Two-Lung and One-Lung Ventilation in Patients - Anesthesia ...

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40 CARDIOVASCULAR ANESTHESIA BARDOCZKY ET AL. ANESTH ANALG POSITION AND Fio 2 DURING OLV 2000;90:35–41 not cause more of an increase in shunt. Pao 2 during TLV may also be a determining factor of oxygenation during OLV (18). Second, we did not study OLV for long periods (more than two hours) with high Fio 2 values, but according to the study of Barker et al. (19), late hypoxemia occurs (mean OLV time, 170 minutes) when ventilating with 100% oxygen, which may be in part caused by absorption atelectasis. High Fio 2 can lead to arteriovenous shunting in areas of airway closure and, further, cause absent ventilation in lung units with low ventilation/perfusion ratios. Third, if we consider that the lateral TLV/OLV always followed the supine TLV/OLV sequence, one can argue that a time effect could influence the present results. Concerning the time course of the HPV response, many experimental and clinical studies have been performed, with sometimes contradictory results. Benumof (20) showed that intermittent hypoxic challenges potentiated the hypoxic vasoconstriction in the left lower lobe of open-chest dog lungs, but the preparation and manipulation of the animals required considerable instrumentation and manipulation, which may have interfered with the HPV. Carlsson et al. (21) found maximal HPV response within 15 minutes of hypoxia in a human study, which agrees with observations in animal studies. Tucker and Reeves (22) were unable to maintain HPV during acute hypoxia in anesthetized dogs. During one-lung hypoxia in dogs, Domino et al. (23) studied HPV in closedchest dogs and found a maximal level from the very first hypoxic challenge. Thus, there is a wide variation in the results obtained concerning the influence of time on HPV. In our study, the experimental procedure was almost identical to the procedure performed by Carlsson et al. (21) or by Domino et al. (23), who concluded that the time factor should not be a hindrance to manipulative studies on the HPV response once a maximal response has been evoked, normally in 10–15 minutes. Fourth, if we consider that, after the period of supine TLV, we have only declamped the tracheal limb of the DLT and closed it, without sighing the nondependent lung, the 5-mL/kg gas distributed to that lung will not reverse the amount of atelectasis. So, our study may be comparable to the study of Fiser et al. (9), but as significant changes were found in the lateral position, we can argue that if HPV was maximal after the first 15 min of hypoxia, there is another factor, probably gravity, that could contribute to flow redistribution. Nevertheless, in the particular conditions of the present study—patients with mild COPD, closed chest, mixed locoregional/general balanced anesthesia—increased HPV responses in the lateral position cannot be excluded as explanations of Pao 2 values observed in the second OLV episode. Paco 2, especially at high values, influences the level HPV response (24). Thus, the Paco 2 values of the studied patients were always maintained within normal limits in the different periods of blood gas measurements. Another factor that may influence hypoxia during OLV is the side of the surgery. Left thoracotomy has a better Pao 2 during OLV than right thoracotomy, because the left lung normally receives 10 percent less cardiac output than the right lung (18). In our study, there were no statistical differences concerning the side of surgery in the three groups or among the three groups. Gravity is a major, pharmacologically and physiopathologically, independent determinant of regional pulmonary blood flow distribution. The extent of blood flow redistribution depends on the local relationship between pulmonary arterial, venous, and airway pressures. In the lateral position, regional blood flow increases from the nondependent to the dependent thoracic wall (8). Unfortunately, the design of our study did not permit us to distinguish between the direct effects of HPV on blood flow and the effects of gravitational redistribution of blood flow. The differences observed among the three groups of patients supports the hypothesis of Benumof et al. (25), who demonstrated, on a canine left lower lobe preparation, that if Fio 2 changes cause secondary changes in Pao 2, and in the mixed venous oxygen tension, then the mixed venous oxygen tension is a new and important determinant of the magnitude of HPV. This suggests that when one compartment Fio 2 is 1.0 and the other compartment is hypoxic, HPV in the hypoxic compartment is maximal. The method used to ventilate the dependent lung is an important determinant of the blood flow distribution during OLV. High airway pressures can compress lung vessels, diverting blood flow from ventilated to nonventilated regions. However, hypoventilation of the dependent lung during OLV is associated with lower airway pressure, and the ventilated lung pulmonary vascular resistance may decrease, thus promoting HPV in the nonventilated lung (7). This mechanism of improved Pao 2 was unlikely in the present investigation, as ventilatory settings were kept constant, inspiratory airway pressures were not changed, and the mechanical characteristics of the dependent lung remained unaltered (Tables 2–4) after changing the position. These findings indicate that the improved Pao 2 cannot be attributed to an altered HPV caused by change in ventilatory pattern. Surgical compression and retraction may also contribute to the passive reduction of nondependent lung blood flow (15). However, in our study, there was no mechanical effect on lung parenchyma, as the data
ANESTH ANALG CARDIOVASCULAR ANESTHESIA BARDOCZKY ET AL. 41 2000;90:35–41 POSITION AND Fio 2 DURING OLV were collected before chest opening. Therefore, surgical manipulation could not influence the amount of shunt occurring. We conclude that, in addition to HPV, the augmented redistribution of perfusion caused by gravitational forces is probably responsible for the higher Pao 2 during OLV in the lateral position. The finding of significantly lower Pao 2 values occurring when OLV was initiated in the supine position may predict more frequent intraoperative hypoxemia when thoracic surgery requiring OLV is performed with patients in the supine position. If severe hypoxemia occurs during OLV in the lateral position, higher Fio 2 values might be used. References 1. Pasque MK, Cooper JD, Kaiser L, et al. Improved technique for bilateral lung transplantation: rationale and initial clinical experience. Ann Thorac Surg 1990;49:785–91. 2. Cooper JD, Patterson GA, Sundaresan RS, et al. Results of 150 consecutive bilateral lung volume reduction procedures in patients with severe emphysema. J Thorac Cardiovasc Surg 1996; 112:1319–30. 3. Lima O, Ramos L, DiBiasi P, Judice L. Median sternotomy for bilateral resection of emphysematous bullae. J Thorac Cardiovasc Surg 1981;82:892–7. 4. Wasnick JD, Acuff T. Anesthesia and minimally invasive thoracoscopically assisted coronary artery bypass: a brief clinical report. J Cardiothorac Vasc Anesth 1997;11:552–5. 5. Urschel HC, Razzuk MA. Median sternotomy as a standard approach for pulmonary resection. Ann Thorac Surg 1986;41: 130–4. 6. Benumof JL. One-lung ventilation and hypoxic pulmonary vasoconstriction: implications for anesthetic management. Anesth Analg 1985;64:821–33. 7. Benumof JL. Physiology of the lateral decubitus position, the open chest and one-lung ventilation. In: Kaplan JA, ed. Thoracic anesthesia. New York: Churchill Livingstone, 1993:193–221. 8. Arborelius M, Lundin G, Svanberg L, Defares JG. Influence of unilateral hypoxia on blood flow through the lungs in man in lateral position J Appl Physiol 1960;15:595–7. 9. Fiser WP, Friday CD, Read RC. Changes in arterial oxygenation and pulmonary shunt during thoracotomy with endobronchial anesthesia. J Thorac Cardiovasc Surg 1982;83:523–31. 10. Hannalah MS, Benumof JL, McCarthy PO, et al. Comparison of three techniques to inflate the bronchial cuff of left polyvinylchloride double-lumen tubes. Anesth Analg 1993;77:990–4. 11. Deleted in proof. 12. Rehder K, Wenthe FM, Sessler AD. Function of each lung during mechanical ventilation with ZEEP and with PEEP in man anesthetized with thiopental-meperidine. Anesthesiology 1973; 39:597–606. 13. Gayes JM, Emery RW. The MIDCAB experience: a current look at evolving surgical and anesthetic approaches. J Cardiothorac Vasc Anesth 1997;11:625–8. 14. Marshall BE. Hypoxic pulmonary vasoconstriction. Acta Anaesthesiol Scand 1990;34:37–41. 15. Alfery DD, Benumof JL, Trousdale FR. Improving oxygenation during one-lung ventilation in dogs: the effects of positive endexpiratory pressure and blood-flow restriction to the nonventilated lung. Anesthesiology 1981;55:381–5. 16. Boldt J, Muller M, Uphus D, et al. Cardiorespiratory changes in patients undergoing pulmonary resection using different anesthetic management techniques. J Cardiothorac Vasc Anesth 1996;7:854–9. 17. Rehder K, Knopp TJ, Sessler AD, Didier EP. Ventilationperfusion relationship in young healthy awake and anesthetized-paralyzed man. J Appl Physiol 1979;47:745–53. 18. Slinger P, Suissa S, Adam J, Triolet W. Predicting arterial oxygenation during one-lung ventilation with continuous positive airway pressure to the nonventilated lung. J Cardiothorac Anesth, 1990;4:436–40. 19. Barker SJ, Clarke C, Trivedi N, et al. Anesthesia for thoracoscopic laser ablation of bullous emphysema. Anesthesiology 1993;78:44–50. 20. Benumof JL. Intermittent hypoxia increases lobar hypoxic pulmonary vasoconstriction. Anesthesiology 1983;58:399–404. 21. Carlsson AJ, Bindslev L, Santesson J, et al. Hypoxic pulmonary vasoconstriction in the human lung: the effect of prolonged unilateral hypoxic challenge during anaesthesia. Acta Anaesthesiol Scand 1985;29:346–51. 22. Tucker A, Reeves JT. Non-sustained pulmonary vasoconstriction during acute hypoxia in anesthetized dogs. Am J Physiol 1977;42:889–99. 23. Domino K, Chen L, Alexander C, et al. Time course and responses of sustained hypoxic pulmonary vasoconstriction in the dog. Anesthesiology 1984;60:562–6. 24. Benumof JL, Mathers JM, Wahrenbrock EA. Cyclic hypoxic pulmonary vasoconstriction induced by concomitant carbon dioxide changes. J Appl Physiol 1976;41:466–9. 25. Benumof JL, Pirlo AF, Johanson I, Trousdale FR. Interaction of PVO2 with PAO2 on hypoxic pulmonary vasoconstriction. J Appl Physiol 1981;51:871–4.
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