Resting Arterial Oxygen Tension Influences Pulmonary Vascular Resistance in Heart Failure

2006 ◽  
Vol 12 (6) ◽  
pp. S11
Author(s):  
Thomas P. Olson ◽  
Robert P. Frantz ◽  
Kathy A. O'Malley ◽  
Bruce D. Johnson
1999 ◽  
Vol 91 (4) ◽  
pp. 945-945 ◽  
Author(s):  
Albert Benzing ◽  
Torsten Loop ◽  
Georg Mols ◽  
Klaus Geiger

Background Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide. Methods Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated. Results During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air. Conclusions Unintended inhalation of nitric oxide increases arterial oxygen tension and decreases pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. The unintended nitric oxide inhalation interferes with the therapeutic use of nitric oxide.


1980 ◽  
Vol 44 (9) ◽  
pp. 749-754 ◽  
Author(s):  
KINJI ISHIKAWA ◽  
KEN KANAMASA ◽  
TETSU YAMAKADO ◽  
YASUYUKI KOHASHI ◽  
ARATA KATO ◽  
...  

1987 ◽  
Vol 25 (3) ◽  
pp. 199-208 ◽  
Author(s):  
STEVEN J. BARKER ◽  
KEVIN K. TREMPER

1996 ◽  
Vol 23 (2) ◽  
pp. 75-77
Author(s):  
P. Dobromylskyj ◽  
P.M. Taylor ◽  
J.C. Brearley ◽  
C.B. Johnson ◽  
S.P.L. Luna

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 219-228
Author(s):  
Henrique Rigatto ◽  
June P. Brady

We studied nine healthy preterm infants during the first 35 days of life to define the relationship between periodic breathing, apnea, and hypoxia. For this purpose we compared ventilation/apnea (V/A), minute ventilation, and alveolar and capillary blood gases during periodic breathing induced by hypoxia and during spontancous periodic breathing in room air. We induced periodic breathing by giving the baby in sequence 21, 19, 17, and 15% O2 to breathe for 5 minutes each, and also by giving 21, 15, and 21% O2. We measured ventilation with a nosepiece and a screen flowmeter. With a decrease in arterial oxygen tension, preterm infants (1) hypoventilated, (2) breathed periodically more frequently, and (3) showed a decrease in V/A due to an increase in the apneic interval. In one baby this led to apnea lasting 30 seconds. These findings support our hypothesis that preterm infants breathing periodically hypoventilate and suggest that hypoxia may be a primary event leading to periodic breathing and apnea.


1974 ◽  
Vol 85 (2) ◽  
pp. 254-261 ◽  
Author(s):  
Arnold W. Strauss ◽  
Marilyn Escobedo ◽  
David Goldring

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