Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model

1997 ◽  
Vol 82 (6) ◽  
pp. 1963-1971 ◽  
Author(s):  
Thierry Busso ◽  
Peter A. Robbins
Keyword(s):  
Gas Exchange ◽  
Lung Model ◽  
Gas Composition ◽  
Breathing Patterns ◽  
Alveolar Volume ◽  
Gas Concentration ◽  
Pulmonary Capillaries ◽  
Partial Pressures ◽  
End Tidal ◽  
Alveolar Gas Exchange

Busso, Thierry, and Peter A. Robbins. Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model. J. Appl. Physiol. 82(6): 1963–1971, 1997.—The purpose of this study was to evaluate algorithms for estimating O2 and CO2 transfer at the pulmonary capillaries by use of a nine-compartment tidally ventilated lung model that incorporated inhomogeneities in ventilation-to-volume and ventilation-to-perfusion ratios. Breath-to-breath O2 and CO2 exchange at the capillary level and at the mouth were simulated by using realistic cyclical breathing patterns to drive the model, derived from 40-min recordings in six resting subjects. The SD of the breath-by-breath gas exchange at the mouth around the value at the pulmonary capillaries was 59.7 ± 25.5% for O2 and 22.3 ± 10.4% for CO2. Algorithms including corrections for changes in alveolar volume and for changes in alveolar gas composition improved the estimates of pulmonary exchange, reducing the SD to 20.8 ± 10.4% for O2 and 15.2 ± 5.8% for CO2. The remaining imprecision of the estimates arose almost entirely from using end-tidal measurements to estimate the breath-to-breath changes in end-expiratory alveolar gas concentration. The results led us to suggest an alternative method that does not use changes in end-tidal partial pressures as explicit estimates of the changes in alveolar gas concentration. The proposed method yielded significant improvements in estimation for the model data of this study.

A model evaluation of estimates of breath-to-breath alveolar gas exchange

1983 ◽  
Vol 55 (6) ◽  
pp. 1936-1941 ◽  
Author(s):  
G. D. Swanson ◽  
D. L. Sherrill
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Indirect Measurement ◽  
Alveolar Volume ◽  
Gas Concentration ◽  
Inherent Error ◽  
Sinusoidal Flow ◽  
End Tidal ◽  
Exercise In Humans ◽  
Alveolar Gas Exchange

A mathematical model has been implemented for evaluation of methods for estimating breath-to-breath alveolar gas exchange during exercise in humans. This model includes a homogeneous alveolar gas exchange compartment, a dead space compartment, and tissue spaces for CO2 (alveolar and dead space). The dead space compartment includes a mixing portion surrounded by tissue and an unmixed (slug flow) portion which is partitioned between anatomical and apparatus contributions. A random sinusoidal flow pattern generates a breath-to-breath variation in pulmonary stores. The Auchincloss algorithm for estimating alveolar gas exchange (Auchincloss et al., J. Appl. Physiol. 21: 810-818, 1966) was applied to the model, and the results were compared with the simulated gas exchange. This comparison indicates that a compensation for changes in pulmonary stores must include factors for alveolar gas concentration change as well as alveolar volume change and thus implies the use of end-tidal measurements. Although this algorithm yields reasonable estimates of breath-to-breath alveolar gas exchange, it does not yield a “true” indirect measurement because of inherent error in the estimation of a homogeneous alveolar gas concentration at the end of expiration.

Expiratory and arterial partial pressure relations under different ventilation-perfusion conditions

1983 ◽  
Vol 54 (6) ◽  
pp. 1745-1753 ◽  
Author(s):  
A. Zwart ◽  
S. C. Luijendijk ◽  
W. R. de Vries
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Gas Analysis ◽  
Lung Model ◽  
Breathing Patterns ◽  
Tracer Gas ◽  
Physiological Dead Space ◽  
Arterial Partial Pressure ◽  
The Difference ◽  
End Tidal

Inert tracer gas exchange across the human respiratory system is simulated in an asymmetric lung model for different oscillatory breathing patterns. The momentary volume-averaged alveolar partial pressure (PA), the expiratory partial pressure (PE), the mixed expiratory partial pressure (PE), the end-tidal partial pressure (PET), and the mean arterial partial pressure (Pa), are calculated as functions of the blood-gas partition coefficient (lambda) and the diffusion coefficient (D) of the tracer gas. The lambda values vary from 0.01 to 330.0 inclusive, and four values of D are used (0.5, 0.22, 0.1, and 0.01). Three ventilation-perfusion conditions corresponding to rest and mild and moderate exercise are simulated. Under simulated exercise conditions, we compute a reversed difference between PET and Pa compared with the rest condition. This reversal is directly reflected in the relation between the physiological dead space fraction (1--PE/Pa) and the Bohr dead space fraction (1--PE/PET). It is argued that the difference (PET--Pa) depends on the lambda of the tracer gas, the buffering capacity of lung tissue, and the stratification caused by diffusion-limited gas transport in the gas phase. Finally some determinants for the reversed difference (PET--Pa) and the significance for conventional gas analysis are discussed.

Breathing volumes and gas exchange during simulated rapid free ascent from 100 msw

1993 ◽  
Vol 74 (3) ◽  
pp. 1293-1298 ◽  
Author(s):  
D. Linnarsson ◽  
H. Ornhagen ◽  
M. Gennser ◽  
H. Berg
Keyword(s):  
Gas Exchange ◽  
Surface Pressure ◽  
Time Course ◽  
Decompression Sickness ◽  
Dilution Method ◽  
Gas Composition ◽  
Arterial Pco2 ◽  
End Tidal ◽  
Gas Expansion ◽  
The Brain

The crew of a disabled submarine can be rescued by means of free ascent through the water to the surface. Pulmonary gas exchange was studied during simulated rapid free ascent in subjects standing immersed to the neck in a pressure chamber. The pressure was rapidly increased to 1.1 MPa [100 meters seawater (msw)] followed by decompression at 0.03 MPa/s (3 msw/s). Effective inspired tidal volume, as estimated by an Ar dilution method, fell gradually to zero during decompression from 20 to 0 msw. Directly determined expired tidal volumes were increased up to two to three times at the time of return to surface pressure compared with pre- and postdecompression volumes. End-tidal PCO2 was increased on compression and fell to a nadir of 3.4 kPa (25 Torr) at the time of return to surface pressure. Thus, intrapulmonary gas expansion caused simultaneous inspiratory hypoventilation and expiratory hyperventilation. If O2-enriched gas is to be used to reduce the risk of decompression sickness, it should be administered early during decompression to alter the intrapulmonary gas composition. The time course of arterial PCO2 changes as reflected by end-tidal values during short-lasting compression/decompression would act to promote inert gas supersaturation in the brain.

Breath-by-breath alveolar gas exchange

1983 ◽  
Vol 55 (2) ◽  
pp. 583-590 ◽  
Author(s):  
D. Giezendanner ◽  
P. Cerretelli ◽  
P. E. Di Prampero
Keyword(s):  
Gas Exchange ◽  
Open Circuit ◽  
Single Breath ◽  
Alveolar Level ◽  
Expired Gas ◽  
The Difference ◽  
Computer Monitors ◽  
End Tidal ◽  
Breath Measurement ◽  
Alveolar Gas Exchange

A method is described for breath-by-breath measurement of alveolar gas exchange corrected for changes of lung gas stores. In practice, the subject inspires from a spirometer, and each expired tidal volume is collected into a rubber bag placed inside a rigid box connected to the same spirometer. During the inspiration following any given expiration the bag is emptied by a vacuum pump. A computer monitors inspiratory and expiratory tidal volumes, drives four solenoid valves allowing appropriate operation of the system, and memorizes end-tidal gas fractions as well as mixed expired gas composition analyzed by mass spectrometer. Thus all variables for calculating alveolar gas exchange, based on the theory developed by Auchincloss et al. (J. Appl. Physiol. 21: 810-818, 1966), are obtained on a single-breath basis. Mean resting and steady-state exercise gas exchange data are equal to those obtained by conventional open-circuit measurements. Breathing rates up to 30 X min-1 can be followed. The breath-to-breath variability of O2 uptake at the alveolar level is less (25-35%) than that measured at the mouth as the difference between the inspired and expired volumes, both at rest and during exercise up to 0.7 of maximum O2 consumption.

Gas exchange in a three-compartment lung model analyzed by forcing sinusoids of N2O

1993 ◽  
Vol 75 (4) ◽  
pp. 1863-1876 ◽  
Author(s):  
C. E. Hahn ◽  
A. M. Black ◽  
S. A. Barton ◽  
I. Scott
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Dead Space ◽  
Animal Studies ◽  
Lung Model ◽  
Distribution Model ◽  
Mixed Venous Blood ◽  
Blood Gas ◽  
Partial Pressures ◽  
Wide Range

A mathematical gas exchange model, using sinusoidal forcing functions of inert inspired gas (A. Zwart, R. C. Seagrave, and A. Van Dieren. J. Appl. Physiol. 41: 419#x2013;424, 1976), has been extended by us to include dead space (VD), a single alveolar compartment (VA) perfused with blood flow (Qp), and a shunt (Qs). In this new work we use N2O as the indicator gas in the mathematical model and in the experimental studies, in low enough concentrations [<6% (vol/vol)] to avoid anesthetic effects. Mathematical relationships between the inspired and expired N2O gas partial pressures, the blood gas N2O partial pressures, and their variation with forcing frequency are derived for a continuous ventilation uptake and a conventional anesthetic gas distribution model. We show that these gas and blood gas N2O relationships give direct derivation of cardiorespiratory parameters such as VA, Qp, the dead space-to-total ventilation ratio (VD/VT), and the shunt-to-total blood flow ratio (Qs/QT) without altering the subject's oxygenation and that they are essentially free from recirculation effects at high forcing frequencies > or = 2 min-1. Theoretical results from the model are presented for a wide range of forcing frequencies between 2 x 10(-2) and 10 min-1 (sinusoid periods 30#x2013;0.1 min), and these show that VA, Qp, and VD/VT can all be measured by N2O forcing frequencies > or = 1 min-1. We also present results from five animal studies, with an experimental inspired gas forcing frequency range of 0.125 to 2 min-1, which show qualitative agreement with the predictions of the continuous ventilation model. During these animal studies both mass spectrometric N2O respiratory gas measurements and intravascular polarographic arterial and mixed venous blood N2O partial pressure measurements were made, and examples of these in vivo measurements are presented, together with examples of the calculations derived from them.

scholarly journals End-tidal to Arterial Gradients and Alveolar Deadspace for Anesthetic Agents

2020 ◽  
Vol 133 (3) ◽  
pp. 534-547
Author(s):  
Philip J. Peyton ◽  
Jan Hendrickx ◽  
Rene J. E. Grouls ◽  
Andre Van Zundert ◽  
Andre De Wolf
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Compartment Model ◽  
Lung Model ◽  
Anesthetic Agents ◽  
Partial Pressures ◽  
Three Compartment Model ◽  
Log Normal ◽  
End Tidal ◽  
Blood Solubility

Background According to the “three-compartment” model of ventilation-perfusion () inequality, increased scatter in the lung under general anesthesia is reflected in increased alveolar deadspace fraction (Vda/Va) customarily measured using end-tidal to arterial (a-a) partial pressure gradients for carbon dioxide. a-a gradients for anesthetic agents such as isoflurane are also significant but have been shown to be inconsistent with those for carbon dioxide under the three-compartment theory. The authors hypothesized that three-compartment Vda/Va calculated using partial pressures of four inhalational agents (Vda/Vag) is different from that calculated using carbon dioxide (Vda/Vaco2) measurements, but similar to predictions from multicompartment models of physiologically realistic “log-normal” distributions. Methods In an observational study, inspired, end-tidal, arterial, and mixed venous partial pressures of halothane, isoflurane, sevoflurane, or desflurane were measured simultaneously with carbon dioxide in 52 cardiac surgery patients at two centers. Vda/Va was calculated from three-compartment model theory and compared for all gases. Ideal alveolar (Pag) and end-capillary partial pressure (Pc’g) of each agent, theoretically identical, were also calculated from end-tidal and arterial partial pressures adjusted for deadspace and venous admixture. Results Calculated Vda/Vag was larger (mean ± SD) for halothane (0.47 ± 0.08), isoflurane (0.55 ± 0.09), sevoflurane (0.61 ± 0.10), and desflurane (0.65 ± 0.07) than Vda/Vaco2 (0.23 ± 0.07 overall), increasing with lower blood solubility (slope [Cis], –0.096 [–0.133 to –0.059], P &lt; 0.001). There was a significant difference between calculated ideal Pag and Pc’g median [interquartile range], Pag 5.1 [3.7, 8.9] versus Pc’g 4.0[2.5, 6.2], P = 0.011, for all agents combined. The slope of the relationship to solubility was predicted by the log-normal lung model, but with a lower magnitude relative to calculated Vda/Vag. Conclusions Alveolar deadspace for anesthetic agents is much larger than for carbon dioxide and related to blood solubility. Unlike the three-compartment model, multicompartment scatter models explain this from physiologically realistic gas uptake distributions, but suggest a residual factor other than solubility, potentially diffusion limitation, contributes to deadspace. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Direct effect of PaCO2 on respiratory sinus arrhythmia in conscious humans

2002 ◽  
Vol 282 (3) ◽  
pp. H973-H976 ◽  
Author(s):  
Nobuko Sasano ◽  
Alex E. Vesely ◽  
Junichiro Hayano ◽  
Hiroshi Sasano ◽  
Ron Somogyi ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Direct Effect ◽  
Respiratory Sinus Arrhythmia ◽  
Random Order ◽  
Mean Amplitude ◽  
Frequency Component ◽  
Pulmonary Gas Exchange ◽  
High Frequency Component ◽  
Sinus Arrhythmia ◽  
End Tidal

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2directly affects RSA in conscious humans even when changes in tidal volume (VT) and breathing frequency ( F B), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal Pco 2 (Pet CO2 ) to 30, 40, or 50 mmHg in random order at constant VT and F B. The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with Pet CO2 ( P < 0.001). Mean R-R interval did not differ at Pet CO2 of 40 and 50 mmHg but was less at 30 mmHg ( P < 0.05). Because VT and F B were constant, these results support our hypothesis that increased CO2directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.

Inspiratory Speech as a Management Option for Spastic Dysphonia

1992 ◽  
Vol 101 (5) ◽  
pp. 375-382 ◽  
Author(s):  
Gordon A. Harrison ◽  
Richard H. Troughear ◽  
Pamela J. Davis ◽  
Alison L. Winkworth
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Voice Quality ◽  
Management Option ◽  
Communication Problems ◽  
Partial Pressures ◽  
The Subject ◽  
And Control ◽  
Laryngeal Resistance

A case study is reported of a subject who has used inspiratory speech (IS) for 6 years as a means of overcoming the communication problems of long-standing adductor spastic dysphonia (ASD). The subject was studied to confirm his use of IS, determine the mechanisms of its production, investigate its effects on ventilatory gas exchange, and confirm that it was perceptually preferable to ASD expiratory speech (ES). Results showed that the production and control of a high laryngeal resistance to airflow were necessary for usable IS. Voice quality was quantitatively and perceptually poor; however, the improved fluency and absence of phonatory spasm made IS the preferred speaking mode for both the listener and the speaker. Transcutaneous measurements of the partial pressures of oxygen and carbon dioxide in the subject's blood were made during extended speaking periods. These measurements indicated that ventilation was unchanged during IS, and that ventilation during ES was similar to the “hyperventilation” state of normal speakers. The reasons for the absence of phonatory spasm during IS are discussed, and the possibility of its use as a noninvasive management option for other ASD sufferers is addressed.

Ventilatory response to 8 h of isocapnic and poikilocapnic hypoxia in humans

1995 ◽  
Vol 78 (3) ◽  
pp. 1092-1097 ◽  
Author(s):  
L. S. Howard ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Progressive Increase ◽  
Nasal Catheter ◽  
Partial Pressures ◽  
End Tidal ◽  
Almost All ◽  
And Control

Almost all studies of the effects of prolonged hypoxia on ventilation (VE) in humans have been performed with the end-tidal PCO2 (PETCO2) left uncontrolled. The purpose of this study was to compare the effects of 8 h of hypoxia with PETCO2 held constant with 8 h of hypoxia with PETCO2 left uncontrolled. Ten subjects completed the study. Each was seated inside a chamber in which the inspired gas could be controlled so as to maintain the desired partial pressures of end-tidal gases (sampled via nasal catheter) constant (see L.S.G.E. Howard et al. J. Appl. Physiol. 78:1088–1091, 1995.). Three 8-h protocols were employed: 1) isocapnic hypoxia, at an end-tidal PO2 of 55 Torr with PETCO2 held at the subject's resting value; 2) poikilocapnic hypoxia, at the same end-tidal PO2; and 3) control, where the inspired gas was air. VE was measured (over 3 min) at 0 and 20 min and at hourly intervals between 1.5 and 7.5 h. There was a rise in VE during isocapnic hypoxia [from an initial VE of 16.2 +/- 1.3 (SE) l/min to a final VE of 24.8 +/- 1.6 l/min], which was significant compared with poikilocapnic hypoxia and control values (P < 0.001, analysis of variance). There was no significant progressive rise in VE during poikilocapnic hypoxia compared with control values. These results show that isocapnic hypoxia produces a progressive increase in VE when sustained over an 8-h period. The onset of this response is faster than has been noted in studies of the progressive rise in VE associated with the poikilocapnic hypoxia of altitude.

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