Distribution Of Ventilation-perfusion Ratios Research Articles

Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man

Blood gases, hemodynamics and ventilation were measured in 7 healthy volunteers at baseline while breathing room air (F i O 2 0.21), during hypoxia (F i O 2 0.125, 15 min) and after nifedipine 20 mg sublingually at F i O 2 0.21 (45 min) and at F i O 2 (15 min). Distributions of ventilation-perfusion ratios (V̇ a/Q̇) were determined, using the multiple inert gas elimination technique, at baseline, during hypoxia, and again during hypoxia after nifedipine intake. Hypoxia was associated with an average increase in pulmonary vascular resistances by 104%, which was partialaly inhibited by nifedipine. The inert gas data showed a mild deterioration in the distribution of V̇ a/Q̇ ratios during hypoxia. However, when blood flow and ventilation were constrained to the baseline normoxic values in the distributions recovered during hypoxia (‘normalization procedure’) a slight improvement in V̇ a/Q̇ matching could be evidenced, which was blunted during hypoxia after nifedipine. This was interpreted as the functional of hypoxic pulmonary vasoconstriction (HPV). Using the ‘normalized’ distributions, we computed the relationship between the decrease in compartmental blood flow that occurred during hypoxia and the corresponding alveolar P O 2 , and calculated the gain due to HPV feedback using equations of the control theory. The contribution of HPV to the stability of compartmental V̇ a/Q̇ was greatest for alveolar P O 2 values around 60 mm Hg, but at best the feedback had only a moderate efficiency.

Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema.

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

Pulmonary gas exchange during exercise in patients with chronic obliterative pulmonary hypertension.

The effect of exercise on pulmonary gas exchange was investigated in 7 patients with pulmonary hypertension resulting from primary pulmonary hypertension or recurrent pulmonary emboli. During supine bicycle exercise averaging 2.4 times baseline O2 consumption there was a significant fall in the arterial PO2 (64 +/- 1.1 to 56 +/- 5.4) and widening of the alveolar-arterial gradient for O2 (50 +/- 4.6 to 62 +/- 5.5). Measurement of the distribution of ventilation-perfusion (VA/Q) ratios by the multiple inert gas technique demonstrated no increase in VA/Q inequality. The increased hypoxemia was due to the fall in the mixed venous PO2 and its impact on the end-capillary blood of the shunt and low VA/Q units present at both rest and exercise. A concomitant shift in the mean VA/Q ratio for the normal lung units mitigated but could not eliminate the fall in the arterial PO2. We conclude that the increased hypoxemia seen during exercise in these patients is due to the widened arterial-venous O2 difference expected with exercise and its effect on the mild VA/Q inequality characteristic of this disorder.

IMPROVED ARTERIAL OXYGENATION BY ALMITRINE IN CYSTIC FIBROSIS ADOLESCENTS

Chronic hypoxemia following long lasting bronchial obstruction in adolescent C/F is a new problem since improved survival. Serious disconfort as headache, loss of intellectual fitness and even cor pulmonale results. As chronic oxygen therapy is mostly not accepted in mild cases we looked for almitrine, a proven peripheral chemo-receptor aganist, which has been shown efficient in old patients with COPD. It was given to 5 patients with a mean age of 15 years. Before and 20 min after IV almi-trine (0.25 mg/kg/h) gazometric, hemodynamic and lung mechanic parameters were measured and the distribution of ventilation-perfusion ratios were determined by the multiple inert gas elimination technique. During almitrine infusion oxygenation (pa O2 varied from 63.0±3.1 to 72.0 ± 2.5 mm Hg, p < 0.02) improved. Alveolar to arterial pO2 gradient (from 36.5 ± 3.3 to 30.8 ± 2.4 mmHg, p = 0.10) and venous admixture (from 19.0 ± 3.1 to 13.3 ± 1.6%, p = 0.07) decreased slightly. Pulmonary arterial mean pressure (from 20.3 ± 1.8 to 23.1 ± 1.7, p < 0.01) and pulmonary vascular resistance index (from 254 ± 13 to 300 ± 8 dyne.1 cm-5.m2, p < 0.02) increased significantly. Minute ventilation (from 8.2 ± 0.7 to 8.1 ± 0.6 1/min, N.S.) did not change. We conclude that almitrine increases arterial oxygenation in C/F by improvement of VA/Q matching. This improvement of gas exchange function of the lung appeared to be related to an increased vascular tone which was well tolerated. These preliminary results deserve to be confirmed by chronic oral treatment.

Lung Volume and VA/Q Distribution Response to Intravenous versus Inhalation Anesthesia in Sheep

The effects of intravenous pentobarbital versus nitrous oxide/halothane inhalation anesthesia on blood gases, distribution of ventilation-perfusion ratios (VA/Q), and lung volume (FRC) were compared in 8 tracheostomized sheep in the lateral decubitus position. Pentobarbital anesthesia produced no significant changes (from awake control) in arterial blood PO2 or PCO2, ventilation-perfusion inequality, intrapulmonary shunt, or FRC during either spontaneous breathing or mechanical ventilation with muscle paralysis. With inhalation anesthesia, PaO2 decreased from 132 +/- 13 mmHg awake to 106 +/- 11 mmHg and 104 +/- 6 mmHg (FIO2 all 0.3) during spontaneous and mechanical ventilation. Shunt increased from 1.4 +/- 1.0% awake to 10.6 +/- 4.5 and 13.9 +/- 5.3%, respectively. Mean VA/Q decreased from 0.39 +/- 0.07 awake, to 0.21 +/- 0.06 and 0.29 +/- 0.07. Log standard deviation of VA/Q increased from 0.66 +/- 0.12 awake to 0.83 +/- 0.28 and 0.89 +/- 0.15. FRC decreased from 1.66 +/- 0.65 1 to 1.46 +/- 0.62 and 1.22 +/- 0.63 1, respectively. Differences in response to intravenous versus inhalation anesthesia for the above variables all were statistically significant at P less than 0.05. FRC and shunt changes with anesthesia showed significant correlation for both spontaneous (r = -0.80) and mechanical ventilation (r = 0.77), P less than 0.005 for both. We therefore propose that the differences between lung volume and gas exchange effects of intravenous versus inhalation anesthesia in sheep may have been related causally.

The mechanisms of arterial hypoxemia during hemodialysis.

Hypoxemia during hemodialysis has variously been attributed to worsening ventilation-perfusion (VA/Q) relationships, alveolar hypoventilation combined with a reduced respiratory quotient, increased right-to-left shunting, and diffusion impairment. It is difficult to separate out these various effects, which explains lack of agreement in the literature. To more critically evaluate the causes of hypoxemia during hemodialysis, we used a multiple inert gas elimination technique to determine the distribution of ventilation-perfusion ratios during hemodialysis in 8 patients with chronic renal failure. Measurements were made before, during (at 60, 120, and 210 min), and after hemodialysis. Whereas arterial PO2 fell from 87 to 74 mmHg by 120 min, ventilation-perfusion relationships actually improved. Cardiac output fell from 5.3 to 4.0 L/min over the same time. Alveolar ventilation, respiratory quotient, and alveolar PO2 all fell, and the alveolar arterial PO2 difference remained essentially unchanged. These findings suggest that the hypoxemia observed during hemodialysis is primarily due to a decrease in alveolar ventilation and respiratory quotient associated with removal of metabolic CO2 in the dialyzer. Secondary factors affecting arterial PO2 were the slight improvement in ventilation-perfusion relationships tending to increase it, and the decrease in cardiac output tending to decrease it. There was no evidence for diffusion impairment because the measured VA/Q inequality accounted for the degree of hypoxemia.

Regional distribution of ventilation-perfusion ratios in acute pulmonary embolism.

Regional ventilation perfusion ratios have been computed in 44 patients with acute pulmonary embolism with a gamma-camera using Krypton 81m, a short-life radionuclide delivered by inhalation and infusion. This noninvasive technique is performed during tidal breathing and can be easily repeated. High V/Q's are detected in the embolic regions and low V/Q's in the nonembolic regions with a shift of the perfusion distribution towards these low values. This pattern disappears with recovery. This technique can be used in clinical practice for diagnostic purposes.

Effects of high-frequency breathing on pulmonary ventilation and gas exchange.

The effects of spontaneous high-frequency breathing (HFB) on lung function were evaluated in three subjects highly trained in the practice of yoga. Transpulmonary pressure was measured by an esophageal balloon catheter and gas flow by pneumotachography. The abdominal and rib cage contributions to tidal breathing were measured separately by respiratory inductive plethysmography. Gas exchange was studied by the conventional technique and by multiple inert gas elimination. During HFB, respiratory rate increased to 232 cycles/min with a tidal volume of 0.35 liter. This resulted in a more than 10-fold increase in expired minute ventilation to approximately 90 1/min. The transpulmonary pressure varied by 20 cmH2O, with the calculated elastic, resistive, and accelerative components varying by 2, 20, and 8 cmH2O, respectively. Respiratory work increased more than 200-fold in comparison with resting ventilation. A phase shift between thoracic and abdominal breathing was observed and was interpreted as a volume displacement of approximately 30 1/min between the two parts of the respiratory system. Arterial oxygen and carbon dioxide tension remained normal. Bohr dead space increased, while acetone dead space remained unaltered. A bimodal distribution of ventilation-perfusion ratios (VA/Q) was observed, with one mode in normal and another in "high" VA/Q regions.

Alveolar stability during anaesthesia for reconstructive vascular surgery in the leg.

Alveolar stability was studied during prolonged enflurane anaesthesia by using a multiple inert-gas elimination technique for the assessment of the "continuous" distribution of ventilation-perfusion ratios (VA/Q). All 10 patients (mean age: 61 years, six smokers) presented with increased VA/Q mismatching during anaesthesia, with a redistribution of lung blood flow to regions with low or high VA/Q. Five patients had perfusion of units with VA/Q less than or equal to 0.07 which may cause unstable alveoli with the presently used inspiratory gas mixture. However, only two patients displayed increasing shunting suggestive of alveolar collapse during the 3.5 h observation period. This lower than expected incidence may indicate protective mechanisms against atelectasis, such as mechanical interdependence between lung units, or collateral ventilation.

Observation of VA/Q distribution in the artifical ventilation therapy for the acute pulmonary insufficiency

Using six inert gas elimination method, the change of distribution of ventilation-perfusion ratio (VA/Q) was observed on 2 cases of the artificial ventilation treatment of acute pulmonary insufficiency.In case 1 who developed acute pulmonary insufficiency following the cardiac arrest in acute poisoning of agricultural agent and who showed the large intrapulmonary shunting and bimodal VA/Q imbalance. On the 4th date after the commencement of the artificial ventilation, intrapulmonary shunting was considerably improved and at the 24th date VA/Q imbalance was also improved.In case 2 who developed acute pulmonary insufficiency following the multiple rib fracture and pulmonary contusion and who showed unimodal widely distributed VA/Q imbalance in addition to the large intrapulmonary shunting, the improvement of intrapulmonary shunting was obtained also at the 4th date of artificial ventilation therapy and at 8th date VA/Q imbalance was improved.The results obtained were also confirmed by the finding on the chest x ray and those obtained in arterial blood gas analysis.As a conclusion it will be reasonably stated that in the case of acute pulmonary insufficiency, following the artificial ventilation therapy, the improvement of intrapulmonary shunting will be first obtained then VA/Q imbalance will be improved.

Pulmonary gas exchange during acute myocardial ischaemia a study in the closed chest anaesthetized dog.

The occurrence and the cause of arterial hypoxaemia were studied in spontaneously breathing dogs in which myocardial ischaemia was induced during anaesthesia. Changes in several circulatory and ventilatory variables and in parameters of gas exchange were assessed in twelve dogs in the two 1st h after the intervention; these included changes in the distribution of ventilation-perfusion ratios determined with an inert tracer gas method. Eight out of 12 dogs developed haemodynamic signs of an acute myocardial infarction after occlusion of a branch of the left coronary artery; the circulatory changes were moderate in 6 and severe in 2 animals. A drop in Pa,O2 occurred in 5 dogs. In one without significant haemodynamic changes it was largely due to a decrease in alveolar ventilation. The ventilation-perfusion ratio distribution in the other 4 dogs did not change in a consistent way; appreciable shunt circulation (6.6%) developed in one dog. Neither ventilation-perfusion mismatch nor shunt circulation contributed much to the hypoxaemia. The most consistent finding in the 5 dogs in whom Pa,O2 fell, was a drop in Pv,O2 (mean 1.3 kPa); it accounted for 86% of the drop in Pa,O2.

Distributions of V̇ A/Q̇ in dog lungs obtained with the 50 compartment and the log normal approach

From the lungs wash-out ratios of six inert gases that were intravenously administered to 26 anaesthetized normal dogs, 120 distributions of ventilation-perfusion ratios (V̇ A/Q̇) were determined, using two different techniques: the 50 compartment approach developed by Wagner et al. (1974a) and a least squares curve fitting method, comparing observed and calculated inert gas data corresponding to a single log normal distribution. The latter is defined by three parameters, the (geometric) mean V̇ A/Q̇, the standard deviation of log V̇ A/Q̇ and s shunt fraction. A unimodal log normal fit was almost always obtained, but in 14 cases the 50 compartment approach yielded a bimodal distribution, which gave a better fit to the data in 7 cases. In almost other cases the log normal distribution fitted better; the mean V̇ A/Q̇'s were about equal, but the standard deviations obtained from the log normal fit were often much less. It appears that, whereas in the log normal approach distributions of any sharpness can be fitted, the computer technique used in the 50 compartment approach, involving a smoothing algorithm, shortens and broadens any sharp and narrow peak in them. The effect of different smoothing factors in the 50 compartment approach was investigated. The Pa O 2 predicted from either distribution was about the same and somewhat less than the acute Pa O 2 , so that one model is not superior to the other in describing oxygen transfer in the lung.

Ventilation-perfusion distributions in the adult respiratory distress syndrome.

The distribution of ventilation-perfusion ratios, as determined by the multiple inert gas elimination technique, was measured in 16 patients with the adult respiratory distress syndrome. In each case, the distribution of ventilation-perfusion ratios was bimodal. The upper mode consisted of units with normal ventilation-perfusion ratios that received a mean of 52% of the cardiac output. The lower mode, which received the remainder of the cardiac output, consisted of either pure shunt or shunt plus a small number of units with very low ventilation-perfusion ratios (less than 0.01). The measured arterial PO2 and that predicted from the distribution of ventilation-perfusion ratios were very closely correlated (r = 0.93), indicating that the hypoxemia was completely explained by the measured ventilation-perfusion inequality. In 12 patients, the effect of positive end-expiratory pressure on the distribution of ventilation-perfusion ratios was also determined. The addition of positive end-expiratory pressure uniformly resulted in a decrease in blood flow to the lower mode and an increase in the ventilation of unperfused alveoli. Increasing positive end-expiratory pressure also led to a uniform decrease in cardiac output. We conclude that the hypoxemia of the adult respiratory distress syndrome is caused by the presence of shunt or units of very low ratio of ventilation to perfusion and that positive end-expiratory pressure increases the arterial PO2 by decreasing the perfusion of unventilated lung. The mechanism of this decrease is yet to be defined.

Gas exchange after pulmonary fat embolism in dogs

Gas exchange following moderately severe experimental pulmonary fat embolism was studied in nine dogs. A new method designed to describe the distribution of ventilation-perfusion ratios in the lung was applied before and after intravenous injection of homologous neutral fat. The dose of fat (0.75 ml/kg) was low enough to produce a small but significant decrease in arterial PO2 (mean change of 10 mm Hg) in the first 15 minutes after the embolism but high enough to result in the death of two of the four dogs that were allowed to survive the initial postembolism period. Pulmonary artery pressure and pulmonary vascular resistance both rose significantly within 5 minutes of the fat injection and remained elevated for the 2 hour experimental period. Immediately after the embolism there was an increase in the percentage of the total ventilation going to areas of the lung with ventilation-perfusion ratios between 10 and 100, which usually appeared as a discrete mode in the ventilation distribution. This mismatching of ventilation and perfusion partially resolved within 2 hours after the embolism, as indicated by the gradual disappearance of this population of gas exchanging units with relatively decreased blood flow. At no time within 2 hours after the embolism was there a significant increase in shunt or in ventilation to totally unperfused lung. The gas exchange pattern in the two dogs that subsequently died was indistinguishable from that of the other seven in the immediate postembolism period.

Redistribution of pulmonary blood flow in the dog with PEEP ventilation

The effects of positive end-expiratory pressure (PEEP) at 20 cmH2O on the distribution of pulmonary blood flow was studied in intact dogs and isolated lung preparations. Measurements were made of a) the continuous distribution of ventilation-perfusion ratios (VA/Q), b) the vertical distribution of pulmonary blood flow, and c) the dimensions of the microvasculature. Without PEEP the distributions of ventilation and perfusion were unimodal and centered on a VA/Q close to one. Dependent regions received 5-10 times more of cardiac output than uppermost regions. With PEEP the distribution showed a bimodal character, one mode of normal VA/Q and the other comprising one-third of ventilation, lying between VA/Q of 10 and 100. Cardiac output was reduced two- to threefold and blood flow in the uppermost regions was grossly reduced but not eliminated. Bimodal distributions were also found in isolated lungs with PEEP, and histological examination of rapidly frozen lung tissue showed that alveolar capillaries were closed in the uppermost, poorly perfused regions, whereas alveolar corner vessels remained open. We suggest that the blood flow through these corner vessels is responsible for the additional, high VA/Q mode during PEEP.

Topographical ventilation and perfusion distribution during IPPB in the lateral posture.

We measured topographical ventilation and perfusion distribution in the gravity field using 133Xe in 5 normal subjects either during natural breathing or during intermittent positive pressure ventilation (IPPB) in the lateral decubitus posture. The ratio of ventilation of upper regions to that of lower regions increased from 0.61 +/- 0.10 (mean +/- SE) during natural breathing to 0.95 +/- 0.08 during IPPB. In contrast, the ratio of regional perfusion was unchanged in the 2 conditions. Consequently, distribution of regional ventilation-perfusion ratios became less homogeneous during IPPB. Whereas during natural breathing the ratio of ventilation-perfusion of upper regions to that of lower regions was 1.09 +/- 0.18, during IPPB this ratio was 1.52 +/- 0.14. Despite the differences in regional ventilation distribution between natural breathing and IPPB, analysis of multiple-breath 133Xe washouts measured at the mouth did not reveal any difference. The results are consistent with the hypothesis that the magnitude of diaphragmatic tension is the main determinant of topographical ventilation distribution in the lateral posture.

Gas exchange during acute experimental canine asthma.

The inert gas infusion technique was used to recover distributions of ventilation-perfusion ratios in anesthetized dogs during 17 episodes of acute asthma produced experimentally by broncho-provocation with aerosolized Ascaris suum extract, methacholine, or histamine. Regardless of the agent used, 2 general patterns of ventilation/perfusion maldistribution were observed. During mild attacks of bronchospasm, a broadening of the normal unimodal distribution of ventilation-perfusion ratios occurred. During more severe attacks, the ventilation/perfusion distributions were clearly bimodal (with true right-to-left shunt of more than 4 per cent present on only one occasion), suggesting that there are, in general, 2 populations of gas-exchanging units in the lung under these conditions. One population has approximately normal ratios of ventilation to blood flow. The second is a population centered on a low ventilation-perfusion ratio (average, 0.14) that can be explained by ventilation of lung units with completely obstructed bronchi via collateral pathways. The postmortem appearances of the lungs and the time course of the gas-exchange abnormalities suggest that the chief cause of the bronchial occlusion responsible for the low ventilation-perfusion units was excessive mucus in the lumen. The presence of collateral pathways of ventilation in the canine lung appeared to protect the animals from developing areas of true shunt under these conditions. The ventilation/perfusion distributions were similar to those seen in human patients with bronchial asthma.

Chromatographic Analysis of Multiple Tracer Inert Gases in the Presence of Anesthetic Gases

A gas chromatographic method for simultaneous analysis of multiple tracer inert gases in blood and expired gas samples is described. The method enables determination of the distribution of ventilation-perfusion ratios in the lungs during anesthesia with nitrous oxide and halothane. In addition, simultaneous analysis of anesthetic gas concentration in blood permits calculation of the amount of uptake or elimination of anesthetic gases from the Fick principle.

Ventilation/Blood Flow and Gas Exchange.

Introduction Oxygen transport from air to tissues Inequality of blood flow and ventilation in the normal lung Ventilation-perfusion ratio inequality and regional gas exchange Ventilation-perfusion ratio inequality and overall gas exchange Methods of measuring ventilation-perfusion ration inequality Distributions of ventilation-perfusion ratios Appendixes: How to talk the Va/Q language How to draw a Va/Q line Suggestions for further reading References Index

Inert gas elimination characteristics of the normal and abnormal lung

ARTICLESInert gas elimination characteristics of the normal and abnormal lungM. P. Hlastala, and H. T. RobertsonM. P. Hlastala, and H. T. RobertsonPublished Online:01 Feb 1978https://doi.org/10.1152/jappl.1978.44.2.258MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMeasurement of the distribution of ventilation-perfusion ratios in the human lung with proton MRI: comparison with the multiple inert-gas elimination techniqueRui Carlos Sá*, A. Cortney Henderson*, Tatum Simonson, Tatsuya J. Arai, Harrieth Wagner, Rebecca J. Theilmann, Peter D. Wagner, G. Kim Prisk, and Susan R. Hopkins18 July 2017 | Journal of Applied Physiology, Vol. 123, No. 1Multiple inert gas elimination technique by micropore membrane inlet mass spectrometry—a comparison with reference gas chromatographyMoritz Kretzschmar, Thomas Schilling, Andreas Vogt, Hans Ulrich Rothen, João Batista Borges, Thomas Hachenberg, Anders Larsson, James E. Baumgardner, and Göran Hedenstierna15 October 2013 | Journal of Applied Physiology, Vol. 115, No. 8Hypoxic Pulmonary VasoconstrictionJ. T. Sylvester, Larissa A. Shimoda, Philip I. Aaronson, and Jeremy P. T. Ward1 January 2012 | Physiological Reviews, Vol. 92, No. 1Point:Counterpoint: Exercise-induced intrapulmonary shunting is imaginary vs. realSusan R. Hopkins, I. Mark Olfert, and Peter D. Wagner1 September 2009 | Journal of Applied Physiology, Vol. 107, No. 3Pulmonary PhysiologyCO2 relaxes parenchyma in the liquid-filled rat lungMichael J. Emery, Randy L. Eveland, Seong S. Kim, Jacob Hildebrandt, and Erik R. 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Glenny1 June 2000 | Journal of Applied Physiology, Vol. 88, No. 6Imaging obstructed ventilation with NMR using inert fluorinated gasesDean O. Kuethe, Arvind Caprihan, H. Michael Gach, Irving J. Lowe, and Eiichi Fukushima1 June 2000 | Journal of Applied Physiology, Vol. 88, No. 6Measurement of cardiac output during exercise by open-circuit acetylene uptakeRebecca C. Barker, Susan R. Hopkins, Nancy Kellogg, I. Mark Olfert, Tom D. Brutsaert, Timothy P. Gavin, Pauline L. Entin, Anthony J. Rice, and Peter D. Wagner1 October 1999 | Journal of Applied Physiology, Vol. 87, No. 4Pulmonary embolization causes hypoxemia by redistributing regional blood flow without changing ventilationWilliam A. Altemeier, H. Thomas Robertson, Steve McKinney, and Robb W. Glenny1 December 1998 | Journal of Applied Physiology, Vol. 85, No. 6Pulmonary gas-exchange analysis by using simultaneous deposition of aerosolized and injected microspheresWilliam A. Altemeier, H. Thomas Robertson, and Robb W. Glenny1 December 1998 | Journal of Applied Physiology, Vol. 85, No. 6Pulmonary Blood Flow Redistribution with Low Levels of Positive End-expiratory PressureAnesthesiology, Vol. 88, No. 5Shunt and ventilation-perfusion distribution during partial liquid ventilation in healthy pigletsElisabeth A. Mates, Jacob Hildebrandt, J. Craig Jackson, Peter Tarczy-Hornoch, and Michael P. Hlastala1 March 1997 | Journal of Applied Physiology, Vol. 82, No. 3Gas Exchange during Gas and Liquid Ventilation1 November 1996 | Journal of Intensive Care Medicine, Vol. 11, No. 6Gas exchange and regional redistribution of pulmonary blood flow during resuscitation of acute pulmonary bead embolizationPulmonary Pharmacology, Vol. 5, No. 4Dynamics of soluble gas exchange in the airways: II. Effects of breathing conditionsRespiration Physiology, Vol. 83, No. 3The matching of ventilation and perfusion in the lung of the Tegu lizard, Tupinambis nigropunctatusRespiration Physiology, Vol. 60, No. 3Interaction of series and parallel dead space in the lungRespiration Physiology, Vol. 54, No. 1Resolution of the multiple inert gas method for estimating V̇a/Q̇ maldistributionRespiration Physiology, Vol. 49, No. 3Interpretation of inert gas retention and excretion in the presence of stratified inhomogeneityRespiration Physiology, Vol. 46, No. 3Inert gas elimination from lungs with stratified inhomogeneity: TheoryRespiration Physiology, Vol. 44, No. 3Gas exchange abnormalities produced by venous gas emboliRespiration Physiology, Vol. 36, No. 1 More from this issue > Volume 44Issue 2February 1978Pages 258-266 Copyright & PermissionsCopyright © 1978 the American Physiological Societyhttps://doi.org/10.1152/jappl.1978.44.2.258PubMed204617History Published online 1 February 1978 Published in print 1 February 1978 Metrics