Allocating global package pricing. The example of bypass surgery.

When health care organizations announce a change in rates paid to physicians, determining how to equitably distribute the new allocation can be a problem. Package pricing requires practitioners to justify their fees or costs to their colleagues and negotiate for a "specific piece of the pie." While this approach has many models, there are few actual examples. When some successful ones are developed, they should include an economic model which allows a practice to make business decision about marginal production opportunities that are in the best interest of all parties involved. Steps include determining actual costs, historical charge patterns, historical payment patterns and Medicare payment rates.

How physicians can create their future.

This article responds to the need for physicians to become proactive, using strategic planning to address changing conditions in the health care field. Strategic planning purposes are defined and a common process of strategic planning is presented. A case study analysis includes commentary on the need for planning, the context of planning in a larger system, process and procedure, a sample plan, benefits and actions to date, and future uses of the plan. Implications of this case of strategic planning for other physicians are discussed.

Erroneous mass spectrometer data caused by a faulty patient sampling tube: case report and laboratory study.

We report an error due to faulty sampling of gas for mass spectrometry by side-stream analysis that occurred during a general anesthetic for a surgical procedure. Two defects in the patient sampling tube were present. First, a crack was discovered in the polyvinylchloride tubing at the connection to the patient circuit. Second, secretions had accumulated in the end of the tubing that caused a partial obstruction to gas sampling. This combination promoted the contamination of respiratory gases sampled from the anesthesia circuit with entrained room air. This entrainment, however, occurred only during exhalation while ventilation was being controlled with a descending (during exhalation) bellows. The particular sampling error was reproduced and characterized in a mock circuit to simulate the sampling tube defects. It was determined that both a leak and a partial obstruction were necessary conditions for the sampling error to exist.

The influence of ketamine on regional brain glucose use.

The purpose of this study was to determine the effect of different doses of ketamine on cerebral function at the level of individual brain structures as reflected by glucose use. Rats received either 5 or 30 mg/kg ketamine intravenously as a loading dose, followed by an infusion to maintain a steady-state level of the drug. An additional group received 30 mg/kg as a single injection only, and was studied 20 min later, by which time they were recovering consciousness (withdrawal group). Regional brain energy metabolism was evaluated with [6-14C]glucose and quantitative autoradiography during a 5-min experimental period. A subhypnotic, steady-state dose (5 mg/kg) of ketamine caused a stimulation of glucose use in most brain areas, with an average increase of 20%. At the larger steady-state dose (30 mg/kg, which is sufficient to cause anesthesia), there was no significant effect on most brain regions; some sensory nuclei were depressed (inferior colliculus, -29%; cerebellar dentate nucleus, -18%; vestibular nucleus, -16%), but glucose use in the ventral posterior hippocampus was increased by 33%. In contrast, during withdrawal from a 30-mg/kg bolus, there was a stimulation of glucose use throughout the brain (21-78%), at a time when plasma ketamine levels were similar to the levels in the 5 mg/kg group. At each steady-state dose, as well as during withdrawal, ketamine caused a notable stimulation of glucose use by the hippocampus.

Comparison of the effects of volatile anesthetics on brain glucose metabolism in rats.

The objective of this investigation was to compare the effects of the commonly used volatile anesthetics on concentrations of plasma and cerebral glucose and cerebral intermediary metabolites. Fasted male Long-Evans rats were anesthetized with a volatile anesthetic and, after tracheostomy and paralysis, were mechanically ventilated. Each of three groups received one MAC concentration of anesthesia with halothane, enflurane, or isoflurane. At the end of 60-75 min of anesthesia, blood was sampled for arterial blood gas and plasma glucose analysis, and the brain was rapidly sampled and frozen for analysis of energy metabolites. Physiologic variables were maintained as follows: PaCO2 30-40 mmHg, pHa 7.20-7.40, PaO2 greater than 60 mmHg, MAP greater than 60 mmHg, and rectal temperature 37.5-38.5 degrees C. Mean plasma glucose concentrations in the three groups were as follows (muMol/ml +/- SEM): halothane, 7.45 /- .62; enflurane, 6.95 +/- .22; isoflurane, 10.11 +/- 1.00. Mean brain glucose concentrations in the three groups were (muMol/gm wet weight): halothane, 2.04 +/- .20; enflurane, 2.07 +/- .26; isoflurane, 3.04 +/- .31. Plasma and brain glucose levels were significantly increased in the isoflurane group compared to the other two groups (P less than .05) with no differences occurring in the brain/plasma glucose ratio among the three groups. No differences were present between groups in brain lactate, pyruvate, fructose diphosphate, malate, alpha-ketoglutarate, phosphocreatine, or adenine nucleotides. Thus, at one MAC concentration, major differences between volatile anesthetics on brain energy availability are not present, although isoflurane raised cerebral glucose levels.

Failure of glucose and branched-chain amino acids to normalize brain glucose use in portacaval shunted rats.

Several abnormalities in brain and plasma amino acid concentrations caused by portacaval shunting in rats return toward normal after 4 days of intravenous infusion with either glucose or glucose with branched-chain amino acids. To assess the effect of such treatment on brain energy metabolism, regional brain glucose use was measured using [14C]glucose and autoradiography, 5 weeks after portacaval shunting. In one experiment intravenous glucose or glucose with branched-chain amino acids was given for 4 days. In a separate experiment the treatment was given orally for 2 weeks, and in addition to glucose use, brain monoamines and amino acids were measured. No other food was provided; the rats had free access to water. Normally fed shunted rats and sham-operated rats served as controls. Both types of oral treatment lowered the high concentrations of tyrosine, phenylalanine, and glutamine in plasma and brain. Glucose without amino acids normalized brain tryptophan. Levels of brain norepinephrine, 5-hydroxytryptamine (serotonin), and 5-hydroxyindoleacetic acid were significantly raised after shunting. Treatment had no effect on norepinephrine but the glucose diet brought the indoles into the normal range. In contrast, neither intravenous nor oral treatment affected brain glucose use, which remained depressed by 25-30% in all brain areas examined.

Regional brain glucose utilization in rats during etomidate anesthesia.

The influence of etomidate on regional cerebral function as reflected by regional cerebral glucose utilization (rCMRGlc) was studied. Three experiments were performed. In the first, rats had both left femoral vessels cannulated and were placed in restraining cages. Etomidate was infused intravenously (12 mg/kg) at a rate of 6 mg X kg-1 X min-1. This large dose had a modest effect on blood pressure and heart rate, which could be explained by the elimination of stress in restrained rats, and no effect on body temperature, Pao2, PaCo2, or pH. A second group of rats were used to determine the effect of etomidate on the ratio of brain glucose to plasma glucose, which is necessary for calculating rCMRGlc. In the third experiment rCMRGlc was measured in unstressed rats. The rats were anesthetized with an intravenous dose of 1, 2, 6, or 12 mg/kg etomidate infused at a rate of 6 mg X kg-1 X min-1. Etomidate had a marked effect on glucose consumption in many, but not all, cerebral structures. The forebrain (telencephalon and diencephalon) was most affected (-25% to -35%) while the hindbrain was minimally affected. There was no demonstrable dose dependency; 1 mg/kg depressed rCMRGlc as much as 12 mg/kg. The pattern of rCMRGlc depression is in accord with the minimal effects observed on physiologic variables and similar to that caused by the steroid anesthetic Althesin, although the depression seen was not as severe. The pattern of metabolic depression produced by etomidate differs markedly from that produced by barbiturates, which affect all brain regions to a similar degree.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional cerebral glucose utilization during Althesin anesthesia.

The effect of Althesin, an anesthetic comprising two steroids, on regional cerebral function was determined by measurement of regional cerebral glucose utilization. Rats were anesthetized with an intravenous dose of 4, 8, or 20 mg total steroid/kg. These doses produced anesthesia for 12, 18, and 37 min, respectively. There were no physiologically significant effects of Althesin (20 mg/kg) on body temperature, blood pH, or blood gases. Blood pressure and heart rate decreased slightly after administration of Althesin. Althesin had a profound effect on glucose consumption in many, but not all, cerebral structures. The forebrain (especially cerebral cortex) was affected most, while the hindbrain was much less so or not at all. This pattern of functional depression is in accord with the minimal effects observed on physiologic variables. The effects of Althesin differ from those of other known anesthetics and suggest a unique mechanism. The possibility of action through naturally occurring steroid receptors is considered.

Portacaval anastomosis: brain and plasma metabolite abnormalities and the effect of nutritional therapy.

Rats with portacaval shunts were used as a model of hepatic encephalopathy and compared to shamoperated controls. First, the changes in intermediary metabolites and amino acids in blood and whole brain were characterized and found to be similar at 4 and 7 weeks after shunting. Second, the effects of nutritional therapy on selected metabolites and tryptophan transport into brain were assessed in rats 5 weeks after surgery. Ordinary food was removed and the rats were treated with glucose given either by mouth or intravenously, or intravenous glucose plus branched chain amino acids. Several abnormalities in plasma amino acid concentrations were reversed by treatment. The abnormally high brain uptake index of tryptophan, a consequence of portacaval shunting, was not lowered by any of the treatment regimens; it was even higher in the groups given glucose by mouth and glucose plus amino acids. Calculated competition for entry of tryptophan, phenylalanine, and tyrosine into brain was unchanged (glucose plus amino acids), or reduced (glucose alone). Brain glutamine content was brought to near normal by all treatments. Infusion of glucose plus branched chain amino acids normalized brain content of tryptophan, phenylalanine, and tyrosine, even though the brain uptake index of tryptophan was higher in this group. Thus, partial or complete reversal of several abnormalities found after portacaval shunting was achieved by removal of oral food and administration of glucose. The addition of branched chain amino acids to the glucose infusion restored brain content of three aromatic amino acids to near normal, by a mechanism which appeared to be unrelated to transport across the blood-brain barrier.

Ammonia selectively stimulates neutral amino acid transport across blood-brain barrier.

The response to increased blood NH4+ of three blood-brain barrier transport systems, which are altered after portacaval anastomosis, was studied. NH4+ acetate was infused for 4 or 22 h to raise blood and brain NH4+, and brain glutamine, to levels similar to those observed after portacaval anastomosis. While brain glutamine content was much higher (16-20 mumol/g) than normal (6 mumol/g) at both times, the permeability of the blood-brain barrier to the neutral amino acid [14C]tryptophan was greater only after 22 h of infusion. After discontinuing the infusion for 5 h, tryptophan transport returned to normal, whereas brain glutamine remained elevated (13 mumol/g). Thus there seemed to be no relationship between the rate of transport and glutamine content. The permeability to [14C]sucrose was unaltered, showing that the integrity of the blood-brain barrier was maintained. Other changes that are characteristic of portacaval shunting, such as decreased basic amino acid ([14C]lysine) and monocarboxylic acid (3-[14C]hydroxybutyrate) transport, were not reproduced by 22 h of infusion. The results demonstrated that the continued presence of NH4+ could be responsible for the change in at least one of the transport systems that are affected by portacaval shunting.

Regional cerebral glucose utilization in rats with portacaval anastomosis.

Regional cerebral glucose utilization was measured using [2-14C]glucose in rats with an end-to-side portacaval anastomosis. The experiments were conducted in two groups of rats 4 to 8 weeks after portacaval shunting was established. One group was paralyzed and given N2O:O2 (70:30), whereas the other was conscious, unstressed, and unaware of the experiment. In both groups the rate of glucose utilization was decreased in almost all brain structures by an average of 20% after portacaval shunting. The results showed definitively that cerebral energy metabolism was reduced at a time when there were no obvious neurological abnormalities.