A Theoretical Analysis of the Continuous Distribution of Specific Tidal Volume Throughout the Lung with Special Reference to Anatomical Dead Space

1976 ◽  
Vol BME-23 (2) ◽  
pp. 110-117 ◽  
Author(s):  
Henri F. Lecocq
Keyword(s):  
Theoretical Analysis ◽  
Special Reference ◽  
Tidal Volume ◽  
Dead Space ◽  
Continuous Distribution ◽  
Anatomical Dead Space

scholarly journals Nasal high flow reduces minute ventilation during sleep through a decrease of carbon dioxide rebreathing

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Ventilation ◽  
Control Ventilation ◽  
High Flow ◽  
Carbon Dioxide Rebreathing ◽  
Anatomical Dead Space

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.

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 The principle of upper airway unidirectional flow facilitates breathing in humans

2008 ◽  
Vol 105 (3) ◽  
pp. 854-858 ◽  
Author(s):  
Yandong Jiang ◽  
Yafen Liang ◽  
Robert M. Kacmarek
Keyword(s):  
Respiratory Distress ◽  
Tidal Volume ◽  
Dead Space ◽  
Breathing Pattern ◽  
Heat Removal ◽  
Upper Airway ◽  
Random Order ◽  
Water Evaporation ◽  
Breathing Patterns ◽  
Anatomical Dead Space

Upper airway unidirectional breathing, nose in and mouth out, is used by panting dogs to facilitate heat removal via water evaporation from the respiratory system. Why some humans instinctively employ the same breathing pattern during respiratory distress is still open to question. We hypothesized that 1) humans unconsciously perform unidirectional breathing because it improves breathing efficiency, 2) such an improvement is achieved by bypassing upper airway dead space, and 3) the magnitude of the improvement is inversely proportional to the tidal volume. Four breathing patterns were performed in random order in 10 healthy volunteers first with normal breathing effort, then with variable tidal volumes: mouth in and mouth out (MMB); nose in and nose out (NNB); nose in and mouth out (NMB); and mouth in and nose out (MNB). We found that unidirectional breathing bypasses anatomical dead space and improves breathing efficiency. At tidal volumes of ∼380 ml, the functional anatomical dead space during NMB (81 ± 31 ml) or MNB (101 ± 20 ml) was significantly lower than that during MMB (148 ± 15 ml) or NNB (130 ± 13 ml) (all P < 0.001), and the breathing efficiency obtained with NMB (78 ± 9%) or MNB (73 ± 6%) was significantly higher than that with MMB (61 ± 6%) or NNB (66 ± 3%) (all P < 0.001). The improvement in breathing efficiency increased as tidal volume decreased. Unidirectional breathing results in a significant reduction in functional anatomical dead space and improvement in breathing efficiency. We suggest this may be the reason that such a breathing pattern is preferred during respiratory distress.

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.

A self-retaining nasal flowmeter for preterm infants

1980 ◽  
Vol 48 (3) ◽  
pp. 569-571 ◽  
Author(s):  
R. T. Brouillette ◽  
B. T. Thach
Keyword(s):  
Stainless Steel ◽  
Tidal Volume ◽  
Preterm Infants ◽  
Dead Space ◽  
Nasal Cannula ◽  
Light Weight ◽  
Low Resistance ◽  
Respiratory Airflow ◽  
The Subject ◽  
Compact Design

A nasal flowmeter suitable for preterm infants is described. It is made from a commercially available nasal cannula and 400-mesh stainless steel screen. Low dead space (0.35 ml) and low resistance (1.3 cmH2O . 100 ml-1 . s) are advantages. Light weight and compact design have eliminated the need for extensive restraint of the subject. Also, the investigator need not hold the flowmeter in place. These features make accurate measurement of respiratory airflow and tidal volume possible during polygraphic monitoring studies lasting several hours.

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.

Effects of Combined Abdominal and Thoracic Airsac Occlusion on Respiration in Domestic Fowl

1990 ◽  
Vol 152 (1) ◽  
pp. 93-100 ◽  
Author(s):  
JOHN BRACKENBURY ◽  
JANE AMAKU
Keyword(s):  
Metabolic Rate ◽  
Tidal Volume ◽  
Dead Space ◽  
Domestic Fowl ◽  
Detrimental Effect ◽  
Minute Ventilation ◽  
Respiratory Pattern ◽  
Blood Gas ◽  
Control Value ◽  
Air Sacs

Ventilation and respiratory and blood gas tensions were monitored at rest and during running exercise, following bilateral occlusion of the cranial and caudal thoracic and the abdominal air sacs. This represents a removal of approximately 70% of the total air-sac capacity. At rest, the birds were strongly hypoxaemic/hypercapnaemic. Ventilation was maintained at its control value but respiratory frequency was significantly increased and tidal volume diminished. The birds were capable of sustained running at approximately three times the pre-exercise metabolic rate. Minute ventilation during exercise was the same as that of the controls, but breathing was faster and shallower. Exercise had no effect on blood gas tensions in either the control or the experimental birds. There was no evidence of a detrimental effect of air-sac occlusion on the effectiveness of inspiratory airflow valving in the lung: hypoxaemia appeared to be due to the altered respiratory pattern, which resulted in increased dead-space inhalation.

scholarly journals Management of hypercapnia in critically ill mechanically ventilated patients—A narrative review of literature

2020 ◽  
Vol 21 (4) ◽  
pp. 327-333
Author(s):  
Ravindranath Tiruvoipati ◽  
Sachin Gupta ◽  
David Pilcher ◽  
Michael Bailey
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Dead Space ◽  
Hypercapnic Acidosis ◽  
Mechanically Ventilated ◽  
Mechanically Ventilated Patients ◽  
Low Tidal Volume ◽  
Volume Ventilation ◽  
Low Volume ◽  
Ventilated Patients

The use of lower tidal volume ventilation was shown to improve survival in mechanically ventilated patients with acute lung injury. In some patients this strategy may cause hypercapnic acidosis. A significant body of recent clinical data suggest that hypercapnic acidosis is associated with adverse clinical outcomes including increased hospital mortality. We aimed to review the available treatment options that may be used to manage acute hypercapnic acidosis that may be seen with low tidal volume ventilation. The databases of MEDLINE and EMBASE were searched. Studies including animals or tissues were excluded. We also searched bibliographic references of relevant studies, irrespective of study design with the intention of finding relevant studies to be included in this review. The possible options to treat hypercapnia included optimising the use of low tidal volume mechanical ventilation to enhance carbon dioxide elimination. These include techniques to reduce dead space ventilation, and physiological dead space, use of buffers, airway pressure release ventilation and prone positon ventilation. In patients where hypercapnic acidosis could not be managed with lung protective mechanical ventilation, extracorporeal techniques may be used. Newer, minimally invasive low volume venovenous extracorporeal devices are currently being investigated for managing hypercapnia associated with low and ultra-low volume mechanical ventilation.

Uneven gas mixing during rebreathing assessed by simultaneously measuring dead space

1982 ◽  
Vol 53 (4) ◽  
pp. 930-939 ◽  
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.

Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Tidal Volume ◽  
Lung Volume ◽  
Dead Space ◽  
Control Level ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Diffusing Capacity ◽  
Fixed Rate

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

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