Intra‐pulmonary arteriovenous anastomoses and pulmonary gas exchange: evaluation by microspheres, contrast echocardiography and inert gas elimination

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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Intrapulmonary shunting and pulmonary gas exchange during normoxic and hypoxic exercise in healthy humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00208.2007 ◽

2008 ◽

Vol 104 (5) ◽

pp. 1418-1425 ◽

Cited By ~ 88

Author(s):

Andrew T. Lovering ◽

Lee M. Romer ◽

Hans C. Haverkamp ◽

David F. Pegelow ◽

John S. Hokanson ◽

...

Keyword(s):

Gas Exchange ◽

Contrast Echocardiography ◽

Pulmonary Gas Exchange ◽

Pulmonary Vasculature ◽

Long Term Effects ◽

Arteriovenous Shunting ◽

Healthy Humans ◽

Intrapulmonary Shunting ◽

Exercise Induced

Exercise-induced intrapulmonary arteriovenous shunting, as detected by saline contrast echocardiography, has been demonstrated in healthy humans. We have previously suggested that increases in both pulmonary pressures and blood flow associated with exercise are responsible for opening these intrapulmonary arteriovenous pathways. In the present study, we hypothesized that, although cardiac output and pulmonary pressures would be higher in hypoxia, the potent pulmonary vasoconstrictor effect of hypoxia would actually attenuate exercise-induced intrapulmonary shunting. Using saline contrast echocardiography, we examined nine healthy men during incremental (65 W + 30 W/2 min) cycle exercise to exhaustion in normoxia and hypoxia (fraction of inspired O2 = 0.12). Contrast injections were made into a peripheral vein at rest and during exercise and recovery (3–5 min postexercise) with pulmonary gas exchange measured simultaneously. At rest, no subject demonstrated intrapulmonary shunting in normoxia [arterial Po2 (PaO2) = 98 ± 10 Torr], whereas in hypoxia (PaO2 = 47 ± 5 Torr), intrapulmonary shunting developed in 3/9 subjects. During exercise, ∼90% (8/9) of the subjects shunted during normoxia, whereas all subjects shunted during hypoxia. Four of the nine subjects shunted at a lower workload in hypoxia. Furthermore, all subjects continued to shunt at 3 min, and five subjects shunted at 5 min postexercise in hypoxia. Hypoxia has acute effects by inducing intrapulmonary arteriovenous shunt pathways at rest and during exercise and has long-term effects by maintaining patency of these vessels during recovery. Whether oxygen tension specifically regulates these novel pathways or opens them indirectly via effects on the conventional pulmonary vasculature remains unclear.

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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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Reproduction of inert gas and oxygenation data: a comparison of the MIGET and a simple model of pulmonary gas exchange

Intensive Care Medicine ◽

10.1007/s00134-010-1981-7 ◽

2010 ◽

Vol 36 (12) ◽

pp. 2117-2124 ◽

Cited By ~ 19

Author(s):

Stephen E. Rees ◽

S. Kjærgaard ◽

S. Andreassen ◽

G. Hedenstierna

Keyword(s):

Simple Model ◽

Gas Exchange ◽

Pulmonary Gas Exchange ◽

Inert Gas

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

Anesthesiology ◽

10.1097/00000542-200112000-00022 ◽

2001 ◽

Vol 95 (6) ◽

pp. 1422-1426 ◽

Cited By ~ 12

Author(s):

Axel Kleinsasser ◽

Karl H. Lindner ◽

Christoph Hoermann ◽

Andreas Schaefer ◽

Christian Keller ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Porcine Model ◽

Minimum Alveolar Concentration ◽

Pulmonary Gas Exchange ◽

Inert Gas ◽

Sevoflurane Anesthesia ◽

Isoflurane Anesthesia ◽

Volatile Anesthesia ◽

Normal Ventilation

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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Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.4.1686 ◽

1988 ◽

Vol 65 (4) ◽

pp. 1686-1692 ◽

Cited By ~ 3

Author(s):

A. A. Balgos ◽

D. C. Willford ◽

J. B. West

Keyword(s):

Gas Exchange ◽

Blood Gases ◽

Normal Subjects ◽

Pulmonary Gas Exchange ◽

Inert Gas ◽

Base Line ◽

Slight Improvement ◽

Arterial Blood ◽

The Mean ◽

Arterial Po2

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

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AltitudeOmics: effect of reduced barometric pressure on detection of intrapulmonary shunt, pulmonary gas exchange efficiency, and total pulmonary resistance

Journal of Applied Physiology ◽

10.1152/japplphysiol.00474.2017 ◽

2018 ◽

Vol 124 (5) ◽

pp. 1363-1376 ◽

Cited By ~ 5

Author(s):

Frank A. Petrassi ◽

James T. Davis ◽

Kara M. Beasley ◽

Oghenero Evero ◽

Jonathan E. Elliott ◽

...

Keyword(s):

Blood Flow ◽

Gas Exchange ◽

Sea Level ◽

Oxygen Tension ◽

Pulmonary Blood Flow ◽

Contrast Echocardiography ◽

Barometric Pressure ◽

Arteriovenous Anastomoses ◽

Pulmonary Resistance ◽

Flow Through

Blood flow through intrapulmonary arteriovenous anastomoses (QIPAVA) occurs in healthy humans at rest and during exercise when breathing hypoxic gas mixtures at sea level and may be a source of right-to-left shunt. However, at high altitudes, QIPAVA is reduced compared with sea level, as detected using transthoracic saline contrast echocardiography (TTSCE). It remains unknown whether the reduction in QIPAVA (i.e., lower bubble scores) at high altitude is due to a reduction in bubble stability resulting from the lower barometric pressure (PB) or represents an actual reduction in QIPAVA. To this end, QIPAVA, pulmonary artery systolic pressure (PASP), cardiac output (QT), and the alveolar-to-arterial oxygen difference (AaDO2) were assessed at rest and during exercise (70–190 W) in the field (5,260 m) and in the laboratory (1,668 m) during four conditions: normobaric normoxia (NN; [Formula: see text] = 121 mmHg, PB = 625 mmHg; n = 8), normobaric hypoxia (NH; [Formula: see text] = 76 mmHg, PB = 625 mmHg; n = 7), hypobaric normoxia (HN; [Formula: see text] = 121 mmHg, PB = 410 mmHg; n = 8), and hypobaric hypoxia (HH; [Formula: see text] = 75 mmHg, PB = 410 mmHg; n = 7). We hypothesized QIPAVA would be reduced during exercise in isooxic hypobaria compared with normobaria and that the AaDO2 would be reduced in isooxic hypobaria compared with normobaria. Bubble scores were greater in normobaric conditions, but the AaDO2 was similar in both isooxic hypobaria and normobaria. Total pulmonary resistance (PASP/QT) was elevated in HN and HH. Using mathematical modeling, we found no effect of hypobaria on bubble dissolution time within the pulmonary transit times under consideration (<5 s). Consequently, our data suggest an effect of hypobaria alone on pulmonary blood flow. NEW & NOTEWORTHY Blood flow through intrapulmonary arteriovenous anastomoses, detected by transthoracic saline contrast echocardiography, was reduced during exercise in acute hypobaria compared with normobaria, independent of oxygen tension, whereas pulmonary gas exchange efficiency was unaffected. Modeling the effect(s) of reduced air density on contrast bubble lifetime did not result in a significantly reduced contrast stability. Interestingly, total pulmonary resistance was increased by hypobaria, independent of oxygen tension, suggesting that pulmonary blood flow may be changed by hypobaria.

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