Lung tissue and airway impedances during pulmonary edema in normal range of breathing

1995 ◽  
Vol 78 (5) ◽  
pp. 1889-1897 ◽  
Author(s):  
G. M. Barnas ◽  
J. Sprung ◽  
R. Kahn ◽  
P. A. Delaney ◽  
M. Agarwal
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Tissue ◽  
Airway Pressure ◽  
Alveolar Pressure ◽  
Mean Airway Pressure ◽  
Normal Range ◽  
Normal Breathing ◽  
The Right ◽  
Severe Pulmonary Edema

How pulmonary edema affects lung tissue and airway properties is not clear. From measurements of airway pressure and flow, we measured lung elastance (EL) and resistance (RL) in 5 anesthetized-paralyzed open-chested dogs during sinusoidal forcing in the frequency (f) and tidal volume (VT) ranges of normal breathing. RL was divided into its tissue (Rti) and airway (Raw) components from measurements of alveolar pressure through capsules glued to the lung surface. After induction of severe pulmonary edema by injection of oleic acid into the right atrium, forcing was repeated at the same mean airway pressure (Paw) as in control animals (11 cmH2O) and at a higher Paw (14 cmH2O), as would occur in closed-chested dogs during edema (G. M. Barnas, D. Stamenovic, and K. R. Lutchen. J. Appl. Physiol. 73: 1040–1046, 1992). Edema increased EL, and this increase was greater at Paw = 14 cmH2O (P < 0.05). The f dependences of EL and Rti were increased by edema (P < 0.05), and there was a large negative dependence of EL on VT at Paw = 14 cmH2O. Edema increased RL (P < 0.05), but this increase depended on f, VT, and Paw. The increase in RL was due largely to increases in Rti at Paw = 14 cmH2O and to increases in Raw at Paw = 11 cmH2O. We conclude that the functional effects of oleic acid-induced pulmonary edema on RL are due mostly to changes in lung tissue.

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

1992 ◽  
Vol 73 (3) ◽  
pp. 1040-1046 ◽  
Author(s):  
G. M. Barnas ◽  
D. Stamenovic ◽  
K. R. Lutchen
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Chest Wall ◽  
Mean Airway Pressure ◽  
Normal Range ◽  
Normal Ranges ◽  
Before And After ◽  
Measured Resistance ◽  
The Right ◽  
Severe 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.

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

1994 ◽  
Vol 76 (2) ◽  
pp. 560-564 ◽  
Author(s):  
G. M. Barnas ◽  
P. B. Randalls ◽  
F. C. Forrest ◽  
B. H. Hoff ◽  
P. L. Donahue ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Rate Constant ◽  
Airway Pressure ◽  
Esophageal Pressure ◽  
Gas Transfer ◽  
Before And After ◽  
The Right ◽  
Severe Pulmonary Edema ◽  
133Xe Washout

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.

Lung Tissue and Airway Impedances during Pulmonary Edema in the Normal Range of Breathing

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A1423 ◽  
Author(s):  
J. Sprung ◽  
G. M. Barnas ◽  
R. Kahn ◽  
P. A. Delaney
Keyword(s):  
Pulmonary Edema ◽  
Lung Tissue ◽  
Normal Range

Alveolar pressure in fluid-filled occluded lung segments during permeability edema

1983 ◽  
Vol 55 (4) ◽  
pp. 1098-1102
Author(s):  
J. P. Kohler ◽  
C. L. Rice ◽  
G. S. Moss ◽  
J. P. Szidon
Keyword(s):  
Oleic Acid ◽  
Hydrostatic Pressure ◽  
Pulmonary Edema ◽  
Intravenous Injection ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Base Line ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Permeability Pulmonary Edema

In a model of increased hydrostatic pressure pulmonary edema Parker et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267-276, 1978) demonstrated that alveolar pressure in occluded fluid-filled lung segments was determined primarily by interstitial fluid pressure. Alveolar pressure was subatmospheric at base line and rose with time as hydrostatic pressure was increased and pulmonary edema developed. To further test the hypothesis that fluid-filled alveolar pressure is determined by interstitial pressure we produced permeability pulmonary edema-constant hydrostatic pressure. After intravenous injection of oleic acid in dogs (0.01 mg/kg) the alveolar pressure rose from -6.85 +/- 0.8 to +4.60 +/- 2.28 Torr (P less than 0.001) after 1 h and +6.68 +/- 2.67 Torr (P less than 0.01) after 3 h. This rise in alveolar fluid pressure coincided with the onset of pulmonary edema. Our experiments demonstrate that during permeability pulmonary edema with constant capillary hydrostatic pressures, as with hemodynamic edema, alveolar pressure of fluid-filled segments seems to be determined by interstitial pressures.

scholarly journals Ventilation inhomogeneity in oleic acid-induced pulmonary edema

1997 ◽  
Vol 82 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
John Y. C. Tsang ◽  
Michael J. Emery ◽  
Michael P. Hlastala
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Phase Iii ◽  
Lung Water ◽  
Peripheral Airways ◽  
Ventilation Inhomogeneity ◽  
Distal Airway ◽  
Tissue Compliance ◽  
Permeability Pulmonary Edema ◽  
The Right

Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala. Ventilation inhomogeneity in oleic acid-induced pulmonary edema. J. Appl. Physiol.82(4): 1040–1045, 1997.—Oleic acid causes permeability pulmonary edema in the lung, resulting in impairment of gas-exchange and ventilation-perfusion heterogeneity and mismatch. Previous studies have shown that by using the multiple-breath helium washout (MBHW) technique, ventilation inhomogeneity (VI) can be quantitatively partitioned into two components, i.e., convective-dependent inhomogeneity (cdi) and diffusive-convective-dependent inhomogeneity (dcdi). Changes in VI, as represented by the normalized slope of the phase III alveolar plateau, were studied for 120 min in five anesthetized mongrel dogs that were ventilated under paralysis by a constant-flow linear motor ventilator. These animals received oleic acid (0.1 mg/kg) infusion into the right atrium at t = 0. MBHWs were done in duplicate for 18 breaths every 40 min afterward. Three other dogs that received only normal saline served as controls. The data show that, after oleic acid infusion, dcdi, which represents VI in peripheral airways, is responsible for the increasing total VI as lung water accumulates progressively over time. The cdi, which represents VI between larger conductive airways, remains relatively constant throughout. This observation can be explained by increases in the heterogeneity of tissue compliance in the periphery, distal airway closure, or by decreases in ventilation through collateral channels.

Rebreathing lung tissue volume of sheep with normal and edematous lungs

1986 ◽  
Vol 61 (3) ◽  
pp. 1132-1138 ◽  
Author(s):  
G. J. Huchon ◽  
A. Lipavsky ◽  
J. M. Hoeffel ◽  
J. F. Murray
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Blood Volume ◽  
Lung Tissue ◽  
Extravascular Lung Water ◽  
Lung Water ◽  
Lung Weight ◽  
Tissue Volume ◽  
Accuracy Of Measurements ◽  
Permeability Pulmonary Edema

To determine the accuracy of measurements of lung tissue volume (Vlt) by rebreathing acetylene in normal and edematous lungs, we compared gravimetric values of total lung weight (Ql) and extravascular lung water (Qwl) with Vlt in anesthetized control sheep (C) and sheep with hydrostatic pulmonary edema (HPE) or oleic acid-induced permeability pulmonary edema (PPE), five animals each. In eight additional sheep we determined that acetylene solubility in blood (0.117 +/- 0.010 ml X 100 ml-1 X Torr-1) differed significantly from that in lung-blood homogenates (0.095 +/- 0.009 ml X 100 ml-1 X Torr-1, P = 0.0017). The latter value was used in all calculations. In C, Vlt was 194% of Qwl and 98% of Ql; in HPE, Vlt was 144% of Qwl and 87% of Ql; and in PPE, Vlt was 112% of Qwl and 77% of Ql. We conclude that when the lungs are normal, Vlt reasonably measures Ql not Qwl. However in both HPE and PPE, Vlt progressively underestimates Ql and cannot differentiate between increased blood volume and increased Qwl.

Mean airway pressure as an index of mean alveolar pressure.

1996 ◽  
Vol 153 (6) ◽  
pp. 1825-1830 ◽  
Author(s):  
P Valta ◽  
C Corbeil ◽  
M Chassé ◽  
J Braidy ◽  
J Milic-Emili
Keyword(s):  
Airway Pressure ◽  
Alveolar Pressure ◽  
Mean Airway Pressure

Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung

1979 ◽  
Vol 46 (1) ◽  
pp. 31-35 ◽  
Author(s):  
J. Pavlin ◽  
F. W. Cheney
Keyword(s):  
Pulmonary Edema ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Rabbit Model ◽  
Dry Weight ◽  
Pleural Space ◽  
Positive Pressure ◽  
Unilateral Pulmonary Edema ◽  
Reexpansion Pulmonary Edema ◽  
The Right

The effects of the mode of reinflation and of the duration of prior collapse on the development of unilateral pulmonary edema following reexpansion of collapsed lung were studied in a rabbit model simulating the human syndrome of “reexpansion pulmonary edema.” The right lungs of rabbits were maintained in an atelectatic state for 0.5 h to 8 days, by injection of air into the pleural space. Reexpansion was achieved in 2 h by application of positive pressure to the airway while a chest tube was connected to underwater seal, or by application of negative pressure (-20 to -100 Torr) to a screened window in the partietal pleura. The lung surface pressures we actually applied by the two methods are not known. Animals were then killed and pulmonary edema was determined by wet-to-dry weight ratios. The incidence of unilateral pulmonary edema increased as the duration of prior collapse was increased (85% after 7--8 days; 17% after 3 days; and 0% after 0,5 h) when reinflated with -100 Torr applied to the pleural window. Although the incidence was less, it also occurred following the use of pleural window pressure less negative than -100 Torr, and after reinflation by positive airway pressure.

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