Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Decompression”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed1991

Doppler detection of decompression bubbles with computer assisted digitization of ultrasonic signals.

Precordial Doppler ultrasonic monitoring is routinely used for detection of venous gas bubbles resulting from decompression in hypobaric or hyperbaric applications. Bubble scoring codes have been devised in an attempt to quantify the number of audible bubble signals heard over the background sounds of the cardiac cycle. The audio interpretation of these ultrasonic backscatter signals remains the most common method for decompression evaluation. We report on the use of an inexpensive, commercially available audio digitizer in conjunction with a personal computer to digitize Doppler bubble signals for visual and electronic evaluation. This device can be operated simultaneously with Doppler audio monitoring. Precordial and arterial Doppler recordings of gas bubbles were obtained from anesthetized dogs after intravascular infusion or following decompression. Additional evaluations were conducted on Doppler bubble recordings obtained from human decompression studies. The device can be used in real-time or for later signal analysis. Accompanying menu-driven software provides for numerous signal modification options and visual displays. This device can provide a simultaneous visual display of Doppler signals normally only available for audio evaluation.

Animals↗
PubMed1990

Rapid decompression of a transport aircraft cabin: protection against hypoxia.

The hypoxic hazard after rapid decompression in transport aircraft was evaluated as a function of the current means of protection, including the role of the inhaled oxygen fraction (FIO2) prior to decompression. The decompressions were made in 2 s; the initial altitude was 8,000 ft and the final altitude was 16,000-45,000 ft. The physiological measurements were arterial oxygen saturation, heart rate, ventilatory frequency, and gaseous analysis in the mask. Results show that FIO2 prior to decompression is not very significant, but the delay before donning the oxygen system seems to be the most limiting factor against tolerance to hypoxia.

Aerospace Medicine↗
PubMed1989

Ethanol treatment for acute decompression sickness in rabbits.

Rabbits developed acute decompression sickness after staying at 6 ATA for 30 min followed by decompression to 1 ATA in 20 min or less. If the rabbits received an i.v. injection of 25% ethanol upon surfacing, all survived, whereas half the untreated control group died within 15-35 min after decompressing. In ethanol-treated animals, no bubbles were seen in blood vessels of visceral organs, muscles, and subcutaneous tissues at autopsy 60 min after treatment. Decompression reduced platelet counts markedly in all rabbits, but in the control group the count stayed low, whereas with ethanol treatment the counts had reached the precompression level after 1 h and 24 h.

Animals↗
PubMed1986

Decompression sickness incidence over 63 months of hypobaric chamber operation.

U.S. Army hypobaric chamber operations over a 63-month period were retrospectively reviewed, and incidence rates for decompression sickness were calculated. The overall incidence rate was 1.38/1000 exposures. The rate for interior technicians monitoring chamber operations was 6.16/1000 exposures. The rate for students was 0.64/1000 exposures. The increased incidence of decompression sickness for technicians was especially pronounced for the 10,668-m and 13,106-m flight profiles. Rapid decompression after the 7,620-m flight profile did not appear to increase the incidence of decompression sickness.

Altitude↗
PubMed1985

Origin and time course of gas bubbles following rapid decompression in the hamster.

Because conflicting results have been obtained in studies of the hamster (Mesocricetus auratus) microcirculation following rapid decompression, we were interested in the origin of bubbles in the cheek-pouch preparation. The hamster cheek-pouch and surgically exposed femoral vessels were observed under the microscope, before and immediately following rapid decompression. The animals were placed in a hyperbaric chamber and exposed to an increased pressure of 7 ATA for 1 h. They were then decompressed at a rate of 18 m/min until reaching 1 ATA. This hyperbaric exposure produced an LD50 in 100 hamsters examined in this study. In 40% of these animals "bubbles" were seen entering the cheek-pouch artery after a delay of from 3 to 6 min following decompression. Before observing bubbles in the cheek-pouch artery, bubbles were always seen in the femoral vein. Those animals that had observable bubbles in the cheek-pouch usually demonstrated a tachypnea, followed by gasping and apnea. When bubbles were seen in the arterial circulation, few animals survived for more than 10 min following the hyperbaric exposure. Postmortem examination of these animals revealed massive gas emboli in the large venous vessels, right ventricle, and fewer bubbles in the left ventricle. Postmortem examination of surviving animals revealed that the majority of the gas was in the venous vessels and right heart. These data support the hypothesis that bubbles first form on the venous side of the circulation and, if they exceed a certain volume, move through the pulmonary circulation into the systemic arterial vessels.

Animals↗
PubMed1979

Bubble production in agarose gels subjected to different decompression schedules.

The relative effectiveness of seven different (military, commercial, and experimental) decompression schedules in reducing bubble formation within aqueous gels has been evaluated quantitatively under rigorously controlled conditions. Specifically, visual counts have been conducted of the bubbles formed in highly purified agarose gels subjected to the different decompression schedules. The order of effectiveness among these schedules in reducing bubble formation in the agarose gel samples was as follows: Model 1 greater than Royal Naval Physiological Laboratory approximately French Ministry of Labor greater than Yount et al. greater than Japanese Department of Labor greater than United States Navy greater than French Navy. It was concluded that the depth at which slow decompression commences is a major factor, along with the total decompression time, in determining the extent of bubble formation.

Decompression↗
PubMedDate not supplied

[Blood-brain barrier disorders and changes in intracranial pressure in cats with surgical brain wound following sudded brain decompression].

The condition of the blood-brain barrier and changes in intracranial pressure were studied in cats with surgical brain wounds and after sudded decompression. It was found that evident disturbances of the barrier function appeared only 48 hours after removal of brain tissue and were affecting mainly the white matter. Sudden decompression led to disturbances of blood-brain function when it was proceded by at least 2 hours of epidural compression. Changes developed in the cortex and basal ganglia. After 48 hours from tissue removal a significant rise of pressure was observed in the cisterna magna to a mean value of 11.5 mm Hg. Decompression caused a fall of cerebrospinal pressure, often below zero, and this was followed by a rise to values significantly exceeding the level before decompression.

Animals↗
PubMed1983

Cardiovascular effects of induced decompression sickness in sheep fetus.

Ten chronically catheterized near-term sheep fetuses were used to study the effect of induced intravascular bubbling on fetal placental vascular dynamics and fetal regional blood flows. Fetal blood pressure and heart rate were measured, and radioactive microspheres were administered to fetuses before and 5, 10, 15, and 20 min after a simulated no-decompression dive to 100 fsw (4 ATA) for 25 min. A decrease in brain blood flow was the only effect observed 5 min after decompression. Fifteen minutes later arterial hypertension was evident. Eight fetuses displayed arrhythmia, but there was no significant change in heart rate, myocardial blood flow, or resistance. There was a reduction in blood flow, and a concomitant increase in vascular resistance, in the gut, kidneys, placental membranes, and skeletal muscle, as well as in the brain. Total placental blood flow was unchanged throughout the postdive period, although placental vascular resistance was elevated 20 min after surfacing. Analysis of the placental blood flow at the cotyledonary level in 6 animals revealed no uniform response to decompression. The results are consistent with the hypothesis that the instrumented fetus suffers widespread vascular embolization and disruption of organ blood flows. We conclude that the observed changes in the fetal cardiovascular system, however, are not precipitated by an initial effect of decompression on the fetal placental circulation.

Animals↗
PubMed1984

Factitious decompression sickness.

The diagnosis of decompression sickness is made largely by history; there are few physical findings and no radiographic or laboratory tests to support the diagnosis. We present three cases of factitious decompression sickness in which patients fabricated an appropriate history and underwent compression therapy. Due to the potential severity of decompression sickness and the relative safety of compression therapy, the initiation of therapy must not be delayed in a case of decompression sickness. Once therapy is begun, investigation into the particulars of a suspicious case can be made.

Adult↗
PubMed1980

Respiratory gas exchange during positive pressure breathing and rapid decompression to simulated altitudes of 18.3 and 24.4 km.

Respiratory gas exchange was studied, using the technique of mass spectrometry, during events of slow and rapid decompression of human subjects to simulated altitudes of 60,000 and 80,000 ft (18.3 and 24.4 km, respectively). Positive breathing pressures and G-suit counterpressures were employed in three series of decompression experiment. Low levels of inspired carbon dioxide and nitrogen reflected the rebreathing of gases throughout the experiments. Application of a positive breathing pressure of 70 torr, accompanied by a jerkin pressure equal to breathing pressure and a G-suit counterpressure of four times the breathing pressure on the trunk and limbs, respectively, maintained alveolar oxygen at physiologically safe levels during decompression to 60,000 ft (18.3 km) altitude. Similarly, 80 torr positive breathing pressure, in combination with four times the breathing pressure in the G suit, adequately satisfied the requirements for oxygen during rapid decompression to 80,000 ft (24.4 km) simulated altitude.

Aerospace Medicine↗
PubMed1978

Decompression sickness in the goat: nature of brain and spinal cord lesions at 48 hours.

An investigation was undertaken to determine whether permanent damage to the central nervous system (CNS) is associated with transient decompression sickness in the goat. Twelve goats were compressed in air at 100 fsw for one hour. After decompression over a period of 2.5 min, seven animals showed signs of decompression sickness and four of these were treated by recompression in oxygen. Residual clinical signs after 12 h were present in one animal only. The seven affected goats were killed 48 h after decompression. Lesions in the CNS (other than hemorrhage) were confined to the spinal cord of three animals that had shown paralysis, and consisted of infarction of white matter with occasional microthrombi and perivascular proteinaceous edema of the gray matter. In all seven animals, there was hemorrhage in the spinal cord and in four, hemorrhage in the brain. Infarction of the spinal cord was not present in the four animals that had shown only slight clinical signs (limping); one of these goats had been treated by recompression in oxygen.

Animals↗
PubMed1978

Intracardial gas bubbles and decompression sickness while flying at 9,000 m within 12-24 h of diving.

Intracardial gas bubbles, detected with Doppler ultrasound, and symptoms of decompression sickness were registered at 9,000 m simulated altitude within 12, 18, and 24 h of exposures to 15 or 39 m simulated water depth allowing no stage decompression. With a time interval of 12 h between diving and flying, the earliest intracardial bubbles were found in some subjects already during the first minutes at altitude, and the earliest symptoms of decompression sickness some minutes afterwards. With an 18-h interval, the earliest bubbles and symptoms as well as their average time onsets appeared somewhat later. With a 24-h interval, the earliest bubbles and symptoms were detected slightly later, i.e. after 17 min and 23 min, respectively. Thus, a safe time interval between no-stage decompression dives and flying at 9,000 m cabin altitude for a maximum of 15 min appears to be 24 h. For prolonged such flights, a longer time interval seems to be necessary.

Adult↗
PubMed1980

Amelioration of decompression sickness in mice by pretreatment with cyproheptadine.

Substances that stimulate smooth muscle have been previously implicated in the pathogenesis of decompression sickness. This concept was strongly supported by the demonstration that compounds that combine activities against histamine, bradykinin, and serotonin prevent or ameliorate decompression sickness. This communication deals with the prophylactic effect of cyproheptadine (Periactin), a drug exhibiting such pharmacologic properties. More than 500 obese mice were used. Experimental groups, subcutaneously injected with cyproheptadine (0.5-40 mg/kg) prior to compression, and corresponding control animals were simultaneously subjected to 75 psig air pressure for 6 h and then rapidly decompressed. Most control animals exhibited signs of decompression sickness (chokes, scratching, twitching, convulsions, paralysis) and died. Gross and histologic examination revealed gas bubbles in vessels and tissues, perivascular edema, and other changes. In cyproheptadine-treated animals the incidence and severity of clinical manifestations and pathologic alterations were reduced, and mortality was marked decreased. Statistically significant results were obtained with doses of 2.5-10.0 mg/kg. The 5-mg/kg does lowered mortality by 45.9%. These results support the proposed pathogenetic concept and suggest a potential preventive treatment for human subjects.

Animals↗
PubMed1978

The kangaroo rat as a model for type I decompression sickness.

This study involved 720 exposures of 70 kangaroo rats trapped in West Texas and showed that decompression-induced tail biting in this animal provides a good animal model for marginal limb bends in man. That this phenomenon can be reversed by recompression and pathological examination of the tail both indicated that a similar mechanism is probably involved in kangaroo rats and humans. Quantitatively, the most susceptible 20% of kangaroo rats can reproduce the no-stop decompression limits for man for exposure times ranging from 5 min to 8 h, for both air and helium-oxygen. Even the average minimum no-tail-biting depth of 46.2 fsw (2.40 ATA) for this species is much closer to the minimum bends depth of man than to the equivalent depth for other animals of its size, and is as good as the goats'. Its size and habits make the kangaroo rat much more convenient than other animals to use as a model for marginal decompression sickness, and particularly attractive economically for testing long helium-oxygen schedules and other means of decompression sickness prevention.

Animals↗
PubMed1995

Diving at altitude: a review of decompression strategies.

Diving at altitude requires different tables from those at sea level due to the reduction in surface ambient pressure. Several algorithms extrapolating sea-level diving experimental data have been proposed to construct altitude diving tables. The rationale for these algorithms is reviewed together with the conservatism of the resulting tables and decompression computer outputs. All algorithms are based on the adaptation of critical tissue tensions to altitude. These are linear extrapolation (LEM), constant ratio translation (CRT), and constant ratio extrapolation (CRE) of maximum permissible tissue tensions (M values). Either new tables using the altitude-adapted M values were put forward or sea-level tables are to be used through an operation called correction. In this review it is shown that for a given set of M values, CRT and CRE give the same result for no-decompression-stop dives; they always yield more conservative results than LEM. When decompression stops are used, CRT is more conservative than CRE. When applied to different sets of M values, the conservatism becomes a function of bottom time, depth, and altitude. The analysis shows that the tables derived using CRT of U.S. Navy (USN) schedules and CRE Boni et al. tables give more conservative results than LEM Bühlmann tables for higher altitude, longer bottom time, and deeper dives. Aviation altitude exposure decompression sickness (DCS) data are also addressed to compare different model outputs. When applied to USN and Royal Navy tables, LEM yields an altitude DCS limit of 8,581 and 8,977 m, respectively. On the other hand, the altitude limit calculated using CRE applied to USN M values and LEM Bühlmann tables is found to be below 6,000 m.

Aerospace Medicine↗
PubMed1996

Vascular-decompression surgery for severe tinnitus.

Vascular compression of the eighth cranial nerve is increasingly recognised as a possible cause of incapacitating audiovestibular symptoms. There have been few reports of the efficacy of surgical microvascular decompression for tinnitus, and the practise is controversial. During the last 6 years, investigation by air computed tomography (CT) cisternography initially, and fast spin-echo magnetic resonance imaging (MRI) latterly has resulted in the diagnosis of cochlear nerve vascular compression in nine patients with a primary complaint of severe tinnitus who have subsequently undergone vascular-decompression surgery. The duration of symptoms ranged between 1 and 10 years, whilst their subjective tinnitus perception varied between 30 to 60 dB above threshold. Microvascular decompression was carried out by a retrolabyrinthine approach in four and by a retrosigmoid approach in the remaining five cases, with a postoperative follow-up of 1.3 to 5 years. Tinnitus was completely abolished in three (33%), very significantly improved to a sensation level of < or = 10 dB in four (33%), significantly improved to a level of 15 dB in one (11%), and unchanged in two (22%). Both failures had had tinnitus for 6 years and had transient abolition for 10 days after surgery. Subsequent revision decompression surgery was also unsuccessful. This small study suggests that cochleovestibular vascular compression may result in severe tinnitus, which can often be ameliorated surgically.

Adult↗
PubMed1977

Altitude decompression sickness: hyperbaric therapy results in 145 cases.

Most cases of decompression sickness that occur at altitude resolve upon descent to lower altitudes. Before the use of hyperbaric therapy, cases that did not resolve accounted for some of the most difficult medical management problems in military aerospace medicine. On 27 March, 1941, the U.S. Navy Diving School successfully used hyperbaric therapy for a case of altitude-induced decompression sickness that did not resolve on return to ground level. Since then, over 145 such cases have been treated by hyperbaric therapy. At first, treatments involved using compressed air, with varying success. Current medical management of altitude-induced decompression sickness requires immediate compression to 2.8 ATA, equivalent to 60 ft of sea water (FSW) pressure, and a series of intermittent oxygen and air breathing periods during the subsequent slow decompression to surface. This report confirms the treatment recommendations set forth by Behnke and Downey, and crystallized by Goodman in 1964. Conclusions are based on treatment experience in the management of 120 cases in U.S. Air Force hyperbaric chambers, and a survey of hyperbaric facilities which have treated 25 other cases.

Adult↗
PubMedDate not supplied

[Rare case of brain damage in a primary decompression sickness in a diver].

Pressure disease causes very infrequently multifocal injury to the cerebral hemispheres with resulting organic brain disease. The described case was observed in a diver who after correctly performed decompression without any evident faults in decompressions during several years of diving suffered diffuse, multifocal injury to the cerebral hemispheres and right vestibular nuclei. The authors stress the fact that decompression tables differ in various countries. There is no uniform safety decompression table for the divers. Besides that, such factors as individual sensitivity and resistance of the diver to the effects of raised pressure should be taken into consideration.

Brain Diseases↗