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 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.

Prediction of the Physiological Dead-Space in Resting Normal Subjects

1973 ◽  
Vol 45 (3) ◽  
pp. 375-386 ◽  
Author(s):  
E. A. Harris ◽  
Mary E. Hunter ◽  
Eve R. Seelye ◽  
Margaret Vedder ◽  
R. M. L. Whitlock
Keyword(s):  
Tidal Volume ◽  
Multiple Regression ◽  
Dead Space ◽  
Predictive Accuracy ◽  
Volume Ratio ◽  
Normal Subjects ◽  
Physiological Dead Space ◽  
Dead Space Volume ◽  
Made In ◽  
Space Volume

1. Two-hundred and forty duplicate estimations of physiological dead-space volume (VD) were made in forty-eight healthy subjects (twenty-four men and twenty-four women) aged from 20 to 74 years, to assess the predictive accuracy of various standards. 2. The VD/VT (physiological dead-space volume/tidal volume) ratio standard was least precise, but could be improved by allowing for sex and age. 3. The best prediction could be made by multiple regression of VD on age, height, tidal volume (VT) and the reciprocal of respiratory frequency (f), which gave an estimate with a standard deviation of 24·7 ml. 4. Theoretical and practical arguments favour the abandonment of the VD/VT ratio standard. Simple regression of VD on VT also is unsatisfactory, giving a much less precise estimate of VD than a multiple regression on VT and other variables.

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.

Effects of chest compression on reflex ventilatory drive and pulmonary function

1962 ◽  
Vol 17 (4) ◽  
pp. 701-705 ◽  
Author(s):  
Malcolm B. McIlroy ◽  
John Butler ◽  
Theodore N. Finley
Keyword(s):  
Chest Compression ◽  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Lung Compliance ◽  
External Compression ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Ventilatory Drive ◽  
Anatomical Dead Space

External compression of the chest sufficient to reduce the lung volume (FRC) by 1 liter in eight normal subjects interfered with the mechanical function of the lungs. We have confirmed the findings of Caro et al. ( J. Clin. Invest. 39: 573, 1960), who showed a decrease in lung compliance and an increase in respiratory rate. Neither returned to normal when the compressing force was removed, and it was not until the subject took a deep breath that the lungs returned to their control state. We also found a reduction in anatomical dead space and alveolar hyperventilation. Arterial blood gas tensions showed evidence of complex ventilation-perfusion abnormalities, which could not be explained by any single factor. We think the hyperventilation associated with chest compression is reflex in origin and related to a decrease in lung volume rather than to any change in transpulmonary pressure. Submitted on January 4, 1962

Physiological dead space and effective parabronchial ventilation in ducks

1986 ◽  
Vol 60 (1) ◽  
pp. 85-91 ◽  
Author(s):  
R. H. Hastings ◽  
F. L. Powell
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Current Model ◽  
Arterial Occlusion ◽  
Physiological Dead Space ◽  
Pekin Ducks ◽  
Dead Space Volume ◽  
Effective Ventilation ◽  
Pulmonary Arterial ◽  
Cross Current

Gas exchange in avian lungs is described by a cross-current model that has several differences from the alevolar model of mammalian gas exchange [e.g., end-expired PCO2 greater than arterial PCO2 (PaCO2)]. Consequently the methods available for estimating effective ventilation and physiological dead space (VDphys) in alveolar lungs are not suitable for an analysis of gas exchange in birds. We tested a method for measuring VDphys in birds that is functionally equivalent to the conventional alveolar VDphys. A cross-current O2-CO2 diagram was used to define the ideal expired point (PEi) and VDphys was calculated as from the equation, VDphys = [(PEiCO2--PECO2)/PEiCO2]. VT, where VT is tidal volume. In seven Pekin ducks VDphys was 13.8 ml greater than anatomic dead space and measured changes in the instrument dead space volume. VDphys also reflected changes in ventilation-perfusion inequality induced by temporary unilateral pulmonary arterial occlusion. Bohr dead space, calculated by substituting end-expired PCO2 for PEiCO2, was insensitive to such inhomogeneity. Enghoff dead space, calculated by substituting PaCO2 for PEiCO2, is theoretically incorrect for cross-current gas exchange and was often less than anatomic dead space. We conclude that VDphys is a useful index of avian gas exchange and propose a standard definition for effective parabronchial ventilation (VP) analogous to alveolar ventilation (i.e., VP = VE--VDphys, where VE is total ventilation).

Distribution of Dead Space Volume in the Human Lung

1984 ◽  
Vol 67 (5) ◽  
pp. 493-497 ◽  
Author(s):  
George Tatsis ◽  
Keith Horsfield ◽  
Gordon Cumming
Keyword(s):  
Dead Space ◽  
Distribution Curve ◽  
Normal Subjects ◽  
Bronchial Tree ◽  
Data Smoothing ◽  
Dead Space Volume ◽  
Data Points ◽  
Stationary Interface ◽  
The Right ◽  
Space Volume

1. The first four breaths from a multi-breath nitrogen wash-out have been analysed in 20 normal subjects by differentiation and data smoothing of phase II of the expired concentrations of nitrogen and carbon dioxide. 2. This procedure yields a distribution curve which is skewed to the right, the mode of which represents the usual value of dead space. The minimum and maximum values were found by excluding 2.5% of data points at each end of the distribution. 3. The values of minimum, mode and maximum in men were 67.6, 147 and 300 ml. For women the values were 55.4, 109 and 235 ml. 4. It is suggested that this distribution reflects the asymmetrical nature of the bronchial tree and comparison with anatomical data suggests that anatomy is the principal determinant of the distribution of dead space. 5. The contribution made by the spread of the stationary interface within individual bronchioles is evident but small.

Revised Standards for Normal Resting Dead-Space Volume and Venous Admixture in Men and Women

1978 ◽  
Vol 55 (1) ◽  
pp. 125-128 ◽  
Author(s):  
E. A. Harris ◽  
Eve R. Seelye ◽  
R.M.L. Whitlock
Keyword(s):  
Oxygen Tension ◽  
Dead Space ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Venous Admixture ◽  
Men And Women ◽  
Physiological Dead Space ◽  
Dead Space Volume ◽  
Previous Series ◽  
Space Volume

1. Data have been combined from three previous series to provide revised standards for the prediction of physiological dead-space volume (VD), arterial oxygen tension (Pa,o2), alveolar-to-arterial oxygen-tension difference (Pa,o2 - Pa,o2) and venous admixture fraction (Q̇va/Q̇t) in the sitting position. 2. These standards, based on measurements in 96 healthy men and women aged from 20 to 74 years, largely confirm conclusions drawn from the first series of 48 subjects. 3. VD is best predicted on age, height, tidal volume and the reciprocal of respiratory frequency. Pa,o2, (Pa,o2 - Pa,o2) and Q̇va/Q̇t are adequately predicted on age alone.

Correction of inert gas washin or washout for gas solubility in blood

1988 ◽  
Vol 65 (4) ◽  
pp. 1598-1603 ◽  
Author(s):  
E. A. Harris ◽  
R. M. Whitlock
Keyword(s):  
Lung Volume ◽  
Washout Period ◽  
Dead Space ◽  
Inert Gas ◽  
Gas Solubility ◽  
Ventilation Distribution ◽  
Ventilation And Perfusion

We show that when an inert gas is washed into the lungs its retention in the blood during any one breath is approximately proportional to its solubility. This relationship makes possible the correction of washin or washout data for blood uptake or release, provided that two gases of different solubility are used simultaneously. The method automatically allows for the characteristics of an individual washin or washout and for the occurrence of recirculation within a fairly short washin or washout period. It has been tested in models with nonuniform ventilation and perfusion and closely approximates the behavior of a truly insoluble gas. In the derived ventilation distribution, gas solubility appears as ventilation to units of low turnover. In the case of N2 this effect is small but causes appreciable overestimation of lung volume. The recovered dead space and main alveolar distribution are insignificantly affected.

Respiratory dead space and arterial to end-tidal CO2 tension difference in anesthetized man

1960 ◽  
Vol 15 (3) ◽  
pp. 383-389 ◽  
Author(s):  
J. F. Nunn ◽  
D. W. Hill
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Artificial Respiration ◽  
Physiological Dead Space ◽  
Anatomical Dead Space ◽  
The Subject ◽  
The Mean ◽  
The Difference ◽  
End Tidal ◽  
End Tidal Co2

Observations were made during both spontaneous and artificial respiration on 12 fit patients anesthetized for routine surgical procedures. Above a tidal volume of 350 ml (BTPS), the anatomical dead space was close to the predicted normal value for the subject. Below 350 ml, it was reduced in proportion to the tidal volume. The physiological dead space (below the carina) approximated to 0.3 times the tidal volume for tidal volumes between 163 and 652 ml (BTPS). Throughout the range the physiological dead space was considerably in excess of the anatomical dead space measured simultaneously. The difference (alveolar dead space) varied from 15 to 231 ml, being roughly proportional to the tidal volume. The mean arterial to end-tidal CO2 tension difference was 4.6 (S.D. ±2.5) mm Hg and not related to tidal volume or arterial CO2 tension. None of the findings appeared to depend on whether the respiration was spontaneous or artificial. Submitted on September 25, 1959

scholarly journals End-tidal to arterial PCO2 ratio: a bedside meter of the overall gas exchanger performance

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Matteo Bonifazi ◽  
Federica Romitti ◽  
Mattia Busana ◽  
Maria Michela Palumbo ◽  
Irene Steinberg ◽  
...  
Keyword(s):  
Ct Scan ◽  
Dead Space ◽  
Progressive Increase ◽  
Venous Admixture ◽  
Perfect Gas ◽  
Alveolar Dead Space ◽  
Physiological Dead Space ◽  
End Tidal ◽  
The Right ◽  
The Ideal

Abstract Background The physiological dead space is a strong indicator of severity and outcome of acute respiratory distress syndrome (ARDS). The “ideal” alveolar PCO2, in equilibrium with pulmonary capillary PCO2, is a central concept in the physiological dead space measurement. As it cannot be measured, it is surrogated by arterial PCO2 which, unfortunately, may be far higher than ideal alveolar PCO2, when the right-to-left venous admixture is present. The “ideal” alveolar PCO2 equals the end-tidal PCO2 (PETCO2) only in absence of alveolar dead space. Therefore, in the perfect gas exchanger (alveolar dead space = 0, venous admixture = 0), the PETCO2/PaCO2 is 1, as PETCO2, PACO2 and PaCO2 are equal. Our aim is to investigate if and at which extent the PETCO2/PaCO2, a comprehensive meter of the “gas exchanger” performance, is related to the anatomo physiological characteristics in ARDS. Results We retrospectively studied 200 patients with ARDS. The source was a database in which we collected since 2003 all the patients enrolled in different CT scan studies. The PETCO2/PaCO2, measured at 5 cmH2O airway pressure, significantly decreased from mild to mild–moderate moderate–severe and severe ARDS. The overall populations was divided into four groups (~ 50 patients each) according to the quartiles of the PETCO2/PaCO2 (lowest ratio, the worst = group 1, highest ratio, the best = group 4). The progressive increase PETCO2/PaCO2 from quartile 1 to 4 (i.e., the progressive approach to the “perfect” gas exchanger value of 1.0) was associated with a significant decrease of non-aerated tissue, inohomogeneity index and increase of well-aerated tissue. The respiratory system elastance significantly improved from quartile 1 to 4, as well as the PaO2/FiO2 and PaCO2. The improvement of PETCO2/PaCO2 was also associated with a significant decrease of physiological dead space and venous admixture. When PEEP was increased from 5 to 15 cmH2O, the greatest improvement of non-aerated tissue, PaO2 and venous admixture were observed in quartile 1 of PETCO2/PaCO2 and the worst deterioration of dead space in quartile 4. Conclusion The ratio PETCO2/PaCO2 is highly correlated with CT scan, physiological and clinical variables. It appears as an excellent measure of the overall “gas exchanger” status.

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