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 ◽  
...  

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.

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov

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.


2020 ◽  
pp. 471-477
Author(s):  
T.A. MIROSHKINA ◽  
◽  
S.A. SHUSTOVA ◽  

The article provides information on the lung dead space – a part of the respiratory volume that does not participate in gas exchange. The anatomical and alveolar dead spaces jointly together form the physiological dead space. The article describes methods for determining the volume of dead spaces using the capnovolumetry. The volume of physiological dead space is calculated using the C. Bohr equation. The volume of anatomical dead space can be determined using the equal area method proposed by W.S. Fowler. The volume of the alveolar dead space is the difference of volumes of the physiological and anatomical dead spaces. In pathology, the volume of the alveolar space and, consequently, physiological dead space can increase significantly. Determination of the volume of dead space is the significant criterion for diagnostic and predicting the outcome of a number of diseases. Keywords: Physiological dead space , anatomical dead space , alveolar dead space , capnovolumetry, volumetric capnography.


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.


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.


2021 ◽  
Author(s):  
Quangang Yang

Background: In mechanical ventilation, there are still some challenges to turn a modern ventilator into a fully reactive device, such as lack of a comprehensive target variable and the unbridged gap between input parameters and output results. This paper aims to present a state ventilation which can provide a measure of two primary, but heterogenous, ventilation support goals. The paper also tries to develop a method to compute, rather than estimate, respiratory parameters to obtain the underlying causal information. Methods: This paper presents a state ventilation, which is calculated based on minute ventilation and blood gas partial pressures, to evaluate the efficacy of ventilation support and indicate disease progression. Through mathematical analysis, formulae are derived to compute dead space volume/ventilation, alveolar ventilation, and CO2 production. Results: Measurements from a reported clinical study are used to verify the analysis and demonstrate the application of derived formulae. The state ventilation gives the expected trend to show patient status, and the calculated mean values of dead space volume, alveolar ventilation, and CO2 production are 158mL, 8.8L/m, and 0.45L/m respectively for a group of patients. Discussions and Conclusions: State ventilation can be used as a target variable since it reflects patient respiratory effort and gas exchange. The derived formulas provide a means to accurately and continuously compute respiratory parameters using routinely available measurements to characterize the impact of different contributing factors.


1976 ◽  
Vol 51 (4) ◽  
pp. 323-333 ◽  
Author(s):  
Christine A. Bradley ◽  
E. A. Harris ◽  
Eve R. Seelye ◽  
R. M. L. Whitlock

1. Physiological dead-space volume (VD) was measured in twenty-four healthy men and women aged from 20 to 71 years, at rest and at two rates of work on a treadmill, whilst breathing air and breathing oxygen. 2. The effect of correction of arterial carbon dioxide tension (Pa,co2) to pulmonary capillary temperature on the resulting value for VD was investigated. We find that the effect is substantial and that a correction should be made. 3. Equations have been derived for the prediction of normal VD during exercise. The best prediction was given by a regression on height, age, carbon dioxide output, ventilation and respiratory frequency, with an upper 95% confidence limit of +81 ml.


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.


2018 ◽  
Vol 104 (3) ◽  
pp. F321-F323
Author(s):  
Ashley Nieves ◽  
Ashley Cozzo ◽  
Zora Kosoff ◽  
Chani Traube ◽  
Alan M Groves

High flow therapy works partly by washout of airway dead space, the volume of which has not been quantified in newborns. This observational study aimed to quantify airway dead space in infants and to compare efficacy of washout between high flow devices in three-dimensional (3D) printed airway models of infants weighing 2.5–3.8 kg. Nasopharyngeal airway dead space volume was 1.5–2.0 mL/kg in newborns. A single cannula device produced lower carbon dioxide (CO2) levels than a dual cannula device (33.7, 31.2, 23.1, 15.9, 10.9 and 6.3 mm Hg vs 36.8, 35.5, 32.1, 26.8, 23.1 and 18.8 mm Hg at flow rates of 1, 2, 3, 4, 6 and 8 L/min, respectively; p<0.0001 at all flow rates). Airway pressure was 1 mm Hg at all flow rates with the single cannula but increased at higher flow rates with the dual cannula.Relative nasopharyngeal airway dead space volume is increased in newborns. In 3D-printed airway models, a single cannula high flow device produces improved CO2 washout with lower airway pressure.


Author(s):  
Santiago C. Arce ◽  
Fernando Chiodetti ◽  
Eduardo L. De Vito

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