Pulmonary Hemodynamics and Gas Exchange During Venoarterial Bypass with Membrane-Lung Oxygenation

1979 ◽  
pp. 258-266
Author(s):  
F. Jardin ◽  
B. Regnier ◽  
H. Gastine ◽  
F. Lemaire
Keyword(s):  
Gas Exchange ◽  
Pulmonary Hemodynamics ◽  
Membrane Lung

scholarly journals Superoxide Dismutase Improves Gas Exchange and Pulmonary Hemodynamics in Premature Lambs

2005 ◽  
Vol 172 (6) ◽  
pp. 745-749 ◽  
Author(s):  
John P. Kinsella ◽  
Thomas A. Parker ◽  
Jonathan M. Davis ◽  
Steven H. Abman
Keyword(s):  
Superoxide Dismutase ◽  
Gas Exchange ◽  
Pulmonary Hemodynamics

Effect of inhaled nitric oxide on pulmonary hemodynamics after acute lung injury in dogs

1994 ◽  
Vol 76 (3) ◽  
pp. 1356-1362 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Dead Space ◽  
Left Ventricular ◽  
Right Atrial ◽  
Adrenergic Blockade ◽  
Pulmonary Hemodynamics ◽  
Beta Adrenergic

Increased pulmonary vascular resistance (PVR) and mismatch in ventilation-to-perfusion ratio characterize acute lung injury (ALI). Pulmonary arterial pressure (Ppa) decreases when nitric oxide (NO) is inhaled during hypoxic pulmonary vasoconstriction (HPV); thus NO inhalation may reduce PVR and improve gas exchange in ALI. We studied the hemodynamic and gas exchange effects of NO inhalation during HPV and then ALI in eight anesthetized open-chest mechanically ventilated dogs. Right atrial pressure, Ppa, and left ventricular and arterial pressures were measured, and cardiac output was estimated by an aortic flow probe. Shunt and dead space were also estimated. The effect of 5-min exposures to 0, 17, 28, 47, and 0 ppm inhaled NO was recorded during hyperoxia, hypoxia, and oleic acid-induced ALI. During ALI, partial beta-adrenergic blockade (propranolol, 0.15 mg/kg i.v.) was induced and 74 ppm NO was inhaled. Nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) levels were measured. During hyperoxia, NO inhalation had no measurable effects. Hypoxia increased Ppa (from 19.8 +/- 6.1 to 28.3 +/- 8.7 mmHg, P < 0.01) and calculated PVR (from 437 +/- 139 to 720 +/- 264 dyn.s.cm-5, P < 0.01), both of which decreased with 17 ppm NO. ALI decreased arterial PO2 and increased airway pressure, shunt, and dead space ventilation. Ppa (19.8 +/- 6.1 vs. 23.4 +/- 7.7 mmHg) and PVR (437 +/- 139 vs. 695 +/- 359 dyn.s.cm-5, P < 0.05) were greater during ALI than during hyperoxia. No inhalation had no measureable effect during ALI before or after beta-adrenergic blockade. MetHb remained low, and NO-Hb was unmeasurable. Bolus infusion of nitroglycerin (15 micrograms) induced an immediate decrease in Ppa and PVR during ALI.(ABSTRACT TRUNCATED AT 250 WORDS)

EFFECTS OF WOUND EXCISION ON PULMONARY HEMODYNAMICS AND GAS EXCHANGE IN BURNED PATIENTS

1988 ◽  
Vol 67 (Supplement) ◽  
pp. 81
Author(s):  
S. Gregoretti ◽  
S. Gelman ◽  
A. R. Dimick
Keyword(s):  
Gas Exchange ◽  
Pulmonary Hemodynamics ◽  
Wound Excision

Effect of Lung Volume Reduction Surgery on Gas Exchange and Pulmonary Hemodynamics at Rest and during Exercise

1998 ◽  
Vol 158 (4) ◽  
pp. 1020-1025 ◽  
Author(s):  
MONIQUE OSWALD-MAMMOSSER ◽  
ROMAIN KESSLER ◽  
GILBERT MASSARD ◽  
JEAN-MARIE WIHLM ◽  
EMMANUEL WEITZENBLUM ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Volume Reduction ◽  
Lung Volume Reduction Surgery ◽  
Lung Volume Reduction ◽  
Pulmonary Hemodynamics

Acid-base status affects gas exchange in canine oleic acid pulmonary edema

1991 ◽  
Vol 260 (4) ◽  
pp. H1080-H1086 ◽  
Author(s):  
S. Brimioulle ◽  
J. L. Vachiery ◽  
P. Lejeune ◽  
M. Leeman ◽  
C. Melot ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Metabolic Acidosis ◽  
Gas Exchange ◽  
Pulmonary Edema ◽  
Sulfur Hexafluoride ◽  
Respiratory Acidosis ◽  
Pulmonary Gas Exchange ◽  
Intrapulmonary Shunt ◽  
Pulmonary Hemodynamics ◽  
Acid Base Status

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.

Hypoxic pulmonary vasoconstriction and gas exchange in acute canine pulmonary embolism

1996 ◽  
Vol 80 (4) ◽  
pp. 1240-1248 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
F. Vermeulen ◽  
R. Naeije
Keyword(s):  
Pulmonary Embolism ◽  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Blood Clot ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Autologous Blood ◽  
Response Curves ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Hypoxic pulmonary vasoconstriction (HPV) is inhibited in several models of acute lung injury. Whether HPV is preserved in pulmonary embolism is unknown. We investigated the effects of a reduction in the fraction of inspired O2 (FIO2) on pulmonary hemodynamics and gas exchange in anesthetized dogs before and after autologous blood clot pulmonary embolism. In a first group of 14 dogs, stimulus-response curves for HPV were constructed as pulmonary arterial pressure (Ppa) vs. FIO2 varied between 1.0 and 0.06 at a cardiac output (Q) kept constant at 3.5 l.min-1.m-2. Gas exchange was evaluated by using the multiple inert-gas elimination technique at FIO2 of 1.0, 0.4, and 0.1. Embolism decreased the relative magnitude of HPV, expressed as the gradient between Ppa and pulmonary arterial occluded pressure in hypoxia divided by (Ppa-pulmonary arterial occluded pressure) at FIO2 of 1.0, from 1.8 to 1.2 (P < 0.05). Retention minus excretion gradients for sulfur hexafluoride and ethane were increased by decreased FIO2 (P < 0.005 and P < 0.05, respectively) before but not after embolism. Hypoxia-induced deterioration in gas exchange before embolism was related to the amount of baseline very low ventilation-perfusion (VA/Q) ratios. Similar results were obtained in a second group of seven dogs with Q decreased to maintain Ppa at the same average value as before embolism. However, gas exchange was not affected by inspiratory hypoxia before as well as after embolism in this group, which presented with a lesser amount of baseline very low VA/Q. In both groups of dogs, increase in the FIO2 from 0.4 to 1.0 did not affect gas exchange. We conclude that 1) pulmonary embolism is associated with a partial inhibition of HPV, 2) HPV does not contribute to preserve gas exchange in pulmonary embolism, and 3) a strong HPV may deteriorate gas exchange in severe hypoxia in the presence of minor very low VA/Q inequality.

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