Pulmonary hemodynamics and venous admixture in severe pulmonary edema due to edema permeability

1976 ◽  
Vol 4 (2) ◽  
pp. 95
Author(s):  
A. Harari ◽  
F. Lemaire ◽  
B. Teisseire ◽  
B. Regnier
Keyword(s):  
Pulmonary Edema ◽  
Venous Admixture ◽  
Pulmonary Hemodynamics ◽  
Severe Pulmonary Edema

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 edema and hemodynamic changes on extravascular thermal volume of the lung

1984 ◽  
Vol 56 (4) ◽  
pp. 878-890 ◽  
Author(s):  
B. A. Gray ◽  
R. C. Beckett ◽  
R. C. Allison ◽  
D. R. McCaffree ◽  
R. M. Smith ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Mean Transit Time ◽  
Hemodynamic Changes ◽  
Pulmonary Hemodynamics ◽  
Indocyanine Green Dye ◽  
Pulmonary Arterial ◽  
The Mean ◽  
The Difference ◽  
Acute Changes ◽  
Thermal Dilution

The extravascular thermal volume of the lung (ETV) has been measured in dogs as the difference between mean transit time (t) volumes for heat and indocyanine green dye across the pulmonary circulation, calculated as the product of thermal dilution cardiac output (CO) and the difference in t for aortic indicator-dilution curves generated by right and left atrial injections. ETV measurements were compared with the extravascular lung mass (ELM): in 21 normal dogs, ETV/ELM = 1.11 +/- 0.14 (SD); in 17 dogs with hydrostatic pulmonary edema (up to 21 g/kg), ETV/ELM = 0.90 +/- 0.11; and in 27 dogs with alloxan pulmonary edema (up to 51 g/kg); ETV/ELM = 0.93 +/- 0.13. For all 65 dogs the mean ETVELM was 0.98 +/- 0.15, and the liner regression was ETV (ml/kg) = 0.90 ELM (g/kg) + 0.86 +/- 2.25 (SEE; r = 0.96). Calculations based on measurements of lung specific heat predict that ETV/ELM should equal 0.984. With acute changes in pulmonary hemodynamics, ETV was reduced by reductions in pulmonary arterial pressure (Ppa) sufficient to produce zone 1 conditions at the top of the lung. However, ETV was not affected by increases in CO (mean = 50%) produced by nitroprusside or by increases in Ppa and pulmonary blood volume (mean = 27%) produced by partial mitral valve obstruction. Distortion of the thermal dilution curve due to position of the arterial thermistor appears to be the greatest source of variability and overestimation. Simultaneous measurements from pairs of thermistors differed by 14% (range 0.4–50%).

Effects of pulmonary edema on regional pulmonary perfusion in the intact dog lung

1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg
Keyword(s):  
Blood Flow ◽  
Pulmonary Edema ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Weight Ratio ◽  
Flow Distribution ◽  
Base Line ◽  
Dependent Lung ◽  
Lung Water ◽  
Pulmonary Hemodynamics

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.

Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema

1990 ◽  
Vol 68 (3) ◽  
pp. 912-918 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Pulmonary Edema ◽  
Canine Model ◽  
Neurogenic Pulmonary Edema ◽  
Plasma Catecholamine ◽  
Pulmonary Hemodynamics ◽  
Lung Lobe ◽  
Pulmonary Vasoconstriction ◽  
Lower Lung ◽  
Severe Degree ◽  
Plasma Catecholamine Concentrations

The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL) perfusion of seven splenectomized (to keep hematocrit and blood viscosity constant) dogs was isolated so the LLL could be perfused at constant flow and outflow pressure with blood pumped from the pulmonary artery. The LLL was denervated by removing it from the dog. Veratrine (40-160 micrograms/kg) increased LLL arterial pressure by 39.2% and produced large increases in plasma catecholamine concentrations. The double-occlusion technique indicated that 74% of the increase in the LLL arteriovenous pressure gradient was due to an increase in venous tone. This pattern of vasoconstriction was similar to that previously observed during the infusion of exogenous catecholamines and suggested that catecholamines mediated the LLL response. The more severe degree of PH observed in the intact animal in NPE, however, suggests that passive rather than active changes in pulmonary hemodynamics are predominantly responsible for the development of PH in this disorder.

Effect of blood and albumin on pulmonary hypertension and edema in perfused rabbit lungs

1995 ◽  
Vol 78 (2) ◽  
pp. 499-504 ◽  
Author(s):  
S. A. Kraft ◽  
S. Fujishima ◽  
G. P. McGuire ◽  
J. S. Thompson ◽  
T. A. Raffin ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
Nitrogen Mustard ◽  
Blood Perfusion ◽  
Leukocyte Activation ◽  
Buffer Solution ◽  
Edema Formation ◽  
Pulmonary Hemodynamics ◽  
Buffer Solutions ◽  
Macromolecular Permeability

Perfusate composition may alter pulmonary hemodynamics and edema formation in perfused lungs. Perfusion for 3 h with Krebs-Henseleit solution with 3% bovine serum albumin did not produce pulmonary hypertension, pulmonary edema (assessed by lung wet-to-dry wt ratio), or increased macromolecular permeability (assessed by 125I-albumin uptake). Addition of blood to hematocrit levels of 10 or 20% resulted in pulmonary hypertension during the final hour of perfusion but not pulmonary edema or increased macromolecular permeability. Pulmonary hypertension during blood perfusion was primarily due to increased precapillary resistance. Perfusion with buffer solution without albumin produced edema and increased macromolecular permeability but not pulmonary hypertension. In lungs perfused with blood (20% hematocrit), thromboxane B2 levels increased in parallel with the pulmonary hypertension, and inhibition of cyclooxygenase or thromboxane synthase with indomethacin or dazmegrel prevented pulmonary hypertension. Perfusion with leukopenic blood (from prior nitrogen mustard administration or from filtration) also prevented pulmonary hypertension. We conclude that blood perfusion produces pulmonary hypertension via thromboxane A2 generation, which depends on leukocyte activation, and that perfusion with buffer solutions without albumin produces edema and increased permeability without pulmonary hypertension.

Severe Pulmonary Edema due to Hyponatremia after Hysteroscopy; Rapid and Full Recovery

2014 ◽  
Vol 3 (3) ◽  
pp. 375
Author(s):  
Akcan Akkaya ◽  
Ahmet Karatas ◽  
Abdullah Demirhan ◽  
Tulay Ozlu ◽  
Murat Bilgi ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Full Recovery ◽  
Severe Pulmonary Edema

Severe Pulmonary Edema Related to Dextran 40

2002 ◽  
Vol 49 (2) ◽  
pp. 221-222 ◽  
Author(s):  
Ferit Demirkan ◽  
??akir ??nal ◽  
Emrah Arslan ◽  
Mukadder ??alko??lu ◽  
??zlem Kandemir
Keyword(s):  
Pulmonary Edema ◽  
Dextran 40 ◽  
Severe Pulmonary Edema

scholarly journals STUDIES ON PULMONARY EDEMA

1937 ◽  
Vol 66 (4) ◽  
pp. 405-411 ◽  
Author(s):  
Sidney Farber
Keyword(s):  
Guinea Pig ◽  
Pulmonary Edema ◽  
Guinea Pigs ◽  
Artificial Respiration ◽  
Vasomotor Control ◽  
Pulmonary Vessels ◽  
Cervical Vagotomy ◽  
Vasomotor Nerves ◽  
Bilateral Vagotomy ◽  
Severe Pulmonary Edema

1. Guinea pigs die shortly after bilateral cervical vagotomy, even when continuous artificial respiration effected through a tracheal cannula is carried out. Death is caused by severe pulmonary edema and congestion. 2. Direct observation of the lungs after bilateral vagotomy demonstrates that pulmonary edema develops gradually and increases slowly in amount and severity. Congestion precedes and accompanies the development of the edema. 3. Neuropathic pulmonary edema in the guinea pig is caused by disturbance to or abolition of the pulmonary vasomotor nerves. 4. The evidence obtained by experiments on animals suggests that neuropathic pulmonary edema in man is caused by disturbances, either central or peripheral, to the vasomotor control of the pulmonary vessels.

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