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Case Reports  |   July 2000
Compliance and Capnography Monitoring during Independent Lung Ventilation: Report of Two Cases
Author Affiliations & Notes
  • Gilda Cinnella, M.D.
    *
  • Michele Dambrosio, M.D., Ph.D.
  • Nicola Brienza, M.D., Ph.D.
    *
  • Francesco Bruno, M.D.
  • Antonio Brienza, M.D.
    §
  • *Assistant Professor of Anesthesiology and Intensive Care. †Associate Professor of Anesthesiology and Intensive Care. ‡Professor of Anesthesiology and Intensive Care. §Director, Intensive Care Unit, Professor of Anesthesiology and Intensive Care.
Article Information
Case Reports
Case Reports   |   July 2000
Compliance and Capnography Monitoring during Independent Lung Ventilation: Report of Two Cases
Anesthesiology 7 2000, Vol.93, 275-278. doi:
Anesthesiology 7 2000, Vol.93, 275-278. doi:
INDEPENDENT lung ventilation (ILV) has been applied in severe asymmetrical or unilateral lung injury to improve hypoxemia refractory to conventional mechanical ventilation and positive end-expiratory pressure. 1–6 The most commonly used approach is to deliver the same tidal volume (Vt) to each lung. 1,3,6–8 However, this setting produces higher plateau airway pressure (Pplat) in the more injured lung. 2–4,7 
We describe two patients with unilateral lung injury successfully treated using ILV. Unlike other cases reported, Vt was initially set in each lung at a value generating a Pplat less than or equal to 26 cm H2O and then progressively reset on the basis of single-lung static compliance (Cst) variations. Capnography of each lung was continuously performed, and end-tidal carbon dioxide (ETCO2) was measured to follow the ventilation–perfusion (V/Q) matching.
Case Reports
Case 1
A 25-yr-old woman experienced thoracic trauma. Intubation was performed with use of an orotracheal tube, and the patient was transferred to the intensive care unit. Computed tomography showed left lung contusion. Major asymmetry in lung expansion was observed, with poor aeration of the left lung. The patient underwent ventilation using square wave flow, respiratory rate 16 breaths/min, Vt 700 ml, fractional inspired oxygen tension (FiO2) 100%, and inspiratory–expiratory ratio 0.33. Pplat was 40 cm H2O and Cst was 13 cm H2O/ml. The capnogram wave had an irregularly shaped plateau with an ETCO2of 30 mmHg. Arterial oxygen saturation was 90%, arterial oxygen tension (PaO2) was 50 mmHg, arterial carbon dioxide tension was 34 mmHg, and respiration (p  H) was 7.47.
Independent lung ventilation was instituted via  a double-lumen tube: each lung was initially ventilated with respiratory rate 16 breaths/min, Vt 350 ml, inspiratory–expiratory ratio 0.33, and FiO2100%. A positive end-expiratory pressure of 5 cm H2O was applied to the left lung. In the right lung, Pplat recorded 30 min later was 18 cm H2O, Cst was 19.4 cm H2O/ml, and the capnogram was regular, with ETCO2of 35 mmHg. On the left side, Pplat was 36 cm H2O, Cst was 11.2 cm H2O/ml, expiratory carbon dioxide waveform was irregular with a biphasic plateau, and ETCO2was 22 mmHg. Consequently, ventilatory settings for the right lung remained unmodified, whereas Vt to the left lung was decreased to 230 ml. With this setting, Pplat was 26 cm H2O and Cst was 10.9 cm H2O/ml. The capnogram remained irregular and ETCO2increased to 24 mmHg. Arterial oxygen saturation was 98%. Vt to the left lung was progressively increased and set to obtain a Pplat less than or equal to 26 cm H2O, as shown in figures 1A–C. ILV was discontinued after 48 h, at which point there was no difference in Vt and, consequently, in Cst between the two lungs. At the same time, the capnogram of the left lung had a steady plateau, and there was no difference in ETCO2. After ILV was discontinued, the patient received ventilation via  an orotracheal single-lumen tube and was transferred to the unit after mechanical ventilation was discontinued.
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C  ) case 1, (D–F  ) case 2. (A  and B  ) static compliance, (C  and D  ) tidal volume, and (E  and F  ) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C 
	) case 1, (D–F 
	) case 2. (A 
	and B 
	) static compliance, (C 
	and D 
	) tidal volume, and (E 
	and F 
	) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C  ) case 1, (D–F  ) case 2. (A  and B  ) static compliance, (C  and D  ) tidal volume, and (E  and F  ) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
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Case 2
A 59-yr-old man was admitted to the intensive care unit with multiple right-sided rib fractures, diffuse right lung contusion, and right arm fracture. The patient was intubated with an orotracheal monolumen tube and received ventilation with square wave flow, respiratory rate 16 breaths/min, Vt 850 ml, FiO2100%, and inspiratory–expiratory ratio 0.33. Pplat was 46 cm H2O and Cst was 18.4 cm H2O/ml. The capnography wave was irregularly shaped with a positive slope, and ETCO2was 35 mmHg. Arterial oxygen saturation was 90%, PaO2was 65 mmHg, arterial carbon dioxide tension was 38 mmHg, and respiration was 7.44.
Independent lung ventilation was instituted via  an orotracheal double-lumen tube, and each lung was ventilated with respiratory rate 16 breaths/min, Vt 400 ml, inspiratory–expiratory ratio 0.33, and FiO2100%. A positive end-expiratory pressure of 7 cm H2O was applied to the right lung. In the left lung, Pplat recorded 30 min later was 22 cm H2O, Cst was 18.2 cm H2O/ml, and the capnogram was regular, with an ETCO2of 40 mmHg. In the right lung, Pplat was 42 cm H2O, Cst was 11.4 cm H2O/ml, expiratory carbon dioxide waveform was irregular with a positive slope, and ETCO2was 28 mmHg.Ventilatory settings for the left lung remained unmodified, and Vt to the right lung was reduced to 245 ml. With this setting, Pplat was 26 cm H2O, Cst was 12.9 cm H2O/ml, the capnogram plateau did not change, and ETCO2was 30 mmHg. PaO2was 85 mmHg, arterial carbon dioxide tension was 50 mmHg, and p  H was 7.52. A Swann–Ganz catheter was inserted, and the measured Qs/Qt was 26%. Vt to the right lung was progressively increased and set to obtain a Pplat less than or equal to 26 cm H2O, as shown in figures 1D, E, and F. ILV was discontinued after 84 h, at which point there was no difference in Vt and, consequently, in Cst between the two lungs. At the same time, the capnogram of the right lung had a steady plateau, and there was no difference in ETCO2. The measured Qs/Qt was 10%.
After ILV was stopped, the patient received ventilation via  an orotracheal single lumen tube and was transferred to the hospital ward after mechanical ventilation was discontinued.
Discussion
The main aspect of unilateral lung injury is the development of asymmetric lung disease, producing differences in compliance between the two lungs. 1,2,5,6 As a consequence, during conventional lung ventilation, Vt is mostly diverted toward the more compliant lung, resulting in overinflation and increased ventilation–perfusion ratio (dead space). 2,3,8 Lung overdistension causes a Starling resistor mechanism on normal alveolar capillaries, with the diversion of blood flow toward the underventilated injured lung, increasing blood shunting. 1–7 During such conditions, ILV is indicated to ventilate the diseased lung while avoiding hyperinflation in the normal lung. 1–8 
The two patients described herein were treated by setting Vt in both lungs at a value generating a Pplat less than or equal to 26 cm H2O and progressively increasing it on the basis of Pplat variations, and the patients were monitored using the continuous measurement of single-lung capnography.
Until now, equal Vt in the two lungs has been considered in most published studies to be the setting that produces the best oxygenation. 1,3–7 In an experimental study, East et al.  3 compared different Vt delivery patterns and found that the highest PaO2:FiO2ratio was obtained when equal Vt was given in both lungs. However, this pattern led to levels of Pplat higher than 30 cm H2O in the diseased lung, as also reported in a clinical study by Zandstra et al.  , 7 because in unilateral lung injury, by definition, the contused lung is less compliant than the normal lung. This ventilatory strategy was based on the assumption that the aim of ILV is only to separate the ventilation of each lung, allowing the lung with contusion to receive its Vt. The angiographic data of Carlon et al.  , 1 showing that the shunt fraction in the lung with contusion decreased considerably as soon as ILV was instituted, confirmed this hypothesis.
However, some data in the literature seem to show that a different ventilatory strategy, i.e.  , to set for each lung ventilation modeled to its mechanical properties, can be applied with good results in terms of the PaO2:FiO2ratio, avoiding additional lung injury caused by volutrauma. 2,8,9 Siegel et al.  2 proposed to measure the pressure–volume of each lung to set ventilation more appropriately. The pressure–volume curve measurement can be too complex to be performed many times a day, as would be necessary in such patients. Therefore, in our patients, mechanics of each lung were measured by the static compliance, and Vt was set at a value generating a Pplat less than 26 cm H2O, which is the threshold level accepted by many authors to avoid additional volutrauma. 9 This ventilatory schema allowed a stable PaO2:FiO2ratio in our two patients.
The second aspect to be outlined in these two patients is the expiratory capnograph monitoring. A few experimental and clinical studies showed that, during ILV, ETCO2is lower and the waveform is irregular in the lung with contusion. 2,3,8 The absence of a steady plateau on the capnogram may indicate intrapulmonary gas maldistribution, and an irregularly shaped plateau can reflect differences between the time constants of different alveolar regions. 10 The difference in carbon dioxide waveform and ETCO2value can be explained by the dyshomogeneity proper to lung injury, characterized by coexistence in the same lung of alveolar regions with different time constants. 10 A high Vt in the diseased lung probably accentuates this dyshomogeneity. These data were confirmed for our patients. During the course of ILV, in the lungs with contusion, together with improvement of the lung damage, the airway pressure developed by a given Vt was reduced, whereas ETCO2increased. Vt was increased stepwise until the Pplat was equal in both lungs, and by this time there was no difference in ETCO2between the two lungs. Moreover, in the patient in case 2, the measured shunt fraction was reduced from 26 to 10%.
We believe that the ventilatory setting used in these two cases could allow a stable PaO2:FiO2ratio and that the ETCO2measurement could be a useful tool to monitor patients during ILV.
References
Carlon GC, Kahn R, Howland WS, Baron R, Ramaker J: Acute life-threatening ventilation perfusion inequality: An indication for independent lung ventilation. Crit Care Med 1978; 6:380–3Carlon, GC Kahn, R Howland, WS Baron, R Ramaker, J
Siegel JH, Stoklosa JC, Borg U, Wiles CE, Sganga G, Geisler FH, Belzberg H, Wedel S, Blevins S, Goh CK: Quantification of asymmetric lung pathophysiology as a guide to the use of simultaneous independent lung ventilation in post-traumatic and septic ARDS. Ann Surg 1985; 202:425–39Siegel, JH Stoklosa, JC Borg, U Wiles, CE Sganga, G Geisler, FH Belzberg, H Wedel, S Blevins, S Goh, CK
East TD, Pace NL, Westenskow DR, Lund K: Differential lung ventilation with unilateral PEEP following unilateral hydrochloric acid aspiration in the dog. Acta Anaesthesiol Scand 1983; 27:356–60East, TD Pace, NL Westenskow, DR Lund, K
Alberti A, Valenti S, Gallo F, Vincenti E: Differential lung ventilation with a double-lumen tracheostomy tube in unilateral refractory atelectasis. Intensive Care Med 1992; 18:479–84Alberti, A Valenti, S Gallo, F Vincenti, E
Siegel JH, Giovannini I, Coleman B: Ventilation/perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis. J Trauma 1979; 19:432–60Siegel, JH Giovannini, I Coleman, B
Carlon GC, Ray C, Klein R, Goldiner PL, Miodonownik KS: Criteria for selective positive end expiratory pressure and independent synchronized ventilation of each lung. Chest 1978; 74:501–7.Carlon, GC Ray, C Klein, R Goldiner, PL Miodonownik, KS
Zandstra DF, Stoutenbeek CP, Bams JL: Monitoring lung mechanics and airway pressures during differential lung ventilation (ILV)with emphasis on weaning from ILV. Intensive Care Med 1989; 15:458–63Zandstra, DF Stoutenbeek, CP Bams, JL
Cinnella G, Dambrosio M, Brienza N, Ranieri M: Reexpansion pulmonary edema with acute hypovolemia. Intensive Care Med 1998; 24:1117Cinnella, G Dambrosio, M Brienza, N Ranieri, M
Roupie E, Dambrosio M, Servillo G, Mentec H, El Atrous S, Beydon L, Brun-Buisson C, Lemaire F, Brochard L: Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome. Am J Resp Crit Care Med 1995; 152:121–8Roupie, E Dambrosio, M Servillo, G Mentec, H El Atrous, S Beydon, L Brun-Buisson, C Lemaire, F Brochard, L
Blanch L, Fernandez R, Artigas A: The expiratory capnogram in mechanically ventilated patients, Update in Intensive Care and Emergency Medicine. Edited by Vincent JL. Berlin, Springer, 1993, pp 411–5
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C  ) case 1, (D–F  ) case 2. (A  and B  ) static compliance, (C  and D  ) tidal volume, and (E  and F  ) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C 
	) case 1, (D–F 
	) case 2. (A 
	and B 
	) static compliance, (C 
	and D 
	) tidal volume, and (E 
	and F 
	) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
Fig. 1. (Open triangles) normal lung and (closed squares) diseased lung. Single points indicate values measured 30 min after setting independent lung ventilation with the same tidal volume on both lungs. Solid lines indicate values measured during ILV set with a lower tidal volume on the diseased lung. (A–C  ) case 1, (D–F  ) case 2. (A  and B  ) static compliance, (C  and D  ) tidal volume, and (E  and F  ) end-tidal carbon dioxide of normal (open triangles) and diseased lung (closed squares) during independent lung ventilation.
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