Effect of posture on pulmonary dead space in man

1959 ◽  
Vol 14 (3) ◽  
pp. 339-344 ◽  
Author(s):  
R. L. Riley ◽  
S. Permutt ◽  
S. Said ◽  
M. Godfrey ◽  
T. O. Cheng ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Upright Posture ◽  
Alveolar Dead Space ◽  
Erect Posture ◽  
Arterial Blood ◽  
Physiologic Dead Space ◽  
Expired Gas ◽  
The Difference ◽  
Normal Men

Physiologic dead space was determined in the supine and upright postures by simultaneous sampling and subsequent analysis of arterial blood and expired gas for Pco2. In seven normal men there was invariably a higher dead space in the upright than in the supine position. The difference averaged 83 ml and was statistically significant (S.E. 25 ml and P < 0.01). The ratio of dead space to tidal volume also invariably increased on assuming the upright posture. Evidence is presented for believing that most of the change in physiologic dead space resulted from a change in alveolar dead space. Estimated changes in the ratio of alveolar dead space to alveolar tidal volume suggest that approximately one seventh of the total number of alveoli became nonperfused on changing from the supine to the erect posture. These findings are consistent with bronchospirometric and hemodynamic evidence that the apex of the lung is virtually nonperfused in the resting human subject in the upright posture. Submitted on November 12, 1958

Sources of carbon dioxide in penguin air sacs

1985 ◽  
Vol 248 (6) ◽  
pp. R748-R752 ◽  
Author(s):  
F. L. Powell ◽  
S. C. Hempleman
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Respiratory Rate ◽  
Dead Space ◽  
Arterial Blood ◽  
Air Sacs ◽  
Expired Gas ◽  
The Difference

CO2 tensions in the caudal air sacs of birds cannot be quantitatively predicted by current models of avian respiration, mainly because the contribution of neopulmonic parabronchial gas exchange has not been determined. To overcome this problem we studied penguins that have purely paleopulmonic lungs. Three penguins were anesthetized, intubated, and ventilated at a constant respiratory rate and different tidal volumes (VT). PO2 and PCO2 were measured in arterial blood and end-expired, mixed-expired, interclavicular air sac, and caudal thoracic air sac gas. Interclavicular air sac and end-expired gas had similar compositions. Caudal thoracic air sac gas was intermediate in composition to end-expired and inspired gas, and its PCO2 was 1.5–3.5 times greater than the value predicted from reinhaled dead space. This difference between measured and predicted caudal thoracic air sac PCO2 increased with VT but showed no relationship to changes in dead space-to-VT ratio. The difference is not explained by stratification or diffusive gas exchange across air sac walls. The results can be explained by postulating that inspired gas passes over exchange surfaces on its path to caudal air sacs. This is unexpected in the purely paleopulmonic lungs of penguins and suggests that airflow may not be caudocranial in all paleopulmonic parabronchi.

A New Equal Area Method to Calculate and Represent Physiologic, Anatomical, and Alveolar Dead Spaces

2006 ◽  
Vol 104 (4) ◽  
pp. 696-700 ◽  
Author(s):  
Yongquan Tang ◽  
Martin J. Turner ◽  
A Barry Baker
Keyword(s):  
Carbon Dioxide ◽  
Dead Space ◽  
Graphical Method ◽  
Mean Difference ◽  
Equal Area ◽  
Area Method ◽  
Physiologic Dead Space ◽  
Anatomical Dead Space ◽  
The Mean ◽  
The Difference

Background Physiologic dead space is usually estimated by the Bohr-Enghoff equation or the Fletcher method. Alveolar dead space is calculated as the difference between anatomical dead space estimated by the Fowler equal area method and physiologic dead space. This study introduces a graphical method that uses similar principles for measuring and displaying anatomical, physiologic, and alveolar dead spaces. Methods A new graphical equal area method for estimating physiologic dead space is derived. Physiologic dead spaces of 1,200 carbon dioxide expirograms obtained from 10 ventilated patients were calculated by the Bohr-Enghoff equation, the Fletcher area method, and the new graphical equal area method and were compared by Bland-Altman analysis. Dead space was varied by varying tidal volume, end-expiratory pressure, inspiratory-to-expiratory ratio, and inspiratory hold in each patient. Results The new graphical equal area method for calculating physiologic dead space is shown analytically to be identical to the Bohr-Enghoff calculation. The mean difference (limits of agreement) between the physiologic dead spaces calculated by the new equal area method and Bohr-Enghoff equation was -0.07 ml (-1.27 to 1.13 ml). The mean difference between new equal area method and the Fletcher area method was -0.09 ml (-1.52 to 1.34 ml). Conclusions The authors' equal area method for calculating, displaying, and visualizing physiologic dead space is easy to understand and yields the same results as the classic Bohr-Enghoff equation and Fletcher area method. All three dead spaces--physiologic, anatomical, and alveolar--together with their relations to expired volume, can be displayed conveniently on the x-axis of a carbon dioxide expirogram.

Postural variations in dead space and CO2 gradients breathing air and O2

1962 ◽  
Vol 17 (3) ◽  
pp. 417-420 ◽  
Author(s):  
C. P. Larson ◽  
J. W. Severinghaus
Keyword(s):  
Dead Space ◽  
Normal Limit ◽  
Healthy Adult ◽  
Sitting Position ◽  
Alveolar Dead Space ◽  
Vascular Bed ◽  
Postural Changes ◽  
Physiologic Dead Space ◽  
Pulmonary Vascular Bed

Effects of postural changes on anatomic and physiologic dead space and arterial-alveolar CO2gradients were studied in 11 healthy, adult subjects breathing air and O2. Results indicate that, on moving from the supine to the sitting position, Vads and Vpds increased by corresponding amounts (42 and 37 ml) with no increase in alveolar dead space or volume of lung which is nonperfused. Arterial-alveolar CO2 gradients were unaffected by posture, but more than doubled with O2 breathing, suggesting that O2 may relax the pulmonary vascular bed and diminish perfusion of highest lung segments. Isoproterenol aerosol (0.5%) produced significant bronchodilatation (27 ml increase in Vads), but only small and inconsistent increases in alveolar dead space and CO2 gradients. The PDS/Vt ratio in these subjects while sitting, breathing air, averaged 31 ± 6%, which is higher than the normally accepted value of 30%. As a result, the upper normal limit for PDS/Vt has been increased to 40% in our laboratories. Submitted on January 22, 1962

Alveolar gas exchange during exercise: a single-breath analysis

1984 ◽  
Vol 57 (6) ◽  
pp. 1704-1709 ◽  
Author(s):  
C. J. Allen ◽  
N. L. Jones ◽  
K. J. Killian
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Heavy Exercise ◽  
Single Breath ◽  
Arterial Blood ◽  
Co2 Output ◽  
Dead Space Volume ◽  
Airway Dead Space ◽  
Male Subjects ◽  
Alveolar Gas Exchange

Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.

A Breath of Fresh Air—Ventilation

2011 ◽  
pp. 101-107
Author(s):  
James R. Munis
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Breathing Circuit ◽  
Alveolar Ventilation ◽  
Air Ventilation ◽  
Expired Gas ◽  
Space Ratio ◽  
Normal Ventilation

The sine qua non of ventilation is arterial carbon dioxide. If you want to know about ventilation, just check the PaCO2. If it is low or normal, ventilation is fine, regardless of any other parameter, including respiratory rate, tidal volume, or dead space ratio. However, if PaCO2 is high, then alveolar ventilation (VA) is impaired (relative to the carbon dioxide load being presented to the lungs). In a conventional breathing circuit, dead space ends at the Y-shaped junction of the inspiratory and expiratory arms of the circuit and the endotracheal tube. On the machine side of that junction, the inspiratory and expiratory limbs see only fresh inspired or expired gas, respectively, but not both. You should know 2 other things about ventilation. One is the Bohr equation, which estimates the ratio of dead space to tidal volume. The anatomic dead space is estimated as the expired volume that coincides with half maximal nitrogen content. The second thing is the effect of gravity on the distribution of ventilation within the lung.

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

Inspiratory airway CO2 loading in the pony

1984 ◽  
Vol 57 (4) ◽  
pp. 1097-1103 ◽  
Author(s):  
H. W. Shirer ◽  
J. A. Orr ◽  
J. L. Loker
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Blood Gases ◽  
Minute Volume ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Airway Dead Space ◽  
Arterial Po2 ◽  
Stimulation Of

To determine if CO2-sensitive airway receptors are important in the control of breathing, CO2 was preferentially loaded into the respiratory airways in conscious ponies. The technique involved adding small amounts of 100% CO2 to either the latter one-third or latter two-thirds of the inspiratory air in an attempt to raise CO2 concentrations in the airway dead space independent of the arterial blood. Arterial blood gas tensions (PCO2 and PO2) and pH, as well as respiratory output (minute volume, tidal volume, and respiratory rate), were measured in a series of 20 experiments on 5 awake ponies. Elevation of airway CO2 to approximately 12% by addition of CO2 to the latter portion of the inspiratory tidal volume did not alter either ventilation or arterial blood gases. When CO2 was added earlier in the inspiratory phase to fill more of the airway dead space, a small but significant increase in minute volume (2.1 l X min-1 X m-2) and tidal volume (0.1 l X m-2) was accompanied by an increase in arterial PCO2, arterial PO2, and a fall in pH (0.96 Torr, 10.5 Torr, 0.007 units, respectively). A second series of 12 experiments on 6 awake ponies using radiolabeled 14CO2 determined that the increases in breathing were minimal when compared with the large increase that occurred when these animals inhaled 6% 14CO2 (12.7 l X min-1 X m-2). Also, stimulation of systemic arterial or central nervous system chemoreceptors cannot be eliminated from the response since significant amounts of 14CO2 were present in the arterial blood when this marker gas was added to the latter two-thirds of the inspiratory tidal volume. The results, therefore, provide no evidence for CO2-sensitive airway receptors that can increase breathing when stimulated during the latter part of the inspiratory cycle.

Alveolar dead space does not affect indirect Fick cardiac output determinations

1990 ◽  
Vol 68 (2) ◽  
pp. 787-791 ◽  
Author(s):  
J. M. Badgwell ◽  
J. E. Heavner
Keyword(s):  
Nitrous Oxide ◽  
Cardiac Output ◽  
Tidal Volume ◽  
Dead Space ◽  
Glass Beads ◽  
Alveolar Dead Space ◽  
Volume Fractions ◽  
Noninvasive Cardiac Output ◽  
Wide Range ◽  
Dead Space Ventilation

We examined the influence of three variables (different breathing circuits, breath selected for analysis, and alveolar dead space ventilation) on the accuracy of noninvasive cardiac output determinations with the Fick CO2 (indirect) equation. We compared noninvasive determinations with invasive thermodilution measurements over a wide range of cardiac outputs in 17 2-mo-old pigs anesthetized with halothane and nitrous oxide and paralyzed with either pancuronium or d-tubocurare. We found that rebreathing and nonrebreathing circuits provide accurate cardiac output determinations and that the optimal breath for analysis with either the rebreathing or nonrebreathing technique appears to depend on the cardiac output. When alveolar dead space was increased by using positional changes and the intracardiac administration of glass beads, there was still a good correlation between noninvasive and invasive cardiac output determinations. We conclude that both rebreathing and nonrebreathing techniques of indirect Fick cardiac output determinations correlate well with thermodilution measures over a wide range of cardiac outputs and alveolar dead space/tidal volume fractions.

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