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PubMed1984

Mechanisms of gas transport during ventilation by high-frequency oscillation.

Ventilation by high-frequency oscillation (HFO) presents some difficulties in understanding exactly how gas is transported in the lung. However, at a qualitative level, five modes of transport may be identified: 1) direct alveolar ventilation in the lung units situated near the airway opening; 2) bulk convective mixing in the conducting airways as a result of recirculation of air among units of inhomogeneous time constants; 3) convective transport of gases as a result of the asymmetry between inspiratory and expiratory velocity profiles; 4) longitudinal dispersion caused by the interaction between axial velocities and radial transports due to turbulent eddies and/or secondary swirling motions; and 5) molecular diffusion near the alveolocapillary membrane. These modes of transport are not mutually exclusive and certainly interact. It is therefore difficult to make quantitative predictions about the overall rate of transport. Qualitatively, it may now be stated with confidence that convective transport in the tracheobronchial tree is very important during HFO as in normal breathing and that increasing tidal volume is more effective than increasing frequency in improving gas exchange during HFO. To optimize the gas transport efficiency of HFO, future research should focus on identifying the rate-limiting mode of transport for a given set of geometric and dynamic conditions.

Animals↗
PubMed1984

Unilateral acute lung injury induced by ethchlorvynol in anesthetized dogs.

Ethchlorvynol (ECV) was used to induce unilateral acute lung injury in anesthetized dogs. Measurements of extravascular thermal volume by double-indicator (thermal-dye) dilution with and without left main pulmonary arterial occlusion permitted sequential estimates of extravascular lung water (EVLW) for each lung. Determinations of EVLW by thermal-dye and gravimetric methods were highly correlated (r = 0.80). ECV (9-15 mg/kg) administered into the right pulmonary circulation produced progressive increases in right lung EVLW, which by 120 min post-ECV was increased 152 +/- 22% (SE) over control (P less than 0.001). Left lung EVLW remained unchanged. Similarly, right, but not left, peak airway pressure was increased. Thermal dilution, coupled with electromagnetic methods, permitted estimates of blood flow to each lung. Despite redistribution of flow to the uninjured lung, systemic PO2 decreased (P less than 0.001) and venous admixture increased (P less than 0.05), suggesting impaired matching of ventilation and perfusion. In summary, introduction of ECV into one lung produced unilateral acute lung injury. EVLW increased solely in the injured lung as did peak airway pressure. Although there was a partial redistribution of blood flow away from the injured lung to the uninjured one, it was apparently inadequate to prevent impaired oxygenation of the blood.

Animals↗
PubMed1985

Model of gas transport during high-frequency ventilation.

We analyze gas exchange during high-frequency ventilation (HFV) by a stochastic model that divides the dead space into N compartments in series where each compartment has a volume equal to tidal volume (V). We then divide each of these compartments into alpha subcompartments in series, where each subcompartment receives a well-mixed concentration from one compartment and passes a well-mixed concentration to another in the direction of flow. The number of subcompartments is chosen on the basis that 1/alpha = (sigma t/-t)2, where -t is mean transit time across a compartment of volume, and sigma t is standard deviation of transit times. If (sigma t/-t)D applies to the transit times of the entire dead space, the magnitude of gas exchange is proportional to (sigma t/-t)D, frequency, and V raised to some power greater than unity in the range where V is close to VD. When V is very small in relation to VD, gas exchange is proportional to (sigma t/-t)2D, frequency, and V raised to a power equal to either one or two depending on whether the flow is turbulent or streamline, respectively. (sigma t/-t)D can be determined by the relation between the concentration of alveolar gas at the air outlet and volume expired as in a Fowler measurement of the volume of the dead space.

Humans↗
PubMed1985

Increased cardiac output increases shunt: role of pulmonary edema and perfusion.

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6-29%, O2 technique) and extravascular thermal volume (ETV, 2.6-7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.

Animals↗
PubMed1986

Diffusion-related differences in elimination of inert gases from the lung.

Partial pressures of intravenously infused acetylene, Freon 22, and isoflurane (gases with similar solubilities in blood but differing molecular weights) were compared in arterial and mixed venous blood and mixed expired gas of 13 anesthetized mongrel dogs to determine whether gas molecular weight influenced gas exchange. Analysis of covariance was used to account for the variables of ventilation-perfusion ratio, partition coefficient, and experimental run before individual gas effects were sought. A gas effect difference was observed such that the arterial fractional retention of isoflurane (mol wt 184.5) would be 12% higher than that of acetylene (mol wt 26) if the two gases had identical partition coefficients. This effect was neither significantly increased by positive end-expiratory pressure nor decreased by high-frequency oscillatory ventilation. To test whether the individual gas effect was greater with gases with disparate erythrocyte and plasma partition coefficients, the exchange of ethyl iodide (erythrocyte-to-plasma solubility ratio 8.1) and diethyl ether (solubility ratio 0.95) was compared in five dogs. A larger difference between the elimination of the two gases was observed than predicted from the differences in molecular weight. The observed individual gas effect appears to be diffusion related, influenced both by the molecular weight of a gas and its erythrocyte-plasma partition coefficient ratio.

Acetylene↗
PubMed1988

Single-breath DLCO maneuver causes cardiac output to fall during and after cycling.

The purpose of this study was to evaluate the influence of the single-breath pulmonary diffusing capacity (DLCO) breath-hold maneuver on central hemodynamics. Ten men (mean age 24 yr) were studied at rest, during 40 min of cycling at 40 and 60% of peak O2 uptake, and 10 min into recovery. DLCO was measured in the seated position during a 10-s breath hold at total lung capacity. At rest the breath hold caused a significant fall in stroke volume (SV, -16%) and an increase in heart rate (HR, +20%) with no change in cardiac output (Q). The resting DLCO of 36.5 ml.min-1.mmHg-1 increased by 28 and 48%, respectively, during the low- and moderate-intensity cycling. The breath hold while cycling caused a significant decrease in SV and Q, but HR did not change. Likewise, during recovery SV and Q fell with the breath hold but again HR did not change. A significant fall in systolic (-17%), diastolic (-12.5%), and mean arterial pressure (-15%) occurred during the breath hold at rest and during and after the exercise. The reduction observed in SV and blood pressure most likely reflected a decrease in venous return. The differences observed in the HR response before, compared with during and after exercise, were consistent with a resetting or shift in the operating point of the arterial baroreflex. Because blood flow fell during the exercise and recovery breath-hold maneuver, the "true" DLCO may have been underestimated during and after cycling.

Adult↗
PubMed1990

Exercise tolerance and pulmonary gas exchange after deep saturation dives.

Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

High-frequency ventilation in dogs with three gases of different densities.

Dogs were ventilated with a high-frequency oscillation device varying the frequency (5-15 Hz), the tidal volume (25-100 ml), and the resident gas (He, N2, SF6). Tidal volume was measured with a body plethysmograph. Blood gases were measured after a quasi-steady state was established. The kinematic viscosity of the breathing gas mixture, which changed by 1,700%, was found to have little effect on arterial PO2 and PCO2. The results are consistent with findings in a branched model that consisted of tubes with a diameter of 1 cm and with the theory of Taylor-type diffusion in turbulent flow. In addition, experiments were performed reducing and increasing the equipment dead space. This resulted in changes of PO2 and PCO2 that were appreciably less than those resulting from variations of tidal volume of the same magnitude.

Animals↗
PubMed1992

Convective and diffusive gas transport in canine intrapulmonary airways.

The significance of convective and diffusive gas transport in the respiratory system was assessed from the response of combined inert gas and particle boluses inhaled into the conducting airways. Particles, considered as "nondiffusing gas," served as tracers for convection and two inert gases with widely different diffusive characteristics (He and SF6) as tracers for convection and diffusion. Six-milliliter boluses labeled with monodisperse di-2-ethylhexyl sebacate droplets of 0.86-microns aerodynamic diameter, 2% He, and 2% SF6 were inspired by three anesthetized mechanically ventilated beagle dogs to volumetric lung depths up to 170 ml. Mixing between inspired and residual air caused dispersion of the inspired bolus, which was quantified in terms of the bolus half-width. Dispersion of particles increased with increasing lung depth to which the boluses were inhaled. The increase followed a power law with exponents less than 0.5 (mean 0.39), indicating that the effect of convective mixing per unit volume was reduced with depth. Within the pulmonary dead space, the behavior of the inert gases He and SF6 was similar to that of the particles, suggesting that gas transport was almost solely due to convection. Beyond the dead space, dispersion of He and SF6 increased more rapidly than dispersion of particles, indicating that diffusion became significant. The gas and particle bolus technique offers a suitable approach to differential analysis of gas transport in intrapulmonary airways of lungs.

Animals↗
PubMed1993

Determinants of maximal oxygen uptake in rats acclimated to simulated altitude.

The effect of acclimation to hypoxia on maximal O2 uptake (VO2max), maximal cardiac output (Qmax), and arteriovenous O2 concentration difference (a-vCO2) was studied in male Sprague-Dawley rats acclimated for 3 wk to a barometric pressure of approximately 380 Torr (A rats). Nonacclimated control animals were pair-fed littermates maintained at an ambient barometric pressure of approximately 740 Torr (NA rats). Both A and NA rats exercised maximally on a treadmill with inspired PO2 maintained at either approximately 72 or 145 Torr. Arterial blood O2 concentration was significantly higher in A than in NA rats (16.0 +/- 0.6 vs. 12.4 +/- 0.3 ml/dl in hypoxia and 28.4 +/- 1.5 vs. 20.1 +/- 0.9 ml/dl in normoxia, respectively; both P < 0.05). During hypoxic exercise VO2max was slightly but significantly higher in A than in NA subjects (55.3 +/- 1.3 vs. 48.8 +/- 1.1 ml STPD.min-1 x kg-1; P < 0.05). In hypoxia a-vCO2 was 16.6 +/- 0.6 and 12.4 +/- 0.4 ml/dl and Qmax was 401 +/- 17 and 489 +/- 9 ml.min-1 x kg-1 in A and NA subjects, respectively (both P < 0.05). A rats showed both lower maximal heart rate and lower maximal stroke volume during hypoxic exercise. In normoxia there was no significant difference in VO2max between A and NA rats (71.8 +/- 2.7 vs. 73.9 +/- 3.1 ml.min-1 x kg-1). As with hypoxia, in normoxia a-vCO2 was significantly higher and Qmax was significantly lower in A than in NA animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1994

Superresistance against hypoxia after preliminary adaptation to repeated stress.

The study investigated the influence of adaptation to stress on resistance to hypoxia. After rats were adaptated to moderate restraint stress, they were anesthetized and exposed to 6% O2. Adaptation increased tidal volume by 2.6-fold, lung and alveolar ventilation by 1.6- and 1.8-fold, respectively, and O2 consumption by 1.6-fold; limited lactate accumulation in the liver by 2-fold, in the heart by 34%, in the lung by 36%, and in the blood by 36%; and elevated pH. At the same time, preliminary adaptation to stress inhibited the hypoxic activation of lipolysis and peroxidation in all tissues. The concentration of lipid peroxides decreased after adaptation by 1.3- to 1.5-fold in different organs, whereas the content of free fatty acids diminished by 1.7- to 2.3-fold. Finally, after adaptation, mortality decreased under severe hypoxia by 6.5-fold. Thus, the data suggest that the cross-protective effect of adaptation was achieved by the economization of respiration and circulation, by marked augmentation in the ability of tissue to utilize blood O2, and by the limitation of processes that are able to damage tissue membranes, namely, acidosis, lipolysis, and lipid peroxidation.

Acid-Base Equilibrium↗
PubMed1998

Stop-flow studies of distribution of filtration in rat lungs.

The stop-flow approach was used to investigate where filtration occurs in the pulmonary vasculature after elevation of left atrial pressure and aspiration of HCl. Rat lungs were perfused for 11 min at zero left atrial pressures, and then flow was stopped for 10 min and left atrial pressures were increased to 20 cmH2O. Thereafter, 3HOH was instilled into the air spaces, and the pulmonary vasculature was flushed by perfusing it from the pulmonary artery to left atrium (anterograde flush) or in the opposite direction (retrograde flush). Increases in fluorescein isothiocyanate (FITC)-dextran (molecular weight 2,000,000) indicated filtration, and these preceded increases in 3HOH after anterograde but not retrograde flushes. This suggests that some filtration occurred through vessels that were relatively venous compared with those through which 3HOH exchange had occurred. Filtration increased fivefold after instillation of 0.1 N HCl in isotonic saline into the air spaces before perfusion. Increases in Evans blue-labeled albumin concentrations were < 40% those of FITC-dextran, indicating loss from the vasculature, but increases in unlabeled albumin and FITC-albumin were comparable.

Animals↗
PubMed1999

Modeling diffusion limitation of gas exchange in lungs containing perfluorocarbon.

We reported changes in alveolar-arterial PO2 gradient, ventilation-perfusion heterogeneity, and arterial-alveolar PCO2 gradient during partial liquid ventilation (PLV) in healthy piglets (E. A. Mates, P. Tarczy-Hornoch, J. Hildebrandt, J. C. Jackson, and M. P. Hlastala. In: Oxygen Transport to Tissue XVII, edited by C. Ince. New York: Plenum, 1996, vol. 388, p. 585-597). Here we develop two mathematical models to predict transient and steady-state (SS) gas exchange conditions during PLV and to estimate the contribution of diffusion limitation to SS arterial-alveolar differences. In the simplest model, perfluorocarbon is represented as a uniform flat stirred layer and, in a more complex model, as an unstirred spherical layer in a ventilated terminal alveolar sac. Time-dependent solutions of both models show that SS is established for various inert and respiratory gases within 5-150 s. In fluid-filled unventilated terminal units, all times to SS increased sometimes by hours, e.g., SF6 exceeded 4 h. SS solutions for the ventilated spherical model predicted minor end-capillary disequilibrium of inert gases and significant disequilibrium of respiratory gases, which could explain a large portion of the arterial-alveolar PCO2 gradient measured during PLV (14). We conclude that, during PLV, diffusion gradients for gases are generally small, except for CO2.

Algorithms↗
PubMed1999

Pulmonary gas exchange during exercise in pigs.

Increased ventilation-perfusion (VA/Q) inequality is observed in approximately 50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O2 difference (A-aDO2). Despite extensive investigation, the cause remains unknown. As a first step to more direct examination of this problem, we developed an animal model. Eight Yucatan miniswine were studied at rest and during treadmill exercise at approximately 30, 50, and 85% of maximal O2 consumption (VO2 max). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-aDO2 increased from 0 +/- 3 (SE) Torr at rest to 14 +/- 2 Torr during the heaviest exercise level, but arterial PO2 (PaO2) remained at resting levels during exercise. There was normal VA/Q inequality [log SD of the perfusion distribution (log) = 0.42 +/- 0.04] at rest, and moderate increases (log = 0.68 +/- 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. The VA/Q inequality changes are similar to those reported in highly trained humans. However, in swine, unlike in humans, there was no inert gas evidence for pulmonary end-capillary diffusion limitation during heavy exercise; there was no systematic difference in the measured PaO2 and the PaO2 as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise-induced VA/Q inequality.

Anaerobic Threshold↗