Saturation and desaturation with N2 and He at 4 atm.
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Adolescent↗
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Results for “DECOMPRESSION SICKNESS”
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Circulatory impairment during exposure to ambient pressures of 4 mm Hg and 55 mm Hg.
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Animals↗
Absorption of gas bubbles in flowing blood.
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Absorption↗
A new gas lesion syndrome in man, induced by "isobaric gas counterdiffusion".
Normal men have been found to develop pruritus and gas bubble lesions in the skin, and disruption of vestibular function, when breathing nitrogen or neon with oxygen while surrounded by helium at increased ambient pressure. This phenomenon, which occurs at stable ambient pressures, at 1 or many ATA, has been designated the "isobaric gas counterdiffusion syndrome." In a series of analyses and experiments in vivo and in vitro the cause of the syndrome has been established as due to gas accumulation and development of gas bubbles in tissues as a result of differences in selective diffusivities, for various respired and ambient gases, in the tissue substances between capillary blood and the surrounding atmosphere. The phenomenon here described in man is an initial stage of a process shown later in animals to progress to continuous, massive, lethal, intravascular gas embolization.
Atmosphere Exposure Chambers↗
Decompression limits for compressed air determined by ultrasonically detected blood bubbles.
The direct decompression limits for a group of divers over a range of pressure-time air exposures was determined using ultrasonic detection of venous gas emboli (VGE). In addition to dry chamber exposures, ranging from 233 ft for 7 min to 25 ft for 720 min, we exposed six divers to open ocean dives at 165 ft for 10 min. Findings demonstrated a strong individual propensity to form VGE, correlating with susceptibility to bends. No bends developed without the prior detection of precordial VGE. The present concept of no problems after any period of time at 30 fsw was not confirmed. Isopleths of equal percentage occurrence of VGE were computed between 10 and 60%. Open ocean exposures increased the percentage of VGE and bends, when compared to dry chamber exposures. Limiting tissue half times computed from the 20% VGE isopleth suggested that saturation exposures are controlled by a greater sensitivity of the short-half-time tissues than previously appreciated, rather than by additionally extended half times.
Adult↗
The lung as a filter for microbubbles.
A new ultrasonic Doppler device has been used noninvasively over the femoral artery of anesthetized dogs to prove that it can detect carefully calibrated microbubbles of 14--189 micrometers diam when these are infused directly into the aorta. The same evaluated technique has then been employed to detect any bubbles escaping into the arterial system when gas was infused into the venous system either as microbubbles or as a bolus. Results from 18 dogs showed that, under normal conditions, the lungs are a superb filter for bubbles and that any cutoff diameter is less than 22 micrometers. However, bubbles escaped entrapment when the lungs were severely overloaded with gas (20 ml) or were pretreated with a pulmonary vasodilator (aminophylline). The dog preparation and arterial Doppler device appear to be ideal for future studies to determine what other factors might compromise the capability of the lungs to filter microbubbles. Physiological parameters showed dramatic changes when bubbles were detected as escaping into the arterial system by comparison with their effect when retained within the lungs. Changes in respiration profile indicated that they may offer a useful index of the degree of venous embolization and, hence, a warning of impending overload leading to arterial embolization.
Air↗
Stochastic description of inert gas exchange.
Data from experiments measuring the rate of uptake and elimination of nonmetabolic gas in living organs are usually analyzed by several exponential time constants or their equivalent half-times (i.e, exponential series analysis). To avoid the limitations of this technique, we have formulated a method that combines analysis by moments of distribution with transfer function techniques, which makes the analysis independent of any mechanistic model. This method is an improvement over previous methods because it allows better comparison of gas exchange experiments and better prediction of gas exchange in the formulation of diver decompression schedules. Measurements of radioxenon uptake and elimination in two areas of a dog are presented. Analysis of the same organ response by both methods showed a fivefold variation in derived exponential time constants compared with less than 10% variation among moment descriptors.
Animals↗
Responses of fetal sheep to simulated no-decompression dives.
The effect of simulated standard no-decompression dives to 60 and 100 ft of seawater was tested in 12 near term sheep carrying 16 fetuses. In the immediate postdive period there were no significant changes in fetal blood pressure or fetal placental or renal blood flow, but the maternal blood pressure was elevated and the maternal placental blood flow was depressed. Six surgically prepared fetuses were dived to 100 ft. Five died within 20 min of ascent and the sixth suffered severe cardiac arrhythmia and hypotension. At autopsy all fetuses were observed to have massive bubbling in the arterial system and heart. Five fetuses were dived to 100 ft without surgery. Two were alive 3 h later and no bubbles were present at autopsy, and three were born alive at term. With the 60-ft dives, three fetuses were subjected to surgery and all suffered massive bubbling. Two fetuses were dived to 60 ft without surgery; one was alive after 3 h and the other was born alive at term. We conclude that surgery and monitoring result in the formation of postdive gas bubbles that would not otherwise appear.
Animals↗
Pathophysiology of inner ear dysfunction in the squirrel monkey in rapid decompression.
More than 90 squirrel monkeys with bilateral myringotomies (a small hole in each ear drum) were rapidly decompressed in a hyperbaric chamber according to a special diving profile in which 35% of attempts produced disorders ("hits") confined to the inner ear. Monkeys receiving inner ear hits (as determined by the sudden onset of vigorous head or eye nystagmus during decompression) were tested and killed at times ranging from 1 h to more than 12 mo following the dive. Histologically, in monkeys killed 1 mo or less after the hit, hemorrhage and/or a deep purple-staining precipitated material were frequently found in the otic fluid spaces. In those monkeys killed more than 1 mo after a hit, ectopic new bone growth in the arms of the semicircular canals was a common sequela. New bone growth never appeared in the cochlea. In unaffected ears, and in both ears of control animals, the precipitated material was somewhat less than in ears damaged by decompression; and, furthermore, new bone growth did not occur. Behaviorally, the hit monkeys showed vestibular deficits that were consistent with the structural damage revealed by histology.
Animals↗
Central venous bubbles and mixed venous nitrogen in goats following decompression.
Decompression of awake goats from saturation at 1, 2, and 3 ATA of air has been carried out using ultrasonic Doppler bubble detection, central venous blood inert gas measurement, and cardiac output measurement. The results of these experiments indicate that the decrease in nitrogen elimination rate as an apparent result of decompression cannot be due to excessive cardiac output or mass transport of a large amount of inert gas to the lungs as bubbles. Rather, the rapid drop in mixed venous nitrogen content is consistent with a generalized decrease in tissue-to-blood nitrogen elimination. This in turn appears to be due to a cardiovascular response to the decompression insult as was previously reported for dogs (D'Aoust et al., J. Appl. Physiol. 41: 348--355, 1976) at 1, 2, and 3 ATA; addition of ultrasonic Doppler monitoring and cardiac output in the present studies allowed measurement of the degree of latency in the appearance of bubbles at a central venous location. This time period includes that required for bubble formation, growth, and vascular transport of the bubbles to the Doppler detector. All results of these studies are consistent with the interpretation that due to a decompression insult, which probably includes bubble formation, some degree of hemostasis, and other hematologic sequelae, the transport of tissue inert gas to the capillary venous blood is retarded, thus providing the rapid apparent decrease in mixed venous blood inert gas content. These results demonstrate what is most likely a general response to a severe but not crucial decompression by the cardiovascular system.
Animals↗
Bubble formation in crabs induced by limb motions after decompression.
In vivo bubble formation was studied in the megalopal stage of the crab Pachygrapsus crassipes. The animals were equilibrated with elevated argon, nitrogen, or helium pressures then rapidly decompressed to atmospheric pressure. Voluntary motions induced bubble nucleation in leg joints after exposures to as low as 2 atm nitrogen (gauge pressure). Delays of several minutes sometimes passed between decompression and bubble formation. Mechanically stimulating the animals to move their legs increased this bubble formation, whereas immobilizing the legs before gas equilibration prevented it, even in animals decompressed from 150 atm nitrogen. We conclude that preformed nuclei are not responsible for bubbles developing in the legs of this animal. Instead, tribonucleation of bubbles apparently occurs as a result of limb motions at relatively low gas supersaturations.
Animals↗
Morphological and physiological responses of the lungs of dogs to acute decompression.
The lung's response to decompression was studied in dogs anesthetized with pentobarbital sodium. Arterial pressure, hematocrit, right ventricular pressure, left ventricular end-diastolic pressure (LVEDP), dynamic compliance (CL), pulmonary resistance (RL), and arterial PO2, PCO2, and pH were measured prior to and for 3 h after a simulated air dive to 300 feet of seawater. Bronchoscopy was performed predive and at 3 h postdive. At 3 h animals were killed, and sections of lung were excised for histological examination. The decompression profile used regularly produced pulmonary hypertension, systemic hypotension, hemoconcentration, and arterial hypoxemia. CL fell in all but one dived animal. RL was more variable but remained unchanged postdive in most animals. The decompression stress did not alter the bronchoscopic and histological appearance of the airway mucosa. Pulmonary edema was regularly observed in histological sections and occurred without elevations of LVEDP. We concluded that noncardiac pulmonary edema is the principal response of the lung to decompression stress.
Animals↗
Isoproterenol infusion promotes nitrogen washout in rats under normobaric conditions.
Cardiac output and the rate of N2 elimination were measured simultaneously in unanesthetized rats during isobaric desaturation with 100% O2. Whole-body N2-washout curves for the rat are characterized by three compartment half times derived by exponential stripping, representing the slow, intermediate, and fast components of the system. During saline infusion (control) the respective half times for these compartments were 120, 15, and 2 min. Isoproterenol infusion increased cardiac output by 40% and the volume of N2 eliminated by 10% over a 2-h washout. More importantly, the half time of the slowest compartment decreased from 120 to 70 min. The intermediate compartment half time shortened from 15 to 13 min, while the fast compartment was unaffected. The decrease in slow compartment half time will contribute significantly to the shortening of the duration of stay during decompression. A plot of slow compartment rate constants vs. measured cardiac output (range 280-690 ml X min-1 X kg-1) demonstrated a linear relationship between perfusion and the tissue-blood gas exchange rate. The results indicate that enhanced cardiac output and generalized vasodilation shorten the time required to desaturate the slower body tissues. Various maneuvers or drugs that demonstrate similar cardiovascular responses should be beneficial during prolonged decompression procedures involved in saturation diving.
Animals↗
Fatty acids in human platelets and plasma. Fish oils decrease sensitivity toward N2 microbubbles.
Platelet aggregation induced by N2 microbubbles (simulating microbubbles developed during deep diving) was measured in seven volunteers before and after intake of ethyl-eicosapentaenoate (-EPA, 3.5 g/day) and ethyl-docosahexaenoate (-DHA, 2.5 g/day) for 2 wk. The relative content of arachidonic acid (AA) decreased in platelets from all individuals, whereas the content of EPA and DHA increased. The decrease of AA was almost identical with the increase of EPA plus DHA. In plasma the AA content was unchanged, while EPA and DHA increased. The N2 microbubble-induced aggregation showed a significant negative correlation with the DHA content both in platelets and in plasma. Less aggregation was also observed with high EPA content in platelets or plasma. A significant correlation between AA content in platelets and aggregation was seen. Intake of marine oils may be beneficial to divers under deep diving and to patients during extracorporeal circulation, because this may reduce the microbubble-induced aggregation.
Adult↗
Variability over time of complement activation induced by air bubbles in human and rabbit sera.
Complement activation induced by air bubbles in rabbit and human sera was studied by measuring the generation of anaphylatoxin des-Arg-C5a. des-Arg-C5a was quantified by sandwich enzyme-linked immunosorbent assays based on neoepitope-specific anti-des-Arg-C5a monoclonal antibodies. Air bubbles were continuously introduced to serum via a calibrated microflowmeter, and the serum was incubated at 37 degrees C for 30 min. Air bubbles clearly generated increased amounts of des-Arg-C5a compared with corresponding levels in control serum, and a dose-dependent effect was also noted. Strong positive correlations between des-Arg-C5a concentrations in control sera and sera incubated with air bubbles at a flow of 0.5 ml/min were found. To study variation over time, serum was obtained at regular intervals from six rabbits and from six healthy humans during 66- and 196-day periods, respectively. A pronounced intraindividual variability over time was thus observed. The reason for the large variability is at present unknown. We conclude that the sensitivity of complement to activation by air bubbles is not an inherent, static feature of the complement system of an individual. Therefore single-point analysis of complement activation by air bubbles appears to be an inappropriate parameter by which to differentiate a "sensitive" or "insensitive" complement system between individuals.
Air↗
Bubbles in circulating blood: stabilization and simulations of cyclic changes of size and content.
Surface tension, blood pressure, and inherent unsaturation due to O2 metabolism promote diffusion of gases out of bubbles in the bloodstream. We review the mechanisms that can overcome the absorptive tendencies so small spherical bubbles can persist. One general type of stabilizer is a mechanical structure at the gas-liquid interface that can support a negative pressure so that gases inside can be in diffusion equilibrium with their counterparts outside; one possibility for mechanical stabilizers are surfactant films. We show that a slowly permeating gas is analogous to a mechanical stabilizer; it allows equilibration of other gases inside-to-outside by diluting the gases inside. By using numerically solved equations based on physics of diffusion, we demonstrate how nonrigid stabilized bubbles change size as they move through the circulatory system. In small pulmonary vessels, the bubbles enlarge because blood pressure is low, there is no inherent unsaturation, and O2 and N2 diffuse from lung gas into the bubble; these gases diffuse out again in the systemic circulation.
Absorption↗
Effect of a short-acting NO donor on bubble formation from a saturation dive in pigs.
It has previously been reported that a nitric oxide (NO) donor reduces bubble formation from an air dive and that blocking NO production increases bubble formation. The present study was initiated to see whether a short-acting NO donor (glycerol trinitrate, 5 mg/ml; Nycomed Pharma) given immediately before start of decompression would affect the amount of vascular bubbles during and after decompression from a saturation dive in pigs. A total of 14 pigs (Sus scrofa domestica of the strain Norsk landsvin) were randomly divided into an experimental (n = 7) and a control group (n = 7). The pigs were anesthetized with ketamine and alpha-chloralose and compressed in a hyperbaric chamber to 500 kPa (40 m of seawater) in 2 min, and they had 3-h bottom time while breathing nitrox (35 kPa O(2)). The pigs were all decompressed to the surface (100 kPa) at a rate of 200 kPa/h. During decompression, the inspired Po(2) of the breathing gas was kept at 100 kPa. Thirty minutes before decompression, the experimental group received a short-acting NO donor intravenously, while the control group were given equal amounts of saline. The average number of bubbles seen during the observation period decreased from 0.2 to 0.02 bubbles/cm(2) (P < 0.0001) in the experimental group compared with the controls. The present study gives further support to the role of NO in preventing vascular bubble formation after decompression.
Animals↗
Magnetic resonance signal abnormalities and neuropsychological deficits in elderly compressed-air divers.
We investigated the association between MR signal abnormalities of the central nervous system, neuropsychologic performance and exposure indices in 20 experienced elderly compressed-air divers who had no history of neurological decompression illness (DCI). Results of MRI of the brain and psychometric testing were compared with 20 matched healthy commercial employees who never dived: 60% of the divers and 45% of the controls had hyperintense MR abnormalities. Among divers, both the number and the size of abnormalities correlated with hours diving in the deep air-diving range of 40-60 m (p < 0.05). Divers' mental flexibility and visual tracking performance were decreased in comparison with controls (p < 0.05 and p < 0.01). Divers thus are at risk of detrimental long-term effects of compressed-air diving on the central nervous system even in the absence of a history of neurological DCI.
Barotrauma↗