Tissue Gas Tensions Research Articles

Radiological Investigation of Gas Embolism in the East Asian Finless Porpoise (Neophocaena asiaeorientalis sunameri)

Cetaceans have long been considered biologically adapted to suffer no adverse effects from diving-related tissue gas tension. However, increasing reports of gas embolism in cetaceans inhabiting European, Mediterranean and American waters have challenged the conventional understanding of marine mammal diving physiology. In human hyperbaric medicine, virtopsy techniques such as post-mortem computed tomography (PMCT) facilitate the visualization of gas embolism and could be performed adjunct to conventional autopsy. This research presents the first case of gas embolism identified in an East Asian finless porpoise inhabiting Asian waters. Massive gas embolic lesions were found in the liver, which had been compressing both the lungs and abdominal organs, and signs of pneumonia and parasitic infection were observed in both lungs. It is hypothesized that this porpoise might have been unable to expelin vivogas bubbles from its circulation due to pulmonary dysfunction. Consequently, gas bubbles agglomerated in the liver, resulting in the development of gas embolic lesions. The findings of the present study provide insights into the occurrence of gas embolism in the East Asian finless porpoise, highlighting the potential of PMCT as a promising tool for the diagnosis of gas embolism in stranded cetaceans.

Monitoring the biomechanical and physiological effects of postural changes during leisure chair sitting

BackgroundIndividuals with limited mobility can spend prolonged periods in leisure chairs, increasing their risk of developing a seated acquired pressure ulcer. The present study aims to use objective measures of posture and tissue viability to identify the associated risks of leisure chair related pressure ulcers. MethodsHealthy participants (n = 13) were recruited to sit on a leisure chair with either a viscoelastic foam or air cushion. Participants were asked to adopt four different postures for a period of 10 min followed by a 10 min refractory period. Measurements at the leisure chair-participant interface included interface pressure, transcutaneous tissue gas tensions at the ischial tuberosities, accelerometer data collected from the sternum and subjective comfort levels. ResultsResults indicated that interface pressures remained consistent, with peak pressure index values of less than 60 mmHg across all conditions. A proportion of participants exhibited decreased oxygen tensions associated with increased carbon dioxide tensions during one or more test condition. This was particularly prevalent during the right lean posture on the air cushion (46%). In all cases, normal tissue viability was restored during standing. The accelerometer was able to detect significant changes (p < 0.05) in relative trunk angles during slump and right lean when compared to optimal sitting posture. ConclusionCommercially available leisure chairs have little evidence to support their pressure relieving properties. This study revealed that a proportion of healthy individuals demonstrated a compromised tissue viability in specific postures. Further research is required to assess the impact of these sitting conditions in vulnerable individuals.

Decompression sickness ('the bends') in sea turtles.

Decompression sickness (DCS), as clinically diagnosed by reversal of symptoms with recompression, has never been reported in aquatic breath-hold diving vertebrates despite the occurrence of tissue gas tensions sufficient for bubble formation and injury in terrestrial animals. Similarly to diving mammals, sea turtles manage gas exchange and decompression through anatomical, physiological, and behavioral adaptations. In the former group, DCS-like lesions have been observed on necropsies following behavioral disturbance such as high-powered acoustic sources (e.g. active sonar) and in bycaught animals. In sea turtles, in spite of abundant literature on diving physiology and bycatch interference, this is the first report of DCS-like symptoms and lesions. We diagnosed a clinico-pathological condition consistent with DCS in 29 gas-embolized loggerhead sea turtles Caretta caretta from a sample of 67. Fifty-nine were recovered alive and 8 had recently died following bycatch in trawls and gillnets of local fisheries from the east coast of Spain. Gas embolization and distribution in vital organs were evaluated through conventional radiography, computed tomography, and ultrasound. Additionally, positive response following repressurization was clinically observed in 2 live affected turtles. Gas embolism was also observed postmortem in carcasses and tissues as described in cetaceans and human divers. Compositional gas analysis of intravascular bubbles was consistent with DCS. Definitive diagnosis of DCS in sea turtles opens a new era for research in sea turtle diving physiology, conservation, and bycatch impact mitigation, as well as for comparative studies in other air-breathing marine vertebrates and human divers.

Tissue gas tensions and tissue metabolites for detection of organ hypoperfusion and ischemia

The aim of this study was to evaluate how tissue gas tensions and tissue metabolites measured in situ can detect hypoperfusion and differentiate between aerobic and anaerobic conditions during hemorrhagic shock. We hypothesized that tissue PCO(2) (PtCO(2)) would detect hypoperfusion also under aerobic conditions and detect anaerobic metabolism concomitantly with or earlier than other markers. Prospective experimental animal study with eight anesthetized pigs subjected to a continuous blood loss ∼8% of total blood volume per hour until death. We measured cardiac index, organ blood flows, and tissue levels of PO(2), PCO(2), glucose, pyruvate, lactate, and glycerol in intestine, liver, kidney, and skeletal muscle. With reduction in blood flow to the organs under aerobic conditions, PtCO(2) increased ∼1-4 kPa from baseline. With the onset of tissue hypoxia there was a pronounced increase of PtCO(2), lactate, lactate-pyruvate (LP) ratio, and glycerol. Tissue pH and bicarbonate decreased significantly, indicating that metabolic acid was buffered by bicarbonate to generate CO(2). Moderate tissue hypoperfusion under aerobic conditions is associated with increased PtCO(2), in contrast to metabolic parameters of ischemia (lactate, LP ratio, and glycerol) which remain low. From the onset of ischemia there is a much more rapid and pronounced increase in PtCO(2), lactate, and LP ratio. PtCO(2) can be used as a marker of hypoperfusion under both aerobic and anaerobic conditions; it gives an earlier warning of hypoperfusion than metabolic markers and increases concomitantly with or earlier than other markers at the onset of tissue anaerobiosis.

Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation

Inner ear decompression sickness has been strongly associated with the presence of right-to-left shunts. The implied involvement of intravascular bubbles shunted from venous to arterial circulations is inconsistent with the frequent absence of cerebral symptoms in these cases. If arterial bubbles reach the labyrinthine artery, they must also be distributing widely in the brain. This discrepancy could be explained by slower inert gas washout from the inner ear after diving and the consequent tendency for arterial bubbles entering this supersaturated territory to grow because of inward diffusion of gas. Published models for inner ear and brain inert gas kinetics were used to predict tissue gas tensions after an air dive to 4 atm absolute for 25 min. The models predict half-times for nitrogen washout of 8.8 min and 1.2 min for the inner ear and brain, respectively. The inner ear remains supersaturated with nitrogen for longer after diving than the brain, and in the simulated dive, for a period that corresponds with the latency of typical cases. It is therefore plausible that prolonged inner ear inert gas supersaturation contributes to the selective vulnerability of the inner ear to short latency decompression sickness in divers with right-to-left shunt.

Response of heart rate and cloacal ventilation in the bimodally respiring freshwater turtle, Rheodytes leukops, to experimental changes in aquatic PO2

Changes in heart rate (f(H)) and cloacal ventilation frequency (f(C)) were investigated in the Fitzroy turtle, Rheodytes leukops, under normoxic (17.85 kPa) and hypoxic (3.79 kPa) conditions at 25 degrees C. Given R. leukops' high reliance on aquatic respiration via the cloacal bursae, the objective of this study was to examine the effect of varying aquatic PO(2) levels upon the expression of a bradycardia in a freely diving, bimodally respiring turtle. In normoxia, mean diving f(H) and f(C) for R. leukops remained constant with increasing submergence length, indicating that a bradycardia failed to develop during extended dives of up to 3 days. Alternatively, exposure to aquatic hypoxia resulted in the expression of a bradycardia as recorded by a decreasing mean diving f(H) with increasing dive duration. The observed bradycardia is attributed to a hypoxic-induced metabolic depression, possibly facilitated by a concurrent decrease in f(C). Results suggest that R. leukops alters its strategy from aquatic O(2) extraction via cloacal respiration in normoxia to O(2) conservation when exposed to aquatic hypoxia for the purpose of extending dive duration. Upon surfacing, a significant tachycardia was observed for R. leukops regardless of aquatic PO(2), presumably functioning to rapidly equilibrate blood and tissue gas tensions with alveolar gas to reduce surfacing duration.

HYPERBARIC OXYGEN FOR THE TREATMENT OF FOURNIER’S GANGRENE

Fournier's gangrene is a necrotizing fasciitis of the genitalia that is associated with high morbidity and mortality. Groups at many institutions have initiated routine adjuvant hyperbaric oxygen (HBO) therapy. We examined whether HBO has made a difference in the morbidity, mortality and costs associated with treating this disease. We also analyzed predictors of extended hospital stay and mortality. The records of patients with the hospital discharge diagnoses of Fournier's gangrene, necrotizing fasciitis, gangrene of the genitalia and scrotal gangrene from 1993 to 2002 were reviewed. Data concerning clinical presentation characteristics, hospital stay, complications, hospital charges and outcomes, including graft failure and death, were analyzed. A total of 42 patients were identified and followed a median 4.2 years. Of the patients 16 underwent surgical debridement and antibiotic therapy alone, and 26 were treated with HBO plus surgery and antibiotics. Overall disease specific mortality was 21.4%, that is 12.5% in the nonHBO group and 26.9% in the HBO group. Three or more complications occurred in 13% of nonHBO and in 19% of HBO cases, of which the most common was myocardial infarction. The skin graft failure rate was 6% (nonHBO) and 8% (HBO). Physical disability was a statistically significant predictor of extended hospital stay (p <0.01). There was a trend toward a correlation between known coronary artery disease and death (p = 0.2). A statistically significant difference was noted in average daily hospital charges in nonHBO vs HBO cases ($2,552 vs $3,384 daily, p <0.01). These data do not support routine HBO in the treatment of Fournier's gangrene. There was a trend toward higher morbidity and mortality in the HBO group, suggesting that treatment may have been given to patients who were more ill.

Physiological control of diving behaviour in the Weddell sealLeptonychotes weddelli: a model based on cardiorespiratory control theory

Despite being obligate air breathers, many species of marine mammal are capable of spending most of their lives submerged in water. How they do this has been a subject of intense interest to physiologists for over a century, yet we still do not have a detailed understanding of the physiological mechanisms underlying this behaviour. What are the proximate mechanisms that trigger the 'decisions' to submerge and return to the surface? The present study proposes a model intended to address this question, based on fundamental concepts of cardiorespiratory control. Two basic hypotheses are examined by computer simulation, using a mathematical model of the mammalian cardiorespiratory control system with parameter values for an adult Weddell seal: (1) that the control of diving can be considered to be a respiratory control problem, and (2) that dives are initiated and maintained by disfacilitation of respiratory drive, not inhibition. Computer simulations confirmed the plausibility of these hypotheses. Simulated diving behaviour and physiological responses (ventilation, cardiac output, blood and tissue gas tensions) were consistent with published data from freely diving Weddell seals. Dives up to the estimated aerobic dive limit (ADL, 18-25 min) could be simulated without the need for active inhibition of breathing in this model. This theoretical analysis suggests that the most important physiological adjustments occur during the surface interval phase of the dive cycle and include hyperventilation accompanied by high cardiac output, appropriate regulation of cerebral blood flow and central chemoreceptor threshold shifts. During dives, cardiac output, distribution of peripheral blood flow, splenic contraction and peripheral chemoreflex drives were found to modulate physiological and behavioural responses, but were not essential for simulated dives to occur. The main conclusion from this study is that the central chemoreceptor may be an important mechanism involved in the regulation of diving behaviour, implying that CO2, not O2, is the key regulatory variable in this model. This model includes and extends the ADL concept and suggests an explicit mechanism by which the respiratory control system may play a central role in the regulation of diving behaviour. It is likely that respiratory mechanisms are an important component of a hierarchical behavioural control system and further studies are required to test the qualitative and quantitative validity of the model.

Subcutaneous gas tensions closely track ileal mucosal gas tensions in a model of endotoxaemia without anaerobism

Few comparative data exist on the responses of the subcutaneous and splanchnic circulations to evolving endotoxic shock. We therefore compared continuous subcutaneous pO(2) (pO(2sc)) and pCO(2) (pCO(2sc)) with simultaneous continuous gut luminal pCO(2) (pCO(2gi)) in an animal model of endotoxaemia and examined whether changes in gas tensions track tissue energy charge (EC). Prospective observational study. Fourteen anaesthetized rats, 7 controls and 7 experimental. Controls were injected with saline, the experimental group with 20 mg/kg Klebsiella endotoxin. pCO(2sc), pO(2sc), and pCO(2gi) were measured continuously. Plasma lactate concentrations were measured at defined periods during the study. After 2 h ileal segments were snap frozen and assayed for tissue EC. Endotoxaemia resulted in a significant decrease in mean arterial blood pressure (132+/-9 to 71+/-20 mmHg) and pO(2sc) (71+/-23 to 33+/-22 torr) and a significant increase in pCO(2gi) (58+/-10 to 90+/-20 torr) and pCO(2sc) (56+/-6 to 81+/-25 torr). During endotoxaemia pCO(2gi) was directly correlated with pCO(2sc) (R (2)=0.5) and inversely correlated with pO(2sc) (R (2)=0.63). Plasma lactate concentrations were significantly elevated from baseline in the endotoxin limb. The mean EC was not significantly different in the two groups. Both subcutaneous tissue gas tensions and intestinal luminal carbon dioxide tensions are rapidly responsive during evolving hypodynamic endotoxic shock. Alterations in tissue gas tensions were not associated with dysoxia.

Monitoring Tissue Gas Tensions in Critical Illness

Monitoring Tissue Gas Tensions in Critical Illness

Comparison of brain tissue and local cerebral venous gas tensions and pH

Neurosurgical monitoring devices have recently become available which are capable of measuring cerebral tissue gas tensions and pH. Brain tissue sensors have not been conclusively demonstrated to correlate with other measurements of regional cerebral gas tensions or pH. The present study was undertaken to correlate sensor values for p 02/ p C02 and pH with blood samples taken concurrently from local cerebral veins. Adult mongrel dogs were anesthetized and a craniotomy was performed. A small gyral vein was isolated and cannulated. Adjacent to the venous catheter tip, a Neurotrend® brain tissue probe was inserted in an intracortical location. Each subject received a sequence of manipulations in inspired oxygen and end tidal carbon dioxide conditions. Under each experimental condition, samples of arterial and gyral venous blood were obtained and blood gas analysis performed. Concurrent brain probe measurements of tissue p02, pC02 and pH were recorded. Statistical analysis determined that local tissue and cerebral venous blood values for p02, pC02 and pH were highly correlated (Rs= 0.62-0.82; p 0.001). This indicates that there exists a confirmable monotonic relationship between tissue values and conditions in the post-capillary venous bed. Tissue sensors such as the Neurotrend® probe can offer reliable trend indications in brain tissue gas tensions and pH. [Neurol Res 2000; 22: 642-644

Cerebral hypoxia after etomidate administration and temporary cerebral artery occlusion.

Neurovascular surgical procedures often require temporary cerebral arterial occlusion. Although clinical validation is lacking, etomidate has often been used to attenuate the effects of cerebral ischemia in this setting. The purpose of this study was to evaluate the effects of etomidate and temporary cerebral arterial occlusion on human brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH during intracranial aneurysm surgery. We studied nine patients presenting for cerebral aneurysm surgery. A Paratrend probe was used to determine brain tissue pH and gas tensions. Etomidate was administered to produce electroencephalographic burst suppression before temporary cerebral arterial occlusion. After etomidate administration in nine patients, brain tissue PO2 decreased 30% compared with baseline (P < 0.05). During temporary brain artery occlusion in 8 patients, tissue PO2 decreased 32% below preclip values (P < 0.05) in conjunction with a tissue PCO2 increase of 23% (P < 0.05) and a 0.1-unit decrease in pH (P < 0.05). In patients in whom PO2 decreased below 10 mm Hg during temporary clipping, tissue pH decreased, compared with patients in whom PO2 remained above 10 mm Hg (P < 0.05). These results demonstrate that etomidate administration during cerebral aneurysm surgery decreases tissue PO2 and that in these patients, tissue PO2 does not increase with increases in inspired oxygen concentration. Low tissue PO2 during temporary clipping significantly increases the risk of tissue acidosis. Etomidate administration alone resulted in cerebral deoxygenation. Subsequent temporary cerebral artery occlusion resulted in additional tissue deoxygenation and acidosis. These results suggest that etomidate enhances hypoxic risk in the setting of cerebral ischemia.

Adipose tissue metabolism in humans determined by vein catheterization and microdialysis techniques

A technique for catheterization of a vein draining abdominal subcutaneous tissue and a microdialysis technique that allows measurements of intercellular water concentrations in adipose tissue in humans have recently been described. In the present study, we compare the two techniques during an oral glucose load. In addition a technique using microdialysis for measurement of tissue oxygen and carbon dioxide tensions is described. Microdialysis and vein catheterization were performed in the same region on the abdomen, and the subcutaneous adipose tissue blood flow was measured by the local 133Xe washout method. The results show that subcutaneous adipose tissue gas tensions are on level with gas tensions measured in abdominal venous blood. Comparison of metabolite concentrations measured in the venous blood and venous blood concentrations calculated from microdialysis data shows that there is good agreement between the concentrations obtained by the two techniques with respect to glucose and glycerol, whereas lactate concentrations are very different. With regard to substrate fluxes calculated by Fick's principle, the catheterization technique is probably the most reliable, considering the numerous assumptions on which calculations of venous concentrations from microdialysis data are based. Advantages and disadvantages of the two techniques are discussed.

Hypoxic survival differs between two mole rat species ( Spalax ehrenbergi) of humid and arid habitats

1. 1. Two chromosomal species, 2 n = 52 and 2 n =60 of the mole rat superspecies ( Spalax ehrenbergi), occupy humid (2 n = 52) and arid (2 n = 60) habitats in Israel. 2. 2. Gas conductivity of the soil of the 2 n = 52 mole rat is lower than that of the 2 n = 60 mole rat, and the 2 n = 52 mole rat is better adapted to hypoxia. 3. 3. The hypothesis that the 2 n = 52 mole rat can survive to a lower pO 2 than the 2 n = 60 mole rat was tested. 4. 4. Terminal pO 2 (Torr) of four females 2 n = 52 was lower, 18.0 ± 2.9 (SD), than the terminal pO 2 of five females 2 n = 60, 28.2 ± 5.1 (SD). 5. 5. The hypoxic survival of the 2 n = 52 mole rat as compared to that of the 2 n = 60 mole rat correlates with other physiological traits: breathing and heart frequencies, blood hemoglobin and tissue gas tensions.

Renal tissue gas tensions during hemorrhagic shock.

To evaluate the development of renal hypoxia during hemorrhagic shock, fourteen dogs were induced in this study. The animals were divided equally into a group in which mean arterial pressure (MAP) was kept at 50 mmHg (group 1), and into another where MAP was kept at 40 mmHg for 180 min (group 2). Renal tissue gas tensions were determined by a mass spectrometer. In the 50-mmHg group, renal tissue oxygen tension (PrO2) dropped for 15 min following hemorrhage, remained constant for 90 min, then fell further for 150 min before a plateau was established. In the 40-mmHg group, the PrO2 dropped for 90 min before reaching a plateau. The second PrO2 decline occurred at the same level in both the 50-mmHg group and the 40-mmHg group. The point at which the same PrO2 level occurred for each group suggests the cessation of oxygen consumption and the conditions of renal hypoxia. It is assumed that renal hypoxia occurs in 120 min at a MAP of 50-mmHg and in 60 min at a MAP of 40 mmHg.

Effects of vasopressors on renal tissue gas tensions during hemorrhagic shock in dogs.

Effects of dopamine, epinephrine, and norepinephrine on renal tissue gas tension changes during hemorrhagic shock in dogs were investigated. The changes in the renal tissue gas tension were determined by the use of a Teflon membrane mass spectrometer. The animals were bled to a mean arterial pressure (MAP) of 50 mm Hg and maintained for one hour. Then, vasopressors were administered to maintain the MAP above 100 mm Hg. After the infusion of dopamine, the renal tissue oxygen tension (PrO2) was elevated for 20 min and tissue CO2 tension (PrCO2) decreased for 70 min. Neither PrO2 nor PrCO2 returned to the control levels. When epinephrine was infused, there was an initial slight transient rise in PrO2, which decreased gradually while PrCO2 decreased for 30 min and then gradually rose. When norepinephrine was infused, there was also an initial slight transient elevation in PrO2 which then decreased, while PrCO2 decreased transiently and then rose rapidly. These results suggest that although dopamine was the most useful vasopressor for improving renal tissue gas exchange during hemorrhagic shock, it did not restore completely oxygen delivery.

Effects of phenylephrine on tissue gas tension, bleeding, infection, and lidocaine absorption.

In an attempt to find a vasoconstrictor with less detrimental local and systemic effects than epinephrine, the effects of phenylephrine, a pure alpha agonist, on tissue gas tension, bleeding, infection rates, and lidocaine absorption were studied. All concentrations of phenylephrine significantly reduced tissue PO2 within 10 minutes of injection, and reduction of PO2 was dose-dependent. Phenylephrine 1:10,000 produced significant bacterial growth when simultaneously injected with 6 X 10(6) Staphylococcus aureus. Bacterial growth was insignificant with 1:20,000 phenylephrine and absent with 1:40,000 phenylephrine. Blood loss from a standard wound was significantly reduced at all concentrations of phenylephrine. Lidocaine absorption was significantly reduced with 1:20,000 and 1:40,000 phenylephrine. In a rat model, 1:40,000 phenylephrine significantly reduced blood loss and lidocaine absorption, produced minimal reduction of tissue PO2, and did not enhance bacterial invasion.

Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia.

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO2) and carbon dioxide (PCO2) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions, PO2 was significantly lower in the subendocardium (13.5 +/- 4.5 mm Hg) than in the subepicardium (20.7 +/- 2.3 mm Hg), whereas PCO2 did not differ significantly (43 +/- 8.8 and 51 +/- 9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardial PO2 decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardial PO2 was 4.1 +/- 6.3 mm Hg while subepicardial PO2 was 6.7 +/- 15.0 mm Hg (P less than 0.05). PCO2 reached peak values of 56 +/- 25 mm Hg subendocardial and 82 +/- 22 mm Hg subepicardial at 2.67 +/- 0.71 min and 3.43 +/- 0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows while PO2 recovered with different kinetics. Subendocardial PO2 increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.

Irradiation-induced hypoxia in bones and soft tissues: an experimental study.

Bone marrow and subcutaneous tissue pO2 and pCO2 were measured by means of implanted tissue tonometers in irradiated and nonirradiated rabbit hind limbs. The x-ray dose was 500, 1000, 1500, 2000, and 3000 rads. Tissue gas tensions were measured 1 day and 5 and 11 weeks after radiation. The pCO2 changes in both tissues were slight but not statistically significant. The subcutaneous tissue pO2 decreased during the acute phase of irradiation injury, and the effect of irradiation was dose-dependent. Later on, irradiation had no significant effects on the subcutaneous pO2, although light microscopy of the affected tissues showed fibrosis and blood vessel changes. The response of the subcutaneous pO2 to systemic hyperoxia also increased in the chronic phase of irradiation injury as a sign of improved microcirculation. The bone marrow showed a high radiosensitivity. Irradiation caused a rapid dose-dependent decrease of the marrow pO2, and the marrow pO2 decreased with time during the chronic phase of irradiation injury. The marrow pO2 responded slowly and marginally to an increment of arterial pO2 during breathing 100% oxygen as further evidence of impaired vascular pattern. The results showed that irradiation causes only a transient impairment of tissue perfusion in the skin. However, irradiation-damaged marrow was characterized by progressive tissue hypoxia.

Effects of positive end-expiratory pressure on tissue gas tensions and oxygen transport.

To determine whether positive end-expiratory pressure (PEEP) impairs peripheral tissue oxygenation, hemodynamic variables including blood and subcutaneous tissue gas tensions were measured at 0, 5, 10, 15, and 20 cm H2O of PEEP, in 9 patients who were being mechanically ventilated for acute pulmonary failure. Increasing the level of PEEP produced parallel decreases in cardiac output and oxygen delivery (DO2 = cardiac output X arterial oxygen content); however, there were no significant changes in mean arterial blood pressure (MAP), oxygen consumption (VO2), mixed-venous oxygen tension (PvO2), pH, or base excess. Subcutaneous tissue oxygen (PtO2) and carbon dioxide (PtCO2) tensions, which were directly measured in the femoral region by a mass spectrometer, also remained at their baseline levels (zero end-expiratory pressure). We concluded that peripheral tissue oxygenation is not impaired up to the level of 20 cm H2O of PEEP, even though DO2 significantly decreases.