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Deep sea divers, aviators and astronauts are at risk of decompression sickness when the ambient pressure reductions exceed a critical threshold. Venous bubbles associated with decompression sickness have the potential to react with the vascular membrane and adjacent blood products, eliciting an inflammatory cascade. Preventive measures usually involve careful decompression procedures to avoid or reduce bubble formation. De-nitrogenation with 100% oxygen pre-breathing as a preventive measure has been well established at least in altitude decompression exposures. The objective of this study was to determine the physiological and biochemical effects of Hyperbaric Oxygen Pre-breathe (HBOP) upon decompression from a hyperbaric exposure. Male Sprague-Dawley rats were randomly assigned to one of eight groups. Two experimental groups received HBOP at 1 and 18 hours prior to decompression, as compared with ground level oxygen or non-treated groups that still experienced decompression stress, and the associated non-decompressed controls. The results showed decreased extravascular lung water (pulmonary edema), bronchoalveolar lavage and pleural protein and arterial, broncho-alveolar lavage, and urine leukotriene E4 (LKE4) levels in both the 1Hr and 18Hr HBOP decompressed rats compared to non-oxygenated decompressed rats, as well as a decreased overall expression of signs of decompression sickness. This study indicates that HBOP-treated rats exhibit fewer signs and complications of decompression sickness compared with non-treated or ground level oxygen treated rats.

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OBJECTIVES: To monitor PO2, PCO2, and pH in the interstitium of skeletal muscle (PmO2, PmCO2, and pHm) during hemorrhage, shock, and resuscitation using fiber-optic sensors and to compare Pco2 and pH in the interstitium of gastric mucosa (PrCO2 and pHi) obtained using gastric CO2 tonometry. DESIGN: Prospective, controlled observational study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Nine mongrel dogs (20 to 35 kg). INTERVENTIONS: Anesthesia was induced with pentobarbital (25 mg/kg iv) and maintained (10 mg/hr) after hemorrhagic shock. Mechanical ventilation was established to maintain baseline PaCO2 approximately 35 torr. Arterial, venous, and pulmonary artery catheters were placed. Blood flow probes were placed around the right femoral artery and vein. A probe (0.5 mm in diameter) with fiber-optic PO2, PCO2, and pH sensors was placed percutaneously in the adductor muscle of the right thigh. A gastric tonometer catheter was placed in the stomach lumen. After baseline data collection, controlled hemorrhage to mean arterial pressure (MAP) of 45 to 50 mm Hg was maintained for 1 hr. Shed blood was then reinfused. Blood gas, hemodynamic, and gastric tonometric data were collected during shock and reinfusion at 30-min intervals and hourly after reinfusion for 4 hrs. Normothermia was maintained. MEASUREMENTS AND MAIN RESULTS: PmO2 decreased rapidly from 42 +/- 13 torr (mean +/- sD) to 13 +/- 9 torr within 15 mins and to 6 +/-4 torr within 30 mins of MAP reaching 45 mm Hg, and it recovered to baseline with reinfusion. pHm decreased gradually from 7.23 +/-0.09 to 6.89 +/- 0.25 during the 1-hr shock period and increased slowly toward baseline after reinfusion. pHi decreased from 7.43 +/- 0.14 to 6.91 +/- 0.23, and on average it returned to baseline 2 hrs after reinfusion. PmCO2 increased from 50 +/- 12 to 113 +/- 49 torr, increased further to 124 +/- 73 torr during reinfusion, and returned slowly toward baseline after reinfusion. PrCO2 increased from 35 +/- 8 to 60 +/- 19 torr and returned to baseline within 15 mins after reinfusion. During shock and reinfusion, oxygen delivery, mixed venous PO2, mixed venous oxygen saturation, and PmO2 responded with similar time courses. After reinfusion, on average, PmO2 exceeded baseline PmO2 and mixed venous PO2, and oxygen availability exceeded demand, suggesting an oxygen consumption defect. On average, PmCO2 and pHm did not return to baseline values 4 hrs after reinfusion, suggesting the persistence of anaerobic metabolic effects in skeletal muscle beyond the relatively short time that is required to reestablish baseline MAP, blood flow rates, oxygen delivery, PrCO2, and pHi. CONCLUSIONS: PmO2, PmCO2, and pHm, monitored simultaneously using fiber-optic sensors in a single, small probe placed percutaneously, appear to indicate greater severity of shock and more prolonged resuscitation than conventional systemic or gastric tonometric variables.

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BACKGROUND: Although evidence of systemic vasoconstriction has been reported both in animal models and in humans, the regional hemodynamic effects of hyperbaric hyperoxia have not been well characterized. METHODS: In the present study, we report the effects of hyperoxia (normobaric and hyperbaric) on simultaneous measurements of cardiac and regional hemodynamics in the chronically instrumented conscious dog. RESULTS: Hyperbaric hyperoxia (202 kPa) produced significant decreases in heart rate (12%) and cardiac output (20%) and a significant increase in systemic vascular resistance (30%). Carotid artery blood flow decreased significantly (18%) whereas coronary, hepatic, renal and mesenteric flows remained unchanged. CONCLUSIONS: Our data show that the hyperoxic vasoconstriction is limited to the cerebral and peripheral vascular beds. Additionally, blood flow to major organs is well preserved in the face of hyperoxia-induced decreases in cardiac output. Consequently, we postulate that a redistribution of blood flow from peripheral vascular beds (e.g., skin, muscle, bone) to major organs occurs during hyperbaric hyperoxia.

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OBJECTIVE: To test fiber-optic PO2, PCO2, and pH sensors placed in skeletal muscle as monitors of hemorrhage, shock, and resuscitation, compared with mean arterial blood pressure, cardiac output, and blood gas variables. DESIGN: Observational study in physiology laboratory, using a canine controlled hemorrhagic shock model. MATERIALS AND METHODS: Mongrel dogs (20-35 kg; n = 10) were monitored with arterial, venous, and pulmonary artery catheters. A probe (0.5 mm in diameter) with fiber-optic PO2, PCO2, and pH sensors was placed percutaneously in the adductor muscle of the right medial thigh. Mean arterial blood pressure of 45 to 50 mm Hg was maintained for 1 hour with controlled hemorrhage, after which shed blood was reinfused. The animals were monitored for 4 hours after reinfusion. MEASUREMENTS AND MAIN RESULTS: Skeletal muscle PO2 (PmO2) decreased from 31+/-9 to 5+/-4 mm Hg during shock and recovered with reinfusion. Skeletal muscle pH (pHm) decreased from 7.24+/-0.10 to 6.94+/-0.12 during shock, to 6.90+/-0.13 with reinfusion, and recovered to near baseline 2 hours after reinfusion. PmCO2 increased from 48+/-14 to 134+/-86 mm Hg during shock, to 138+/-92 mm Hg with a time course inverse to pHm, and recovered to near baseline 30 minutes after reinfusion. On average, skeletal muscle PCO2 (PmCO2) and pHm did not recover to baseline, possibly indicating persistent anaerobic metabolic effects. O2 delivery, mixed venous PO2, mixed venous O2, saturation and PmO2 responded with similar time courses. CONCLUSION: PmO2, PmCO2, and pHm can be monitored simultaneously for several hours with fiber-optic sensors in a single, small probe. PmO2 may provide information comparable to O2 delivery. PmCO2 may reflect adequacy of perfusion. pHm may indicate success of resuscitation. This technology may offer new insight into the extent of injury and refinement of shock resuscitation and monitoring.

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Physiological studies of the effects of high altitude on man often require the use of a hypobaric chamber to simulate the reduced ambient pressures. Typical "altitude" chambers in use today require complex mechanical vacuum systems to evacuate the chamber air, either directly or via reservoir system. Use of these pumps adds to the cost of both chamber procurement and maintenance, and service of these pumps requires trained support personnel and regular upkeep. In this report we describe use of venturi vacuum pumps to perform the function of mechanical vacuum pumps for human and experimental altitude chamber operations. Advantages of the venturi pumps include their relatively low procurement cost, small size and light weight, ease of installation and plumbing, lack of moving parts, and independence from electrical power sources, fossil fuels and lubricants. Conversion of three hyperbaric chambers to combined hyper/hypobaric use is described.

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Decompression-induced venous bubble formation has been linked to increased neutrophil counts, endothelial cell injury, release of vasoactive eicosanoids, and increased vascular membrane permeability. These actions may account for inflammatory responses and edema formation. Increasing the intracellular cAMP has been shown to decrease eicosanoid production and edema formation in various models of lung injury. Reduction of decompression-induced inflammatory responses was evaluated in decompressed rats pretreated with saline (controls) or dibutyryl cAMP (DBcAMP, an analog of cAMP). After pretreatment, rats were exposed to either 616 kPa for 120 min or 683 kPa for 60 min. The observed increases in extravascular lung water ratios (pulmonary edema), bronchoalveolar lavage, and pleural protein in the saline control group (683 kPa) were not evident with DBcAMP treatment. DBcAMP pretreatment effects were also seen with the white blood cell counts and the percent of neutrophils in the bronchoalveolar lavage. Urinary levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were significantly increased with the 683 kPa saline control decompression exposure. DBcAMP reduced the decompression-induced leukotriene E4 production in the urine. Plasma levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were increased with the 683-kPa exposure groups. DBcAMP treatment did not affect these changes. The 11-dehydrothromboxane B2 and leukotriene E4 levels in the bronchoalveolar lavage were increased with the 683 kPa exposure and were reduced with the DBcAMP treatment. Our results indicate that DBcAMP has the capability to reduce eicosanoid production and limit membrane permeability and subsequent edema formation in rats experiencing decompression sickness.

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BACKGROUND: Previous studies demonstrated gas emboli formation during rewarming from hypothermia on cardiopulmonary bypass when the temperature gradient exceeded a critical threshold. It also has been suggested that formation of arterial gas emboli may occur during cooling on cardiopulmonary bypass when cooled oxygenated blood exiting the heat exchanger is warmed on mixture with the patient's blood. The purpose of this study was to determine under what circumstances gas emboli formation would occur during cooling on cardio-pulmonary bypass. METHODS: Eight anesthetized mongreal dogs were placed on cardiopulmonary bypass using a roller pump, membrane oxygenator, and arterial line filter. For emboli detection, we positioned a transesophageal echocardiographic probe at the aortic arch distal to the aortic cannula and Doppler probes at the common carotid artery and the arterial line. Cooling gradients between normothermic blood and cooled arterial perfusate of 5 degrees, 10 degrees, 15 degrees, 20 degrees, and 0 degree C (isothermal controls) were investigated. In addition to preestablished temperature gradients, we investigated the effect of rapid cooling (maximal flow through the heat exchanger at a water bath temperature of 4 degrees C) after the initiation of normothermic cardiopulmonary bypass. RESULTS: Minimal gas emboli were detected at the aortic arch at gradients of 10 degrees C or greater. The incidence of emboli was related directly to the magnitude of the temperature gradient (p < 0.01). No emboli were detected at the carotid artery. During rapid cooling, no emboli were observed either at the aorta or at the carotid artery. CONCLUSIONS: Cooling gradients of 10 degrees C or greater may be associated with gas emboli formation, but they may be of limited clinical significance because no emboli were detected distal to the aortic arch. During the application of rapid cooling, no emboli formation was observed.

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BACKGROUND: Current therapy for massive venous air embolism (VAE) may include the use of the left lateral recumbent (LLR) position, although its effectiveness has been questioned. This study used transesophageal echocardiography to evaluate the effect of body repositioning on intracardiac air and acute cardiac dimension changes. METHODS: Eighteen anesthetized dogs in the supine position received a venous air injection of 2.5 ml/kg at a rate of 5 ml/ s. After 1 min the dogs were repositioned into either the LLR, LLR 10 degrees head down (LLR-10 degrees), right lateral recumbence, or remained in the supine position. RESULTS: Repositioning after VAE resulted in relocation of intracardiac air to nondependent areas of the right heart. Peak right ventricular (RV) diameter increase and mean arterial pressure decrease were greater in the repositioned animals compared with those in the supine position (P < 0.05). Right ventricular diameter and mean arterial pressure showed an inverse correlation (r = 0.81). Peak left atrial diameter decrease was greater in the LLR and LLR-10 degrees positions compared with the supine position (P < 0.05). Repositioning did not influence peak pulmonary artery pressure increase, and no correlation was found between RV diameter and pulmonary artery pressure. All animals showed electrocardiogram and echocardiographic changes reconcilable with myocardial ischemia. CONCLUSIONS: In dogs, body repositioning after VAE provided no benefit in hemodynamic performance or cardiac dimension changes, although relocation of intracardiac air was demonstrated. Right ventricular air did not appear to result in significant RV outflow obstruction, as pulmonary artery pressure increased uniformly in all groups and was not influenced by the relocation of intracardiac air. The combination of increased RV afterload and arterial hypotension, possibly with subsequent RV ischemia rather than RV outflow obstruction by an airlock appeared to be the primary mechanism for cardiac dysfunction after VAE.

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OBJECTIVES: 1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult. DESIGN: Prospective, controlled, animal study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Fourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated. INTERVENTIONS: Anesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FiO2 0.21). Mechanical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FiO2 0.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximately 40 mm Hg produced with isoflurane approximately 4%). After 45 mins, carotid artery occlusion was released, FiO2 was reset to 0.21, and anesthetic was returned to halothane (approximately 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult. MEASUREMENTS AND MAIN RESULTS: Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximately 1-hr intervals. Baseline data agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2 continued to decrease rapidly after brain insult and then remained approximately 52 +/- 10 torr (approximately 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2 increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximately 35 +/- 10 torr (approximately 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult. CONCLUSIONS: Intracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO2, and pH in dogs for periods lasting > 8 hrs. Significant changes in brain p

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BACKGROUND: Astronauts conducting extravehicular activities undergo decompression to a lower ambient pressure, potentially resulting in gas bubble formation within the tissues and venous circulation. Additionally, exposure to microgravity produces fluid shifts within the body leading to cardiovascular deconditioning. A lower incidence of decompression illness in actual spaceflight compared with that in ground-based altitude chamber flights suggests that there is a possible interaction between microgravity exposure and decompression illness. HYPOTHESIS: The purpose of this study was to evaluate the cardiovascular and pulmonary effects of simulated hypobaric decompression stress using a tail suspension (head-down tilt) model of microgravity to produce the fluid shifts associated with weightlessness in conscious, chronically instrumented rats. METHODS: Venous bubble formation resulting from altitude decompression illness was simulated by a 3-h intravenous air infusion. Cardiovascular deconditioning was simulated by 96 h of head-down tilt. Heart rate, mean arterial blood pressure, central venous pressure, left ventricular wall thickening and cardiac output were continuously recorded. Lung studies were performed to evaluate edema formation and compliance measurement. Blood and pleural fluid were examined for changes in white cell counts and protein concentration. RESULTS: Our data demonstrated that in tail-suspended rats subjected to venous air infusions, there was a reduction in pulmonary edema formation and less of a decrease in cardiac output than occurred following venous air infusion alone. Mean arterial blood pressure and myocardial wall thickening fractions were unchanged with either tail-suspension or venous air infusion. Heart rate decreased in both conditions while systemic vascular resistance increased. CONCLUSIONS: These differences may be due in part to a change or redistribution of pulmonary blood flow or to a diminished cellular response to the microvascular insult of the venous air embolization.

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Sprague-Dawley rats were compressed to 616 kPa (a) for 120 min then decompressed at 38 kPa/min to assess the cardiovascular and pulmonary responses to moderate decompression stress. In one series of experiments the rats were chronically instrumented with Doppler ultrasonic probes for simultaneous measurement of blood pressure, cardiac output, heart rate, left and right ventricular wall thickening fraction, and venous bubble detection. Data were collected at baseline, throughout the compression/decompression protocol, and for 120 min post decompression. In a second series of experiments the pulmonary responses to the decompression protocol were evaluated in non-instrumented rats. Analyses included blood gases, pleural and bronchoalveolar lavage (BAL) protein and hemoglobin concentration, pulmonary edema, BAL and lung tissue phospholipids, lung compliance, and cell counts. Venous bubbles were directly observed in 90% of the rats where immediate post-decompression autopsy was performed and in 37% using implanted Doppler monitors. Cardiac output, stroke volume, and right ventricular wall thickening fractions were significantly decreased post decompression, whereas systemic vascular resistance was increased suggesting a decrease in venous return. BAL Hb and total protein levels were increased 0 and 60 min post decompression; pleural and plasma levels were unchanged. BAL white blood cells and neutrophil percentages were increased 0 and 60 min post decompression and pulmonary edema was detected. Venous bubbles produced with moderate decompression profiles give detectable cardiovascular and pulmonary responses in the rat.

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We describe the case of a 33-year-old woman who suffered a delayed-onset arterial gas embolism following a significant venous air embolism during surgery to remove an acoustic neuroma. We report the management of the problem and discuss the mechanisms by which this event might have occurred.

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BACKGROUND: Continuous venous air emboli have been detected in the inferior vena cava and smaller veins using transesophageal echocardiography in patients with positive pressure ventilation and associated pulmonary barotrauma. The authors hypothesized that gas entered the venous circulation, following dissection of small vessels at several sites in the subcutaneous or retro-peritoneal soft tissues. OBJECTIVE: The present study was designed to determine if a comparable venous gas embolism occurred in anesthetized dogs, after creation of a pneumomediastinum. DESIGN: Using transesophageal echocardiography, we observed 11 anesthetized dogs mechanically ventilated with positive end-expiratory pressure, while mediastinal air was introduced through a catheter at a rate of 0.5 ml/kg/min. RESULTS: A continuous stream of bubbles appeared in the inferior vena cava in 8/11 dogs (73%) after an infusion period of 280 +/- 81 min. A surge of bubbles was commonly observed following abdominal massage and was often associated with a transient decrease of end-tidal carbon dioxide tensions. In two dogs the air infusion rate was reduced to 0.25 mg/kg/min, and bubbles were detected in the inferior vena cava for as long as 16 consecutive hours. CONCLUSION: We conclude that in anesthetized dogs mechanically ventilated with positive end-expiratory pressure, unremitting pneumomediastinum is usually followed by continuous venous air embolism. A mechanism hypothesized for venous gas entry in the clinical condition of positive end-expiratory pressure ventilation with subcutaneous gas is suggested by this model.

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OBJECTIVE: The esophageal-tracheal Combitube (Sheridan, Inc., Argyle, NY) is a unique double lumen tube that has been introduced as an emergency intubation device. Since it is placed blindly, proper use requires determination of which lumen can be successfully used for ventilation. The Easycap (Nellcor, Inc., Pleasanton, CA) is a colorimetric carbon dioxide detector that reacts with exhaled gas to indicate proper tracheal tube location. The purpose of this study was to determine if the Easycap can be used to identify which Combitube lumen is patent to the trachea after blind placement in dogs. METHODS AND RESULTS: The study was conducted using 8 anesthetized dogs. In each of 15 blind insertions of the Combitube, the Easycap device responded appropriately by changing color from purple to yellow when connected to the lumen communicating with the trachea. When the Easycap device was connected to the alternate lumen, no color change was appropriately observed in 9 out of 15 cases (60%) after 6 breaths; in 4 of the remaining 6 (87%, total), no color change was noted after 12 breaths. In the 2 remaining cases, the color change indicated the need of further verification of the tube location. In separate experiments, 10 direct tracheal and esophageal insertions of the Combitube were correctly verified by the appropriate Easycap color change. CONCLUSIONS: Our results suggest that the Easycap device may be useful with the Combitube, although human data are required.

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Transesophageal echocardiography was used to evaluate venous bubbles produced in nine anesthetized dogs following decompression from 2.84 bar after 120 min at pressure. In five dogs a pulsed Doppler cuff probe was placed around the inferior vena cava for bubble grade determination. The transesophageal echo images demonstrated several novel or less defined events. In each case where the pulmonary artery was clearly visualized, the venous bubbles were seen to oscillate back and forth several times, bringing into question the effect of coincidental counting in routine bubble grade analysis using precordial Doppler. A second finding was that in all cases, extensive bubbling occurred in the portal veins with complete extraction by the liver sinusoids, with one exception where a portal-to-hepatic venous anastomosis was observed. Compression of the bowel released copious numbers of bubbles into the portal veins, sometimes more than were released into the inferior vena cava. Finally, large masses of foam were routinely observed in the non-dependent regions of the inferior vena cava that not only delayed the appearance of bubbles in the pulmonary artery but also allowed additional opportunity for further reaction with blood products and for coalescence to occur before reaching the pulmonary microcirculation. These novel observations are discussed in relation to the decompression process.

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Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow patency. We evaluated the effects of: a) venous gas embolism (0.025, 0.05 and 0.15 ml.kg-1.min-1 for 180 min.); b) hyperbaric decompression; and c) hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.

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Gas microbubbles were detected in the left ventricle of a supine subject being screened for an atrial septal defect as a participant of a hypobaric decompression study. This determination was made using the saline echocontrast procedure. We found provocation by a Valsalva maneuver not to be necessary in this individual for right-to-left passage of contrast microbubbles into the left heart and middle cerebral artery. When this same individual underwent hypobaric decompression to a simulated altitude of 21,000 ft, numerous gas microbubbles were detected in the right heart, but no gas bubbles were detected in either the left ventricular outflow tract or in the middle cerebral artery. This observation appears to be a novel finding, not previously reported.

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