Hemodilution during Venous Gas Embolization Improves Gas Exchange, without Altering V̇A/Q̇ or Pulmonary Blood Flow Distributions 

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 < 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.

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 < 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 < 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 < 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 < 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 < 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 < 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.


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.


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.


1999 ◽  
Vol 14 (3) ◽  
pp. 154-160 ◽  
Author(s):  
Masao Tayama ◽  
Nobuaki Hirata ◽  
Tohru Matsushita ◽  
Tetsuya Sano ◽  
Norihide Fukushima ◽  
...  

2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P &lt; 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P &lt; 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.


PEDIATRICS ◽  
1967 ◽  
Vol 40 (6) ◽  
pp. 937-938
Author(s):  
M. E. A.

THE elegant studies reported by Led-better, Homma, and Farhi in this issue are entitled `'Readjustment in Distribution of Alveolar Ventilation and Lung Perfusion in the Newborn." It must come as a great surprise to the reader to discover that the only measurement actually made was the partial pressure of nitrogen in the infants' urine. How could one conclude that there were significant imbalances between the distribution of alveolar ventilation and pulmonary blood flow (VA/Q) in the first days of life in normal infants from a urine sample? It is all the more astounding in the light of previous (and seemingly more direct) studies of alveolar-arterial oxygen and carbon dioxide differences which led others to consider the differences largely explained by anatomical right-to-left shunts.


2004 ◽  
Vol 287 (4) ◽  
pp. L867-L878 ◽  
Author(s):  
Kai Heckel ◽  
Rainer Kiefmann ◽  
Martina Dörger ◽  
Mechthild Stoeckelhuber ◽  
Alwin E. Goetz

Permeability of the endothelial barrier to large molecules plays a pivotal role in the manifestation of early acute lung injury. We present a novel and sensitive technique that brings microanatomical visualization and quantification of microvascular permeability in line. White New Zealand rabbits were anesthetized and ventilated mechanically. Rabbit serum albumin (RSA) was labeled with colloidal gold particles. We quantified macromolecular leakage of gold-labeled RSA and thickening of the gas exchange distance by electron microscopy, taking into account morphology of microvessels. The control group receiving a saline solution represented a normal gas exchange barrier without extravasation of gold-labeled albumin. Infusion of lipopolysaccharide (LPS) resulted in a significant displacement of gold-labeled albumin into pulmonary cells, the lung interstitium, and even the alveolar space. Correspondingly, intravital fluorescence microscopy and digital image analysis indicated thickening of width of alveolar septa. The findings were accompanied by a deterioration of alveolo-arterial oxygen difference, whereas wet/dry ratio and albumin concentration in the bronchoalveolar lavage fluid failed to detect that early stage of pulmonary edema. Inhibition of the nuclear enzyme poly(ADP-ribose) synthetase by 3-aminobenzamide prevented LPS-induced microvascular injury. To summarize: colloidal gold particles visualized by standard electron microscopy are a new and very sensitive in vivo marker of microvascular permeability in early acute lung injury. This technique enabling detailed microanatomical and quantitative pathophysiological characterization of edema formation can form the basis for evaluating novel treatment strategies against acute lung injury.


2000 ◽  
Vol 16 (2) ◽  
pp. 288 ◽  
Author(s):  
T.V. Brogan ◽  
R.G. Hedges ◽  
S. McKinney ◽  
H.T. Robertson ◽  
M.P. Hlastala ◽  
...  

Respiration ◽  
1974 ◽  
Vol 31 (4) ◽  
pp. 289-295
Author(s):  
M. Arborelius, jr. ◽  
V. Lopéz-Majano ◽  
R.C. Reba ◽  
T.K. Natarajan

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