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J Appl Physiol 83: 1517-1521, 1997;
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Vol. 83, Issue 5, 1517-1521, 1997

Gas compression in lungs decreases peak expiratory flow depending on resistance of peak flowmeter

O. F. Pedersen1, T. F. Pedersen2, and M. R. Miller2

1 Department of Environmental and Occupational Medicine, University of Aarhus, DK-8000 Aarhus C, Denmark; and 2 Department of Medicine, University of Birmingham, Selly Oak Hospital, Birmingham B29 6JD, United Kingdom

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES

ABSTRACT

Pedersen, O. F., T. F. Pedersen, and M. R. Miller. Gas compression in lungs decreases peak expiratory flow depending on resistance of peak flowmeter. J. Appl. Physiol. 83(5): 1517-1521, 1997.---It has recently been shown (O. F. Pedersen T. R. Rasmussen, Ø. Omland, T. Sigsgaard, P. H. Quanjer, and M. R. Miller. Eur. Respir. J. 9: 828-833, 1996) that the added resistance of a mini-Wright peak flowmeter decreases peak expiratory flow (PEF) by ~8% compared with PEF measured by a pneumotachograph. To explore the reason for this, 10 healthy men (mean age 43 yr, range 33-58 yr) were examined in a body plethysmograph with facilities to measure mouth flow vs. expired volume as well as the change in thoracic gas volume (Vb) and alveolar pressure (PA). The subjects performed forced vital capacity maneuvers through orifices of different sizes and also a mini-Wright peak flowmeter. PEF with the meter and other added resistances were achieved when flow reached the perimeter of the flow-Vb curves. The mini-Wright PEF meter decreased PEF from 11.4 ± 1.5 to 10.3 ± 1.4 (SD) l/s (P < 0.001), PA increased from 6.7 ± 1.9 to 9.3 ± 2.7 kPa (P < 0.001), an increase equal to the pressure drop across the meter, and caused Vb at PEF to decrease by 0.24 ± 0.09 liter (P < 0.001). We conclude that PEF obtained with an added resistance like a mini-Wright PEF meter is a wave-speed-determined maximal flow, but the added resistance causes gas compression because of increased PA at PEF. Therefore, Vb at PEF and, accordingly, PEF decrease.

peak flow-determining factors; thoracic gas compression; added expiratory resistance

INTRODUCTION

IT HAS RECENTLY BEEN SHOWN that the added resistance of a mini-Wright peak flowmeter decreases peak expiratory flow (PEF) by ~8% compared with PEF measured by a pneumotachograph (8). Furthermore, there is evidence that PEF is determined by the wave-speed flow-limiting mechanism in most healthy and probably also asthmatic subjects (6). Fry and Hyatt (3) observed that an added resistance shifts the isovolume pressure-flow curves to the right. The alveolar pressure at PEF must therefore be increased by adding the pressure drop across the PEF meter. The total pressure necessary to reach a given PEF may therefore be so large that it cannot be achieved even with maximum effort. The purpose of this study is to determine whether the decrease in PEF is because of insufficient driving pressure or to increased alveolar pressure, causing decreased thoracic gas volume at PEF (5) and thereby lowering the wave-speed-determined maximal flow.

MATERIALS AND METHODS

Equipment. We used a pressure-corrected flow body plethysmograph consisting of a 500-liter modified mercury plethysmograph (Glasgow, Scotland). Box pressure was measured across a 64-cm2 single layer 400-mesh screen in the wall of the plethysmograph by use of a Validyne MP45 transducer with a ±0.2-kPa membrane to provide box flow. Mouth flow was measured by use of an unheated Fleisch-type pneumotachograph with a diameter of 5 cm, normally used by Vitalograph Compact (Buckingham, UK). The pressure across the pneumotachograph head was measured by another similar Validyne transducer. The pneumotachograph head was provided with a conical inlet containing a wire screen and was tested as described previously (7) with steady and dynamic flows. It was linear up to 16 l/s [r2 = 0.9994, residual standard deviation (RSD) from regression line through the origin = 0.11 l/s]. The signals from the transducers were low-pass filtered at 40 Hz (18 dB/octave) and fed to an IBM AT3 computer supplied with an analog-to-digital conversion board (Dash-16, Metrabyte, Taunton, MA). Data acquisition and calculation applied Asyst software (version 1.56, McMillan, CA). The sampling rate was 500 Hz for the first 200 ms and subsequently was 200 Hz. Total sampling time was 4.45 s.

Calibration was performed in the following manner. By use of a calibration device delivering 7.89 liters during an explosive decompression (7), flow entered the box via the mouth pneumotachograph, which during calibration was inverted so that the flow was in the expiratory direction. The delivered flow continued through the box and out of the screen. Damping of the box flow because of the capacitance of the air in the box was corrected for by adding a signal proportional to the first derivative of box pressure vs. time to the pressure signal used in the box-flow recording (10). Box flow was displayed against mouth flow, and the correction was adjusted so that a closed loop was obtained. Box flow was matched to mouth flow by using a third-degree polynomial, making the reading of the box flow identical to that of the mouth flow during the calibration procedure. Electronic and thermal drift were carefully corrected for before each subsequent measurement.

Determination of alveolar pressure. Because of compression of the alveolar air during forced expiration, the amount of air leaving the box through the mouth pneumotachograph will be less than the amount entering the box via the screen, which changes during the expiration, the difference being Delta V. With the assumption of isothermal conditions, alveolar pressure can be determined by application of Boyle's law
P<SC>a</SC> = &Dgr;V(P<SC>b</SC> − P<SC>h</SC><SUB>2</SUB><SC>o</SC>)/(TLC − Vb) (1)
where PA is alveolar pressure, PB is barometric pressure, PH2O is the pressure of saturated water vapor at 37°C, TLC is the total lung capacity from which the expiration starts, and Vb is the volume entering the box during the expiration. This equation is essentially the same as was applied by Ingram and Schilder (5) and Zamel et al. (11).

Validation of pressure measurements. A servo-controlled calibration pump recently developed at the University of Birmingham was placed in the plethysmograph. An artificial flow profile was delivered by the pump with a PEF of 9.99 l/s, time from 10 to 90% PEF of 30 ms, and dwell time of flow >90% PEF of 20 ms. The pump expired through stiff tubing (3.5 cm2 internal diameter), a slide valve with orifices of different sizes, and the mouth pneumotachograph. With no extra resistance the pressure drop across the mouthpiece assembly depended on flow (V) as described by the equation P = 0.0148(V)1.57 kPa (r2 = 0.9996, RSD = 2.1%). Alternatively, an encased mini-Wright PEF meter could replace the slide valve and be used as an added resistance. This increased the pressure across the mouthpiece assembly to 0.189(V)1.11 kPa (r2 = 0.9996, RSD = 1.4%). The volume reduction in the pump because of expiration and compression of air was replaced by air entering the box via the screen. "Alveolar" pressure was directly measured in the pump by using a Validyne transducer with a ±20-kPa diaphragm and sampled in the same way as the mouth and box flow measurements, after calibration with a mercury manometer at 10 kPa. Measured alveolar pressure at PEF was compared with alveolar pressure calculated from Eq. 1 and multiplied by 1.4 to account for adiabatic conditions in the pump. This was done with and without the added resistances described above.

Subjects and measurements. We examined 10 healthy male subjects (two smokers), mean age 43 yr (range 31-58 yr), mean height 178 cm (range 172-185 cm). By using a conventional plethysmographic technique (9), the TLC was first determined. Still seated in the plethysmograph, the subjects performed at least three satisfactory forced vital capacity (FVC) blows, as done with the servo pump, through orifices of different sizes and an encased mini-Wright PEF meter. Flow-volume curves were recorded with mouth flow vs. mouth volume change as well as vs. box volume change. Furthermore, alveolar pressure was recorded vs. box volume change. On-line calculations included the following: PEF and forced expiratory volume in 1 s (FEV1) at the mouth (PEFm and FEV1 m, respectively); PEF of thoracic gas displacement (PEFb); mouth volume expired at PEFm; thoracic volume displaced at PEFb; thoracic volume displaced at PEFm; rise time to PEFm; rise time to PEFb; FVC at the mouth (FVCm); and FVC of thoracic gas displacement (FVCb) and of mouth flows at 5% intervals from 80% FVCm and 80% FVCb to low in the vital capacity. Alveolar pressure values were calculated for PEFm. Baseline spirometry was evaluated according to European standards (9). The BTPS factor was determined for the first six subjects as FVC measured by the box after relaxation of the expiratory muscles divided by FVCm.

Statistics. The on-line calculated data were evaluated by use of the SPSS/PC statistical package (Norusis, Chicago, IL). Because of the effect of gas compression on the flow-volume curve obtained at the mouth (5), we decided to use the mean values from the three satisfactory blows from each subject instead of applying any special selection criteria (9). Mean flow-volume curves and pressure-volume curves for all subjects were constructed for blows with the different added resistances. Paired differences were analyzed by t-tests, and the overall differences between orifices were analyzed by analysis of variance. P <=  0.05 was considered significant.

RESULTS

Test of calibration. PEF for the mouth flow calibration was 18.97 ± 0.19 (SD) l/s (n = 10), and for the corrected box flow calibration it was 18.73 ± 0.94 l/s. The time from 10 to 90% of PEFm was 51 ± 8 ms, and that of the corrected box flow was 54 ± 9 ms. The facts that the loop could be closed and that the rise times recorded are close to the lower fifth percentile of rise times in a population study (7) indicate that the frequency response was adequate. Validation of the pressure measurements by using the servo-controlled calibration pump showed that the maximum error of derived pressure was an underestimate at the highest pressure (highest resistance) of 0.4 kPa. The percentage of absolute error was generally <3%.

Subject data. Table 1 describes baseline data for the individual subjects. Deviation from predicted values is described by standardized residuals (SRD) by using predicted values from the European standard (9). Although perfectly healthy, subject 10 has a PEF equal to 1.64 RSD below the predicted value, which is considered borderline abnormal (9). All other values were within normal limits.

Table  1.   Baseline data for individual subjects
Subject No. PEF
FEV1
FVC
TLC
Liters/s SRD Liters/s SRD Liters SRD Liters SRD
1 12.0 0.10 3.61  -0.15 4.35  -0.36 5.61  -0.67
2 10.7  -0.65 3.51  -0.52 4.24  -0.71 6.70  -0.85
3 11.3 0.07 3.02 0.03 3.92  -0.49 6.89  -0.75
4 10.2  -0.96 3.31  -0.11 4.88  -0.24 7.71  -1.05
5 11.8  -0.04 3.79  -0.06 4.54  -0.27 6.52  -0.61
6 10.5  -0.56 3.32  -0.08 4.59  -0.10 7.41  -0.95
7 14.1 0.89 4.67 0.68 4.71  -0.32 8.29 0.89
8 11.1  -0.60 4.37 0.16 5.02  -0.15 7.82  -0.19
9 12.0 1.45 3.92 0.81 4.92 0.62 8.53  -0.15
10 8.66  -1.64 3.10  -0.83 4.45  -0.31 6.22  -1.03
PEF, peak expiratory flow; FEV1, forced expiratory volume in 1 s; FVC, forced vital capacity; TLC, total lung capacity; SRD, standard residual, i.e., deviation from predicted divided by residual standard deviation for prediction equation (RSD).

Flow-volume and pressure-volume curves. From 105 measurements in 6 subjects, the BTPS correction factor was determined to be 1.07 ± 0.04 (mean ± SD). This mean value was used to correct all the mouth flows.

Figure 1 shows mean mouth flows for all 10 subjects through the different added resistances plotted against expired volume (%FVCm). It is seen that the PEF meter has almost the same effect as the 13-mm orifice. The peaks of curves obtained with added resistances appear to be inside the perimeter of the flow-volume curves. Paired comparisons of peak flows with added resistances on the one hand, and interpolated values on the curve with no added resistance on the other, however, showed no significant deviation for orifice 1 and the PEF meter, borderline significant difference for orifice 2 (P = 0.07), and significant deviation for orifice 3 (P = 0.01).
Fig. 1. Mouth flow vs. expired volume for forced expiratory maneuvers through added resistances. Orif, orifice; Orif 0, no added resistance; Orif 1, 13-mm orifice; Orif 2, 10.5-mm orifice; Orif 3, 8.5-mm orifice; PEF, peak expiratory flow; FVC, forced vital capacity. Values are means for 10 subjects. See Table 2 for details.
[View Larger Version of this Image (20K GIF file)]

Figure 2 similarly shows mean mouth flows plotted against thoracic gas volume change (%FVCb). The peaks appear closer to the perimeter. Only the peak for orifice 3 is different from the perimeter (P = 0.05).
Fig. 2. Mouth flow vs. thoracic gas volume change measured by plethysmograph. Values are means for 10 subjects. Abbreviations and symbols are defined as in legend for Fig. 1. See Table 2 for details.
[View Larger Version of this Image (22K GIF file)]

Figure 3 shows mouth flow vs. alveolar pressure. Increased resistance causes PEFm to decrease and alveolar pressure at PEF to increase systematically.
Fig. 3. Mouth flow vs. alveolar pressure determined by plethysmograph. Values are means for 10 subjects. Abbreviations and symbols are defined as in legend for Fig. 1. See Table 2 for details.
[View Larger Version of this Image (17K GIF file)]

Table 2 summarizes essential features from Figs. 1, 2, 3 and other calculations. Apart from the findings seen in Figs. 1, 2, 3, Table 2 shows that the PEF entering the box (i.e., PEFb) is considerably larger than PEFm but that it also decreases with increasing resistance. The rise time to PEFm increases with increasing resistance, but the rise time to PEFb remains unchanged. This indicates an increasing time lag between box flow and mouth flow.

Table  2.   Effect of added expiratory resistance on PEF
Control PEF Meter Difference from Control Orifice 1  Orifice 2  Orifice 3  ANOVA
PEFm, l/s 11.4 ± 1.5  10.3 ± 1.4  P = 0.00  10.0 ± 1.2  8.2 ± 1.1  6.7 ± 0.7  P = 0.00 
PEFb, l/s 19.0 ± 4.4  17.7 ± 5.7  NS 17.2 ± 4.1  15.0 ± 4.2  14.0 ± 3.8  P = 0.00 
Mouth volume expired at PEFm, liters 0.47 ± 0.09  0.56 ± 1.4  P = 0.01  0.58 ± 0.14  0.77 ± 0.29  0.82 ± 0.20  P = 0.00 
Thoracic volume displaced at PEFb, liters 0.88 ± 0.12  0.86 ± 0.16  NS 0.81 ± 0.18  0.70 ± 0.16  0.64 ± 0.14  P = 0.00 
Thoracic volume displaced at PEFm, liters 0.89 ± 0.15  1.13 ± 0.19  P = 0.00  1.18 ± 0.24  1.50 ± 0.29  1.65 ± 0.22  P = 0.00 
Rise time to PEFm, ms 59 ± 14  69 ± 17  P = 0.01  70 ± 12  98 ± 18  113 ± 20  P = 0.00 
Rise time to PEFb, ms 65 ± 11  66 ± 14  NS 62 ± 12  64 ± 16  64 ± 13  NS
Alveolar pressure at PEFm, kPa 6.7 ± 1.9  9.3 ± 2.7  P = 0.00  9.7 ± 2.9  12.6 ± 3.7  14.8 ± 4.0  P = 0.00
Values are means ± SD; n = 10 subjects. PEFm, PEF measured at mouth; PEFb, peak of flow entering box (PEF of thoracic volume displacement); ANOVA, analysis of variance; NS, not significant.

Addition of the PEF meter influences the flow at the mouth so that PEFm decreases, mouth volume expired at PEFm increases, thoracic volume displaced at PEFm increases, rise time to PEFm increases, and alveolar pressure at PEFm increases. It is remarkable that flow, and accordingly volume, measured by the box is not significantly influenced by the PEF meter. The PEF meter causes the alveolar pressure at PEFm to increase by 2.6 ± 1.3 kPa, a value that is not different from the pressure drop across the PEF meter, determined by separate experiments to be 1.9 ± 0.3 kPa for the same values of PEFm (P = 0.12). The increase in alveolar pressure causes thoracic gas volume at PEFm to decrease by 0.24 ± 0.09 liter (P < 0.001).

DISCUSSION

Although plethysmographic determination of alveolar pressure is not a new method, it has not been thoroughly evaluated for determination of rapid pressure events. The initial calibration and tuning of the box applied explosive decompression, delivering ~19 l/s, which is the same as the mean PEFb in Table 2. The rise time of the calibration signal was ~55 ms and was also comparable to the means of the subjects shown in Table 2. Because the linearity of the mouth pneumotachograph on a previous occasion had been found to be linear up to at least 16 l/s, we believe that linearity as well as frequency response was adequate for the study performed. We found it very important that box flow during calibration was identical to mouth flow and that this could be ensured by matching the two flows by use of a third-degree polynomial.

To further test the algorithm for calculation of alveolar pressure, we used a demanding flow profile to run a servo-controlled calibration pump installed in the plethysmograph. Although the input from this pump remained uninfluenced by increasing outflow resistance, this was not true for the output flow measured by the mouth pneumotachograph. For the smallest orifice tested with the pump (5.5 mm), PEFm fell to 3.0 l/s and the rise time increased to 116 ms. At a given pressure, flow cannot exceed that determined by the pressure-flow characteristics of the resistor. The difference between the input flow generated by the piston and mouth flow is the rate of gas compression in the pump. This compression accounts for the delay of PEFm compared with PEFb, increasing with resistance. The servo-controlled pump did not provide data about the validity of the box-derived alveolar pressure for all pressure and flow combinations in the experiment, but it served to demonstrate that, in principle, correct pressures can be derived. The experiments support that this is the case. We assumed adiabatic conditions in the pump. When measurements are made in subjects, the heat dissipation is efficient and the conditions are isothermal, as discussed by Zamel et al. (11). Assuming isothermal conditions, they found good agreement between measured esophageal pressure and derived alveolar pressure during forced expirations in subjects with use of the plethysmograph.

There were several similarities between results obtained by using the pump and those obtained in the subjects. The thoracic flow profile, like the input flow profile of the pump, changed little with increased outflow resistance. Rise times to PEFb were not influenced in either instance, but the load caused PEFb to decrease in the human subjects without use of the pump. In subjects both with and without use of the pump, rise time to PEFm increased with resistance, causing an increased time lag between PEFm and PEFb. There was no flow limitation in the pump because it had no airways that could be dynamically compressed. Therefore, pressure-flow curves comparable to those in Fig. 3 were closed loops, with pressure and flow in phase and maximum flow at maximum pressure. The fact that pressure continued to increase as flow fell after PEFm was reached (Fig. 3) indicates that PEFm was achieved with most of the added resistors when wave-speed flow limitation occurred somewhere in the airway (6).

The decrease in mouth flow with increasing alveolar pressure is probably secondary to the concomitant decrease in lung volume and therefore does not give information about force-velocity properties of the respiratory muscles, which, however, can be obtained from a similar plot of box flow vs. alveolar pressure. Hyatt and Flath (4) were not aware of this distinction and used both plots to express force-velocity properties of the muscles.

A decreased PEF due to the added resistance of a PEF meter could be because of a decreased driving pressure across the airways upstream from the resistor. This does not seem to be the case, because the alveolar pressure at PEF increases by an amount equal to the pressure across the resistor; i.e., the respiratory muscles are able to cope with this added resistance.

The higher alveolar pressure, however, causes the thoracic gas volume to decrease because of compression. PEF with the PEF meter is lower but still on the envelope of the flow-volume curve showing mouth flow vs. thoracic gas volume change. This indicates that PEF with the flowmeter is determined by the wave-speed flow-limiting mechanism, as indicated in a previous study (6).

According to the theory of flow limitation at wave speed (2), the maximum flow will decrease when the elastic recoil of the lung decreases, when the cross-sectional area at the flow-determining site decreases, when the airway compliance therein increases, and when the pressure loss upstream increases. Among these factors, we believe that the decreased PEF with the PEF meter is primarily because of decreased lung elastic recoil pressure caused by compression of the thoracic gas volume. This, in combination with increased upstream pressure loss due to decreased lung volume, decreases the distending pressure at the flow-determining site and, accordingly, the cross-sectional area. This causes a smaller wave-speed flow and accordingly a smaller PEF. Similar arguments would hold also for orifice 2, which has a considerably larger resistance. In 1957, Campbell et al. (1) determined esophageal pressure at PEF, to distinguish between mechanisms of airway obstruction in emphysema and asthma. In three normal subjects, they found a mean PEF of 10.6 l/s, a value not different from our mean value, and the corresponding mean esophageal pressure, which they called "the maximum effective intrathoracic pressure," was 5.6 kPa. If an estimated elastic recoil pressure of 1-2 kPa is added to their esophageal pressure, the calculated alveolar pressure at PEF for their data of 6-7 kPa would not be different from our mean value of 6.7 kPa (Table 2). They also demonstrated curves in which the pressure increases considerably after PEF was reached. This can be taken as evidence of flow limitation at PEF.

We have only examined healthy normal men but believe that the same mechanisms are operating in women and patients with airway obstruction. In five emphysematous subjects with a mean PEF of 2.3 l/s, Campbell et al. found a mean maximum effective intrathoracic pressure of only 1.8 kPa. This indicates that because of flow limitation, these patients can only use a fraction of the expiratory pressure to generate PEF. A lower alveolar pressure at PEF will diminish gas compression in the lungs of emphysematous patients, but this is counterbalanced by an increased thoracic gas volume, giving more compression for the same increase in alveolar pressure. A previous study (8) indicates that the resistance of a mini-Wright meter decreases PEF almost proportionally to PEF. A study similar to the present one, using patients with emphysema and chronic airflow limitation, would help to clarify the mechanism.

We conclude that PEF, when recorded with a peak flowmeter that imposes an added resistance to expiration, is smaller than PEF obtained by using a low-resistance pneumotachograph. The added resistance of the PEF meter causes an increased alveolar pressure at PEF, which leads to more thoracic gas compression, so the lungs are at a lower lung volume when PEF is achieved. Therefore, the decrease in PEF can be explained in accordance with the wave-speed theory of flow limitation. These findings have implications for the interpretation of PEF and stress the importance of standardization of peak flowmeter resistance to optimize comparison of PEF obtained with different types of PEF meters.

ACKNOWLEDGEMENTS

This study was supported by the European Steel and Coal Community (agreement no. 7280/03/056) and the European Economic Community (agreement MAT1-CT 93032).

FOOTNOTES

Address for reprint requests: O. F. Pedersen, Institute of Environmental and Occupational Medicine, Bldg. 180, Univ. of Aarhus, DK-8000 Aarhus N, Denmark (E-mail ofp{at}mil.aau.dk).

Received 8 April 1997; accepted in final form 7 July 1997.

REFERENCES

1. Campbell, E. J., H. B. Martin, and R. L. Riley. Mechanisms of airway obstruction. Bull. Johns Hopkins Hosp. 101: 329-343, 1957. [Medline]
2. Dawson, S. V., and E. A. Elliott. Wave-speed limitation on expiratory flow---a unifying concept. J. Appl. Physiol. 43: 498-515, 1977[Abstract/Free Full Text].
3. Fry, D. L., and R. E. Hyatt. Pulmonary mechanics: a unified relationship between pressure, volume and gasflow in the lungs of normal and diseased human subjects. Am. J. Med. 29: 672-689, 1960. [Medline]
4. Hyatt, R. E., and R. E. Flath. Relationship of air flow to pressure during maximal respiratory effort in man. J. Appl. Physiol. 21: 477-482, 1966[Free Full Text].
5. Ingram, R. H., Jr., and D. P. Schilder. Effect of thoracic gas compression on the flow-volume curve of the forced vital capacity. Am. Rev. Respir. Dis. 94: 56-63, 1966[Medline].
6. Pedersen, O. F., H. J. L. Brackel, J. M. Bogaard, and K. F. Kerrebijn. Wave-speed-determined flow limitation at peak flow in normal and asthmatic subjects. J. Appl. Physiol. 83: 1721-1732, 1997[Abstract/Free Full Text].
7. Pedersen, O. F., T. R. Rasmussen, S. K. Kjaergaard, M. R. Miller, and P. H. Quanjer. Frequency response of variable orifice peak flow meters: requirements and testing. Eur. Respir. J. 8: 849-855, 1995[Abstract].
8. Pedersen, O. F., T. R. Rasmussen, Ø. Omland, T. Sigsgaard, P. H. Quanjer, and M. R. Miller. Peak expiratory flow and the resistance of the mini-Wright peak flow meter. Eur. Respir. J. 9: 828-833, 1996[Abstract].
9. Quanjer, P. H, G. J. Tammeling, and J. E. Cotes, O. F. Pedersen, R. Peslin, and Y.-C. Yernault. Lung volumes and forced ventilatory flows. Official statement of the European Respiratory Society. Eur. Respir. J. 6, Suppl. 16: 5-40, 1993.
10. Stanescu, D. C., P. De Sutter, and K. P. van de Woestijne. Pressure corrected flow body plethysmograph. Am. Rev. Respir. Dis. 105: 304-305, 1972[Medline].
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0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society


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