Despite changes in volume of respiration, physiologic dead space to tidal volume ratios remained constant

1968 ◽  
Vol 29 (1) ◽  
pp. 178-178
Author(s):  
J. F. Nunn ◽  
D. W. Hill
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Physiologic Dead Space

Unanesthetized dogs with increased respiratory dead space

1960 ◽  
Vol 15 (5) ◽  
pp. 838-842 ◽  
Author(s):  
Thomas B. Barnett ◽  
Richard M. Peters
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Volume ◽  
Alveolar Ventilation ◽  
Physiologic Dead Space ◽  
Consistent Change ◽  
The Dead ◽  
Animal Preparation ◽  
Respiratory Dead Space

A method is described for maintaining a permanent tracheostomy in dogs. This animal preparation has been used to study the effects of artificially increased respiratory dead space. Trained dogs with tracheostomies have made possible measurements of ventilation without anesthesia. It has been found that additions to the respiratory dead space in the form of tubing of frac34 in. i.d. result in an increase in physiologic dead space of the same magnitude as the volume of tubing added. Increasing the dead space in this manner resulted in an increased minute volume which was accomplished principally by an increase in tidal volume without a significant or consistent change in respiratory rate. Alveolar ventilation remained unchanged even with large additions to the dead space (20–30 cc/kg of animal wt.). Arterial pCO2 was significantly higher in these animals than in the controls. The CO2 tension was similarly elevated when extra dead space of lesser volume (5–20 cc/kg) was allowed to remain on the dogs for more than 48 hours. Submitted on April 13, 1960

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

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

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.

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.

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