Effect of altered gas diffusivity on alveolar gas exchange-a theoretical study

1980 ◽  
Vol 48 (1) ◽  
pp. 147-153 ◽  
Author(s):  
W. Nixon ◽  
A. Pack

Experimental studies have established that alveolar gas exchange is inversely relation to the molecular diffusivity of gas in the lung airways. The mechanism underlying this relationship is, however, unclear. To investigate this phenomenon, the conditions relevant to the experimental studies are simulated using a computational model of pulmonary gas transport. Results from these simulations suggest that the inverse relationship found experimentally can largely be explained on the basis of the intra-acinar stratification of blood flow and gas concentrations. Gas having a relatively low molecular diffusivity is not transported as far into the acinus as gas having a higher diffusivity. When these relative intra-acinar gas distributions interact with the blood flow distribution, which has been shown experimentally to be weighted towards the proximal alveoli, more gas exchange occurs in the low molecular diffusivity mixture. Consideration of the various other mechanisms that have been proposed to explain the experimental findings.he inverse dependence suggests that they are of little significance. In particular, our studies remove the need to invoke Taylor diffusion to explain the experimental findings.

1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


1999 ◽  
Vol 91 (6) ◽  
pp. 1861-1861 ◽  
Author(s):  
Steven Deem ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Richard G. Hedges ◽  
Erik R. Swenson

Background Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. Methods Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). Results Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P &lt; 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. Conclusions Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear.


2000 ◽  
Vol 89 (6) ◽  
pp. 2263-2267 ◽  
Author(s):  
Robb W. Glenny ◽  
H. Thomas Robertson ◽  
Michael P. Hlastala

To determine whether vasoregulation is an important cause of pulmonary perfusion heterogeneity, we measured regional blood flow and gas exchange before and after giving prostacyclin (PGI2) to baboons. Four animals were anesthetized with ketamine and mechanically ventilated. Fluorescent microspheres were used to mark regional perfusion before and after PGI2 infusion. The lungs were subsequently excised, dried inflated, and diced into ∼2-cm3 pieces ( n = 1,208–1,629 per animal) with the spatial coordinates recorded for each piece. Blood flow to each piece was determined for each condition from the fluorescent signals. Blood flow heterogeneity did not change with PGI2 infusion. Two other measures of spatial blood flow distribution, the fractal dimension and the spatial correlation, did not change with PGI2 infusion. Alveolar-arterial O2 differences did not change with PGI2 infusion. We conclude that, in normal primate lungs during normoxia, vasomotor tone is not a significant cause of perfusion heterogeneity. Despite the heterogeneous distribution of blood flow, active regulation of regional perfusion is not required for efficient gas exchange.


1982 ◽  
Vol 53 (6) ◽  
pp. 1411-1417 ◽  
Author(s):  
J. H. Jones

Ostriches (Struthio camelus) are the only birds known that can increase post-dead space ventilation during severe heat stress without experiencing hypocapnia and respiratory alkalosis. To determine whether this phenomenon occurs due to redistribution of pulmonary blood flow during panting, thus creating an extreme ventilation-perfusion (V/Q) imbalance, the distributions of pulmonary blood flow in ostriches at rest (15 degrees C) and in severe panting (45 degrees C) were determined using radioactively labeled microspheres. Blood flow distribution at rest was greatest in the neopulmo [18% greater than mean pulmonary blood flow (MPBF)] and the cranial (23% greater than MPBF) and distal (12% greater than MPBF) regions of the paleopulmo. During panting blood flow was not shunted around the lung, and flow to the neopulmo decreased to MPBF, became more homogeneous along the craniocaudal axis, and remained nonhomogeneous along the mediolateral axis. The results suggest that the observed decrease in gas exchange during panting is probably due primarily to shunting of the increased ventilation around the parabronchial exchange region rather than to alterations in the patterns of V/Q within the lung.


2004 ◽  
Vol 97 (6) ◽  
pp. 2104-2111 ◽  
Author(s):  
William A. Altemeier ◽  
Steve McKinney ◽  
Melissa Krueger ◽  
Robb W. Glenny

Although recent high-resolution studies demonstrate the importance of nongravitational determinants for both pulmonary blood flow and ventilation distributions, posture has a clear impact on whole lung gas exchange. Deterioration in arterial oxygenation with repositioning from prone to supine posture is caused by increased heterogeneity in the distribution of ventilation-to-perfusion ratios. This can result from increased heterogeneity in regional blood flow distribution, increased heterogeneity in regional ventilation distribution, decreased correlation between regional blood flow and ventilation, or some combination of the above (Wilson TA and Beck KC, J Appl Physiol 72: 2298–2304, 1992). We hypothesize that, although repositioning from prone to supine has relatively small effects on overall blood flow and ventilation distributions, regional changes are poorly correlated, resulting in regional ventilation-perfusion mismatch and reduction in alveolar oxygen tension. We report ventilation and perfusion distributions in seven anesthetized, mechanically ventilated pigs measured with aerosolized and injected microspheres. Total contributions of pulmonary structure and posture on ventilation and perfusion heterogeneities were quantified by using analysis of variance. Regional gradients of posture-mediated change in ventilation, perfusion, and calculated alveolar oxygen tension were examined in the caudocranial and ventrodorsal directions. We found that pulmonary structure was responsible for 74.0 ± 4.7% of total ventilation heterogeneity and 63.3 ± 4.2% of total blood flow heterogeneity. Posture-mediated redistribution was primarily oriented along the caudocranial axis for ventilation and along the ventrodorsal axis for blood flow. These mismatched changes reduced alveolar oxygen tension primarily in the dorsocaudal lung region.


2002 ◽  
Vol 97 (3) ◽  
pp. 652-659 ◽  
Author(s):  
Christian Putensen ◽  
Jukka Räsänen ◽  
Gabriele Putensen-Himmer ◽  
John B. Downs

Background Rapid recovery and weaning from ventilatory support and cardiovascular stability are suggested advantages of isoflurane inhalation, in concentrations ranging from 0.1 to 0.6 vol%, for long-term sedation in mechanical ventilated patients. This study was designed to determine whether isoflurane in low concentrations impairs pulmonary gas exchange by increasing ventilation and perfusion (V(A)/Q) mismatch during lung injury. Methods Fourteen anesthetized dogs received in random order 0, 0.25, or 0.5 vol% end-tidal isoflurane before and after induction of lung injury with oleic acid. Gas exchange was assessed by blood gas analysis and by estimating the V(A)/Q distributions using the multiple inert gas elimination technique. Results Administration of oleic acid produced a lung injury with severe V(A)/Q mismatch and 38 +/- 4% intrapulmonary shunting of blood. During lung injury, isoflurane accounted for a dose-related increase in blood flow to shunt units from 38 +/- 4 to 42 +/- 3 (0.25 vol%) and 48 +/- 4% (0.5 vol%) (P &lt; 0.05), dispersion pulmonary blood flow distribution from 0.94 +/- 0.07 to 1.01 +/- 0.09 (0.25 vol%) and 1.11 +/- 0.11% (0.5 vol%) (P &lt; 0.05), and a decrease in perfusion of normal V(A)/Q units from 58 +/- 5 to 55 +/- 4 (0.25 vol%) and 50 +/- 4% (0.5 vol%) (P &lt; 0.05) (mean +/- SE). Isoflurane decreased arterial oxygen partial pressure from 72 +/- 4 to 62 +/- 4 mmHg (0.25 vol%) and 56 +/- 4 mmHg (0.5 vol%) (P &lt; 0.05) and oxygen delivery from 573 +/- 21 to 529 +/- 19 ml. kg. min (0.25 vol%) and 505 +/- 22 ml. kg. min (0.5 vol%) (P &lt; 0.05). Gas exchange, perfusion of shunt and normal V(A)/Q units, and pulmonary blood flow distribution was similar in absence of lung injury with and without isoflurane. Isoflurane 0.5 vol% lowered cardiac output during all conditions (P &lt; 0.05). CONCLUSIONS Inhalation of low concentrations of isoflurane contributed to increased V(A)/Q mismatch and decreased systemic blood flow and oxygen delivery in mechanically ventilated animals with injured lungs.


2020 ◽  
Vol 22 (2) ◽  
pp. 619-636 ◽  
Author(s):  
Zbigniew Tyfa ◽  
Damian Obidowski ◽  
Krzysztof Jóźwik

AbstractThe primary objective of this research can be divided into two separate aspects. The first one was to verify whether own software can be treated as a viable source of data for the Computer Aided Design (CAD) modelling and Computational Fluid Dynamics CFD analysis. The second aspect was to analyze the influence of the Ventricle Assist Device (VAD) outflow cannula positioning on the blood flow distribution in the brain-supplying arteries. Patient-specific model was reconstructed basing on the DICOM image sets obtained with the angiographic Computed Tomography. The reconstruction process was performed in the custom-created software, whereas the outflow cannulas were added in the SolidWorks software. Volumetric meshes were generated in the Ansys Mesher module. The transient boundary conditions enabled simulating several full cardiac cycles. Performed investigations focused mainly on volume flow rate, shear stress and velocity distribution. It was proven that custom-created software enhances the processes of the anatomical objects reconstruction. Developed geometrical files are compatible with CAD and CFD software – they can be easily manipulated and modified. Concerning the numerical simulations, several cases with varied positioning of the VAD outflow cannula were analyzed. Obtained results revealed that the location of the VAD outflow cannula has a slight impact on the blood flow distribution among the brain supplying arteries.


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