Pulmonary mechanics during induced pulmonary edema in anesthetized dogs

1959 ◽  
Vol 14 (2) ◽  
pp. 177-186 ◽  
Author(s):  
C. D. Cook ◽  
J. Mead ◽  
G. L. Schreiner ◽  
N. R. Frank ◽  
J. M. Craig
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Tidal Range ◽  
Pulmonary Mechanics ◽  
Vascular Congestion ◽  
Anesthetized Dogs ◽  
Trapped Gas ◽  
Aortic Obstruction ◽  
Gas Volume ◽  
Normal Lungs

In order to study the mechanisms underlying the changes in the mechanical properties of the lungs during pulmonary edema, pulmonary vascular congestion was produced in spontaneously breathing, anesthetized dogs by partial aortic obstruction and intravenous infusion. Brief periods of congestion were associated with small changes in the lung compliance compared with the progressive and striking compliance reduction (-78%) noted with more prolonged congestion. Lung volume at end-expiration showed little change if edema fluid and trapped gas as well as the ventilated gas volume were taken into account. When edematous lungs were forcibly inflated beyond the tidal range, it was found that the overall compliance at a distending pressure of 30 cm H2O was not much less (-6%) than that of normal lungs. Furthermore, edematous lungs manifested marked ‘static’ hysteresis during such maneuvers. These findings suggested that surface phenomena were responsible for the mechanical behavior of edematous lungs rather than vascular congestion, per se, or intrinsic tissue changes. This was borne out by experiments on excised lungs which showed that the elastic properties of edematous lungs were not significantly different from normal lungs when surface forces were minimized. Submitted on August 25, 1958

THE EFFECT OF ACUTE PULMONARY EDEMA UPON LUNG COMPLIANCE

PEDIATRICS ◽  
1964 ◽  
Vol 33 (1) ◽  
pp. 55-62
Author(s):  
Theresa B. Haddy ◽  
Francis J. Haddy
Keyword(s):  
Pulmonary Edema ◽  
Airway Pressure ◽  
Lung Compliance ◽  
Acute Pulmonary Edema ◽  
Vascular Volume ◽  
Bronchial Mucus ◽  
Pressure Independent ◽  
Relationship Of ◽  
Gas Volume ◽  
The Relationship

Thirty-eight puppies were paired according to weight and one of each pair was infused intravenously with normal saline and levarterenol in order to produce acute pulmonary edema. The lungs were immediately excised and the relationship of gas volume to airway pressure was examined in either the natural or gas-free postmortem state. The edematous lungs consistently opened at lower pressures than did the nonedematous lungs. After opening had occurred, the rise in airway pressure for a given increase in gas volume was often, but not invariably, greater in the edematous lung. The effect of change in pulmonary vascular volume was studied in eight excised adult dog lungs. In the absence of pulmonary edema, an increase in vascular volume [SEE FIG. 5. IN SOURCE PDF] caused a slight increase in airway pressure. In the same lungs, massive pulmonary edema increased airway pressure independent of vascular pressure. [SEE FIG 4 IN SOURCE PDF] These findings suggest that changes in the bronchial mucus-alveolar lining layer complex, parenchyma, and vascular volume all contribute to the changes in compliance seen in acute pulmonary edema. The change in the bronchial mucus-alveolar lining layer complex is of such a nature as to increase compliance, whereas the changes in the parenchyma and pulmonary blood volume decrease compliance.

Pulmonary exchange as related to altered pulmonary mechanics in anesthetized dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 659-664 ◽  
Author(s):  
Clarence R. Collier ◽  
Jere Mead
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lung Compliance ◽  
Surface Forces ◽  
Pulmonary Mechanics ◽  
Diffusing Capacity ◽  
Venous Admixture ◽  
Diffusion Capacity ◽  
Air Space ◽  
Anesthetized Dogs

Pulmonary mechanics and gas exchange were studied in supine anesthetized dogs, with and without periodic hyperinflations of the lungs, and after a single forced deflation. After a period without hyperinflations the lung compliance decreased to 66% of control values and patchy atelectasis was observed, but no changes were observed in diffusing capacity (Dl) or per cent venous admixture ( Qva/ Qt). Following a single forced deflation the compliance was 40% of control. Dl was 40% and Qva/ Qt 180% of control values, respectively. These data could be accounted for if there was an accompanying shift of blood flow from atelectatic to nonatelectatic areas, the compensation being very nearly complete for moderate, but less than complete for marked reductions in compliance. Alternative explanations of the apparent compensation are: 1) preferential initial atelectasis of regions with high ventilation-perfusion ratios (as proposed by Farhi) and 2) substantial reductions in compliance without closure of air space, as might result from changes in surface forces with time. aerotonometer; atelectasis; venous admixture; mechanics of breathing; compliance of dog lungs; diffusion capacity of dog lungs; ventilation perfusion; relationships of dog lungs Submitted on October 28, 1963

scholarly journals Effect of cardiogenic and noncardiogenic pulmonary edema on histamine responsiveness in sheep

1998 ◽  
Vol 85 (5) ◽  
pp. 1635-1642 ◽  
Author(s):  
James R. Snapper ◽  
Peter L. Lefferts ◽  
Weixuan Lu ◽  
Young Sil Hwang ◽  
Jonathan D. Plitman
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Cardiogenic Pulmonary Edema ◽  
Local Effects ◽  
Permeability Changes ◽  
Vascular Congestion ◽  
Before And After ◽  
Dynamic Lung Compliance ◽  
Histamine Challenge ◽  
Intravenous Atropine

We compared the effects of cardiogenic pulmonary edema, brief pulmonary vascular congestion without frank edema, and noncardiogenic pulmonary edema on responsiveness to inhaled histamine in chronically instrumented awake sheep. Histamine responsiveness was measured before and after 1) cardiogenic pulmonary edema induced by raising left atrial pressure to 35 cmH2O (↑Pla) for 3.5 h by partial obstruction of flow across the mitral valve, 2) brief cardiogenic congestion via ↑Pla for 0.5 h, 3) noncardiogenic pulmonary edema induced by 25 mg/kg intravenous perilla ketone (PK), and 4) 3.5 h of monitoring without ↑Pla or PK (controls). Treatment for 3.5 h with ↑Pla ( n = 9) and PK ( n = 11) each significantly lessened the histamine dose required to cause a fall to 65% of baseline dynamic lung compliance (ED65Cdyn), i.e., increased responsiveness. Sheep treated for 0.5 h with ↑Pla ( n = 7) and controls ( n = 5) showed no significant change in ED65Cdyn. Intravenous atropine (0.1 mg/kg) before the second histamine challenge altered neither the reduction of ED65Cdyn in ↑Pla ( n = 8) and PK ( n = 9) sheep nor the ED65Cdyn level of controls ( n = 9). These data imply that the local effects of edema, rather than bronchial vascular hemodynamics, cholinergic reflexes, and permeability changes, are germane to lung hyperresponsiveness during pulmonary edema in sheep.

On-Line Calculation of Pulmonary Mechanics by Digital Computer

1978 ◽  
Vol 17 (04) ◽  
pp. 261-272 ◽  
Author(s):  
Y. Brault ◽  
G. Atlan ◽  
H. Lorino ◽  
A. Harf ◽  
A.-M. Lorino ◽  
...  
Keyword(s):  
Time Pressure ◽  
Lung Compliance ◽  
Pulmonary Mechanics ◽  
Close Correspondence ◽  
Standard Equipment ◽  
On Demand ◽  
On Line ◽  
The Subject ◽  
Ventilatory Mechanics ◽  
Computerized System

A system was built up around a minicomputer to process in real time pressure and flow signals collected during the course of three ventilatory mechanics tests: the calculation of the lung volume, the evaluation of the static lung compliance, the analysis of the forced expiratory performance. The subject is seated in an open body Plethysmograph, which allows for the instantaneous calculation of changes in the volume of his thorax and abdomen. The system is controlled through a graphics console which displays the sampled curves and the results of data processing. In addition, the signals can be stored on demand onto a magnetic tape so that the method can be tested and improved off line. The results obtained in healthy volunteers are highly reproducible. A close correspondence is found both in patients and volunteers between computer-derived and hand-calculated results. The computerized system has become a standard equipment of our Lung Function Department, where it allows for a rapid quantitative analysis of lung volumes, lung elasticity and bronchial airflow.

Measurement of pulmonary edema in intact dogs by transthoracic gamma-ray attenuation

1979 ◽  
Vol 47 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
D. S. Simon ◽  
J. F. Murray ◽  
N. C. Staub
Keyword(s):  
Pulmonary Edema ◽  
Time Course ◽  
Gamma Ray ◽  
High Sensitivity ◽  
Lung Edema ◽  
Lung Water ◽  
Vascular Congestion ◽  
Isolated Lung ◽  
Wide Range ◽  
Gamma Ray Attenuation

We evaluated the attenuation of the 122 keV gamma ray of cobalt-57 across the thorax of anesthetized dogs as a method for following the time course of lung water changes in acute pulmonary edema induced by either increased microvascular permeability or increased microvascular hydrostatic pressure. The gamma rays traversed the thorax centered on the seventh rib laterally where the lung mass in the beam path was greatest. Calibration measurements in isolated lung lobes demonstrated the high sensitivity and inherent accuracy of the method over a wide range of lung water contents. In control dogs reproducibility averaged +/-3%. Increased permeability edema led to large rapid increases in the transthoracic gamma ray attenuation (TGA), while increased pressure caused an immediate, modest increase in TGA (vascular congestion) followed by a slow further increase over 2 h. There was a fairly good correlation between the increase in extravascular lung water and the change in TGA. The method is simple, safe, and noninvasive and appears to be useful for following the time course of lung water accumulation in generalized lung edema in anesthetized animals.

Cardiorespiratory effects of rapid saline infusion in normal man

1975 ◽  
Vol 38 (5) ◽  
pp. 786-775 ◽  
Author(s):  
A. L. Muir ◽  
D. C. Flenley ◽  
B. J. Kirby ◽  
M. F. Sudlow ◽  
A. R. Guyatt ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Control Period ◽  
Lung Compliance ◽  
Saline Infusion ◽  
Tidal Range ◽  
Closing Volume ◽  
Rapid Infusion ◽  
Pulmonary Arterial

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

Combination of constant-flow and continuous positive-pressure ventilation in canine pulmonary edema

1989 ◽  
Vol 67 (2) ◽  
pp. 817-823 ◽  
Author(s):  
J. I. Sznajder ◽  
C. J. Becker ◽  
G. P. Crawford ◽  
L. D. Wood
Keyword(s):  
Pulmonary Edema ◽  
Positive Pressure Ventilation ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Constant Flow ◽  
Positive End Expiratory Pressure ◽  
Ventilatory Mode ◽  
Continuous Positive Pressure ◽  
Bronchoscopic Guidance ◽  
Normal Lungs

Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.

"Closing volume" changes in alloxan-induced pulmonary edema in anesthetized dogs

1975 ◽  
Vol 39 (2) ◽  
pp. 235-241 ◽  
Author(s):  
R. Lemen ◽  
J. G. Jones ◽  
P. D. Graf ◽  
G. Cowan
Keyword(s):  
Pulmonary Edema ◽  
Control Group ◽  
Closing Volume ◽  
Base Line ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Period 2 ◽  
System Pressure ◽  
Before And After ◽  
Anesthetized Dogs

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.

Evidence for increased intrathoracic fluid volume in man at high altitude

1979 ◽  
Vol 47 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. J. Jaeger ◽  
J. T. Sylvester ◽  
A. Cymerman ◽  
J. J. Berberich ◽  
J. C. Denniston ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Transpulmonary Pressure ◽  
Fluid Volume ◽  
Pulmonary Mechanics ◽  
Volume Curve ◽  
Extravascular Fluid ◽  
Pressure Volume Curve ◽  
Transthoracic Electrical Impedance ◽  
Extravascular Fluid Volume

To determine if subclinical pulmonary edema occurs commonly at high altitude, 25 soldiers participated in two consecutive 72-h field exercises, the first at low altitude (200–875 m) and the second at high altitude (3,000–4,300 m). Various aspects of ventilatory function and pulmonary mechanics were measured at 0, 36, and 72 h of each exercise. Based on physical examination and chest radiographs there was no evidence of pulmonary edema at high altitude. There was, however, an immediate and sustained decrease in vital capacity and transthoracic electrical impedance as well as a clockwise rotation of the transpulmonary pressure-volume curve. In contrast, closing capacity and residual volume did not change immediately upon arrival at high altitude but did increase later during the exposure. These observations are consistent with an abrupt increase in thoracic intravascular fluid volume upon arrival at high altitude followed by a more gradual increase in extravascular fluid volume in the peribronchial spaces of dependent lung regions.

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