Measurement of respiratory function: gas exchange

Oxygen passes from the atmosphere to the cells along a concentration gradient (down a cascade) via the alveoli, the arteries and the capillaries. Arterial (and thus cellular) oxygenation depends on the efficient matching of ventilation with pulmonary blood flow. Over-perfused and under-ventilated or non-ventilated alveoli lead to hypoxaemia and over-ventilated, under-perfused alveoli to wasted ventilation (dead space). The average (or ideal) partial pressure of oxygen in arterial blood can be calculated. Gas exchange and its impairments can be assessed from measurements of gas volumes and partial pressures in arterial and mixed venous blood and in expired air. Alveolar-arterial gradients, pulmonary shunt and physiological dead space can all be calculated. There are more complex and sophisticated ways of assessing gas exchange, such as scanning blood flow and ventilation with radionuclides and the use of gases with varying solubilities to assess gas exchange, but these are not commonly used in clinical anaesthetic practice.     

Fluid balance and non-respiratory functions of the lung

The primary function of the lung is gas exchange between alveolar gas and the blood flowing through the nearby capillaries. This stage of gas exchange takes place by diffusion. Because gases such as oxygen diffuse relatively slowly through liquids it is essential that the fluid barrier is kept as short as possible. Furthermore, it is vital that interstitial fluid does not escape into the alveoli because this would abolish gas exchange in the flooded alveoli and lead to shunt. A number of physiological mechanisms normally ensure that fluid that does leave the pulmonary microvasculature is quickly removed and hence gas transfer is not impaired. The lungs, in addition, perform a number of other important functions, including modification of circulating levels of a range of biologically active materials, filtration of blood and serving as a reservoir of blood for rapid adjustment of input to the left atrium when needed.     

Fluid balance and non-respiratory functions of the lung

The primary function of the lung is gas exchange between alveolar gas and the blood flowing through the nearby capillaries. This stage of gas exchange takes place by diffusion. Because gases such as oxygen diffuse relatively slowly through liquids it is essential that the fluid barrier is kept as short as possible. Furthermore, it is vital that interstitial fluid does not escape into the alveoli because this would abolish gas exchange in the flooded alveoli and lead to shunt. A number of physiological mechanisms normally ensure that fluid that does leave the pulmonary microvasculature is quickly removed and hence gas transfer is not impaired. The lungs, in addition, perform a number of other important functions, including modification of circulating levels of a range of biologically active materials, filtration of blood and serving as a reservoir of blood for rapid adjustment of input to the left atrium when needed.     

Effects of inflammation and fibrosis on pulmonary function in diffuse lung fibrosis.

To investigate the relation between lung function and inflammation and fibrosis in patients with diffuse lung fibrosis, a study was made of untreated patients without appreciable airway obstruction (14 patients with cryptogenic fibrosing alveolitis and seven with pneumoconiosis). Quantitative assessment of inflammatory infiltration and fibrosis was carried out on open lung biopsy specimens and compared with lung volumes, carbon monoxide transfer factor (TLCO), TLCO corrected for alveolar volume (TLCO/VA), and arterial blood gases at rest and during exercise. The degree of fibrosis and the degree of cellular infiltration were positively correlated. Lung volumes and TLCO were correlated with the grades of fibrosis and cellular infiltration of alveoli; arterial blood gases during exercise tended to correlate with both fibrosis and infiltration (p less than 0.06). In contrast, morphological data were not correlated with gas exchange at rest or with TLCO/VA. It is concluded that, in untreated patients with diffuse lung fibrosis, lung volumes, TLCO, and arterial blood gases during exercise reflect the lung lesions, and that the pulmonary function tests used cannot discriminate between fibrosis and infiltration of the lung by inflammatory cells.     

Apnoeic diving safety--experimental approaches to oxygen augmentation

A study was undertaken to determine whether a volume of oxygen injected from a 100 ml syringe and inhaled during a 10 m ascent would be exhaled again fully or partially by two experienced male divers. Each performed one apnoeic dive with and another without O2 augmentation. Analyses of mouth gas showed that the injected O2 had disappeared when the divers reached the surface. Any movement of the injected O2 to the alveoli through an open glottis probably resulted from simple diffusion as well as from agitation and mixing of gases by simulated respiratory activity. High-frequency positive-pressure ventilation applied by several authors, whereby sufficient gas exchange is achieved by oscillating small tidal volumes at frequencies of up to 900 per minute, may substantiate this possibility. The injected O2 was found also to have disappeared from the alveolar gas, shown by a comparison of O2 fraction differences between augmented and non-augmented dives. Injection and inhalation of the additional O2 will raise the partial pressure of O2 in the alveoli and increase oxygen transfer across the alveolar membrane into the blood, with more molecules being taken up within seconds during the ascent time. O2 augmentation in larger volumes during apnoeic diving could lead to a burst lung and must be regarded with suspicion. There is evidence that O2 augmentation by means of a small syringe attached to a trained diver's snorkel will help prevent apnoeic blackout.     

Spontaneous gas bubbling in microporous oxygenators

During operation of the microporous membrane oxygenators at some conditions, gas microbubbles penetrate into the blood. This effect, so-called spontaneous bubbling, takes place even when the blood pressure is higher than the gas pressure. This phenomenon was confirmed experimentally both in a model cell with hydrophobic microporous hollow fibers being used in the oxygenators and in in vitro tests on the actual microporous hollow fiber oxygenator. We proposed a mechanism of spontaneous gas bubbling into liquid that contains dissolved gases. Because of a partial pressure gradient, the dissolved gases and water vapors are transported from blood into the gas pore. This causes Stefans gas flow directed from the liquid-gas interface. Because of the high hydraulic resistance of the micropores, gas pressure at the meniscus increases up to gas bubbling. A mishandled priming of the oxygenator as well as the blood pressure pulsation caused by the roller pump operation contribute to spontaneous gas bubbling in the microporous oxygenators. The flow and pressure in the hydrophobic pores were calculated for various gases.     

Respiration: gas transfer

Oxygen and carbon dioxide move passively between the alveoli and the pulmonary blood down concentration gradients, as described by Fick’s law of diffusion. Lungs are thin enough and offer a sufficiently large surface area for equilibrium to be achieved well before the blood has left them. As a result, the exchange of these gases is normally limited by the cardiac output. Both ventilation and perfusion of the lungs show gradients in the upright individual, with lower values at the apex than at the base. These gradients are caused by gravity, though the details of these effects differ between ventilation and perfusion. There is a ventilation-perfusion gradient down the lung, with the highest values at the apex; apical alveoli are over-ventilated and basal ones over-perfused. Such imbalances are normally minimized by local reflexes involving airway constriction (apex) and vascular constriction (base). One of the main functions of haemoglobin is to transport oxygen from the lungs to the tissues. The properties of this molecule are such that: small falls in the partial pressure of alveolar oxygen do not reduce the saturation of blood leaving the lungs; increased release of oxygen to the tissues is accomplished with small falls below the normal partial pressure of oxygen; and raised acidity and temperature in exercising tissues promote oxygen unloading. Haemoglobin is also involved in the carriage of carbon dioxide, directly (by the formation of carbaminohaemoglobin) and indirectly (by acting as a buffer for hydrogen ions produced during the formulation of carbaminohaemoglobin and by dissociation of carbonic acid formed at the erythrocyte membrane).     

How often should we perform arterial blood gas analysis during thoracoscopic surgery?

STUDY OBJECTIVES: To continuously measure arterial blood gases (ABGs), to calculate the percentage of anticipated changes over time, and to develop recommendations for sampling frequencies of arterial blood gases in patients undergoing thoracoscopic surgery. DESIGN: Prospective, observational clinical trial. SETTING: University hospital. PATIENTS: 43 consecutive elective patients undergoing thoracoscopic surgery with one-lung ventilation. INTERVENTIONS AND MEASUREMENTS: A Paratrend 7 probe for continuous arterial partial pressure of oxygen and arterial partial pressure of carbon dioxide measurement was introduced through a radial artery cannula in the awake patient before surgery. Data were collected throughout the procedure until patients left the operating room. Afterward, time courses of arterial blood gas values were transformed into frequency space by fast Fourier transform analysis, and the expected deviations in arterial blood gases were calculated over time. MAIN RESULTS: Forty-three consecutive patients undergoing thoracoscopic surgery were included, and arterial blood gas values were measured during a total of 141.5 h. Critical arterial partial pressure of oxygen values 相似文献   

Why is the patient still hypoxic despite being ventilated?

The passage of oxygen from the atmosphere to the mitochondria is a complex process. Pathological conditions may affect this transfer at any step. The patient on the intensive care unit is particularly likely to be affected by disease or iatrogenic intervention. Hypoxia may be caused by an abnormal supply of oxygen, abnormalities of gas exchange, deficient transport in the blood or alterations in localized tissue utilization. An understanding of the principles involved will enable effective interpretation and subsequent management of the hypoxic patient.     

Efficacy of Continuous Insufflation of Oxygen Combined with Active Cardiac Compression-Decompression during Out-of-hospital Cardiorespiratory Arrest

Background: During experimental cardiac arrest, continuous insufflation of air or oxygen (CIO) through microcannulas inserted into the inner wall of a modified intubation tube and generating a permanent positive intrathoracic pressure, combined with external cardiac massage, has previously been shown to be as effective as intermittent positive pressure ventilation (IPPV).

Methods: After basic cardiorespiratory resuscitation, the adult patients who experienced nontraumatic, out-of-hospital cardiac arrest with asystole, were randomized to two groups: an IPPV group tracheally intubated with a standard tube and ventilated with standard IPPV and a CIO group for whom a modified tube was inserted, and in which CIO at a flow rate of 15 l/min replaced IPPV (the tube was left open to atmosphere). Both groups underwent active cardiac compression-decompression with a device. Resuscitation was continued for a maximum of 30 min. Blood gas analysis was performed as soon as stable spontaneous cardiac activity was restored, and a second blood gas analysis was performed at admission to the hospital.

Results: The two groups of patients (47 in the IPPV and 48 in the CIO group) were comparable. The percentages of patients who underwent successful resuscitation (stable cardiac activity; 21.3 in the IPPV group and 27.1% in the CIO group) and the time necessary for successful resuscitation (11.8 +/- 1.8 and 12.8 +/- 1.9 min) were also comparable. The blood gas analysis performed after resuscitation (8 patients in the IPPV and 10 in the CIO group) did not show significant differences. The arterial blood gases performed after admission to the hospital and ventilation using a transport ventilator (seven patients in the IPPV group and six in the CIO group) showed that the partial pressure of arterial carbon dioxide (PaCO2) was significantly lower in the CIO group (35.7 +/- 2.1 compared with 72.7 +/- 7.4 mmHg), whereas the p H and the partial pressure of arterial oxygen (PaO2) were significantly higher (all P < 0.05).     

Cardiovascular actions of desflurane with and without nitrous oxide during spontaneous ventilation in humans.

We investigated the cardiovascular actions of desflurane (formerly I-653) during spontaneous ventilation. We gave 0.8-0.9, 1.2-1.3, and 1.6-1.7 MAC desflurane in oxygen (n = 6) and in 60% nitrous oxide, balance oxygen (n = 6) to unmedicated healthy male volunteers. Both anesthetic regimens decreased ventilation, increased partial pressure of arterial carbon dioxide, and produced similar cardiovascular changes. In comparison with values obtained when the volunteers were conscious, desflurane anesthesia with spontaneous ventilation decreased systemic vascular resistance and mean arterial blood pressure. Cardiac index, heart rate, stroke volume index, and central venous blood pressure increased. Left ventricular ejection fraction increased at 0.83 MAC desflurane in oxygen, and otherwise did not differ from the conscious value. The velocity of ventricular circumferential fiber shortening, estimated by echocardiography, increased with desflurane in oxygen but did not change with desflurane in nitrous oxide. Oxygen consumption increased during desflurane and oxygen anesthesia, but not when nitrous oxide plus oxygen was the background gas. Desflurane increased oxygen transport, the ratio of oxygen transport to oxygen consumption, mixed venous partial pressure of oxygen, and oxyhemoglobin saturation. The cardiovascular changes with desflurane during spontaneous ventilation differ from those during controlled ventilation. With both background gases, spontaneous ventilation, in comparison with controlled ventilation, increased cardiac index, stroke volume, central venous pressure, left ventricular ejection fraction, velocity of circumferential fiber shortening, oxygen transport, and the ratio of oxygen transport to oxygen consumption but did not change mean arterial blood pressure except at 1.66 MAC desflurane in oxygen (when it was higher with spontaneous than with controlled ventilation).     

Efficacy of continuous insufflation of oxygen combined with active cardiac compression-decompression during out-of-hospital cardiorespiratory arrest

BACKGROUND: During experimental cardiac arrest, continuous insufflation of air or oxygen (CIO) through microcannulas inserted into the inner wall of a modified intubation tube and generating a permanent positive intrathoracic pressure, combined with external cardiac massage, has previously been shown to be as effective as intermittent positive pressure ventilation (IPPV). METHODS: After basic cardiorespiratory resuscitation, the adult patients who experienced nontraumatic, out-of-hospital cardiac arrest with asystole, were randomized to two groups: an IPPV group tracheally intubated with a standard tube and ventilated with standard IPPV and a CIO group for whom a modified tube was inserted, and in which CIO at a flow rate of 15 l/min replaced IPPV (the tube was left open to atmosphere). Both groups underwent active cardiac compression-decompression with a device. Resuscitation was continued for a maximum of 30 min. Blood gas analysis was performed as soon as stable spontaneous cardiac activity was restored, and a second blood gas analysis was performed at admission to the hospital. RESULTS: The two groups of patients (47 in the IPPV and 48 in the CIO group) were comparable. The percentages of patients who underwent successful resuscitation (stable cardiac activity; 21.3 in the IPPV group and 27.1% in the CIO group) and the time necessary for successful resuscitation (11.8 +/- 1.8 and 12.8 +/- 1.9 min) were also comparable. The blood gas analysis performed after resuscitation (8 patients in the IPPV and 10 in the CIO group) did not show significant differences. The arterial blood gases performed after admission to the hospital and ventilation using a transport ventilator (seven patients in the IPPV group and six in the CIO group) showed that the partial pressure of arterial carbon dioxide (PaCO2) was significantly lower in the CIO group (35.7 +/- 2.1 compared with 72.7 +/- 7.4 mmHg), whereas the pH and the partial pressure of arterial oxygen (PaO2) were significantly higher (all P < 0.05). CONCLUSIONS: Continuous insufflation of air or oxygen alone through a multichannel open tube was as effective as IPPV during out-of-hospital cardiac arrest. A significantly greater elimination of carbon dioxide and a better level of oxygenation in the group previously treated with CIO probably reflected better lung mechanics.     

Hemodilution during Venous Gas Embolization Improves Gas Exchange, without Altering V̇A/Q̇ or Pulmonary Blood Flow Distributions

Background: Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization.

Methods: Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion ( A/ ) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence).

Results: Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall A/ distribution and a predominance of high A/ areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30 +/- 1% to 11 +/- 1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375 +/- 61 mmHg at 30% hematocrit to 218 +/- 12.8 mmHg at 15% hematocrit, but increased again (301 +/- 33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P< 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in A/ or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution.     

Side effects of nitrous oxide (author's transl)]

When nitrous oxide is breathed the alvolar partial pressure will cause it to diffuse into the blood, tissues and gas-containing spaces within the body until equilibrium is reached. At the same time nitrogen will be excreted from tissues and blood to alveolar gas. There is a 35 fold difference in the blood-gas partition coefficient between nitrous oxide (0.47) and nitrogen (0.013). For every molecule of nitrogen that is removed from the aircontaining space in the body, 35 molecules of nitrous oxide are transferred from the blood to the air space. This differential solubility of nitrogen and nitrous oxide results either in an increase in the volume of the gas space if the space is compliant (gastrointestinal tract, pneumothorax, air embolus, cuff of the endotracheal tube), or in an increase in the pressure if the space is non-compliant (pneumencephalography, middle ear, sinus). The clinical significance of these side effects of nitrous oxide and experimental studies are discussed.     

Vom Isofluran zum Perfluorhexan? Perfluorkarbone – Therapiemöglichkeiten beim akuten Lungenversagen

The introduction of Perfluorochemicals into medicine and especially into the treatment of severe lung injury is a fascinating scientific task. Many recall the famous experiments from Clark et al. in 1966 when he demonstrated "liquidventilation with perfluorocarbons" in the mammal species for the first time. After this hallmark, perfluorocarbons were subsequently introduced in research of acute lung injury by the techniques of Total- and Partial-Liquid-Ventilation (TLV; PLV). Perfluorocarbons (saturated organofluorids) have unique chemical and physical properties which made them attractive substances for intraalveolar application. The strong C-F bindings in the perfluorocarbon molecules are responsible for their chemical stability, biochemical inertness, high capacity to dissolve respiratory gases, low surface tension and high vapor pressures. Furthermore, the high density of the PFC lead to radio-opacity and their distribution to dependent lung areas. The efficacy of PFC liquid, applied by TLV/PLV has been demonstrated in numerous animal studies using different models of acute lung injury. Currently, several mechanisms of action of perfluorocarbon fluids in acute lung injury are discussed: recruitment of atelectatic alveoli, prevention of endexpiratory collapse of alveoli ("liquid PEEP"), redistribution of perfusion, oxygen transport, surfactant like effects and decrease of inflammation. Since total liquid ventilation has been used only in experimental models of lung injury, partial liquid ventilation has been introduced successfully into clinical trials (phase I-II). However, the results of the first randomised, controlled study of PLV in 90 adult patients suffering from severe respiratory failure (ALI/ARDS) showed no differences between PLV and conventional treatment. Furthermore, the instillation of relatively large amounts of liquid into the lungs poses several technical challenges and may be associated with complications such as liquithoraces, pneumothoraces and hypoxia. Since mammal lungs are evolutionary specialised to gas exchange using atmospheric oxygen, the application of liquids, even if they transport respiratory gases very well is not physiologic. To overcome these unwanted side effects, we developed a technique of perfluorocarbon vaporisation in analogy to the application of inhalation anaesthetic agents. After resolving some technical issues, this application technique was used successfully in an animal model of acute lung injury. Vaporisation of perfluorohexane in a concentration of 18 Vol.% of inspired gas improved significantly oxygenation and lung compliance. Though these results are promising, mechanisms of action, dose-efficacy relation, surfactant-perfluorocarbon interaction or anti-inflammatory effects of vaporised perfluorohexane are still unclear. These questions need to be clarified before this technique can be applied clinically. However, the inhalation of vapor, a technique already familiar to anaesthesiologists should avoid risks of large amounts of fluids in the bronchoalveolar space. Furthermore, this technique can be administered by established anaesthetic equipment with the advantage of exact dosing, continuous monitoring, and demand application in a way near to clinical routine.     

Special article: general anesthetic gases and the global environment

General anesthetics are administered to approximately 50 million patients each year in the United States. Anesthetic vapors and gases are also widely used in dentists' offices, veterinary clinics, and laboratories for animal research. All the volatile anesthetics that are currently used are halogenated compounds destructive to the ozone layer. These halogenated anesthetics could have potential significant impact on global warming. The widely used anesthetic gas nitrous oxide is a known greenhouse gas as well as an important ozone-depleting gas. These anesthetic gases and vapors are primarily eliminated through exhalation without being metabolized in the body, and most anesthesia systems transfer these gases as waste directly and unchanged into the atmosphere. Little consideration has been given to the ecotoxicological properties of gaseous general anesthetics. Our estimation using the most recent consumption data indicates that the anesthetic use of nitrous oxide contributes 3.0% of the total emissions in the United States. Studies suggest that the influence of halogenated anesthetics on global warming will be of increasing relative importance given the decreasing level of chlorofluorocarbons globally. Despite these nonnegligible pollutant effects of the anesthetics, no data on the production or emission of these gases and vapors are publicly available. The primary goal of this article is to critically review the current data on the potential effects of general anesthetics on the global environment and to describe possible alternatives and new technologies that may prevent these gases from being discharged into the atmosphere.     

BLOOD GAS AND ELECTROLYTE DETERMINATIONS DURING EXPOSURE TO ULTRASONIC NEBLIZED AEROSOLS

Blood gas, electrolyte and blood volume changes were followedduring 12-hour exposure to aerosols generated from ultrasonicnebulizers. While blood volume and electrolytes remained relativelystable, significant changes in blood gases and A-aDO₂ were found.These experiments indicate that atelectasis with increased shuntof blood through perfused but non-ventilated alveoli can resultfrom chronic exposure to high output of ultrasonic aerosols.It was concluded that while ultrasonic nebulizers are an importantclinical tool in aerosol therapy, prolonged exposure to suchaerosols must be viewed with caution.     

Effect of graded hemorrhage on renal cortical perfusion in dogs

Renal cortical tissue gas tensions, systemic oxygen supply and some features of energy metabolism and central hemodynamics were recorded in splenectomized dogs during graded hemorrhage and subsequent reinfusion of shed blood. Renal cortical partial pressure of oxygen and carbon dioxide responded rapidly to changes in blood volume and cardiac output. Lowest cortical partial pressure of oxygen values and highest cortical partial pressure of carbon dioxide levels were achieved at a maximal 50 percent blood loss. The decrease in arterial pressure, blood hemoglobin and hematocrit as well as the increase in blood lactate concentration lagged behind blood loss. Renal cortical partial pressure of oxygen, arterial pressure and cardiac output responded rapidly to reinfusions of withdrawn blood, while the cortical partial pressure of carbon dioxide, heart rate, arterial pH and blood lactate concentration returned to initial levels more slowly. Arterial blood gases remained normal throughout the observation period and did not provide an adequate index of tissue oxygenation. In contrast, the partial pressure of oxygen of the renal cortex proved an excellent and sensitive indicator of renal perfusion during hemorrhagic shock and its management.     

Transport von Blutgasproben

BACKGROUND: Transport of blood gas samples via a pneumatic tube system and subsequent analysis in the central laboratory can reduce costs and errors compared to on-site testing in the operating theatre or the intensive care unit. In this study, a modern pneumatic tube transport system was tested for its usability for this purpose. METHODS: A total of 4 consecutive blood gas samples were obtained intraoperatively from 54 different patients and sent to the central laboratory. Of these, 3 samples were transferred using the pneumatic tube system but by different methods and 1 sample was transported personally which served as a reference. The results of sample analysis concerning blood gases, electrolytes and haemoglobin were compared and examined for differences. RESULTS: No statistically significant differences could be determined between the different modes of transportation. CONCLUSION: Transport of samples for blood gas analysis via a modern pneumatic tube system is safe when samples are correctly prepared.     

Hemodilution during venous gas embolization improves gas exchange, without altering V(A)/Q or pulmonary blood flow distributions

BACKGROUND: Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. METHODS: Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). RESULTS: Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P < 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. CONCLUSIONS: Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear.