Effect of rib cage and abdominal restriction on total respiratory resistance and reactance

In 14 healthy male subjects we studied the effects of rib cage and abdominal strapping on lung volumes, airway resistance (Raw), and total respiratory resistance (Rrs) and reactance (Xrs). Rib cage, as well as abdominal, strapping caused a significant decrease in vital capacity (respectively, -36 and -34%), total lung capacity (TLC) (-31 and -27%), functional residual capacity (FRC) (-28 and -28%), and expiratory reserve volume (-40 and -48%) and an increase in specific airway conductance (+24 and +30%) and in maximal expiratory flow at 50% of control TLC (+47 and +42%). The decrease of residual volume (RV) was significant (-12%) with rib cage strapping only. Abdominal strapping resulted in a minor overall increase in Rrs, whereas rib cage strapping produced a more marked increase at low frequencies; thus a frequency dependence of Rrs was induced. A similar pattern, but with lower absolute values, of Rrs was obtained by thoracic strapping when the subject was breathing at control FRC. Xrs was decreased, especially at low frequencies, with abdominal strapping and even more with thoracic strapping; thus the resonant frequency of the respiratory system was shifted toward higher frequencies. Partitioning Rrs and Xrs into resistance and reactance of lungs and chest wall demonstrated that the different effects of chest wall and abdominal strapping on Rrs and Xrs reflect changes mainly of chest wall mechanics.     

Influence of posture on lung volumes and impedance of respiratory system in healthy smokers and nonsmokers

In 105 adults we investigated the influence of the body positions, sitting with respect to supine, on lung volumes and on the input resistance, (Rrs) and reactance (Xrs) of the respiratory system. Rrs and Xrs were measured between 2 and 26 Hz by means of a forced oscillation technique. Vital capacity (VC) and expiratory reserve volume (ERV) are smaller in the supine position; this reduction decreases with age and is less for ERV in male smokers than in nonsmokers. The Rrs values are larger in the supine position, and the slope of the Rrs-frequency curves tends to become less positive or negative, depending on sex, age, and smoking habits. Xrs decreases at lower frequencies. The changes in Rrs due to posture are larger in young smokers than in young nonsmokers. This is not explained by changes in ERV and may reflect changes in the intrinsic properties of the airways induced by smoking.     

Changes of respiratory input impedance during breathing in humans.

Changes of total respiratory resistance (Rrs) and reactance (Xrs) were studied between 8 and 32 Hz at five moments during the respiratory cycle in healthy adults (group A) and children (group B) and in patients with chronic obstructive lung disease (group C) and with upper airway obstruction (group D). Two forced oscillation techniques were used: the conventional one and the head generator, with the oscillations applied at the mouth and around the head of the subject, respectively. Both techniques yielded similar results. Rrs is lowest during the transition from inspiration to expiration and highest in the course of expiration, except in group D. Mean Xrs is highest at the transitions from inspiration to expiration or vice versa and lowest during expiration, except in group D. In groups C and D, the increases of Rrs are accompanied by a more pronounced negative frequency dependence of Rrs. The variations of Rrs and Xrs appear to be markedly flow dependent and may be a consequence of the interaction of breathing with oscillatory flows.     

Respiratory input impedance in anesthetized paralyzed patients

Respiratory impedance (Zrs) was measured between 0.25 and 32 Hz in seven anesthetized and paralyzed patients by applying forced oscillation of low amplitude at the inlet of the endotracheal tube. Effective respiratory resistance (Rrs; in cmH2O.l-1.s) fell sharply from 6.2 +/- 2.1 (SD) at 0.25 Hz to 2.3 +/- 0.6 at 2 Hz. From then on, Rrs decreased slightly with frequency down to 1.5 +/- 0.5 at 32 Hz. Respiratory reactance (Xrs; in cmH2O.l-1.s) was -22.2 +/- 5.9 at 0.25 Hz and reached zero at approximately 14 Hz and 2.3 +/- 0.8 at 32 Hz. Effective respiratory elastance (Ers = -2pi x frequency x Xrs; in cmH2O/1) was 34.8 +/- 9.2 at 0.25 Hz and increased markedly with frequency up to 44.2 +/- 8.6 at 2 Hz. We interpreted Zrs data in terms of a T network mechanical model. We represented the proximal branch by central airway resistance and inertance. The shunt pathway accounted for bronchial distensibility and alveolar gas compressibility. The distal branch included a Newtonian resistance component for tissues and peripheral airways and a viscoelastic component for tissues. When the viscoelastic component was represented by a Kelvin body as in the model of Bates et al. (J. Appl. Physiol. 61: 873-880, 1986), a good fit was obtained over the entire frequency range, and reasonable values of parameters were estimated. The strong frequency dependence of Rrs and Ers observed below 2 Hz in our anesthetized paralyzed patients could be mainly interpreted in terms of tissue viscoelasticity. Nevertheless, the high Ers we found with low volume excursions suggests that tissues also exhibit plasticlike properties.     

Effect of upper airway shunt and series properties on respiratory impedance measurements

Because of the contradictory statements published about the influence of the shunt properties of the upper airway on the measurements of the respiratory impedence by means of the forced oscillation technique, this influence has been reevaluated. In healthy adults and children and in patients with obstructive lung disease, the total respiratory impedance was measured by applying oscillations at the mouth (conventional technique) or around the head (head generator technique), with the cheeks either supported by the hands or not. In healthy adults the two techniques (conventional cheeks supported and head generator) yield similar results for respiratory resistance (Rrs) and a more pronounced increase of respiratory reactance (Xrs) with frequency with the head generator. In children and in patients with moderate airway obstruction, the negative frequency dependence of Rrs observed with the conventional technique tends to disappear with the head generator. This is not observed in patients with severe airway obstruction. The differences between the two techniques can be explained by the influence of the shunt impedance of the upper airway on Rrs and Xrs. Correction for this influence by subtracting the impedance measured during a Valsalva maneuver is not satisfactory, since the Valsalva maneuver itself modifies the upper airway shunt. The head generator technique reduces the influence of the upper airway shunt but does not suppress it altogether; the residual error is small, however.     

Effects of tidal volume and methacholine on low-frequency total respiratory impedance in dogs

The frequency dependence of respiratory impedance (Zrs) from 0.125 to 4 Hz (Hantos et al., J. Appl. Physiol. 60: 123-132, 1986) may reflect inhomogeneous parallel time constants or the inherent viscoelastic properties of the respiratory tissues. However, studies on the lung alone or chest wall alone indicate that their impedance features are also dependent on the tidal volumes (VT) of the forced oscillations. The goals of this study were 1) to identify how total Zrs at lower frequencies measured with random noise (RN) compared with that measure with larger VT, 2) to identify how Zrs measured with RN is affected by bronchoconstriction, and 3) to identify the impact of using linear models for analyzing such data. We measured Zrs in six healthy dogs by use of a RN technique from 0.125 to 4 Hz or with a ventilator from 0.125 to 0.75 Hz with VT from 50 to 250 ml. Then methacholine was administered and the RN was repeated. Two linear models were fit to each separate set of data. Both models assume uniform airways leading to viscoelastic tissues. For healthy dogs, the respiratory resistance (Rrs) decreased with frequency, with most of the decrease occurring from 0.125 to 0.375 Hz. Significant VT dependence of Rrs was seen only at these lower frequencies, with Rrs higher as VT decreased. The respiratory compliance (Crs) was dependent on VT in a similar fashion at all frequencies, with Crs decreasing as VT decreased. Both linear models fit the data well at all VT, but the viscoelastic parameters of each model were very sensitive to VT. After methacholine, the minimum Rrs increased as did the total drop with frequency. Nevertheless the same models fit the data well, and both the airways and tissue parameters were altered after methacholine. We conclude that inferences based only on low-frequency Zrs data are problematic because of the effects of VT on such data (and subsequent linear modeling of it) and the apparent inability of such data to differentiate parallel inhomogeneities from normal viscoelastic properties of the respiratory tissues.     

A modified measurement of respiratory resistance by forced oscillation during normal breathing.

We have modified the measurements of the resistance of the respiratory system, Rrs, by the forced oscillation technique and we have developed equipment to automatically compute Rrs. Flow rate and mouth pressure are treated by selective averaging filters that remove the interference of the subject's respiratory flow on the imposed oscillations. The filtered mean Rrs represents a weighted ensemble average computer over both inspiration and expiration. This method avoids aberrant Rrs values, decreases the variability, and yields an unbiased mean Rrs. Rrs may be measured during slow or rapid spontaneous breathing, in normals and in obstructive patients, over a range of 3-9 Hz. A good reproducibility of Rrs at several days' interval was demonstrated. Frequency dependence of Rrs was found in patients with obstructive lung disease but not in healthy nonsmokers.     

Effect of body posture on respiratory impedance

The effects of posture on the mechanics of the respiratory system are not well known, particularly in terms of total respiratory resistance. We have measured respiratory impedance (Zrs) by the forced random noise excitation technique in the sitting and the supine position in 24 healthy subjects. Spirometry and lung volumes (He-dilution technique) were also measured in both postures. The equivalent resistance (Rrs), compliance (Crs), and inertance (Irs) were also calculated by fitting each measured Zrs to a linear series model. When subjects changed from sitting to the supine position, the real part of Zrs increased over the whole frequency band. The associated equivalent resistance, Rrs, increased by 28.2%. The reactance decreased for frequencies lower than 18 Hz and increased for higher frequencies. Consequently, Crs decreased by 38.7% and Irs increased by 15.6%. All of these parameter differences were significant (P less than 0.001). A covariance analysis showed that a significant amount of the postural change in Rrs and Crs can be explained by the reduction of functional residual capacity (FRC). This indicates that the observed differences on Zrs can in part be explained be a shift of the operating point of the respiratory system induced by the decrease in the FRC.     

Forced oscillatory impedance of the respiratory system at low frequencies

Respiratory mechanical impedances were determined during voluntary apnea in five healthy subjects, by means of 0.25- to 5-Hz pseudo/random oscillations applied at the mouth. The total respiratory impedance was partitioned into pulmonary (ZL) and chest wall components with the esophageal balloon technique; corrections were made for the upper airway shunt impedance and the compressibility of alveolar gas. Neglect of these shunt effects did not qualitatively alter the frequency dependence of impedances but led to underestimations in impedance, especially in the chest wall resistance (Rw), which decreased by 20-30% at higher frequencies. The total resistance (Rrs) was markedly frequency dependent, falling from 0.47 +/- 0.06 (SD) at 0.25 Hz to 0.17 +/- 0.01 at 1 Hz and 0.15 +/- 0.01 kPa X l-1 X s at 5 Hz. The changes in Rrs were caused by the frequency dependence of Rw almost exclusively between 0.25 and 2 Hz and in most part between 2 and 5 Hz. The effective total respiratory (Crs,e) and pulmonary compliance were computed with corrections for pulmonary inertance derived from three- and five-parameter model fittings of ZL. Crs,e decreased from the static value (1.03 +/- 0.18 l X kPa-1) to a level of approximately 0.35 l X kPa-1 at 2-3 Hz; this change was primarily caused by the frequency-dependent behavior of chest wall compliance.     

Comparison of plethysmographic methods for obtaining thoracic gas volume in anesthetized dogs

In dogs, respiratory system resistance (Rrs) is frequency independent, and during high-frequency oscillatory ventilation (HFO) the relationship between CO2 elimination (VCO2) and frequency is linear. In contrast, we found in rabbits a large frequency-dependent decrease in Rrs with increasing frequency along with a nonlinear relationship between frequency and VCO2 (J. Appl. Physiol. 57: 354-359, 1984). We proposed that frequency dependent mechanical properties of the lung account for inter-species differences in the frequency dependence of gas exchange during HFO. In the current study we tested this hypothesis further by measuring VCO2 and Rrs as a function of frequency in a species of monkey (Macaca radiata). In these monkeys, Rrs decreased minimally between 4 and 8 Hz and in general increased at higher frequencies, whereas VCO2 was linearly related to frequency. This is further evidence supporting the hypothesis that nonlinear frequency-VCO2 behavior during HFO is related to frequency-dependent behavior in Rrs.     

Changes in the mechanical properties of the respiratory system during the development of interstitial lung edema

Background

Pulmonary edema induces changes in airway and lung tissues mechanical properties that can be measured by low-frequency forced oscillation technique (FOT). It is preceded by interstitial edema which is characterized by the accumulation of extravascular fluid in the interstitial space of the air-blood barrier. Our aim was to investigate the impact of the early stages of the development of interstitial edema on the mechanical properties of the respiratory system.

Methods

We studied 17 paralysed and mechanically ventilated closed-chest rats (325–375 g). Total input respiratory system impedance (Zrs) was derived from tracheal flow and pressure signals by applying forced oscillations with frequency components from 0.16 to 18.44 Hz distributed in two forcing signals. In 8 animals interstitial lung edema was induced by intravenous infusion of saline solution (0.75 ml/kg/min) for 4 hours; 9 control animals were studied with the same protocol but without infusion. Zrs was measured at the beginning and every 15 min until the end of the experiment.

Results

In the treated group the lung wet-to-dry weight ratio increased from 4.3 ± 0.72 to 5.23 ± 0.59, with no histological signs of alveolar flooding. Resistance (Rrs) increased in both groups over time, but to a greater extent in the treated group. Reactance (Xrs) did not change in the control group, while it decreased significantly at all frequencies but one in the treated. Significant changes in Rrs and Xrs were observed starting after ~135 min from the beginning of the infusion. By applying a constant phase model to partition airways and tissue mechanical properties, we observed a mild increase in airways resistance in both groups. A greater and significant increase in tissue damping (from 603.5 ± 100.3 to 714.5 ± 81.9 cmH₂O/L) and elastance (from 4160.2 ± 462.6 to 5018.2 ± 622.5 cmH₂O/L) was found only in the treated group.

Conclusion

These results suggest that interstitial edema has a small but significant impact on the mechanical features of lung tissues and that these changes begin at very early stages, before the beginning of accumulation of extravascular fluid into the alveoli.     

Impedance measurement during air and He-O2 breathing before and after salbutamol in normal subjects

Total respiratory resistance and reactance from 4 to 52 Hz were determined by the method of forced pseudorandom noise oscillation in 20 normal male subjects before and after inhalation of 0.200 mg salbutamol (albuterol) and before and after the subjects were equilibrated with 80% He-20% O2. During air breathing, there was a statistically significant decrease of resistance values at lower frequencies after inhalation of salbutamol. When the subject was equilibrated with 80% He-20% O2, total respiratory resistance markedly decreased at all frequencies, and a negative frequency dependence of resistance was observed between 8 and 20 Hz. Resistance values further decreased during He-O2 breathing after inhalation of salbutamol. After inhalation of salbutamol, reactance values increased during air and He-O2 breathing. The density-dependent decrease of the real part of impedance can be explained by a decrease of turbulence in the larger airways. The bronchodilating effect of salbutamol was not influenced by a change in the physical properties of the inhaled gas. During He-O2 breathing, reactance values significantly decreased, resulting in an increase of resonant frequency due to a decrease of inductive reactance. It is concluded that an increase in the capacitance of the respiratory system must be supposed to explain the increase in reactance values after inhalation of the beta-adrenergic agonist salbutamol.     

Effects of continuous negative airway pressure on lung volume and respiratory resistance.

This study was designed to determine the responses of lung volume and respiratory resistance (Rrs) to decreasing levels of continuous negative airway pressure (CNAP). Twenty normal subjects were studied in the basal state and under CNAP levels of -5, -10, and -15 hPa. Rrs was measured by the forced oscillation technique (4-32 Hz). End-expiratory lung volume (EELV) and tidal volume (VT) were measured by whole body plethysmography. Rrs was extrapolated to 0 Hz (R(0)) and estimated at 16 Hz (R(16)) by linear regression analysis of Rrs vs. frequency. Specific Rrs, SR(0) and SR(16), were then calculated as R(0) (EELV + VT/2) and R(16) (EELV + VT/2), respectively. EELV significantly decreased, whereas R(0), R(16), SR(0), and SR(16) significantly increased, as the CNAP level decreased (P < 0.0001 for all). At the lowest CNAP level, R(0) and R(16) reached 198 +/- 13 and 175 +/- 9% of their respective basal values. The CNAP-induced increase in R(0) was significantly higher than that in R(16) (P < 0.004). Our results demonstrate that the CNAP-induced increase in Rrs does not result from a direct lung volume effect only and strongly suggest the involvement of other factors affecting both intrathoracic and extrathoracic airway caliber.     

Broadband frequency dependence of respiratory impedance in rats.

Past studies in humans and other species have revealed the presence of resonances and antiresonances, i.e., minima and maxima in respiratory system impedance (Zrs), at frequencies much higher than those commonly employed in clinical applications of the forced oscillation technique (FOT). To help understand the mechanisms behind the first occurrence of antiresonance in the Zrs spectrum, the frequency response of the rat was studied by using FOT at both low and high frequencies. We measured Zrs in both Wistar and PVG/c rats using the wave tube technique, with a FOT signal ranging from 2 to 900 Hz. We then compared the high-frequency parameters, i.e., the first antiresonant frequency (far,1) and the resistive part of Zrs at that frequency [Rrs(far,1)], with parameters obtained by fitting a modified constant-phase model to low-frequency Zrs spectra. The far,1 was 570 +/- 43 (SD) Hz and 456 +/- 16 Hz in Wistar and PVG/c rats, respectively, and it did not shift with respiratory gases of different densities (air, heliox, and a mixture of SF(6)). The far,1 and Rrs(far,1) were relatively independent of methacholine-induced bronchoconstriction but changed significantly with increasing transrespiratory pressures up to 20 cmH(2)O, in the same way as airway resistance but independently of changes to tissue parameters. These results suggest that, unlike the human situation, the first antiresonance in the rat is not primarily dependent on the acoustic dimensions of the respiratory system and can be explained by interactions between compliances and inertances localized to the airways, but this most likely does not include airway wall compliance.     

Respiratory transfer impedance and derived mechanical properties of conscious rats.

A setup is described for measuring the respiratory transfer impedance of conscious rats in the frequency range 16-208 Hz. The rats were placed in a restraining tube in which head and body were separated by means of a dough neck collar. The restraining tube was placed in a body chamber, allowing the application of pseudorandom noise pressure variations to the chest and abdomen. The flow at the airway opening was measured in a small chamber connected to the body chamber. The short-term reproducibility of the transfer impedance was tested by repeated measurements in nine Wistar rats. The mean coefficient of variation for the impedance did not exceed 10%. The impedance data were analyzed using different models of the respiratory system of which a three-coefficient resistance-inertance-compliance model provided the most reliable estimates of respiratory resistance (Rrs) and inertance (Irs). The model response, however, departed systematically from the measured impedance. A nine-coefficient model best described the data. Optimization of this model provided estimates of the respiratory tissue coefficients and upper and lower airway coefficients. Rrs with this model was 13.6 +/- 1.0 (SD) kPa.l-1.s, Irs was 14.5 +/- 1.3 Pa.l-1.s2, and tissue compliance (Cti) was 2.5 +/- 0.5 ml/kPa. The intraindividual coefficient of variation for Rrs and Irs was 11 and 18%, respectively. Because most of the resistance and inertance was located in the airways (85 and 81% of Rrs and Irs, respectively), the partitioning in tissue and upper and lower airway components was rather poor. Our values for Rrs and Irs of conscious rats were much lower and our values for Cti were higher than previously reported values for anesthetized rats.     

Lung and chest wall impedances in the dog: effects of frequency and tidal volume.

Dependences of the mechanical properties of the respiratory system on frequency (f) and tidal volume (VT) in the normal ranges of breathing are not clear. We measured, simultaneously and in vivo, resistance and elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) of five healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml, 0.2-2 Hz) delivered at a constant mean lung volume. Each dog showed the same f and VT dependences. The Ers and Ecw increased with increasing f to 1 Hz and decreased with increasing VT up to 200 ml. Although EL increased slightly with increasing f, it was independent of VT. The Rcw decreased from 0.2 to 2 Hz at all VT and decreased with increasing VT. Although the RL decreased from 0.2 to 0.6 Hz and was independent of VT, at higher f RL tended to increase with increasing f and VT (i.e., as peak flow increased). Finally, the f and VT dependences of Rrs were similar to those of Rcw below 0.6 Hz but mirrored RL at higher f. These data capture the competing influences of airflow nonlinearities vs. tissue nonlinearities on f and VT dependence of the lung, chest wall, and total respiratory system. More specifically, we conclude that 1) VT dependences in Ers and Rrs below 0.6 Hz are due to nonlinearities in chest wall properties, 2) above 0.6 Hz, the flow dependence of airways resistance dominates RL and Rrs, and 3) lung tissue behavior is linear in the normal range of breathing.     

Low-frequency pulmonary impedance in rabbits and its response to inhaled methacholine.

We assessed pulmonary mechanics in six open-chest rabbits (3 young and 3 adult) by the forced oscillation technique between 0.16 and 10.64 Hz. Under control conditions, pulmonary resistance (RL) decreased markedly between 0.16 and 4 Hz, after which it became reasonably constant. Measurements of alveolar pressure from two alveolar capsules in each rabbit showed that the large decrease of RL with increasing frequency below 4 Hz was due to lung tissue rheology and that tissue resistance was close to zero above 4 Hz. Estimates of resistance and elastance, also obtained by fitting tidal ventilation data at 1 Hz to the equation of the linear single-compartment model, gave values for RL motion that were slightly higher than those obtained by forced oscillations at the same frequency, presumably because of the flow dependence of airways resistance. After treatment with increasing doses of aerosolized methacholine, RL and pulmonary elastance between 0.16 and 1.34 Hz progressively increased, as did the point at which the pulmonary reactance crossed zero (the resonant frequency). The alveolar pressure measurements showed the lung to become increasingly inhomogeneously ventilated in all six animals, whereas in the three younger rabbits lobar atelectasis developed at high methacholine concentrations and the alveolar capsules ceased to communicate with the central airways. We conclude that the low-frequency pulmonary impedance of rabbits exhibits the same qualitative features observed in other species and that it is a sensitive indicator of the changes in pulmonary mechanics occurring during bronchoconstriction.     

Resonant frequency of the chest-lung system by analysis of the respiratory flow curve

1. Resonant frequency of the chest-lung system in six tracheotomized, spontaneously breathing dogs was determined by analyzing the shape of the respiratory flow curve. 2. The resonant frequency was calculated from the periodic deviations from a sinusoidal flow pattern observed in the inspiratory phase of the breathing cycle. 3. Mean (+/- S.D.) resonant frequency was 6.1 +/- 0.9 Hz which was very close to the panting frequency (5.7 Hz) of the same dogs. 4. Resonant frequencies of the respiratory system in various species are compared.     

Respiratory modulation of human autonomic rhythms

We studied the influence of three types of breathing [spontaneous, frequency controlled (0.25 Hz), and hyperventilation with 100% oxygen] and apnea on R-R interval, photoplethysmographic arterial pressure, and muscle sympathetic rhythms in nine healthy young adults. We integrated fast Fourier transform power spectra over low (0.05-0.15 Hz) and respiratory (0.15-0.3 Hz) frequencies; estimated vagal baroreceptor-cardiac reflex gain at low frequencies with cross-spectral techniques; and used partial coherence analysis to remove the influence of breathing from the R-R interval, systolic pressure, and muscle sympathetic nerve spectra. Coherence among signals varied as functions of both frequency and time. Partialization abolished the coherence among these signals at respiratory but not at low frequencies. The mode of breathing did not influence low-frequency oscillations, and they persisted during apnea. Our study documents the independence of low-frequency rhythms from respiratory activity and suggests that the close correlations that may exist among arterial pressures, R-R intervals, and muscle sympathetic nerve activity at respiratory frequencies result from the influence of respiration on these measures rather than from arterial baroreflex physiology. Most importantly, our results indicate that correlations among autonomic and hemodynamic rhythms vary over time and frequency, and, thus, are facultative rather than fixed.