Breath by Breath Measurement of Anatomical Dead Space Volume: Cyclic Variations Due to Bronchomotor Activity

2015 ◽  
pp. 25-30
Author(s):  
W. K. R. Barnikol ◽  
K. Diether ◽  
E. Eissfeller
Keyword(s):  
Dead Space ◽  
Dead Space Volume ◽  
Anatomical Dead Space ◽  
Cyclic Variations ◽  
Breath Measurement ◽  
Space Volume

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.

scholarly journals MEASUREMENT OF LUNG DEAD SPACE VOLUME BY CAPNOVOLUMETRY

2020 ◽  
pp. 471-477
Author(s):  
T.A. MIROSHKINA ◽  
◽  
S.A. SHUSTOVA ◽  
Keyword(s):  
Dead Space ◽  
Alveolar Dead Space ◽  
Volumetric Capnography ◽  
Equal Area ◽  
Physiological Dead Space ◽  
Dead Space Volume ◽  
Anatomical Dead Space ◽  
The Difference ◽  
Space Volume

The article provides information on the lung dead space – a part of the respiratory volume that does not participate in gas exchange. The anatomical and alveolar dead spaces jointly together form the physiological dead space. The article describes methods for determining the volume of dead spaces using the capnovolumetry. The volume of physiological dead space is calculated using the C. Bohr equation. The volume of anatomical dead space can be determined using the equal area method proposed by W.S. Fowler. The volume of the alveolar dead space is the difference of volumes of the physiological and anatomical dead spaces. In pathology, the volume of the alveolar space and, consequently, physiological dead space can increase significantly. Determination of the volume of dead space is the significant criterion for diagnostic and predicting the outcome of a number of diseases. Keywords: Physiological dead space , anatomical dead space , alveolar dead space , capnovolumetry, volumetric capnography.

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.

Labeled carbon dioxide (C18O2): an indicator gas for phase II in expirograms

2004 ◽  
Vol 97 (5) ◽  
pp. 1755-1762 ◽  
Author(s):  
Holger Schulz ◽  
Anne Schulz ◽  
Gunter Eder ◽  
Joachim Heyder
Keyword(s):  
Carbon Dioxide ◽  
Phase Ii ◽  
Dead Space ◽  
Moment Analysis ◽  
Cumulative Distribution ◽  
Breath Holding ◽  
Power Moment ◽  
Single Breath ◽  
Dead Space Volume ◽  
Space Volume

Carbon dioxide labeled with 18O (C18O2) was used as a tracer gas for single-breath measurements in six anesthetized, mechanically ventilated beagle dogs. C18O2 is taken up quasi-instantaneously in the gas-exchanging region of the lungs but much less so in the conducting airways. Its use allows a clear separation of phase II in an expirogram even from diseased individuals and excludes the influence of alveolar concentration differences. Phase II of a C18O2 expirogram mathematically corresponds to the cumulative distribution of bronchial pathways to be traversed completely in the course of exhalation. The derivative of this cumulative distribution with respect to respired volume was submitted to a power moment analysis to characterize volumetric mean (position), standard deviation (broadness), and skewness (asymmetry) of phase II. Position is an estimate of dead space volume, whereas broadness and skewness are measures of the range and asymmetry of functional airway pathway lengths. The effects of changing ventilatory patterns and of changes in airway size (via carbachol-induced bronchoconstriction) were studied. Increasing inspiratory or expiratory flow rates or tidal volume had only minor influence on position and shape of phase II. With the introduction of a postinspiratory breath hold, phase II was continually shifted toward the airway opening (maximum 45% at 16 s) and became steeper by up to 16%, whereas skewness showed a biphasic response with a moderate decrease at short breath holding and a significant increase at longer breath holds. Stepwise bronchoconstriction decreased position up to 45 ± 2% and broadness of phase II up to 43 ± 4%, whereas skewness was increased up to twofold at high-carbachol concentrations. Under all circumstances, position of phase II by power moment analysis and dead space volume by the Fowler technique agreed closely in our healthy dogs. Overall, power moment analysis provides a more comprehensive view on phase II of single-breath expirograms than conventional dead space volume determinations and may be useful for respiratory physiology studies as well as for the study of diseased lungs.

Alveolar and Dead Space Volume Measured by Oscillations of Inspired Oxygen in Awake Adults

1997 ◽  
Vol 156 (6) ◽  
pp. 1834-1839 ◽  
Author(s):  
E. M. WILLIAMS ◽  
R. M. HAMILTON ◽  
L. SUTTON ◽  
J. P. VIALE ◽  
C. E. W. HAHN
Keyword(s):  
Dead Space ◽  
Dead Space Volume ◽  
Inspired Oxygen ◽  
Space Volume

Infusion Set Characteristics Such as Antireflux Valve and Dead-Space Volume Affect Drug Delivery

2010 ◽  
Vol 111 (6) ◽  
pp. 1427-1431 ◽  
Author(s):  
Damien Lannoy ◽  
Bertrand Décaudin ◽  
Sophie Dewulf ◽  
Nicolas Simon ◽  
Alexandre Secq ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Dead Space ◽  
Dead Space Volume ◽  
Antireflux Valve ◽  
Space Volume

Measurements of the dead space volume

1979 ◽  
Vol 47 (2) ◽  
pp. 319-324 ◽  
Author(s):  
C. J. Martin ◽  
S. Das ◽  
A. C. Young
Keyword(s):  
Phase I ◽  
Lung Volume ◽  
Dead Space ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Inert Gas ◽  
Physiological Dead Space ◽  
Dead Space Volume ◽  
Anatomical Dead Space ◽  
Frequency Changes

The “anatomical” dead space is commonly measured by sampling an inert gas (N2) and volume in the exhalation following a large breath of oxygen (VD(F)). It may also be measured from an inert gas washout (VD(O)) that describes both volume and the delivery of VD(O) throughout the expiration. VD(O) is known to increase with age and is enlarged in some obstructive syndromes. VD(O) was appreciably larger than VD(F) in our normal subjects. Both measures increased with lung volume, the increase being entirely due to an increase in the volume of phase I. Physiological dead space (VD(p)) however, did not change significantly with lung volume, showing “alveolar” dead space to diminish as a result. An increase in VD(O) occurred with increasing respiratory frequency that was explained by the increase in volume of phase I. Although an increase in VD(F) occurred with frequency, this was significantly less than that seen by VD(O), i.e., VD(F) did not see the progressive increase in phase I volume with frequency. No lung volume or frequency changes, parasympatholytic or sympathomimetic drugs, or altered patterns of breathing simulated the late delivery of dead space seen in age and some obstructive syndromes.

scholarly journals Computerized Dead-Space Volume Measurement of Face Masks Applied to Simulated Faces

2015 ◽  
Vol 60 (9) ◽  
pp. 1247-1251 ◽  
Author(s):  
I. Amirav ◽  
A. S. Luder ◽  
A. Halamish ◽  
C. Marzuk ◽  
M. Daitzchman ◽  
...  
Keyword(s):  
Dead Space ◽  
Volume Measurement ◽  
Dead Space Volume ◽  
Space Volume
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