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.     

Selected contribution: airway caliber in healthy and asthmatic subjects: effects of bronchial challenge and deep inspirations.

In 9 healthy and 14 asthmatic subjects before and after a standard bronchial challenge and a modified [deep inspiration (DI), inhibited] bronchial challenge and after albuterol, we tracked airway caliber by synthesizing a method to measure airway resistance (Raw; i.e., lung resistance at 8 Hz) in real time. We determined the minimum Raw achievable during a DI to total lung capacity and the subsequent dynamics of Raw after exhalation and resumption of tidal breathing. Results showed that even after a bronchial challenge healthy subjects can dilate airways maximally, and the dilation caused by a single DI takes several breaths to return to baseline. In contrast, at baseline, asthmatic subjects cannot maximally dilate their airways, and this worsens considerably postconstriction. Moreover, after a DI, the dilation that does occur in airway caliber in asthmatic subjects constricts back to baseline much faster (often after a single breath). After albuterol, asthmatic subjects could dilate airways much closer to levels of those of healthy subjects. These data suggest that the asthmatic smooth muscle resides in a stiffer biological state compared with the stimulated healthy smooth muscle, and inhibiting a DI in healthy subjects cannot mimic this.     

Signal Transduction in Smooth Muscle: Selected Contribution: Airway caliber in healthy and asthmatic subjects: effects of bronchial challenge and deep inspirations

In 9 healthy and 14 asthmatic subjects before and after astandard bronchial challenge and a modified [deep inspiration (DI), inhibited] bronchial challenge and after albuterol, we tracked airwaycaliber by synthesizing a method to measure airway resistance (Raw;i.e., lung resistance at 8 Hz) in real time. We determined the minimumRaw achievable during a DI to total lung capacity and the subsequentdynamics of Raw after exhalation and resumption of tidal breathing.Results showed that even after a bronchial challenge healthy subjectscan dilate airways maximally, and the dilation caused by a single DItakes several breaths to return to baseline. In contrast, at baseline,asthmatic subjects cannot maximally dilate their airways, and thisworsens considerably postconstriction. Moreover, after a DI, thedilation that does occur in airway caliber in asthmatic subjectsconstricts back to baseline much faster (often after a single breath).After albuterol, asthmatic subjects could dilate airways much closer tolevels of those of healthy subjects. These data suggest that theasthmatic smooth muscle resides in a stiffer biological state comparedwith the stimulated healthy smooth muscle, and inhibiting a DI inhealthy subjects cannot mimic this.

     

Maintenance of airway caliber in isolated airways by deep inspiration and tidal strains.

Deep inspirations (DIs) are large periodic breathing maneuvers that regulate airway caliber and prevent airway obstruction in vivo. This study characterized the intrinsic response of the intact airway to DI, isolated from parenchymal attachments and other in vivo interactions. Porcine isolated bronchial segments were constricted with carbachol and subjected to transmural pressures of 5-10 cmH2O at 0.25 Hz (tidal breathing) interspersed with single DIs of amplitude 5-20 cmH2O, 5-30 cmH2O, or 5-40 cmH2O (6-s duration) or DI of amplitude 5-30 cmH2O (30-s duration). Tidal breathing was ceased after DI in a subset of airways and in control airways in which no DI was performed. Luminal cross-sectional area was measured using a fiber-optic endoscope. Bronchodilation by DI was amplitude dependent; 5-20 cmH2O DIs produced less dilation than 5-30 cmH2O and 5-40 cmH2O DIs (P=0.003 and 0.012, respectively). Effects of DI duration were not significant (P=0.182). Renarrowing after DI followed a monoexponential decay function to pre-DI airway caliber with time constants between 27.4+/-4.3 and 36.3+/-6.9 s. However, when tidal breathing was ceased after DI, further bronchoconstriction occurred within 30s. This response was identical in both the presence and absence of DI (P=0.919). We conclude that the normal bronchodilatory response to DI occurs as a result of the direct mechanical effects of DI on activated ASM in the airway wall. Further bronchoconstriction occurs by altering the airway wall stress following DI, demonstrating the importance of continual transient strains in maintaining airway caliber.     

Halothane decreases both tissue and airway resistances in excised canine lungs

Studies of the anesthetic effects on the airway often use pulmonary resistance (RL) as an index of airway caliber. To determine the effects of the volatile anesthetic, halothane, on tissue and airway components of RL, we measured both components in excised canine lungs before and during halothane administration. Tissue resistance (Rti), airway resistance (Raw), and dynamic lung compliance (CL, dyn) were determined at constant tidal volume and at ventilatory frequencies ranging from 5 to 45 min-1 by an alveolar capsule technique. Halothane decreased RL at each breathing frequency by causing significant decreases in both Raw and Rti but did not change the relative contribution of Rti to RL at any frequency. Halothane increased CL,dyn at each breathing frequency, although there was little change in the static pressure-volume relationship. The administration of isoproterenol both airway and tissue components of RL; it may act by relaxing the contractile elements in the lung. Both components must be considered when the effects of volatile anesthetics on RL are interpreted.     

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.     

Viscoelastic behavior of lung and chest wall in dogs determined by flow interruption

Pulmonary and chest wall mechanics were studied in six anesthetized paralyzed dogs, by use of the technique of rapid airway occlusion during constant flow inflation. Analysis of the pressure changes after flow interruption allowed us to partition the overall resistance of the lung (Rl) and chest wall (Rw) and total respiratory system (Rrs) into two components, one (Rinit) reflecting in the lung airway resistance (Raw), the other (delta R) reflecting primarily the viscoelastic properties of the pulmonary and chest wall tissues. The effects of varying inspiratory flow and inflation volume were interpreted in terms of frequency dependence of resistance, by using a spring-and-dashpot model previously proposed and substantiated by Bates et al. (Proc. 9th Annu. Conf. IEEE Med. Biol. Soc., 1987, vol. 3, p. 1802-1803). We observed that 1) Raw and Rw,init were nearly equal and small relative to Rl and Rw (both were unaffected by flow); 2) Rrs,init decreased slightly with increasing volume; 3) both delta Rl and delta Rw decreased with increasing flow and increased with increasing lung volume. These changes were manifestations of frequency dependence of delta R, as it is predicted by the model; 4) Rrs, Rl, and Rw followed the same trends as delta R. These results corroborate data previously reported in the literature with the use of different techniques to measure airways and pulmonary tissue resistances and confirm that the use of Rl to assess bronchial reactivity is problematic. The interrupter techniques provides a convenient way to obtain Raw values, as well as analogs of lung and chest wall tissue resistances in intact dogs.     

Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans.

Lung mechanics and airway responsiveness to methacholine (MCh) were studied in seven volunteers before and after a 20-min intravenous infusion of saline. Data were compared with those of a time point-matched control study. The following parameters were measured: 1-s forced expiratory volume, forced vital capacity, flows at 40% of control forced vital capacity on maximal (Vm(40)) and partial (Vp(40)) forced expiratory maneuvers, lung volumes, lung elastic recoil, lung resistance (Rl), dynamic elastance (Edyn), and within-breath resistance of respiratory system (Rrs). Rl and Edyn were measured during tidal breathing before and for 2 min after a deep inhalation and also at different lung volumes above and below functional residual capacity. Rrs was measured at functional residual capacity and at total lung capacity. Before MCh, saline infusion caused significant decrements of forced expiratory volume in 1 s, Vm(40), and Vp(40), but insignificantly affected lung volumes, elastic recoil, Rl, Edyn, and Rrs at any lung volume. Furthermore, saline infusion was associated with an increased response to MCh, which was not associated with significant changes in the ratio of Vm(40) to Vp(40). In conclusion, mild airflow obstruction and enhanced airway responsiveness were observed after saline, but this was not apparently due to altered elastic properties of the lung or inability of the airways to dilate with deep inhalation. It is speculated that it was likely the result of airway wall edema encroaching on the bronchial lumen.     

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.     

Relating maximum airway dilation and subsequent reconstriction to reactivity in human lungs.

Measures of airway resistance (Raw) during deep inspiration (DI) suggest that asthmatic subjects possess stiffer, more reactive airway smooth muscle. There is evidence that one can enhance airway reactivity in healthy lungs by prohibiting DI for an extended period. The present study had two goals. First, we determined whether the maximum dilation capacity of asthmatic subjects depended on the rate of the DI. Second, we investigated whether the enhanced reactivity in healthy humans might derive from additional mechanisms not present in asthmatic subjects. For the first goal, we tracked Raw in seven healthy and seven asthmatic subjects during a noncoached DI, a DI with a 5- to 10-s breath hold at total lung capacity, and a rapid DI. We found that the minimum resistance achieved at total lung capacity was independent of the manner in which the DI was performed. For the second goal, we tracked the rate of return of Raw after a DI as well as dynamic lung elastance before and after the DI, at baseline and after bronchial challenge. A drop in lung elastance post-DI would indicate reopening of lung regions and/or reduced heterogeneities. The data show that constricted healthy but not asthmatic subjects produce longer lasting residual dilation. Hence, a portion of the enhanced reactivity in a healthy subject's response to prohibition of DIs is likely due to airway closure and/or atelectasis that can be ablated with a DI. We conclude that preventing DIs does not ensure that healthy subjects will transition entirely to an asthmatic-like hyperreactive lung state.     

Partitioning of pulmonary resistance in dogs: effect of tidal volume and frequency

To determine the sensitivity of pulmonary resistance (RL) to changes in breathing frequency and tidal volume, we measured RL in intact anesthetized dogs over a range of breathing frequencies and tidal volumes centering around those encountered during quiet breathing. To investigate mechanisms responsible for changes in RL, the relative contribution of airway resistance (Raw) and tissue resistance (Rti) to RL at similar breathing frequencies and tidal volumes was studied in six excised, exsanguinated canine left lungs. Lung volume was sinusoidally varied, with tidal volumes of 10, 20, and 40% of vital capacity. Pressures were measured at three alveolar sites (PA) with alveolar capsules and at the airway opening (Pao). Measurements were made during oscillation at five frequencies between 5 and 45 min-1 at each tidal volume. Resistances were calculated by assuming a linear equation of motion and submitting lung volume, flow, Pao, and PA to a multiple linear regression. RL decreased with increasing frequency and decreased with increasing tidal volume in both isolated and intact lungs. In isolated lungs, Rti decreased with increasing frequency but was independent of tidal volume. Raw was independent of frequency but decreased with tidal volume. The contribution of Rti to RL ranged from 93 +/- 4% (SD) with low frequency and large tidal volume to 41 +/- 24% at high frequency and small tidal volume. We conclude that the RL is highly dependent on breathing frequency and less dependent on tidal volume during conditions similar to quiet breathing and that these findings are explained by changes in the relative contributions of Raw and Rti to RL.     

Effects of posture and bronchoconstriction on low-frequency input and transfer impedances in humans.

We simultaneously evaluated the mechanical response of the total respiratory system, lung, and chest wall to changes in posture and to bronchoconstriction. We synthesized the optimal ventilation waveform (OVW) approach, which simultaneously provides ventilation and multifrequency forcing, with optoelectronic plethysmography (OEP) to measure chest wall flow globally and locally. We applied an OVW containing six frequencies from 0.156 to 4.6 Hz to the mouth of six healthy men in the seated and supine positions, before and after methacholine challenge. We measured mouth, esophageal, and transpulmonary pressures, airway flow by pneumotachometry, and total chest wall, pulmonary rib cage, and abdominal volumes by OEP. We computed total respiratory, lung, and chest wall input impedances and the total and regional transfer impedances (Ztr). These data were appropriately sensitive to changes in posture, showing added resistance in supine vs. seated position. The Ztr were also highly sensitive to lung constriction, more so than input impedance, as the former is minimally distorted by shunting of flow into alveolar gas compression and airway walls. Local impedances show that, during bronchoconstriction and at typical breathing frequencies, the contribution of the abdomen becomes amplified relative to the rib cage. A similar redistribution occurs when passing from seated to supine. These data suggest that the OEP-OVW approach for measuring Ztr could noninvasively track important lung and respiratory conditions, even in subjects who cannot cooperate. Applications might range from routine evaluation of airway hyperreactivity in asthmatic subjects to critical conditions in the supine position during mechanical ventilation.     

Partitioning of respiratory mechanics in halothane-anesthetized humans

In five spontaneously breathing anesthetized subjects [halothane approximately 1 minimal alveolar concentration (MAC), 70% N2O, 30% O2], flow, changes in lung volume, and esophageal and airway opening pressure were measured in order to partition the elastance (Ers) and flow resistance (Rrs) of the total respiratory system into the lung and chest wall components. Ers averaged (+/- SD) 23.0 +/- 4.9 cmH2O X l-1, while the corresponding values of pulmonary (EL) and chest wall (EW) elastance were 14.3 +/- 3.2 and 8.7 +/- 3.0 cmH2O X l-1, respectively. Intrinsic Rrs (upper airways excluded) averaged 2.3 +/- 0.2 cmH2O X l-1 X s, the corresponding values for pulmonary (RL) and chest wall (RW) flow resistance amounting to 0.8 +/- 0.4 and 1.5 +/- 0.5 cmH2O X l-1 X s, respectively. Ers increased relative to normal values in awake state, mainly reflecting increased EL. Rw was higher than previous estimates on awake seated subjects (approximately 1.0 cmH2O X l-1 X s). RL was relatively low, reflecting the fact that the subjects had received atropine (0.3-0.6 mg) and were breathing N2O. This is the first study in which both respiratory elastic and flow-resistive properties have been partitioned into lung and chest wall components in anesthetized humans.     

Responsiveness of the isolated airway during simulated deep inspirations: effect of airway smooth muscle stiffness and strain.

In vivo, breathing movements, including tidal and deep inspirations (DIs), exert a number of beneficial effects on respiratory system responsiveness in healthy humans that are diminished or lost in asthma, possibly as a result of reduced distension (strain) of airway smooth muscle (ASM). We used bronchial segments from pigs to assess airway responsiveness under static conditions and during simulated tidal volume oscillations with and without DI and to determine the roles of airway stiffness and ASM strain on responsiveness. To simulate airway dilations during breathing, we cycled the luminal volume of liquid-filled segments. Volume oscillations (15 cycles/min) were set so that, in relaxed airways, they produced a transmural pressure increase of approximately 5-10 cmH(2)O for tidal maneuvers and approximately 5-30 cmH(2)O for DIs. ACh dose-response curves (10(-7)-3 x 10(-3) M) were constructed under static and dynamic conditions, and maximal response and sensitivity were determined. Airway stiffness was measured from tidal trough-to-peak pressure and volume cycles. ASM strain produced by DI was estimated from luminal volume, airway length, and inner wall area. DIs produced substantial ( approximately 40-50%) dilation, reflected by a decrease in maximal response (P < 0.001) and sensitivity (P < 0.05). However, the magnitude of bronchodilation decreased significantly in proportion to airway stiffening caused by contractile activation and an associated reduction in ASM strain. Tidal oscillations, in comparison, had little effect on responsiveness. We conclude that DI regulates airway responsiveness at the airway level, but this is limited by airway stiffness due to reduced ASM strain.     

A comparison of the dose-response behavior of canine airways and parenchyma

We compared the histamine responsiveness of canine airways and parenchymal tissues in six anesthetized paralyzed open-chest mongrel dogs, partitioning total lung resistance (RL) into airway resistance (Raw) and tissue viscance (Vti). Pressure was measured during tidal breathing (frequency was 0.3 Hz) at the trachea and in three alveolar regions by use of alveolar capsules. Measurements were taken before and after the delivery of increasing concentrations of aerosolized histamine (0.1-30 mg/ml). We found that Vti accounted for 78 +/- 8% of RL under base-line conditions; this proportion remained relatively constant throughout the histamine concentration-response curve. There was a significant correlation between percent change in Vti and percent change in Raw at all levels of histamine-induced constriction (P less than 0.001). Moreover, the sensitivity of the tissues and airways (defined as the concentration of histamine required to double resistance) was remarkably similar. We conclude that, at this frequency of ventilation, Vti accounts for the major portion of RL both under base-line conditions and after histamine-induced constriction. Although increases in RL cannot be attributed solely to events occurring in the airways, the close correlation between changes in Raw and Vti and the similar sensitivities of the two support the use of indexes reflecting changes in airway caliber as an indicator of overall lung histamine responsiveness.     

Head position modifies upper airway resistance in men

We measured in healthy volunteers airway resistance (R(aw)), resistance of the respiratory system (Rrs), and supralaryngeal resistance (Rsl) in the following head positions: neutral, extended, and partially and fully flexed. Sagittal magnetic resonance images of the upper airways were recorded in neutral and flexed head positions. We observed significant increases in Raw (P less than 0.01), Rrs (P less than 0.001), and Rsl (P less than 0.001) in the flexed position, with respect to the neutral one, and corresponding decreases of specific airway and specific respiratory conductances. Resistances decreased (although not significantly) when the subjects' heads were extended. A decrease in both diameter and surface area of the hypopharyngeal airways (as shown by magnetic resonance images) with total head flexion was accompanied by significant increases in all measured resistances. Changes in the caliber of hypopharynx appear to be responsible for the increase in resistance during head flexion.     

Interrupter technique for measurement of respiratory mechanics in anesthetized cats

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg ip), airflow, changes in lung volume, and tracheal and esophageal pressures were measured. Airflow was interrupted by brief airway occlusions during relaxed expirations (elicited via the Breuer-Hering inflation reflex) and throughout spontaneous breaths. A plateau in tracheal pressure occurred throughout relaxed expirations and the latter part of spontaneous expirations indicating respiratory muscle relaxation. Measurement of tracheal pressure, immediately preceding airflow, and corresponding volume enabled determination of respiratory system elastance and flow resistance. These were partitioned into lung and chest wall components using esophageal pressure. Respiratory system elastance was constant over the tidal volume range, divided approximately equally between the lung and chest wall. While the passive pressure-flow relationship for the respiratory system was linear, those for the lung and chest wall were curvilinear. Volume dependence of chest wall flow resistance was demonstrated. During inspiratory interruptions, tracheal pressure increased progressively; initial tracheal pressure was estimated by backward extrapolation. Inspiratory flow resistance of the lung and total respiratory system were constant. Force-velocity properties of the contracting inspiratory muscles contributed little to overall active resistance.     

Effects of volume history and vagotomy on pulmonary and chest wall mechanics in cats

Using the technique of rapid airway occlusion during constant-flow inflation, we studied the effects of inflation volume, different baseline tidal volumes (10, 20, and 30 ml/kg), and vagotomy on the resistive and elastic properties of the lungs and chest wall in six anesthetized tracheotomized paralyzed mechanically ventilated cats. Before vagotomy, airway resistance decreased significantly with increasing inflation volume at all baseline tidal volumes. At any given inflation volume, airway resistance decreased with increasing baseline tidal volume. After vagotomy, airway resistance decreased markedly and was no longer affected by baseline tidal volume. Prevagotomy, pulmonary tissue resistance increased progressively with increasing lung volume and was not affected by baseline tidal volume. Pulmonary tissue resistance decreased postvagotomy. Chest wall tissue resistance increased during lung inflation but was not affected by either baseline tidal volume or vagotomy. The static volume-pressure relationships of the lungs and chest wall were not affected by either baseline tidal volume or vagotomy. The data were interpreted in terms of a linear viscoelastic model of the respiratory system (J. Appl. Physiol. 67: 2276-2285, 1989).     

Tracking of airway and tissue mechanics during TLC maneuvers in mice.

A tracking impedance estimation technique was developed to follow the changes in total respiratory impedance (Zrs) during slow total lung capacity maneuvers in six anesthetized and mechanically ventilated BALB/c mice. Zrs was measured with the wave-tube technique and pseudorandom forced oscillations at nine frequencies between 4 and 38 Hz during inflation from a transrespiratory pressure of 0-20 cmH2O and subsequent deflation, each lasting for approximately 20 s. Zrs was averaged for 0.125 s and fitted by a model featuring airway resistance (Raw) and inertance, and tissue damping and elastance (H). Lower airway conductance (Glaw) was linearly related to volume above functional residual capacity (V) between 0 and 75-95% maximum V, with a mean slope of dGlaw/dV = 13.6 +/- 4.6 cmH2O-1. s-1. The interdependence of Raw and H was characterized by two distinct and closely linear relationships for the low- and high-volume regions, separated at approximately 40% maximum V. Comparison of Raw with the highest-frequency resistance of the total respiratory system revealed a marked volume-dependent contribution of tissue resistance to total respiratory system resistance, resulting in the overestimation of Raw by 19 +/- 8 and 163 +/- 40% at functional residual capacity and total lung capacity, respectively, whereas the lowest frequency reactance was proportional to H; these findings indicate that single-frequency resistance values may become inappropriate as surrogates of Raw when tissue impedance is changing.     

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.