Agreement between an ingestible telemetric sensor system and a mercury thermometer before and after linear regression correction.

OBJECTIVES: To evaluate the use of the CorTemp ingestible sensor system to monitor athletes in the prevention of thermal injuries, 3 objectives were established: (1) to determine the agreement between the system and a mercury thermometer and quantify the effect of exceeding the recommended yearly manufacturer calibration, (2) to establish the effect of individual sensor correction on agreement, and (3) to determine the quantity of data required for effective correction. DESIGN: Validation study. PARTICIPANTS: Ninety-four ingestible sensors. INTERVENTIONS: (1) Five comparisons were made between each sensor and a mercury thermometer across the range of 33 to 41 degrees C. This was performed immediately, and 14 to 18 months, after factory calibration. (2) Linear regression equations were created and used to correct sensor readings at approximately 37 degrees C; the corrected value was compared with the mercury thermometer. (3) Linear regression equations were created for each sensor using 2 to 5 data points. MAIN OUTCOME MEASURES: Systematic bias and random error (95%). RESULTS: (1) Systematic bias + or - random error (95%) was 0.73% + or - 0.23% ( approximately 0.27 + or - 0.09 degrees C) and 0.54% + or - 0.28% ( approximately 0.22 + or - 0.11 degrees C) immediately and 14 to 18 months post factory calibration, respectively. (2) Regression correction improved agreement through reductions in systematic bias. (3) Individualized equations using a minimum of 3 comparisons were required to reduce agreement to + or - 0.10 degrees C; the use of 5 comparisons minimized the number of readings exceeding + or - 0.10 degrees C. CONCLUSIONS: (1) The CorTemp system inflates temperature measurements compared with a mercury thermometer. (2) Individual sensor calibration is warranted. (3) Correction equations should use a minimum of 3, preferably 5, comparisons. After regression correction, the system displays satisfactory accuracy for preventative monitoring.

Diurnal normobaric moderate hypoxia raises serum erythropoietin concentration but does not stimulate accelerated erythrocyte production.

This study was performed to examine the effect of diurnal normobaric hypoxia on hematological parameters. Eleven healthy male volunteers were randomly selected to be in either the hypoxic group (n=6) or the control group (n=5). The hypoxic group was exposed to 8 h of normobaric hypoxia in hypoxic tent systems that elicited a target peripheral O(2) saturation of 81+/-2% on three consecutive days. The control group spent three consecutive 8-h days in modified tent systems that delivered normoxic air into the tent. Venous blood samples were collected before the exposure (days -5, 0), after each day of the exposure (days 1, 2, 3), and for 3 weeks after the exposure (days 7, 10, 13, 17, 24). Serum erythropoietin concentration significantly increased from 9.1+/-3.3 U.L(-1) to 30.7+/-8.6 U.L(-1) in the hypoxic group. Although there were significant increases in hematocrit (4%), hemoglobin concentration (5%), red blood cell count (4%) on day 7 in the hypoxic group, these observations were likely due to dehydration or biological variation over time. There was no significant change in early erythropoietic markers (reticulocyte counts or serum ferritin concentration), which provided inconclusive evidence of accelerated erythroid differentiation and proliferation. The results suggest that the degree of hypoxia was sufficient to stimulate increased erythropoietin production and release. However, the duration of hypoxic exposure was insufficient to propagate the erythropoietic cascade.

Effect of five nights of normobaric hypoxia on cardiovascular responses to acute isocapnic hypoxia in humans: relationship to ventilatory chemosensitivity.

The aim of this study was to elucidate (1) the cardiovascular responses to acute isocapnic hypoxia stimuli following five nights of normobaric poikilocapnic hypoxia, and (2) whether the changes in the cardiovascular responses to hypoxia are correlated to the change in acute hypoxic ventilatory (AHVR) chemosensitivity. Twelve male subjects [26.6 +/- 4.1 (SD) years] slept 8-9 h day(-1) overnight for five consecutive days at a simulated altitude of 4300 m (FiO2 = approximately 13.8%). Using the technique of dynamic end-tidal forcing, the AHVR was assessed twice, prior to and immediately after the hypoxic exposure. During each AHVR test, mean arterial blood pressure (MAP) and heart rate (HR) were measured continuously using finger photoplethysmography and an ECG monitor, respectively. Immediately following the exposure, AHVR and MAP sensitivities were increased by 1.80 +/- 1.30 l min(-1) %(-1) (p < 0.01) and 0.69 +/- 0.40 mmHg %(-1) (p < 0.05), respectively, and there were significant correlations between the increases in the AHVR and MAP sensitivities (r = 0.67; p < 0.05). In summary, following five nights of normobaric hypoxia, there is an enhanced MAP response to hypoxic stimuli. The relationship between the enhanced AHVR and MAP sensitivity raises the possibility of a common pathway in the regulation of peripheral chemosensitivity and MAP responses during periods of isocapnic hypoxia.

The effects of systemic hypoxia on colon anastomotic healing: an animal model.

PURPOSE: Acute postoperative systemic hypoxia occurs frequently in the clinical setting following intestinal resection, as a result of complications such as pneumonia, pulmonary edema, or the acute respiratory distress syndrome. Although it is well established that oxygen is essential for metabolism in general and intestinal anastomotic healing, the mechanisms by which systemic hypoxia affect this process are not clear. The purpose of this study was to establish an animal model to simulate acute systemic hypoxia and to examine the effects on anastomotic healing. We investigated the hypothesis that systemic hypoxia impairs anastomotic healing in the colon by disrupting revascularization via changes in the expression of two putative angiogenic factors: inducible nitric oxide synthase and vascular endothelial growth factor. METHODS: Phase I: Juvenile male Sprague-Dawley rats underwent carotid artery cannulation. In a controlled environment the FiO2 was incrementally decreased from 21 to 9 percent and the resultant PaO2 measured. Phase II: Animals underwent colonic transection with immediate reanastomosis and were placed in either a normoxic (FiO2 21 percent) or hypoxic (FiO2 11 percent) environment for seven days. Perianastomotic in vivo tissue oxygen saturation was measured before segmental colon resection in each of the animals and at seven days before measurement of anastomotic bursting pressure. Perianastomotic tissue samples were assessed by Western blot assay for the expression of vascular endothelial growth factor and inducible nitric oxide synthase protein. Sections from each tissue sample were taken and evaluated by a pathologist blinded to treatment group for determination of anastomotic healing score. RESULTS: Phase I: Incrementally decreasing the FiO2 resulted in a progressive decrease in PaO2 (r2 = 0.77). Phase II: Animals maintained in a hypoxic environment had a significant decrease in tissue oxygen saturation (73 +/- 9 percent vs. 94 +/- 3 percent; P < 0.0001) and anastomotic bursting pressure (118 +/- 18 mmHg vs. 207 +/- 30 mmHg; P < 0.0001) compared with normoxic controls. Systemic hypoxia induced a significant increase, when compared with normoxic controls, in vascular endothelial growth factor (247.1 +/- 9.5 vs. 142.2 +/- 10.6; P < 0.0001) and inducible nitric oxide synthase (259.6 +/- 21.1 vs. 120.2 +/- 10.9; P < 0.0001) protein expression and led to a significant decrease in the overall wound-healing score. CONCLUSION: This study validates a new animal model to study the effects of acute systemic hypoxia on colonic anastomotic healing. In this model, systemic hypoxia directly translated into local tissue hypoxia, and anastomotic healing was impaired. Contrary to our original hypothesis, hypoxia led to a significant increase in vascular endothelial growth factor and inducible nitric oxide synthase protein expression at the colonic anastomotic site. Impairment in anastomotic integrity despite upregulation of these angiogenic factors could be a result of the inability of wounded tissue to respond to vascular endothelial growth factor and inducible nitric oxide synthase or alternatively, hypoxia may adversely affect collagen synthesis and deposition directly.

Protocol to measure acute cerebrovascular and ventilatory responses to isocapnic hypoxia in humans.

This study describes a protocol to determine acute cerebrovascular and ventilatory (AHVR) responses to hypoxia. Thirteen subjects undertook a protocol twice, 5 days apart. The protocol started with 8 min of eucapnic euoxia (end-tidal P(CO2) (PET(CO2)= 1.5 Torr) above rest; end-tidal P(O2) (PET(O2)) = 88 Torr) followed by six descending 90 s hypoxic steps (PET(O2) = 75.2, 64.0, 57.0, 52.0, 48.2, 45.0 Torr). Then, PET(O2) was elevated to 300 Torr for 10 min while PET(O2) remained at eucapnia (5 min) then raised by 7.5 Torr (5 min). Peak blood flow velocity in the middle cerebral artery (MCA) and regional cerebral oxygen saturation (Sr(O2)) were measured with transcranial Doppler ultrasound and near-infrared spectroscopy, respectively, and indices of acute hypoxic sensitivity were calculated (AHR(CBF) and AHRSr(O2)). Values for AHR(CBF), AHRSr(O2) and AHVR were 0.43 cm s(-1) % desaturation(-1), 0.80% % desaturation(-1) and 1.24l min(-1) % desaturation(-1), respectively. Coefficients of variation for AHR(CBF), AHRSr(O2) and AHVR were small (range = 8.0-15.2%). This protocol appears suitable to quantify cerebrovascular and ventilatory responses to acute isocapnic hypoxia.

Validation of pulse oximetry during progressive normobaric hypoxia utilizing a portable chamber.

Validation of pulse oximetry in commercially available normobaric hypoxic chambers (NHC) has not been previously reported. The present study examined the validity of pulse oximetry (SpO2) against direct measurements of arterial oxygen saturation (SaO2) via co-oximetry (AVOXimeter 4000) in 13 young adults age 21.3 +/- 0.6 years. Over a period of 2.5 hrs, the inspired fraction of oxygen inside a NHC (Hypoxico, Inc.) was progressively reduced from 20.9% to 11.5%. Measurements of SaO2 at baseline and at 15, 30, 60, 90, 120, and 150 min during the hypoxic exposures were compared with SpO2 estimates of oxygen saturation (Nellcor 295) using reflectance (RS-10, temporal) and transmission (D-25, finger) sensors. Regression analysis and methods for assessing agreement (bias, b; precision, p) of SaO2 with SpO2 were similar (R2 = 0.92, 0.89; b = 0.016, -0.47; p = 2.47, 3.03; RS-10 and D-25, respectively). When SaO2 < 85%, RS-10 had greater validity than D-25 (R2 = 0.73, 0.56; b = 1.38, 1.13; p = 2.72, 4.34; RS-10 and D-25, respectively). In light of these findings, caution should be exercised when monitoring individuals with pulse oximetry during desaturation episodes below 85%. When employing frequent NHC exposures, a priori validation of SpO2 utilized to assess blood oxygen status appears warranted.

Effects of five consecutive nocturnal hypoxic exposures on the cerebrovascular responses to acute hypoxia and hypercapnia in humans.

The effects of discontinuous hypoxia on cerebrovascular regulation in humans are unknown. We hypothesized that five nocturnal hypoxic exposures (8 h/day) at a simulated altitude of 4,300 m (inspired O2 fraction = approximately 13.8%) would elicit cerebrovascular responses that are similar to those that have been reported during chronic altitude exposures. Twelve male subjects (26.6 +/- 4.1 yr, mean +/- SD) volunteered for this study. The technique of end-tidal forcing was used to examine cerebral blood flow (CBF) and regional cerebral O2 saturation (Sr(O2)) responses to acute variations in O2 and CO2 twice before, immediately after, and 5 days after the overnight hypoxic exposures. Transcranial Doppler ultrasound was used to assess CBF, and near-infrared spectroscopy was used to assess Sr(O2). Throughout the nocturnal hypoxic exposures, end-tidal Pco2 decreased (P < 0.001) whereas arterial O2 saturation increased (P < 0.001) compared with overnight normoxic control measurements. Symptoms associated with altitude illness were significantly greater than control values on the first night (P < 0.001) and second night (P < 0.01) of nocturnal hypoxia. Immediately after the nocturnal hypoxic intervention, the sensitivity of CBF to acute variations in O2 and CO2 increased 116% (P < 0.01) and 33% (P < 0.05), respectively, compared with control values. Sr(O2) was highly correlated with arterial O2 saturation (R2 = 0.94 +/- 0.04). These results show that discontinuous hypoxia elicits increases in the sensitivity of CBF to acute variations in O2 and CO2, which are similar to those observed during chronic hypoxia.

Effects of five nights of normobaric hypoxia on the ventilatory responses to acute hypoxia and hypercapnia.

This study examined the effects of five nights of normobaric hypoxia on ventilatory responses to acute isocapnic hypoxia (AHVR) and hyperoxic hypercapnia (AHCVR). Twelve male subjects (26.6 +/- 4.1 years, standard deviation (S.D.)) slept 8-9 h per day overnight for 5 consecutive days at a simulated altitude of 4,300 m (FiO2= approximately 13.8%). Using the technique of dynamic end-tidal forcing, the AHVR and AHCVR were assessed twice prior to, immediately after, and 5 days following the hypoxic exposure. Immediately following the exposure, AHVR was increased by 1.6 +/- 1.3 L min(-1) %(-1) (P<0.01) when compared with control values. Likewise, after the exposure, ventilation in hyperoxia was increased (P<0.001) and was associated with both an increase in the slope (1.5 +/- 1.4 L min(-1) Torr(-1); P<0.05) and decrease in the intercept (-2.7 +/- 4.3 Torr; P<0.05) of the AHCVR. These results show that five nights of hypoxia can elicit similar perturbations, in both AHVR and AHCVR, as have been reported during more chronic altitude exposures.