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Pulmonary gas exchange in breath-hold diving (BHD) consists of a progressive increase in arterial partial pressures of oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]) during descent. However, recent findings have demonstrated that [Formula: see text] does not consistently rise in all subjects. This study aimed at verifying and explaining [Formula: see text] derangements during BHD analyzing arterial blood gases and searching for pulmonary alterations with lung ultrasound. After ethical approval, 14 fit breath-hold divers were included. Experiments were performed in warm water (temperature: 31°C). We analyzed arterial blood gases immediately before, at depth, and immediately after a breath-hold dive to - 15 m of fresh water (mfw) and - 42 mfw. Signs of lung interstitial edema and atelectasis were searched simultaneously with a marinized lung ultrasound. In five subjects ( - 15 mfw) and four subjects ( - 42 mfw), the [Formula: see text] at depth seems to decrease instead of increasing. [Formula: see text] and lactate showed slight variations. At depth, no lung ultrasound alterations were seen except in one subject (hypoxemia and B-lines at - 15 mfw; B-lines at the surface). Lung interstitial edema was detected in 3 and 12 subjects after resurfacing from - 15 to - 42 mfw, respectively. Two subjects developed hypoxemia at depth and a small lung atelectasis (a focal pleural irregularity of triangular shape, surrounded by thickened B-lines) after resurfacing from - 42 mfw. Current experiments confirmed that some BH divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, which could not be detected in all subjects probably due to limited time available at depth. NEW & NOTEWORTHY During breath-hold diving, arterial partial pressure of oxygen ([Formula: see text]) and arterial partial pressure of carbon dioxide ([Formula: see text]) are believed to increase progressively during descent, as explained by theory, previous end-tidal alveolar gas measurements, and arterial blood gas analysis in hyperbaric chambers. Recent experiments in real underwater environment found a paradoxical [Formula: see text] drop at depth in some divers. This work confirms that some breath-hold divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, as suggested by lung ultrasound findings.

Doppler ultrasound (DU) is used in decompression research to detect venous gas emboli in the precordium or subclavian vein, as a marker of decompression stress. This is of relevance to scuba divers, compressed air workers and astronauts to prevent decompression sickness (DCS) that can be caused by these bubbles upon or after a sudden reduction in ambient pressure. Doppler ultrasound data is graded by expert raters on the Kisman-Masurel or Spencer scales that are associated to DCS risk. Meta-analyses, as well as efforts to computer-automate DU grading, both necessitate access to large databases of well-curated and graded data. Leveraging previously collected data is especially important due to the difficulty of repeating large-scale extreme military pressure exposures that were conducted in the 70-90s in austere environments. Historically, DU data (Non-speech) were often captured on cassettes in one-channel audio with superimposed human speech describing the experiment (Speech). Digitizing and separating these audio files is currently a lengthy, manual task. In this paper, we develop a graphical user interface (GUI) to perform automatic speech recognition and aid in Non-speech and Speech separation. This constitutes the first study incorporating speech processing technology in the field of diving research. If successful, it has the potential to significantly accelerate the reuse of previously-acquired datasets. The recognition task incorporates the Google speech recognizer to detect the presence of human voice activity together with corresponding timestamps. The detected human speech is then separated from the audio Doppler ultrasound within the developed GUI. Several experiments were conducted on recently digitized audio Doppler recordings to corroborate the effectiveness of the developed GUI in recognition and separations tasks, and these are compared to manual labels for Speech timestamps. The following metrics are used to evaluate performance: the average absolute differences between the reference and detected Speech starting points, as well as the percentage of detected Speech over the total duration of the reference Speech. Results have shown the efficacy of the developed GUI in Speech/Non-speech component separation., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Azarang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Doppler ultrasound (DU) measurements are used to detect and evaluate venous gas emboli (VGE) formed after decompression. Automated methodologies for assessing VGE presence using signal processing have been developed on varying real-world datasets of limited size and without ground truth values preventing objective evaluation. We develop and report a method to generate synthetic post-dive data using DU signals collected in both precordium and subclavian vein with varying degrees of bubbling matching field-standard grading metrics. This method is adaptable, modifiable, and reproducible, allowing for researchers to tune the produced dataset for their desired purpose. We provide the baseline Doppler recordings and code required to generate synthetic data for researchers to reproduce our work and improve upon it. We also provide a set of pre-made synthetic post-dive DU data spanning six scenarios representing the Spencer and Kisman-Masurel (KM) grading scales as well as precordial and subclavian DU recordings. By providing a method for synthetic post-dive DU data generation, we aim to improve and accelerate the development of signal processing techniques for VGE analysis in Doppler ultrasound., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Le et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Pulmonary gas exchange during diving or in a dry hyperbaric environment is affected by increased breathing gas density and possibly water immersion. During free diving, there is also the effect of apnea. Few studies have published blood gas data in underwater or hyperbaric environments: this review summarizes the available literature and was used to test the hypothesis that arterial Po 2 under hyperbaric conditions can be predicted from blood gas measurement at 1 atmosphere assuming a constant arterial/alveolar Po 2 ratio (a:A). A systematic search was performed on traditional sources including arterial blood gases obtained on humans in hyperbaric or underwater environments. The a:A was calculated at 1 atmosphere absolute (ATA). For each condition, predicted arterial partial pressure of oxygen ([Formula: see text]) at pressure was calculated using the 1 ATA a:A, and the measured [Formula: see text] was plotted against the predicted value with Spearman correlation coefficients. Of 3,640 records reviewed, 30 studies were included: 25 were reports describing values obtained in hyperbaric chambers, and the remaining were collected while underwater. Increased inspired O 2 at pressure resulted in increased [Formula: see text], although underlying lung disease in patients treated with hyperbaric oxygen attenuated the rise. [Formula: see text] generally increased only slightly. In breath-hold divers, hyperoxemia generally occurred at maximum depth, with hypoxemia after surfacing. The a:A adequately predicted the [Formula: see text] under various conditions: dry ( r = 0.993, P < 0.0001), rest versus exercise ( r = 0.999, P < 0.0001), and breathing mixtures ( r = 0.995, P < 0.0001). In conclusion, pulmonary oxygenation under hyperbaric conditions can be reliably and accurately predicted from 1 ATA a:A measurements.

Divers who wish to prolong their time underwater while carrying less equipment often use devices called rebreathers, which recycle the gas expired after each breath instead of discarding it as bubbles. However, rebreathers' need to replace oxygen used by breathing creates a failure mechanism that can and frequently does lead to hypoxia, loss of consciousness, and death. The purpose of this study was to determine whether a pulse oximeter could provide a useful amount of warning time to a diver with a rebreather after failure of the oxygen addition mechanism. Twenty-eight volunteer human subjects breathed on a mixed-gas rebreather in which the oxygen addition system had been disabled. The subjects were immersed in water in four separate environmental scenarios, including cold and warm water, and monitored using pulse oximeters placed at multiple locations. Pulse oximeters placed on the forehead and clipped on the nasal ala provided a mean of 32 s (±10 s SD) of warning time to divers with falling oxygen levels, prior to risk of loss of consciousness. These devices, if configured for underwater use, could provide a practical and inexpensive alarm system to warn of impending loss of consciousness in a manner that is redundant to the rebreather., (© 2022. The Author(s) under exclusive licence to Biomedical Engineering Society.)

Venous gas emboli (VGE) are often quantified as a marker of decompression stress on echocardiograms. Bubble-counting has been proposed as an easy to learn method, but remains time-consuming, rendering large dataset analysis impractical. Computer automation of VGE counting following this method has therefore been suggested as a means to eliminate rater bias and save time. A necessary step for this automation relies on the selection of a frame during late ventricular diastole (LVD) for each cardiac cycle of the recording. Since electrocardiograms (ECG) are not always recorded in field experiments, here we propose a fully automated method for LVD frame selection based on regional intensity minimization. The algorithm is tested on 20 previously acquired echocardiography recordings (from the original bubble-counting publication), half of which were acquired at rest (Rest) and the other half after leg flexions (Flex). From the 7,140 frames analyzed, sensitivity was found to be 0.913 [95% CI: 0.875-0.940] and specificity 0.997 [95% CI: 0.996-0.998]. The method's performance is also compared to that of random chance selection and found to perform significantly better (p≺0.0001). No trend in algorithm performance was found with respect to VGE counts, and no significant difference was found between Flex and Rest (p>0.05). In conclusion, full automation of LVD frame selection for the purpose of bubble counting in post-dive echocardiography has been established with excellent accuracy, although we caution that high quality acquisitions remain paramount in retaining high reliability., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Decompression sickness (DCS, "bends") is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation). This may occur when ambient pressure is reduced during any of the following: ascent from a dive; depressurization of a hyperbaric chamber; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft; and during space walks., Competing Interests: The author of this paper declares no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Purpose: Adaptations during voluntary breath-hold diving have been increasingly investigated since these athletes are exposed to critical hypoxia during the ascent. However, only a limited amount of literature explored the pathophysiological mechanisms underlying this phenomenon. This is the first study to measure arterial blood gases immediately before the end of a breath-hold in real conditions., Methods: Six well-trained breath-hold divers were enrolled for the experiment held at the "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Before the experiment, an arterial cannula was inserted in the radial artery of the non-dominant limb. All divers performed: a breath-hold while moving at the surface using a sea-bob; a sled-assisted breath-hold dive to 42 m; and a breath-hold dive to 42 m with fins. Arterial blood samples were obtained in four conditions: one at rest before submersion and one at the end of each breath-hold., Results: No diving-related complications were observed. The arterial partial pressure of oxygen (96.2 ± 7.0 mmHg at rest, mean ± SD) decreased, particularly after the sled-assisted dive (39.8 ± 8.7 mmHg), and especially after the dive with fins (31.6 ± 17.0 mmHg). The arterial partial pressure of CO 2 varied somewhat but after each study was close to normal (38.2 ± 3.0 mmHg at rest; 31.4 ± 3.7 mmHg after the sled-assisted dive; 36.1 ± 5.3 after the dive with fins)., Conclusion: We confirmed that the arterial partial pressure of oxygen reaches hazardously low values at the end of breath-hold, especially after the dive performed with voluntary effort. Critical hypoxia can occur in breath-hold divers even without symptoms.

Immersion pulmonary (IPE, also known as swimming-induced pulmonary edema, SIPE) is a condition in which pulmonary edema develops rapidly during a dive or vigorous swim. Symptoms include dyspnea and hemoptysis. Physical exam reveals typical signs of bilateral pulmonary edema, which can be confirmed radiographically or with bedside ultrasound., Competing Interests: The author of this paper declares no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Introduction: Patients with prior primary spontaneous pneumothorax (PSP) frequently seek clearance to dive. Despite wide consensus in precluding compressed-air diving in this population, there is a paucity of data to support this decision. We reviewed the literature reporting the risk of PSP recurrence., Methods: A literature search was performed in PubMed and Web of Science using predefined terms. Studies published in English reporting the recurrence rate after a first PSP were included., Results: Forty studies (n=3,904) were included. Risk of PSP recurrence ranged 0-67% (22 ± 15.5%; mean ± SD). Mean follow-up was 36 months, and 63 ± 39% of recurrences occurred during the first year of follow-up. Elevated height/weight ratio and emphysema-like changes (ELCs) are associated with PSP recurrence. ELCs are present in 59%-89% (vs. 0-15%) of patients with recurrence and can be detected effectively with high-resolution CT scan (sensitivity of 84-88%). Surgical pleurodesis reduces the risk of recurrence substantially (4.0 ± 4% vs. 22 ± 15.5%)., Conclusion2: Risk of PSP recurrence seems to decline over time and is associated to certain radiological and clinical risk factors. This could be incremented by the stresses of compressed-air diving. A basis for informed patient-physician discussions regarding future diving is provided in this review., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Importance: Scuba diving is becoming increasingly popular. However, scuba diving is associated with specific risks; 80% of adults and 85% of juvenile divers (aged 6-17 years) have been reputed to have an ear, nose, or throat complaint related to diving at some point during their diving career. Divers frequently seek advice from primary care physicians, diving physicians, and otorhinolaryngologists, not only in the acute setting, but also related to the long-term effects of diving., Observations: The principles underpinning diving-related injuries that may present to the otorhinolaryngologist rely on gas volume and gas saturation laws, and the prevention of these injuries requires both that the diver is skilled and that their anatomy allows for pressure equalization between the various anatomical compartments. The overlapping symptoms of middle ear barotrauma, inner ear barotrauma, and inner ear decompression sickness can cause a diagnostic conundrum, and a thorough history of both the diver's symptoms and the dive itself are required to elucidate the diagnosis. Correct diagnosis and appropriate treatment result in a more timely return to safe diving., Conclusions and Relevance: The aim of this review is to provide a comprehensive overview of otorhinolaryngological complications during diving. With the increasing popularity of diving and the frequency of ear, nose, or throat-related injuries, it could be expected that these injuries will become more common and this review provides a resource for otorhinolaryngologists to diagnose and treat these conditions.

Importance: Self-contained underwater breathing apparatus (scuba) diving has become increasingly popular with millions of people diving each year. Otorhinolaryngologists are often consulted either by patients or diving physicians regarding fitness to dive, and at present, the guidelines do not provide comprehensive information regarding the evaluation of this patient cohort. The aim of this review is to provide a comprehensive overview of existing otorhinolaryngological guidelines for fitness to dive recreationally., Observations: There is a paucity of guidelines for assessing otorhinolaryngological fitness to dive in the recreational diver. Comprehensive guidelines exist from US, European, and UK regulatory bodies regarding fitness for commercial diving; however, not all of these can be directly extrapolated to the recreational diver. There are also a variety of conditions that are not covered either by the existing fitness for recreational diving guidelines or the commercial regulatory bodies., Conclusions and Relevance: With the paucity of recreational fitness to dive guidelines we must draw on information from the commercial diving regulatory bodies. We have provided our own recommendations on the conditions that are not covered by either of the above, to provide otorhinolaryngologists with the information they require to assess fitness for recreational diving.

Rebreather diving has one of the highest fatality rates per man hour of any diving activity in the world. The leading cause of death is hypoxia, typically from equipment or procedural failures. Hypoxia causes very few symptoms prior to causing loss of consciousness. Additionally, since the electronics responsible for controlling oxygen levels in rebreathers often control their alarm systems, frequently divers do not receive any external warnings. This study investigated the use of a forehead pulse oximeter as an independent warning device in the event of rebreather failure. Ten test subjects (seven male, three female, median age 29, range 26-35) exercised at a targeted rate of 2 L/minute oxygen consumption while on a non-functional rebreather breathing loop (mean consumption achieved 2.09 ± 0.36 L/minute). Each subject was tested both at the surface and at pressurized depth of 77 fsw (starting pO₂=0.7 atm). The data show that a pulse oximeter could be used to provide an Mk 16 rebreather diver with a minimum mean of 49 seconds (± 17 seconds SD) of warning time after a noticeable change in blood oxygen saturation (SpO₂ ≤ 95%) but before any risk of loss of consciousness (calculated SpO₂ ≤ 80%), so that the diver may take mitigating actions. No statistical difference in warning time was found between the tests at surface and at 77 fsw (P=0.46)., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Carbon dioxide (CO₂) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO₂ elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO₂) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO₂ (arterial pressure of PCO₂) can also occur in divers without a change in inspired PCO₂. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO₂ solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO₂. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia in diving, including its measurement, cause, mental and physical effects, and areas for future study., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Diving narcosis results from the complex interaction of gases, activities, and environmental conditions. We hypothesized that these interactions could be separated into their component parts. Where previous studies have tested single cognitive tasks sequentially, we varied inspired partial pressures of CO 2 , N 2 , and O 2 in immersed, exercising subjects while assessing multitasking performance with the Multi-Attribute Task Battery II (MATB-II) flight simulator. Cognitive performance was tested under 20 conditions of gas partial pressure and exercise in 42 male subjects meeting U.S. Navy age and fitness profiles. Inspired nitrogen (N 2 ) and oxygen (O 2 ) partial pressures were 0, 4.5, and 5.6 ATA and 0.21, 1.0, and 1.22 ATA, respectively, at rest and during 100-W immersed exercise with and without 0.075-ATA CO 2 Linear regression modeled the association of gas partial pressure with task performance while controlling for exercise, hypercapnic ventilatory response, dive training, video game frequency, and age. Subjects served as their own controls. Impairment of memory, attention, and planning, but not motor tasks, was associated with N 2 partial pressures >4.5 ATA. Sea level O 2 at 0.925 ATA partially rescued motor and memory reaction time impaired by 0.075-ATA CO 2 ; however, at hyperbaric pressures an unexpectedly strong interaction between CO 2 , N 2 , and exercise caused incapacitating narcosis with amnesia, which was augmented by O 2 Perception of narcosis was not correlated with actual scores. The relative contributions of factors associated with diving narcosis will be useful to predict the effects of gas mixtures and exercise conditions on the cognitive performance of divers. The O 2 effects are consistent with O 2 narcosis or enhanced O 2 toxicity., (Copyright © 2016 the American Physiological Society.)

Water covers over 70% of the earth, has varying depths and temperatures and contains much of the earth's resources. Head-out water immersion (HOWI) or submersion at various depths (diving) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and renal responses. The translocation of blood into the thorax and elevation of plasma volume by autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which result in endocrine changes that return plasma volume and arterial pressure to preimmersion levels. Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output compared to TN; however, they influence heart rate and the distribution of muscle and fat blood flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The properties of water determine the mechanical load and the physiological responses during exercise in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac output. During submersion, compressed gas must be breathed which introduces the potential for oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompression and after may cause pain in joints and the nervous system., (Copyright © 2015 John Wiley & Sons, Inc.)

Purpose: Immersion pulmonary edema (IPE) occurs in swimmers (especially triathletes) and scuba divers. Its pathophysiology and risk factors are incompletely understood. This study was designed to establish the prevalence of preexisting comorbidities in individuals who experience IPE., Methods: From 2008 to May 2010, individuals who had experienced IPE were identified via recruitment for a physiological study. Past medical history and subject characteristics were compared with those available in the current body of literature., Results: At Duke University Medical Center, Durham, NC, 36 subjects were identified (mean age = 50.11 ± 10.8 yr), of whom 72.2% had one or more significant medical conditions at the time of IPE incident (e.g., hypertension, cardiac dysrhythmias or structural abnormality or dysfunction, asthma, diabetes mellitus, overweight or obesity, obstructive sleep apnea, hypothyroidism). Forty-five articles were included, containing 292 cases of IPE, of which 24.0% had identifiable cardiopulmonary risk factors. Within the recreational population, cases with identifiable risk factors comprised 44.9%. Mean age was 47.8 ± 11.3 yr in recreational divers/swimmers and 23.3 ± 6.4 yr in military divers/swimmers., Conclusions: Cardiopulmonary disease may be a common predisposing factor in IPE in the recreational swimming/diving population, whereas pulmonary hypertension due to extreme exertion may be more important in military cases. Individuals with past history of IPE in our case series had a greater proportion of comorbidities compared to published cases. The role of underlying cardiopulmonary dysfunction may be underestimated, especially in older swimmers and divers. We conclude that an episode of IPE should prompt the evaluation of cardiac and pulmonary function.

Diving exposes a person to the combined effects of increased ambient pressure and immersion. The reduction in pressure when surfacing can precipitate decompression sickness (DCS), caused by bubble formation within tissues due to inert gas supersaturation. Arterial gas embolism (AGE) can also occur due to pulmonary barotrauma as a result of breath holding during ascent or gas trapping due to disease, causing lung hyperexpansion, rupture and direct entry of alveolar gas into the blood. Bubble disease due to either DCS or AGE is collectively known as decompression illness. Tissue and intravascular bubbles can induce a cascade of events resulting in CNS injury. Manifestations of decompression illness can vary in severity, from mild (paresthesias, joint pains, fatigue) to severe (vertigo, hearing loss, paraplegia, quadriplegia). Particularly as these conditions are uncommon, early recognition is essential to provide appropriate management, consisting of first aid oxygen, targeted fluid resuscitation and hyperbaric oxygen, which is the definitive treatment. Less common neurologic conditions that do not require hyperbaric oxygen include rupture of a labyrinthine window due to inadequate equalization of middle ear pressure during descent, which can precipitate vertigo and hearing loss. Sinus and middle ear overpressurization during ascent can compress the trigeminal and facial nerves respectively, causing temporary facial hypesthesia and lower motor neuron facial weakness. Some conditions preclude safe diving, such as seizure disorders, since a convulsion underwater is likely to be fatal. Preventive measures to reduce neurologic complications of diving include exclusion of individuals with specific medical conditions and safe diving procedures, particularly related to descent and ascent., (© 2014 Elsevier B.V. All rights reserved.)

The Diving Committee of the Undersea and Hyperbaric Medical Society has reviewed available evidence in relation to the medical aspects of rescuing a submerged unresponsive compressed-gas diver. The rescue process has been subdivided into three phases, and relevant questions have been addressed as follows. Phase 1, preparation for ascent: If the regulator is out of the mouth, should it be replaced? If the diver is in the tonic or clonic phase of a seizure, should the ascent be delayed until the clonic phase has subsided? Are there any special considerations for rescuing rebreather divers? Phase 2, retrieval to the surface: What is a "safe" ascent rate? If the rescuer has a decompression obligation, should they take the victim to the surface? If the regulator is in the mouth and the victim is breathing, does this change the ascent procedures? If the regulator is in the mouth, the victim is breathing, and the victim has a decompression obligation, does this change the ascent procedures? Is it necessary to hold the victim's head in a particular position? Is it necessary to press on the victim's chest to ensure exhalation? Are there any special considerations for rescuing rebreather divers? Phase 3, procedure at the surface: Is it possible to make an assessment of breathing in the water? Can effective rescue breaths be delivered in the water? What is the likelihood of persistent circulation after respiratory arrest? Does the recent advocacy for "compression-only resuscitation" suggest that rescue breaths should not be administered to a non-breathing diver? What rules should guide the relative priority of in-water rescue breaths over accessing surface support where definitive CPR can be started? A "best practice" decision tree for submerged diver rescue has been proposed.

Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water, although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters and studied at 1 atm absolute (ATA) during dry and immersed rest and exercise in thermoneutral (29-31 degrees C) and cold (18-20 degrees C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (P < or = 0.004). Resting MPAP and PAWP values (means +/- SD) were 20 +/- 2.9/13 +/- 3.9 (cold body/cold head), 21 +/- 3.1/14 +/- 5.2 (cold/warm), 14 +/- 1.5/10 +/- 2.2 (warm/warm), and 15 +/- 1.6/10 +/- 2.6 mmHg (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (P < 0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE.

Diving-related pulmonary effects are due mostly to increased gas density, immersion-related increase in pulmonary blood volume, and (usually) a higher inspired Po(2). Higher gas density produces an increase in airways resistance and work of breathing, and a reduced maximum breathing capacity. An additional mechanical load is due to immersion, which can impose a static transrespiratory pressure load as well as a decrease in pulmonary compliance. The combination of resistive and elastic loads is largely responsible for the reduction in ventilation during underwater exercise. Additionally, there is a density-related increase in dead space/tidal volume ratio (Vd/Vt), possibly due to impairment of intrapulmonary gas phase diffusion and distribution of ventilation. The net result of relative hypoventilation and increased Vd/Vt is hypercapnia. The effect of high inspired Po(2) and inert gas narcosis on respiratory drive appear to be minimal. Exchange of oxygen by the lung is not impaired, at least up to a gas density of 25 g/l. There are few effects of pressure per se, other than a reduction in the P50 of hemoglobin, probably due to either a conformational change or an effect of inert gas binding.

During diving, arterial Pco(2) (Pa(CO(2))) levels can increase and contribute to psychomotor impairment and unconsciousness. This study was designed to investigate the effects of the hypercapnic ventilatory response (HCVR), exercise, inspired Po(2), and externally applied transrespiratory pressure (P(tr)) on Pa(CO(2)) during immersed prone exercise in subjects breathing oxygen-nitrogen mixes at 4.7 ATA. Twenty-five subjects were studied at rest and during 6 min 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 P(tr) was varied between +10, 0, and -10 cmH(2)O; breathing gas Po(2) was 0.7, 1.0, and 1.3 ATA; and inspiratory and expiratory breathing resistances were varied using 14.9-, 11.6-, and 10.2-mm-diameter-aperture disks. During exercise, Pa(CO(2)) (Torr) 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 during air breathing and to 49.9 +/- 5.4 (P < 0.001 vs. 1 ATA) during breathing with high external resistance. There was no significant effect of inspired Po(2) or P(tr) on Pa(CO(2)) or minute ventilation (Ve). Ve (l/min) 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 during air breathing and to 49.2 +/- 7.3 (P < 0.001) during breathing with resistance. We conclude that the major contributors to increased Pa(CO(2)) during exercise at 4.7 ATA are increased depth and external respiratory resistance. HCVR and maximal O(2) consumption were also weakly predictive. The effects of P(tr), inspired Po(2), and O(2) consumption during short-term exercise were not significant.

Introduction: First aid oxygen (FAO2) has been widely used as an emergency treatment for diving injuries, but there are few studies supporting its efficacy., Methods: 2,231 sequential diving injury reports collected by the Divers Alert Network (DAN) Injury database from 1998 to 2003 were examined., Results: 47% (1,045) of cases received FAO2. The median time to FAO2 treatment after surfacing was four hours and after symptom onset was 2.2 hours. Persistent complete relief (14%) or improvement (51%) was seen with FAO2 alone (65% overall response; n = 330). After one recompression treatment 67% of FAO2 patients reported complete relief compared to 58% of the no FAO2 group (OR = 1.5, 95% CI = 1.2 -1.8). FAO2 given at any time after surfacing significantly reduced the odds of multiple recompression treatments (OR = 0.83, 0.70-0.98). When FAO2 was given within 4 hours of surfacing, the OR decreased to 0.50 (0.36-0.69) yielding a number needed to treat of 6. Case severity affected urgency of FAO2 treatment. Individuals with more prominent symptoms received prompt treatment. Cardiopulmonary, skin, and serious neurological symptoms had shorter delays to FAO2 (p < 0.001)., Conclusions: FAO2 increased recompression efficacy and decreased the number of recompression treatments required if given within four hours after surfacing.

Insulin-requiring diabetes mellitus (IRDM) is commonly described as an absolute contraindication to scuba diving. A 1993 Divers Alert Network survey, however, identified many active IRDM divers. We report on the plasma glucose response to recreational diving in IRDM divers. Plasma glucose values were collected before and after diving in IRDM and healthy control divers. Time/depth profiles of 555 dives in IRDM divers were recorded. IRDM divers had been diving for a mean of almost nine years and had diabetes for a mean of over 15 years. No symptoms or complications related to hypoglycemia were reported (or observed). Post-dive plasma glucose fell below 70 mg x dL(-1) in 7% (37/555) of the IRDM group dives compared to 1% (6/504) of the controls (p<0.05). Moderate levels of hyperglycemia were also noted in 23 divers with IRDM on 84 occasions. While large plasma glucose swings from pre-dive to post-dive were noted, our observations indicate that plasma glucose levels, in moderately-controlled IRDM, can be managed to avoid hypoglycemia during routine recreational dives under ordinary environmental conditions and low risk decompression profiles.

Background: Severe decompression illness (DCI) could be more likely in cigarette smokers because of airway obstruction or vascular disease. The present study evaluated the severity of DCI as a function of cigarette smoking in recreational divers., Methods: We examined all DCI reports recorded in the Divers Alert Network (DAN) database from 1989 through 1997. Smoking history was quantified as heavy (>15 pack-years), light (0 to 15 pack-years), and never smoked. DCI symptoms were classified as severe (alteration in consciousness, balance or bladder/bowel control, motor weakness, visual symptoms, convulsions), moderate (other neurological symptoms), or mild (pain, skin, or nonspecific symptoms). The proportional odds model and generalized logits were used for the adjusted analysis when accounting for other covariates., Results: There were 4,350 patients included in the analysis. After adjustment for confounding variables, heavy smokers were more likely to have severe vs. mild symptoms than nonsmokers (OR = 1.88) (95% CI 1.36, 2.60) or light smokers (OR = 1.56) (95% CI 1.09, 2.23). Heavy smokers and light smokers were more likely to have severe vs. moderate symptoms than nonsmokers (OR = 1.36) (95% CI 1.06, 1.74) and (1.22) (1.02, 1.46), respectively. Although these data do not reveal whether smoking predisposes to DCI, the results are consistent with a tendency, when DCI occurs, for cigarette smoking to trigger more severe symptoms., Conclusions: The data suggest that when DCI occurs in recreational divers, smoking is a risk factor for increased severity of symptoms.

Physiological dead space (Vds), end-tidal CO(2) (Pet(CO(2))), and arterial CO(2) (Pa(CO(2))) were measured at 1 and 2.8 ATA in a dry hyperbaric chamber in 10 older (58-74 yr) and 10 younger (19-39 yr) air-breathing subjects during rest and two levels of upright exercise on a cycle ergometer. At pressure, Vd (liters btps) increased from 0.34 +/- 0.09 (mean +/- SD of all subjects for normally distributed data, median +/- interquartile range otherwise) to 0.40 +/- 0.09 (P = 0.0060) at rest, 0.35 +/- 0.13 to 0.45 +/- 0.11 (P = 0.0003) during light exercise, and 0.38 +/- 0.17 to 0.45 +/- 0.13 (P = 0.0497) during heavier exercise. During these conditions, Pa(CO(2)) (Torr) increased from 33.8 +/- 4.2 to 35.7 +/- 4.4 (P = 0.0059), 35.3 +/- 3.2 to 39.4 +/- 3.1 (P < 0.0001), and 29.6 +/- 5.6 to 37.4 +/- 6.5 (P < 0.0001), respectively. During exercise, Pet(CO(2)) overestimated Pa(CO(2)), although the absolute difference was less at pressure. Capnography poorly estimated Pa(CO(2)) during exercise at 1 and 2.8 ATA because of wide variability. Older subjects had higher Vd at 1 ATA but similar changes in Vd, Pa(CO(2)), and Pet(CO(2)) at pressure. These results are consistent with an effect of increased gas density.

Recognition of condition attributable to the environmental changes experienced by divers will facilitate appropriate treatment. The diagnosis of these conditions rarely requires sophisticated imaging or electrophysiologic testing. Divers who have suspected DCI, in addition to general supportive measures, should be administered fluids and oxygen and transported to a recompression chamber. For diving-related conditions, on-line consultation is available from the Divers Alert Network, Durham, NC (919-684-8111).

Urinary vasopressin (VP), aldosterone (ALDO), osmotic substances, sodium excretion, and plasma volume were assessed in 4 healthy male divers during 2 predive control days, 2 compression days, 6 days at 46 atm abs, and 26 days of decompression with stops at 37 and 27 atm abs. At pressure the ambient gas was trimix (0.5 atm abs O2:5% N2:remainder He). All urine was collected throughout the dive. Samples were divided into daytime (0700-1900) and nighttime (1900-0700). Indocyanine green dye dilution was used to determine plasma volume at predive 1, 46, and 24 atm abs. In agreement with previous dives at 31 atm abs, there was a decrease in VP excretion during compression lasting until return to 1 atm abs (P less than 0.05). Also similar to the shallower dives at 31 atm abs, the normal diurnal pattern of VP excretion, daytime higher than nighttime (P less than 0.05), disappeared at pressure. Urine osmolality showed alterations compatible with responses to VP. In contrast to previous studies at 31 atm abs, but in agreement with a previous study at 49.5 atm abs, there was no sustained increase in urinary ALDO excretion and only a transient natriuresis during the compression phase, followed by a reduced sodium excretion. In confirmation of earlier conclusions from indirect evidence, direct measurements of plasma volume indicated a reduction of about 20% (P less than 0.05) at 46 atm abs which remained reduced after decompression to 24 atm abs.

Four subjects were compressed to a simulated depth of 450 msw (46 bar) for 37 days in the main research chamber of the German underwater simulator diving facility at the GKSS Research Center, Geesthacht. The ambient gas was trimix. Urine was collected at 0700, 1300, and 1900 h each day for analysis of Na+, K+, volume, osmolality, and creatinine. Urine, antidiuretic hormone (ADH), and aldosterone were analyzed separately. Daily fluid, Na+, and K+ intake were analyzed throughout the dive. The aim of the investigation was to confirm the existence of a diuresis and natriuresis which had been observed in earlier saturation dives to 31 atm abs using He-O2. A significant diuresis was observed during compression despite a decrease in fluid intake. After compression the diuresis decreased somewhat but remained significantly above precompression control levels during the entire hyperbaric exposure. No significant change in fluid intake was observed. Daily Na+ and K+ excretion increased significantly during compression, which was accompanied by a significant increase in nocturnal excretion of Na+ and K+. Daily intake of Na+ and K+ decreased throughout the dive. Daily urine ADH decreased immediately upon compression and was associated with a parallel decrease in urine osmolality. In contrast, urinary aldosterone excretion exhibited no change during the dive despite the increase in Na+ and K+ excretion and decrease in Na+ intake.

Platelet counts were measured in 10 divers during the course of 4 experimental deep dives (450 and 600 m) and different anticoagulants were tested. The use of sodium citrate as an anticoagulant was associated with artifactual thrombocytopenia, whereas ethylenediaminetetraacetic acid proved to be satisfactory. During one of the dives (450 m) the use of fluorocarbon to remove excess dissolved inert gas before decompression of the samples was systematically tested. Mean platelet count decreased from 272,600 +/- 29,400 mm-3 (mean +/- SD) on Day 7 (450 m) to 177,700 +/- 26,400 mm-3 on Day 12 (360 m). Platelet count had recovered to 209,900 +/- 20,700 mm-3 at the time of surfacing. Mean hematocrit (expressed in percent) increased from 44.7 +/- 2.2 predive to 59.4 +/- 2.0 on Day 7 (450 m) to 40.9 +/- 2.8 at the time of surfacing. These changes were statistically significant (P less than 0.05). Platelet counts on samples that had been degassed with fluorocarbon were not different from samples that had been decompressed without degassing.

This descriptive, nonrandomized, multicenter-based study compares the treatment outcomes of two major categories of recompression treatment tables for recreational sport SCUBA divers suffering from decompression sickness and/or arterial gas embolism. Stratified and logistic regression analyses were used to compare the enhanced tables, which use pressures of 165 fsw (feet of salt water) or 60 fsw with extended recompression time, to the regular tables, which use pressures of 60 fsw or less without extended recompression time. A total of 113 cases were treated with enhanced tables, 54 being successes. A total of 214 cases were treated with regular tables, 135 being successes. The final logistic statistical model after adjusting for confounding factors found a significant improvement in successful treatment outcomes for divers treated with tables that use pressures of 60 fsw or less without extended recompression time (OR = 0.47, 95% CI = 0.28-0.78).

30 patients with a history of decompression sickness were examined for the presence of patent foramen ovale by bubble contrast, two-dimensional echocardiography and colour flow doppler imaging. With bubble contrast, 11 (37%) of the patients had right-to-left shunting through a patent foramen ovale during spontaneous breathing. 61% of a subset of 18 patients with serious signs and symptoms had shunting. This number was significantly higher than the 5% prevalence seen with the same diagnostic technique in 176 healthy volunteers. The presence of patent foramen ovale seems to be a risk factor for the development of decompression sickness in divers.

Five male volunteers served as subjects for exercise studies during three dives to pressures of 47 and 66 ATA while breathing gases containing 0.5 ATA PO2 and varying amounts of N2 and He. The inspired gas density ranged from 1.1 g/l (BTPS) at the surface to 17.1 g/l at the highest pressure. Dyspnea at rest and during exercise was evident in all divers and was predominantly inspiratory in nature. Despite the dyspnea, divers were able to perform work requiring an O2 consumption larger than 2 l/min STPD at each depth. Compared with surface measurements, moderate work at depth was associated with alveolar hypoventilation, arterial hypercapnia, very large physiological dead space, and higher levels of arterial lactate and signs of simultaneous respiratory and metabolic acidosis. The increase of ventilation that accompanies the onset of acidemia at the surface was not present at depth. Acidemia at depth was more severe, and its onset occurred at lesser work rates than at 1 ATA. No large differences could be ascertained when a variety of responses obtained with inspired gas having a density of 7.9 g/l at 47 ATA were compared with those obtained with an inspired gas density of 17.1 g/l at 66 ATA. It appears that the major impact of the environment on the physiological responses to work was almost fully manifested at a pressure of 47 ATA with a He-O2 gas mixture. It is cautioned that maximum work tolerance may be an insufficient assessment of the physiological condition of a diver exposed to these high pressures.

Diving accidents related to barotrauma constitute a unique subset of ischemic insults to the CNS. Victims may demonstrate components of arterial gas embolism, which has a propensity for cerebral involvement, and/or decompression sickness, with primarily spinal cord involvement. Fourteen patients with diving-related barotrauma were studied with MR imaging of the brain and spinal cord and with CT of the brain. In four patients with presumed cerebral gas embolism, cranial MR was abnormal in three patients while CT was abnormal in only one. Twelve patients had decompression sickness and spinal cord symptoms. MR documented spinal cord abnormalities in three patients. However, scans obtained early in our study were frequently limited by technical constraints. MR of the brain is more sensitive than conventional CT scanning techniques in detecting and characterizing foci of cerebral ischemia caused by embolic barotrauma to the CNS. Although spinal MR may be less successful in the localization of spinal cord lesions related to decompression sickness, these lesions were previously undetectable by other neuroimaging methods.