Frequency Dependence Of Respiratory Resistance Research Articles

Hyperpolarized 3He magnetic resonance imaging ventilation defects in asthma: relationship to airway mechanics.

In patients with asthma, magnetic resonance imaging (MRI) provides direct measurements of regional ventilation heterogeneity, the etiology of which is not well‐understood, nor is the relationship of ventilation abnormalities with lung mechanics. In addition, respiratory resistance and reactance are often abnormal in asthmatics and the frequency dependence of respiratory resistance is thought to reflect ventilation heterogeneity. We acquired MRI ventilation defect maps, forced expiratory volume in one‐second (FEV 1), and airways resistance (Raw) measurements, and used a computational airway model to explore the relationship of ventilation defect percent (VDP) with simulated measurements of respiratory system resistance (Rrs) and reactance (Xrs). MRI ventilation defect maps were experimentally acquired in 25 asthmatics before, during, and after methacholine challenge and these were nonrigidly coregistered to the airway tree model. Using the model coregistered to ventilation defect maps, we narrowed proximal (9th) and distal (14th) generation airways that were spatially related to the MRI ventilation defects. The relationships for VDP with Raw measured using plethysmography (r = 0.79), and model predictions of Rrs>14 (r = 0.91, P < 0.0001) and Rrs>9 (r = 0.88, P < 0.0001) were significantly stronger (P = 0.005; P = 0.03, respectively) than with FEV 1 (r = −0.68, P = 0.0001). The slopes for the relationship of VDP with simulated lung mechanics measurements were different (P < 0.0001); among these, the slope for the VDP‐Xrs0.2 relationship was largest, suggesting that VDP was dominated by peripheral airway heterogeneity in these patients. In conclusion, as a first step toward understanding potential links between lung mechanics and ventilation defects, impedance predictions were made using a computational airway tree model with simulated constriction of airways related to ventilation defects measured in mild‐moderate asthmatics.

Novel interpretations of respiratory impedance in COPD based on computational fluid dynamics

Although it has been conventionally believed that negative frequency dependence of respiratory resistance and deep decline of respiratory reactance during expiratory phase in COPD are due to ventilation inhomogeneity caused by small airway obstructions, there have been neither experimental theoretical evidence. We have recently confirmed that the airflow limitation site in COPD is the intra-mediastinal airway (intra-thoracic trachea, main bronchi, and right lobar bronchi) whose membranous part is displaced inward during expiration by the use of 4D-CT (see our another presentation) . Therefore, we have hypothesized they are also due to the might occur in the membranous part of the intra-thoracic trachea in emphysema by FOT, because it may be easily flip-flopped. In order to validate this hypothesis theoretically, we constructed an oscillated 4D lung model with tracheal deformation and reproduced the respiratory impedance by the use of computational fluid dynamics.

Inter-individual differences in control of alveolar capillary blood volume in exercise and hypoxia

We compared by non-invasive technique the adaptive response of alveolar capillary network to edemagenic conditions (exercise and high altitude [HA, PIO2 107mmHg] in subjects with different resting sea level (SL) capillary blood volume (normalized to alveolar volume, Vc/Va): Group 1 (N=10, Vc/Va=16.1±6.8ml/L- mean±SD) and Group 2 (N=10, Vc/Va=25±7.7). In Group 1 Vc/Va remained unchanged in HA at rest and increased during exercise at SL (26.3±8.6) and HA (28.75±10.2); in Group 2 Vc/Va significantly decreased in HA (19±6) and did not increase in exercise at SL and HA. We hypothesize that Group2 exerts a tight control on Vc/Va being more exposed to the risk of lung edema due to inborn greater microvascular permeability. Conversely, Group 1 appears more resistant to lung edema given the large capillary recruitment in the most edemagenic condition. The 4-fold increase in frequency dependence of respiratory resistance in Group2 in HA stems for greater proneness for lung water perturbation compared to Group 1.

The origin of frequency dependence of respiratory resistance: An airflow simulation study using a 4D pulmonary lobule model

The origin of frequency dependence of respiratory resistance has been explained by ventilation inhomogeneity; however, it is unclear which components in the respiratory system generate the frequency dependence. The author constructed a 4D pulmonary lobule model and analysed relationships between airflow rate, pressure and airway resistance by the use of computational fluid dynamics. The lobule model contained bifurcated bronchioles with two adjacent acini in which deformable inter-acinar septa and alveolar duct walls were designed. Constrictive conditions of respective bronchioles were designed, too. 4D finite element models for computational fluid dynamics were generated and airflow simulations were performed under moving boundary conditions of the arbitrary Lagrangean-Eulerean method. From the simulation results, airway resistances for various conditions were calculated. Tissue resistance emerged under the condition of different acinar pressures caused by unequal airway resistances. If the inter-acinar septum was shifted so as to cancel the pressure difference, the acinar pressures were equal in spite of unequal airway resistances, and hence, tissue resistances did not emerge. Therefore, the tissue resistance in the former case is thought to be an index of alveolar pressure inequality (which could be cancelled by mechanical interaction of lung parenchyma), rather than a material property of the tissue itself. Inequality of alveolar pressure decreases as the input oscillatory frequency increases. Therefore, frequency dependence of the respiratory resistance should be regarded as a conditional index of the alveolar pressure inequality caused by heterogeneous changes in the intra-pulmonary airway and/or the lung parenchyma.

Relationship between dynamic respiratory mechanics and disease heterogeneity in sheep lavage injury*

Acute respiratory distress syndrome and acute lung injury are characterized by heterogeneous flooding/collapse of lung tissue. An emerging concept for managing these diseases is to set mechanical ventilation so as to minimize the impact of disease heterogeneity on lung mechanical stress and ventilation distribution. The goal of this study was to determine whether changes in lung mechanical heterogeneity with increasing positive end-expiratory pressure in an animal model of acute lung injury could be detected from the frequency responses of resistance and elastance. Prospective, experimental study. Research laboratory at a veterinary hospital. Female sheep weighing 48 +/- 2 kg. In five saline-lavaged sheep, we acquired whole-lung computed tomography scans, oxygenation, static elastance, and dynamic respiratory resistance and elastance at end-expiratory pressure levels of 7.5-20 cm H2O. As end-expiratory pressure increased, computed tomography-determined alveolar recruitment significantly increased but was accompanied by significant alveolar overdistension at 20 cm H2O. An optimal range of end-expiratory pressures (15-17.5 cm H2O) was identified where alveolar recruitment was significantly increased without significant overdistension. This range corresponded to the end-expiratory pressure levels that maximized oxygenation, minimized peak-to-peak ventilation pressures, and minimized indexes reflective of the mechanical heterogeneity (e.g., frequency dependence of respiratory resistance and low-frequency elastance). Static elastance did not demonstrate any significant pressure dependence or reveal an optimal end-expiratory pressure level. We conclude that dynamic mechanics are more sensitive than static mechanics in the assessment of the functional trade-off of recruitment relative to overdistension in a sheep model of lung injury. We anticipate that monitoring of dynamic respiratory resistance and elastance ventilator settings can be used to optimize ventilator management in acute lung injury.

Respiratory resistance and impedance magnitude in healthy children aged 2-18 years.

Two hundred eighteen healthy children aged 2 to 18 years were studied using a modification of the forced oscillation technique. Reference values with height as predictor were determined for total respiratory resistance and impedance during inspiration, expiration, and throughout the whole respiratory cycle at an oscillation frequency of 4 Hz and, in a subpopulation of 61 children, at frequencies of 2 and 12 Hz. Mean total inspiratory resistance, determined at 4 Hz, decreased with growth from 1.3 kPa X 1(-1) X s at 2 years of age to 0.3 kPa X 1(-1) X s at 18 years. Variability in the results between individuals, expressed in terms of coefficient of variation, was found to be +27% and -21%, respectively, and within individuals, 9%. Resistance during expiration was on average 16% higher than during inspiration and the variability within individuals was 11%. A marked decrease in resistance was found in small children when the frequency was increased from 2 to 12 Hz. The frequency dependence of respiratory resistance observed in small children changes gradually with growth, in parallel with the reduction of total respiratory resistance, to an adult pattern in which no significant change in resistance can be noted between frequencies of 2 and 12 Hz.

Upper airway walls impedance measured with head plethysmograph.

Respiratory input impedance (Zrs) measured by forced oscillations needs to be corrected for the motion of extrathoracic airway walls. Two methods of obtaining the impedance of this shunt pathway [upper airway impedance (Zuaw)] were compared in six normal subjects. In the first, flow was measured at the airway opening during Valsalva maneuvers, as described by Michaelson et al. (10). In the second, motions of upper airway walls were directly assessed during respiratory impedance measurements by use of a head plethysmograph. Larger upper airway impedance values were found during Valsalva maneuvers, corresponding to a larger upper airway resistance (Ruaw) (at 20 Hz, Ruaw = 9.1 +/- 4.7 compared with 7.0 +/- 2.1 cmH2O X 1-1 X s with the second method) and inertance (Iuaw) (Iuaw = 0.053 +/- 0.036 vs. 0.025 +/- 0.008 cmH2O X 1-1 X s2, P less than 0.05) and a lower upper airway compliance (Cuaw) (Cuaw = 0.78 +/- 0.33 vs. 1.15 +/- 0.15 ml X cmH2O-1, P less than 0.05). Active contraction of facial muscles during Valsalva maneuvers may be responsible for this finding. As a consequence, respiratory impedance values are undercorrected when using the Valsalva method, leading in normal subjects to an overestimation of respiratory compliance by 30% and an underestimation of inertance by 16% (P less than 0.05) and promoting positive frequency dependence of respiratory resistance. Substantial errors may be avoided by using a head plethysmograph, which permits measuring Zrs and Zuaw simultaneously.

Estimating central and peripheral respiratory resistance: an alternative analysis.

Pimmel et al (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45: 375--380, 1978) recently presented an analysis of the frequency dependence of respiratory resistance (Rrs) based on a simple electrical analog of the respiratory system that allows estimation of the central (Rc) and peripheral (Rp) components of Rrs. The method by which they determine these parameters from the experimental data is based on a number of unproven assumptions. Using the same electrical analog, we present an analysis that allows calculation of these parameters, as well as the corner frequency of the network (f1), without need for similar assumptions. Our technique is based on fitting the resistances (RTh) measured over a range of frequencies (f) to the exact solution of the network given by RTh = Rc + Rpf1(2)/f2 + f1(2)). Using the transformation X = 1/(f2 + f1(2), the equation becomes a linear relationship between RTh and X allowing the resistances to be determined by linear regression. Reanalysis of Pimmel et al.'s data demonstrated that the assumptions of a constant f1, and the equivalence of RTh at 0 Hz to RTh at 1 Hz in invalid under certain conditions. Thus, if one is to use the electrical analog to partition Rrs into its central and peripheral components, one should use the analytic approach suggested here that does not rely on these assumptions.