Functional Reduction of Anatomical Dead Space in the Management of Acute Alveolar Hypoventilation

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.

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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

European Respiratory Journal ◽

10.1183/13993003.02251-2017 ◽

2018 ◽

Vol 51 (5) ◽

pp. 1702251 ◽

Cited By ~ 19

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.

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Uneven gas mixing during rebreathing assessed by simultaneously measuring dead space

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.4.930 ◽

1982 ◽

Vol 53 (4) ◽

pp. 930-939 ◽

Cited By ~ 11

Author(s):

M. F. Petrini ◽

B. T. Peterson ◽

R. W. Hyde ◽

V. Lam ◽

M. J. Utell ◽

...

Keyword(s):

Dead Space ◽

Sulfur Hexafluoride ◽

Breath Holding ◽

Gas Mixing ◽

Pulmonary Tissue ◽

Pulmonary Capillary Blood Flow ◽

Pulmonary Capillary Blood ◽

Anatomical Dead Space ◽

The Difference ◽

Uneven Ventilation

To evaluate the rate of gas mixing in human lungs during rebreathing maneuvers used to measure pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc), we devised a method to determine the dead space during rebreathing (VRD). Required measurements are initial concentration of a foreign inert insoluble gas in the rebreathing bag, first mixed expired concentration, equilibrated concentration, volume inspired, and volume of the first expired breath. In subjects breathing rapidly at 30 breaths/min with inspired volumes in excess of 2 liters, VRD had values three or more times greater than the predicted anatomical dead space (VD). Breath holding after the first inspiration progressively diminished VRD so that after 10–15 s, it approximately equaled predicted VD. VRD measured with helium was smaller than VRD measured with sulfur hexafluoride. The reported degree of uneven ventilation from gravitational forces in normal humans can account for only about one-third of the difference between VRD and VD. These findings support the concept that mixing by diffusion between peripheral parallel airways is incomplete at normal breathing rates in humans and can result in errors as high as 25% in Vt and Qc.

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Anatomical dead space and airway resistance after glycopyrrolate or atropine premedication

Canadian Anaesthetists Society journal / Journal de la Société canadienne des anesthésistes ◽

10.1007/bf03007290 ◽

1981 ◽

Vol 28 (1) ◽

pp. 51-54 ◽

Cited By ~ 2

Author(s):

Alexander W. Gotta ◽

Cole Ray ◽

Colleen A. Sullivan ◽

Paul L. Goldiner

Keyword(s):

Dead Space ◽

Airway Resistance ◽

Anatomical Dead Space

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Effects of forward acceleration on anatomical dead space

Journal of Applied Physiology ◽

10.1152/jappl.1965.20.6.1205 ◽

1965 ◽

Vol 20 (6) ◽

pp. 1205-1210 ◽

Cited By ~ 1

Author(s):

Charles Jacquemin ◽

Jean Demange ◽

Jean Timbal ◽

Pierre Varene

Keyword(s):

Mass Spectrometer ◽

Dead Space ◽

Human Subjects ◽

Alveolar Plateau ◽

Anatomical Dead Space ◽

Ventilation Perfusion Ratio

The effects of transverse acceleration (1–5 G) on anatomical dead space have been studied on four human subjects. Instantaneous analysis of expired gases has been done by mass spectrometer. Half deflection between inspired gases and alveolar plateau levels is considered as the signal for the end of dead-space sweep. It is confirmed that no obstructive syndrome occurs during these accelerations. The airway size is not reduced; on the contrary, the anatomical dead space increases with the level of accelerations. Furthermore, a decreasing slope of the CO2 alveolar plateau has been noted on two subjects. These facts can be interpreted admitting a passive displacement of the pulmonary blood mass under influence of forward acceleration and the adjustment of ventilation to perfusion. transverse acceleration; mass spectrometer; ventilation-perfusion ratio Submitted on February 8, 1965

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Anatomical Dead Space and Airway Resistance After Glycopyrrolate or Atropine Premedication

Survey of Anesthesiology ◽

10.1097/00132586-198112000-00013 ◽

1981 ◽

Vol 25 (6) ◽

pp. 363

Author(s):

A. W. GOTTA ◽

C. RAY ◽

C. A. SULLIVAN ◽

P. L. GOLDINER

Keyword(s):

Dead Space ◽

Airway Resistance ◽

Anatomical Dead Space

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Measurements of the dead space volume

Journal of Applied Physiology ◽

10.1152/jappl.1979.47.2.319 ◽

1979 ◽

Vol 47 (2) ◽

pp. 319-324 ◽

Cited By ~ 18

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.

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