The Relationship Between Anthropometric Measures, Blood Gases, and Lung Function in Morbidly Obese White Subjects

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Abstract

Background

Obesity may cause adverse effects on the respiratory system. The main purpose of this study was to investigate how various measures of obesity are related to arterial blood gases and pulmonary function.

Methods

This is a cross-sectional study of consecutive morbidly obese patients with normal lung function. Blood gas samples were taken from the radial artery after 5 min of rest with subjects sitting upright. Lung function measurements included dynamic spirometry, static lung volumes, and gas diffusing capacity.

Results

The 149 patients (77% women) had a mean (SD) age of 43 years (11 years) and BMI of 45.0 kg/m ² (6.3 kg/m ²). The mean expiratory reserve volume (ERV) was less than half (49%) of predicted value, whilst most other lung function values were within predicted range. Forty-two patients had an abnormally low pO2 value (<10.7 kPa [80 mmHg]), while eight patients had a high pCO2 value (>6.0 kPa [45 mmHg]). All anthropometric measures correlated significantly with decreasing pO2 and increasing pCO2 (all P values < 0.05). BMI, neck circumference (NC), and waist circumference (WC) were negatively correlated with ERV ( r = −0.25, −0.19, −0.21, respectively, all P values < 0.05). Multiple linear regression showed that BMI, WC, and NC were significantly associated with pO2 after adjustments for age, gender, and pack-years (all P values < 0.001). The models explained 34–36% of the variations in pO2. BMI, NC, and WC were also significantly associated with pCO2 (all P values < 0.05).There was no significant association between waist-to-hip ratio and blood gases (both P values > 0.27).

Conclusions

Both central and overall obesity were associated with unfavorable blood gases and low ERV.

Related collections

Most cited references 14

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Body mass index and waist circumference independently contribute to the prediction of nonabdominal, abdominal subcutaneous, and visceral fat.

Donald P. Kotler, Ian Janssen, Steven B Heymsfield … (2002)

It is unknown whether the ability of waist circumference (WC) to predict health risk beyond that predicted by body mass index (BMI) alone is explained in part by the ability of WC to identify those with elevated concentrations of total or abdominal fat. We sought to determine whether BMI and WC independently contribute to the prediction of non-abdominal (total fat - abdominal fat), abdominal subcutaneous, and visceral fat. Fat distribution was measured by magnetic resonance imaging in 341 white men and women. Multiple regression analysis was performed to measure whether the combination of BMI and WC explained a greater variance in non-abdominal, abdominal subcutaneous, and visceral fat than did BMI or WC alone. These fat depots were also compared after a subdivision of the cohort into 3 BMI (normal, overweight, and class I obese) and 3 WC (low, intermediate, and high) categories according to the classification system used to identify associations between BMI, WC, and health risk. Independent of age and sex, the combination of BMI and WC explained a greater variance in non-abdominal, abdominal subcutaneous, and visceral fat than did either BMI or WC alone (P < 0.05). For non-abdominal and abdominal subcutaneous fat, BMI was the strongest correlate; thus, by adding BMI to WC, the variance accrued was greater than when WC was added to BMI. However, when WC was added to BMI, the added variance explained for visceral fat was greater than when BMI was added to WC. Furthermore, within each of the 3 BMI categories studied, an increase in the WC category was associated with an increase in visceral fat (P < 0.05). BMI and WC independently contribute to the prediction of non-abdominal, abdominal subcutaneous, and visceral fat in white men and women. These observations reinforce the importance of using both BMI and WC in clinical practice.

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Obesity and asthma: possible mechanisms.

Stephanie A. Shore (2008)

Epidemiologic data indicate that obesity increases the prevalence and incidence of asthma and reduces asthma control. Obese mice exhibit innate airway hyperresponsiveness and augmented responses to certain asthma triggers, further supporting a relationship between obesity and asthma. Here I discuss several mechanisms that may explain this relationship. In obesity, lung volume and tidal volume are reduced, events that promote airway narrowing. Obesity also leads to a state of low-grade systemic inflammation that may act on the lung to exacerbate asthma. Obesity-related changes in adipose-derived hormones, including leptin and adiponectin, may participate in these events. Comorbidities of obesity, such as dyslipidemia, gastroesophageal reflux, sleep-disordered breathing, type 2 diabetes, or hypertension may provoke or worsen asthma. Finally, obesity and asthma may share a common etiology, such as common genetics, common in utero conditions, or common predisposing dietary factors. Novel therapeutic strategies for treatment of the obese patient with asthma may result from an increased understanding of the mechanisms underlying this relationship.