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Proper placement of the tracheal tube requires confirmation, and the predominant method in addition to clinical signs is the presence of end-tidal carbon dioxide. Such is the importance of confirmation that novel methods may also have a place. We previously demonstrated using ex-vivo swine tissue a unique spectral reflectance characteristic of tracheal tissue that differs from oesophageal tissue. We hypothesised that this characteristic would be present in living swine tissue and human cadavers. Reflectance spectra in the range 500-650 nm were captured using a customised fibreoptic probe, compact spectrometer and white light source from both the trachea and the oesophagus in anesthetised living swine and in human cadavers. A tracheal detection algorithm using ratio comparisons of reflectance was developed. The existence of the unique tracheal characteristic in both in-vivo swine and cadaver models was confirmed (p < 0.0001 for all comparisons between tracheal and oesophageal tissue at all target wavelengths in both species). Furthermore, our proposed tracheal detection algorithm exhibited a 100% positive predictive value in both models. This has potential utility for incorporation into airway management devices.

Loss of a patent airway is a significant cause of prehospital death. Endotracheal intubation is the gold standard of care but has a high rate of failure and complications, making development of new devices vital. We previously showed that tracheal tissue has a unique spectral profile which could be utilized to confirm correct airway device placement. Therefore, the goals of this study were twofold: 1‐ to develop an airway obstruction model and 2‐ use that model to assess how airway compromise affects tissue reflectance. Female swine were anesthetized, intubated, and instrumented. Pigs were allowed to breathe spontaneously and underwent either slow‐ or rapid‐onset obstruction until a real‐time pulse oximeter reading of ≤50%. At baseline, 25%, 50%, 75%, and 100% obstruction, a fiber‐optic reflection probe was inserted into the trachea and esophagus to capture reflectance spectra. Both slow‐ and rapid‐onset obstruction significantly decreased arterial oxygen concentration (sO2) and increased partial pressure of CO2 (pCO2). The presence of the tracheal‐defining spectral profile was confirmed and remained consistent despite changes in sO2 and pCO2. This study validated a model of slow‐ and rapid‐airway obstruction that results in significant hypoxia and hypercapnia. This is valuable for future testing of airway device components that may improve airway management. Additionally, our data support the ability of spectral reflectance to differentiate between tracheal and esophageal tissues in the presence of a clinical condition that decreases oxygen saturation.

The spectral power of low frequency oscillations of systolic arterial pressure (SAP(LF)) has been used as a non-invasive surrogate of muscle sympathetic nerve activity (MSNA) in both experimental and clinical situations. For SAP(LF) to be used in this way, a relationship must exist between SAP(LF) and MSNA within individuals during sympathetic activation. Using progressive central hypovolaemia to induce sympathetic activation, we hypothesised that SAP(LF) would correlate with MSNA in all subjects. ECG, beat-by-beat arterial pressure and MSNA were recorded in humans (n = 20) during a progressive lower body negative pressure (LBNP) protocol designed to cause presyncope in all subjects. Arterial pressure oscillations were assessed in the low frequency (LF; 0.04-0.15 Hz) domain using a Fourier transform. For the entire group, SAP(LF), MSNA burst frequency, and total MSNA increased during LBNP. Values for coefficients of determination (r(2)) describing the linear associations of SAP(LF) with MSNA burst frequency and total MSNA were 0.73 and 0.84, but rose to 0.89 and 0.98 when curvilinear fits were used, indicating that the relationship is curvilinear rather than linear. Associations between SAP(LF) and MSNA within each individual subject, however, varied widely for both MSNA burst frequency and total MSNA, whether derived by linear (r(2) range, 1.7 × 10(-6) to 0.99) or polynomial (r(2) range, 0.09 to 1.0) regression analysis. Similar results were obtained when relationships between low frequency oscillations in diastolic arterial pressure and MSNA were evaluated. These results do not support the use of low frequency oscillations in arterial pressure as a non-invasive measure of sympathetic outflow for individual subjects during sympathetic activation.

Activation of sympathetic efferent traffic is essential to maintaining adequate arterial pressures during reductions of central blood volume. Sympathetic baroreflex gain may be reduced, and muscle sympathetic firing characteristics altered with head-up tilt just before presyncope in humans. Volume redistributions with lower body negative pressure (LBNP) are similar to those that occur during haemorrhage, but limited data exist describing arterial pressure–muscle sympathetic nerve activity (MSNA) relationships during intense LBNP. Responses similar to those that occur in presyncopal subjects during head-up tilt may signal the beginnings of cardiovascular decompensation associated with haemorrhage. We therefore tested the hypotheses that intense LBNP disrupts MSNA firing characteristics and leads to a dissociation between arterial pressure and sympathetic traffic prior to presyncope. In 17 healthy volunteers (12 males and 5 females), we recorded ECG, finger photoplethysmographic arterial pressure and MSNA. Subjects were exposed to 5 min LBNP stages until the onset of presyncope. The LBNP level eliciting presyncope was denoted as 100% tolerance, and then data were assessed relative to this normalised maximal tolerance by expressing LBNP levels as 80, 60, 40, 20 and 0% (baseline) of maximal tolerance. Data were analysed in both time and frequency domains, and cross-spectral analyses were performed to determine the coherence, transfer function and phase angle between diastolic arterial pressure (DAP) and MSNA. DAP–MSNA coherence increased progressively and significantly up to 80% maximal tolerance. Transfer functions were unchanged, but phase angle shifted from positive to negative with application of LBNP. Sympathetic bursts fused in 10 subjects during high levels of LBNP (burst fusing may reflect modulation of central mechanisms, an artefact arising from our use of a 0.1 s time constant for integrating filtered nerve activity, or a combination of both). On average, arterial pressures and MSNA decreased significantly the final 20 s before presyncope (n= 17), but of this group, MSNA increased in seven subjects. No linear relationship was observed between the magnitude of DAP and MSNA changes before presyncope (r= 0.12). We report three primary findings: (1) progressive LBNP (and presumed progressive arterial baroreceptor unloading) increases cross-spectral coherence between arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) withdrawal of MSNA is not a prerequisite for presyncope despite significant decreases of arterial pressure; and (3) reductions of venous return, probably induced by intense LBNP, disrupt MSNA firing characteristics that manifest as fused integrated bursts before the onset of presyncope. Although fusing of integrated sympathetic bursts may reflect a true physiological compensation to severe reductions of venous return, duplication of this finding utilizing shorter time constants for integration of the nerve signal is required.

Relatively large thermal gradients may exist during exposure of an animal to microwaves (MWs), particularly at high frequencies. Differences in thermal gradients within the body may lead to noticeable differences in the magnitude of cardiovascular changes resulting from MW exposure. This study compares the thermal distribution and cardiovascular effects of exposure to a single MW frequency with effects of simultaneous exposure to two frequencies. Ketamine-anesthetized male Sprague-Dawley rats (n = 58) were exposed individually to one of three conditions: 1-GHz, 10-GHz, or combined 1- and 10-GHz MWs at an equivalent whole-body specific absorption rate of 12 W/kg. The continuous-wave irradiation was conducted under far-field conditions with animals in E orientation (left lateral exposure, long axis parallel to the electric field) or in H orientation (left lateral exposure, long axis perpendicular to the electric field). Irradiation was started when colonic temperature was 37.5 degrees C and was continued until lethal temperatures were attained. Colonic, tympanic, left and right subcutaneous, and tail temperatures, and arterial blood pressure, heart rate, and respiratory rate were continuously recorded. In both E and H orientations, survival time (i.e., time from colonic temperature of 37.5 degrees C until death) was lowest in animals exposed at 1-GHz, intermediate in those exposed at 1- and 10-GHz combined, and greatest in the 10-GHz group (most differences statistically significant). At all sites (with the exception of right subcutaneous), temperature values in the 1- and 10-GHz combined group were between those of the single-frequency exposure groups in both E and H orientations. During irradiation, arterial blood pressure initially increased and then decreased until death. Heart rate increased throughout the exposure period. The general, overall patterns of these changes were similar in all groups. The results indicate that no unusual physiological responses occur during multi-frequency MW exposure, when compared with results of single-frequency exposure. Bioelectromagnetics 21:159-166, 2000. Published 2000 Wiley-Liss, Inc.

We investigated the thermal distribution and cardiovascular effects produced by sustained exposure of rats to 94 GHz radio-frequency electromagnetic radiation (RFR). Sixteen ketamine-anesthetized Sprague-Dawley rats were exposed individually at a power density of 75 mW/cm2 under far-field conditions in E orientation. Irradiation began when colonic temperature was 37 degrees C and continued until death. Large, immediate increases in subcutaneous temperature on the irradiated side were accompanied by more moderate, delayed increases in colonic temperature. These body-temperature responses were similar to previous results obtained during 35 GHz RFR exposure. During irradiation, arterial blood pressure initially increased and then precipitously decreased until death. The heart rate increased throughout the exposure period. When comparing the results of these 94 GHz exposures with those in previous studies of lower RFR frequencies, it appears that the patterns of heart-rate and blood-pressure changes that occur before death are similar. We conclude that exposure to 94 GHz RFR produces extreme peripheral heating without similar levels of core heating and that this pattern of heat deposition is sufficient to produce circulatory failure and subsequent death.

Nonuniform heating may result from microwave (MW) irradiation of tissues and is therefore important to investigate in terms of health and safety issues. Hypothalamic (Thyp), cortical (Tctx), tympanic (Tty), and rectal (Tre) temperatures were measured in rats exposed in the far field, k-polarization (i.e., head pointed toward the transmitter horn and E-field in vertical direction) to two power densities of 2.06 GHz irradiation. The high-power density (HPM) was 1700 mW/cm2 [specific absorption rate (SAR): hypothalamus 1224 W/kg; cortex 493 W/kg]; the low-power density (LPM) was 170 mW/cm2 (SAR: hypothalamus 122.4 W/kg; cortex 49.3 W/kg). The increase (rate-of-rise, in degrees C/s) in Thyp was significantly greater than those in Tctx or Tre when rats were exposed to HPM. LPM produced more homogeneous heating. Quantitatively similar results were observed whether rats were implanted with probes in two brain sites or a single probe in one or the other of the two sites. The qualitative difference between regional brain heating was maintained during unrestrained exposure to HPM in the h-polarization (i.e., body parallel to magnetic field). To compare the temperature changes during MW irradiation with those produced by other modalities of heating, rats were immersed in warm water (44 degrees C, WWI); exposed to a warm ambient environment (50 degrees C, WSED); or exercised on a treadmill (17 m/min 8% grade) in a warm ambient environment (35 degrees C, WEX). WWI produced uniform heating in the regions measured. Similar rates-of-rise occurred among regions following WSED or WEX, thus maintaining the pre-existing gradient between Thyp and Tctx These data indicate that HPM produced a 2-2.5-fold difference in the rate-of-heating within brain regions that were separated by only a few millimeters. In contrast, more homogeneous heating was recorded during LPM or nonmicrowave modalities of heating.

Exposure to fast-rise-time ultra-wideband (UWB) electromagnetic pulses has been postulated to result in effects on biological tissue (including the cardiovascular system). In the current study, 10 anesthetized Sprague-Dawley rats were exposed to pulses produced by a Sandia UWB pulse generator (average values of exposures over three different pulse repetition rates: rise time, 174-218 ps; peak E field, 87-104 kV/m; pulse duration, 0.97-0.99 ns). Exposures to 50, 500 and 1000 pulses/s resulted in no significant changes in heart rate or mean arterial blood pressure measured every 30 s during 2 min of exposure and for 2 min after the exposure. The results suggest that acute UWB whole-body exposure under these conditions does not have an immediate detrimental effect on these cardiovascular system variables in anesthetized rats.

1. The purpose of this study was to examine effects of the beta(1)-adrenoreceptor antagonist esmolol (infused at 2 or 4 mg kg-1 body wt min-1) on heart rate, blood pressure, respiratory rate, localized body temperature changes, survival times, and lethal body temperatures that occur during the exposure of anaesthetized rats to 35 GHz microwaves. 2. Forty Sprague-Dawley rats, anaesthetized with ketamine, were exposed to 35 GHz microwaves at a level that resulted in heating and death. During irradiation, a continuous increase in heart rate and a biphasic response in blood pressure (initial increase followed by a decrease) were observed in all groups of animals. 3. Esmolol caused a significant dose-dependent decrease in blood pressure, relative to saline-treated animals, but only a small attenuation of the heat-induced rise in heart rate. In experiments in which esmolol was infused and microwave exposure was continued until death, drug-treated animals survived for significantly shorter periods and died at significantly lower body temperatures. The change in survival may have been related to the lower blood pressure due to esmolol treatment.