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Biomedical subjects

W J Mills

Publications and source records attributed to W J Mills.

14 recordsLinked to original sources
PubMed1992

Field care of the hypothermic patient.

The world literature of sports medicine and mountain medicine has been much concerned with early recognition, emergency on-site care, and rescue transportation of the cold-injured patient. Considerable problems exist for the initial rescuer and first responder, particularly if that person is alone. Thoughts of initial approach and care, are presented, particularly for the first, often untrained in-field rescue responders. The site of rescue and field variables found at that site are presented. Methods in aiding field assessment of the state of hypothermia are listed, particularly the evaluation of signs and symptoms of the victim. Early care and avoidance of further heat loss is discussed. The consideration for the rescuer (and victim) is to 'think heat'. Basic principles of care are stated, particularly for care of the victim 'with no apparent signs of life'.

Body Temperature Regulation↗
PubMed1991

Renal carbonic anhydrase inhibition reduces high altitude sleep periodic breathing.

The efficacy of carbonic anhydrase (CA) inhibitors in amelioration of periodic breathing during sleep at high altitude is not fully understood. Although CA is present in a number of tissues, we hypothesized that selective renal CA inhibition without physiologically important inhibition of other tissue CA, may be sufficient alone by its generation of a mild metabolic acidosis to stimulate ventilation and prevent periodic breathing. We studied benzolamide (3 mg/kg), a selective inhibitor of renal CA, in 4 climbers on ventilation and ventilatory responses at sea level and on arterial O2 saturation (SaO2%) and periodic breathing during sleep at altitude. At sea level, ventilation increased and PaO2 rose accompanied by a mild metabolic acidosis. The isocapnic hypoxic ventilatory response was unchanged but the hyperoxic hypercapnic ventilatory response rose 40%. At high altitude (4400 m), daytime SaO2% improved from 81 to 85 and venous plasma HCO3- fell from 18.9 to 14.8 mM. During sleep, mean SaO2% rose from 76 to 80 and periodic breathing decreased 75%. We conclude that metabolic acidosis occurring with all CA inhibitors is one of the major stimulant actions of these drugs on ventilation while awake and during sleep at high altitude.

Acidosis↗
PubMed1988

Abnormal control of ventilation in high-altitude pulmonary edema.

We wished to determine the role of hypoxic chemosensitivity in high-altitude pulmonary edema (HAPE) by studying persons when ill and upon recovery. We studied seven males with HAPE and seventeen controls at 4,400 m on Mt. McKinley. We measured ventilatory responses to both O2 breathing and progressive poikilocapnic hypoxia. Hypoxic ventilatory response (HVR) was described by the slope relating minute ventilation to percent arterial O2 saturation (delta VE/delta SaO2%). HAPE subjects were quite hypoxemic (SaO2% 59 +/- 6 vs. 85 +/- 1, P less than 0.01) and showed a high-frequency, low-tidal-volume pattern of breathing. O2 decreased ventilation in controls (-20%, P less than 0.01) but not in HAPE subjects. The HAPE group had low HVR values (0.15 +/- 0.07 vs. 0.54 +/- 0.08, P less than 0.01), although six controls had values in the same range. The three HAPE subjects with the lowest HVR values were the most hypoxemic and had a paradoxical increase in ventilation when breathing O2. We conclude that a low HVR plays a permissive rather than causative role in the pathogenesis of HAPE and that the combination of extreme hypoxemia and low HVR may result in hypoxic depression of ventilation.

Adult↗
PubMed1988

The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.

High-altitude pulmonary edema (HAPE), a severe form of altitude illness that can occur in young healthy individuals, is a noncardiogenic form of edema that is associated with high concentrations of proteins and cells in bronchoalveolar lavage (BAL) fluid (Schoene et al., J. Am. Med. Assoc. 256: 63-69, 1986). We hypothesized that acute mountain sickness (AMS) in which gas exchange is impaired to a milder degree is a precursor to HAPE. We therefore performed BAL with 0.89% NaCl by fiberoptic bronchoscopy in eight subjects at 4,400 m (barometric pressure = 440 Torr) on Mt. McKinley to evaluate the cellular and biochemical responses of the lung at high altitude. The subjects included one healthy control (arterial O2 saturation = 83%), three climbers with HAPE (mean arterial O2 saturation = 55.0 +/- 5.0%), and four with AMS (arterial O2 saturation = 70.0 +/- 2.4%). Cell counts and differentials were done immediately on the BAL fluid, and the remainder was frozen for protein and biochemical analysis to be performed later. The results of this and of the earlier study mentioned above showed that the total leukocyte count (X10(5)/ml) in BAL fluid was 3.5 +/- 2.0 for HAPE, 0.9 +/- 4.0 for AMS, and 0.7 +/- 0.6 for controls, with predominantly alveolar macrophages in HAPE. The total protein concentration (mg/dl) was 616.0 +/- 3.3 for HAPE, 10.4 +/- 8.3 for AMS, and 12.0 +/- 3.4 for controls, with both large- (immunoglobulin M) and small- (albumin) molecular-weight proteins present in HAPE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

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.

Adult↗
PubMed1987

Respiratory stimulants and sleep periodic breathing at high altitude. Almitrine versus acetazolamide.

We studied the effects of almitrine, acetazolamide, and placebo on the hypoxic ventilatory response (HVR), sleep periodic breathing, and arterial oxygen saturation (SaO2) in 4 healthy climbers. In a laboratory on Denali (Mt. McKinley) at 4,400 m (PB = 440 mm Hg), we used a double-blind, randomized, three-way crossover design. The HVR was measured during the waking state. Periodic breathing and SAO2% were measured during 3-h sleep studies. Almitrine and acetazolamide both increased SaO2% during sleep, although almitrine increased periodic breathing, whereas acetazolamide decreased periodic breathing. The HVR (delta VE/delta SaO2%) was doubled with almitrine (p less than 0.05), but unchanged with acetazolamide. The HVR was positively related to periodic breathing (p less than 0.05). We conclude that periodic breathing during sleep at high altitude is related to the hypoxic ventilatory response, and that acetazolamide is a superior agent to almitrine for ameliorating periodic breathing.

Acetazolamide↗
PubMed1986

High-altitude pulmonary edema. Characteristics of lung lavage fluid.

To evaluate the cellular and biochemical composition of bronchoalveolar fluid in high-altitude pulmonary edema (HAPE), we performed bronchoalveolar lavage in three climbers with HAPE in a research facility at 4400 m on Mount McKinley. Three healthy climbers were used as controls. The HAPE fluids contained marked increases in high-molecular-weight proteins, erythrocytes, and leukocytes, most of which were alveolar macrophages. The HAPE fluids also contained detectable amounts of leukotriene B4 and other lipoxygenase products of arachidonic acid metabolism, complement fragments (C5a), inhibitors of neutrophil chemotaxis, and acid proteases but not hydroxyproline, a constituent of collagen. The data from this study indicate that HAPE involves a transient "large pore" leak in the pulmonary circulation. Despite the presence of two potent mediators of inflammation, leukotriene B4 and C5a, HAPE is not characterized by the intense neutrophil accumulation that is typical of other forms of acute lung injury.

Adult↗
PubMed1985

A decrease in clonus amplitude by topical anesthesia.

Skin desensitization by topical anesthetic was studied for its effects on the frequency and amplitude of 3 overt involuntary oscillations of the ankle: pathological clonus, physiological clonus, and physiological action tremor. Pathological clonus was studied in two spinal cord patients, physiological clonus in 3 normal subjects following prolonged exercise, and physiological action tremor in 7 normal subjects performing voluntary movements. Topical anesthetic applied to the skin of the leg, ankle and proximal half of the foot resulted in a significant decrease in the amplitude of all 3 oscillations with no significant change in frequency. The effect of topical anesthetic on pathological clonus amplitude was so profound that neither patient could initiate clonus for approximately 30 min, despite repeated attempts to do so. While the mechanism determining the frequencies of these oscillations is a matter of considerable debate, the consistency in their response to topical anesthetic suggests that a common mechanism may exist. A possible clinical application is suggested. Topical anesthetic may be a non-invasive means of attenuating undesirable large amplitude tremors and clonus.

Action Potentials↗
PubMed1985

High altitude pulmonary edema and exercise at 4,400 meters on Mount McKinley. Effect of expiratory positive airway pressure.

Breathing against positive expiratory pressure has been used to improve gas exchange in many forms of pulmonary edema, and forced expiration against resistance during exercise has been advocated for climbing at high altitude as a method to optimize performance. To evaluate the effect of expiratory positive airway pressure (EPAP) on climbers with high altitude pulmonary edema (HAPE) and on exercise at high altitude, we studied four climbers with HAPE at rest and 13 healthy climbers during exercise on a bicycle ergometer at 4400 m. We measured minute ventilation (VI, L/min), arterial oxygen saturation (SaO2 percent), end-tidal carbon dioxide (PACO2, mm Hg), respiratory rate (RR), and heart rate (HR) during the last minute of a five minute interval at rest in the climbers with HAPE, and at rest, 300, and 600 kpm/minute workloads on a bicycle ergometer in the healthy subjects. The HAPE subjects demonstrated an increased SaO2 percent, no change in HR or VI, and a decrease in RR on EPAP as compared to control. In normal subjects, SaO2 percent, VI, and heart rate were significantly higher on EPAP 10 cm H2O than 0 cm H2O control (p less than 0.01, 0.01, and 0.05, respectively). The RR and PaCO2 were not significantly different. In summary, EPAP improves gas exchange in HAPE subjects at rest. The EPAP in normal subjects at high altitude resulted in a higher SaO2 percent at the expense of a higher VI and higher HR. These results suggest that the work of breathing is higher and the stroke volume lower on EPAP. The positive pressure mask may be an effective temporizing measure for victims of HAPE who cannot immediately go to a lower altitude.

Adult↗
PubMed1978

Death on Denali.

Between 1903 and 1975 about 1 percent of climbers on Mount McKinley (Denali) and Mount Foraker in Alaska died. In 1976 a total of ten (1.7 percent) of 587 mountaineers died, but this rate of death was not significantly higher than previously. Nineteen percent of climbers in 1976 suffered major or minor injuries, illness or death. Acute mountain sickness (AMS), frostbite and fractures were common. Thirty-three rescues or retrievals of bodies were mounted at a cost of more than $82,000. Inexperience (particularly with arctic mountaineering), poor leadership, faulty equipment and undue reliance on rescue by helicopter contributed to the alarming incidence of accident, illness and death on big peaks in Mount McKinley National Park in 1976.

Adolescent↗
PubMedDate not supplied

Body composition testing of athletes in the field using bioelectric impedance analysis.

Bioelectric impedance analysis was performed as part of the field testing of seventeen athletes competing in the 1990 Iditarod Sled Dog Race. The purpose was to measure initial body composition and the changes that occurred during this extended performance period under Arctic conditions. Four women and thirteen men aged 26-53 years were tested to measure changes in their lean body weight, total body water, total body fat and percent body water. Study results record average body fat losses of 2.14 kg in the male and 1.02 kg in the female racers. Total body water and lean body mass remained stable, while an increase in body water percentage (men: 4.31%, women: 2.78%) was recorded. Though questions remain, bioelectric impedance analysis demonstrates potential for use in future field research projects.

Adult↗