Computations of State Ventilation and Respiratory Parameters

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.

Volumetric Сapnography As a Tool for Evaluation of Alveolar Ventilation Effectiveness in Clinical Practice

General Reanimatology ◽

10.15360/1813-9779-2018-5-16-24 ◽

2018 ◽

Vol 14 (5) ◽

pp. 16-24 ◽

Cited By ~ 1

Author(s):

P. Török ◽

F. Depta ◽

V. Donic ◽

M. Nosál’ ◽

S. Imrecze ◽

...

Keyword(s):

Minute Ventilation ◽

Artery Bypass ◽

Lung Ventilation ◽

Co2 Exchange ◽

Alveolar Ventilation ◽

Co2 Production ◽

Dead Space Volume ◽

The Relationship ◽

Pressure Controlled ◽

The purpose of the study was to compare the relationship between the dead space volume and tidal volume (VD/VT) using volumetric capnography (VCap) during pressure controlled (PCV) and pressure supported (PSV) ventilation mode in the postoperative period.Materials and methods. 30 randomly assigned cardiac surgical patients undergoing CABG (coronary artery bypass grafting) using ECC (extracorporeal circuit) were included in an observational, prospective study. Patients were connected to the ventilator immediately after ICU admission. After that, monitoring VD/VT, CO2 production (VECO2) as well as ventilation parameters was carried out. The parameters during PCV and PSV mode were statistically evaluated using t-test.Results. Expiratory CO2 (ETCO2) concentration were not significantly different in both PCV or PSV (p=NS), although both VECO2 and minute ventilation (MV) increased during PSV mode (p<0.01). VD/VT in PSV mode was lower than in PCV. Gas exchange represented by alveolar ventilation (VA) was better during PSV (p<0.01). VA was also higher during PSV (p<0.05). The calculated VD/VT ratio differed between PCV and PSV mode (p<0.01).Conclusion. VCap represents a tool for monitoring of CO2 exchange effectivness. We registered a decrease in VD/VT with improved alveolar ventilation (VA) in PSV mode. VCap seems to be a suitable instrument for adjustment of protective lung ventilation.

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 ◽

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.

Effect of centrally administered gamma-aminobutyric acid on metabolic function

10.1152/jappl.1986.61.2.472 ◽

1986 ◽

Vol 61 (2) ◽

pp. 472-476 ◽

Cited By ~ 12

Author(s):

M. P. Kneussl ◽

P. Pappagianopoulos ◽

B. Hoop ◽

H. Kazemi

Keyword(s):

Minute Ventilation ◽

Aminobutyric Acid ◽

Co2 Production ◽

Metabolic Function ◽

Gamma Aminobutyric Acid ◽

Dead Space Volume ◽

Anesthetized Dogs ◽

Gaba Content ◽

The Brain ◽

gamma-Aminobutyric acid (GABA) content of the brain increases during hypoxia and hypercapnia and GABA by itself is a central ventilatory depressant and may depress metabolism as well. Therefore the effect of centrally administered GABA by ventriculocisternal perfusion on O2 consumption (VO2) and CO2 production (VCO2) was studied in pentobarbital-anesthetized dogs. GABA (30 mM) in mock cerebrospinal fluid (CSF) was perfused for 15 min at the rate of 1.0 ml/min followed by perfusion with mock CSF alone. Body temperature, perfusion pressure, and CSF pH were kept constant. Minute ventilation (VE) was kept constant mechanically. Under these conditions, VO2, VCO2, alveolar ventilation (VA), and relative pulmonary dead space volume (VD/VT) were measured. During perfusion with 30 mM GABA, mean VO2 (+/- SE) decreased from 96.5 +/- 3.3 to 81.9 +/- 5.1 ml/min, VCO2 from 72.1 +/- 3.8 to 60.7 +/- 3.0 ml/min, and VA from 1.7 +/- 0.1 to 1.3 +/- 0.1 l/min. VD/VT increased from 0.55 +/- 0.02 to 0.65 +/- 0.01. Perfusion with mock CSF alone restored these parameters to initial levels within 15 min. We conclude that centrally administered GABA depresses VO2 and VCO2. This reduction in metabolic function is independent of the central modulatory effects of GABA on respiration.

Respiration

10.1093/oso/9780197571194.003.0012 ◽

2021 ◽

pp. 261-291

Author(s):

Graham Mitchell

Keyword(s):

Carbon Dioxide ◽

Gas Exchange ◽

Respiratory System ◽

Dead Space ◽

Ventilation Rate ◽

Alveolar Ventilation ◽

Laryngeal Muscles ◽

Dead Space Volume ◽

Recurrent Laryngeal Nerves ◽

This chapter discusses the respiratory system of giraffes. The respiratory system supplies oxygen, removes of carbon dioxide and produces the airflow needed to make sounds. Giraffes do not have the velocity of airflow through the airways to vibrate vocal cords sufficiently to generate sounds able to be heard by humans but can produce sounds able to be heard by giraffes. Air reaches alveoli for gas exchange through a long trachea, which is relatively narrow (~4 cm in diameter). Dead space volume is large. A short trunk and rigid chest wall reduce the capacity of the thorax and consequently lung volume is small. Respiratory rate is low (~10 min-1), but tidal volume is relatively big, and alveolar ventilation rate (VA; ~60 L min-1) delivers sufficient air despite the large dead space volume. Laryngeal muscles act to prevent food from entering the trachea a process controlled by the (short) superior and (long) inferior (recurrent) laryngeal nerves. Air that has been delivered to alveoli comes into contact with pulmonary artery blood (=cardiac output, Q; ~40 L min-1). The VA: Q ratio is ~1.5 (cf 0.8 in humans). Gas exchange occurs by diffusion. The surface area for diffusion is related to the number of alveoli which increase in number during growth from ~1 billion in a newborn giraffe to 11 billion in an adult. Gas carriage of oxygen and carbon dioxide is a function of erythrocytes which are small (MCV = 12 fL) but numerous (12 × 1012 L-1) and each liter of blood contains ~150 g of hemoglobin.

Dead Space Volume in N95 Masks

Archivos de Bronconeumología ◽

10.1016/j.arbres.2020.11.006 ◽

2020 ◽

Author(s):

Santiago C. Arce ◽

Fernando Chiodetti ◽

Eduardo L. De Vito

Keyword(s):

Dead Space ◽

Dead Space Volume ◽

High-frequency ventilation

Physiological Reviews ◽

10.1152/physrev.1984.64.2.505 ◽

1984 ◽

Vol 64 (2) ◽

pp. 505-543 ◽

Cited By ~ 81

Author(s):

J. M. Drazen ◽

R. D. Kamm ◽

A. S. Slutsky

Keyword(s):

Experimental Data ◽

Gas Exchange ◽

Dead Space ◽

Gas Transport ◽

Physical Models ◽

High Frequency Ventilation ◽

General Description ◽

Wide Range ◽

Dead Space Volume ◽

Complete physiological understanding of HFV requires knowledge of four general classes of information: 1) the distribution of airflow within the lung over a wide range of frequencies and VT (sect. IVA), 2) an understanding of the basic mechanisms whereby the local airflows lead to gas transport (sect. IVB), 3) a computational or theoretical model in which transport mechanisms are cast in such a form that they can be used to predict overall gas transport rates (sect. IVC), and 4) an experimental data base (sect. VI) that can be compared to model predictions. When compared with available experimental data, it becomes clear that none of the proposed models adequately describes all the experimental findings. Although the model of Kamm et al. is the only one capable of simulating the transition from small to large VT (as compared to dead-space volume), it fails to predict the gas transport observed experimentally with VT less than equipment dead space. The Fredberg model is not capable of predicting the observed tendency for VT to be a more important determinant of gas exchange than is frequency. The remaining models predict a greater influence of VT than frequency on gas transport (consistent with experimental observations) but in their current form cannot simulate the additional gas exchange associated with VT in excess of the dead-space volume nor the decreased efficacy of HFV above certain critical frequencies observed in both animals and humans. Thus all of these models are probably inadequate in detail. One important aspect of these various models is that some are based on transport experiments done in appropriately scaled physical models, whereas others are entirely theoretical. The experimental models are probably most useful in the prediction of pulmonary gas transport rates, whereas the physical models are of greater value in identifying the specific transport mechanism(s) responsible for gas exchange. However, both classes require a knowledge of the factors governing the distribution of airflow under the circumstances of study as well as requiring detail about lung anatomy and airway physical properties. Only when such factors are fully understood and incorporated into a general description of gas exchange by HFV will it be possible to predict or explain all experimental or clinical findings.

Gas transport during high-frequency ventilation

10.1152/jappl.1983.55.2.472 ◽

1983 ◽

Vol 55 (2) ◽

pp. 472-478 ◽

Cited By ~ 15

Author(s):

V. Brusasco ◽

T. J. Knopp ◽

K. Rehder

Keyword(s):

Stroke Volume ◽

Dead Space ◽

High Frequency ◽

Oscillation Frequency ◽

High Frequency Ventilation ◽

Dead Space Volume ◽

Entire Lung ◽

Frequency Ventilation ◽

Gas Volume ◽

During high-frequency small-volume ventilation (HFV), the transport rate of gas from the mouth to a lung region is a function of two conductances (conductance is the transfer rate of a gas divided by its partial pressure difference): regional longitudinal gas conductance along the airways (Grlongi) and gas conductance between lung regions (Ginter). Grlongi per unit regional lung (gas) volume [Grlongi/(Vr beta g)] was determined during HFV in 11 anesthetized paralyzed dogs lying supine. The distribution of Grlongi/(Vr beta g) was nearly uniform during HFV when stroke volumes were less than approximately two-thirds of the Fowler dead-space volume. By contrast, the distribution of Grlongi/(Vr beta g) was nonuniform when the stroke volume exceeded approximately two-thirds of the Fowler dead-space volume and the oscillation frequency was 5 Hz. Gas conductance along the airways per unit lung gas volume [average Glongi/(V beta g)], for the entire lung, increased with stroke volume at all frequencies, but for a given product of oscillation frequency and stroke volume, the average Glongi/(V beta g) was greater when stroke volume was large and oscillation frequency was low. The average Glongi/(V beta g) increased with frequency up to a maximal value; the frequency at which the maximum occurred depended on the kinematic viscosity of the inspired gas mixture.

Labeled carbon dioxide (C18O2): an indicator gas for phase II in expirograms

10.1152/japplphysiol.01360.2003 ◽

2004 ◽

Vol 97 (5) ◽

pp. 1755-1762 ◽

Cited By ~ 9

Author(s):

Holger Schulz ◽

Anne Schulz ◽

Gunter Eder ◽

Joachim Heyder

Keyword(s):

Carbon Dioxide ◽

Phase Ii ◽

Dead Space ◽

Moment Analysis ◽

Cumulative Distribution ◽

Breath Holding ◽

Power Moment ◽

Single Breath ◽

Dead Space Volume ◽

Carbon dioxide labeled with 18O (C18O2) was used as a tracer gas for single-breath measurements in six anesthetized, mechanically ventilated beagle dogs. C18O2 is taken up quasi-instantaneously in the gas-exchanging region of the lungs but much less so in the conducting airways. Its use allows a clear separation of phase II in an expirogram even from diseased individuals and excludes the influence of alveolar concentration differences. Phase II of a C18O2 expirogram mathematically corresponds to the cumulative distribution of bronchial pathways to be traversed completely in the course of exhalation. The derivative of this cumulative distribution with respect to respired volume was submitted to a power moment analysis to characterize volumetric mean (position), standard deviation (broadness), and skewness (asymmetry) of phase II. Position is an estimate of dead space volume, whereas broadness and skewness are measures of the range and asymmetry of functional airway pathway lengths. The effects of changing ventilatory patterns and of changes in airway size (via carbachol-induced bronchoconstriction) were studied. Increasing inspiratory or expiratory flow rates or tidal volume had only minor influence on position and shape of phase II. With the introduction of a postinspiratory breath hold, phase II was continually shifted toward the airway opening (maximum 45% at 16 s) and became steeper by up to 16%, whereas skewness showed a biphasic response with a moderate decrease at short breath holding and a significant increase at longer breath holds. Stepwise bronchoconstriction decreased position up to 45 ± 2% and broadness of phase II up to 43 ± 4%, whereas skewness was increased up to twofold at high-carbachol concentrations. Under all circumstances, position of phase II by power moment analysis and dead space volume by the Fowler technique agreed closely in our healthy dogs. Overall, power moment analysis provides a more comprehensive view on phase II of single-breath expirograms than conventional dead space volume determinations and may be useful for respiratory physiology studies as well as for the study of diseased lungs.

Alveolar and Dead Space Volume Measured by Oscillations of Inspired Oxygen in Awake Adults

American Journal of Respiratory and Critical Care Medicine ◽

10.1164/ajrccm.156.6.9612082 ◽

1997 ◽

Vol 156 (6) ◽

pp. 1834-1839 ◽

Cited By ~ 7

Author(s):

E. M. WILLIAMS ◽

R. M. HAMILTON ◽

L. SUTTON ◽

J. P. VIALE ◽

C. E. W. HAHN

Keyword(s):

Dead Space ◽

Dead Space Volume ◽

Inspired Oxygen ◽

Distal effects of tracheal gas insufflation: changes with catheter position and oleic acid lung injury

10.1152/jappl.1996.81.3.1121 ◽

1996 ◽

Vol 81 (3) ◽

pp. 1121-1127 ◽

Cited By ~ 16

Author(s):

A. Nahum ◽

S. A. Ravenscraft ◽

A. B. Adams ◽

J. J. Marini

Keyword(s):

Oleic Acid ◽

Lung Injury ◽

Dead Space ◽

Minute Ventilation ◽

Catheter Position ◽

Tracheal Gas Insufflation ◽

Before And After ◽

Dead Space Volume ◽

Catheter Tip ◽

Conducting Airways

We separated distal (turbulence-related) and proximal (dead space washout-related) effects of tracheal gas insufflation (TGI) by comparing the effects of straight and inverted catheters. We reasoned that the inverted catheter was unlikely to remove CO2 from conducting airways distal to its orifice. In six normal dogs during TGI at 10 l/min, advancing the catheters from 10 to 1 cm above the main carina decreased dead space volume by 29 +/- 12 and 12 +/- 6 ml (P < 0.04) with the straight and inverted catheters, respectively. By comparison, the tracheal volume between 10 and 1 cm above the carina was 15 +/- 2 ml. In another set of dogs (n = 5), we examined the distal effects of TGI before and after oleic acid-induced lung injury. During TGI at 10 l/min before and after oleic acid injury, the differences in arterial PCO2 between the straight and inverted catheters were 5 +/- and 9 +/- 6 Torr (P < 0.18), respectively. Our data suggest that distal effects of TGI become more pronounced as the catheter tip is positioned closer to the main carina. The distal effects of TGI were not diminished after oleic acid injury when minute ventilation was maintained constant.