintenance fluid infusion, the left ventricular stroke work index increased to 36.8 +/- 4.2 g X m/M2 (not significant). These data suggest that volume infusion restores ventricular filling in patients with sepsis. Although fluid repletion increases stroke and cardiac output, depressed left ventricular performance appears to be an early finding in septic shock.
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A retrospective study of 50 patients with circulatory shock and serial hemodynamic and metabolic measurements was undertaken. From the patient records, values for first measured cardiac index (CI) (t = 1) and highest CI (t = 2) with concomitantly obtained hemodynamic and metabolic variables and with arterial blood lactate levels (ABL), measured within 1.5 hours of t = 1 and t = 2 were taken. Nineteen patients had nonseptic shock (NSS), and 31 had septic shock (SS). ⋯ In SS, changes in ABL best correlated with changes in SVRI (r = -0.54; p less than 0.01). Our data suggest that anaerobic metabolism, reflected by ABL, decreases in response to an increase in CaO2, CI, and thus DO2 in NSS but not in hyperdynamic SS. Anaerobic metabolism in the latter may relate to peripheral vasodilation, associated with peripheral "functional" shunting of blood transported oxygen, rather than to insufficient DO2.
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The behavior of white blood cells (WBCs) in the capillary network of the cat brain was studied under normal conditions and during acute hemorrhagic hypotension. A small transilluminated area of the cerebral cortex was observed directly, and blood cells flowing through the capillary network were recorded on cinefilm using a high-speed cinecamera. The cell motion was analyzed on the projection screen using a frame-by-frame method. ⋯ RBC velocity in capillaries was reduced. The ST level was increased significantly with a decrease in RBC velocity. These findings suggest that acute hemorrhagic hypotension may induce flow maldistribution in cerebral microcirculation.