Comparison of intraosseous, central, and peripheral routes of crystalloid infusion for resuscitation of hemorrhagic shock in a swine model.

Venous access is often a clinical dilemma in severely hypovolemic children. This study compares fluid resuscitation by central vein, peripheral vein, and the intraosseous route in a hemorrhagic shock model. Hampshire piglets were bled to a mean arterial pressure of 30 mm Hg. This level of shock was sustained for 30 minutes. Resuscitation was carried out with normal saline delivered at 50 mL/min by a manual pressure of 450-475 mm Hg over the ensuing 20 minutes. Bone marrow from two intraosseous-infused animals was harvested immediately after the study for histologic examination. The hemodynamic response to crystalloid resuscitation was comparable among the three groups. There was no significant difference in mean arterial pressure, central venous pressure, cardiac output, pulmonary capillary wedge pressure, mixed venous oxygen saturation, or arterial oxygen saturation. Histologically, cellular washout and necrosis were found in bone marrow immediately adjacent to the intraosseous needle infusion site. For fixed-rate infusion, intraosseous crystalloid resuscitation is as efficacious as that delivered by peripheral or central venous routes in reversing hemorrhagic shock.

The effects of acute sleep deprivation during residency training.

Verbal and symbol concentration, learning, problem solving, clear thinking, manual skills, and memory were tested in 42 surgical residents to assess the effects of acute sleep deprivation on specific neuropsychological parameters. A series of eight neuropsychological tests--digit symbols, digit vigilance, story memory, trail making, PASAT, Raven matrices, delayed story, and pegboard--and a questionnaire on mood states were completed by the residents both when fatigued (less than 4 hours of sleep: mean, 2.0 +/- 1.5 hours) and when rested (more than 4 hours of sleep: mean, 6.5 +/- 1.0 hours), with at least 7 days between tests. In order to eliminate the effects of learning from the first test series, randomization of residents was performed so that one half were first evaluated when rested and one half when fatigued. ANOVA, multiple regression analysis, and the Student t test were used to assess differences. In the acute sleep-deprived state, residents were less vigorous and more fatigued, depressed, tense, confused, and angry (p less than 0.05) than they were in rested state. Despite these changes in mood, however, the responses on all of the functional tests were no different statistically in those who were rested and those who were fatigued (even in those with less than 2 hours' sleep). We conclude that acute sleep deprivation of less than 4 hours alters mood state but does not change performance in test situations in which concentration, clear thinking, and problem solving are important.

Oxygen insufficiency during hypoxic hypoxia in rat brain cortex.

To relate cerebral oxygen sufficiency and insufficiency with arterial oxygen tension, reduction/oxidation responses of the initial and terminal members of the mitochondrial respiratory chain (NADH and cytochrome c oxidase) were recorded in situ by optical techniques when increased cerebral energy use was provoked by direct electrical stimulation. Small decreases in paO2, produced by forced ventilation of hypoxic gas mixtures, resulted in decreased amplitude of the characteristic negative shift in extracellular potential which accompanies such stimulation and smaller oxidative response of NADH and cytochrome oxidase. When paO2 fell below 40-50 Torr, stimulation produced reductive rather than oxidative shifts of the mitochondrial respiratory chain components. The data suggest that when arterial oxygen tension is slightly decreased, compensating mechanisms allow brain function to continue with minimal changes in cortical metabolites and high energy phosphate compounds. When arterial oxygen falls below 40-50 Torr, however, compensation can no longer prevent tissue hypoxia during times of increased energy demand. Thus, hypoxemia is not necessarily synonymous with oxygen insufficiency, but oxygen sufficiency must be defined with due regard to the degree of energy demand.

Norepinephrine depletion alters cerebral oxidative metabolism in the "active" state.

Unilateral chemical lesion of the nucleus locus coeruleus in rats produced unilateral depletion of ipsilateral cortical norepinephrine. Norepinephrine depletion was not associated with changes in "resting" metabolic balance of the cerebral cortex, as determined by in situ reflection spectrophotometry of the redox state of cytochrome oxidase. Norepinephrine depletion, however, caused slowing of the transient metabolic response to sudden increases in energy demand produced by direct cortical electrical stimulation. The effect was apparent in the redox state of both cytochrome oxidase and NAD, the latter being measured, also in situ, by reflection microfluorometry. These results demonstrate that norepinephrine has a role in modulating the response to increased metabolic demand in the cerebral cortex. Norepinephrine may mediate its effect by potentiating Na+, K+-ATPase or through its effects on vascular reactivity, or both.

Cerebral norepinephrine: influence on cortical oxidative metabolism in situ.

Unilateral lesion of the locus coeruleus and the resultant norepinephrine depletion in the ipsilateral cerebrum alters the relationship between cerebral metabolic demands and local delivery of oxygen and substrates. This effect of norepinephrine depletion is demonstrated by slower recovery of the redox ratio of cytochrome a,a3 during increased metabolic demands induced by local cortical stimulation.