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PubMedDate not supplied

Rapid assessment of ventilation by measurement of carbon dioxide elimination during high-frequency ventilation of kittens.

Monitoring of the effectiveness of ventilation is a significant problem during high-frequency ventilation (HFV). The time necessary to achieve equilibrium of the arterial tension of carbon dioxide (Paco2) following step changes in ventilation is appreciable, because of large body stores of CO2. Waiting for Paco2 to reach equilibrium is not only time-consuming but a potentially dangerous means of monitoring ventilator adjustments during HFV. Five kittens of mean +/- SD 1,082 +/- 383 gm weight were studied during HFV, both with normal lungs and lungs injured by saline lavage-induced surfactant depletion. The transcutaneous tension of carbon dioxide (Ptcco2) was monitored continuously to determine the time required to achieve equilibrium of Paco2 following a step change in ventilation. The rate of pulmonary CO2 elimination (VECO2) was measured immediately before and immediately after (less than 12 sec) step changes in ventilation and was used to predict the change in Paco2 achieved once equilibrium was reestablished. With normal lungs, equilibration time following step changes in ventilation was found to be approximately 20 minutes. After step decreases in ventilation of the injured lung, achieving equilibrium state took significantly longer, approximately 30 minutes. The Paco2 predicted was significantly related to the change in Paco2 achieved at equilibrium for both normal and injured lung studies. We concluded that direct monitoring of VECO2 during HFV may be a useful clinical monitoring technique, allowing rapid and accurate assessment of the efficiency of ventilation following step changes in ventilation and potentially assisting in optimizing ventilator settings.

Animals↗
PubMed2006

Exercise induced arterial hypoxemia: the role of ventilation-perfusion inequality and pulmonary diffusion limitation.

Many apparently healthy individuals experience pulmonary gas exchange limitations during exercise, and the term "exercise induced arterial hypoxemia" (EIAH) has been used to describe the increase in alveolar-arterial difference for oxygen (AaDO2), which combined with a minimal alveolar hyperventilatory response, results in a reduction in arterial PO2. Despite more than two decades of research, the mechanisms of pulmonary gas exchange limitations during exercise are still debated. Using data in 166 healthy normal subjects collated from several previously published studies it can be shown that approximately 20% of the variation in PaO2 between individuals can be explained on the basis of variations in alveolar ventilation, whereas variations in AaDO2 explain approximately 80%. Using multiple inert gas data the relative contributions of ventilation-perfusion ("VA/Q") inequality and diffusion limitation to the AaDO2 can be assessed. During maximal exercise, both in individuals with minimal (AaDO2 < 20 Torr, x = 13 +/- 5, means +/- SD, n = 35) and moderate to severe (AaDO2= 25-40 Torr, x = 33 +/- 6, n = 20) gas exchange limitations, VA/Q inequality is an important contributor to the AaDO2. However, in subjects with minimal gas exchange impairment, VA/Q inequality accounts for virtually all of the AaDO2 (12 +/- 6 Torr), whereas in subjects with moderate to severe gas exchange impairment it accounts for less than 50% of the AaDO2 (15 +/- 6 Torr). Using this framework, the difficulties associated with unraveling the mechanisms of pulmonary gas exchange limitations during exercise are explored, and current data discussed.

Diffusion↗
PubMed1990

Continuous distributions of ventilation and gas conductance to perfusion in the lungs.

Theoretical analysis and experimental observations were conducted to establish a method allowing to demonstrate the characteristics of distribution of ventilation (VA) as well as of diffusive conductance (G) to perfusion (Q) in the lungs. O2, CO2 and CO binding to hemoglobin molecules within the erythrocyte together with six inert gases including SF6, ethane, cyclopropane, halothane, diethyl ether and acetone, of varied solubility in blood and different diffusivity in lung tissue, were used as indicator gases. 15 patients with interstitial pneumonia of unknown etiology, placed in the supine position, were given a mixture of 21% O2 and 0.1% CO in N2 as the inspired gas and saline containing appropriate amount of the six inert gases was infused via an antecubital vein. After a steady state was established, the expired gas was collected and the samples of both arterial and mixed venous blood were simultaneously taken through catheters inserted into the femoral and pulmonary artery. The concentrations of the indicator gases in the samples were measured by gas chromatography, with electrodes or with the Scholander gas analyzer. Assuming that the mass transfer efficiency of a given indicator gas at each gas exchange unit would be limited by VA/Q and G/Q ratios, the data obtained from the human subjects were analyzed in terms of a lung model having 20 units along the VA/Q and G/Q axes, respectively. The numerical analysis including the procedure of simultaneous Bohr integration for O2, CO2 and CO in a pulmonary capillary and the method of weighted least-squares combined with constrained optimization permitted the data to be transformed into a virtually continuous distribution of Q against VA/Q and G/Q axes. The numerical procedure was strictly tested using various artificial distributions of VA/Q and G/Q ratios, showing that it could characterize the distributions containing up to at least two modes on VA/Q-G/Q field with a substantial accuracy. Analytical results estimated from the patients with interstitial lung disease revealed the following features. (1) There appears to be bimodal distribution of Q along G/Q axis extending to relatively low G/Q less than 10(-3) ml(STPD)/(ml.Torr), which may limit O2 exchange between alveolar gas and capillary blood. This area of low G/Q receives 10% of total Q. (2) Severe diffusion limitation causing disequilibrium of the inert gas across the blood-gas barrier is solely observed in 2 out of 15 patients and an amount of Q associated with this phenomenon is very small (below 1%).(ABSTRACT TRUNCATED AT 400 WORDS)

Carbon Dioxide↗
PubMed1990

Phase II study of tallysomycin S10b in patients with advanced head and neck cancer.

Twenty patients with advanced head and neck tumors were entered in a phase II trial of tallysomycin S10b given intravenously at weekly doses of 2.5 mg/m2. All patients had received prior chemotherapy +/- radiotherapy. Sixteen patients were evaluable for response. Two had stable disease for 15 and 22 weeks respectively. None exhibited tumor shrinkage. Non-hematologic toxicities primarily consisted of gastrointestinal intolerance. Mild fever was noted in about half of the patients and increase in serum creatinine was observed in four. Other side effects consisted of decrease in pulmonary diffusion capacity and skin changes. In conclusion, tallysomycin S10b has no activity in previously treated head and neck cancer patients and has a toxicity spectrum similar to that of bleomycin.

Aged↗
PubMed1987

Extravascular lung water.

Extravascular lung water (idQw1) is measured in vivo from the difference in mean transit times, computed by extrapolating the dilution curves, of two indicators, one freely diffusible, the other confined to the intravascular space. Using 3H2O it has been shown that idQw1 is smaller than the amount of extravascular water obtained from the difference between wet and dry lung weight (Qw1). Extrapolation allows one to use dilution curves for a short time, i.e., up to onset of obvious recirculation. Clearing the dilution curves or recirculation by deconvolution extends the observation time, which then becomes limited by sampling duration rather than onset of recirculation. This procedure entails recording recirculating tracers in the pulmonary artery (PA). Dilutions of tracers at input in PA and output in a systemic artery must be related to each other as continuous time functions. This is accomplished by means of a convolution integral. Deconvolution yields the frequency function of water molecule transit time in the extravascular lung space, l(t). In dogs and men, in both normal and edematous lungs, l(t) exhibits a knee and a fairly long tail. Extravascular lung water computed from l(t), idcQw1, agrees with Qw1 and correlates with data on the extravascular thermal volume of the lung and with radiographic findings of lung edema. A radiographic score of pulmonary edema may be used clinically to assess extravascular lung water in cardiac patients and in patients with adult respiratory distress syndrome.

Capillary Permeability↗
PubMed1986

Excretion-retention data of steady state gas exchange in tidal breathing. II. Dependency on the diffusion coefficient.

The steady state gas transfer properties of the lung can be derived from excretion-retention (E-R) data of inert tracer gases that are infused intravenously. E = PE/Pv and R = Pa/Pv, where PE, Pa and Pv represent the partial pressures of the tracer gases in mixed expired gas, arterial blood and mixed venous blood, respectively. In this paper, we investigate the influence of diffusive gas mixing in the lung on E and R. To that end, E-R data sets were simulated with a lung model that takes into account tidal breathing, the morphometric geometry of the airways, diffusion limited gas mixing in the alveolar space and gas dissolved in superficial lung tissue. The results show a linear relationship between R/E and D-0.5, where D represents the diffusion coefficient of the tracer gases in the alveolar gas mixture. This is in contrast to the results of simulations with a lung model that describes the different gas transport mechanisms, including diffusion, as a constant rate process, where a linear relationship between R/E and D-1 is predicted. It is further shown that E-R data of helium and sulphur hexafluoride cannot be used to demonstrate diffusion limited gas mixing in the lung, in particular, in the presence of a real shunt fraction. For that purpose, excretion data of pairs of tracer gases with different D but equal, medium blood-gas partition coefficients (1 less than lambda less than 30) should be used. For such pairs of tracer gases, the E values may differ by more than 10% when the D values for the two gases are 0.22 and 0.1 cm2s-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗
PubMed1993

Early effects of short-time cigarette smoking on the human lung: a study of bronchoalveolar lavage fluids.

We investigated the early effects of cigarette smoking in healthy subjects by means of lung lavage, looking at markers of alveolar permeability, the alveolar cell profile, the immunophenotyping of macrophages and lymphocytes, and the level and profile of surfactant phospholipids. Bronchoalveolar lavages (BAL) were performed in 33 healthy subjects [20 nonsmokers (nS), 13 moderate and short-time smokers (S)]. In the acellular supernatants we measured the markers of alveolar permeability (i.e., total proteins, albumin, albumin/urea), the alveolar epithelial lining fluid (AELF), the surfactant amounts and profile, and explored the blood lymphocytes by in vitro exposure. The cell pellet established the alveolar formula and a membrane mapping of macrophages (LFA-1 and HLA-DRII expression) and lymphocytes (CD4, CD8, LFA-1, HLA-DRII expression). We found no significant increase of alveolar permeability in our smokers, but an increased alveolar cellularity (more than 3-fold vs nS, P < 0.05) evenly distributed between sub-populations except for an enhanced number of eosinophils in smokers (P < 0.05 vs nS). Smokers' alveolar macrophages had an overloaded cytoplasm, a decreased percentage of antigen-handling cell expression (HLA DRII: P < 0.05 vs nS) and a low percentage of cell to cell adhesion molecule expression (LFA-1: P < 0.05 vs nS). Smoking history and LFA-1 expression on alveolar macrophages were interrelated. Smokers' alveolar lymphocyte subsets were more often T suppressor cells (CD8+) and had an increased percentage of antigen-presenting cell expression (HLA DRII: P < 0.05 vs nS). Smokers' BAL fluid did not show the inhibitory control of phytohemagglutinin-induced lymphocyte proliferation present in nonsmokers' fluids. Surfactant phospholipid amounts were similar, but phosphatidylethanolamine was raised and the ratio of phosphatidylcholine to sphingomyelin decreased in smokers (P < 0.05 vs nS). We observed specific cellular and biochemical alterations in the lung lavage of short-time smokers. Alveolar macrophage and lymphocyte expression of LFA-1 and HLA-DR II molecules was altered. Smokers' alveolar fluids lost the physiologic regulatory control of T mitogen-induced lymphocyte proliferation. Membrane phospholipids released by cellular damage increased early in tobacco-exposed lung fluids. This profile of alterations may be an early and sensitive marker of smoking-induced lung damage.

Adult↗
PubMed2005

[Hyperpolarized (3)helium gas for functional magnetic resonance imaging of the lung].

Lung imaging is traditionally done using X-ray-based methods, since MRI is limited by low proton density as well as inherent magnetic field inhomogeneities of the lung tissue. After introduction of MRI using hyperpolarized noble gases, a totally new field of MRI of the chest has rapidly evolved. These techniques reveal new functional information of the lungs, which could not be obtained before. The first part of this review describes the underlying MR technology explaining distribution of static ventilation, dynamic distribution of ventilation, lung microstructure (apparent diffusion coefficient [ADC]), measurement of oxygen partial pressure (pO(2)), and safety. The clinical potential is afterwards demonstrated in the second part. Therefore, the effort in normal lungs and the mainly focused diseases chronic obstructive pulmonary disease (COPD), smoker's lung, cystic fibrosis, asthma, lung transplantation, and pulmonary embolism are reported.

Administration, Inhalation↗