Isoflurane and Sevoflurane Anesthesia in Pigs with a Preexistent Gas Exchange Defect

Background Decreased arterial partial pressure of oxygen (PaO2) during volatile anesthesia is well-known. Halothane has been examined with the multiple inert gas elimination technique and has been shown to alter the distribution of pulmonary blood flow and thus PaO2. The effects of isoflurane and sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesized that sevoflurane with a relatively high minimum alveolar concentration (MAC) would result in significantly more gas exchange disturbances in comparison with isoflurane or control. Methods This study was performed in a porcine model with an air pneumoperitoneum that generates a reproducible gas exchange defect. After a baseline measurement of pulmonary gas exchange (multiple inert gas elimination technique) during propofol anesthesia, 21 pigs were randomly assigned to three groups of seven animals each. One group received isoflurane anesthesia, one group received sevoflurane anesthesia, and one group was continued on propofol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or propofol anesthesia, a second measurement (multiple inert gas elimination technique) was performed. Results At the second measurement, inert gas shunt was 15 +/- 3% (mean +/- SD) during sevoflurane anesthesia versus 9 +/- 1% during propofol anesthesia (P = 0.02). Blood flow to normal ventilation/perfusion (V(A)/Q) lung areas was 83 +/- 5% during sevoflurane anesthesia versus 89 +/- 1% during propofol anesthesia (P = 0.04). This resulted in a PaO2 of 88 +/- 11 mmHg during sevoflurane anesthesia versus 102 +/- 15 mmHg during propofol anesthesia (P = 0.04). Inert gas and blood gas variables during isoflurane anesthesia did not differ significantly from those obtained during propofol anesthesia. Conclusions In pigs with an already existent gas exchange defect, sevoflurane anesthesia but not isoflurane anesthesia causes significantly more gas exchange disturbances than propofol anesthesia does.

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Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution

Journal of Applied Physiology ◽

10.1152/jappl.1999.87.1.132 ◽

1999 ◽

Vol 87 (1) ◽

pp. 132-141 ◽

Cited By ~ 39

Author(s):

Steven Deem ◽

Richard G. Hedges ◽

Steven McKinney ◽

Nayak L. Polissar ◽

Michael K. Alberts ◽

...

Keyword(s):

Blood Flow ◽

Fractal Dimension ◽

Gas Exchange ◽

Spatial Correlation ◽

Pulmonary Blood Flow ◽

Minute Ventilation ◽

Flow Distribution ◽

Pulmonary Gas Exchange ◽

Normal Lung ◽

Blood Flow Distribution

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.

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Effects of Vaporized Perfluorocarbon on Pulmonary Blood Flow and Ventilation/Perfusion Distribution in a Model of Acute Respiratory Distress Syndrome

Anesthesiology ◽

10.1097/00000542-200112000-00021 ◽

2001 ◽

Vol 95 (6) ◽

pp. 1414-1421 ◽

Cited By ~ 12

Author(s):

Matthias Hübler ◽

Jennifer E. Souders ◽

Erin D. Shade ◽

Nayak L. Polissar ◽

Carmel Schimmel ◽

...

Keyword(s):

Blood Flow ◽

Oleic Acid ◽

Gas Exchange ◽

Lung Injury ◽

Repeated Measures ◽

Pulmonary Blood Flow ◽

Analysis Of Covariance ◽

Inert Gas ◽

Low Flow ◽

Repeated Measures Analysis

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 < 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 < 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.

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Unilateral lung edema: effects on pulmonary gas exchange, hemodynamics, and pulmonary perfusion distribution

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.4.1513 ◽

2000 ◽

Vol 89 (4) ◽

pp. 1513-1521 ◽

Cited By ~ 8

Author(s):

Klaus Slama ◽

Mareike Gesch ◽

Johannes C. Böck ◽

Sylvia M. Pietschmann ◽

Walter Schaffartzik ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Pulmonary Artery ◽

Venous Pressure ◽

Pulmonary Gas Exchange ◽

The Other ◽

Lung Edema ◽

Pulmonary Perfusion ◽

Central Venous ◽

Fluorescent Microspheres

Two types of unilateral lung edema in sheep were characterized regarding their effects on pulmonary gas exchange, hemodynamics, and distribution of pulmonary perfusion. One edema type was induced with aerosolized HCl (0.15 M, pH 1.0) and the other with NaCl (0.15 M, pH 7.4). Both aerosols were nebulized continuously for 4 h into left lungs. In HCl-treated animals, pulmonary gas exchange deteriorated [from a partial arterial O2 pressure-to-inspired O2 fraction ratio (PaO2 /Fi O2 ) of 254 at baseline to 187 after 4 h HCl]. In addition, pulmonary artery pressure and total pulmonary vascular resistance increased (from 16 to 19 mmHg and from 133 to 154 dyn · s · cm−5, respectively). In NaCl-treated animals, only the central venous pressure significantly increased (from 7 to 9 mmHg). Distribution of pulmonary perfusion (measured with fluorescent microspheres) changed differently in both groups. After HCl application, 6% more blood flow was directed to the treated lung, whereas, after NaCl, 5% more blood flow was directed to the untreated lung. HCl and NaCl treatment both induce an equivalent lung edema, but only HCl treatment is associated with gas exchange alteration and tissue damage. Redistribution of pulmonary perfusion maintains gas exchange during NaCl treatment and decreases it during HCl inhalation.

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Pulmonary gas exchange response to exercise- and mannitol-induced bronchoconstriction in mild asthma

Journal of Applied Physiology ◽

10.1152/japplphysiol.00108.2008 ◽

2008 ◽

Vol 105 (5) ◽

pp. 1477-1485 ◽

Cited By ~ 27

Author(s):

Phillip A. Muñoz ◽

Federico P. Gómez ◽

Hernán A. Manrique ◽

Josep Roca ◽

Joan A. Barberà ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Minute Ventilation ◽

Forced Expiratory Volume ◽

Pulmonary Gas Exchange ◽

Slow Recovery ◽

Airway Narrowing ◽

Asthmatic Patients ◽

Response To Exercise ◽

Blood Flow Redistribution

Both exercise (EIB) and mannitol challenges were performed in asthmatic patients to assess and compare their pulmonary gas exchange responses for an equivalent degree of bronchoconstriction. In 11 subjects with EIB [27 ± 4 (SD) yr; forced expiratory volume in 1 s (FEV1), 86 ± 8% predicted], ventilation-perfusion (V̇a/Q̇) distributions (using multiple inert gas elimination technique) were measured 5, 15, and 45 min after cycling exercise (FEV1 fall, 35 ± 12%) and after mannitol (33 ± 10%), 1 wk apart. Five minutes after EIB, minute ventilation (V̇e; by 123 ± 60%), cardiac output (Q̇t, by 48 ± 29%), and oxygen uptake (V̇o2; by 54 ± 25%) increased, whereas arterial Po2 (PaO2; by 14 ± 11 Torr) decreased due to moderate V̇a/Q̇ imbalance, assessed by increases in dispersions of pulmonary blood flow (log SDQ̇; by 0.53 ± 0.16) and alveolar ventilation (log SDV̇; by 0.28 ± 0.15) (dimensionless) ( P < 0.01 each). In contrast, for an equivalent degree of bronchoconstriction and minor increases in V̇e, Q̇t, and V̇o2, mannitol decreased PaO2 more intensely (by 24 ± 9 Torr) despite fewer disturbances in log SDQ̇ (by 0.27 ± 0.12). Notwithstanding, mannitol-induced increase in log SDV̇ at 5 min (by 0.35 ± 0.15) was similar to that observed during EIB, as was the slow recovery in log SDV̇ and high V̇a/Q̇ ratio areas, at variance with the faster recovery of log SDQ̇ and low V̇a/Q̇ ratio areas. In asthmatic individuals, EIB provokes more V̇a/Q̇ imbalance but less hypoxemia than mannitol, primarily due to postexercise increases in V̇e and Q̇t benefiting PaO2. V̇a/Q̇ inequalities during both challenges most likely reflect uneven airway narrowing and blood flow redistribution generating distinctive V̇a/Q̇ patterns, including the development of areas with low and high V̇a/Q̇ ratios.

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Oxygen-induced alteration of ventilation-perfusion relationships in rats

Journal of Applied Physiology ◽

10.1152/jappl.1979.47.5.1112 ◽

1979 ◽

Vol 47 (5) ◽

pp. 1112-1117 ◽

Cited By ~ 20

Author(s):

W. E. Truog ◽

M. P. Hlastala ◽

T. A. Standaert ◽

H. P. McKenna ◽

W. A. Hodson

Keyword(s):

Gas Exchange ◽

Pulmonary Gas Exchange ◽

Inert Gas ◽

Base Line ◽

Small Animals ◽

Difference Curve ◽

Oxygen Breathing ◽

Anesthetized Rats ◽

Effect Of Oxygen ◽

Breathing Room

The effect of oxygen breathing on shunt and ventilation-perfusion ratios (VA/Q) in anesthetized rats was studied using a modification of the multiple inert gas elimination technique. Base-line analyses showed hypoxemia in some animals breathing room air (arterial O2 tensions 48-70 Torr) associated with intrapulmonary shunts ranging from 0 to 22%, and variable low VA/Q lung regions as determined by calculation of the inert gas arterial-alveolar difference curve. Of nine rats that breathed 100% oxygen for 30 min, three showed increases in shunt (0% leads to 19%, 1.5% leads to 16%, 11% leads to 40%). These three animals had larger preexisting low VA/Q regions than the six that developed no shunt (0.48 +/- 0.15 vs. 0.17 +/- 0.03 (mean +/- SD); P less than 0.05). These data are compatible with the theory of absorption atelectasis. This study documents the usefulness of the inert gas elimination technique for studying pulmonary gas exchange problems in small animals.

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The effect of blood flow and diffusion impairment on pulmonary gas exchange: A computer model

Computers and Biomedical Research ◽

10.1016/0010-4809(87)90037-1 ◽

1987 ◽

Vol 20 (5) ◽

pp. 497-506 ◽

Cited By ~ 6

Author(s):

Wesley M. Granger ◽

David A. Miller ◽

Ina C. Ehrhart ◽

Wendell F. Hofman

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Computer Model ◽

Pulmonary Gas Exchange ◽

And Diffusion

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Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.2.912 ◽

1994 ◽

Vol 77 (2) ◽

pp. 912-917 ◽

Cited By ~ 95

Author(s):

S. R. Hopkins ◽

D. C. McKenzie ◽

R. B. Schoene ◽

R. W. Glenny ◽

H. T. Robertson

Keyword(s):

Gas Exchange ◽

Aerobic Capacity ◽

Maximal Exercise ◽

Cycle Ergometer ◽

Pulmonary Gas Exchange ◽

Inert Gases ◽

Inert Gas ◽

Diffusion Limitation ◽

Maximal Aerobic Capacity ◽

Arterial Blood

To investigate pulmonary gas exchange during exercise in athletes, 10 high aerobic capacity athletes (maximal aerobic capacity = 5.15 +/- 0.52 l/min) underwent testing on a cycle ergometer at rest, 150 W, 300 W, and maximal exercise (372 +/- 22 W) while trace amounts of six inert gases were infused intravenously. Arterial blood samples, mixed expired gas samples, and metabolic data were obtained. Indexes of ventilation-perfusion (VA/Q) mismatch were calculated by the multiple inert gas elimination technique. The alveolar-arterial difference for O2 (AaDO2) was predicted from the inert gas model on the basis of the calculated VA/Q mismatch. VA/Q heterogeneity increased significantly with exercise and was predicted to increase the AaDO2 by > 17 Torr during heavy and maximal exercise. The observed AaDO2 increased significantly more than that predicted by the inert gas technique during maximal exercise (10 +/- 10 Torr). These data suggest that this population develops diffusion limitation during maximal exercise, but VA/Q mismatch is the most important contributor (> 60%) to the wide AaDO2 observed.

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