1Ghent University Hospital, Ghent, 2Erasme University Hospital, 3Free University of Brussels, Brussels, Belgium*Corresponding author: Department of Anaesthesiology, Ghent University Hospital, De Pintelaan 185, B-9000 Ghent, Belgium
Presented in part at the Annual Congress of the European Society of Anaesthesiologists, Lausanne, Switzerland, May 6, 1997.
Accepted for publication: September 9, 2001
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Abstract |
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Methods. We studied 15 patients about to undergo lung surgery, during anaesthesia, and placed in the lateral position. Ventilation was with constant minute volume, inspiratory flow and FIO2. For periods of 15 min, RR of 5, 10, and 15 bpm were applied in a random sequence and recordings were made of lung mechanics and an arterial blood gas sample was taken. Data were analysed with the repeated measures ANOVA and paired t-test with Bonferroni correction.
Results. PaO2 changes were not significant. At the lowest RR, PaCO2 decreased (from 42 (SD 4) mm Hg at RR 1541 (4) mm Hg at RR 10 and 39 (4) mm Hg at RR 5, P<0.01), and end-tidal carbon dioxide increased (from 33 (5) mm Hg at RR 15 to 35 (5) mm Hg at RR 10 and 36 (6) mm Hg at RR 5, P<0.01). Intrinsic positive end-expiratory pressure (PEEPi) was reduced even with larger tidal volumes (from 6 (4) cm H2O at RR 155 (4) cm H2O at RR 10, and 3 (3) cm H2O at RR 5, P<0.01), most probably caused by increased expiratory time at the lowest RR.
Conclusion. A reduction in RR reduces PEEPi and hypercapnia during OLV in anaesthetized patients with chronic obstructive lung disease.
Br J Anaesth 2002; 88: 5660
Keywords: lung, one-lung ventilation; lung, respiratory rate; complications, pulmonary hyperinflation; ventilation, intrinsic positive end-expiratory pressure; complications, chronic obstructive pulmonary disease
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Introduction |
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During the mechanical ventilation of these patients lungs, conditions that impede expiratory flow (increased airway resistance, and the resistance of the double-lumen tube (DLT)) 4 5 or poor settings of the ventilator6 may cause dynamic pulmonary hyperinflation (DPH) and PEEPi. In addition, alveolar overdistension by severe DPH in the ventilated lung may divert pulmonary blood flow to the non-ventilated lung, and impair arterial oxygenation.
Increases in RR, Vt, or a reduction of expiratory time (Te) would encourage the development of PEEPi and DPH.7 Severe DPH causes circulatory depression and pulmonary barotrauma.4 7 8
The settings for mechanical ventilation in patients with COPD during OLV to avoid excessive DPH and hypercapnia have not been clearly identified. Studies performed during OLV have mainly assessed the effect of Vt changes9 10 or the isolated effect of altered RR with unchanged Vt.11 However, with constant RR, a greater Vt would promote PEEPi,6 while a smaller Vt would not be adequate because of dependent lung atelectasis and hypercapnia. If a constant Vt is chosen, with changes in RR, then an increase of RR would cause PEEPi and a decrease of RR would increase hypercapnia because of reduced minute ventilation. We tested if a ventilatory pattern, which combined a reduction in RR with a constant minute volume (with a proportional Vt increase), could control both hypercapnia and PEEPi during OLV of patients with chronic obstructive pulmonary disease.
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Materials and methods |
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From the recorded data, the elastic recoil pressure (Pel,rs) of the dependent lung-thorax was determined by subtracting the recorded PEEPi from the static end-inspiratory pressure. Static compliance of the respiratory system (Cst,rs) was obtained by dividing the expiratory tidal volume by Pel,rs. The exhaled volume was corrected for the compliance of the respiratory circuit (7 ml cm H2O1) to eliminate errors from the volume compressed in the tubing.13
The study was performed in the lateral position, before the surgical procedure started.
Statistical analysis
We used the KolmogorovSmirnov one-sample test to check that the samples were normally distributed. Repeated measures ANOVA was used to test for differences between RRs. Pairwise comparisons between groups were made, using Students paired t-test with the Bonferroni adjustment for multiple comparisons, using the GB-Stat 6.0 for IBM and compatibles (Dynamic Microsystems, Inc., 1996). P-values <0.05 were considered significant. Data are presented as mean (SD).
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Results |
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Pel,rs increased at lower RR (P<0.01, repeated measures ANOVA), but Cst,rs did not change significantly (Table 2). During dependent-lung ventilation, PEEPi values greater than 10 cm H2O were found in only two patients (at RR 10 and RR 15). Zero PEEPi values were recorded in four patients at RR 5 and another one at RR 10. Despite the larger Vt at lower RR, PEEPi was less (P<0.01, repeated measures ANOVA). This value was significantly less at RR 5 compared with RR 10 and RR 15 (P<0.01, Bonferroni t-test), but without statistical significance when comparing RR 15 and RR 10 (Table 2 and Fig. 018F1).
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Discussion |
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Co-existing lung disease is the rule rather than exception in patients undergoing lung surgery. The volume, frequency and timing of gas delivered to the dependent lung can have important, disease-specific effects on the cardiovascular and respiratory systems.14
Until now, a low RR has not been studied during OLV in patients with pulmonary hyperinflation in a randomized fashion. Robinson and co-workers15 describe two ventilator-dependent patients with cystic fibrosis who could not be managed with conventional ventilation during sequential double-lung transplantation. Lung implantation was facilitated by OLV at a slow rate (6 bpm) with a long Ti (5 s) and a long Te (5 s), implantation of donor lung, by decreasing hypercapnia and reducing pulmonary arterial pressure.
Lowering the RR, with unchanged minute volume implies an increase in Vt. In patients without significant pulmonary disease, OLV during general anaesthesia decreases arterial oxygenation because of atelectasis in the dependent lung.9 However, patients with COPD do not develop atelectasis and decrease in FRC during anaesthesia,16 presumably because of long standing hyperinflation.
In obstructive airway disease, lung injury with alveolar leaks may be caused by dynamic hyperinflation during mechanical ventilation. Some authors believe that increased inspiratory airway pressures are necessary to overcome airway resistance when high inspiratory flow rates are used, as a large part of the inspiratory pressure is not transmitted to the alveoli.17 18 Because alveolar distending volume is not readily measured clinically, Pplateau measured during an inspiratory pause is generally accepted as a reasonable estimate of peak alveolar pressure.19 20 During positive pressure ventilation, the Pplateau below which lung injury is unlikely is approximately 35 cm H2O, commonly believed to correspond to an alveolar pressure of approximately 30 cm H2O. For safer OLV conditions, Slinger21 suggested limiting Pplateau to 25 cm H2O. Given this range of opinion, careful monitoring of patients managed with this approach is mandatory. In the present study, the Pplateau was generally less than this value (except a single value of 26 cm H2O at RR 5) despite the Vt increases from 433 (81) ml at RR 15 to 623 (97) ml at RR 10 and 1234 (197) ml at RR 5. The duration of OLV periods in this study was short and the patients were anaesthetized and paralysed, but concern could arise from long-term use of low-rate ventilation.
At large values of Vt, an increased PEEPi might be expected, because in addition to the degree of airflow obstruction, one of the major determinants in the development of PEEPi is the Vt to be exhaled in a fixed fraction of time.22 Nevertheless, besides Vt, the main determinant of dynamic hyperinflation and PEEPi in COPD patients is the absolute value of Te and not the Ti:Ttot ratio per se.4 Therefore, considering a given respiratory system with its specific compliance and its expiratory and inspiratory resistances, for a fixed Ti fraction, PEEPi will increase when RR is raised (reduction of Te) and decrease when the RR is reduced (increase of Te). Small changes in Te did not affect PEEPi because the volume expelled per unit time near the end of exhalation is very small.23 In patients with COPD and acute respiratory failure, while PEEPi was increased by Te shorter than 3 s, prolonging Te more than 3 s had little effect on PEEPi.6 Both studies were of mechanically ventilated patients with an acute exacerbation of COPD, and the effect of prolonging Te on gas exchange were not assessed. In the present study of stable COPD patients during OLV in the lateral position, with constant inspiratory time fraction (Ti=33% of Ttot), a reduced RR and increased Vt, increased the Te from 2.6 s at RR 15 to 4 s at RR 10 and 8 s at RR 5 bpm, respectively. In contrast to the findings of Rossi, because of the parallel increase of Vt in our study, a decrease of PEEPi was observed only at the very long Te associated with the RR 5 bpm (Table 2 and Fig. 018F1).
An insignificant increase of PaO2 when RR was decreased (and Vt increased) supports the results of previous studies.911 Increased inspiratory airway pressures causing increased vascular resistance in the dependent lung of some patients could explain the lack of consistently improved oxygenation during high Vt ventilation.9 24
In this study, the high RR (15 bpm) and small Vt ventilation caused hypercapnia with a mean PaCO2 of 43 mm Hg. When ventilation was performed at low RR (5 bpm) and high Vt, mean PaCO2 decreased significantly to 39 mm Hg. This value approached the preoperative values (38 (4) mm Hg). The reduced PaCO2PE'CO2 suggests altered intrapulmonary gas distribution at low RR, but differences in E'CO2 may also simply reflect the fact that, with a significant positive slope of the capnogram, prolonging expiration itself will increase E'CO2 without necessarily reflecting any change in gas exchange.
This ventilatory patternlowered RR (and increased Vt) with constant minute volumemay represent a simple way to reduce PEEPi and hypercapnia during OLV in patients with pulmonary hyperinflation, as changing RR or Vt alone increases either the PEEPi, or the PaCO2. Careful monitoring of these patients for the risk of barotrauma is mandatory. However, given the lack of significant effect on oxygenation (the hallmark of OLV), it is difficult to recommend the technique of high Vt, low RR OLV for routine practice. This ventilatory management should be reserved for patients with severe COPD in whom PEEPi and hypercapnia would possibly complicate OLV.
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Acknowledgements |
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