Unintended Inhalation of Nitric Oxide by Contamination of Compressed Air 

1999 ◽  
Vol 91 (4) ◽  
pp. 945-945 ◽  
Author(s):  
Albert Benzing ◽  
Torsten Loop ◽  
Georg Mols ◽  
Klaus Geiger
Keyword(s):  
Nitric Oxide ◽  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Vascular Resistance ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Arterial Oxygen Tension ◽  
Compressed Air ◽  
Arterial Oxygen

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.

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
Keyword(s):  
Heart Failure ◽  
Pulmonary Vascular Resistance ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen

Changes in arterial oxygen tension when weaning neonates from inhaled nitric oxide

2001 ◽  
Vol 32 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Gregory M. Sokol ◽  
Naomi S. Fineberg ◽  
Linda L. Wright ◽  
Richard A. Ehrenkranz
Keyword(s):  
Nitric Oxide ◽  
Oxygen Tension ◽  
Arterial Oxygen Tension ◽  
Inhaled Nitric Oxide ◽  
Arterial Oxygen

Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

2002 ◽  
Vol 28 (8) ◽  
pp. 1064-1072 ◽  
Author(s):  
Seow P. Tan ◽  
F. Genc ◽  
E. Delgado ◽  
J. Kellum ◽  
M. Pinsky
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Compressed Air ◽  
Oxide Contamination

Volume loading reduces pulmonary vascular resistance in ventilated animals with acute lung injury: evaluation of RV afterload

2011 ◽  
Vol 300 (3) ◽  
pp. R763-R770 ◽  
Author(s):  
Jamie R. Mitchell ◽  
Christopher J. Doig ◽  
William A. Whitelaw ◽  
John V. Tyberg ◽  
Israel Belenkie
Keyword(s):  
Cardiac Output ◽  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pressure Gradient ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Volume Loading ◽  
External Constraint

During mechanical ventilation, increased pulmonary vascular resistance (PVR) may decrease right ventricular (RV) performance. We hypothesized that volume loading, by reducing PVR, and, therefore, RV afterload, can limit this effect. Deep anesthesia was induced in 16 mongrel dogs (8 oleic acid-induced acute lung injury and 8 controls). We measured ventricular pressures, dimensions, and stroke volumes during positive end-expiratory pressures of 0, 6, 12, and 18 cmH2O at three left ventricular (LV) end-diastolic pressures (5, 12, and 18 mmHg). Oleic acid infusion (0.07 ml/kg) increased PVR and reduced respiratory system compliance ( P < 0.05). With positive end-expiratory pressure, PVR was greater at a lower LV end-diastolic pressure. Increased PVR was associated with a decreased transseptal pressure gradient, suggesting that leftward septal shift contributed to decreased LV preload, in addition to that caused by external constraint. Volume loading reduced PVR; this was associated with improved RV output and an increased transseptal pressure gradient, which suggests that rightward septal shift contributed to the increased LV preload. If PVR is used to reflect RV afterload, volume loading appeared to reduce PVR, thereby improving RV and LV performance. The improvement in cardiac output was also associated with reduced external constraint to LV filling,; since calculated PVR is inversely related to cardiac output, increased LV output would reduce PVR. In conclusion, our results, which suggest that PVR is an independent determinant of cardiac performance, but is also dependent on cardiac output, improve our understanding of the hemodynamic effects of volume loading in acute lung injury.

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