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G M Barnas

Publications and source records attributed to G M Barnas.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effect of surface forces on oscillatory behavior of lungs.

The effect of alveolar surface tension on lung dynamic behavior was investigated by measuring total lung and tissue impedances in excised rabbit lungs at breathing frequencies of 0.2-0.8 Hz and tidal volumes of 10, 20, and 30 ml before and after lavage with 3-dimethyl siloxane, which provided a constant surface tension of 16 dyn/cm. The lungs were oscillated around the mean deflation pressures of 5 (control) and 8 cmH2O (lavaged), i.e., lung volume of 60% of total lung capacity. The total lung impedance was calculated from measurements of pressure and airflow at the trachea, and tissue impedance was measured by the alveolar capsule technique. The airway contribution was obtained as the difference between total lung and tissue impedances. In the lavaged lungs, dynamic elastance (Edyn) decreased and tissue resistance (Rti) increased relative to the control values over the entire frequency range. Airway resistance increased at the higher flow rates only. The decrease in Edyn could be attributed to the absence of surface film elastance in the lavaged lungs. The increase in airway resistance could be attributed to accentuated flow dependence due to changes in airway geometry and residual lavage liquid. However, the most intriguing result was the increase in Rti in the lavaged lungs. It could be attributed to altered mechanics at the alveolar duct level after lavage. It is concluded that dissipative properties of lung tissue are major determinants of Rti, whereas elastic properties of both tissue and surface film are important determinants of Edyn.

Airway Resistance↗
PubMed1995

Effects of PEEP on acinar gas transfer in healthy and lung-injured dogs.

We measured cardiorespiratory variables and 133xenon washout from a nonperfused lung region (XeW) in six anesthetized/paralyzed dogs, mechanically ventilated with 60% O2 at different positive end-expiratory pressures (PEEP). XeW in this technique represents directly measured acinar gas transfer (3). Measurements were repeated after induction of lung injury by lavaging the lungs 11 to 13 times with 600 ml saline. In control dogs, lung compliance (CL), alveolar ventilation (Valv), and XeW all decreased with increasing PEEP from 0 to 25 cm H2O (p < 0.05), while lung resistance (RL) did not change. After lavage, CL, Valv, and XeW below 15 cm H2O PEEP were all less than control values (p < 0.05), while RL was higher than control values. As PEEP increased from 0 to 20 cm H2O, Valv and XeW increased, but CL did not change; RL decreased only from 0 to 5 cm H2O. At 20 cm H2O PEEP, Valv and CL were not different from control values (p > 0.05), and XeW was higher than control values (p < 0.05). At estimated alveolar volumes above 400 ml, values for XeW before and after lavage were similar. We conclude that, during severe lung injury: (1) increasing PEEP to moderate levels will increase acinar gas transfer but, after a certain lung volume is reached, further increases in PEEP will have effects similar to the healthy condition; (2) overall mechanical properties of the lung do not reflect the responses to PEEP of the lung periphery.

Animals↗
PubMed1994

Transfer of gas from the acinus during continuous flow and intermittent positive pressure ventilation.

We used a technique of measuring Xenon133 washout (XeW) from the alveolar space to evaluate transfer of gas from the acinus (Mackenzie et al., J. Appl. Physiol. 68: 2013-2018, 1990) during 2 min of apnea, 2 min of tracheal insufflation with oxygen (TRIO) and 90 sec of intermittent positive pressure ventilation (IPPV) in 6 anesthetized and paralyzed dogs. Xenon133 dissolved in saline was injected into an occluded acinar region through a pulmonary artery catheter, and XeW was measured by gamma scintillation scanning. With this technique, XeW during apnea represents the contribution of cardiogenic oscillations in regional flow. The XeW rate constant (min-1 +/- SE) was 0.37 +/- 0.03 during apnea. This was not different (P > 0.05) with TRIO (0.29 +/- 0.04). With IPPV, the rate constant increased to 3.49 +/- 0.39, faster than with either apnea or TRIO (P < 0.001). We conclude that: (1) TRIO does not increase convective gas transfer from the acini compared to apnea; and (2) transfer of gas out of the acini due to cardiogenic oscillations is a very small portion of the total gas eliminated during IPPV.

Animals↗
PubMed1994

Influence of waveform and analysis technique on lung and chest wall properties.

To test an approach for measuring respiratory system resistance (R) and elastance (E) during non-sinusoidal forcing, we measured airway and esophageal pressures and flow at the trachea of 9 anesthetized-paralyzed dogs during sinusoidal forcing (SF) and 4 types of non-sinusoidal forcings at 0.15 and 0.6 Hz and 300 ml tidal volume. During SF, calculations of E and R of the lungs, chest wall or total system from discrete Fourier transform (DFT) and two other widely used methods (multiple regression and volume-pressure loop analysis) did not differ from each other (P > 0.05). During forcing with sinusoidal or step inspiration with passive expiration (inspiratory to expiratory ratio, I/E, = 1:1), Es from any analysis method were within 10% of values during SF. Although Rs of the lungs, chest wall or total system were not affected by waveform shape with DFT (P > 0.05), the other analysis methods gave values for R during non-SF that differed (P < 0.05) from those during SF by up to 77%. If I/E was changed to 1:2, with or without an added 10% inspiratory pause, values for E and R differed least from values during SF if DFT was used. During severe pulmonary edema induced by infusion of oleic acid in the right atrium, results for lung properties were similar to controls, despite large increases in E and R of the lungs. We conclude that E and R of the lungs and chest wall can be measured by DFT using nonsinusoidal forcing waveforms available on most clinical ventilators, incurring only modest error.

Airway Resistance↗
PubMed1994

Lung and chest wall mechanical properties before and after cardiac surgery with cardiopulmonary bypass.

From measurements of airway and esophageal pressures and flow, we calculated the elastance and resistance of the total respiratory system (Ers and Rrs), chest wall (Ecw and Rcw), and lungs (EL and RL) in 11 anesthetized-paralyzed patients immediately before cardiac surgery with cardiopulmonary bypass and immediately after chest closure at the end of surgery. Measurements were made during mechanical ventilation in the frequency and tidal volume ranges of normal breathing. Before surgery, frequency and tidal volume dependences of the elastances and resistances were similar to those previously measured in awake seated subjects (Am. Rev. Respir. Dis. 145: 110-113, 1992). After surgery, Ers and Rrs increased as a result of increases in EL and RL (P < 0.05), whereas Ecw and Rcw did not change (P > 0.05). EL and RL exhibited nonlinearities (i.e., decreases with increasing tidal volume) that were not seen before surgery, and RL showed a greater dependence on frequency than before surgery. The changes in RL or EL after surgery were not correlated with the duration of surgery or cardiopulmonary bypass time (P > 0.05). We conclude that 1) frequency and tidal volume dependences of respiratory system properties are not affected by anesthesia, paralysis, and the supine posture, 2) open-chest surgery with cardiopulmonary bypass does not affect the mechanical properties of the chest, and 3) cardiac surgery involving cardiopulmonary bypass causes changes in the mechanical behavior of the lung that are generally consistent with those caused by pulmonary edema induced by oleic acid (J. Appl. Physiol. 73: 1040-1046, 1992) and decreases in lung volume.

Adult↗
PubMed1994

Effect of pulmonary edema on transfer of gas from acinus to airways.

We directly measured the effect of progressive pulmonary edema on gas transfer from the acinus by injecting 133Xe dissolved in saline through a pulmonary artery catheter into an acinar region with occluded blood flow and measuring 133Xe washout by gamma scintillation scanning. We measured washout in six anesthetized paralyzed dogs during mechanical ventilation with O2 before and after injection of 0.6 mg/kg of oleic acid into the right atrium, which induces severe pulmonary edema within 2 h. Changes in the elastance and resistance of the lung were also calculated from measurements of airway flow, airway pressure, and esophageal pressure. Before injection of oleic acid, the monoexponential rate constant for 133Xe washout was 3.6 +/- 1.4 (SE) min-1; from this we estimated that the rate of gas transfer of 133Xe from the acini was 1.0 l/min. The rate constant decreased gradually after the injection and was correlated with increases in elastance and resistance (r = -0.66) and decreases in alveolar PO2 (r = 0.71). At 2 h after injection, the rate constant (1.2 +/- 0.8 min-1) was lower than control (P < 0.01), and the rate of gas transfer of 133Xe from the acini was < 0.32 l/min. We conclude that resistance in the acini is increased during pulmonary edema and that it is correlated, in the oleic acid model, with changes in overall lung mechanical properties.

Animals↗
PubMed1994

Gravitational and shear-associated pressure gradients in the abdomen.

The abdomen has been variously characterized as a hydrostatic system, in which pressures exhibit a gravitational gradient and pressure fluctuations are spatially uniform, and as a compartment, in which pressure gradients are not simply gravitational and pressure fluctuations differ markedly from place to place. To characterize the pressures acting on the ventral abdominal wall, we used saline-filled catheters and air-filled balloons in anesthetized dogs in various body positions during spontaneous breathing and mechanical ventilation. Pressures were measured in the stomach and at multiple sites next to the abdominal wall. Under most circumstances, measurements next to the abdominal wall exhibited a hydrostatic gravitational gradient of approximately 0.89 cmH2O/cm height and pressure fluctuations were spatially homogeneous. Deviations from this hydrostatic behavior were seen when abdominal pressures were compared with gastric pressures, when measurements were made with a balloon catheter, and when the lower abdomen was constricted with a binder. Analysis of these and previously published data suggests that the abdomen does, at times, behave like a hydraulic system but can deviate from simple hydrostatic behavior to the extent that shape-stable abdominal viscera are deformed.

Abdomen↗
PubMed1994

Endotracheal tube and tracheobronchial obstruction as causes of hypoventilation with high inspiratory pressures.

Two cases of difficult ventilation are presented, the first caused by endotracheal tube obstruction with nasal turbinate, and the second caused by tracheobronchial obstruction with blood clots. The clinical presentation in each case was characterized by extreme difficulty in ventilating and severe hypercapnia despite vigorous ventilatory efforts with either a mechanical ventilator or resuscitator bag. A simple manipulation of the endotracheal tube cuff helped to differentiate between increased impedance caused by endotracheal tube obstruction as opposed to increased respiratory system impedance beyond the tip of tube. In the second patient, in whom even a short interruption of ventilation was poorly tolerated, simultaneous rigid bronchoscopy (for removal of intratracheal masses) and ventilation via endotracheal tube were successfully performed.

Adult↗
PubMed1993

Effect of posture on lung and regional chest wall mechanics.

BACKGROUND: Little is known about the extent to which changes in postures in clinical situations affect respiratory mechanics, even in humans with healthy respiratory systems. This study tested the hypothesis that posture has only small effects on overall respiratory system mechanics in healthy subjects, despite changes in parts of the respiratory system in some postures. METHODS: Measurements were made of airway flow, airway and esophageal pressures, and rib cage and abdominal volume displacements (with inductance plethysmography) of awake, healthy subjects, relaxed at functional residual capacity, during external forcing at 0.2 Hz with a tidal volume of 8-10 ml/kg. From these measurements, discrete Fourier transform was used to calculate elastances (E) and resistances (R) of the total respiratory system, lungs, total chest wall, and compartments of the chest wall (rib cage, diaphragm-abdomen, and belly wall). Measurements were made while the subjects were in nine different postures: in six of these, the torso was straight; in three, the torso was bent or twisted. RESULTS: Although changes in mechanics of parts of the respiratory system were evident in certain postures, overall respiratory mechanics were not greatly affected by posture. Changing from sitting to supine decreased E and R of the diaphragm-abdomen about 50% (P < .05), but total chest wall E and R changed only slightly. Lung E increased 24% (P < .05), but total respiratory E did not change (P < .05). Lung and total respiratory R increased 40-50% (P < .05) with this same change in posture. As long as the torso was straight, however, changes in orientation of 30 degrees from the horizontal or a shift to lateral posture resulted in only minor changes in the variables measured. Postures in which the torso was twisted or bent increased E of the total chest wall 20-30% compared to supine (P < .05), due to increases in E of one or more compartments. Respiratory system E also increased, at most 14%. Although lung R decreased 30-45% (P < .05) in these postures compared to supine with a straight torso, chest wall and total respiratory R generally were unchanged. CONCLUSIONS: Changes in respiratory system mechanics over a wide range of postures that may be encountered clinically are relatively small in healthy awake subjects due to adaptability of total chest wall mechanical behavior.

Adult↗
PubMed1993

Effect of lung volume on lung resistance and elastance in awake subjects measured during sinusoidal forcing.

BACKGROUND: Although lung volume may be changed by certain procedures during anesthesia and mechanical ventilation, dependence of the dynamic mechanical properties of the lungs on lung volume are not clear. Based on studies in dogs, the authors hypothesized that changes in lung mechanics caused by anesthesia in healthy humans could be accounted for by immediate changes in lung volume and that lung resistance will not be decreased by positive end-expiratory airway pressure if tidal volume and respiratory frequency are in the normal ranges. METHODS: Lung resistance and dynamic lung elastance were measured in six healthy, relaxed, seated subjects during sinusoidal volume oscillations at the mouth (5 mL/kg; 0.4 Hz) delivered at mean airway pressure from -9 to +25 cmH2O. Changes in lung volume from functional residual capacity were measured with inductance plethysmographic belts. RESULTS: Decreases in mean mean airway pressure that caused decreases in lung volume from functional residual capacity comparable to those typically observed during anesthesia were associated with significant increases in both dynamic lung elastance and lung resistance. Increases in mean mean airway pressure that caused increases in lung volume from functional residual capacity did not increase lung resistance and increased dynamic lung elastance only above about 15 cmH2O. CONCLUSIONS: Increases in dynamic lung elastance and lung resistance with anesthesia can be explained by the accompanying, acute decreases in lung volume, although other factors may be involved. Increasing lung volume by increasing mean airway pressure with positive end-expiratory pressure will decrease lung resistance only if the original lung volume is low compared to awake, seated functional residual capacity.

Adult↗
PubMed1993

Effects of mean airway pressure and tidal volume on lung and chest wall mechanics in the dog.

Dependencies of the dynamic mechanical properties of the respiratory system on mean airway pressure (Paw) and the effects of tidal volume (VT) are not completely clear. We measured resistance and dynamic elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) in six healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml; 0.4 Hz) delivered at mean Paw from -9 to +23 cmH2O. Changes in end-expiratory lung volume, estimated with inductance plethysmographic belts, showed a typical sigmoidal relationship to mean Paw. Each dog showed the same dependencies of mechanical properties on mean Paw and VT. All elastances and resistances were minimal between 5 and 10 cmH2O mean Paw. All elastances, Rrs, and RL increased greatly with decreasing Paw below 5 cmH2O. Ers and EL increased above 10 cmH2O. Ecw, Ers, Rcw, and Rrs decreased slightly with increasing VT, but RL and EL were independent of VT. We conclude that 1) respiratory system impedance is minimal at the normal mean lung volume of supine anesthetized paralyzed dogs; 2) the dependency of RL on lung volume above functional residual capacity is dependent on VT and respiratory frequency; and 3) chest wall, but not lung, mechanical behavior is nonlinear (i.e., VT dependent) at any given lung volume.

Air Pressure↗
PubMed1993

Alternative model of respiratory tissue viscoplasticity.

Respiratory tissue impedance exhibits both tidal volume and frequency dependences in the ranges of normal breathing. Hildebrandt argued that these indicate tissue viscoplasticity and offered a model in support of his argument consisting of viscoelastic and plastoelastic compartments, both mechanically in parallel (J. Appl. Physiol. 28: 365-372, 1970). Although the model appears to be qualitatively consistent with oscillatory behavior of a wide variety of respiratory tissues, it yields only moderately good quantitative correspondences despite a relatively large number of parameters, eight. One reason may be the model topology, which implies that rate-dependent and amplitude-dependent processes are decoupled. This is contrary to observed behavior. In this study we offer a model in which viscoelastic and plastoelastic compartments are mechanically coupled through a serial arrangement. The total number of parameters in the model is four. Using a least squares technique, we fitted this model to impedance data of chest wall, healthy lungs, and edematous lungs, all measured in vivo. We found that the model could account for the major, as well as the more subtle, features of the chest wall data with fewer parameters and fewer ad hoc assumptions than Hildebrandt's model. Although it lacks anatomic specifics, the model suggests that the observed chest wall behavior may stem from the actin-myosin cross-bridge kinetics. It also seems applicable to lung tissue, although the requirements for the plastoelastic compartment are less certain. In the case of edematous lungs, the applicability of the model is difficult to establish.

Airway Resistance↗
PubMed1992

Effects of cardiac oscillations on acinar gas mixing during pulmonary edema.

We used a previously reported technique (Mackenzie et al., J. Appl. Physiol. 68: 2013-2018, 1990) to measure the effects of severe pulmonary edema on acinar cardiogenic gas mixing in anesthetized dogs. We also tested how increases in lung volume affected gas mixing in healthy lungs and during pulmonary edema. Cardiogenic gas mixing was evaluated by measurement of the rate of washout of xenon133 injected into an occluded pulmonary artery during apnea. The rate constant of xenon133 washout was 0.40 min-1 (+/- 0.06 SE) in the healthy lung at functional residual capacity. It decreased (P < 0.05) to 0.08 min-1 (+/- 0.03) when lung volume was raised 500 ml. Pulmonary edema was induced by injection of oleic acid (0.06 mg.kg-1) into the right atrium over a 4-min period; clinical signs of severe pulmonary edema were present after 90 min. The rate constant for xenon133 washout (0.07 +/- 0.03 min-1) was less than in the healthy lung (P < 0.05), and was not changed after lung volume was increased (P > 0.05). We conclude that, in the presence of severe pulmonary edema: (1) acinar resistance is increased and/or magnitude of cardiogenic oscillations is decreased; and (2) salutary effects of increased lung volume are not due to enhancement of cardiogenic gas mixing.

Airway Resistance↗
PubMed1992

Effects of analysis method and forcing waveform on measurement of respiratory mechanics.

The respiratory system has been shown to exhibit nonlinear mechanical properties in the frequency (f) range of normal breathing, manifested by tidal volume (Vt) dependence. Calculations of respiratory system resistance (R) and elastance (E) from pressure-flow measurements during external forcing at a given f may be ambiguous, especially if non-sinusoidal forcing waveforms are used. We evaluated the degree to which R and E depended upon: (1) analysis method (Fourier transform, multiple regression and pressure-volume loop analysis) and; (2) shape of the forcing waveform (sinusoidal, quasi-sinusoidal and step). We measured pressure and flow at the mouth of 5 healthy, awake subjects, relaxed at functional residual capacity, during forcing with the three different waveforms in the normal range of f (0.2-0.6 Hz) and Vt (250-750 ml). During sinusoidal forcing, E and R were not affected by analysis method (P greater than 0.2). With Fourier transform and multiple regression, E was not affected by waveform shape (P greater than 0.05); with loop analysis, E was slightly (less than 10%) higher during quasi-sinusoidal and step forcing than during the sine (P less than 0.05). R was least affected by waveform shape with Fourier transform. We conclude that, in the f and Vt range of normal breathing: (1) respiratory system impedance is 'quasi-linear,' i.e. despite dependencies of R and E on Vt, non-linearities are not large enough to restrict interpretation of R and E at a given f and Vt; (2) it may be possible to measure R and E using non-sinusoidal forcing waveforms available on most clinical ventilators, incurring only modest error.

Adult↗
PubMed1992

Lung and chest wall impedances in the dog: effects of frequency and tidal volume.

Dependences of the mechanical properties of the respiratory system on frequency (f) and tidal volume (VT) in the normal ranges of breathing are not clear. We measured, simultaneously and in vivo, resistance and elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) of five healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml, 0.2-2 Hz) delivered at a constant mean lung volume. Each dog showed the same f and VT dependences. The Ers and Ecw increased with increasing f to 1 Hz and decreased with increasing VT up to 200 ml. Although EL increased slightly with increasing f, it was independent of VT. The Rcw decreased from 0.2 to 2 Hz at all VT and decreased with increasing VT. Although the RL decreased from 0.2 to 0.6 Hz and was independent of VT, at higher f RL tended to increase with increasing f and VT (i.e., as peak flow increased). Finally, the f and VT dependences of Rrs were similar to those of Rcw below 0.6 Hz but mirrored RL at higher f. These data capture the competing influences of airflow nonlinearities vs. tissue nonlinearities on f and VT dependence of the lung, chest wall, and total respiratory system. More specifically, we conclude that 1) VT dependences in Ers and Rrs below 0.6 Hz are due to nonlinearities in chest wall properties, 2) above 0.6 Hz, the flow dependence of airways resistance dominates RL and Rrs, and 3) lung tissue behavior is linear in the normal range of breathing.

Airway Resistance↗
PubMed1992

Lung and chest wall impedances in the dog in normal range of breathing: effects of pulmonary edema.

We evaluated the effect of pulmonary edema on the frequency (f) and tidal volume (VT) dependences of respiratory system mechanical properties in the normal ranges of breathing. We measured resistance and elastance of the lungs (RL and EL) and chest wall of four anesthetized-paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml, 0.2-2 Hz), delivered at a constant mean airway pressure. Measurements were made before and after severe pulmonary edema was produced by injection of 0.06 ml/kg oleic acid into the right atrium. Chest wall properties were not changed by the injection. Before oleic acid, EL increased slightly with increasing f in each dog but was independent of VT. RL decreased slightly and was independent of VT from 0.2 to 0.4 Hz, but above 0.4 Hz it tended to increase with increasing flow, presumably due to the airway contribution. After oleic acid injection, EL and RL increased greatly. Large negative dependences of EL on VT and of RL on f were also evident, so that EL and RL after oleic acid changed two- and fivefold, respectively, within the ranges of f and VT studied. We conclude that severe pulmonary edema changes lung properties so as to make behavior VT dependent (i.e., nonlinear) and very frequency dependent in the normal range of breathing.

Airway Resistance↗