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Effect of Acetylsalicylic Acid on Pulmonary Gas Exchange in Patients With Severe Pneumonia : A Pilot Study FREE TO VIEW

Miquel Ferrer; Antoni Torres; Rachel Baer; Carme Hernández; Josep Roca; Robert Rodriguez-Roisin
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From the Servei de Pneumologia i Allèrgia Respiratòria, Hospital Clínic, Departament de Medicina, Universitat de Barcelona, Barcelona, Spain

1997 by the American College of Chest Physicians

Chest. 1997;111(4):1094-1100. doi:10.1378/chest.111.4.1094
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Background: It has been hypothesized that local release of prostacyclin in acute pneumonia may ablate hypoxic pulmonary vasoconstriction, thus contributing to the impairment of pulmonary gas exchange in these patients. Inhibition of cyclooxygenase pathway could prevent this phenomenon by reducing the release of these metabolites.

Methods: A study was designed to assess the effect of IV acetylsalicylic acid (ASA) (2 g) on pulmonary gas exchange in seven patients (age, 64±11 [mean±SD] years) with unilateral severe pneumonia (PaO2/fraction of inspired oxygen, 168±67) needing mechanical ventilation. Respiratory gases, pulmonary and systemic hemodynamics, and ventilation-perfusion (VA/Q) distributions were studied before and 15 and 60 min after the infusion of ASA.

Results: At baseline, the amount of shunt (VA/Q ratios <0.005) was 28±17% of cardiac output, blood flow to areas with low VAQ ratios (<0.1, excluding shunt) was 8±7%, and the dispersion of pulmonary blood flow distribution (second moment, log SD Q) was 1.45±0.49 (normal range, 0.3 to 0.6). Sixty minutes after the infusion of ASA, we observed a mild reduction of the amount of shunt, from 28±17% to 23.5±13% (p<0.05) without changes in arterial oxygenation. This was associated with a significant increase in mean pulmonary artery pressure (from 21.9±3.6 to 24.4±5.1 and 23.9±5.3 mm Hg, p<0.025 and p=0.1) and pulmonary vascular resistance (from 1.4±0.9 to 1.8±0.8 and 1.8±1.3 mm Hg · min · L, p<0.002 and p=0.11) 15 and 60 min after ASA, respectively. The ASA plasma levels were within the normal therapeutic range (120±7 µg/mL, 15 min, and 113±11 µg/mL, 60 min after ASA infusion).

Conclusions: Although there was a modest improvement in intrapulmonary shunt, our results suggest that perfusion of ASA in this small sample of patients with severe pneumonia appears to be of little benefit as complementary treatment for severe hypoxemia.




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