Effectiveness of a health course at influencing preservice teachers' attitudes toward teaching health.

Research has shown that effective school health education depends on the effectiveness of health training for prospective teachers. This research tested the effectiveness of a university course in preparing preservice teachers in the area of school health. Education majors enrolled in the course "Drug and Health Issues for Educators" at Montana State University were administered a pretest/posttest questionnaire at the beginning and end of spring semester 2000 to gather data for testing five hypotheses. Analyses were conducted on 119-paired samples. The course appeared effective at influencing how a preservice teacher values health education in the school, their intentions to include and confidence in including health in their teaching, and their ability to provide a student with information on personal health issues.

Impact of hypoxemia on the performance of cerebral oximeter in volunteer subjects.

Adverse neurological events during hypoxic episodes in high-risk patients or in patients not thought to be at risk while undergoing procedures increase morbidity and mortality. The ability to reliably monitor cerebral oxygenation could serve as an indicator for the need of therapeutic intervention and it's overall effect. This study was designed to verify the reliability of the only commercially available continuous noninvasive monitor, the INVOS 3100 (Somanetics Corp., Troy, MI), in subjects with varying levels of hypoxemia. Six adult volunteer subjects were enrolled. After placement of electrocardiogram (EKG), noninvasive blood pressure (NIBP), pulse oximeter (SpO2), cerebral oximeter (rSO2), a 20 g radial artery catheter, and a 4 F oximetric jugular bulb catheter, the subjects were given hypoxic mixtures to breathe to varying levels of desaturation. Arterial and mixed venous blood was drawn for blood-gas analysis at each level of O2 saturation. The cerebral hemoglobin saturation value from the cerebral oximeter was compared to the combined brain saturation using the formula: estimated field saturation between the light source and the detector (fSO2) = 0.25 x the arterial oxygen saturation (SaO2) + 0.75 x the jugular bulb venous oxygen saturation (SjvO2), (fSO2 = 0.25 SaO2 + 0.75 SjvO2). Statistical analysis demonstrated a correlation of 0.67 between rSO2 and fSO2 and a bias of -3.1% with a precision of 12.1%. Minimal bias of 0.38% and precision of 6.22% were calculated for transitional error. We concluded from the study that rSO2 may serve as a reliable indicator of changes in brain oxygenation induced by hypoxemia.

Cause of metabolic acidosis in prolonged surgery.

OBJECTIVE: The intraoperative development of metabolic acidosis is frequently attributed to hypovolemia, tissue hypoperfusion, and lactic acidosis. In this study, dilutional acidosis was evaluated as a possible mechanism for the routine development of intraoperative acidosis in noncardiac, nonvascular surgery patients. DESIGN: Prospective, observational study. SETTING: University-affiliated Veteran's Affairs Medical Center and a staff model, health maintenance organization hospital. PATIENTS: Twelve patients undergoing prolonged surgical procedures expected to last > or = 4 hrs were enrolled in the study. INTERVENTIONS: Perioperative management was based on the judgment of the attending anesthesiologist and surgeon without knowledge of the study's intent. MEASUREMENTS AND MAIN RESULTS: Arterial blood gas parameters, serum electrolytes, and urine electrolytes were measured pre- and postoperatively. Pulmonary artery catheters were placed for hemodynamic measurement and oxygen delivery calculations. Plasma volume was measured both pre- and postoperatively, using the Evans blue dye dilution technique. Although significant changes in lactate level (1.1 +/- 0.6-1.8 +/- 1.0) occurred, the change was not large enough to explain the degree of change in base excess (0.8 +/- 2.3 to -2.7 +/- 2.9). Chloride levels significantly increased (106 +/- 3-110 +/- 5) with a correlation (r2 = .92; p < .0001) between the degree of change in chloride and the degree of change in base excess. Plasma volume did not change. Furthermore, a correlation between the volume of normal saline administered and the change in base excess was found (r2 = .86; p < .0001), although no correlation was found with Ringer's lactate solution. An even stronger correlation was noted when the total chloride amount administered was compared with the change in base excess (r2 = .93; p < .0001). CONCLUSIONS: In this patient population, a common source of increasing base deficit is related to chloride administration. The largest source of chloride is usually normal saline. Classically, dilutional acidosis would explain the predominance of this acidotic change; however, no increase in plasma volume occurred. The absence of plasma volume change would suggest that the mechanism postulated to result in dilutional acidosis is incomplete. The common treatment of administering more fluid for intraoperative acidosis may be inappropriate, may have caused the acidosis, and may further exacerbate the acidosis. Chloride levels should be assessed whenever a metabolic acidosis is seen perioperatively.