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CARDIOVASCULAR ANESTHESIA: Research Report

Lung Recruitment Improves the Efficiency of Ventilation and Gas Exchange During One-Lung Ventilation Anesthesia

Tusman, Gerardo, MD*; Böhm, Stephan H., MD; Sipmann, Fernando Suárez, MD; Maisch, Stefan, MD

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doi: 10.1213/01.ANE.0000068484.67655.1A
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During one-lung ventilation (OLV) anesthesia in the lateral position, pulmonary shunt ranges from 15% to 40% because of the total collapse of the nondependent lung (1). In addition, there is clear evidence from computerized tomography that zones of compression atelectasis are redirected to the dependent lung when patients are changed from the supine to the lateral position (2,3). Both atelectasis and hypoventilated zones in the dependent lung contribute to a ventilation/perfusion (V̇/𝑄̇) mismatch and have an additive effect to the shunting in the nondependent lung (4).

The V̇/𝑄̇ relationship describes the efficiency of gas exchange and ranges from zero (shunt) to infinite (alveolar dead space; VDalv). Total V̇/𝑄̇ depends on the algebraic sum of the V̇/𝑄̇ ratio in every alveolus, and any deviation from the normal value of 1.0 causes inefficiencies in gas exchange.

Blood oxygenation evaluates shunt, whereas dead space (i.e., inefficient ventilation) is related to the lung's CO2 removal. However, shunt has a close relationship to dead space, and vice versa (5), because both are related to gas exchange but use a different gas for analysis. Thus, gas exchange and ventilation efficiency (4,6,7) during general anesthesia can be evaluated by the analysis of arterial blood gases and by the single-breath test of CO2 (SBT-CO2), the most commonly used tool for dead-space analysis.

We have recently shown that an alveolar recruitment strategy (ARS) improves arterial oxygenation during OLV anesthesia after vascular clipping in lobectomies (8). We hypothesized that improved V̇/𝑄̇ matching in the dependent lung was responsible for the reduced intrapulmonary shunt. The objective of this study was to evaluate the effect of a recruitment maneuver on the gas exchange efficiency during OLV without any kind of pulmonary vascular interruption in the nondependent lung. Ventilatory and gas exchange efficiency was studied by SBT-CO2 and arterial blood gas analysis.

Methods

Twelve patients were studied during general anesthesia for elective open thoracic surgery or thoracoscopy. Patients with acute or chronic uncompensated cardiopulmonary disease were not included in the study. Informed consent was obtained, and the study was approved by the local ethics committee.

For open thoracotomies only, a thoracic epidural catheter was placed at T2 to T4, and a total volume of 0.1 mL/kg of bupivacaine 0.5% without epinephrine was administered. Before the epidural anesthesia, intra-vascular volume was expanded by infusing 7 mL/kg of a colloidal solution (Hemacell™) and maintained at 8 mL · kg−1 · h−1 of normal saline solution.

After 3 min of breathing 100% oxygen, general anesthesia was induced with fentanyl 5 μg/kg, thiopental 3 mg/kg, and vecuronium 0.08 mg/kg IV. Anesthesia was maintained with isoflurane 0.5–0.6 minimum alveolar anesthetic concentration and epidural lidocaine 1% boluses of 5 mL for open thoracotomies. For thoracoscopies and minimally invasive coronary artery bypass graft, anesthesia was maintained with isoflurane 0.7–1 minimum alveolar anesthetic concentration and boluses of fentanyl 2 μg/kg and vecuronium 0.015 mg/kg as clinically necessary.

The trachea and the left bronchus were intubated with a left double-lumen tube (DLT) of the appropriate size (Broncho-Cath™; Mallinckrodt Laboratories, Atholone, Ireland). Air leakage was assessed by introducing the capnograph's sidestream sensor into each lumen of the DLT while maintaining ventilation through the other lumen. Bronchoscopy confirmed the correct position of the DLT before and after the patients were positioned in the lateral position. During OLV, the lumen of the nonventilated side was left open to air.

Lungs were ventilated with a Servo 900 C in a volume-controlled ventilation mode and an inspired oxygen fraction of 1.0. The ventilator delivered a square-wave flow with an inspiratory time of 33% and no end-inspiratory pause. The respiratory rate was set between 10 and 14 breaths/min, tidal volumes (VT) were maintained at 8 mL/kg, and positive end-expiratory pressure (PEEP) was 8 cm H2O throughout the study.

During OLV, VT was reduced to 6 mL/kg to avoid peak pressures more than 30 cm H2O. Respiratory rate was increased to 15–18 breaths/min to maintain the same minute ventilation as during two-lung ventilation (TLV).

Standard monitoring was performed with the Cardiocap II monitor. A Capnomac Ultima monitor was used to measure the following ventilation variables and gas concentrations: peak inspiratory pressure (PIP), PEEP, expired VT, respiratory rate, expired minute volume, and oxygen and CO2 fractions.

Carbon dioxide elimination (V̇CO2) was calculated as the product of alveolar ventilation and the mean expired alveolar fraction of CO2. Oxygen consumption (V̇O2) was calculated as the product of alveolar ventilation times the inspiratory-expiratory oxygen difference. The respiratory quotient (RQ) was calculated by dividing V̇CO2 by V̇O2.

The SBT-CO2 was performed by using the side-stream infrared capnometer and the pneumotachograph of the Capnomac Ultima and a signal processor. Data were recorded and analyzed by a computer. The capnograph and blood gas analyzer were calibrated with a known gas concentration of CO2 (5%). This calibration was performed in each patient before the induction of anesthesia.

Airway flow and pressure measurements are based on the measurement of kinetic gas pressure and are performed by using the Pitot effect. Flow rate is measured and integrated to obtain VT. The Capnomac device restores normal airway volumes from standard condition to body temperature, ambient pressure, and water vapor saturation automatically. Volume calibration was performed with a 700-mL supersyringe before anesthesia induction by following the manufacturer's guidelines.

The sidestream CO2 signal has a time delay compared with the flow signal. The software automatically corrected for the CO2 delay by using mathematical algorithms similar to those described by Breen et al. (9). The VTCO2,br or area under the curve was computed by integrating expired flow and FCO2 in each breath.

Analysis of dead space was performed off-line by using Fowler's analysis (10) and adding the PaCO2 value to the SBT-CO2 curve (Fig. 1, A and B). The mean value of three consecutive SBT-CO2 tests was used for each variable. The apparatus's dead space was 60 mL (10 mL from D-LITE™ plus 50 mL from DLT connections) and was subtracted from the airway dead-space value (VDaw). Dead-space variables are described in Figure 1 and in Table 1. All measurements were performed with the patient in the lateral position. Arterial blood gases, SBT-CO2, and ventilatory and hemodynamic data were recorded at three points:

Table 1
Table 1:
Dead-Space Data
Figure 1.
Figure 1.:
The single-breath test for CO2 (SBT-CO2). A, Classic dead-space subdivisions (6,10). Z = airway dead space (VDaw); Y = alveolar dead space; X = area under the curve; VTalv = alveolar tidal volume; PaCO2 = arterial partial pressure of CO2 (mm Hg); PAECO2 = mean partial pressure of CO2 in alveolar air, defined as the middle of the a-b line. B, Phase I, II, and III of the SBT-CO2. Slopes of Phase II and III were derived from least-squares linear regression by using data points collected between 25% and 75% of the corresponding phase; 50% of the Phase II slope defines the limit between airway and alveolar gas.
  1. TLV: 15 min after placing the patient in the lateral position, with the chest still closed.
  2. OLVPRE: after 20 min of OLV ventilation, before applying the ARS.
  3. OLVARS: 20 min after applying the ARS selectively to the dependent lung.

Patients were studied during OLV before any vascular interruption in the nondependent lung. During OLV, patients were studied at the moment of highest shunt before any vascular clipping in the nondependent lung. The recruitment maneuver was applied selectively to the dependent lung immediately after the measurement at Point 2. First, the ventilator was switched to pressure-control ventilation, adjusting the level of pressure to obtain the same VT as during volume-control ventilation. Ventilation was then allowed to equilibrate for 3 min. Thereafter, the ARS was performed as described previously (8,11) on the basis of the concept described by Lachmann (12). The critical alveolar opening pressure was assumed to be at 40 cm H2O, as described for healthy lungs (11,13).

The ARS protocol was as follows:

  1. Inspiratory time was increased to 50%.
  2. Respiratory frequency was set to 12 breaths/min.
  3. The inspiratory pressure gradient was limited to 20 cm H2O to avoid large VTs during the maneuver. PIP and PEEP were sequentially increased from 30/10 to 35/15 in steps of 5 breaths. The recruitment pressure of 40/20 cm H2O was applied for 10 breaths.
  4. Airway pressures were then gradually decreased, returning to baseline settings but maintaining a PEEP level of 8 cm H2O.

After the ARS was completed, the ventilator was set back to volume control. The ARS took approximately 3 min.

Before the recruitment maneuvers, central venous pressure values were maintained >10 mm Hg to avoid hemodynamic side effects caused by the increased intrathoracic pressures (14). Hemodynamic and ventilatory variables were monitored closely while the ARS was performed. If mean arterial blood pressure or heart rate changed by >15% from baseline, the ARS was discontinued and 500 mL of crystalloid solution was administered. After hemodynamic stability returned, the ARS was tried again.

During surgery, oxygen saturation was maintained >90% at all times. If, during OLV, SpO2 decreased to less than 90%, surgery was temporarily interrupted to resume TLV (intermittent ventilation) until oxygen saturation recovered to at least 97%. Blood samples were processed within 5 min of extraction by the blood gas analyzer ABL 520 (Radiometer, Copenhagen, Denmark), and values were corrected for body temperature. This device was calibrated with the same CO2 concentration as the capnograph (5%).

Descriptive statistical analysis was performed for each variable by using INSTAT 2.0. Comparison of variables between points was performed with repeated-measures analysis of variance. If the analysis of variance F statistic was significant, the Student-Newman-Keuls posttest detected significant differences. Values are reported as mean ± SD, and P < 0.05 was considered significant.

Results

Twelve patients—10 men and 2 women—were included in this study (Table 2). Only Patient 7 received inhaled bronchodilators sporadically as needed.

Table 2
Table 2:
Patient Data

PaO2 was significantly higher during TLV (379 ± 67 mm Hg) compared with OLVPRE (144 ± 73 mm Hg; P < 0.001) and OLVARS (244 ± 89 mm Hg; P < 0.001). During OLV, the difference in PaO2 before and after the ARS also reached significance (Fig. 2).

Figure 2.
Figure 2.:
PaO2 (mm Hg) in all patients during two-lung ventilation (TLV) and during one-lung ventilation before (OLVPRE) and after (OLVARS) the alveolar-recruitment strategy. Each symbol represents one patient in every point of the study. Horizontal bars represent mean values at each point.

Hemoglobin oxygen saturation was lower at OLVPRE (95.5% ± 2.6%) as compared with TLV (98.7% ± 0.4%; P < 0.001) and OLVARS (97.8% ± 0.9%; P < 0.01). Only Patient 8 needed four cycles of intermittent ventilation during OLV before the ARS (SpO2 <90%). Blood gases were taken after the fourth cycle of intermittent TLV immediately before the recruitment maneuver. In this patient, the ARS relieved the arterial hypoxemia instantaneously (SpO2 from 88% to 98%), and no more episodes of hemoglobin desaturation occurred.

PaCO2 was 43 ± 6 mm Hg during OLVARS but was not significantly different from the other conditions. However, PaCO2 was higher during OLVPRE (46 ± 6 mm Hg) compared with TLV (38 ± 4 mm Hg; P < 0.05). ETCO2 and the mean partial pressure of CO2 in alveolar air (PAECO2) were stable during the protocol, without any significant differences among the measurement points. The Pa-ETCO2 difference was significantly higher during OLVPRE (14.2 ± 4.8 mm Hg) compared with TLV (8.8 ± 3.2 mm Hg) and OLVARS (11.6 ± 4.6 mm Hg). The arterial pH remained in the normal range throughout the study period.

All dead-space variables (Table 1) decreased during OLVARS compared with OLVPRE, but differences showed statistical significance only for the dead-space gas volume/VT ratio, Vol I, II, III/VT, and Phase III slope. VTs were higher during TLV (506 ± 83 mL) compared with OLVPRE (377 ± 45 mL) and OLVARS (382 ± 42 mL). Minute ventilation was similar between OLVPRE (5.9 L/min) and OLVARS (5.8 L/min), but both values were significantly smaller than during TLV (7 L/min). PIP values were higher during OLVPRE (25.3 ± 1.7 cm H2O) compared with TLV (20.6 ± 1.7 cm H2O; P < 0.001) and OLVARS (23.2 ± 2 cm H2O; P < 0.05), with no differences between the last two.

Hemodynamic variables, minute CO2 elimination, oxygen consumption, and RQ were similar at all time points. The total time of OLV ranged from 50 to 105 min. No hemodynamic or ventilatory side effects related to the recruitment maneuver were detected.

Discussion

The results of this study indicate an improved efficiency in gas exchange after a lung recruitment maneuver during OLV. This finding agrees with our previous results (8) and can be explained by a recruitment effect on both shunt and dead space, taking into account that hemodynamic, metabolic, and ventilatory conditions were stable along the protocol.

Arterial oxygenation is a common measurement used to describe the extent of lung collapse. Different authors (15,16) propose that a PaO2 >450 mm Hg defines an “open lung” condition during pure oxygen breathing. Arterial oxygenation, however, is an unspecific variable to evaluate the recruitment effect because it depends on the hemodynamic and metabolic status. Because these two conditions remained stable throughout the study period, a true recruitment effect is the most likely explanation for the increases seen in PaO2.

During TLV, a mean PaO2 of 379 ± 67 mm Hg indicated some extent of lung collapse, a common finding during general anesthesia (Fig. 2). Oxygenation was further impaired during OLVPRE but increased after the dependent lung was recruited.

The nomogram of Benatar et al. (17) was used to calculate the approximate shunt in our patients: at TLV, shunt values ranged from 8% to 22% (mean, 16%), values typically seen in general anesthesia. During OLV, they ranged from 18% to 45% (mean, 28%), and during OLVARS they ranged from 12% to 27% (mean, 21%). After lung recruitment, oxygenation was sufficient to maintain hemoglobin saturation >95%.

PaCO2 increased during OLV at the same ETCO2 and PAECO2 values as those observed during TLV. Increases in dead space during OLV can explain this decrease in the efficiency of CO2 removal. Because arterial oxygenation is only one of the variables describing the effects of recruitment in the protocol, we included the dead-space analysis, a well known tool for evaluating the lung's efficiency of gas exchange.

During TLV, the values of dead space-derived variables are larger than normal (18) because of the DLT, lung collapse, open-chest condition, and the use of positive-pressure ventilation.

Surprisingly, VDalv did not change during OLV despite a significant increase in shunt. We cannot explain the absence of an increase in VDalv despite a marked shunt effect (apparent dead space) during OLV compared with TLV. We believe that during TLV, a decrease in the perfusion of the nondependent lung can increase VDalv (real VDalv) despite a lower shunt (6,19).

Large tidal values during TLV result also in absolute large values for VDaw, alveolar tidal volume (VTalv), and physiological dead space than the ones observed during OLV, thus making their direct comparison questionable. Nevertheless, when these variables are adjusted to account for differences in VT, this comparison may become useful.

The variables that represent efficiency of ventilation and CO2 exchange (VTCO2,br, dead-space gas volume/VT ratio, Pa-ETCO2, VTalv, and VDalv/VTalv) were higher during TLV compared with OLV. During OLV, all variables improved only after the recruitment maneuver.

Even more interesting was the behavior of the variables that show the distribution of VT throughout the SBT-CO2 phases. Distribution of volume was most efficient during OLV after the ARS, as indicated by a decrease in Phase I and II volumes and a concomitant increase in Phase III volume. The absolute value of the Phase III/VT ratio observed after recruitment was even higher than during TLV.

Phase II represents a transition between alveolar and airway gas transport (10,20). An increase in the cross-sectional area of the bronchial tree in the lung periphery decreases the linear velocity of the bulk flow until a point where the two transport mechanisms within the lungs—convection and diffusion—are of equal magnitude. This “stationary diffusion front” demarcates the transition between airway and alveolar gas. On expiration, this front corresponds to Phase II and is used to measure VDaw in Fowler's analysis (10).

Changes in inspiratory flow, VT, and peripheral cross-sectional area of bronchioli have an effect on the diffusion front and, thus, on the volume and slope of Phase II (10,19,20). If inspiratory flow and VT are constant, as during OLV, any change in Phase II must be interpreted as a recruitment-related increase in the cross-sectional area of the bronchioli leading to a more homogeneous gas emptying of lung acini.

The slope of Phase II, which depends on the spread of transit time of different lung units, increased during OLV after the recruitment maneuver when compared with the other study conditions. However, differences were not significant. This increase in Phase II slope, in combination with a decrease in its volume, can be considered as a more synchronous and homogeneous emptying of acini during expiration. Both asthma and emphysema have an opposite effect on Phase II (21–23). These conditions show a wide dispersion on the transit time of gas emptying among lung units, making the slope of Phase II flatter and its volume larger.

Diffusion is the most important mechanism of gas transport within the acinus. Phase III volume represents the amount of gas exposed to the capillary bed and therefore depends on an effective pulmonary perfusion and CO2 production. Phase III slope is directly related to the V̇/𝑄̇ relationship and represents the diffusional resistance for CO2 at the alveolar-capillary membrane. Its positive slope is explained by lung pendelluft, continuous evolution of CO2 from the blood into the acini, and a stratified inhomogeneity (19,20,24).

During OLVARS, Phase III volume increased while its slope decreased compared with OLVPRE. Schwardt et al. (24), using a mathematical model, described the effects of independent changes of physiologic variables and acinar structures on the slope of Phase III. Regarding these data and maintaining all variables that can influence diffusional CO2 resistance constant, as in this study, any change in the slope can be explained by a change in the area of gas exchange. Clinical data support our findings: Ream et al. (25) described a decrease in normalized Phase III slope in children during normal growth as a result of an increase in the “alveolated” airway. A decrease in functional lung acini in emphysema is related to an increase in Phase III slope.

We studied patients submitted to different thoracic surgeries, including classical thoracotomies (lobectomies), minimally invasive thoracotomies (minimally invasive coronary artery bypass graft), and closed-chest surgeries (thoracoscopies). Possible differences in lung mechanics can account for the changes in arterial oxygenation and ventilation efficiency among these different type of surgeries. However, oxygenation and dead-space behavior were similar and hemodynamic and metabolic conditions were constant throughout the study period. For these reasons, we believe that the changes in gas exchange and dead space that we observed were related to the therapeutic effect of the recruitment maneuver.

Epidural anesthesia used in open thoracotomies can cause hemodynamic and metabolic changes that could influence gas exchange. However, these conditions were stable, and no differences were seen in PaO2 between open thoracotomies and thoracoscopies without epidural anesthesia. We used empirical values of 40 cm H2O of PIP as an opening pressure and 8 cm H2O of PEEP to keep the lung open (8,11,13) because individual levels of these pressures are difficult to determine at the bedside.

Because of a mediastinal displacement, the surgeon's manipulation and the chest fixation opening and closing pressures in the dependent lung could be higher during thoracic surgery as compared with the other types of surgeries. In addition, PIP may not represent true alveolar pressure when a narrow DLT is used. For this reason, it is possible that true opening and closing pressures were not reached in each patient, which could have resulted in the absence of the maximal effect of the ARS on oxygenation and lung efficiency. The number of patients studied was small, but our main goal was to show the physiologic effect of the lung-recruitment maneuver on gas exchange and dead space during OLV.

We conclude that lung recruitment improves gas exchange and ventilation efficiency during OLV anesthesia. Our results suggest that one simple recruitment maneuver during OLV is enough to increase PaO2 to safer levels, thereby eliminating the need for any additional therapeutic intervention.

References

1. Torda TA, McCulloch CH, O'Brien HD, et al. Pulmonary venous admixture during one-lung anaesthesia: the effect of inhaled oxygen tension and respiratory rate. Anaesthesia 1974;29:272–9.
2. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985;62:422–8.
3. Klingstedt C, Hedenstierna G, Lunquist H, et al. The influence of body position and differential ventilation on lung dimensions and atelectasis formation in anaesthetized man. Acta Anaesthesiol Scand 1990;34:315–22.
4. Hedenstierna G, Tokics L, Strandberg A, et al. Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis. Acta Anaesthesiol Scand 1986;30:183–91.
5. Fletcher R. Deadspace during general anesthesia. Acta Anaesthesiol Scand 1990;34:46–50.
6. Fletcher R, Jonson B. The concept of deadspace with special reference to the single breath test for carbon dioxide. Br J Anaesth 1981;53:77–88.
7. Hofbrand BI. The expiratory capnogram: a measure of ventilation-perfusion inequalities. Thorax 1966;21:518–24.
8. Tusman G, Böhm SH, Melkun F, et al. Alveolar recruitment strategy increases arterial oxygenation during one-lung ventilation. Ann Thorac Surg 2002;73:1204–9.
9. Breen PH, Mazumdar B, Skinner SC. Capnometer transport delay: measurement and clinical implications. Anesth Analg 1994;78:584–6.
10. Fowler WS. Lung function studies. II. The respiratory dead space. Am J Physiol 1948;154:405–16.
11. Tusman G, Böhm SH, Vazquez da Anda G, et al. Alveolar recruitment strategy” improves arterial oxygenation during general anaesthesia. Br J Anaesth 1999;82:8–13.
12. Lachmann B. Open up the lung and keep the lungs open. Intensive Care Med 1992;18:319–21.
13. Rothen HU, Sporre B, Wegenius G, et al. Reexpansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71:788–95.
14. Jellinek H, Krafft P, Fitzgerald R, et al. Right atrial pressure predicts hemodynamic response to apneic positive airway pressure. Crit Care Med 2000;28:672–8.
15. Froese AB, Bryan AC. High frequency ventilation. Am Rev Respir Dis 1987;135:1363–74.
16. Böhm SH, Vazquez de Anda GF, Lachmann B. The open lung concept. In: Vincent JL, ed. Yearbook of intensive care and emergency medicine. 2nd ed. Berlin: Springer-Verlag, 1999:430–40.
17. Benatar SR, Hewlett AM, Nunn JF. The use of iso-shunt lines for control of oxygen therapy. Br J Anaesth 1973;45:711–6.
18. Aström E, Niklason L, Drefeldt B, et al. Partitioning of deadspace: a method and reference value in the awake human. Eur Respir J 2000;16:659–64.
19. Fletcher R, Jonson B. Deadspace and the single breath test for carbon dioxide during anesthesia and artificial ventilation. Br J Anaesth 1984;56:109–19.
20. Englel LA. Gas mixing within acinus of the lung. J Appl Physiol 1983;54:609–18.
21. Schwardt JD, Neufeld GR, Baumgardner JE, et al. Noninvasive recovery of acinar anatomic information from CO2 expirograms. Ann Biomed Eng 1994;22:293–306.
22. Kars AH, Bogard JM, Stijnen T, et al. Deadspace and slope indices from the expiratory carbon dioxide-tension volume curve. Eur Respir J 1997;10:1829–36.
23. You B, Peslin R, Duvivier C, et al. Expiratory capnography in asthma: evaluation of various shape indices. Eur Respir J 1994;7:318–23.
24. Schwardt JF, Gobran SR, Neufeld GR, et al. Sensitivity of CO2 washout to changes in acinar structure in a single-path model of lung airways. Ann Biomed Eng 1991;19:679–97.
25. Ream RS, Screiner MS, Neff JD, et al. Volumetric capnography in children: influence of growth on the alveolar plateau slope. Anesthesiology 1995;82:64–73.
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