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PubMed1998

Differential air sac pressures in diving tufted ducks Aythya fuligula.

The air in the respiratory system of diving birds contains a large proportion of the body oxygen stores, but it must be in the lungs for gas exchange with blood to occur. To test the hypothesis that locomotion induces mixing of air sac air with lung air during dives, we measured differential pressures between the interclavicular and posterior thoracic air sacs in five diving tufted ducks Aythya fuligula. The peak differential pressure between posterior thoracic and interclavicular air sacs, 0.49+/-0.13 kPa (mean +/- s.d.), varied substantially during underwater paddling as indicated by gastrocnemius muscle activity. These data support the hypothesis that locomotion, perhaps through associated abdominal muscle activity, intermittently compresses the posterior air sacs more than the anterior ones. The result is differential pressure fluctuations that might induce the movement of air between air sacs and through the lungs during dives.

Abdominal Muscles↗
PubMed2002

Kinematics of diving Atlantic puffins (Fratercula arctica L.): evidence for an active upstroke.

To examine the propulsion mechanism of diving Atlantic puffins (Fratercula arctica), their three-dimensional kinematics was investigated by digital analysis of sequential video images of dorsal and lateral views. During the dives of this wing-propelled bird, the wings are partly folded, with the handwings directed backwards. The wings go through an oscillating motion in which the joint between the radius-ulna and the hand bones leads the motion, with the wing tip following. There is a large rotary motion of the wings during the stroke, with the wings being pronated at the beginning of the downstroke and supinated at the end of the downstroke/beginning of the upstroke. Calculated instantaneous velocities and accelerations of the bodies of the birds show that, during the downstroke, the birds accelerate upwards and forwards. During the upstroke, the birds accelerate downwards and, in some sequences analysed, also forwards, but in most cases the birds decelerate. In all the upstrokes analysed, the forward/backward acceleration shows the same pattern, with a reduced deceleration or even a forward acceleration during 'mid' upstroke indicating the production of a forward force, thrust. Our results show that the Atlantic puffin can use an active upstroke during diving, in contradiction to previous data. Furthermore, we suggest that the partly folded wings of diving puffins might act as efficient aft-swept wingtips, reducing the induced drag and increasing the lift-to-drag ratio. A movie is available on-line.

Animals↗
PubMed2003

Recreational scuba diving in Caribbean marine protected areas: do the users pay?

There are more than 200 marine protected areas (MPAs) in the Caribbean and Central America that contain coral reefs and are therefore theoretically attractive to scuba divers. One fifth of dive operators in 30 countries were surveyed for their use of MPAs: the majority are located within 20 km of at least one MPA and 46% conduct at least 80% of their diving within a MPA. An estimated 15 million dives take place outside of Florida each year, half of these occurring inside MPAs. Only 25% of MPAs containing coral reefs charge divers an entry or user fee, which is most usually USD 2-3 levied per dive or per diver. The revenue generated by these fees is estimated at USD 1-2 million annually, but the potential for generating income has not been fully realized. A significant contribution to the cost of regional conservation could be achieved if higher fees were applied more widely than at present.

Animals↗
PubMed1976

Role of the chemoreceptor in diving bradycardia in rat.

Responses in heart rate and blood pressure to the dive in unanesthetized rats were studied by submersion of the head in water for 30 sec. During the dive, remarkable bradycardia developed and blood pressure was slightly elevated. Bilateral section of the carotid sinus nerves or selective destruction of the carotid body chemoreceptor by intrasinusal injection of acetic acid attenuated the bradycardic response to the dive, while section of the recurrent nerves or section of the sympathetic trunks at the cervical level together with the superior laryngeal nerves had no effect. These data indicate that the chemoreceptor plays an important role in diving bradycardia in rats.

Animals↗
PubMed1979

Ear damage due to diving.

Diving injury may affect all parts of the ear during all types of diving. Divers are regularly exposed to noise and 120 dB(A) is measured during ventilation of a hyperbaric chamber. Ear canal squeeze, possibly with drum perforation, may give a transient conductive hearing loss. Middle ear squeeze, possibly with drum perforation, also gives a transient conductive loss. Inner ear barotrauma, possibly with perilymph fistula, most often results in transient vertigo and lasting sensorineural high tone loss, often resembling a noise-induced loss. Decompression sickness and gas embolism can also damage the inner ear. A change of breathing gas during deep diving has damaged the labyrinth, most likely due to counter diffusion. The authors have seen two cases of over window perilymph fistula resulting from diving. One of them also suffered a burst ear drum on the same side. His hearing returned to normal after surgical repair.

Barotrauma↗
PubMed1995

Oxygen diving-induced middle ear under-aeration.

Middle ear negative pressure and effusions have been described after oxygen diving. The prevalence, dynamics and pathophysiology of this phenomenon are not clear, and were hence investigated in the present study. Thirty-four oxygen divers with normal otoscopic and tympanometric evaluation participated in the study. The subjects' symptoms were documented, and pneumatic otoscopy and tympanometry were repeated immediately after the completion of a 3 h, 15 feet oxygen dive, and 7 h later on awakening from the night's sleep. Most divers had positive otoscopic findings the morning after the dive, all of which cleared within 4 h of rising. A significant decrease was observed in average middle ear compliance (p = 0.0463, one way ANOVA), and an increase was found in the number of ears with tympanic compliance less than 0.3 ml (p = 0.0001, Kruskal-Wallis non-parametric ANOVA). In addition, 14.7% of the ears had type C, and 27.9% type B tympanograms the morning after the dive (p = 0.0001 chi2). The generalized nature of oxygen-induced middle ear under-aeration, combined with the dynamics of the symptoms and signs observed, make middle ear barotrauma, tympanic cavity oxygen absorption, and middle ear epithelial oxygen toxicity all unlikely explanations. The observed phenomenon and its dynamics might stem from a reversible derangement in a middle ear chemoreceptor reflex arch, which has recently been suggested as regulating middle ear aeration.

Acoustic Impedance Tests↗
PubMed1990

Nitrogen partial pressures in man after decompression from simulated scuba dives.

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.

Arteries↗
PubMed1985

A SCUBA-diving fatality.

An investigation by a Naval Board of Inquiry into the circumstances of a fatal naval diving accident is presented. Although drowning contributed to the fatal outcome, massive arterial gas embolism is thought to have been the principal cause of death, and the value of post-mortem computed tomography scanning for its detection is demonstrated. The possibility is discussed of diver error due to unfamiliarity with equipment and procedures, compounded by nitrogen narcosis. The shortfall in expertise of coronial inquiries into diving deaths is emphasized against a background of increasing popularity of sports diving around Australia. The implications for the offshore industry are obvious and suggest the need for a federal diving inspectorate.

Accidents↗
PubMed1992

Why some people do not drown. Hypothermia versus the diving response.

OBJECTIVE: To examine our present state of knowledge regarding the remarkable survival of some victims from prolonged submersion for an hour or more. Debate continues on the relative importance of the two explanatory theories--diving response and hypothermia. DATA SOURCES: A wide range of physiological, pathophysiological and clinical papers relating to the diving response, hypothermia and near-drowning, with emphasis on the period 1981-1991. DATA SYNTHESIS: The normothermic human brain suffers irreversible damage if subjected to acute asphyxia for longer than 10 minutes. Significant resistance of brain tissue to hypoxia occurs only after its temperature has fallen from 37 degrees C to 30 degrees C or less. Body surface cooling depresses core temperature by only one-third of this drop in 10 minutes. Hence an additional factor, other than hypothermia, is required to explain survival from near-drowning. The idea that ingestion and aspiration of large amounts of cold water produce such a temperature drop lacks quantitative evidence. The diving response seen in marine mammals also occurs in humans but to a lesser extent; however, about 15% of volunteers tested exhibit a profound response. This response which starts immediately upon submersion prevents aspiration of water, redistributes oxygen stores to heart and brain, slows cardiac oxygen use and initiates a hypometabolic state. The possible influence of alcohol on these processes is considered. CONCLUSIONS: Survival from prolonged near-drowning appears to depend upon a specific temporal interplay between the diving response and hypothermia, resulting in a protective state of hypometabolism.

Bradycardia↗
PubMed1976

South African underwater diving accidents, 1969-1976.

Since 1969 a survey of diving accidents involving South African amateur divers was undertaken. The South African Underwater Union diving accident report form was used, and various State agents (SA Police and inquest courts) and individual divers and club instructors were questioned. This survey covers the period up to the end of June 1976. Data acquired during the 8-year period 1969 - 1976 are compared. A conservative estimate from the number of certificates issued to club divers indicates a 25% increase in diver population, while the number of fatilities has decreased from 0,1% in 1971 to 0,016% in 1976, indicating the importance of accident reporting in determining safety trends. In general, a change in pattern is observed during the last 4 years, showing more SCUBA than breath-hold fatalities. The formation of the Decompression Sickness and Diving Accidents Investigation Panel as a further measure to decrease fatal diving accidents is discussed.

Accidents↗
PubMed1999

Effects of repeated apneas on apneic time and diving response in non-divers.

Human breath-hold divers usually perform a series of dives with short intervals. Repeated apneas prolong apneic time, and an accentuated diving response has been suggested to be the cause. The aim of this study was to investigate the effect of repeated apneas on apneic time and diving response in humans. Forty-one subjects performed a series of five apneas with face immersion in water of 10 degrees C, separated by 2-min intervals. Apneas were performed at rest and to individual maximal duration. Heart rate, mean arterial pressure, skin capillary blood flow, and respiratory movements were recorded. Thirty-eight of the subjects were used for analysis of cardiovascular parameters, and in 23 subjects the physiologic breaking point could be detected by the involuntary breathing movements. Heart rate reduction and blood pressure increase were most prominent during the first apneic face immersion, whereas skin capillary blood flow reduction was most intense in the second apneic face immersion. Blood pressure and skin capillary blood flow during recovery from apneic episodes also changed throughout the series. Repetition increased apneic time by 55% and postponed the occurrence of involuntary breathing movements by 27% in subjects passing the physiologic breaking point. We conclude that both physiologic factors, associated with the accumulation of CO2, and psychologic factors, related to the capacity to withstand the respiratory drive, contribute to the prolongation of apneic time whereas an increased diving response does not contribute.

Adult↗
PubMed1999

Cardiac and humoral changes induced by recreational scuba diving.

The aim of this study was to evaluate the prevalence and the possible clinical relevance of circulating bubbles after a recreational scuba dive. Twenty healthy subjects (18 male, 2 female; age range 25-36 yr) underwent a Doppler-echocardiographic study in basal conditions and 1.9+/-0.2 h after a recreational scuba dive. Venous blood samples were taken just before the two ultrasonic studies to obtain leukocyte and platelet counts and plasma activity of angiotensin-converting enzyme (ACE; assumed as pulmonary endothelial damage marker). Circulating bubbles were observed in the right heart chambers of 12 subjects after the dive. The echocardiographic and humoral data were evaluated before and after diving in subjects with and without circulating bubbles. At the postdive evaluation, a significant increase in right ventricular dimensions (37.4+/-3.9 vs. 40.7+/-4.0 mm; P < 0.01) and a significant reduction of early diastolic filling velocities of both right (59.1+/-16.4 vs. 48.9+/-6.9 cm x s-(-1); P < 0.05) and left (76.2+/-9.9 vs. 67.5+/-10.2 cm x s(-1); P < 0.02) ventricle were observed in the group with circulating bubbles. In the same group, significant increases in ACE activity (92.9+/-41.1 vs. 105.9+/-41.7 U x liter(-1); P < 0.05), platelets (217+/-34 vs. 232+/-35 10(3) x microl(-1); P < 0.01), and granulocytes (3,704+/-715 x microl(-1) vs. 5,212+/-1,995 x microl(-1); P < 0.001) were observed. The bubble-free group showed only a postdive significant decrease of left ventricular early diastolic filling velocity (74+/-6.8 vs. 62.6+/-4.5 cm x s(-1); P < 0.005). These data may indicate that circulating gas bubbles are associated with cardiac changes, suggesting a right ventricular overload and an impairment of ventricular diastolic performance. Postdive humoral and hematologic changes are consistent with the hypothesis that "silent" gas bubbles may damage pulmonary endothelium and activate the reactive systems of the human body.

Adult↗
PubMed1999

[Asthma and diving with a cylinder].

Undersea diving is an activity that is practised more and more in holiday clubs. There is no precise legislation on the causes of unfitness of the amateur, in contrast to the professional diver, where the medical criteria are strict and controlled. When diving with a cylinder, on descent, the ventilatory load increases with increase of the ambient pressure and dynamic resistance in the airways increases. "As with an insufficient respiration on the surface, a healthy subject when diving has a ventilatory ability that is drastically reduced". Moreover with cylinder ventilation, the diver has available a reserve of gas under pressure from which he inspires with the aid of a breathing apparatus (regulator): he breathes dry gas that is dried before compression in the reservoirs, chilled by the relief valve on leaving the reservoir. This inhalation of cold, dry air associated with a hyperventilation during the descent produces ideal conditions to trigger exercise induced asthma. All subjects who present a bronchial hyperreactivity have the risk when diving with a cylinder of triggering a bronchospasm that is identical with that of a sporting asthmatic. During surfacing: the re-surfacing diver runs the risk of an accident of pulmonary suppression if he does not expire sufficiently during his return to the surface: the mass of intrapulmonary air of the resurfacer dilates and the excess of volume is exhaled by the diver: a volume of air of 5 l at 10 m depth corresponds to a volume of 10 l on the surface. Therefore the airways must remain free: an obstruction of the peripheral airways associated with an urgent re-surfacing produces a very rapid thoracic dilation which is responsible for pulmonary barotrauma (pulmonary barotrauma is frequently lethal with 30% of accidental deaths).

Asthma↗
PubMed1976

Decompression sickness during saturation dives.

Available Navy saturation diving data were analyzed for an evaluation of the therapeutic adequacy of decompression sickness treatment procedures and for delineation of precipitant factors in the etiology and treatment of decompression sickness during saturation dives. None of the cases of decompression sickness recorded during saturation dives involved more than musculoskeletal or joint pain, and in 96% of the cases the joint pain was confined to the diver's knees. In 89% of the cases symptoms appeared while the divers were still under pressure. The subsequent recompression treatment of these cases resulted in full relief in only 35% of the cases; the remaining 65% completed the therapy and subsequent decompression with residual pain which diminished over a period of weeks. The adequacy of the recompression appears to be inversely proportional to the depth of reported onset of symptoms and the time required to obtain even partial relief is directly related to the magnitude of the recompression ratio used. Four explanations are suggested for the limited recompression therapy common in saturation diving: increase in musculoskeletal pain with recompression, peer pressure to avoid extension of the chamber confinement, lack of severe neurological symptoms, and the tremendous depths required to obtain a reasonable recompression ratio. The author further suggests that future treatment procedures will require a departure from the accepted concept of radically decreasing the volume of inert gas bubbles by increasing pressure.

Analysis of Variance↗
PubMed1999

[Asthma and diving].

Until recently asthma was considered a contraindication for scuba diving due to possible "air trapping" and subsequent barotrauma. However, in view of the wide prevalence and heterogeneity of the illness this is no longer justified. There are, nevertheless, certain prerequisites for diving with asthma: a complete anamnesis and an analysis of the pulmonary function, an exact diagnosis of the trigger factors as well as of the bronchial hyperreactivity in order to correctly ascertain the asthma level. When scuba diving, asthmatics need to observe certain rules. Still, some types of asthma remain incompatible with diving. Among these are the pseudo-allergic, exercise-induced, and psychogenic-induced asthma as well as allergic bronchopulmonal aspergillosis. Asthma due to bronchial infections and GERD are considered relative contraindications.

Accident Prevention↗
PubMed2001

Neurologic complications of scuba diving.

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers. When severe diving injury occurs, the nervous system is frequently involved. In dive-related barotrauma, compressed or expanding gas within the ears, sinuses and lungs causes various forms of neurologic injury. Otic barotrauma often induces pain, vertigo and hearing loss. In pulmonary barotrauma of ascent, lung damage can precipitate arterial gas embolism, causing blockage of cerebral blood vessels and alterations of consciousness, seizures and focal neurologic deficits. In patients with decompression sickness, the vestibular system, spinal cord and brain are affected by the formation of nitrogen bubbles. Common signs and symptoms include vertigo, thoracic myelopathy with leg weakness, confusion, headache and hemiparesis. Other diving-related neurologic complications include headache and oxygen toxicity.

Barotrauma↗
PubMed1996

A priori models in the testing of diving life support equipment.

A priori models have been effectively used at the Navy Experimental Diving Unit (NEDU) to aid in the design of tests for diving equipment. These models are computer simulations conducted prior to the initial testing effort, using mechanistic models derived from first principles or based on prior testing. One example of such a model involves the freeze-up susceptibility of SCUBA regulators used in very cold water at depths to 58 msw (190 fsw). The influence of various dive profiles on the risk of regulator freeze-up was estimated for a variety of model parameters. In a second example, a simple model of CO2 canister duration was used to reveal the relative benefits of various competing diver work/rest profiles. The a priori modeling efforts helped NEDU define relatively efficient and unambiguous designs for testing diving equipment.

Carbon Dioxide↗
PubMed2001

Acute psychosis associated with diving.

There are only a few reported cases of psychiatric disorders presenting a s decompression sickness (DCS). Previous reports indicate that DCS can result in personality change, depression, Munchausen's syndrome, and pseudo stroke. We report two cases of acute psychoses that occurred following diving as suspected DCS and were treated with hyperbaric oxygen, which did not improve the psychotic features. One patient had symptoms of DCS including myalgias, weakness, and fatigue; however the symptoms were inconsistent. The symptom onset and nitrogen loading from his dive profiles made the diagnosis of DCS unlikely. The second patient exhibited mild joint pain, fatigue, and psychosis that was temporally associated with diving but no other symptoms of DCS. Following a detailed medical evaluation we determined that these two patients did not have DCS or arterial gas embolism (AGE). Although it is highly unlikely that a pure psychotic episode will arise as a result of DCS, physicians caring for divers with symptoms of DCS or AGE and acute psychosis may consider a trial of recompression therapy while completing the medical evaluation. Divers with acute psychosis without signs and symptoms and benign dive profiles are unlikely to have DCS or AGE.

Acute Disease↗