1Department of Anaesthesiology and Critical Care Medicine, University of Freiburg, Hugstetterstrasse 55, D-79106 Freiburg, Germany. 2Department of Anaesthesiology and Intensive Care, Zentralklinikum, Augsburg, Germany*Corresponding author
Accepted for publication: September 1, 2000
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2001; 86: 17682
Keywords: complications, acute respiratory distress syndrome; lung, alveolus
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
Methods |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Determination of resistance: volume-dependent Rslice and RMLR
In two patients, gas flow rate was measured with a heated pneumotachograph (Fleisch no. 2; Metabo, Epalinges, Switzerland) connected to the endotracheal tube, which was calibrated with a syringe of 1000 (SD 1) ml (calibration syringe 54500460; Jaeger, Würzburg, Germany). A differential pressure transducer (SPS1, Hoffrichter, Schwerin, Germany) was used to determine the flow proportional pressure difference across the pneumotachograph. Airway pressure was measured by a transducer (1210A; ICSensors, Milpitas, CA, USA) previously tested for linearity between -80 and +80 mbar and calibrated using a Revue Thommen calibrator (Waldenburg, Switzerland). Signals were digitized at 100 Hz with 12-bit resolution (SDM863; Burr Brown, Tucson, AZ, USA). In 14 patients a CP-100 pulmonary monitor (Bicore Monitoring Systems, Irvine, CA, USA), calibrated according to the manufacturers instructions, was used for measurements. The raw data were sampled with 50 Hz and passed to a laptop computer. Thereafter, the raw data from both systems were transmitted to a SparcStation 4 workstation (Sun Microsystems, Palo Alto, CA, USA) to calculate volume-dependent respiratory system resistance (and compliance) using the slice method.5 6
The slice method uses multiple linear regression (MLR).7 Rather than using data derived from end-inspiratory and end-expiratory airway occlusion manoeuvres, MLR uses flow, pressure and volume data of the whole breath. If resistance and compliance are assumed to be constant within the tidal volume range, a simple linear model is usually used for this calculation to give average values of resistance and compliance by analysing inspiration and expiration signals obtained during mechanical ventilation without flow interruption. Consequently, the resulting dynamic resistance and compliance values include pressure components associated with stored viscoelastic energy and the effects of inhomogeneous gas distribution.
The slice method enhances standard MLR because changes in respiratory variables over the volume of interest (usually the VT) can be determined. For this purpose, the VT is first divided into six volume slices of equal size and MLR is done separately for each slice. The resulting plot of Rslice (or Cslice) over the volume slices give volume-dependent resistance (or compliance) within VT.
There are other differences between the slice method and standard MLR. With standard MLR, resistance data are affected by the flow-dependent drop in pressure across the endotracheal tube. With the slice method, this effect is eliminated by continuously calculating tracheal pressure (Ptrach) before the actual slice calcutions.8 9 To ensure the accuracy of the Ptrach calculation in this study, obstruction of the endotracheal tube by secretions or kinking was excluded by suctioning of the airways immediately before the measurements and then monitoring the time constant of passive expiration ().10 The uppermost and lowermost 5% of the pressurevolume loop were excluded from the analysis because of distortions caused by operation of the ventilator valves. Another difference is that the slice method automatically considers intrinsic positive end-expiratory pressure (PEEP).11
The principle of the slice method is shown in an example of a pressurevolume loop (Figure 1). Step 1 involves calculation of Ptrach. The tidal volume is then divided into six slices (step 2) and resistance and compliance are calculated for each slice separately. To assess goodness of fit, the Ptrachvolume loop is reconstructed using calculated respiratory parameters for each slice and measured flow and volume data. The match of the measured and the reconstructed Ptrachvolume loop is shown in part 3 of Figure 1. The absolute deviation (mean plus one SD) of the two loops (P) is shown in part 4 (Figure 1). The quality of the fit and the appropriateness of the model are demonstrated by the small
P; the fit is best in the middle of VT. Since the uppermost (and lowermost) 5% of the loop are not adequately described by a model not including inertance, these parts of the loop were excluded from the analysis.
|
We modified the original slice method5 and did not calculate volume-equidistant data sets from time-equidistant raw data. This computation is time-consuming and requires user intervention, which prevents online calculations of mechanical parameters and hinders clinical application. We therefore no longer use this transformation.2 6 13 All data are given as mean (SD).
![]() |
Results |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
|
|
|
|
![]() |
Discussion |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Methodological considerations
To determine the course of resistance (and compliance) within VT, data from the whole breath, i.e. from inspiration and expiration, were used. The resulting mechanical measurements thus represent both phases of the respiratory cycle. Inspiratory and expiratory resistance can be separated by standard (whole-breath) MLR.7 However, the stability of the fit procedure would have been overstrained by calculation of volume-dependent resistance separately for inspiration and expiration.
The slice method determines resistance as the sum of airway and tissue resistance. The two can be separated with the interrupter technique using sophisticated technical equipment.1518 However, airway resistance data obtained by the interrupter technique inevitably contain the resistance of the endotracheal tube. By contrast, resistance data obtained by the slice method are based on calculated Ptrach after elimination of the resistance of the endotracheal tube.8 9
In the slice method, the pressurevolume loop is divided into six slices of equal volume. Potential effects of the gas flow rate on the mechanical parameters are assumed to be negligible. However, the characteristic decelerating flow pattern of pressure-controlled ventilation used here calls this assumption into question. Therefore, we plotted the absolute mean flow rate in each slice for every patient (Figure 3). While slightly differing from patient to patient, the flow rate was distributed over the slices (i.e. the VT) with a convex pattern. If resistance were to increase with flow rate, a similar pattern would be expected. This pattern was present in patient O and, to a lesser extent, in patients A and H. In all other patients, the course of Rslice within VT was not related to flow values. Consequently, flow has only a minor effect on the course of Rslice within VT. This conclusion supports the findings of Eissa and colleagues,14 who reported resistance to be grossly independent from the gas flow rate in ARDS patients, although their data were obtained by using the interrupter technique.
Interpretation of data
Resistance increased considerably in most patients, as often reported in ALI and ARDS patients.1921 Classically, resistance should decrease during lung inflation,22 so a decrease in Rslice should also be expected even within the small VT. Such a pattern of Rslice occurred only in patient F, whereas in patient O Rslice decreased only at greater lung volume within the tidal volume range. In most of the patients, other patterns of Rslice were found. The constant Rslice (found in six of 16 patients) is relatively easy to interpret. The studied volume range, i.e. the VT, may have been too small for a change of resistance to occur.
Other patterns of Rslice are more interesting. Several investigators reported an increase of resistance with lung inflation in ALI patients.20 21 23 24 In these reports, however, the studied volume range was larger. Eissa and colleagues14 investigated the volume dependence of airway resistance in ARDS patients at different PEEP levels, and hence different lung volumes. Although they studied a volume range that was greater than the tidal volumes studied here, they reported an increase of resistance with lung inflation starting from high PEEP levels (10 or 15 cm H2O). At lower PEEP levels (0 and 5 cm H2O) they observed a concave pattern. These data are not directly comparable because they were obtained with the interrupter technique during constant inspiratory flow. How can we interpret an (unexpected) increase in resistance? Longitudinal stretching of airways at high lung volumes could perhaps decrease their cross sectional area, and thus increase resistance.14
Our data show no apparent association of PEEP with the course of Rslice. This may be because the PEEP was high throughout. Moreover, since larger interindividual differences in lung mechanics exist in ARDS patients, pulmonary overdistension could not be expected at a distinct PEEP level, especially when VT also differs. However, it may be helpful to consider the Cslice data reported previously.2 A decrease in Cslice is interpreted as overdistension. A decreasing Cslice coincided with an increasing Rslice, at least in the upper slices, in eight of 16 patients (C, D, G, I, J, K, M and N). These data may support the interpretation by Eissa and colleagues14 of longitudinal airway stretching at high lung volume. As an alternative explanation for the volume-dependent increase in resistance, Pesenti and colleagues21 suggested an increased tissue resistance caused by inhomogeneity of ventilation at high PEEP levels.
Limitations
This study has two limitations. First, it is an incidental observation. The data were obtained with another end in view, i.e. the analysis of volume-dependent compliance within VT.2 The resistance data reported here were not sampled with an a priori hypothesis and no plan was followed to investigate the volume dependency of resistance after changes in ventilator settings. Secondly, the resistance data presented here represent the behaviour of the whole respiratory system, containing the lungs and chest wall. While the chest walls resistance to airflow can be neglected,20 viscoelastic properties of the chest wall may contribute to the dynamic resistance of the respiratory system. It would only have been possible to separate the resistance of the lung resistance from that of the chest wall by measurement of pleural pressure. It is difficult to measure pleural pressure, so oesophageal pressure is often used as a surrogate. In principle, determination of the lungs inherent resistance based on measurements of oesophageal pressure would be desirable and this could easily be added to the slice method. However, our purpose in measurement of respiratory mechanics with the slice method in this and other studies2 6 13 is to develop a concept that will help clinicians to set the ventilator. A non-invasive approach that could be used in standard ventilator equipment is therefore preferable. Measurement of oesophageal pressure is not suited for routine care, because its application is invasive and requires careful adjustment of the catheters position. Furthermore, oesophageal pressure may not exactly represent pleural pressure, because it is affected by the weight of the mediastinum in the supine position.25
Implications and conclusions
Resistance changes considerably, not only in large volume ranges, but also within the relatively small VT. The method used allows non-invasive and continuous recording of volume-dependent resistance. Clinical benefits for ARDS patients will come only if a thorough explanation of volume-dependent resistance can be derived.
![]() |
Acknowledgements |
---|
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Mols G, Brandes I, Kessler V, et al. Volume-dependent compliance in ARDS: proposal of a new diagnostic concept. Intensive Care Med 1999; 25: 108491[ISI][Medline]
3 Bernard GR, Artigas A, Brigham KL, et al. Report of the AmericanEuropean consensus conference on ARDS: definitions, mechanisms, relevant outcomes and clinical trial coordination. Intensive Care Med 1994; 20: 22532[ISI][Medline]
4 Slutsky AS. Consensus conference on mechanical ventilationJanuary 2830, 1993 at Northbrook, Illinois, USA. Part 2. Intensive Care Med 1994; 20: 15062[ISI][Medline]
5 Guttmann J, Eberhard L, Fabry B, et al. Determination of volume-dependent respiratory system mechanics in mechanically ventilated patients using the new slice method. Technol Health Care 1994; 2: 17591
6 Lichtwarck-Aschoff M, Kessler V, Sjöstrand UH, et al. Static versus dynamic respiratory mechanics for setting the ventilator. Br J Anaesth 2000; 85: 57786
7 Uhl RR, Lewis FJ. Digital computer calculation of human pulmonary mechanics using a least squares fit technique. Comput Biomed Res 1974; 7: 48995[ISI][Medline]
8 Guttmann J, Eberhard L, Fabry B, Bertschmann W, Wolff G. Continuous calculation of intratracheal pressure in tracheally intubated patients. Anesthesiology 1993; 79: 50313[ISI][Medline]
9 Guttmann J, Kessler V, Mols G, Hentschel R, Haberthür C, Geiger K. Calculation of intratracheal pressure in the presence of pediatric endotracheal tubes. Crit Care Med 2000; 28: 101826[ISI][Medline]
10 Guttmann J, Eberhard L, Haberthür C et al. Detection of endotracheal tube obstruction by analysis of the expiratory flow signal. Intensive Care Med 1998; 24: 116372[ISI][Medline]
11 Eberhard L, Guttmann J, Wolff G, et al. Intrinsic PEEP monitored in the ventilated ARDS patient with a mathematical method. J Appl Physiol 1992; 73: 47985[ISI][Medline]
12 Iotti GA, Braschi A, Brunner JX et al. Respiratory mechanics by least square fitting in mechanically ventilated patients: applications during paralysis and during pressure support ventilation. Intensive Care Med 1995; 21: 40613[ISI][Medline]
13 Lichtwarck-Aschoff M, Guttmann J, Eberhard L, Fabry B, Birle J, Adolph M. Delayed derecruitment after removal of PEEP in patients with acute lung injury. Acta Anaesthesiol Scand 1997; 41: 67584[ISI][Medline]
14 Eissa N, Ranieri V, Corbeil C, Chassé M, Braidy J, Milic-Emili J. Effects of positive end-expiratory pressure, lung volume, and inspiratory flow on interrupter resistance in patients with adult respiratory distress syndrome. Am Rev Respir Dis 1991; 144: 53843[ISI][Medline]
15 Bates JHT, Baconnier P, Milic-Emili J. A theoretical analysis of the interrupter technique for measuring respiratory mechanics. J Appl Physiol 1988; 64: 220414
16 Bates JHT, Hunter IW, Sly PD, Okubo S, Filialtrault S, Milic-Emili J. Effect of valve closure time on the determination of respiratory resistance by flow interruption. Med Biol Eng Comput 1987; 25: 13640[ISI][Medline]
17 Kessler V, Mols G, Bernhard H, Haberthür CH, Guttmann J. Interrupter airway and tissue resistance: errors caused by valve properties and respiratory system compliance. J Appl Physiol 1999; 87: 154654
18 Mols G, Kessler V, Benzing A, et al. The traveling shutter wave analyses non-linear compliance during mechanical ventilation. Technol Health Care 1999; 7: 30917[Medline]
19 Eissa NT, Ranieri VM, Corbeil C, et al. Analysis of behavior of the respiratory system in ARDS patients: effects of flow, volume, and time. J Appl Physiol 1991; 70: 271929
20 Pelosi P, Cereda M, Foti G, Giacomini M, Pesenti A. Alterations of lung and chest wall mechanics in patients with acute lung injury: effects of positive end-expiratory pressure. Am J Respir Crit Care Med 1995; 152: 5317[Abstract]
21 Pesenti A, Pelosi P, Rossi N, Virtuani A, Brazzi L, Rossi A. The effects of positive end-expiratory pressure on respiratory resistance in patients with the adult respiratory distress syndrome and in normal anesthetized subjects. Am Rev Respir Dis 1991; 144: 1017[ISI][Medline]
22 Nunn JF. Nunns Applied Respiratory Physiology, 4th Edn. Oxford: Butterworth-Heinemann, 1993
23 Tantucci C, Corbeil C, Chasse M, et al. Flow and volume dependence of respiratory system flow resistance in patients with adult respiratory distress syndrome. Am Rev Respir Dis 1992; 145: 35560[ISI][Medline]
24 Auler JOJ, Saldiva PH, Martins MA, et al. Flow and volume dependence of respiratory system mechanics during constant flow ventilation in normal subjects and in adult respiratory distress syndrome. Crit Care Med 1990; 18: 10806[ISI][Medline]
25 Ranieri VM, Brienza N, Santostasi S, et al. Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome: role of abdominal distension. Am J Respir Crit Care Med 1997; 156: 108291
26 Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988; 138: 7203[ISI][Medline]