| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
Departments of
*Anesthesiology and
Thoracic Surgery, Hôpital Foch, Suresnes, Université Paris-Ouest, France
Address correspondence and reprint requests to Marc Fischler, MD, Département d’Anesthésie, Hôpital Foch, 40 rue Worth, 92150 Suresnes, France. Address e-mail to m.fischler{at}hopital-foch.org
 |
Introduction |
|---|
 Top Introduction Case ReportDiscussionReferences |
|---|
Hypoxemia can be so severe that bronchopulmonary lavage may require extracorporeal membrane oxygenation (5,6). New therapeutics, such as nitric oxide (NO) and almitrine, provide a nonventilatory technique for treating hypoxemia, especially in patients suffering from acute respiratory distress syndrome and hypoxia during one-lung ventilation (7). We used these therapeutics in a case of bronchopulmonary lavage.
|
Case Report |
|---|
|
TopIntroductionCase ReportDiscussionReferences |
|---|
After anesthetic induction with 1 µg/kg sufentanil and 3 mg/kg propofol, rocuronium (1 mg/kg) was given to induce neuromuscular block. A 39-mm, left-sided, double-lumen endotracheal tube was placed without difficulty. Correct position was verified using auscultation and direct visualization with fiberoptic bronchoscopy. Complete lung separation was confirmed by the absence of a leak from the nondependent lung using the bubble technique (8). A 20-gauge cannula was placed into the left radial artery, and a triple-lumen, thermistor-tipped 7.5F pulmonary artery catheter was placed into the right internal jugular vein. The tip of the catheter was located in the left pulmonary artery (preoperative chest radiograph). Anesthesia was maintained by using boluses of sufentanil, propofol, and rocuronium as required. The patient was placed in the right lateral position to decrease the risk of saline dispersion in the left ventilated lung, the right lung was deflated, and the patient’s lungs were mechanically ventilated with 100% oxygen. Ventilatory variables during two-lung and one-lung ventilation included a tidal volume of 500 mL at a rate of 12 breaths/min. The bronchopulmonary lavage was performed as previously described (3). Because PaO2 was <80 mm Hg during the second phase of lung emptying (Table 1) despite pure oxygen ventilation, it was decided to use inhaled NO and/or almitrine to maintain the one-lung ventilation. The following sequences were successively performed during empty and filling phases: inhalation of 20 ppm NO, IV infusion of 4 µg · kg-1 · min-1 almitrine, association of 20 ppm NO and of 4 µg · kg-1 · min-1 almitrine, IV infusion of 16 µg · kg-1 · min-1 almitrine, association of 20 ppm NO and 16 µg · kg · min-1 almitrine. As a long-acting substance, almitrine makes returning to a zero pharmacological set of measurements impossible. Inhaled NO was administered as previously described (7).
|
PaO2 and shunt were 82 mm Hg and 29%, respectively, at the end of the first stage of one-lung ventilation with the other lung emptied. At the end of the first lung filling, PaO2 had increased (454 mm Hg). An increase in PaO2 during empty phases was obtained only during a large-dose almitrine infusion either with (171 mm Hg) or without (133 mm Hg) simultaneous NO inhalation; the shunt was 23% and 27%, respectively, at corresponding times.
A slight increase in systemic arterial pressure, mean pulmonary arterial pressure, and capillary wedge pressure was noticed throughout the procedure, even during the filling phases.
Lavage was repeated until the effluent was clear. A total volume of 13.5 L was infused, and 12.4 L was recovered.
At the end of the procedure, as is usual in our institution, the trachea was intubated with a regular endotracheal tube, and ventilation was maintained to facilitate suctioning to remove remaining fluid and to reexpand the lungs. Extubation was uneventful. The postextubation blood gas values were pHa 7.41, PaO2 83 mm Hg, and PaCO2 37.8 mm Hg. The patient’s condition improved to a large extent. No other bronchopulmonary lavage was planned.
|
Discussion |
|---|
|
TopIntroductionCase ReportDiscussionReferences |
|---|
Pulmonary artery vasculature pharmacological manipulation has been studied extensively in patients suffering from acute respiratory distress syndrome. The pulmonary arterial bed can be dilated using inhaled NO (10) or aerosolized prostacyclin (11), both locally acting pulmonary arterial vasodilators. The pulmonary arterial bed can be vasoconstricted using IV almitrine (12), a selective pulmonary arterial vasoconstrictor, or phenylephrine (13), an 
-receptor agonist. All of these drugs can be used alone or in association, especially the NO-almitrine association (14–16).
Few studies have been performed during one-lung ventilation (OLV). Most clinical studies have demonstrated no improvement in PaO2 during NO inhalation (7,17,18), and only one reported a positive effect.1 Furthermore, it has been demonstrated that delivering50 ppm inhaled NO into the hyperoxic lung increases its perfusion from 70% to 75% of cardiac output by redistributing the blood flow when the opposite lung is hypoxic (19). Because the baseline level of pulmonary vascular resistance is one of the factors that determine NO-induced improvement in arterial oxygenation in patients with acute respiratory failure (20), the fact that NO has no, or only a slightly beneficial, effect during OLV could be explained by pulmonary vascular resistance remaining unchanged or somewhat increasing in this particular situation (21). Sole almitrine administration was studied only in a canine model with normal lungs ventilated with a hyperoxic gas on one side and a hypoxic mixture on the other: a small-dose almitrine infusion (3 µg · kg-1 · min-1) increased PaO2 (22), whereas a large dose (14.3 µg · kg-1 · min-1) was detrimental (23). The combination of 20 ppm inhaled NO and 16 µg · kg-1 · min-1 IV almitrine was studied during OLV in a clinical situation and was shown to reduce the decrease of PaO2 (7).
In our case, an increase in PaO2 was obtained during almitrine infusion, but only when given at a large dose (16 µg · kg-1 · min-1); this is contradictory to the experimental data obtained in dogs (22,23). Furthermore, our patient’s PaO2 increased from 133 to 171 mm Hg when NO was associated with large-dose almitrine. The beneficial effect of the NO-almitrine association may be explained by almitrine’s increasing pulmonary artery pressure, as was suggested in patients suffering from acute lung injury (16,20).
In this case report, the improvement of PaO2 was surely related to the nonventilatory treatment of a such severe hypoxemia for two main reasons. First, the entire study was performed during OLV; therefore, any effect of the bronchopulmonary lavage on oxygenation could not be seen. Second, neither PaO2 nor venous admixture in OLV during bronchopulmonary lavage showed any evolution over the entire procedure (3,24).
During OLV, continuous positive airway pressure for the nonventilated lung is recommended when PaO2 remains low despite ventilation with pure oxygen (25). However, nonventilatory treatment of hypoxemia, such as with a NO-almitrine combination, could be an alternative, especially during bronchopulmonary lavage and selected cases of thoracoscopic procedures, because continuous positive airway pressure could interfere with surgical exposure. Further studies including more patients are required to demonstrate that bronchopulmonary lavage could also be an indication for such treatment, as shown in this case report.
|
Footnotes |
|---|
|
References |
|---|
|
TopIntroductionCase ReportDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  M.-J. Nadeau, D. Cote, and J. S. Bussieres The Combination of Inhaled Nitric Oxide and Pulmonary Artery Balloon Inflation Improves Oxygenation During Whole-Lung Lavage Anesth. Analg., September 1, 2004; 99(3): 676 - 679. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. C. Dietrich and J. D. Tobias Intraoperative Administration of Nitric Oxide J Intensive Care Med, May 1, 2003; 18(3): 146 - 149. [Abstract] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
