Circulatory shock
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Peritonitis-induced septic shock in the neonate is associated with a high mortality. Because there exists no clinically relevant model to study resuscitation of these patients, a model using the neonatal pig was developed. After arterial and central venous cannulation, and placement of a left pulmonary-artery thermodilution catheter, 12 anesthetized neonatal pigs were "resuscitated" with fluids (5% albumin in lactated Ringer's solution at 15 ml/kg/hr), antibiotics, and correction of acidemia. ⋯ These changes in cardiac index were accompanied by a continuous decline in mean arterial pressure, central venous pressure, pulmonary artery pressure, and systemic vascular resistance index, while pulmonary vascular resistance index showed a gradual continuous rise. The observed changes in hemodynamic and laboratory data mimic those anticipated in the human neonate with peritonitis-induced septic shock. This model proves reliable and reproducible, and shows promise as a tool to study the resuscitation of neonates with septic shock.
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Recent evidence has suggested a relationship between the endogenous opioid peptides and the pathophysiology of various shock states. In the present study, we investigated the relationship between the effectiveness of naloxone (an opiate antagonist) and nalbuphine (an opiate agonist/antagonist), and the changes in circulating levels of catecholamines in the nonhuman primate subjected to hemorrhagic shock. Plasma levels of catecholamines were measured using high-performance liquid chromatography (HPLC) during hemorrhagic shock in 15 female baboons. ⋯ Improvements in hemodynamics were maintained with a constant infusion of naloxone (5 mg/kg/hr), which also caused a further significant increase in plasma epinephrine (p less than 0.01). Administration of a single bolus of the opiate agonist/antagonist nalbuphine (5 mg/kg) dramatically decreased cardiac output and mean arterial pressure and had no effect on circulating catecholamines. Our results suggest that (1) the beneficial action of high-dose naloxone in primate hemorrhagic shock may be attributable in part to a drug-induced increase in circulating endogenous catecholamines; and (2) the failure of high-dose nalbuphine to improve cardiovascular function may be related to its partial agonist (cardiodepressant) properties at higher doses.
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This study was designed to evaluate the effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during experimental lactic acid acidosis in dogs. During the normal acid-base state (pH 7.4, PCO2 40 mm Hg), cardiac output and stroke volume were significantly increased and systemic vascular resistance was decreased by the infusion of dopamine or dobutamine 20 mcg/kg/min. Dobutamine produced identical changes in cardiac output, stroke volume, and systemic vascular resistance even during severe lactic acid acidosis (pH 7.0, PCO2 40 mm Hg). ⋯ Dobutamine infusion did not affect the plasma norepinephrine level during normal acid-base state but reduced the level during lactic acid acidosis. The marked increase in plasma norepinephrine following dopamine infusion may explain both the decrease in cardiac output and the increase in systemic vascular resistance in response to dopamine infusion during severe lactic acid acidosis. These results indicate that dobutamine may be more useful than dopamine in improving cardiac output during severe acidosis.
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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.