scholarly journals A model-based approach to interpreting multibreath nitrogen washout data

2018 ◽  
Vol 124 (5) ◽  
pp. 1155-1163 ◽  
Author(s):  
Jason H. T. Bates ◽  
Ubong Peters
Keyword(s):  
Functional Residual Capacity ◽  
Dead Space ◽  
Test Subject ◽  
Phase Iii ◽  
Nitrogen Washout ◽  
Model Based ◽  
Dead Space Volume ◽  
Residual Capacity ◽  
The Subject ◽  
Space Volume

The multibreath nitrogen washout (MBNW) test, as it is currently practiced, provides parameters of potential physiological significance that are derived from the relationship between the volume-normalized Phase III slope of the exhaled nitrogen fraction ([Formula: see text]) vs. the cumulative change in lung volume (V). Reliable evaluation of these parameters requires, however, that the subject breathe deeply and evenly, so that Phase III can be clearly identified in every breath. This places a burden on the test subject that may prove troublesome for young children and those with lung disease. Furthermore, the determination of the slope of Phase III requires that a decision be made as to when Phase II ends and Phase III begins. In an attempt to get around these methodological limitations, we develop here an alternative method of analysis based on a multicompartment model of the lung that accounts for the entire exhaled nitrogen profile, including Phases I, II, and III. Fitting this model to [Formula: see text] and V measured during a MBNW provides an estimate of the coefficient of variation of specific ventilation, as well as functional residual capacity, dead space volume, and a parameter that reflects structural asymmetry at the acinar level in the lung. In the present study, we demonstrate the potential utility of this modeling approach to the analysis of MBNW data. NEW & NOTEWORTHY The multibreath nitrogen washout test potentially provides important physiological information about regional ventilation heterogeneity throughout the lung, but the conventional analysis requires the subject to breathe deeply and regularly, which is not always practical. We have developed a model-based analysis method that avoids this limitation and that also provides measures of functional residual capacity and dead space volume, thereby expanding the applicability and scope of the method.

scholarly journals Physiological signature of late-onset nonallergic asthma of obesity

2020 ◽  
Vol 6 (3) ◽  
pp. 00049-2020
Author(s):  
Anne E. Dixon ◽  
Ubong Peters ◽  
Ryan Walsh ◽  
Nirav Daphtary ◽  
Erick S. MacLean ◽  
...  
Keyword(s):  
Forced Vital Capacity ◽  
Vital Capacity ◽  
Late Onset ◽  
Nitrogen Washout ◽  
Dead Space Volume ◽  
Residual Capacity ◽  
Obese Subjects ◽  
Obese Control ◽  
Asthma Group ◽  
Space Volume

IntroductionObesity can lead to a late-onset nonallergic (LONA) form of asthma for reasons that are not understood. We sought to determine whether this form of asthma is characterised by any unique physiological features.MethodsSpirometry, body plethysmography, multiple breath nitrogen washout (MBNW) and methacholine challenge were performed in four subject groups: Lean Control (n=11), Lean Asthma (n=11), Obese Control (n=11) and LONA Obese Asthma (n=10). The MBNW data were fitted with a novel computational model that estimates functional residual capacity (FRC), dead space volume (VD), the coefficient of variation of regional specific ventilation (CV,V′E) and a measure of structural asymmetry at the level of the acinus (sacin).ResultsBody mass index and waist circumference values were similar in both obese groups, and significantly greater than in lean asthmatic individuals and controls. Forced vital capacity was significantly lower in the LONA Asthma group compared with the other groups (p<0.001). Both asthma groups exhibited similar hyperresponsiveness to methacholine. FRC was reduced in the Obese LONA Asthma group as measured by MBNW, but not in obese controls, whereas FRC was reduced in both obese groups as measured by plethysmography. VD, CV,V′E and sacin were not different between groups.ConclusionsChronic lung compression characterises all obese subjects, as reflected by reduced plethysmographic FRC. Obese LONA asthma is characterised by a reduced ability to recruit closed lung units, as seen by reduced MBNW FRC, and an increased tendency for airway closure as seen by a reduced forced vital capacity.

Dead Space Volume in N95 Masks

2020 ◽  
Author(s):  
Santiago C. Arce ◽  
Fernando Chiodetti ◽  
Eduardo L. De Vito
Keyword(s):  
Dead Space ◽  
Dead Space Volume ◽  
Space Volume

High-frequency ventilation

1984 ◽  
Vol 64 (2) ◽  
pp. 505-543 ◽  
Author(s):  
J. M. Drazen ◽  
R. D. Kamm ◽  
A. S. Slutsky
Keyword(s):  
Experimental Data ◽  
Gas Exchange ◽  
Dead Space ◽  
Gas Transport ◽  
Physical Models ◽  
High Frequency Ventilation ◽  
General Description ◽  
Wide Range ◽  
Dead Space Volume ◽  
Space Volume

Complete physiological understanding of HFV requires knowledge of four general classes of information: 1) the distribution of airflow within the lung over a wide range of frequencies and VT (sect. IVA), 2) an understanding of the basic mechanisms whereby the local airflows lead to gas transport (sect. IVB), 3) a computational or theoretical model in which transport mechanisms are cast in such a form that they can be used to predict overall gas transport rates (sect. IVC), and 4) an experimental data base (sect. VI) that can be compared to model predictions. When compared with available experimental data, it becomes clear that none of the proposed models adequately describes all the experimental findings. Although the model of Kamm et al. is the only one capable of simulating the transition from small to large VT (as compared to dead-space volume), it fails to predict the gas transport observed experimentally with VT less than equipment dead space. The Fredberg model is not capable of predicting the observed tendency for VT to be a more important determinant of gas exchange than is frequency. The remaining models predict a greater influence of VT than frequency on gas transport (consistent with experimental observations) but in their current form cannot simulate the additional gas exchange associated with VT in excess of the dead-space volume nor the decreased efficacy of HFV above certain critical frequencies observed in both animals and humans. Thus all of these models are probably inadequate in detail. One important aspect of these various models is that some are based on transport experiments done in appropriately scaled physical models, whereas others are entirely theoretical. The experimental models are probably most useful in the prediction of pulmonary gas transport rates, whereas the physical models are of greater value in identifying the specific transport mechanism(s) responsible for gas exchange. However, both classes require a knowledge of the factors governing the distribution of airflow under the circumstances of study as well as requiring detail about lung anatomy and airway physical properties. Only when such factors are fully understood and incorporated into a general description of gas exchange by HFV will it be possible to predict or explain all experimental or clinical findings.

Gas transport during high-frequency ventilation

1983 ◽  
Vol 55 (2) ◽  
pp. 472-478 ◽  
Author(s):  
V. Brusasco ◽  
T. J. Knopp ◽  
K. Rehder
Keyword(s):  
Stroke Volume ◽  
Dead Space ◽  
High Frequency ◽  
Oscillation Frequency ◽  
High Frequency Ventilation ◽  
Dead Space Volume ◽  
Entire Lung ◽  
Frequency Ventilation ◽  
Gas Volume ◽  
Space Volume

During high-frequency small-volume ventilation (HFV), the transport rate of gas from the mouth to a lung region is a function of two conductances (conductance is the transfer rate of a gas divided by its partial pressure difference): regional longitudinal gas conductance along the airways (Grlongi) and gas conductance between lung regions (Ginter). Grlongi per unit regional lung (gas) volume [Grlongi/(Vr beta g)] was determined during HFV in 11 anesthetized paralyzed dogs lying supine. The distribution of Grlongi/(Vr beta g) was nearly uniform during HFV when stroke volumes were less than approximately two-thirds of the Fowler dead-space volume. By contrast, the distribution of Grlongi/(Vr beta g) was nonuniform when the stroke volume exceeded approximately two-thirds of the Fowler dead-space volume and the oscillation frequency was 5 Hz. Gas conductance along the airways per unit lung gas volume [average Glongi/(V beta g)], for the entire lung, increased with stroke volume at all frequencies, but for a given product of oscillation frequency and stroke volume, the average Glongi/(V beta g) was greater when stroke volume was large and oscillation frequency was low. The average Glongi/(V beta g) increased with frequency up to a maximal value; the frequency at which the maximum occurred depended on the kinematic viscosity of the inspired gas mixture.

scholarly journals Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls

2018 ◽  
Vol 51 (5) ◽  
pp. 1702251 ◽  
Author(s):  
Paolo Biselli ◽  
Kathrin Fricke ◽  
Ludger Grote ◽  
Andrew T. Braun ◽  
Jason Kirkness ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Dead Space ◽  
Minute Ventilation ◽  
High Flow ◽  
Physiological Dead Space ◽  
Copd Patients ◽  
Dead Space Volume ◽  
Anatomical Dead Space ◽  
Dead Space Ventilation ◽  
Space Volume

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min−1) intermittently for periods of 5–10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min−1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min−1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.

Mode shift of an inhaled aerosol bolus is correlated with flow sequencing in the human lung

2002 ◽  
Vol 92 (3) ◽  
pp. 1232-1238 ◽  
Author(s):  
Christopher N. Mills ◽  
Chantal Darquenne ◽  
G. Kim Prisk
Keyword(s):  
Vital Capacity ◽  
Normal Subjects ◽  
Phase Iii ◽  
Mode Shift ◽  
Nitrogen Washout ◽  
Single Breath ◽  
Posture Change ◽  
Supine Posture ◽  
Residual Capacity ◽  
Phase Iii Slope

We studied the effects on aerosol bolus inhalations of small changes in convective inhomogeneity induced by posture change from upright to supine in nine normal subjects. Vital capacity single-breath nitrogen washout tests were used to determine ventilatory inhomogeneity change between postures. Relative to upright, supine phase III slope was increased 33 ± 11% (mean ± SE, P < 0.05) and phase IV height increased 25 ± 11% ( P < 0.05), consistent with an increase in convective inhomogeneity likely due to increases in flow sequencing. Subjects also performed 0.5-μm-particle bolus inhalations to penetration volumes (Vp) between 150 and 1,200 ml during a standardized inhalation from residual volume to 1 liter above upright functional residual capacity. Mode shift (MS) in supine posture was more mouthward than upright at all Vp, changing by 11.6 ml at Vp = 150 ml ( P < 0.05) and 38.4 ml at Vp = 1,200 ml ( P < 0.05). MS and phase III slope changes correlated positively at deeper Vp. Deposition did not change at any Vp, suggesting that deposition did not cause the MS change. We propose that the MS change results from increased sequencing in supine vs. upright posture.

Relation between anatomic respiratory dead space and body size and lung volume

1963 ◽  
Vol 18 (3) ◽  
pp. 519-522 ◽  
Author(s):  
M. C. Hart ◽  
M. M. Orzalesi ◽  
C. D. Cook
Keyword(s):  
Surface Area ◽  
Functional Residual Capacity ◽  
Dead Space ◽  
Technical Assistance ◽  
Newborn Infants ◽  
Early Period ◽  
Somatic Growth ◽  
Normal Subjects ◽  
Significant Difference ◽  
Residual Capacity

The respiratory anatomic dead space has been measured by the single breath nitrogen washout method of Fowler in 73 normal subjects ranging from 4 to 42 years of age. The volume of the anatomic dead space correlated closely with height (Vd (ml) = 7.585 x Ht (cm)2.363 x 10-4·ɣ = .917), but also with body weight, surface area, and functional residual capacity. When compared on the basis of any of these parameters there was no significant difference between the anatomic dead space values for males and females. Comparisons with available data for newborn infants suggest that the value of the anatomic dead space has a relatively constant relation to height from birth to adulthood. Dead space appears to increase more rapidly than weight, surface area, and functional residual capacity during, at least, the early period of somatic growth. Note: (With the Technical Assistance of J. H. Shaw) Submitted on October 25, 1962

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