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).

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.

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.

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.

Physiological dead space during high-frequency ventilation in dogs

1984 ◽  
Vol 57 (3) ◽  
pp. 881-887 ◽  
Author(s):  
G. G. Weinmann ◽  
W. Mitzner ◽  
S. Permutt
Keyword(s):  
Gas Exchange ◽  
Tidal Volume ◽  
Dead Space ◽  
High Frequency ◽  
Minute Ventilation ◽  
Alveolar Ventilation ◽  
High Frequency Ventilation ◽  
Physiological Dead Space ◽  
Frequency Ventilation ◽  
Normal Ventilation

Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. We found that VD was relatively constant at tidal volumes associated with normal ventilation (7–15 ml/kg) but fell sharply as VT was reduced further to tidal volumes associated with HFV (less than 7 ml/kg). The frequency required to maintain constant alveolar ventilation increased slowly as tidal volume was decreased from 15 to 7 ml/kg but rose sharply with attendant rapid increases in minute ventilation as tidal volumes were decreased to less than 7 ml/kg. At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.

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.

Pulmonary gas exchange and its determinants during sustained microgravity on Spacelabs SLS-1 and SLS-2

1995 ◽  
Vol 79 (4) ◽  
pp. 1290-1298 ◽  
Author(s):  
G. K. Prisk ◽  
A. R. Elliott ◽  
H. J. Guy ◽  
J. M. Kosonen ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pulmonary Gas Exchange ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

Lung cytokinetics after exposure to hypobaria and/or hypoxia and undernutrition in growing rats

1995 ◽  
Vol 79 (4) ◽  
pp. 1299-1309 ◽  
Author(s):  
H. S. Sekhon ◽  
W. M. Thurlbeck
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Normal Gravity ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

Spatial pattern of ventilation-perfusion mismatch following acute pulmonary thromboembolism in pigs

2005 ◽  
Vol 98 (5) ◽  
pp. 1862-1868 ◽  
Author(s):  
John Y. C. Tsang ◽  
Wayne J. E. Lamm ◽  
Ian R. Starr ◽  
Michael P. Hlastala
Keyword(s):  
Dead Space ◽  
Pulmonary Thromboembolism ◽  
Venous Catheter ◽  
Physiological Dead Space ◽  
Mean Pulmonary Arterial Pressure ◽  
Blood Clots ◽  
Acute Pulmonary Thromboembolism ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Vascular Obstruction

We studied the spatial distribution of the abnormal ventilation-perfusion (V̇a/Q̇) units in a porcine model of acute pulmonary thromboembolism (APTE), using the fluorescent microsphere (FMS) technique. Four piglets (∼22 kg) were anesthetized and ventilated with room air in the prone position. Each received ∼20 g of preformed blood clots at time t = 0 min via a large-bore central venous catheter, until the mean pulmonary arterial pressure reached 2.5 times baseline. The distributions of regional V̇a and blood flow (Q̇) at five time points ( t = −30, −5, 30, 60, 120 min) were mapped by FMS of 10 distinct colors, i.e., aerosolization of 1-μm FMS for labeling V̇a and intravenous injection of 15-μm FMS for labeling Q̇. Our results showed that, at t = 30 min following APTE, mean V̇a/Q̇ (V̇a/Q̇ = 2.48 ± 1.12) and V̇a/Q̇ heterogeneity (log SD V̇a/Q̇ = 1.76 ± 0.23) were significantly increased. There were also significant increases in physiological dead space (11.2 ± 12.7% at 60 min), but the shunt fraction (V̇a/Q̇ = 0) remained minimal. Cluster analyses showed that the low V̇a/Q̇ units were mainly seen in the least embolized regions, whereas the high V̇a/Q̇ units and dead space were found in the peripheral subpleural regions distal to the clots. At 60 and 120 min, there were modest recoveries in the hemodynamics and gas exchange toward baseline. Redistribution pattern was mostly seen in regional Q̇, whereas V̇a remained relatively unchanged. We concluded that the hypoxemia seen after APTE could be explained by the mechanical diversion of Q̇ to the less embolized regions because of the vascular obstruction by clots elsewhere. These low V̇a/Q̇ units created by high flow, rather than low V̇a, accounted for most of the resultant hypoxemia.

Gas Exchange during Exercise in Healthy People: I. the Physiological Dead-Space Volume

1976 ◽  
Vol 51 (4) ◽  
pp. 323-333 ◽  
Author(s):  
Christine A. Bradley ◽  
E. A. Harris ◽  
Eve R. Seelye ◽  
R. M. L. Whitlock
Keyword(s):  
Carbon Dioxide ◽  
Dead Space ◽  
Confidence Limit ◽  
Carbon Dioxide Tension ◽  
Physiological Dead Space ◽  
Carbon Dioxide Output ◽  
Pulmonary Capillary ◽  
Dead Space Volume ◽  
Capillary Temperature ◽  
Space Volume

1. Physiological dead-space volume (VD) was measured in twenty-four healthy men and women aged from 20 to 71 years, at rest and at two rates of work on a treadmill, whilst breathing air and breathing oxygen. 2. The effect of correction of arterial carbon dioxide tension (Pa,co2) to pulmonary capillary temperature on the resulting value for VD was investigated. We find that the effect is substantial and that a correction should be made. 3. Equations have been derived for the prediction of normal VD during exercise. The best prediction was given by a regression on height, age, carbon dioxide output, ventilation and respiratory frequency, with an upper 95% confidence limit of +81 ml.

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.

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