The esophageal detector device: a rapid and accurate method for assessing tracheal versus esophageal intubation in a porcine model.

STUDY OBJECTIVES: To assess time and accuracy of the esophageal detector device (EDD), disposable end-tidal CO2 monitor (ETCO2), and standard clinical methods for detection of endotracheal tube placement. DESIGN: Prospective, randomized, single-blinded, controlled laboratory investigation. METHODS: Thirty airway managers (physicians, nurse anesthetists, and paramedics) used one pig (Sus scrofa) as the intubated, respiratory depressed/arrest model. INTERVENTIONS: Part 1: A standard 7.5-mm endotracheal tube was placed in either the esophagus or the trachea of the anesthetized swine. Anatomic location was verified by bronchoscopy. Airway managers blinded to the endotracheal tube location were assigned randomly to identify tube position by one of three methods (EDD, ETCO2, or clinical methods). Speed and accuracy of the assessment were recorded. Part 2: A second identical tube was placed, so that both the esophagus and the trachea were intubated; then, the esophageal tube was bag-ventilated for one minute. Each blinded airway manager, using only the EDD, determined placement site of both tubes. RESULTS: Part 1: Mean time to determine tube placement for group A (EDD) was 13.8 seconds; group B (ETCO2), 31.5 seconds; and group C (clinical methods), 39 seconds. Comparison by analysis of variance yielded a value of P less than .001. Both groups A and B were 100% accurate, whereas 30% of the subjects from group C mistakenly assessed an esophageal tube as in the trachea. Part 2: The EDD remained 100% sensitive and specific despite prior ventilation of the esophageal tube. CONCLUSION: In this porcine model, the EDD and ETCO2 were more accurate than clinical methods in determining endotracheal tube placement. The EDD demonstrated a significant time advantage over both ETCO2 and clinical methods. Prior ventilation of the esophageal tube does not interfere with the accuracy of the EDD.

Altitude symptomatology and mood states during a climb to 3,630 meters.

Ascents to altitudes above 3,050 m have been shown to cause adverse changes in symptoms and moods. The severity of these changes may depend not only on the altitude and rate of climb, but also on the length of stay and the effort expended to reach the desired altitude. In order to better understand how these factors influence symptom and mood changes during a climb, this study systematically assessed symptoms and moods during an ascent to 3,630 m. Self-rated symptoms and moods were determined in seven male volunteers over a period of 7 days (d) during a climb to 3,630 m of Mount Sanford, AK. The subjects were tested five times--twice at 2,225 m, then at 2,530, 3,080, and 3,630 m. Symptoms and moods were assessed with the Environmental Symptoms Questionnaire (ESQ) and the Profile of Mood States (POMS), respectively. Seven symptom factors and two mood factors were found to be adversely affected over time by the changes in altitude. More specifically, the subjects experienced more respiratory acute mountain sickness (AMS), exertion stress, and muscular discomfort and they were also colder, less alert, less vigorous, and more fatigued at higher elevations. These changes occurred primarily at 3,630 m and most also occurred at 3,080 m.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon monoxide poisoning at high altitudes.

Carbon monoxide (CO) poisoning is a common problem encountered in a wide variety of settings, including both suicide attempts and accidental exposures. Fatal CO exposure occurred in two young, healthy mountain climbers who succumbed to fumes generated by a small cook stove in the enclosed space of their tent at 14,200 feet on Mount McKinley. There is the potential for confusing mild to moderate CO poisoning with the signs and symptoms of altitude illness. Physicians who deal with wilderness and environmental emergencies should be aware of this serious hazard.

Dexamethasone for prevention and treatment of acute mountain sickness.

We wished to determine in a field study the effectiveness of dexamethasone for prevention and treatment of acute mountain sickness (AMS). Prevention Trial: We transported 15 subjects from sea level to 4,400 m (PB = 400 mm Hg) on Denali (Mt. McKinley) by means of a 1-h helicopter flight. In a randomized, double-blind fashion we gave eight subjects a placebo and seven subjects 2 mg dexamethasone orally every 6 h, starting 1 h before take-off. The entire placebo group and five of the dexamethasone group developed AMS within 5 h, and became progressively more ill until 12 h when the trial was terminated. We concluded that 2 mg of dexamethasone every 6 h did not prevent AMS in active soldiers rapidly transported to high altitude. Treatment Trial: We treated 11 of those with moderate to severe AMS (symptom score 4.5 +/- 0.7, range 3 to 11) with 4 mg of dexamethasone every 6 h orally or intramuscularly for 24 h. All were markedly improved at 12 h (symptom score 1.0 +/- 0.3, p less than 0.001, range 0 to 3), but symptoms increased after the drug was discontinued at 24 h (symptom score = 2.4 +/- 0.5). We conclude that dexamethasone in a dosage of 4 mg PO or IM every 6 h is an effective treatment for AMS, but that illness may recur with abrupt discontinuation of the drug.

Lack of efficacy of naloxone in a fixed-volume hemorrhage model.

Animal studies using a reservoir model of hemorrhagic shock have shown the narcotic antagonist naloxone to be of value in reversing the hemodynamic effects of severe hemorrhage. We conducted a study to evaluate the ability of naloxone to limit the deleterious effects of a fixed-volume hemorrhage. Fifteen mongrel dogs were bled 50% of their estimated blood volumes during one hour. This was followed by a one-hour stabilization period; reinfusion during a 30-minute period; and finally, an additional one-hour monitoring period. Eight dogs received 2 mg/kg IV naloxone 30 minutes prior to hemorrhage and 2 mg/kg/hr for the duration of the study. Seven control dogs received an equivalent volume of saline without naloxone. Pulmonary capillary wedge pressure, central venous pressure, cardiac output, heart rate, blood pressure, arterial and mixed venous blood gases, and serum lactate were measured at 19 intervals throughout the study period. Mean arterial pressure, cardiac index, and systemic vascular resistance were calculated for each sampling period. With the exception of serum lactates, which were higher in the naloxone group, there were no significant differences between the groups in the mean values calculated for each sampling interval (P less than .05, two-tailed independent t test). Furthermore, the changes in hemodynamic parameters observed during the hemorrhage, stabilization, reinfusion, and monitoring periods were not significantly different. We conclude that in this fixed-volume hemorrhage model, naloxone does not prevent or reverse hemodynamic deterioration.

Phenytoin and acute mountain sickness on Mount Everest.

Twenty-one climbers who were members of the American Ultima Thule Everest Expedition participated in a double-blind, randomized clinical trial of phenytoin prophylaxis for acute mountain sickness during the approach to the northeast ridge of Mount Everest. The study was carried out between Beijing and base camp at 16,800 feet. Time spent ascending from Beijing to base camp averaged 13 days. High-altitude symptom questionnaires were filled out beginning in Lhasa at 11,800 feet and in Xigatse at 12,000 feet, in Xegar at 14,000 feet, and at base camp. Computer analysis of the questionnaire answers performed by an impartial analyst revealed that climbers who took phenytoin were less likely to have headaches at base camp. No other statistically significant differences were observed, but the power of the sample size was low.

Transcutaneous oxygen tension measurements during graded hemorrhage and reinfusion.

Measurement of transcutaneous oxygen tension (PtCO2) has been suggested as a useful monitoring tool in the hypovolemic patient. Our study was undertaken to evaluate changes in PtCO2 that occur during graded hemorrhage and reinfusion, and to compare PtCO2 values to standard cardiorespiratory and biochemical parameters during hypovolemia. Seven mongrel dogs were bled 50% of their estimated blood volume (44 mL/kg) over one hour. This was followed by a one-hour monitoring period, a 30-minute reinfusion period, and an additional one-hour monitoring period. Pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), cardiac output (CO), mean arterial pressure (MAP), mixed venous oxygen tension (MvO2), arterial blood gases, and PtCO2 were measured serially throughout the study period. Cardiac index (CI), peripheral vascular resistance (PVR), O2 consumption, delivery, and percentage of extraction were calculated for each sampling period. A statistically significant fall in CI, MvO2 and PCWP occurred following the first 10% of blood loss; PtCO2 and MAP fell significantly after 20% hemorrhage; CVP fell after 30% hemorrhage. PtCO2 rose significantly after the first 10% of reinfusion, and it continued to rise during the entire reinfusion period, as did MvO2, CO, MAP, CVP, and PCWP. In contrast to the other measured variables, the elevations in PtCO2, and MvO2 were more pronounced early in the reinfusion period. During postreinfusion monitoring, PtCO2, MvO2, CO, and PCWP fell significantly despite maintenance of prehemorrhage MAP and CVP. Overall PtCO2 correlated well with MvO2 and the O2 extraction ratio, and to a lesser extent with CI, MAP, and O2 delivery.(ABSTRACT TRUNCATED AT 250 WORDS)