Circulatory shock
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Cellular membrane destabilization induced by endotoxin and endogenous inflammatory mediators contributes significantly to the progression of metabolic and hemodynamic dysfunction in endotoxemia. Owing to its membrane-stabilizing properties, lidocaine may prove beneficial in the treatment of endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular venous and carotid arterial catheters. ⋯ U-14C-glucose-derived glucose recycling was increased above the lidocaine group's preendotoxin control period and reached values twice those of the untreated pigs' endotoxin infusion period. Compared to their own control period and the untreated group's endotoxin infusion period, percentage lactate/glucose was decreased from 40 min on. Lidocaine treatment elicited modest improvements in systemic arterial blood pressure and reduced relative glucose utilization and gluconeogenesis, but in itself, was not a sufficient therapy for endotoxic shock in this model.
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Review Comparative Study
Oxygen consumption in septic shock: collective review.
That a decline in oxygen consumption (VO2) might herald onset of septic shock prior to hemodynamic collapse is suggested by previous observations in humans and animals in which VO2 appeared to be suppressed in systemic sepsis, despite normal or supranormal cardiac output, and in cellular and mitochondrial preparations exposed to endotoxin, despite adequate flow of perfusate. That a supranormal VO2 might be one of the best predictors of ultimate survival is suggested by data collected from humans during various stages of septic shock. To evaluate VO2 as an early indicator of sepsis, the effect of endotoxemia was observed in 20 rhesus monkeys divided into groups according to hypodynamic, normodynamic, and hyperdynamic blood flow states; the effect of sepsis was observed in seven preterminal septic humans during the final hours of their lives. ⋯ Probability of survival in sepsis appears to be enhanced by VO2 and cardiac output that are supranormal; yet even when VO2 is elevated, death can ensue within minutes to hours. Significant decline in VO2 is a grave prognostic sign, almost always preceded by a relatively easily detected hemodynamic change. Systemic VO2 appears to represent neither a specific early indicator of sepsis nor a certain prognosticator of survival outcome; it might provide useful information regarding adequacy of resuscitation.
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Comparative Study
Increased pulmonary edema with crystalloid compared to colloid resuscitation of shock associated with increased vascular permeability.
Physiologic effects of colloidal (5% albumin, 6% hydroxyethylstarch, 6% dextran-70) and crystalloidal (Ringer's lactate) fluids were examined in rats (six in each fluid group) after infusion of an LD99 of rattlesnake venom, previously shown to produce shock secondary to increased vascular permeability. Venom infusion (iv, 2.0 mg/kg, 30 min) was followed by fluid infusion (iv, 30 min) in quantities sufficient to reverse venom-induced hemoconcentration. Venom infusion decreased mean arterial pressure, increased blood lactate, and increased hematocrit in all animals (p less than .01). ⋯ In spite of the development of pulmonary edema in the crystalloid-treated animals, survival was similar for each group (6/6 for albumin and dextran, 5/6 for hydroxyethylstarch and Ringer's lactate). We thus conclude that both colloidal and crystalloidal fluid resuscitation leads to survival in permeability shock. Resuscitation with crystalloidal fluid, however, requires significantly greater volumes and is associated with the development of pulmonary edema.
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Review Comparative Study
Effects of glucose-insulin-potassium (GIK) on myocardial blood flow and metabolism in canine endotoxin shock.
Glucose-insulin-potassium (GIK) has beneficial effects during endotoxin shock, possibly through improvement of myocardial function, but the mechanism is not clear. We have studied the effects of GIK on left ventricular function, coronary flow, and oxygen consumption in controls and dogs treated with endotoxin (1.5 mg/kg-1). The animals were anaesthetized (etomidate 4 mg/kg-1/hr-1) and ventilated (N2O:O2 = 2:1). ⋯ Endotoxin decreased the ratio of endo- to epicardial flow. GIK did not change this ratio. However, for the same endo to epi ratio, increased CBF implies increased flow to endocardium.
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Reductions in hepatosplanchnic blood flow and oxygen delivery contribute to the hepatic metabolic dysfunction observed in endotoxemia. Through its membrane-stabilizing activity, systemic lidocaine therapy may modify visceral hemodynamics and preserve hepatocellular metabolic function in endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular, portal, hepatic venous and carotid arterial catheters, and hepatic arterial and portal venous flow cuffs to quantitate portosystemic and transhepatic kinetics. ⋯ Transhepatic lactate kinetics were unaffected by treatment, but net hepatic pyruvate uptake in the lidocaine-treated group increased as compared to the untreated group by 140 min postendotoxin, being significantly greater at 220, 280, and 320 min. Hepatic oxygen input was significantly reduced by 25-30% in both groups within 1 h of the onset of endotoxemia, but hepatic oxygen extraction efficiency increased two-to-three-fold, thereby maintaining net hepatic oxygen uptake. Despite the maintenance of hepatic oxygen uptake and improved hepatic pyruvate extraction in lidocaine treated endotoxemic pigs, no significant improvements in glucose homeostasis were incurred, leading to the conclusion that lidocaine therapy offered few significant advantages in the treatment of overall metabolic derangements during acute endotoxemia.