Effect of inspired CO2 on ventilation and perfusion heterogeneity in hyperventilated dogs

1993 ◽  
Vol 75 (3) ◽  
pp. 1306-1314 ◽  
Author(s):  
K. B. Domino ◽  
E. R. Swenson ◽  
N. L. Polissar ◽  
Y. Lu ◽  
B. L. Eisenstein ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Partial Pressure ◽  
Respiratory Rate ◽  
Dead Space ◽  
Pressure Difference ◽  
Inert Gas ◽  
Ventilation Distribution ◽  
Pentobarbital Sodium ◽  
Ventilation And Perfusion ◽  
Paco2 Level

We studied the effect of inspired CO2 on ventilation-perfusion (VA/Q) heterogeneity in dogs hyperventilated under two different tidal volume (VT) and respiratory rate conditions with the use of the multiple inert gas elimination technique. Dogs anesthetized with pentobarbital sodium were hyperventilated with an inspired fraction of O2 of 0.21 by using an increased VT (VT = 30 ml/kg at 18 breaths/min) or an increased respiratory rate (VT = 18 ml/kg at 35 breaths/min). The arterial CO2 tension (PaCO2) was varied to three levels (20, 35, and 52 Torr) by altering the inspired PCO2. The orders of type of ventilation and PaCO2 level were randomized. Compared with normocapnia, VA/Q heterogeneity was increased during hypocapnia induced by increased respiratory rate ventilation, which was indicated by an increase in dispersion indexes and arterial-alveolar inert gas partial pressure difference areas (P < 0.01). In contrast, VA/Q heterogeneity was not affected by hypocapnia when a large VT ventilation was used. Under the conditions of our study, hypercapnia did not result in statistically significant changes in VA/Q heterogeneity with either type of ventilation. Increased VT ventilation reduced dead space at all PaCO2 levels (P < 0.01) and reduced the log standard deviation of the ventilation distribution during normocapnia (P < 0.05) and hypocapnia (P < 0.01). We conclude that hypocapnia increased VA/Q heterogeneity when hyperventilation was achieved with a rapid respiratory rate. Therefore, a lack of improvement in VA/Q matching with inhaled CO2 may be associated with the use of a large VT. These data suggest that hypocapnic bronchoconstriction may be important in mediating hypocapnia-induced VA/Q inequality in dogs.

Correction of inert gas washin or washout for gas solubility in blood

1988 ◽  
Vol 65 (4) ◽  
pp. 1598-1603 ◽  
Author(s):  
E. A. Harris ◽  
R. M. Whitlock
Keyword(s):  
Lung Volume ◽  
Washout Period ◽  
Dead Space ◽  
Inert Gas ◽  
Gas Solubility ◽  
Ventilation Distribution ◽  
Ventilation And Perfusion

We show that when an inert gas is washed into the lungs its retention in the blood during any one breath is approximately proportional to its solubility. This relationship makes possible the correction of washin or washout data for blood uptake or release, provided that two gases of different solubility are used simultaneously. The method automatically allows for the characteristics of an individual washin or washout and for the occurrence of recirculation within a fairly short washin or washout period. It has been tested in models with nonuniform ventilation and perfusion and closely approximates the behavior of a truly insoluble gas. In the derived ventilation distribution, gas solubility appears as ventilation to units of low turnover. In the case of N2 this effect is small but causes appreciable overestimation of lung volume. The recovered dead space and main alveolar distribution are insignificantly affected.

Effects of acetone in heparin on the multiple inert gas elimination technique

1985 ◽  
Vol 58 (4) ◽  
pp. 1143-1147 ◽  
Author(s):  
F. L. Powell ◽  
F. A. Lopez ◽  
P. D. Wagner
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Room Temperature ◽  
Inert Gas ◽  
Published Data ◽  
Physiological Mechanisms ◽  
Heparinized Saline ◽  
Partial Pressures ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

We have detected acetone in several brands of heparin. If uncorrected, this leads to errors in measuring acetone in blood collected in heparinized syringes, as in the multiple inert gas elimination technique for measuring ventilation-perfusion ratio (VA/Q) distributions. Error for acetone retention [R = arterial partial pressure-to-mixed venous partial pressure (P-V) ratio] is usually small, because R is normally near 1.0, and the error is similar in arterial and mixed venous samples. However, acetone excretion [E = mixed expired partial pressure (P-E)-to-P-V ratio] will appear erroneously low, because P-E is accurately measured in dry syringes, but P-V is overestimated. A physical model of a homogeneous alveolar lung at room temperature and without dead space shows: the magnitude of acetone E error depends upon the ratio of blood sample to heparinized saline volumes and acetone partial pressures, without correction, acetone E can be less than that of less soluble gases like ether, a situation incompatible with conventional gas exchange theory, and acetone R and E can be correctly calculated using the principle of mass balance if the acetone partial pressure in heparinized saline is known. Published data from multiple inert gas elimination experiments with acetone-free heparin, in our labs and others, are within the limits of experimental error. Thus the hypothesis that acetone E is anomalously low because of physiological mechanisms involving dead space tissue capacitance for acetone remains to be tested.

Variance of ventilation during exercise

2001 ◽  
Vol 90 (6) ◽  
pp. 2151-2156 ◽  
Author(s):  
Kenneth C. Beck ◽  
Theodore A. Wilson
Keyword(s):  
Standard Deviation ◽  
Normal Distribution ◽  
Ventilation Distribution ◽  
Cycle Exercise ◽  
Expired Gas ◽  
Highly Correlated ◽  
Log Normal ◽  
Male Subjects ◽  
Log Normal Distribution ◽  
Ventilation And Perfusion

Expired gas concentrations were measured during a multibreath washin of He in one female and seven male subjects at rest (seated) and during cycle exercise at work rates of 70–210 W. In a computational model, the ventilation distribution was represented as a log-normal distribution with standard deviation (ςV˙); values of ςV˙ were obtained by fitting the output of the model to the data. At rest, ςV˙ was 0.89 ± 0.18; during exercise, ςV˙ was 0.60 ± 0.13, independent of the level of exercise. These values for the width of the functional ventilation distribution at the scale of the acinus are approximately two times larger than those obtained from anatomic measurements in animals at a scale of 1 cm3. The values for ςV˙, together with data from the literature on the width of the functional ventilation-perfusion distribution, show that ventilation and perfusion are highly correlated at rest, in agreement with anatomic data. The structural sources of nonuniform ventilation and perfusion and of the correlation between them are unknown.

Mechanism of improvement in pulmonary gas exchange during growth in awake piglets

1988 ◽  
Vol 65 (3) ◽  
pp. 1055-1061 ◽  
Author(s):  
P. J. Escourrou ◽  
B. P. Teisseire ◽  
R. A. Herigault ◽  
M. O. Vallez ◽  
A. J. Dupeyrat ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pressure Difference ◽  
Age Groups ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Significant Difference ◽  
Arterial Po2 ◽  
And Diffusion

Previous studies have shown a lower arterial PO2 (PaO2) in infants and young animals than in adults. To investigate the mechanism of this impairment of gas exchange we studied 13 piglets from 12 to 65 days of age. Two days after instrumentation we measured the distribution of ventilation-perfusion ratios (VA/Q) by use of the multiple inert gas technique on awake animals. We showed that PaO2 is lower in young animals, increasing from 72 +/- 11.5 Torr before 2 wk to 102 Torr at 2 mo. This hypoxemia is due to an enlarged alveolar-arterial O2 pressure difference that significantly decreases with age. This impairment in gas exchange is not due to shunting (0.6 +/- 1.3%). Mean dead space (36 +/- 11%) was not related to age. Mean modes of perfusion and ventilation did not differ significantly between age groups. However, the dispersion of perfusion as expressed by its logSD decreased significantly with age, whereas dispersion of ventilation remained constant. Furthermore, in the young animals only, a significant difference was evidenced between measured alveolar-arterial PO2 gradient and the value predicted by the inert gas model. We therefore conclude that the impairment of gas exchange in piglets is due to two mechanisms: VA/Q mismatch and diffusion limitation for O2.

Effects of common dead space on inert gas exchange in mathematical models of the lung

1979 ◽  
Vol 47 (4) ◽  
pp. 896-906 ◽  
Author(s):  
J. B. Fortune ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Dead Space ◽  
The Other ◽  
Inert Gas ◽  
Mixed Gas ◽  
Space Model ◽  
Different Types ◽  
The Dead ◽  
Ventilation And Perfusion

Theoretical gas exchange is compared in lung models having two different types of dead space. In one, the dead space of a lung unit is “personal” and contains gas equivalent in composition to its own alveolar gas; in the other, the dead space is “common” and contains mixed gas from all gas-exchanging units. Formal algebraic analysis of tracer inert gas exchange in two-compartment models shows that values of compartmental ventilation and perfusion can be found that establish one and only one personal dead-space model equivalent for every common dead-space model. When the total dead space and distribution of blood flow and ventilation in the two models are the same, common dead space will always result in improved inert gas elimination. Under these conditions, the amount of improvement is usually greatest when the partition coefficient of the inert gas is between 0.1 and 1.0 and when there is greatest disparity in the ventilation-perfusion ratios (VA/Q). In the inert gas elimination technique that analyzes all dead space as personal, the presence of common dead space consistently causes the recovered VA/Q distributions to be narrower than the actual distributions, but the resultant error is small.

Patient-ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation

1996 ◽  
Vol 81 (1) ◽  
pp. 426-436 ◽  
Author(s):  
V. M. Ranieri ◽  
R. Giuliani ◽  
L. Mascia ◽  
S. Grasso ◽  
V. Petruzzelli ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Dead Space ◽  
Pressure Support ◽  
Esophageal Pressure ◽  
Respiratory Drive ◽  
Resistive Load ◽  
Proportional Assist Ventilation ◽  
Pressure Time ◽  
Pressure Time Product ◽  
Stimulation Of

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.

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.

Reference Values for Respiratory Rate in the First 3 Years of Life

PEDIATRICS ◽  
1994 ◽  
Vol 94 (3) ◽  
pp. 350-355
Author(s):  
Franca Rusconi ◽  
Manuela Castagneto ◽  
Norberto Porta ◽  
Luigi Gagliardi ◽  
Gualtiero Leo ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Young Children ◽  
Respiratory Rate ◽  
Respiratory Infections ◽  
Severe Disease ◽  
Normal Range ◽  
Degree Polynomial ◽  
Percentile Curves ◽  
Polynomial Curve ◽  
Infants And Young Children

Background. Raised respiratory rate is a useful sign to diagnose lower respiratory infections in childhood. However, the normal range for respiratory rate has not been defined in a proper, large sample. Objective. To assess the respiratory rate in a large number of infants and young children in order to construct percentile curves by age; to determine the repeatability of the assessment using a stethoscope and compare it with observation. Methods. Respiratory rate was recorded for 1 minute with a stethoscope in 618 infants and children, aged 15 days to 3 years old, without respiratory infections or any other severe disease when awake and calm and when asleep. In 50 subjects we compared respiratory rate taken 30 to 60 minutes apart to assess repeatability, and in 50 others we compared simultaneous counts obtained by stethoscope versus observation. Results. Repeatability was good as the standard deviation of differences was 2.5 breaths/minute in awake and 1.7 breaths/minute in asleep children. Respiratory rate obtained with a stethoscope was systematically higher than that obtained by observation (mean difference 2.6 breaths/minute in awake and 1.8 breaths/minute in asleep children; P = .015 and P &lt; .001, respectively). A decrease in respiratory rate with age was seen for both states, and it was faster in the first few months of life when also a greater dispersion of values was observed. A second degree polynomial curve accurately fitted the data. Reference percentile values were developed from these data. Conclusions. The repeatability of respiratory rate measured with a stethoscope was good. Percentile curves would be particularly helpful in the first months of life when the decline in respiratory rate is very rapid and prevents to use cut off values for defining "normality."

Ventilation-perfusion relationship in young healthy awake and anesthetized-paralyzed man

1979 ◽  
Vol 47 (4) ◽  
pp. 745-753 ◽  
Author(s):  
K. Rehder ◽  
T. J. Knopp ◽  
A. D. Sessler ◽  
E. P. Didier
Keyword(s):  
Blood Flow ◽  
Healthy Volunteers ◽  
Dead Space ◽  
Flow Distribution ◽  
Blood Flow Distribution ◽  
Alveolar Dead Space ◽  
Awake State ◽  
Lateral Decubitus ◽  
Inspired Oxygen ◽  
Ventilation And Perfusion

Distributions of ventilation and perfusion relative to Va/Q were determined in seven young healthy volunteers (24–33 yr) while they were either in the supine or right lateral decubitus position. The subjects were studied first awake and then while anesthetized-paralyzed and breathing 30% oxygen and again while breathing 100% oxygen. In the awake state, no statistically significant differences were observed in the distribution of ventilation and perfusion relative to Va/Q between the supine and right lateral decubitus positions or on changing the inspired oxygen concentrations. After induction of anesthesia-paralysis, Va/Q mismatching increased significantly but only small right-to-left intrapulmonary shunts developed. Ventilating the lungs with 100% oxygen further increased the dispersion of blood flow distribution during anesthesia-paralysis; lung units with low Va/Q or right-to-left intrapulmonary shunts (or both) developed. With induction of anesthesia-paralysis and intubation of the trachea, the anatomic dead space was decreased and the alveolar dead space increased.

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.

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