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

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.

1960 ◽  
Vol 15 (5) ◽  
pp. 826-828 ◽  
Author(s):  
Philip Samet ◽  
Eugene M. Fierer ◽  
William H. Bernstein

The basic purpose of this investigation was to determine whether salicylates increase the sensitivity of the respiratory center to inhaled CO2. The problem was approached by noting the effect of salicylates upon ventilation and arterial blood Co2 tension and pH during inhalation of compressed air and 3% and 5% Co2 in air. These studies were performed in 30 subjects, 15 of whom ingested 2.1 gm salicylate; the other 15 ingested 3.6 gm. The results demonstrate that the ventilatory response to CO2 was increased only by the larger dose of salicylate. Variations in dead-space volume secondary to increments in tidal volume were observed. Dead-space volume increased in approximately linear fashion with increase in tidal volume. Submitted on October 28, 1959


2018 ◽  
Vol 51 (5) ◽  
pp. 1702251 ◽  
Author(s):  
Paolo Biselli ◽  
Kathrin Fricke ◽  
Ludger Grote ◽  
Andrew T. Braun ◽  
Jason Kirkness ◽  
...  

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.


1979 ◽  
Vol 47 (2) ◽  
pp. 319-324 ◽  
Author(s):  
C. J. Martin ◽  
S. Das ◽  
A. C. Young

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.


Burns ◽  
1995 ◽  
Vol 21 (5) ◽  
pp. 337-339 ◽  
Author(s):  
R.P. Mlcak ◽  
M.H. Desai ◽  
E. Robinson ◽  
R.L. McCauley ◽  
J. Richardson ◽  
...  

1984 ◽  
Vol 67 (5) ◽  
pp. 493-497 ◽  
Author(s):  
George Tatsis ◽  
Keith Horsfield ◽  
Gordon Cumming

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.


1978 ◽  
Vol 55 (1) ◽  
pp. 125-128 ◽  
Author(s):  
E. A. Harris ◽  
Eve R. Seelye ◽  
R.M.L. Whitlock

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.


Author(s):  
Stylianos Michaelides ◽  
George Bablekos ◽  
George Ionas ◽  
Dimitrios Papadopoulos ◽  
Petros Bakakos ◽  
...  

1976 ◽  
Vol 4 (3) ◽  
pp. 203-204 ◽  
Author(s):  
A. Morton ◽  
P. Mahoney ◽  
P. Hansen ◽  
M. McBride ◽  
A. B. Baker

Many studies have shown that after uncomplicated abdominal surgery arterial hypoxaemia frequently occurs because of regional underventilation in relation to perfusion. This paper produces evidence that shows a small increase in physiological dead space to tidal volume ratio following general anaesthesia for abdominal surgery. This increase is thought to be due to tachypnoea rather than alteration in pulmonary blood flow.


2013 ◽  
Vol 115 (9) ◽  
pp. 1268-1274 ◽  
Author(s):  
Constanze Dassow ◽  
David Schwenninger ◽  
Hanna Runck ◽  
Josef Guttmann

Volumetric capnography is a standard method to determine pulmonary dead space. Hereby, measured carbon dioxide (CO2) in exhaled gas volume is analyzed using the single-breath diagram for CO2. Unfortunately, most existing CO2 sensors do not work with the low tidal volumes found in small animals. Therefore, in this study, we developed a new mainstream capnograph designed for the utilization in small animals like rats. The sensor was used for determination of dead space volume in healthy and surfactant-depleted rats ( n = 62) during spontaneous breathing (SB) and mechanical ventilation (MV) at three different tidal volumes: 5, 8, and 11 ml/kg. Absolute dead space and wasted ventilation (dead space volume in relation to tidal volume) were determined over a period of 1 h. Dead space increase and reversibility of the increase was investigated during MV with different tidal volumes and during SB. During SB, the dead space volume was 0.21 ± 0.14 ml and increased significantly at MV to 0.39 ± 0.03 ml at a tidal volume of 5 ml/kg and to 0.6 ± 0.08 ml at a tidal volume of 8 and 11 ml/kg. Dead space and wasted ventilation during MV increased with tidal volume. This increase was mostly reversible by switching back to SB. Surfactant depletion had no further influence on the dead space increase during MV, but impaired the reversibility of the dead space increase.


1963 ◽  
Vol 18 (2) ◽  
pp. 284-288 ◽  
Author(s):  
June M. Raine ◽  
J. M. Bishop

Alveolar-arterial difference in oxygen tension (A-aD) and physiological dead space/tidal volume ratio (Vd/Vt) were measured in normal subjects aged 17–66 years, in the supine and sitting postures. Paoo2 decreased and A-aD increased with age. A-aD was not affected by posture, but increased with Paoo2. Regression equations relating Paoo2 and A-aD to age, and Paoo2 were calculated. Vd/Vt increased with age in the supine position, but when sitting the increase with age was small and barely significant. Consequently, although Vd/Vt was greater when sitting than when supine in young subjects, there was no such difference in the older subjects. Possible reasons for the effect of age and body position are discussed. Submitted on August 6, 1962


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