Clinical Program

The Center for Hyperbaric Medicine and Environmental Physiology is a multidisciplinary organization involved in clinically treating patients with hyperbaric oxygen; researching in the fields of oxygen biology and environmental physiology (especially diving and altitude physiology); and providing information and medical services for recreational divers through the Divers Alert Network (DAN).

DAN is an organization devoted to promoting recreational diving safety via accident and mortality data collection, research, and education. In addition, DAN provides a 24-hour phone consultation service for diving accidents. A dedicated section on DAN can be found here.

The Center consists of several components. The F.G Hall Environmental Laboratory contains a seven-chamber, 254 cu m complex with a 5,660 cu m compressed air storage field; three 3 cu m/min air compressors; a 2,633 cu m liquid oxygen system; two vacuum pumps; and a complete gas mixing facility. These chambers were designed to simulate environments ranging from an altitude of 47,000 m (155,000 feet) to a depth of 1,100 m of sea water (3,600 ft of sea water).

The chambers are outfitted with environmental control units that regulate temperature, humidity, and CO 2 accumulation. The facility is capable of conducting studies of subjects immersed in water. Invasive monitoring of patients or experimental subjects under pressure or at simulated altitude is readily available. Studies have been performed in humans incorporating invasive measurement of arterial and pulmonary arterial pressures, transcranial Doppler blood velocity, precordial Doppler monitoring for vascular bubbles, and in vivo near infrared spectroscopy of tissue oxygenation. In addition to the chambers, a human physiology laboratory is available for human studies at 1 ATA. An electronics shop and machine shop provide in-house design and construction facilities.

Studies on whole animals and tissues are performed in our Oxygen Transport Laboratory, which incorporates an operating room and facilities capable of maintaining anesthetized animals under continuous monitoring for several days. It is equipped with an environmental exposure facility, biochemistry, and molecular biology laboratories, and microscopy and darkroom facilities.

Twenty-four hour coverage is provided for hyperbaric emergencies and elective treatment of patients with hyperbaric oxygen. The call team consists of an intern, resident, or fellow, an attending physician, a nurse, and a chamber operator. The call schedule also includes “hotline” coverage of emergency diving calls from throughout the world.

Two hundred and ninety-nine new patients were evaluated for hyperbaric therapy in 2004 for conditions such as decompression sickness, air embolism, carbon monoxide poisoning, necrotizing soft tissue infections, refractory osteomyelitis, threatened flaps, radiation necrosis, and selected ischemic problem wounds. There were 4,111 patient treatments during the year.

In addition, eight therapeutic lung lavages for patients with pulmonary alveolar proteinosis were carried out under general anesthesia inside “C” chamber. For this procedure, hyperbaric oxygen provides a convenient mechanism for treating hypoxemia. We also provide regular “fitness-to-diving” consultations. All patient data are maintained on a computerized database, which is accessible from anywhere within the Medical Center.

Training Program

For the fifth consecutive year, faculty gave a 37-hour-long graduate and medical school level course on the physiology of extreme environments. In addition to lectures on the physiology of high pressure, hyperoxia, hypoxia, immersion and hypothermia, the course included practical laboratories on diagnosing and managing hyperbaric- and diving-related emergencies. The course was made available not only for the fellows and students working in the Center but also for faculty, residents, interns and fellows in the department and for students with special interest from other Duke programs. The Center also participated in teaching for the Anesthesiology and Environmental Physiology section of the third-year medical student curriculum.

Anesthesia interns regularly rotate onto the Hyperbaric Service, as do fellows in critical care and numerous medical students.

DAN has conducted a three-month summer Research Internship Program for college and medical school students since 1999, with the following objectives: (1) expanding data collection from recreational divers for improving diving safety; (2) educating the diving public about DAN and diving safety; and (3) providing experiences that might motivate young people towards careers in diving science or diving related fields. Interns undergo a 25-hour training course at DAN in diving physiology, diving data collection procedures, diving emergency management, and DAN operations. After training, they are placed with a diving operator along the East or West Coast or in the Caribbean to collect data. This year, five interns participated in the program, which is funded by donations to DAN, and interns can earn college credit for their participation.

Undergraduate interns are also supported from research grants to gain experience in operational/ environmental physiology research. Three research interns participated in 2004.

A workshop on adjunctive therapy for decompression illness was held in April of this year. A consensus formed the basis for the Undersea and Hyperbaric Medical Society Recommendations.

In conjunction with DAN, two one-week courses for Diving Medical Technicians were held in the spring and fall. Similarly, three CME-accredited courses on Diving Medicine were held, one at Duke Medical Center, and one each in the spring and fall held in the Caribbean.

Research Program

The investigators in the Hyperbaric Center are pursuing studies on the mechanisms by which altered environmental conditions (altitude and diving) affect human physiology and the biology of oxygen and nitric oxide at different gas pressures. The following projects were underway in 2004.

Acute Lung Injury-Mechanisms and Therapy (Drs. Piantadosi, Welty-Wolf, Carraway). Animal models have been developed to study acute lung injury due to oxygen toxicity and sepsis. Methods of assessment include gas exchange (blood gases and multiple inert gas elimination), mechanics, lung morphometry, and measurement of pulmonary inflammatory responses and activation of the coagulation system. In addition, mechanisms or systemic organ injury, particularly those involving mitochondria, are being investigated.

Effect of Altitude Acclimatization on Lung NO and CO Concentration and Vascular Tone in Humans (Drs. Bar-Yosef, Piantadosi, Moon). A joint study with members from the Department of Medicine examining the hypothesis that PO 2-related changes in pulmonary and systemic vascular resistance in humans are mediated by changes in pulmonary NO and CO content. Analysis is in progress of data obtained from a prolonged exposure to 15,000 ft altitude in which volunteers are instrumented with arterial and pulmonary artery catheters.

Epidemiological Modeling of Acute Mountain Sickness (AMS) (Drs. Vann and Pollock). AMS is an environmental illness caused by altitude exposure that is susceptible to analysis using standard statistical methodology. With the support of the U.S. Army, we have developed methodology that allows the probability of AMS to be estimated as a function of any general altitude exposure. The Army has gathered additional data that are presently being analyzed.

Flying after Diving (FAD) (Drs. Thalmann, Pollock, Freiberger, Vann). This is a follow-on study to the DAN FAD study funded by the Navy that will investigate dives that are of particular interest to the Navy that were not tested in the DAN study. Our experimental findings to date indicate the FAD guidelines in the U.S. Navy Diving Manual are overly conservative, with the caveat that the experiments were conducted with dry, resting subjects, and the effects of immersion and exercise, which are currently unknown, may be important.

Hyperbaric Oxygen Preconditioning for Hypoxic and Ischemic Brain Injury (Drs. Freiberger, Warner, Sulimann, Piantadosi). The ability of tissues to withstand hypoxic and or ischemic stress can be augmented by preconditioning with a sub-lethal episode hypoxia or ischemia. Based on previous studies in other animal models, we believe that hyperbaric oxygen can have a beneficial preconditioning effect without the obvious dangers of hypoxia and ischemia. We are using the Rice-Vannuci model in neonatal rat pups to measure neuroprotection after both hyperbaric and hypoxic-ischemic preconditioning. We are also studying the elaboration of the biochemical pathways involved in this model to expand our understanding of both hypoxic and hyperoxic oxidant biology and to transition to clinical studies of the use of HBO for preconditioning.

Molecular Biology of Anti-Oxidant Enzymes in the Lung and Brain (Drs. Suliman, Carraway, Gutsaeva, Freiberger, Warner, Lyman, Piantadosi). Oxygen toxicity involving the lungs and brain produces a range of compensatory molecular changes that may have benefit in terms of protecting from subsequent similar or new oxidative stressors. These studies are exploring the mechanisms of regulation, cellular location, and effects of altered expression of key anti-oxidant enzymes on injury during exposure to changes in oxygen partial pressure across a wide spectrum of environments in both animal and cell culture models.

Molecular Responses to Endogenous CO Production and Exogenous CO Exposure: Physiological Versus Pathological Implications for Mitochondrial and Cell Function (Drs. Piantadosi, Suliman, Carraway). This study is exploring the intracellular effects of CO as a signaling molecule in the brain and heart. Carbon monoxide is produced endogenously as a product of the heme degradation pathway and may play a role in regulating several important biochemical processes involving heme metabolism and mitochondrial function. In addition, the cellular uptake of CO may interfere with one or more of these processes during exogenous exposure to CO.

Prevention of Decompression Sickness in Space (Drs. Vann, Pollock). Efforts will continue with NASA support to develop more efficient means of preventing DCS in astronauts during extravehicular activity (EVA) in space flight. Our DCS risk models, for example, can now support real-time staged decompressions of the EVA suit, which could reduce the need for lengthy and costly pre-EVA oxygen breathing without compromising either safety or the astronaut. Our protocol has been used for 34 EVAs from the Space Station to date. We are presently testing a revised protocol that would reduce logistic requirements of current procedures.

Project Dive Exploration (Drs. Vann, Denoble, Freiberger). DAN has worked with the dive computer manufacturers to develop a prospective observational study called Project Dive Exploration, which records depth/time profiles from recreational divers who volunteer to carry recording dive computers during their open-water dives. Additional data are collected on demographics, medical history, dive conditions, and medical outcome of the dives. To date, DAN has collected data on over 100,000 individual dives during which 33 divers were treated for decompression illness. Analysis of this data has shown that the dive conditions, in addition to the dive profile, have important effects on decompression risk. The data collected will better define the risks associated with different diving practices and will help establish guidelines for risk exposure.

Prospective Analysis of the Effectiveness of Hyperbaric Oxygen Treatment for Radiation Necrosis of the CNS (Drs. Dear, Moon, Stolp, Piantadosi, Carraway, Friedman*, Logue‡, Dunn‡) [*Department of Pediatrics; ‡ Department of Psychiatry and Behavioral Sciences]. Hyperbaric oxygen therapy (HBO) has been shown to be a highly effective treatment for radiation necrosis of bone and soft tissue. Anecdotal evidence supports its efficacy in radiation injury to peripheral nerve and the central nervous system. Clinical data are being collected on a consecutive series of patients with radiation-induced CNS injury treated with HBO.

Regulation of Cerebral Blood Flow in Hyperoxia, Hypercarbia, Hypoxia, and CO Hypoxia (Drs. Demchenko, Allen, Bennett, Piantadosi). This team of investigators is performing investigations on the role of endogenous nitric oxide and carbon monoxide in the regulation of cerebral blood flow in under a range of environmental stresses using genetically altered mice. These studies have provided the first direct evidence that hyperoxic vasoconstriction in the brain is a result of decreased NO availability due to the overproduction of the superoxide anion.

Nitric Oxide and CNS-Pulmonary Interactions in O2 Toxicity NO and O 2 Toxicity (Drs. Piantadosi, Demchenko, Allen and Welty-Wolf). This study is testing the hypothesis in animals that a critical difference between pulmonary oxygen toxicity at sea level, which is primarily mediated by inflammation, and that in the hyperbaric range of 2 to 3 ATA is the stimulation of nitroxidergic nerves in the brain and brainstem that generate adverse effects on pulmonary airway and vascular function in vivo.

Effects of Exercise, Gas Density, and Static Lung Loads on End Tidal-Arterial PCO 2 Differences Breathing N 2-O 2 Mixtures during Immersed Prone Exercise (Drs. Moon, Pollock, Freiberger, Stolp). During heavy exercise underwater hypercapnia can occur due to the combined effects of high breathing resistance, nitrogen narcosis, static lung load and high inspired PO 2. Ideally, PCO 2 is measured in arterial blood (PaCO 2). However, in practice end tidal CO 2 (P etCO 2) is generally used as an estimate of PaCO 2. During diving, P etCO 2 may over or underestimate the PaCO 2 depending on the depth, inspired PO 2, static lung load, and exercise level. This study will measure PaCO 2 and P etCO 2 simultaneously during exercise at 1 ATA dry and immersed at 120 fsw. The effect of static lung loads (-10, 0, +10 cmH 2O), inspired PO 2 (0.7-1.3 ATA) high flow resistances and heavy exercise will be conducted in volunteers instrumented with arterial and pulmonary artery catheters. A method of determining PaCO 2 from PETCO 2, taking into account the various breathing environment parameters will be devised.

Utilization of a Deep Stop to Prevent Neurological Decompression Sickness in Scuba Divers (Drs. Bennett and Marroni). In spite of many modifications to decompression schedules, the incidence of neurological (Type II) decompression sickness has remained the same. Our hypothesis was that by combining a deep stop at half the depth of dive with the standard safety stop at 15-20 ft, such decompression sickness can be avoided. Using 22 volunteer Italian scuba divers, this was tested with a matrix of dives with no stop, shallow stop and deep and shallow stop. Doppler measurements and computer calculated tissue gas tensions showed a significant reduction of Doppler bubbles together with the fast 5- and 10-min tissues compatible with the spinal cord tissue half time of 12.5 min. We are presently testing deep-to-shallow dives with the introduction of a deep stop.

Predictors of Increased PaCO2 During Immersed Prone Exercise at 4.7 ATA (Drs. Cherry, Moon, Freiberger, Stolp) During diving, arterial PCO2 (PaCO2) levels can increase and contribute to psychomotor impairment and unconsciousness. This study was designed to investigate the effects of hypercapnic ventilatory response (HCVR), exercise, inspired PO2, and externally applied transrespiratory pressure (Ptr) on PaCO2 during immersed prone exercise breathing oxygen-nitrogen mixes at 4.7 ATA. Methods: Twenty-five subjects were studied at rest and during 6 minutes of exercise while dry and submersed at 1 ATA and during exercise submersed at 4.7 ATA. At 4.7 ATA, subsets of the 25 subjects (9-10 for each condition) exercised as Ptr was varied between +10, 0 and -10 cm H2O; breathing gas PO2 was 0.7, 1.0 and 1.3 ATA; and inspiratory and expiratory breathing resistances were varied using disks with three differrent sizes of circular apertures. During exercise, PaCO2 (mmHg) increased from 31.5±4.1 (mean±SD for all subjects) dry to 34.2±4.8 (P=0.02) submersed, to 46.1±5.9 (P<0.001) at 4.7 ATA breathing air, and to 49.9±5.4 (P<0.001 vs. 1 ATA) with high external breathing resistance. There was no significant effect of inspired PO2 or Ptr on PaCO2 or minute ventilation (V E). V E (l·min-1) decreased from 89.2±22.9 dry to 76.3±20.5 (P=0.02) submersed, to 61.6±13.9 (P<0.001) at 4.7 ATA breathing air, and to 49.2±7.3 (P<0.001) with resistance. We conclude that the major contributors to increased PaCO2 during exercise at 4.7 ATA are the increased depth and external respiratory resistance. HCVR and V O2 max values were also weakly predictive. The effects of Ptr, inspired PO2, and V O2 during short term exercise were not significant.

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Richard E. Moon, MD, CM, M.Sc., FRCPC, FACP, FCCP

Medical Director, Center for Hyperbaric Medicine and Environmental Physiology
Professor of Anesthesiology
Associate Professor of Medicine

Faculty

Martha Sue Carraway, MD (Medicine)
Guy de Lisle Dear, MB
John J. Freiberger, MD, MPH
Claude A. Piantadosi, MD (Medicine)
Bret W. Stolp, MD, PhD

Fellows

Otto Boneta, MD
John Longphre, MD
Diana Gutsaeva, PhD (Research Fellow)
Ciuying Wang, PhD (Research Fellow)

Researchers

Barry Allen, PhD
Richard Auten, PhD (Pediatrics)
Shahar Bar-Yosef , MD
Peter Bennett, PhD, D.Sc.
Martha Sue Carraway, MD (Medicine)
Guy de Lisle Dear, MB
Ivan Demchenko, PhD
Peter Denoble, MD, PhD
John J. Freiberger, MD, MPH
Y.C. Tony Huang, MD (Medicine)
Tim McMahon, MD (Medicine)
Carl Pieper, DPH (Biometry)
Claude Piantadosi, MD (Medicine)
Neal Pollock, PhD
Herbert Saltzman, MD (Medicine)
Nicola Scafetta (Physics)
Bret Stolp, MD, PhD (Cell Biology)
Hagir Suliman, DVM, PhD
Jennifer Turi, MD (Pediatric Critical Care)
Donna Uguccioni, M.Sc
Richard Vann, PhD
David Warner, MD
Richard Whorton, PhD (Pharmacology)
Karen Welty-Wolf, MD (Medicine)

Nursing Staff

Kevin Kraft, RN (Head Nurse)
Roberta Brave, RN
Rebecca Padilla-Burgos, RN
John Rice, RN
Aaron Walker, NA

Support Staff

Eric Alford
Albert Boso
Barry Castle
Benjamin Comfort
Owen Doar
Paul Edwards
Deborah Kraft
Craig Marshall
Lori Merritt
Michael Natoli
Eric Schinazi
Mark Wright
Tony Lee, EMTs