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Original Research: Pulmonary Physiology |

Ventilation/Perfusion Distribution Abnormalities In Morbidly Obese Subjects Before and After Bariatric SurgeryVentilation/Perfusion Imbalance and Morbid Obesity FREE TO VIEW

Eva Rivas, MD; Ebymar Arismendi, MD; Alvar Agustí, MD; Marcelo Sanchez, MD; Salvadora Delgado, MD; Concepción Gistau, MsC; Peter D. Wagner, MD; Roberto Rodriguez-Roisin, MD
Author and Funding Information

From Servei d’Anestesiologia (Dr Rivas); Institut d’investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Fundació Clínic per a la Recerca Biomédica (FCRB) (Drs Rivas, Arismendi, Agustí, Sanchez, Delgado, and Rodriguez-Roisin); Servei de Pneumologia (Institut Clínic del Tòrax [ICT]) (Drs Agustí and Rodriguez-Roisin and Ms Gistau); CIBER Enfermedades Respiratorias (CIBERES) (Drs Arismendi, Agustí, and Rodriguez-Roisin and Ms Gistau); Centre de Diagnòstic per la Imatge (CDI) (Dr Sanchez); Servei de Cirurgia Gastrointestinal (Dr Delgado), Hospital Clínic, Universitat de Barcelona, Barcelona, Spain; and the Department of Medicine (Dr Wagner), University of California, San Diego (UCSD), San Diego, CA.

CORRESPONDENCE TO: Roberto Rodriguez-Roisin, MD, Servei Pneumologia (Institut del Tòrax), Hospital Clínic, Villarroel 170, 08036-Barcelona, Spain; e-mail: rororo@clinic.ub.es


Part of this study has been presented in abstract form at the American Thoracic Society Annual Meeting, May 21, 2014, San Diego CA.

FUNDING/SUPPORT: This study was funded by the Fondo de Investigación Sanitaria (FIS) PI 080311, CIBERES, the Generalitat de Catalunya [2014SGR661], and a grant-in-aid from Almirall.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(4):1127-1134. doi:10.1378/chest.14-1749
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BACKGROUND:  Obesity is a global and growing public health problem. Bariatric surgery (BS) is indicated in patients with morbid obesity. To our knowledge, the effects of morbid obesity and BS on ventilation/perfusion (V. a/Q. ) ratio distributions using the multiple inert gas elimination technique have never before been explored.

METHODS:  We compared respiratory and inert gas (V. a/Q.  ratio distributions) pulmonary gas exchange, breathing both ambient air and 100% oxygen, in 19 morbidly obese women (BMI, 45 kg/m2), both before and 1 year after BS, and in eight normal-weight, never smoker, age-matched, healthy women.

RESULTS:  Before BS, morbidly obese individuals had reduced arterial Po2 (76 ± 2 mm Hg) and an increased alveolar-arterial Po2 difference (27 ± 2 mm Hg) caused by small amounts of shunt (4.3% ± 1.1% of cardiac output), along with abnormally broadly unimodal blood flow dispersion (0.83 ± 0.06). During 100% oxygen breathing, shunt increased twofold in parallel with a reduction of blood flow to low V. a/Q.  units, suggesting the development of reabsorption atelectasis without reversion of hypoxic pulmonary vasoconstriction. After BS, body weight was reduced significantly (BMI, 31 kg/m2), and pulmonary gas exchange abnormalities were decreased.

CONCLUSIONS:  Morbid obesity is associated with mild to moderate shunt and V. a/Q.  imbalance. These abnormalities are reduced after BS.

Figures in this Article

Obesity has become a global and rising public health challenge, affecting millions of adults and children. Current estimates indicate that > 12% of the world population is obese, as defined by a BMI > 30 kg/m2, and that this figure is on the rise.1,2 Bariatric surgery (BS) causes a significant and sustained reduction of BMI, with minor morbidity and mortality, in morbidly obese subjects.3,4

Many previous studies have investigated the effects of obesity on lung function. The excess adipose tissue in the abdomen and around the rib cage reduces functional residual capacity, as shown by a marked decrease in the expiratory reserve volume (ERV).5 In addition, a widened alveolar-arterial Po2 difference (a-aPo2) is frequently reported in morbidly obese subjects.6 However, to our knowledge, except for radioactive measurements of regional ventilation/perfusion (V. a/Q. ) distributions in a few obese subjects,7 the effects of obesity on V. a/Q.  relationships and the potential influence of BS have not before been reported.

We hypothesized that (1) morbid obesity is associated with abnormal V. a/Q.  ratio distributions and (2) BS reduces them. To test this hypothesis, we used the multiple inert gas elimination technique (MIGET) in morbidly obese individuals, before and after BS, breathing ambient air and 100% oxygen to further explore the pulmonary vascular response. The results of this study have been reported previously in abstract form.8

Participants, Study Design, and Ethics

Morbidly obese BS candidates (BMI ≥ 40 kg/m2 or ≥ 35 kg/m2, with obesity-related comorbidities) were recruited prospectively and studied 24 h prior to and 1 year after BS (median, 51 weeks). Exclusion criteria were the presence of moderate to severe sleep apnea9 (by polysomnography) and other chronic respiratory (asthma, COPD, bronchiectasis), cardiovascular, and/or mental illnesses. Normal-weight, sex- and age-matched never smokers were enrolled and served as control subjects. Obese subjects and control subjects were studied while seated at rest, during ambient air and 100% oxygen breathing (30 min each), in random order, after they had refrained from any medication during the prior 24 h. One hundred percent oxygen breathing, inert gas, and hemodynamic measurements were not determined in control individuals. All participants signed informed consent. The study was approved by the ethics committee of the Hospital Clínic (Protocol 2008/4015).

Measurements
Lung Function:

Forced spirometry (before and after bronchodilation), static lung volumes by body plethysmography, and single-breath diffusing capacity of the lung for carbon monoxide (Dlco) (Master Screen Body; Jaeger, CareFusion) were determined before and after BS according to international guidelines. Reference values were those of a Mediterranean population.1012

Respiratory Gas Exchange:

Arterial and mixed venous blood sample gases were analyzed in duplicate for pH, Po2, and Pco2 (Ciba Corning 800), and a-aPo2 values were calculated using a standard formula.13 Oxygen uptake and CO2 production were calculated from mixed expired fractions of oxygen and CO2 (Medical Graphics Corporation), respectively. Minute ventilation was measured using a Wright spirometer and corrected to body temperature and pressure saturated (Respirometer MK8; BOC Healthcare).

Hemodynamic Measurements:

Heart rate and systemic and pulmonary arterial pressures were continuously monitored (HP 1001A-1006A monitor; Hewlett-Packard Company) as previously described.13 Systemic and pulmonary vascular resistances were calculated according to standard formulae.

V.a/Q. Distributions:

The MIGET was used to estimate the distributions of V. a/Q.  ratios within the 24 h prior to surgery, as reported previously.13,14 To calculate these, we used arterial, mixed venous, and mixed expired inert gas concentrations, and cardiac output (Q. t) determined by thermodilution, in obese patients with Pao2 < 80 mm Hg (range, 55-79 mm Hg; n = 13), whereas they were estimated without mixed venous sampling, and Q. t was determined by bioimpedance (PhysioFlow; Manatec Biomedical), as described previously15 in those with normal Pao2 (range, 82-97 mm Hg; n = 6).

Circulating Inflammatory Biomarkers:

Serum samples were obtained by centrifugation of venous blood and were stored at −80°C until analysis. C-reactive protein was quantified using an immunoturbidimetry method (Advia Chemistry; Siemens AG) and leptin, adiponectin, soluble tumor necrosis factor-receptor 1, and IL-8 serum levels were measured using an enzyme-linked immunosorbent assay (Diagnostics Biochem Canada Inc, US BIOLOGIC, IBL International, and Anogen), respectively.

Statistical Analysis

Results are presented as mean ± SE, median, or percentage, as appropriate. To compare obese and control subjects, we used the unpaired Student t test (or the Mann-Whitney test for nonnormally distributed data) and the χ2 test. Obese individuals before and after surgery were compared using the paired Student t test (or the Wilcoxon test for nonnormally distributed data) and the McNemar test. Pearson and Spearman tests were used, as appropriate, to explore bivariate correlations among variables of interest. A P value < .05 was considered statistically significant.

Characterization of Participants

We studied 19 middle-aged, morbidly obese women (17 never smokers and two former smokers) and eight normal-weight, never smoker, healthy women. Table 1 presents their main demographic, serum biomarker, and lung function values at recruitment. As expected, both BMI and waist circumference were greater in obese than in control subjects. The prevalence of arterial hypertension (42% vs 0%), diabetes mellitus (26% vs 0%), and metabolic syndrome (37% vs 0%) (P < .05 each) was also higher in obese participants. The apnea/hypopnea index in obese individuals was 10 ± 2/h. All serum biomarker concentrations except adiponectin were significantly higher in obese than in control individuals (Table 1).

Table Graphic Jump Location
TABLE 1 ]  Demographic, Inflammatory Biomarker, and Lung Function Findings

Data are presented as mean ± SE or median (interquartile range) unless indicated otherwise. a-aPo2 = alveolar-arterial Po2 difference; BS = bariatric surgery; Dlco = diffusing capacity of the lung for carbon monoxide; ERV = expiratory reserve volume; FRC = functional residual capacity; sTNF-R1 = soluble tumor necrosis factor-receptor 1; TLC = total lung capacity.

a 

P values for comparisons between control and obese individuals before surgery.

b 

P values for comparisons between pre- and postoperative conditions in obese individuals.

Findings Before BS
Ambient Air Breathing:

All dynamic and static lung volume (except ERV) and Dlco values in obese participants were lower than in control subjects but were still within their normal reference value range (Table 1). Bronchodilator response was negative. Compared with control subjects, obese participants had enlarged a-aPo2 and lower Pao2, with normal Paco2 and pH. In obese subjects, the mean shunt (V. a/Q.  ratios < 0.005) was mildly to moderately increased (range, 1% to 16% Q. t), and the dispersion of pulmonary blood flow distribution (Log SDQ) (upper normal limit ≤ 0.60)16 was abnormally broad, albeit unimodal (range, 0.43-1.35) (Fig 1), with negligible amounts of low V. a/Q.  ratio areas (< 0.1, excluding shunt) (1.5% ± 0.5% Q. t) (Table 2). The dispersion of alveolar ventilation distribution (Log SDV) (upper normal limit ≤ 0.65) was also unimodal and abnormally broad (range, 0.45-0.98),16 and alveolar units with V. a/Q.  ratios > 100, expressed as a percentage of alveolar volume (dead space) were reduced. A global index of V. a/Q.  inequality that combines Log SDQ and Log SDV (DISP R-E*),17 was moderately to severely increased (9.2 ± 0.7; range, 4.0-15.4) (upper normal limit ≤ 3.0). There was no oxygen diffusion limitation, as reflected by the close agreement between predicted Pao2 by the MIGET and measured Pao2. The median residual sum of squares, the descriptor of the quality of MIGET results, was 2.3, below the expected value of 5.4, indicating a high quality of inert gas data.14

Figure Jump LinkFigure 1 –  Ambient air. Distributions of alveolar ventilation (open blue circles) and pulmonary blood flow (solid red circles) plotted against V. A/Q.  ratio from a representative, mildly hypoxemic, obese participant (age, 56 y; BMI, 42 kg/m2) during ambient air breathing. A, Before bariatric surgery (BS). B, After BS. Before surgery, the pattern of V. A/Q.  ratio distributions was abnormally broadly unimodal, with mild to moderate shunt. Note that after surgery (BMI, 29 kg/m2), shunt decreases without noticeable changes in Log SDQ and Log SDV. AaPO2 = alveolar-arterial Po2 difference; DS = dead space; Log SDQ = dispersion of blood flow distribution; Log SDV = dispersion of alveolar ventilation distribution; V. A/Q.  = ventilation/perfusion.Grahic Jump Location
Table Graphic Jump Location
TABLE 2 ]  Pulmonary Gas Exchange, Ventilatory, Hemodynamic, and Metabolic Findings Breathing Ambient Air and Oxygen-Induced Changes in Obese Individuals Before and After BS

Data are presented as mean ± SE. Log SDQ = dispersion of blood flow distribution; Log SDV = dispersion of alveolar ventilation distribution; NA = not available; O2 = oxygen; PAP = mean pulmonary artery pressure; PCWP = pulmonary capillary wedge pressure; Psa = mean systemic arterial pressure; Pv¯ o2 = mixed venous Po2; PVR = pulmonary vascular resistance; Q. t = cardiac output; SVR = systemic vascular resistance; V. a = alveolar volume V. e = minute ventilation; V. o2 = oxygen consumption. See Table 1 for expansion of other abbreviations.

a 

Breathing ambient air.

b 

Breathing 100% oxygen.

c 

P values for comparisons during ambient air breathing between pre- and postoperative conditions.

d 

P values for comparisons between pre- and postoperative differences from 21% to 100% oxygen breathing.

e 

P < .05 for comparisons before surgery, between ambient air and 100% O2 breathing.

f 

P < .05 for comparisons after surgery, between ambient air and 100% O2 breathing.

g 

Unventilated units (V. a/Q.  ratios < 0.005), expressed as % of Q. t.

h 

Alveolar units with V. a/Q.  ratios > 100, expressed as % of V. a.

Ventilatory, systemic and pulmonary hemodynamics, and metabolic variables were within normal limits in all obese participants (Table 2). We observed that the waist to hip ratio correlated with Pao2 (ρ, −0.72), a-aPo2 (ρ, 0.67), and shunt (ρ, 0.57) (P < .05 each) (Fig 2); likewise, waist circumference was correlated with shunt (ρ, 0.57; P < .02). As expected, shunt was correlated with both Pao2 (ρ, −0.70) (Fig 2) and a-aPo2 (ρ, 0.70) (P < .002 each). Similarly, a lower ERV was associated with more arterial hypoxemia (ρ, 0.52; P < .05).

Figure Jump LinkFigure 2 –  Preoperative correlations between gas exchange descriptors and central obesity and between gas exchange indexes. The greater the waist to hip ratio, the worse the gas exchange abnormalities. A, Lower arterial Po2. B, Greater AaPO2. C, Intrapulmonary shunt. D, Likewise, the lower the arterial Po2, the greater the amount of shunt. Q. T = cardiac output. See Figure 1 legend for expansion of other abbreviation.Grahic Jump Location
100% Oxygen Breathing:

On the on hand, 100% oxygen breathing increased arterial and mixed venous Po2 and a-aPo2 (that already reached full equilibration at 15 min), without changes in Paco2, pH, or ventilatory parameters, and systemic arterial pressure and systemic vascular resistance. In parallel, 100% oxygen breathing reduced Q. t, cardiac index, pulmonary artery pressure, and pulmonary vascular resistance (Table 2). Moreover, shunt increased twofold as compared with ambient air, an increase that was inversely related to the reduction of Log SDQ (Fig 3) and the increase in Pao2 (r = −0.63, P < .01).

Figure Jump LinkFigure 3 –  Pre- and postoperative correlations between oxygen-induced changes in shunt, expressed as a percentage of Q. t, (y-axis) and in Log SDQ (x-axis) (dimensionless). A, Before surgery. B, After surgery. Preoperative oxygen-induced increases in shunt (dark gray circles) were inversely associated with reductions in Log SDQ, a correlation (light gray circles) that was lost postoperatively. See Figure 1 and 2 legends for expansion of other abbreviations.Grahic Jump Location
Findings After BS

Two standard BS procedures, sleeve gastrectomy (n = 13) and Roux-en-Y gastric bypass (n = 6) were used as clinically indicated. There were no differences in any of the outcomes using the two procedures. All obese individuals were discharged from hospital after BS without complications. BMI decreased from 45 ± 1 kg/m2 to 31 ± 1 kg/m2 (P < .001), representing a percentage of excess weight loss, a common surrogate marker of BS success, of 70% ± 4%.4 Arterial hypertension (except in two subjects), diabetes mellitus, and metabolic syndrome were resolved in all obese individuals. All inflammatory serum biomarkers except adiponectin decreased significantly, although fibrinogen, leptin, and soluble tumor necrosis factor-receptor 1 levels remained slightly elevated (like BMI) after surgery (Table 1).

Ambient Air Breathing:

As compared with preoperative conditions, forced spirometry, static lung volumes, Dlco, Pao2, and a-aPo2improved significantly, without changes in Paco2 and pH (Tables 1, 2). Similarly, most of the abnormal V. a/Q.  descriptors improved, as shown by the significant decreases in intrapulmonary shunt without changes in Log SDQ (Fig 1, Table 2). By contrast, Log SDV increased (deteriorated), and dead space remained unchanged. The increased Log SDV could be related to the significant fall in pulmonary artery pressure. This suggests less apical perfusion in the lung, hence facilitating the development of high V. a/Q.  regions after surgery, which would increase the Log SDV, other things being equal. The DISP R-E* descriptor remained moderately abnormal (8.7 ± 0.9; range, 3.3-17.2). Except for systemic vascular resistance, ventilatory, metabolic, and hemodynamic outcomes decreased after BS (Table 2).

The reduction in BMI after BS was significantly related to higher functional residual capacity (ρ, −0.64) and lower Log SDQ (ρ, 0.54) (improvement) values (P < .05 each). The increase in Pao2 after BS was related to Log SDQ reduction (ρ, −0.52; P < .01). The increase in ERV after BS was associated with lower leptin levels (ρ, −0.59; P < .01).

100% Oxygen Breathing:

As compared with ambient air, arterial and mixed venous Po2, arterial pH, and a-aPo2 increased, without accompanying changes in Paco2. It is of note that the increase in Pao2 observed during 100% oxygen breathing was significantly higher than that observed before surgery (P < .01), in keeping with a lower increase in shunt (P < .01) (Table 2). While breathing 100% oxygen, systemic hemodynamic changes were close to those observed during ambient air breathing, except for a greater increase in systemic vascular resistance (Table 2), without changes in pulmonary hemodynamics. The negative preoperative correlation observed between oxygen-induced changes in shunt and Log SDQ was lost after surgery (r = −0.45, P = .06) (Fig 3).

The principal results of this study confirm our working hypothesis by showing that morbidly obese subjects exhibit mild to moderate shunt, together with an abnormal pulmonary blood flow dispersion, that are reduced after BS.

Previous Studies

Although several previous papers have investigated the effects of obesity and BS on lung function, to our knowledge this is the first study that uses the MIGET to investigate V. a/Q.  ratio distributions under these clinical circumstances. In keeping with some,5,6 but not all, of them,18,19 we observed that static lung volumes were relatively well preserved in the subjects studied herein (Table 1). Discrepancies are likely explained by our stringent recruitment criteria, which excluded the coexistence of moderate to severe comorbidities, such as sleep apnea. Previous studies also reported the presence of widened a-aPo2 and mild arterial hypoxemia in obese subjects,6,20 in keeping with our observations (Table 1), as well as significant associations between waist circumference and waist to hip ratio with lung volumes and gas exchange indexes,21 also in agreement with our current findings. Although no previous study has used the MIGET to investigate the distribution of V. a/Q.  ratios in these patients, a study in the 1960s reported oxygen-shunt measurements in a few obese individuals and indicated that arterial hypoxemia was related to perfusion of unventilated areas (ie, shunt).22 Another study using radioactive tracer, also in a few obese subjects, demonstrated that perfusion was maximal in the lower zones, whereas ventilation was significantly reduced, a regional V. a/Q.  imbalance closely associated with the parallel reduction in ERV.7 The amounts of shunt observed in our study are in agreement with these findings.

Interpretation of Findings

Three main novel gas exchange findings of our study deserve specific discussion: (1) the pattern of pulmonary gas exchange abnormalities observed before BS, (2) the differential effects of 100% oxygen breathing before and after BS, and (3) the observation that all V. a/Q.  abnormalities except the Log SDV values were significantly ameliorated after BS.

First, despite minor impairment of lung volumes, very severe obesity was associated with mild to moderate shunt and increased dispersion of both Log SDQ and Log SDV. This pattern of gas exchange disturbances is similar to that shown in patients with pleural effusion that physically compresses the underlying normal lung parenchyma.23 Accordingly, we propose that the excessive adipose tissue that accumulates in morbid obesity causes an excessive and unopposed intraabdominal pressure that compresses the dependent regions of the lungs and results in mild amounts of shunt and low V. a/Q.  ratios (increased Log SDQ). Alternatively, systemic inflammation can alter pulmonary vascular tone,24 hence also influencing V. a/Q.  ratio distributions. Unfortunately, we cannot unravel which of these mechanisms is more relevant, because BS reduced both body weight and systemic inflammation (Table 1).

Second, during oxygen breathing, the increase in shunt was paralleled by a fall in Log SDQ, hence indicating pulmonary blood flow redistribution. This dynamic response mimics that shown in patients with acute lung injury and is likely to be related to the development of reabsorption atelectasis without reversion of hypoxic pulmonary vasoconstriction.25,26 Our contention is that this may reflect weaker and more rigid pulmonary vessels because of excessive adipose tissue-induced endothelial dysfunction,24 because both leptin and adiponectin modulate vascular tone by increasing nitric oxide bioavailability in healthy but not obese individuals.27 Our findings are, therefore, consistent with abnormal pulmonary vascular contractility in morbidly obese subjects.24

Finally, in parallel with weight loss and reduction of systemic inflammation after BS, abnormal V. a/Q.  distributions were also significantly reduced but not abolished, akin to the remnant of mild obesity and systemic inflammation. Although mechanical factors can undoubtedly play a role, the fact that the correlation between oxygen-induced changes in shunt and Log SDQ after BS (Fig 3) was lost suggests improvement in pulmonary blood flow redistribution. This would be in keeping with experimental evidence indicating that perivascular adipose tissue-induced vasodilatation of small arteries can be restored after BS.24 Hence, our observations could support a causal role of obesity on pulmonary gas exchange and vascular tone abnormalities.

Strengths and Limitations

Our study has strengths and limitations. Among the former is the fact that we used the MIGET for the first time to assess pulmonary gas exchange disturbances in this clinical scenario. The MIGET is the most robust tool to investigate the pulmonary and nonpulmonary determinants of gas exchange in humans. Among the latter is the fact that we studied only women because of the sex differences described in pulmonary gas exchange in morbidly obese individuals28,29 and the higher prevalence of this disease in females. Hence, our results may not be extrapolated directly to men.

This study shows that even in the absence of major lung volume alterations, morbidly obese individuals have abnormal V. a/Q.  distributions that are reduced after BS.

Author contributions: R. R.-R. is the guarantor of the manuscript and takes responsibility for the integrity of the data and the accuracy of the data analysis. E. R., E. A., M. S., S. D., C. G., and R. R.-R. contributed to the conduction of the experimental work and the acquisition and analysis of the data; E. R., A. A., P. D. W., and R. R.-R. contributed to the conception and design of the study and interpretation of the data; E. R., E. A., M. S., S. D., C. G., and R. R.-R. contributed to the planning and coordination of the study; and E. R., A. A., P. D. W., and R. R.-R. contributed to the writing of the article and/or had substantial involvement in its critical revision before submission.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Rodriguez-Roisin has received grant money from Almirall for a postdoctoral fellowship. Drs Rivas, Arismendi, Agustí, Sanchez, Delgado, Wagner, and Ms Gistau have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: FIS supported financially all fungible expenses of the study. CIBERES supported in part the salary of Dr Arismendi. Generalitat de Catalunya and Almirall supported in part the salaries of technical staff.

Other contributions: The authors thank all participants in the study for their willingness to contribute to medical research. Likewise, the support of Josep Maria Montserrat, MD (Laboratori del Son, Servei de Pneumologia, ICT); Lluis de Jover, PhD (Departament de Salut Pública, Facultat de Medicina, Universitat de Barcelona); Felip Burgos, PhD; Yolanda Torralba, MsC; Concepción Ruiz, MsC (Centre de Diagnostic Respiratori, Servei de Pneumologia, ICT); Antonio Maria de Lacy, MD; Josep Vidal, MD; and Jaume Balust, MD (Unitat d’Obesitat); is very much appreciated. Our special thanks to Isaac Cano, PhD (Centre de Diagnostic Respiratori, Servei de Pneumologia, ICT) for the improvements in the MIGET programme.

a-aPo2

alveolar-arterial Po2 difference

BS

bariatric surgery

Dlco

diffusing capacity of the lung for carbon monoxide

ERV

expiratory reserve volume

Log SDQ

dispersion of blood flow distribution

Log SDV

dispersion of alveolar ventilation distribution

MIGET

multiple inert gas elimination technique

Q. t

cardiac output

V. a/Q. 

ventilation/perfusion

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Dantzker DR, Wagner PD, West JB. Instability of lung units with low Va/Q ratios during O2breathing. J Appl Physiol. 1975;38(5):886-895.
 
Santos C, Ferrer M, Roca J, Torres A, Hernández C, Rodriguez-Roisin R. Pulmonary gas exchange response to oxygen breathing in acute lung injury. Am J Respir Crit Care Med. 2000;161(1):26-31. [CrossRef] [PubMed]
 
Greenstein AS, Khavandi K, Withers SB, et al. Local inflammation and hypoxia abolish the protective anticontractile properties of perivascular fat in obese patients. Circulation. 2009;119(12):1661-1670. [CrossRef] [PubMed]
 
Zavorsky GS, Wilson B. Sex, girth, waists and hips (what matters for gas exchange in extreme obesity?). Respir Physiol Neurobiol. 2010;170(1):120-122. [CrossRef] [PubMed]
 
Zavorsky GS, Christou NV, Kim do J, Carli F, Mayo NE. Preoperative gender differences in pulmonary gas exchange in morbidly obese subjects. Obes Surg. 2008;18(12):1587-1598. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Ambient air. Distributions of alveolar ventilation (open blue circles) and pulmonary blood flow (solid red circles) plotted against V. A/Q.  ratio from a representative, mildly hypoxemic, obese participant (age, 56 y; BMI, 42 kg/m2) during ambient air breathing. A, Before bariatric surgery (BS). B, After BS. Before surgery, the pattern of V. A/Q.  ratio distributions was abnormally broadly unimodal, with mild to moderate shunt. Note that after surgery (BMI, 29 kg/m2), shunt decreases without noticeable changes in Log SDQ and Log SDV. AaPO2 = alveolar-arterial Po2 difference; DS = dead space; Log SDQ = dispersion of blood flow distribution; Log SDV = dispersion of alveolar ventilation distribution; V. A/Q.  = ventilation/perfusion.Grahic Jump Location
Figure Jump LinkFigure 2 –  Preoperative correlations between gas exchange descriptors and central obesity and between gas exchange indexes. The greater the waist to hip ratio, the worse the gas exchange abnormalities. A, Lower arterial Po2. B, Greater AaPO2. C, Intrapulmonary shunt. D, Likewise, the lower the arterial Po2, the greater the amount of shunt. Q. T = cardiac output. See Figure 1 legend for expansion of other abbreviation.Grahic Jump Location
Figure Jump LinkFigure 3 –  Pre- and postoperative correlations between oxygen-induced changes in shunt, expressed as a percentage of Q. t, (y-axis) and in Log SDQ (x-axis) (dimensionless). A, Before surgery. B, After surgery. Preoperative oxygen-induced increases in shunt (dark gray circles) were inversely associated with reductions in Log SDQ, a correlation (light gray circles) that was lost postoperatively. See Figure 1 and 2 legends for expansion of other abbreviations.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Demographic, Inflammatory Biomarker, and Lung Function Findings

Data are presented as mean ± SE or median (interquartile range) unless indicated otherwise. a-aPo2 = alveolar-arterial Po2 difference; BS = bariatric surgery; Dlco = diffusing capacity of the lung for carbon monoxide; ERV = expiratory reserve volume; FRC = functional residual capacity; sTNF-R1 = soluble tumor necrosis factor-receptor 1; TLC = total lung capacity.

a 

P values for comparisons between control and obese individuals before surgery.

b 

P values for comparisons between pre- and postoperative conditions in obese individuals.

Table Graphic Jump Location
TABLE 2 ]  Pulmonary Gas Exchange, Ventilatory, Hemodynamic, and Metabolic Findings Breathing Ambient Air and Oxygen-Induced Changes in Obese Individuals Before and After BS

Data are presented as mean ± SE. Log SDQ = dispersion of blood flow distribution; Log SDV = dispersion of alveolar ventilation distribution; NA = not available; O2 = oxygen; PAP = mean pulmonary artery pressure; PCWP = pulmonary capillary wedge pressure; Psa = mean systemic arterial pressure; Pv¯ o2 = mixed venous Po2; PVR = pulmonary vascular resistance; Q. t = cardiac output; SVR = systemic vascular resistance; V. a = alveolar volume V. e = minute ventilation; V. o2 = oxygen consumption. See Table 1 for expansion of other abbreviations.

a 

Breathing ambient air.

b 

Breathing 100% oxygen.

c 

P values for comparisons during ambient air breathing between pre- and postoperative conditions.

d 

P values for comparisons between pre- and postoperative differences from 21% to 100% oxygen breathing.

e 

P < .05 for comparisons before surgery, between ambient air and 100% O2 breathing.

f 

P < .05 for comparisons after surgery, between ambient air and 100% O2 breathing.

g 

Unventilated units (V. a/Q.  ratios < 0.005), expressed as % of Q. t.

h 

Alveolar units with V. a/Q.  ratios > 100, expressed as % of V. a.

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Dantzker DR, Wagner PD, West JB. Instability of lung units with low Va/Q ratios during O2breathing. J Appl Physiol. 1975;38(5):886-895.
 
Santos C, Ferrer M, Roca J, Torres A, Hernández C, Rodriguez-Roisin R. Pulmonary gas exchange response to oxygen breathing in acute lung injury. Am J Respir Crit Care Med. 2000;161(1):26-31. [CrossRef] [PubMed]
 
Greenstein AS, Khavandi K, Withers SB, et al. Local inflammation and hypoxia abolish the protective anticontractile properties of perivascular fat in obese patients. Circulation. 2009;119(12):1661-1670. [CrossRef] [PubMed]
 
Zavorsky GS, Wilson B. Sex, girth, waists and hips (what matters for gas exchange in extreme obesity?). Respir Physiol Neurobiol. 2010;170(1):120-122. [CrossRef] [PubMed]
 
Zavorsky GS, Christou NV, Kim do J, Carli F, Mayo NE. Preoperative gender differences in pulmonary gas exchange in morbidly obese subjects. Obes Surg. 2008;18(12):1587-1598. [CrossRef] [PubMed]
 
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