Ann Thorac Surg 2010;89:981-983. doi:10.1016/j.athoracsur.2009.07.059
© 2010 The Society of Thoracic Surgeons
Case Reports
Inhaled Epoprostenol During One-Lung Ventilation
Karthik Raghunathan, MD, MPHa,*,
Neil Roy Connelly, MDa,
Larry D. Robbins, DOa,
Rose Ganim, MDb,
Gary Hochheiser, MDb,
Rebecca DiCampli, DOa
a Department of Anesthesiology, Baystate Medical Center, Tufts University School of Medicine, Springfield, Massachusetts
b Division of Thoracic Surgery, Department of Surgery, Baystate Medical Center, Tufts University School of Medicine, Springfield, Massachusetts
Accepted for publication July 10, 2009.
* Address correspondence to Dr Raghunathan, Department of Anesthesia, Tufts University School of Medicine, Baystate Medical Center, 759 Chestnut St, Springfield, MA 01199 (Email: karthik.raghunathan{at}bhs.org).
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Abstract
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We used inhaled epoprostenol (with intravenous phenylephrine) during one-lung ventilation to improve oxygenation in a patient with severe interstitial lung disease undergoing video-assisted thoracoscopic surgery. The pharmacologic manipulation of pulmonary blood flow remains an underused strategy for the management of hypoxemia during one-lung ventilation.
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Introduction
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Ventilation-perfusion matching and the prevention of hypoxemia remain a central concern during one-lung ventilation (OLV) [1]. We describe a case in which inhaled epoprostenol (Flolan, GlaxoSmithKline, Research Triangle Park, NC) and intravenous phenylephrine were used to dramatically improve oxygenation during video-assisted thoracoscopic surgery (VATS). The use of this combination of pharmacologic agents in this setting has not been previously described.
A 57-year-old man (height, 177 cm; weight, 102 kg) presented for flexible fiberoptic bronchoscopy and VATS. His history included increasing shortness of breath on home O2 at 2 to 4 L/min. His arterial blood gas analysis at baseline showed a pH of 7.46, PaCO2 of 34 mm Hg, and PaO2 of 62 mm Hg. Pulmonary function testing showed a forced expiratory volume in 1 second of 2.7 L (74% predicted) and forced expiratory volume in 1 second to forced vital capacity ratio of 107% predicted. The ventilation adjusted diffusing lung capacity for carbon monoxide was markedly abnormal at 36% predicted. Transthoracic echocardiography was notable for moderate pulmonary hypertension. High resolution computed tomographic scan of the chest revealed moderate to severe interstitial changes with the differential diagnosis encompassing a broad range of conditions, ranging from usual interstitial pneumonia, desquamative interstitial pneumonia, cryptogenic organizing pneumonia, hypersensitivity pneumonitis, to diffuse bronchioloalveolar carcinoma. The surgical plan was to attempt lung biopsies through a VATS approach while an open lung biopsy (with two-lung ventilation and a well placed mini-thoracotomy incision) was the back-up plan.
Preoperative vital signs were normal except for pulse oximetry (SpO2) of 92% on 3 L/min nasal O2. Nebulized albuterol was given prior to induction, and standard monitors including a radial arterial line were placed. Anesthesia was induced with intravenous fentanyl, propofol, and rocuronium, and was maintained with sevoflurane in 100% oxygen with intermittent boluses of fentanyl and rocuronium. After uneventful flexible fiberoptic bronchoscopy, a 39F left-sided Robertshaw double-lumen endobronchial tube was placed. At this time we briefly attempted one-lung ventilation, but the SpO2 promptly decreased to well below 80%, at which point we quickly returned to two-lung ventilation. To increase the tolerability of OLV in this seriously ill patient, we decided to trial inhaled epoprostenol with intravenous phenylephrine. The patient was first placed in a right lateral decubitus position for the left-sided VATS procedure. We established OLV just prior to incision (ventilation of only the right lung). Immediately we started the administration of epoprostenol through a MiniHEART low-flow nebulizer (Westmed, Tucson, AZ) to the dependent ventilated right lung, whereas the nondependent nonventilated left lung was open to the atmosphere. A volumetric infusion pump delivered epoprostenol into the nebulizer (0.75 mg in 50 cc sterile diluent) at 8 cc/hr. With an oxygen flow rate of 2 L/min (Fig 1), the targeted epoprostenol delivery was achieved [2]. Simultaneously, an intravenous infusion of phenylephrine was initiated and titrated to maintain the diastolic blood pressure at baseline pre-induction values. The ventilator (GE Avance S/5 Carestation, GE Healthcare, Piscataway, NJ) was set to a pressure control mode and the fixed bypass of oxygen flow was accounted for at 2 L/min. Peak inspiratory pressure and positive end-expiratory pressure settings of 20 cm H20 and 8 cm H20 were used. Delivered tidal volumes were about 6 cc/kg predicted body weight (450 cc). The lowest SpO2 recorded during this period was 92% (approximately 75 minutes of one-lung ventilation). At the conclusion of the uneventful surgery, the inhaled epoprostenol and intravenous phenylephrine were both discontinued, and the patient remained on one-lung ventilation in the lateral position. After approximately 12 minutes, the patient became severely hypoxemic. An arterial blood sample was drawn at this time, and two-lung ventilation was promptly reinstituted. SpO2 rapidly recovered to >92% with reinflation of the left lung. The patient was extubated and taken to the post-anesthetic care unit. The patient was able to maintain oxygenation on usual levels of support when discharged on postoperative day 1.
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Fig 1. (1) MiniHeart nebulizer with valved tee-adapter (WestMed, Tucson, AZ). (2) Oxygen tubing carrying 2 L/min flow into the nebulizer. (3) Nebulizer interface on the inspiratory limb of the anesthesia circuit. (4) Volumetric infusion of epoprostenol delivered into the nebulizer.
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Histopathology showed marked interstitial fibrosis with the usual interstitial pneumonia pattern, with features suggestive of acceleration. The patient was readmitted within 4 days of discharge secondary to rapid progression to acute respiratory distress syndrome. He suffered cardiac arrest secondary to refractory hypoxemia on postoperative day 17.
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Comment
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In the acute respiratory distress syndrome (ARDS) literature, inhaled epoprostenol has been shown to vasodilate the pulmonary vascular bed and increase blood flow to the ventilated areas of the lung [2]. This effect is largely limited to the pulmonary vasculature and there is rapid inactivation in the lungs (elimination half-life, 6 min). The similarities between OLV and ARDS have also been recognized [3, 4]. The use of inhaled epoprostenol has been described in anesthetized unilaterally ventilated pigs [5], but not yet in human subjects during OLV.
Our patient's markedly reduced diffusing lung capacity implied limited ability to oxygenate during OLV [1, 3]. We also hypothesized that extensive interstitial lung disease might severely affect the ability to redirect blood flow from the nonventilated lung to the ventilated lung by usual hypoxic pulmonary vasoconstriction mechanisms [6]. Empirically we observed this as profound desaturation during an initial attempt at OLV. Consequently, we decided to conduct a trial of inhaled epoprostenol during OLV. Our goal was to induce selective pulmonary vasodilatation in the ventilated lung and to improve ventilation-perfusion matching. In addition, although we had no evidence that it was necessary, we used an intravenous phenylephrine infusion to ameliorate any systemic vasodilatory effects of the epoprostenol, and hypothetically increase pulmonary vascular resistance in the nonventilated lung. The PaO2/FiO2 ratio doubled during OLV (Table 1), and the patient tolerated the procedure well.
Inhaled nitric oxide and intravenous almitrine have been described as the definitive answer to hypoxemia during OLV [7]. Comparative studies of inhaled nitric oxide versus epoprostenol in ARDS have indicated identical efficacy [2]. However, the delivery system for inhaled nitric oxide is more complex and it is also more expensive (direct pharmacy costs of epoprostenol are $30 versus approximately $200 for an equivalent duration of inhaled nitric oxide [8]). Thus, inhaled epoprostenol might increase the tolerability of one-lung ventilation and it might allow wedge resection or segmentectomy for carcinoma in "marginal" patient populations, or the avoidance of cardiopulmonary bypass in some transplant patients. We want to emphasize that when faced with hypoxemia during OLV, clinicians should always first address readily remediable causes (such as a malpositioned double-lumen tube, reduction in dependent-lung functional residual capacity, and so forth) prior to attempting the manipulation of pulmonary perfusion. In conclusion, inhaled epoprostenol (with intravenous phenylephrine) was efficacious and cost-effective for the prevention of hypoxemia during one-lung ventilation in this seriously ill patient. Randomized, clinical trials are required to qualify the efficacy of this therapy and identify patients who would receive the greatest benefit.
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Acknowledgments
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The authors acknowledge that no grants, financial support, technical, or other assistance was received from any extra-mural source.
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References
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Abstract
Introduction
