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The diving accident (decompression incident, DCI) occurs in the decompression phase of dives. The DCI can either be caused by an arterial gas embolism (AGE) subsequent to a pulmonary barotrauma or by the formation of inert gas bubbles subsequent to a reduction of ambient pressure during the ascent from depth. In contrast to the traditional assumption that decompression incidents only occur if decompression rules are neglected, recent data indicate that a vast amount of diving accidents occur even though divers adhered to the rules. Hence, there is a large inter- and intraindividual variability in the predisposition for diving accidents. Within the past few years, the molecular understanding of the pathophysiology of diving accidents has improved considerably. It is now well accepted that pro-inflammatory and pro-coagulatory mechanisms play a central role. Moreover, microparticles are increasingly discussed in the pathogenesis of diving accidents. These new molecular findings have not yet resulted in new therapeutic approaches. However, new approaches of preconditioning before the dive have been developed which are intended to reduce the risk of diving accidents. The symptoms of a diving accident show a large variability and range. They reach from pruritus over tension in the female breast, marbled skin and pain in the joints to severe neurological disability like paraplegia or hemiplegia. Furthermore, pulmonary symptoms can be a result of a pulmonary gas embolism and/or a tension pneumothorax. Extreme cases can also manifest as generalized, difficult-to-treat seizures, loss of consciousness or even death. The evidence-based therapy of diving accidents consists of an immediate application of 100% inspiratory O2. This can be performed via a demand valve, face mask with reservoir bag or ventilation bag connected to a reservoir bag. Fluid substitution is performed by i. v. infusion of 500-1000ml/h of cristalloids. If consciousness is not impaired, the diver is positioned in a supine position, in case of impaired or absent consciousness in a lateral recovery position. Especially in severe cases of DCI a fast transfer to a qualified hyperbaric center and the earliest possible hyperbaric O2-therapy is essential., (© Georg Thieme Verlag Stuttgart · New York.)

Introduction: Full-face-masks (FFM) prevent the diver's face from cold and can support nasal breathing underwater. The aim of the study was to evaluate the effect of the use of FFMs on lung function and wellbeing., Methods: Twenty-one, healthy, non-asthmatic divers performed two cold-water dives (4⁰C, 25 min, 10 metres' depth) - one with a FFM and the other with a standard scuba regulator (SSR). Spirometry was performed before and after each dive and well-being and cold sensation were assessed after the dives., Results: Significant decreases in forced vital capacity (FVC), forced expiratory volume in one second (FEV₁) and midexpiratory flow at 75% of FVC (MEF₇₅) occurred after both FFM and SSR dives. Changes in FVC and FEV₁ did not differ significantly between FFM and SSR dives. However, the mid-expiratory flows measured at 50% and 25% of FVC (MEF₅₀ and MEF₂₅) were significantly lower 10 minutes after the FFM dive compared to 10 minutes after the SSR dive. The wellbeing and cold sensation of the divers were significantly improved with FFM dives compared to SSR dives., Conclusions: Cold-water dives during wintertime can be associated with airway narrowing. During cold-water dives, the use of a FFM appears to reduce the cold sensation and enhance the well-being of the divers. However, a FFM does not appear to prevent airway narrowing in healthy, non-asthmatic subjects.

Introduction: In water resuscitation has been reported to enhance the outcome of drowning victims. Mouth-to-mouth ventilation during swimming is challenging. Therefore, the efficacy of ventilation utilities was evaluated., Methods: Ventilation was assessed with the Oxylator ventilator, as well as the consecutive self-contained underwater breathing apparatus (SCUBA) regulators using an anaesthetic test lung: Poseidon Cyklon 5000, Poseidon XStream, Apeks TX 100, Spiro Arctic, Scubapro Air2 and Buddy AutoAir., Results: Oxylator, Apeks TX 100, Arctic and Buddy AutoAir delivered reliable peak pressures and tidal volumes. In contrast, the ventilation parameters remarkably depended on duration and depth of pressing the purge button in Poseidon Cyklon 5000, Poseidon XStream and Scubapro Air2. Critical peak pressures occurred during ventilation with all these three regulators., Discussion: The use of Poseidon Cyklon 5000, Poseidon XStream and Scubapro Air2 regulators is consequently not recommended for in-water ventilation. With the limitation that the devices were tested with a test lung and not in a human field study, Apeks TX 100, Spiro Arctic and Buddy AutoAir might be used for emergency ventilation and probably ease in-water resuscitation for the dive buddy of the victim. Professional rescue divers could be equipped with the Oxylator and an oxygen tank to achieve an early onset of efficient in-water ventilation in drowning victims.

Introduction: In-water resuscitation has recently been proposed in the European resuscitation guidelines. Initiation of mechanical ventilation underwater might be considered when an immediate ascent to the surface is impossible or dangerous. The present study evaluated the feasibility of such ventilation underwater., Methods: A resuscitation manikin was ventilated using an Interspiro® MK II full-face mask or with an Oxylator® ventilator via a facemask or a laryngeal tube, or with mouth-to-tube inflation. Tidal volumes achieved by the individual methods of ventilation were assessed. The ventilation tests were performed during dives in the wet compartment of a recompression chamber and in a lake. Ventilation was tested at 40, 30, 20, 12, 9 and 6 metres' depth., Results: Ventilation was impossible with the cuffed mask and only sufficient after laryngeal intubation for a small number of breaths. Laryngeal tube ventilation was associated with the aspiration of large amounts of water and the Oxylator failed during the ascent. Efficient ventilation with the MK II full-face mask was also possible only for a short period. An absolutely horizontal position of the manikin was required for successful ventilation, which is likely to be difficult to achieve in open water. Leakage at the sealing lip of the full-face mask and the cuff of the laryngeal tube led to intrusion of water and resulted in subsequent complete failure of ventilation., Conclusions: The efficacy of underwater ventilation seems to be poor with any of the techniques trialed. Water aspiration frequently makes ventilation impossible and might foster emphysema aquosum-like air trapping and, therefore, increase the risk of pulmonary barotrauma during ascent. Because the limitations of underwater ventilation are substantial even under ideal conditions, it cannot be recommended presently for real diving conditions.

Recompression during decompression has been suggested to possibly reduce the risk of decompression sickness (DCS). The main objective of the current study was to investigate the effects of FLIRT (First Line Intermittent Recompression Technique) on bubble detection in man. 29 divers underwent 2 simulated dives in a dry recompression chamber to a depth of 40 msw (500 kPa ambient pressure) in random order. A Buehlmann-based decompression profile served as control and was compared to an experimental profile with intermittent recompression during decompression (FLIRT). Circulating bubbles in the right ventricular outflow tract (RVOT) were monitored by Doppler ultrasound and quantified using the Spencer scoring algorithm. Heat shock protein 70 (HSP70), thrombocytes, D-Dimers and serum osmolarity were analyzed before and 120 min after the dive. Both dive profiles elicited bubbles in most subjects (range Spencer 0-4). However, no statistically significant difference was found in bubble scores between the control and the experimental dive procedure. There was no significant change in either HSP70, thrombocytes, and D-Dimers. None of the divers had clinical signs or symptoms suggestive of DCS. We conclude that FLIRT did not significantly alter the number of microbubbles and thus may not be considered superior to classical decompression in regards of preventing DCS., (© Georg Thieme Verlag KG Stuttgart · New York.)

Unlabelled: Diving with self-contained underwater breathing apparatus (SCUBA) has become a popular recreational activity in children and adolescents. This article provides an extensive review of the current literature., Conclusions: Medical contraindications to SCUBA diving for adults apply to children and adolescents, too, but must be adapted. Additional restrictions to the fitness to dive must apply to both, children and adolescents. Children should always be accompanied by a trained adult when diving., (© 2011 The Author(s)/Acta Paediatrica © 2011 Foundation Acta Paediatrica.)

The purpose of this study was to monitor heart rate (HR) and rhythm during open water SCUBA dives. Nine children performed 25-min open water SCUBA dives to 8 m depth. Before, during and after these dives, ECG was recorded. Compared with predive heart rate, heart rate declined by -24 ± 8% (range -36%; -15%) during the dive. In some children a further decline in HR was observed within the last minutes of the dive. Older and taller subjects and those with a high initial HR showed a more pronounced decline in HR. Furthermore singular supraventricular and ventricular extrasystoles were observed in some children. Immersion as well as facial and skin cooling presumably account for the initial decline in heart rate. A further drop in HR within the last minutes of the dive might be related to mild hypothermia. Single supraventricular and ventricular extrasystoles might occur in healthy children during dives.

An increasing number of children and adolescents is diving with Self-Contained Underwater Breathing Apparatus (SCUBA). SCUBA diving is associated with health risks such as pulmonary barotrauma, especially in children and in individuals with airflow limitation. As no data has been published on the effects of open-water diving on pulmonary function in children, the objective of this study was to evaluate the effects of SCUBA dives on airflow in children. 16 healthy children aged 10-13 years underwent spirometry and a cycle-exercise challenge while breathing cold air. They subsequently performed dives to 1-m and 8-m depth in random order. Pulmonary function was measured before and after the exercise challenge and the dives. There were statistically significant decreases in FEV1, FVC, FEV1/FVC, MEF25 and MEF50 after the cold-air exercise challenge and the dives. Changes in lung function following the exercise challenge did not predict the responses to SCUBA diving. In 3 children the post-dive decrements in FEV1 exceeded 10%. These children had a lower body weight and BMI percentile. SCUBA diving in healthy children may be associated with relevant airflow limitation. A low body mass might contribute to diving-associated bronchoconstriction. In the majority of subjects, no clinically relevant airway obstruction could be observed., (© Georg Thieme Verlag KG Stuttgart · New York.)

The incidence and nature of cardiac arrhythmias during static apnea were studied by monitoring the electrocardiogram (ECG) and oxygen saturation (SaO(2)) of 16 recreational breath-hold divers. All subjects completed a maximal apnea with a mean (+/-SD) breath-hold duration of 281 (+/-73) s without clinical complications. Both heart rate (HR) and SaO(2) decreased significantly with breath-hold duration. The decline in SaO(2) was inversely related to the decline in HR (r = -0.55, P < 0.05). Cardiac arrhythmias (supraventricular and ventricular premature complexes, right bundle branch block) occurred in 12/16 (77%) subjects and were related to breath-hold duration. Subjects with atrial premature complexes (n = 9) had a reduced BMI (P = 0.016) and a higher decline of the terminal SaO(2) (P = 0.01). In conclusion, ectopic arrhythmias were common during maximal static apneas for training purposes. The results indicate that the occurrence of ectopic beats is associated with individual factors such as the tolerable SaO(2) decrease.

A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O(2)(*-)) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O(2)(*-) production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage.

Competitive breath-hold divers (BHD) employ glossopharyngeal insufflation (GI) to increase intrapulmonary oxygen stores and prevent the lungs from dangerous compressions at great depths. Glossopharyngeal insufflation is associated with inflation of the lungs beyond total lung capacity (TLC). It is currently unknown whether GI transiently over-distends the lungs or adversely affects lung elastic properties in the long-term. Resting lung function, ventilatory drive, muscle strength, and lung compliance were measured in eight BHD who performed GI since 5.5 (range 2-6) years on average, eight scuba divers, and eight control subjects. In five BHD subsequent measures of static lung compliance (Cstat) were obtained after 1 and 3 min following GI. Breath-hold divers had higher than predicted ventilatory flows and volumes and did not differ from control groups with regard to gas transfer, inspiratory muscle strength, and lung compliance. A blunted response to CO2 was obtained in BHD as compared to control groups. Upon GI there was an increase in mean vital capacity (VCGI) by 1.75 +/- 0.85 (SD) L compared to baseline (p < 0.001). In five BHD Cstat raised from 3.7 (range 2.9-6.8) L/kPa at baseline to 8.1 (range 3.4-21.2) L/kPa after maximal GI and thereafter gradually decreased to 5.6 (range 3.3-8.1) L/kPa after 1 min and 4.2 (range 2.7-6.6) L/kPa after 3 min (p < 0.01). We conclude that in experienced BHD there is a transient alteration in lung elastic recoil. Resting lung function did not reveal a pattern indicative of altered lung ventilatory or muscle function.

About 10% of all sport scuba divers are children and adolescents. Little is known about the particular risks and consequences of this sport on a child's health. Due to the peculiarities of childhood anatomy and physiology, certain restrictions apply to the diving fitness of children and adolescents. Before starting scuba training, the presence of particular cognitive abilities must be demonstrated and eustachian tube dysfunction must be ruled out by a specialist. Medical contra-indications to scuba diving for adults apply to children too but must be adapted. Relative risks for adults may translate to absolute contra-indications in children and adolescents. When planning dives, there should be rigorous limitations as to depth and time. Experienced adult divers must always assist with dive planning and accompany children and adolescents when scuba diving.

In diving mammals splenic contraction increases circulating red cell volume, whereas in humans increased haemoglobin concentrations have been reported. It is unknown, however, whether repetitive apnea diving also comprises an adaptive increase in total red cell volume as reported in endurance athletes. The first aim of the study therefore was to investigate the effect of repeated apnea dives on splenic size and putative red cell release in trained apnea divers (n = 10) and control subjects (SCUBA divers performing apneas without long-term apnea training, n = 7). Long-term effects of repetitive apnea diving may elevate the oxygen transport capacity by an adaptive increase in total haemoglobin mass as reported in endurance athletes. The second goal, therefore, was to compare the trained apnea divers' and the control divers' total haemoglobin mass (tHb-mass) with that of endurance-trained (n = 9) and untrained (n = 10) non-divers. Before and immediately after a series of five dives to a depth of 4 m in a heated pool, spleen volume was assessed with ultrasound tomography. tHb-mass and plasma volume were measured using the CO-rebreathing method. In the trained apnea divers, repeated apnea dives resulted in a 25% reduction of spleen size (P < 0.001), whereas no significant effect was observed in the control subjects. While tHb-mass did not differ between trained apnea divers, untrained SCUBA divers performing apneas and untrained non-divers, it was 30% lower than in endurance-trained non-divers. We conclude that prolonged apnea training causes marked apnea-induced splenic contraction. In contrast to athletes in endurance sports, the trained apnea divers did not present with increased total haemoglobin mass and, hence, no increase in blood oxygen stores.

Diving accidents represent a departure from the routine practice of emergency physicians. The incidence of non-fatal diving accidents is reported as 1-2 per 10,000 dives. Apart from adequate intravenous hydration, oxygen is the only medication with a proven effect in the treatment of diving accidents. After a typical diving accident, administration of oxygen at an inspired concentration (F(I)O(2) 1.0) as high as possible is recommended. Many divers bring along their own oxygen administration systems to the diving sites and these are often better suited for the treatment of diving accidents than the oxygen systems of many emergency responders. Pressure regulators supplying low constant flow oxygen, nasal prongs and inhalation masks are inappropriate. When using artificial ventilation bags with face masks, an oxygen flow of at least 15 l/min should be used. Demand regulators are simple to use and able to deliver a F(I)O2 of 1.0. Their ease of use has earned them high marks in the emergency management of diving accidents and their similarity to standard diving equipment has also aided relatively widespread acceptance. Circulation breathing systems are more technologically complex oxygen delivery systems which permit CO2 absorption and re-breathing at low oxygen flow. In contrast to the demand modules, the likelihood of mistakes during their usage is higher. In diving accidents, the administration of normobaric oxygen, already begun in the field, is the most important therapy and should not be interrupted. Presented with an inadequate supplemental oxygen supply, the inspired oxygen concentration should not be decreased, rather the duration of the oxygen administration should be reduced. Hyperbaric oxygen therapy should be the mainstay of further treatment.

Study Objectives: Obstructive changes in lung function have been reported with cumulative scuba diving exposure. The aim of this study was to investigate the decline in FEV1 in scuba divers over time., Design: Prospective controlled cohort study., Setting: German Naval Medical Institute., Patients: Four hundred sixty-eight healthy, male, military scuba divers and 122 submariners (control subjects) were entered., Measurements and Results: Pulmonary function tests were performed in all subjects on at least three occasions with a minimum interval of 1 year between first and last measurement. The decline in FEV1 was investigated fitting a general linear model to FEV1 across time with a factorial main-effects model for slopes and intercepts with respect to the factors group, smoking status, and baseline FEV1. Mean baseline age of all subjects was 32 years (SD, 9.1), and mean body mass index was 24.7 kg/m2 (SD, 2.4). Subjects were followed up for 5 years (range, 1 to 9 years) on average. Baseline FEV1 exceeded the predicted values in both divers and nondiving control subjects. There was no significant difference in the decline of FEV1 between divers and control subjects. Over time, FEV1 declined more rapidly in smokers than in nonsmokers (p = 0.0064) and declined more rapidly also in subjects with a baseline FEV1 above average compared to subjects below average (p < 0.0001). The annual decline of FEV1 peaked in smoking divers who had a high FEV1 at baseline., Conclusions: The data indicate that scuba diving is not associated with an accelerated decline in FEV1. Combined exposure to diving and smoking contributes to the fall of FEV1; therefore, smoking cessation is advised for divers.

It is increasingly recognized that professional diving may elicit adverse long-term effects on the lungs, but conflicting results have been reported from distinct diving cohorts. This study reports the longitudinal change in lung function in professional divers who employ closed-circuit oxygen rebreathing apparatuses. All oxygen divers who attended the German Naval Medical Institute between 1994 and 1999 for regular medicals underwent spirometry and were entered if they had at least two follow-up examinations. Forced expiratory flows and volumes at baseline and at maximum follow up were compared. There were 39 divers who presented at least 3 times during a median period of 5.8 (2.7-8) yr. Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) amounted to 4.86 +/- 0.62 L and 5.89 +/- 0.67 L at baseline, and 4.83 +/- 0.64 L and 5.87 +/- 0.69 L at maximum follow up, respectively. The change over time was statistically not significant. Substantial exposure to elevated oxygen partial pressure while diving is not associated with an accelerated decline in lung function. Factors other than hyperoxia (e.g., venous gas microemboli and altered breathing gas characteristics) may account for the long-term effects that have been found in professional divers.

Apnea diving is a fascinating example of applied physiology. The record for apnea diving as an extreme sport is 171 meters, 8:58 minutes. The short time beneath the surface induces profound cardiovascular and respiratory effects. Variations of blood-gas tensions result from the interaction of metabolism and the rapid sequence of compression and decompression. Decompression sickness is possible. Apnea divers can reach depths beyond the theoretic physiologic limit by using the lung-packing maneuver. Apnea divers exhibit a fall in heart rate, which can be trained and is an oxygen-conserving effect, but increases the incidence of ventricular arrhythmia.

This study aimed to establish epidemiological data on diving habits and outcome of subjects with respiratory diseases who are considered at increased risk for diving injuries. We conducted a cross-sectional demographics and prevalence study by distribution of an anonymous questionnaire with an issue of a widespread sport diving magazine. The questionnaire was designed to obtain medical and diving history data with an emphasis on respiratory diseases and complaints. The investigational population comprised sport scuba divers of any age and gender from Austria, Germany, and Switzerland. Two hundred and twenty-six male and 96 female divers sent completed questionnaires. Of the respondents 8.7 % indicated that they currently have asthma. Two thirds of asthmatics complained about regular dyspnoea. However, only 42.4 % used drugs relieving or controlling their symptoms regularly and 27.3 % used them in a prophylactic manner before diving. Five percent and 4.7 % of all divers reported a history of respiratory disease other than asthma or dyspnoea respectively. The divers with respiratory illness or complaints had logged a total of 17,386 dives. There were no cases of serious diving injuries. Despite the well-known limitations of postal surveys assessing self reported data, this study indicates that there is a population of subjects diving uneventfully with respiratory diseases that are considered medical contraindications to diving. These subjects deserve particular guidance on related risks and disease management.

The diving fitness medical examination serves to show and reveal medical conditions that are a contraindication for diving or to evaluate the risk of preexisting conditions. For this reason, it should never have the character of a certification given as a matter of courtesy. Fitness to dive is given if the candidate is healthy and when there are no pathological findings. Even with deviations from the norm, diving is still possible, but with restrictions. Important organ systems for the diving fitness examination are the cardiovascular system, the respiratory organs and the ears. In addition, adequate eyesight is important. The German Society of Diving and Hyperbaric Medicine (GTOUM) has drawn up recommendations on the examination of scuba divers to assist the physician (www.gtuem.org).

Fundamentally, accident mechanisms during the isopression phase of diving are primarily dependent upon the partial pressures of the respiratory gases. An increased nitrogen partial pressure leads to compressed-air intoxication; an increased oxygen partial pressure while diving with oxygen-enriched gas mixtures can trigger an oxygen-induced convulsion. Elevated pCO2 can be provoked by inadequate breathing and/or physical exertion at greater diving depths. Through an adjusted diving behavior and observation of the limits, these problems could be easily avoided.

Barotraumas are caused by pressure differences. As described by Boyle's Law, barotraumas develop during the descent phase of diving (and much more rarely during the ascent). The most frequently affected are the ears and paranasal sinuses, in addition to the facial skin and eyes. The most important preventive measure is performing pressure compensation in the affected body cavities. Barotrauma is treated symptomatically.

A decompression accident occurs during uncontrolled dive ascent with diving equipment. Through the rapid decrease in the surrounding pressure, gas bubbles form in the blood and tissues. Depending upon the mechanism of onset, the decompression illness (DCI) is classified as decompression sickness (DCS) or arterial gas embolism (AGE). The therapy consists of administering, as quickly as possible, 100% oxygen as well as a volume substitution. The treatment is continued in a recompression chamber.

Scuba diving vacations in tropical surroundings belong to the repertoire of most divers. In addition to carefully making travel plans and taking care of the necessary vaccinations and appropriate malaria prophylaxis, the following points also must be observed. The flight itself affects diving safety. In particular, a too short time interval between diving and the return flight can lead to decompression problems. Because most of the diving areas are reached by ship, many divers need a prophylaxis against motion sickness. Moreover, external otitis occurs more frequently while diving in the tropics. Finally, there is potential danger from the sea inhabitants, primarily from scorpion fishes, Portuguese Man-of-Wars, box jellyfishes as well as cone snails.

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.

Elite apnea divers have considerably extended the limits of dive depth and duration but the mechanisms allowing humans to tolerate the compression- and decompression-induced changes in alveolar gas partial pressures are still not fully understood. Therefore we measured arterial blood gas tensions and acid-base-status in two elite apnea divers during simulated wet dives lasting 3 : 55 and 5 : 05 minutes, respectively. Arterial pO2 followed the compression-(from 13.8/16.9 kPa before the dive to 30 kPa at the start of the bottom time) and decompression-induced (from 13.7/21.0 kPa to 3.3/4.9 kPa immediately after surfacing) variations of ambient pressure, while the arterial pCO2 remained within the physiologic range (3.0/3.9 kPa before diving vs. 5.7/5.9 kPa at the end of the bottom time), probably due to the CO2 storage capacity of the blood. These findings may help to explain why humans can sustain deep and long apnea dives without major increases in respiratory drive.

An increasing number of asthmatics participate in recreational scuba diving. This activity presents unique physical and physiological challenges to the respiratory system. This review addresses the susceptibility of divers with asthma to diving accidents, acute asthmatic attacks, and long-term exacerbation of their disease. Recommendations on fitness to dive with asthma and airway hyperresponsiveness are provided.

As the use of oxygen enhances the resorption of gas bubbles in decompression illness, it is recommended and generally accepted that the inspired oxygen concentration in emergency treatment of diving accidents has to be as close to 100% as possible. Therefore, several emergency oxygen devices are offered to the diving community but only with little data in literature on the efficacy of these devices. We tested four emergency oxygen devices with respect to efficacy of oxygen supply and breathing comfort at rest. Nine blinded volunteers had to breathe from the four systems with face mask and mouthpiece as well. Gases were measured with mass spectrometry during a 3 min interval from a capillary port close to the subject. The results showed that none of the systems was able to deliver 100% oxygen all the time, but in three systems inspiratory oxygen values were achieved, although in one system the nitrogen wash-out was slowed due to air contamination during inspiration. The fourth tested system frequently supplied the subjects simply with air while breathing at rest. We conclude from our study that it is difficult to achieve oxygen levels close to 100% in practice. Even in a perfectly working system, the interface between device and subject is a source of entrained air, especially when oxygen breathing has to be performed over a longer period of time. In addition, two of four systems had conceptional problems to supply the subjects with pure O2 during inspiration. None of the tested systems was perfectly designed to serve in such emergencies.

A 43-year-old female recreational scuba diver presented to the emergency department 1 hour after a rapid, uncontrolled ascent. Her presentation included progressing confusion, slow and slurred speech, and complaints of headache and hypesthesia over her forearms and anterior thighs bilaterally. Differential diagnosis included arterial gas embolism and decompression sickness. She underwent recompression therapy with US Navy Table 6 within 120 minutes of her ascent. After recompression therapy, the patient had signs and symptoms consistent with severe rhabdomyolysis, including creatine kinase levels of 36,000 U/L and myoglobinuria.

Decompression injuries are potentially life-threatening incidents, generated by a rapid decline in ambient pressure. Although typically seen in divers, they may be observed in compressed air workers and others exposed to hyperbaric environments. Decompression illness (DCI) results from liberation of gas bubbles in the blood and tissues. DCI may be classified as decompression sickness (DCS) or arterial gas embolism (AGE), depending on where the gas bubbles lodge. DCS occurs after longer exposures to a hyperbaric environment with correspondingly larger up-take of inert gas. DCS may be classified into type 1 with cutaneous symptoms and musculoskeletal pain only or type 2 with neurologic and/or pulmonary symptoms as well. AGE usually results from a pulmonary barotrauma, and with cerebral arterial involvement, the symptoms are similar to a stroke. The most important therapy, in the field, is oxygen resuscitation with the highest possible concentration and volume delivered. The definitive treatment is rapid recompression with hyperbaric oxygen therapy. Additional therapeutic measures are discussed.

In five subjects we examined the effect of exercise on the pattern of central venous (right atrial) N2 tensions (PVN2) after ascent from simulated non-decompression dives. The dives consisted of exposure to air at 3 bar for 20 min with 10 min of exercise (workload 75 W) at depth to achieve near-complete N2 saturation of the muscles. After the dive the subjects rested or, on another day, exercised for 30 min (workload 100 W) starting 10 min after completing the ascent. Blood samples taken every 10 min until the 60th min and 90 min after the dive were analyzed for PVN2 using a manometric Van Slyke apparatus. The amount of N2 eliminated was estimated from the PVN2 by adapting the Fick principle. Immediately after the ascent, PVN2 were 950 +/- 39 and 942 +/- 27 mmHg, respectively, in the rest and experiment series. In the rest experiments PVN2 continuously decreased to 606 +/- 8 mmHg 90 min after the dive, remaining significantly higher (P < 0.05) than before the dive. Exercise caused the PVN2 to increase beyond the corresponding levels of the rest experiments (P < 0.05 at 20 and 30 min exercise). After the exercise PVN2 rapidly declined, reaching predive levels 60 min after the ascent. Exercise increased N2 elimination to 970 +/- 143 ml, whereas it had been 311 +/- 61 ml (P < 0.05) in the corresponding phase of the rest experiments. We conclude that if extensive supersaturation and bubble formation can be avoided, such as probably was the case in our shallow non-decompression dives, exercise after the ascent accelerates N2 elimination.

We report a case of transient circulatory depression due to inadvertent apnea of a subject during decompression from a stimulated dive. The dive consisted of exposure to air at 5 bar and subsequent decompression stops. Arterial blood pressure and a lead II ECG were recorded continuously. During decompression from 1.6 to 1.3 bar, the subject inadvertently held his breath. Arterial pressure fell rapidly from 120/80 to 60/53 mmHg within 20 s. Recognizing that the subject held his breath, one of the supervisors ordered him to resume breathing, and arterial blood pressure was restored rapidly. This circulatory depression was probably due to reduced stroke volume such as described for the syncope of ascent: with the subject retaining his breath, the expanding lung volume increased intrathoracic pressure resulting in impaired venous return.

In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.

In five subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure at rest to air at 6 bar for 30 min. corresponding to a depth of 50 m. Afterwards the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6 and 1.3 bar with a total decompression time of 73 min. Immediately after decompression and every 40 min. until the 240th min. arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min. after decompression indicating still incomplete nitrogen wash-out at least two hours after decompression had been accomplished. Bubble formation is discussed as a cause for prolonged nitrogen elimination. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest.