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

1996 ◽  
Vol 81 (3) ◽  
pp. 1121-1127 ◽  
Author(s):  
A. Nahum ◽  
S. A. Ravenscraft ◽  
A. B. Adams ◽  
J. J. Marini

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.

1993 ◽  
Vol 75 (3) ◽  
pp. 1238-1246 ◽  
Author(s):  
A. Nahum ◽  
S. A. Ravenscraft ◽  
G. Nakos ◽  
A. B. Adams ◽  
W. C. Burke ◽  
...  

Tracheal gas insufflation (TGI) improves the efficiency of CO2 elimination by replacing CO2 in the anatomic dead space proximal to the catheter tip with fresh gas during expiration. Turbulence generated by gas exiting the catheter tip may also contribute to alveolar ventilation. To separate distal (turbulence-related) and proximal (washout of dead space) effects of TGI, we compared the efficacy of a straight and an inverted catheter during continuous and expiratory TGI in six mechanically ventilated dogs. We reasoned that the inverted catheter cannot improve CO2 elimination from more distal conducting airways. During continuous TGI with the straight catheter, arterial PCO2 (PaCO2) decreased significantly from baseline (without TGI) of 56 +/- 10 Torr to 38 +/- 8, 36 +/- 8, and 35 +/- 8 Torr at catheter flow rates (Vcath) of 5, 10, and 15 l/min, respectively. For the same conditions, PaCO2 was always higher (P < 0.001) with the inverted catheter (42 +/- 10, 41 +/- 10, and 41 +/- 10 Torr). PaCO2 was lower with the straight (40 +/- 9 Torr) than with the inverted catheter (44 +/- 10 Torr, P < 0.001) during TGI delivered only during expiration at a Vcath of 10 l/min. End-expiratory lung volume relative to baseline increased during continuous, but not during expiratory, TGI and was significantly greater with the straight than with the inverted catheter (P < 0.0001). Our data confirm that the primary mechanism of TGI is expiratory washout of the proximal anatomic dead space but also suggest a minor contribution of turbulence beyond the tip of the straight catheter.


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.


1995 ◽  
Vol 23 (2) ◽  
pp. 348-356 ◽  
Author(s):  
Avi Nahum ◽  
Amit Chandra ◽  
Jamshid Niknam ◽  
Sue A. Ravenscraft ◽  
Alexander B. Adams ◽  
...  

1998 ◽  
Vol 84 (5) ◽  
pp. 1566-1572 ◽  
Author(s):  
Paul G. Gauger ◽  
Michael C. Overbeck ◽  
Sean D. Chambers ◽  
Christine I. Cailipan ◽  
Ronald B. Hirschl

Gas exchange is improved during partial liquid ventilation with perfluorocarbon in animal models of acute lung injury. The specific mechanisms are unproved. We measured end-expiratory lung volume (EELV) by null-point body plethysmography in anesthetized sheep. Measurements of gas exchange and EELV were made before and after acute lung injury was induced with intravenous oleic acid to decrease EELV and worsen gas exchange. Measurements of gas exchange and EELV were again performed after partial liquid ventilation with 30 ml/kg of perfluorocarbon and compared with gas-ventilated controls. Oxygenation was significantly improved during partial liquid ventilation, and EELV (composite of gas and liquid) was significantly increased, compared with preliquid ventilation values and gas-ventilated controls. We conclude that partial liquid ventilation may directly recruit consolidated alveoli in the lung-injured sheep and that this may be one mechanism whereby gas exchange is improved.


1990 ◽  
Vol 68 (4) ◽  
pp. 1386-1392 ◽  
Author(s):  
C. M. Wiener ◽  
W. Kirk ◽  
R. K. Albert

Although oxygenation improves in patients with the adult respiratory distress syndrome and in animals with oleic acid- (OA) induced acute lung injury when they are turned from the supine to the prone position, the mechanism(s) by which this improvement occurs is not known. Several groups have speculated that this improvement results from preferential edema accumulation in the dorsal lung regions and redistribution of perfusion away from these regions when the patients are turned to the prone position. We used radiolabeled microspheres to measure the regional distribution of perfusion (Qr) to the dorsal, mid, and ventral lungs of eight dogs in vivo in the supine and prone positions, before and after inducing acute lung injury with OA, and correlated the Qr observed after injury with the degree of regional extravascular lung water (EVLWr). Before OA, Qr increased along the gravitational gradient when the animals were supine but was more uniformly distributed when they were prone. After OA, Qr again followed a gravitational gradient when the animals were supine but was preferentially distributed to the nondependent regions when they were prone. EVLWr was similar in all regions, regardless of whether OA was injected when the animals were supine or prone. The gravitational Qr gradient is markedly reduced in the prone position, both before and after lung injury. The prone position-induced improvement in oxygenation is not the result of redistribution of Qr away from areas in which edema preferentially develops.


1987 ◽  
Vol 73 (4) ◽  
pp. 351-359 ◽  
Author(s):  
E. A. Harris ◽  
P. R. Buchanan ◽  
R. M. L. Whitlock

1. Incomplete mixing of alveolar gas may be expressed as an equivalent alveolar dead space serving a remaining alveolar space in which mixing is regarded as complete. Calculation of this dead space during multiple-breath, inert gas wash-in or wash-out leads to an estimate of ‘multiple-breath alveolar mixing efficiency’ (MBME). 2. We measured MBME in 25 healthy subjects and six patients with chronic airflow limitation (CAL), and in three asthmatic patients before and after bronchial provocation with histamine aerosol, from successive breaths during open-circuit, multiple-breath wash-in of a mixture containing helium (He) and sulphur hexafluoride (SF6). The simultaneous use of a light and a heavy gas helps to identify diffusive mechanisms. 3. MBME fell almost linearly with log Z, the proportion of total wash-in remaining uncompleted. For a given Z, MBME was always lower for SF6 than for He in the same subject. In health the lowest MBME (52.2%) was seen for SF6 in a man aged 21 years. The same wash-in yielded a ventilation distribution with an extreme range of specific ventilation of less than 1 decade. MBME of this order is thus consistent with estimates of ventilation distribution in health. 4. Patients with CAL showed a big increase in the volume of the conducting airways or ‘series dead space’ (VDS) for both gases, and VDS was always bigger for SF6 than for He. This very large VDS appears to be the main reason for wash-in delay in these patients, followed by impaired diffusive mixing in the peripheral air spaces. Ventilation maldistribution may play little part in the mixing defect. 5. In asthma, bronchoconstriction by histamine reduced VDS and MBME, but MBME did not differ between He and SF6. This suggests a shortening of diffusion distances beyond the narrowed bronchioles which may help to mitigate the (here predominant) effects of maldistribution on mixing efficiency.


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.


1990 ◽  
Vol 69 (1) ◽  
pp. 293-298 ◽  
Author(s):  
M. Leeman ◽  
P. Lejeune ◽  
J. Closset ◽  
J. L. Vachiery ◽  
C. Melot ◽  
...  

It has recently been suggested that pulmonary hypertension secondary to oleic acid lung injury mainly results from an increase in the critical closing pressure of the pulmonary vessels [Boiteau et al., Am. J. Physiol. 251 (Heart Circ. Physiol. 20): H1163-H1170, 1986]. To further test this hypothesis, we studied 1) the pulmonary arterial pressure- (Ppa) flow (Q) relationship with left atrial pressure (Pla) kept constant (n = 7) and 2) the Ppa-Pla relationship with Q kept constant (n = 9) in intact anesthetized and ventilated dogs before and after lung injury induced by oleic acid (0.09 ml/kg iv). Q was manipulated by use of a femoral arteriovenous bypass and a balloon catheter inserted in the inferior vena cava. Pla was manipulated with a balloon catheter placed by thoracotomy in the left atrium. Ppa-Q plots were rectilinear before as well as after oleic acid. Before oleic acid, the extrapolated pressure intercept of the Ppa-Q plots approximated Pla. Oleic acid administration resulted in a parallel shift of the Ppa-Q plots to higher pressure; i.e., the pressure intercept increased, whereas the slope was not modified. Increasing Pla at constant Q before oleic acid led to a proportional augmentation of Ppa. After oleic acid, however, changes in Pla over the same range affected Ppa only at the highest levels of Pla. These results suggest that oleic acid lung injury increases the critical closing pressure that exceeds Pla, becomes the effective outflow pressure of the pulmonary circulation, and is responsible for the pulmonary hypertension.


2006 ◽  
Vol 101 (3) ◽  
pp. 826-832 ◽  
Author(s):  
S. E. Rees ◽  
S. Kjærgaard ◽  
S. Andreassen ◽  
G. Hedenstierna

The multiple inert-gas elimination technique (MIGET) is a complex mathematical model and experimental technique for understanding pulmonary gas exchange. Simpler mathematical models have been proposed that have a limited view compared with MIGET but may be applicable for use in clinical practice. This study examined the use of a simple model of gas exchange to describe MIGET retention and excretion data in seven pigs before and following lung damage caused by oleic acid infusion and subsequently at different levels of positive end-expiratory pressure. The simple model was found to give, on average, a good description of MIGET data, as evaluated by a χ2 test on the weighted residual sum of squares resulting from the model fit ( P > 0.2). Values of the simple model's parameters (dead-space volume, shunt, and the fraction of alveolar ventilation going to compartment 2) compared well with the similar MIGET parameters (dead-space volume, shunt, log of the standard deviation of the perfusion, log of the standard deveation of the ventilation), giving values of bias and standard deviation on the differences between dead-space volume and shunt of 0.002 ± 0.002 liter and 7.3 ± 2.1% (% of shunt value), respectively. Values of the fraction of alveolar ventilation going to compartment 2 correlated well with log of the standard deviation of the perfusion ( r2 = 0.86) and log of the standard deviation of the ventilation ( r2 = 0.92). These results indicate that this simple model provides a good description of lung pathology following oleic acid infusion. It remains to be seen whether physiologically valid values of the simple model parameters can be obtained from clinical experiments varying inspired oxygen fraction. If so, this may indicate a role for simple models in the clinical interpretation of gas exchange.


1995 ◽  
Vol 10 (3) ◽  
pp. 115-121 ◽  
Author(s):  
Avi Nahum ◽  
Sue A. Ravenscraft ◽  
Alexander B. Adams ◽  
John J. Marini

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