| The Effects of Dependent Ventilated Lung Nitric Oxide in Patients with Normal Baseline Pulmonary Vascular Resistance. |
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Jeong Won Lee, Tae Sung Kim, Hyun Soo Kim, Kwang Min Kim |
1Department of Anesthesiology, Hallym University Medical Center, Seoul, Korea.
2Department of Anesthesiology, College of Medicine, Seoul National University, Seoul, Korea. |
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| Abstract |
BACKGROUND
Inhaled nitric oxide (NO) is a selective and potent pulmonary vasodilator. The authors hypothesized that inhaled NO at 40 ppm would improve parameters of oxygenation and pulmonary hemodynamics in patients undergoing one-lung ventilation in the lateral decubitus position by causing selective ventilated lung vasodilation.
METHODS
Six patients scheduled for thoracotomy operations were anesthetized with a thoracic epidural lidocaine (2%, 8ml/hr), intravenous fentanyl (2-5 ug/kg/min) and inhaled isoflurane (0.5 1.0%), and were monitored with radial and pulmonary artery catheters. After the patients were tumed into in the lateral decubitus position, the dependent lung was ventilated with 70% O2 and 30% N2 for 15 min for the control one-lung ventilation condition. For the study of one-lung ventilation condition, the dependent lung was ventilated with the same gas concentration with NO at 40 ppm for 15 min. During all conditions, pulmonary and systemic hemodynamics, intrapulmonary shunt and other parameters of ventilation were measured in a double blind method.
RESULTS
Baseline pulmonary vascular resistance during two-lung ventilation was 146.8+50.3 (SD) dynes sec cm.
Administration of inhaled NO did not affect right-to-left intrapulmonary shunt, pulmonary vascular resistance, mean arterial pressure or systemic vascular resistance. Mean pulmonary arterial pressure remained unchanged during the administration of inhaled NO.
CONCLUSIONS
Inhaled NO at 40 ppm does not significantly decrease ventilated lung PVR or improve oxygenation during one-lung ventilation in the lateral decubitus position in patients with normal pulmonary vascular resistance. This may be attributed to the inability of inhaled NO to further decrease normal baseline PVR exhibited by all patients enrolled in our study. |
| Key Words:
Arteries; Pulmonary; Vasodilation; Nitric oxide; Ventilation; one-lung |
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