Critical care medicine
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Critical care medicine · Aug 1995
Cerebral hemodynamics and distribution of left ventricular output during inhalation of nitric oxide.
Inhaled nitric oxide is being utilized as a selective pulmonary vasodilator in the treatment of persistent pulmonary hypertension of the newborn. However, the effects of inhaled nitric oxide on cerebral hemodynamics and distribution of left ventricular output in newborn subjects have not been studied. This study was designed to measure quantitatively the effect of inhaled nitric oxide on the distribution of left ventricular output and on cerebral hemodynamics in a perinatal animal model. ⋯ Acute pulmonary vasodilation caused by inhalation of nitric oxide does not change left ventricular output, cerebral blood flow, or cerebral oxygen consumption, despite an increased systemic-to-pulmonary shunt across the ductus arteriosus.
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To determine the prevalence of, and factors associated with, burnout among pediatric intensivists across a variety of practice settings. ⋯ We found that a high degree of burnout exists in pediatric critical care medicine, with 50% of pediatric intensivists at risk or burned out. Overall, there was no association between Burnout Scores and training, practice specialties, or practice settings, nor was there an association with aspects of practice that are physically taxing. However, perceptions about the value of their work and feelings of success and satisfaction were highly associated with those respondents classified as burned out. Routine exercise (a strategy used by some for stress reduction) was associated with lower Burnout Scores. Further studies are necessary to evaluate the trends that we have reported and to identify causal factors.
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Critical care medicine · Aug 1995
Clinical TrialMethylene blue increases myocardial function in septic shock.
To study whether the circulatory changes of human septic shock are mediated in part by nitric oxide. ⋯ After initial resuscitation from human septic shock, a single dose of methylene blue transiently increases mean arterial pressure and oxygen uptake, associated with a decrease in arterial compliance and increases in myocardial function and oxygen delivery. Hence, nitric oxide may be a mediator of the circulatory changes of human septic shock.
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Critical care medicine · Aug 1995
Comparative StudyConcentrations of prolactin and prostaglandins during and after cardiopulmonary resuscitation.
To assess differences in plasma prolactin and prostaglandin concentrations in resuscitated and nonresuscitated patients during cardiopulmonary resuscitation (CPR), and to compare changes of prostaglandin and prolactin concentrations with hemodynamic variables in the immediate postresuscitation phase. ⋯ Prolactin and prostaglandin concentrations were increased during cardiac arrest and CPR. Successful initial resuscitation was associated with increased prolactin and prostaglandin F2 alpha concentrations during CPR. Decreased concentrations in non-resuscitated patients may have been a result of exhaustion of the neuroendocrine and eicosanoid systems, or may be due to differences in bioavailability at the site of blood sampling based upon differences in hemodynamics.
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Critical care medicine · Aug 1995
Effect of volume support, antibiotic therapy, and monoclonal antiendotoxin antibodies on mortality rate and blood concentrations of endothelin and other mediators in fulminant intra-abdominal sepsis in rats.
To study the therapeutic effects of volume support, antibiotics, and a monoclonal antiendotoxin antibody on the mortality rate and blood concentrations of endothelin and other mediators in fulminant intra-abdominal sepsis in rats. ⋯ The concentration of plasma endothelin was increased during fulminant intra-abdominal sepsis in rats. Combining volume support with antibiotic therapy reduced the mortality rate, but did not modify concentrations of plasma endothelin-1. The monoclonal antiendotoxin antibody E5 reduced the mortality rate and concentrations of endotoxin, TNF, and endothelin-1, but not big endothelin. This finding indicates that E5 therapy inhibits the conversion of big endothelin to 21-residue endothelin-1.