Eur Respir J 2001; 18:491-498
Copyright ©ERS Journals Ltd 2001
Effects of PEEP on inspiratory resistance in mechanically ventilated COPD patients
C. Guérin1,
G. Fournier1 and
J. Milic-Emili2
1 Medical Intensive Care Unit, Lyon Sud Hospital and Claude Bernard Lyon I University, Lyon, France, and 2 Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada
CORRESPONDENCE: C. Guérin, Service de Reanimation Medicale et d'Assistance Respiratoire, Hopital de la Croix-Rousse, 103 Grande Rue de la Croix-Rousse, 69004, Lyon, France. Fax: 33 472071774
Keywords: chronic obstructive pulmonary disease, interrupter technique, positive end-expiratory pressure, pulmonary hyperinflation, tissue resistance, volume dependence of respiratory resistance
Received: August 11, 2000
Accepted May 7, 2001
This work was supported by a grant from the Hospices Civils de Lyon.
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Abstract
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This study aimed to investigate the effect of increased lung volume with positive end-expiratory pressure (PEEP) on respiratory resistance in patients with chronic obstructive pulmonary disease (COPD).
Ten patients with COPD were mechanically ventilated for acute respiratory failure. PEEP was set at 0, 5, 10 and 15 cmH2O. Using the rapid airway occlusion technique, the total inspiratory resistance of the respiratory system was partitioned into interrupter (Rint,rs) and additional effective (
Rrs) resistances. At each level of PEEP, at constant inflation flow, the inflation volume (V) was varied from 0.2–1 L, and, at constant V, the inflation flow was varied from 0.2–1.2 L·s–1. The changes in end-expiratory lung volume (EELV) induced by PEEP were also measured.
The difference between the EELV and the relaxation volume of the respiratory system (FRC) increased significantly with PEEP of 10 and 15 cmH2O as compared to a PEEP of 0, the increase being associated with a significant reduction of Rint,rs. By contrast, Rrs was independent of FRC. At constant V, Rint,rs fitted Rohrer's equation (Rint,rs =K1+K2xflow). While K2 significantly declined with FRC, K1 did not change. At all levels of PEEP, Rrs was not influenced by FRC.
With increasing lung volume induced by positive end-expiratory pressure, the inspiratory airway resistance decreased, whereas the viscoelastic behaviour of the respiratory system, as reflected by additional effective resistance, did not change.
In recent years, the rapid airway occlusion (RAO) technique has been extensively used in mechanically ventilated subjects to partition the total inspiratory resistance (Rrs) into: 1) the interrupter resistance (Rint,rs), which in humans mainly reflects airway resistance; and 2) the additional effective inspiratory resistance (Rrs) that results from dynamic pressure dissipation due to the viscoelastic properties of the thoracic tissues and time constant inequality within the lung 1, 2. These studies have shown that Rrs represents a large fraction of Rrs in both normal subjects and patients 1–3. In normal subjects, both at zero end-expiratory pressure (ZEEP) and at increased lung volume with positive end-expiratory pressure (PEEP) of 8 cmH2O, the changes in Rrs with flow and volume can be satisfactorily explained by a simple four-parameter linear viscoelastic model of the respiratory system 4. In contrast, in patients with acute respiratory distress syndrome (ARDS), even on ZEEP, the model fails to account for the changes in Rrs when the inflation volume exceeds 0.7 L 5. Whether this reflects nonlinear viscoelastic behaviour of the stress relaxation units of the injured lung, or other factors, remains to be elucidated. In mechanically ventilated patients with chronic obstructive pulmonary disease (COPD), the effect of PEEP on Rrs has also been studied. In one study, by experimental design, the maximal applied PEEP was limited to 86% of the intrinsic PEEP 6. Under the latter conditions, the changes in end-expiratory lung volume (EELV) were necessarily very small (mean of 0.13 L), and accordingly in that study, there was little or no change of Rrs and Rint,rs. In another study, PEEP was applied up to 15 cmH2O 7. The authors observed a significant reduction of lung interrupter resistance (Rint) and a significant increase of lung additional resistance with PEEP 7. However, these measurements were performed at fixed inflation flow and volume 7. In addition, in the latter study 7 the authors did not assess the change in lung volume elicited by PEEP. Consequently, the volume-dependence of Rrs in COPD patients remains to be determined in experiments in which high levels of PEEP are applied to induce marked changes in lung volume.
The purpose of the present investigation was to assess in COPD patients, using the RAO technique, the effects of increasing lung volume with PEEP up to 15 cmH2O on Rrs and Rint,rs, and to analyse the data in terms of the four-parameter linear viscoelastic model of the respiratory system 1, 8.
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Methods
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Ten male COPD patients with acute respiratory failure (ARF) requiring tracheal intubation and mechanical ventilation were investigated. Their anthropometric characteristics are given in table 1
. Patients were studied 1–10 days after the onset of mechanical ventilation (mean±sd: 3±2.5 days). The diagnosis of COPD was made according to clinical history, chest radiography and pulmonary function tests. The mean values of forced expiratory volume in one second (FEV1) and vital capacity (VC) before ARF were 0.89±0.36 L (31±18 % pred) and 2.13±0.72 L (51±21 % pred), respectively 9. ARF had been triggered by lower respiratory tract infection in four patients, pneumonia in three and pleural effusion in one; no aetiological factor was found in the remaining two patients. The investigation was approved by the Institutional Ethics Committee in Lyon, and informed consent was obtained from the next of kin for each patient. The effects of PEEP on alveolar recruitment, closing volume and haemodynamics on the patients of this study have been previously reported 10.
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Table 1— Anthropometric characteristics and baseline ventilatory settings of 10 chronic obstructive pulmonary disease (COPD) patients
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The patients were orotracheally intubated (Mallinckrodt® cuffed-endotracheal tube of 7.5, 8 or 8.5 mm internal diameter (ID) and 35 cm length; Mallinckrodt laboratories, Athlone, Ireland) and mechanically ventilated in synchronized intermittent mandatory volume (SIMV) mode with a square-wave inspiratory flow (Siemens-Elema 900 C Servo-Ventilator; Solna, Sweden). During the study all patients were sedated with midazolam (0.2 mg·kg–1) and paralyzed with atracurium (0.3–0.6 mg·kg–1). The baseline ventilatory settings, which were kept constant throughout the experiment, are listed in table 1
. The inspiratory duty cycle (tI/ttot) was 0.25±0.03. Airflow (V') was measured with a heated pneumotachograph (Fleisch No.2; Fleisch, Lausanne, Switzerland) inserted between the endotracheal tube and the Y-piece of the ventilator. The pressure drop across the two ports of the pneumotachograph was measured with a differential piezoelectric pressure transducer (163PC01D36, ±12.7 cmH2O; Micro switch Freeport, IL, USA). The response of the pneumotachograph was linear over the experimental range of V'. Pressure at the airway opening (Pao) was measured proximal to the endotracheal tube with a piezoelectric pressure transducer (143PC03D, ±176 cmH2O; Micro switch). Tracheal pressure (Ptr) was measured via a polyethylene catheter (1.5 mm ID) with multiple side holes and an occluded end hole, placed 2 cm past the carinal end of the endotracheal tube and connected to a piezoelectric pressure transducer (143PC03D, ±176 cm H2O; Micro switch). With the system used to measure Pao and Ptr, there was no appreciable shift or alteration in amplitude up to 20 Hz. The equipment dead space (not including the endotracheal tube) was 150 mL. All variables were recorded on an IBM compatible computer by a 12-bit analogue-digital board (DT2801-A) interfaced with data acquisition software (LabdatTM RHT-Infodat Inc., Montreal, Canada) at a sample frequency of 100 Hz. Subsequent data analysis was made with Anadat Tb (RHT-Infodat Inc.). In this analysis, V was obtained by digital integration of the V' signal. Special care was taken to avoid gas leaks in the equipment and around the tracheal cuff.
Measurements were made at four nominal levels of PEEP (0, 5, 10, 15 cmH2O), except for patient No. 2, in whom 15 cmH2O PEEP was not applied. PEEP was applied in random order for 15–20 min. Patients were judged to have reached a steady state by stability of haemodynamic measurements and pulse oximetry records. During the study, a physician not involved in the experiment was always present to provide patient care.
Procedure and data analysis
Patients were investigated supine. The measurements of respiratory mechanics were made at the end of each 15–20 min period of PEEP. Respiratory mechanics were assessed by the constant-flow RAO method 1–3. The two following sets of experiments were performed in each subject at each level of PEEP. 1) Iso-V experiment: while baseline V was kept constant, V' was varied randomly from 0.2–1.2 L·s–1 for single test breaths, by regulating tI with the appropriate knob of the ventilator. 2) Iso-V' experiment: while baseline V' was kept constant, V was changed randomly from 0.2–1 L for single test breaths by changing the frequency of the ventilator.
The end-inspiratory occlusion, obtained by pressing the end-inspiratory hold knob on the ventilator, lasted 5 s. Before each test breath an end-expiratory occlusion was performed by pressing the end-expiratory hold knob on the ventilator. This allowed quantification of intrinsic positive end-expiratory pressure (PEEPi) and to start the test breath from a fixed static elastic equilibrium condition. When PEEP was applied, the end-expiratory occlusion pressure was the sum of the PEEP set by the ventilator and PEEPi. This sum was termed total PEEP (PEEPt). It should be noted that on ZEEP, the ventilator generated a slight PEEP, averaging 0.9±0.6 cmH2O. Accordingly, PEEPt was also measured on ZEEP. Since PEEPi implies dynamic pulmonary hyperinflation (i.e. that EELV during mechanical ventilation exceeds the relaxation volume of the respiratory system (Vr)), the difference between EELV and Vr (termed FRC here) was also measured by reducing the ventilator frequency to its lowest value (1 breath·min–1) during the baseline expiration on SIMV, thus prolonging expiratory duration to allow the patient to exhale to Vr. The Vr was achieved when expiratory flow became nil and end-expiratory occlusion resulted in no change in airway pressure (i.e. no PEEPi). After each test breath, the baseline ventilation was resumed until V, V' and pressures returned to their baseline values (usually in a few breaths). Each measurement was carried out twice.
After end-inspiratory airway occlusions, Ptr and Pao exhibited an initial rapid drop (maximal pressure (Pmax)-P1) followed by a slow decay to an apparent plateau pressure (Pst,rs). During this period, the contribution of reduction in pressure due to volume loss by continuing gas exchange should be negligible. By dividing (maximal tracheal pressure(Pmax,tr)-Pst,rs) by the V' immediately preceding the end-inspiratory occlusion, the total inspiratory resistance of the respiratory system (Rrs) was obtained. By dividing (Pmax,tr-P1,tr) by the V' immediately preceding the end-inspiratory occlusion, Rint,rs was obtained. After airway occlusion, Ptr showed some oscillations due to inertia (immediately after occlusion) and heart beats; these were allowed for by fitting a smooth curve to the pre- and postocclusion portions of the Ptr signal and by back extrapolation of the curvilinear computer-fitted curves to the point in time when the occlusion valve was half closed to obtain Pmax and P1, respectively 2, 11. This was achieved by using Anadat (RHT-lnfodat). In computing Rint,rs, the errors caused by the closing time of the ventilator valve were corrected as previously described 12. The Rrs was computed as the difference between Rrs and Rint,rs. The static elastance of the respiratory system (Est,rs) was computed dividing (Pst,rs-PEEPt) by V.
Model and curve fitting
Data were analysed in terms of the viscoelastic model of the respiratory system depicted in figure 1 1. This model comprises two parallel compartments. The first is a dashpot representing Rint,rs, which explains the initial fast drop observed in respiratory system pressure (Prs) immediately after the end-inspiratory occlusion. Rint,rs is the sum of the interrupter resistance of lung and chest wall. Contrary to in dogs 13, in normal anaesthetized paralysed humans 2 and in COPD patients 3, the chest wall does not contribute substantially to Rint,rs, and essentially reflects the airway resistance. The second compartment of the model in figure 1 is a Kelvin body, which consists of a standard static elastance (Est,rs) in parallel with a Maxwell body, i.e. a spring, E2, and a dashpot, R2, arranged serially. In normal anaesthetized, paralysed subjects and in COPD patients, E2 and R2 mainly reflect the viscoelastic properties of the tissues of the lungs and chest wall 2. In COPD patients, however, part of E2 and R2 is also due to time constant inequalities in the lungs 3.
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Fig. 1.— Scheme of spring-and-dashpot model for interpretation of respiratory mechanics during constant flow interruption. The respiratory system consists of standard resistance (Rint,rs) in parallel with standard elastance (Est,rs) and a series of spring-and-dashpot body (E2 and R2, respectively) that represents stress adaptation units. Distance between the two horizontal bars is the analogue of lung volume (V) and tension between these bars is the analogue of pressure at the airway opening (Pao).
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During constant-V' inflation, the model in figure 1 predicts that Rrs should increase with tI according to the following function 1:
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where the time constant (
2) is equal to R2/E2.
Since during constant-V' inflation Tl=V/V', equation 1 can be rewritten 1:
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The values of R2 and T2 were obtained by fitting the experimental data to equations 1 and 2.
Statistical analysis
Regression analysis was performed using a mixed linear model with random intercept and random slope. The values of respiratory mechanics obtained at the different levels of PEEP were compared using two-way analysis of variance for repeated measures (ANOVA). The values at each level of PEEP were compared to those on ZEEP using the paired t-test of Dunnett 14. Comparison between groups was made using the Student's t-test. A p-value <0.05 was accepted as statistically significant. Values are expressed as mean±sd.
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Results
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The difference between end-expiratory lung volume and the relaxation volume of the respiratory system
As shown in table 2, FRC increased at all levels of PEEP, but the increase was significant only at PEEP >5 cmH2O. The latter reflects the marked difference in the magnitude of PEEPi among the COPD patients (range 2–16 cmH2O). In fact, with 5 cmH2O PEEP, PEEPt was not significantly increased, reflecting the fact that in most of the patients, the applied PEEP had merely replaced PEEPi, and consequently there was little increase in FRC 10, 15.
Interrupter resistance of the respiratory system
At all PEEP levels, the values of Rint,rs at baseline V' and V (table 1) were not significantly different among the iso-V' and iso-V experiments and, hence, were averaged (table 2). While Rint,rs did not change significantly with PEEP (table 2), it decreased significantly with increasing FRC (fig. 2a). This indicates that PEEP can affect Rint,rs only through its effect on FRC. At constant V, Rint,rs increased linearly with V' at all levels of PEEP, according to the following function 1, 3:
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Where K1 and K2 are Rohrer's constants 16. While K1 was independent of FRC (fig. 3a), K2 decreased significantly with FRC (fig 3b).
Additional tissue resistance
The baseline values of Rrs during the iso-V' and iso-V experiments were similar and, hence, were averaged. As shown in table 2, the mean values of Rrs did not change significantly with PEEP. There was also no significant correlation between Rrs and FRC (fig. 2b).
At each level of PEEP, the data of Rrs obtained in the iso-V' and iso-V experiments could be fitted, in all patients, to a single function of tI (equation 1), as shown in figure 4 for a representative subject. The values of R2, 2 and E2 (=R2/2) thus derived, did not vary significantly with either PEEP or FRC (fig. 5).
Respiratory system resistance
As shown in figure 2c, Rrs did not change significantly with FRC, reflecting the concomitant decrease in Rint,rs (fig. 2a) and increase in Rrs (fig. 2b). Similarly, Rrs did not change with PEEP (table 2).
Static elastance of the respiratory system
The baseline values of Est,rs were not different between the two sets of experiments and did not change with either PEEP (table 2) or FRC (fig. 6).
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Discussion
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The main new finding of the present study was that, in COPD patients mechanically ventilated for ARF, the "viscoelastic" behaviour of the respiratory system as reflected by Rrs, does not change with increased lung volume while Rint,rs decreases.
Interrupter resistance of the respiratory system
In normal, anaesthetized paralysed humans, Rint,rs has been found to decrease with PEEP 4, 17, probably reflecting the increased size of the airways as a result of the concomitant increase in lung volume 18. In the present study, Rint,rs was presented both in relation to PEEP, as is commonly done, and FRC, which is the important parameter. Because the effect of PEEP on FRC depends on PEEPi, it is obvious that the results obtained with PEEP in different subjects or studies are not comparable. In fact, the absence of a significant decrease in Rint,rs with PEEP in the patients of the present study (table 2) stems from the complex interplay between PEEPi, dynamic hyperinflation and applied PEEP. Indeed, in COPD patients with tidal expiratory flow limitation, PEEP increases the lung volume only when it approaches or exceeds the PEEPi on ZEEP 10, 14. Since the present study applied fixed incremental levels of PEEP to all patients, rather than levels tailored to the individual values of PEEPi on ZEEP, which varied markedly among patients (range 2–16 cmH2O), the effect of any given PEEP on FRC varied markedly among patients (fig. 7). In contrast, when Rint,rs was referred to FRC, a significant negative correlation was found (fig. 2a).
As previously found in COPD patients with RF in iso-V experiments on ZEEP 3, Rint,rs decreased linearly with inflation volume (equation 4), the correlation being significant in seven patients. With increasing PEEP, the changes become smaller and patients exhibited a significant correlation. This could reflect progressive longitudinal stretching and narrowing of the airways at high lung volume, as previously described in RDS patients 5. An increase in the interrupter resistance of the chest wall (Rint,w) could also explain the rise in Rint,rs at high lung volume. However, in a previous study on COPD patients on ZEEP, which included measurement of oesophageal pressure, no appreciable Rint,w was found 3.
On ZEEP, the values of K1 and K2 were significantly greater in the COPD patients than in normal subjects (table 3), as previously described 3. While in normal subjects K1, but not K2, decreased significantly with increasing lung volume 4, the opposite was found in the COPD patients (fig. 3). The reason for this discrepancy is not clear. It should be noted, however, that K2 is thought to be generated mainly by turbulent flow in the central airways 15. Using another method, Tantucci et al. 19 also found that in COPD patients on ZEEP, K2 decreased with increasing lung volume. The K2 values of the COPD patients were higher than those obtained in previous studies 3, 19. This may be due, at least in part, to the fact that the present COPD patients were investigated at an earlier stage of ARF than in the previous studies. High values of K2 have also been reported in stable COPD patients 20.
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Table 3— Values of K1 and K2 of respiratory system in normal subjects and chronic obstructive pulmonary disease (COPD) patients on zero end-expiratory pressure
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Additional tissue resistance
The experimental relationships of Rrs to tI closely fitted equations 1 and 2 in both iso-V' and iso-V experiments at all four levels of PEEP (fig. 4), as previously found on ZEEP in COPD patients 3 and in normal subjects both on ZEEP and PEEP 4, 21. These results suggest that, in both COPD patients and normal subjects, the "viscoelastic" behaviour of the respiratory system is independent of lung volume, at least over the volume range used during the iso-V' and iso-V experiments (V up to 1 L).
Beydon et al. 22, however, studied two COPD patients with ARF, both on ZEEP and PEEP, and found that the results could be adequately fitted to equation 1 in only one patient on ZEEP. In the other instances, the "viscoelastic" behaviour during constant-flow inflation did not accord with the linear viscoelastic model (constant R2 and E2) but implied a markedly volume-dependent elastic element. This discrepancy with the present and previous results 3 may be due to different methodology or patient population. Beydon et al. 22 occluded the airway at different V' for only 2 s, as compared to 5 s in the present and previous studies 3, 4, 21. This short pause is not long enough to allow the viscoelastic pressure to decay to insignificant values according to the values of 2 in figure 5b. In view of the complexity and diversity of the pathological changes in the lung of COPD patients, it cannot be excluded that in some instances, the linear viscoelastic model (equation 1) may not be adequate to explain the non-Newtonian behaviour of the respiratory system during constant-flow inflation. In the present patients, however, this is not the case. Furthermore, in the present patients, the values of the viscoelastic constants (fig. 5) and Rrs (fig. 2b) did not change significantly with the PEEP-induced changes in FRC.
The values of the viscoelastic constants of the present study, both on ZEEP and PEEP, are significantly higher than those found previously in 16 normal subjects on ZEEP 1, in whom R2, 2 and E2 averaged 4.2±0.6 cmH2O·L–1·s, 0.9±0.3 s and 5.1±1.2 cmH2O·L–1, respectively. This could reflect a loss of pulmonary tissue, either anatomical (emphysema) or functional (airway closure) and, in the absence of rheological changes of the remaining tissue, should result in a proportional increase of R2 and E2 without a change in 2 3. The latter, however, was significantly higher (p<0.01) in the COPD patients than in normal subjects, probably effecting the complex structural changes and increased time constant inequality within the lungs in COPD patients. However, based on the present results and those of D'Angelo et al. 21 on normal subjects it can be concluded that these differences were not due to the characteristic pulmonary hyperinflation of COPD. In fact, in both COPD and normal subjects, the simple linear viscoelastic model in figure 1 fits the experimental results at all lung volumes studied. This, however, is not the case in ARDS patients in whom, even on ZEEP, the model in figure 1 failed to fully describe the experimental relationships of Rrs to tI when inflation volume exceeded 0.71 5.
Since, in the present COPD patients, the viscoelastic behaviour was independent of FRC, it is not surprising that in COPD the viscoelastic work per breath does not change with PEEP-induced changes in lung volume 23.
In conclusion, this is the first systematic study on the effects of high positive end-expiratory pressure on respiratory mechanics in chronic obstructive pulmonary disease patients with acute respiratory failure. The results indicate that respiratory system interrupter resistance decreases with increasing lung volume due to positive end-expiratory pressure, while the viscoelastic behaviour of the respiratory system, as reflected by the additional tissue resistance, is not altered.
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Acknowledgements
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The authors thank the physicians and nursing staff of the Medical Intensive Care Unit of the Centre Hospitalier Lyon-Sud for their valuable cooperation and M. Rabilloud for her help with statistical analysis.
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TOP
Abstract
Methods
), 10 (
) and 15 (
) cmH2O positive end-expiratory pressure (PEEP) of 10 chronic obstructive pulmonary disease patients. Regression lines over all the experimental points are shown: a) y=10.1–2.3x, r=–0.42, p=0.003; b) y=6.8+2.4x, r=0.31. p=ns; c) y=17.0–0.2x, r=0.03, p=ns.
) experiments. Solid lines are the regression lines of the fitting of the experimental points to equation 1
