Obesity: Pulmonary Manifestations

Key Points

The global prevalence of obesity has been steadily increasing over the last few decades, and nearly two-thirds of adults are predicted to carry a diagnosis of overweight or obese by 2050.
Increased thoracic and abdominal adiposity impairs pulmonary function by reducing lung volumes (expiratory reserve volume [ERV], closing volume), capacities (functional residual capacity [FRC], vital capacity, total lung capacity [TLC]), and lung compliance.
Patients with obesity are at risk of chronic hypercapnia, hypoxemia, atelectasis, sleep-disordered breathing, and ultimately obesity hypoventilation syndrome (OHS) and pulmonary hypertension.
Management aims to identify respiratory abnormalities, optimize airway patency, lung compliance, oxygenation, and ventilation, and minimize pulmonary hypertension and right ventricular strain.

Introduction

Obesity is a chronic disease stemming from multifactorial causes, leading to an imbalance of energy intake and expenditure, and resulting in excess fat accumulation and increased risk for adverse health outcomes.¹
In the US, around 42% of adults are considered obese, and obesity has been recognized as a public health epidemic.¹
- Obesity disproportionately affects people identifying as Black or African American and Hispanic/Latino ethnicity, as well as women compared to men.²
Obesity in adults is typically defined as a body mass index (BMI) greater than 30 kg/m² or a waist circumference greater than 102 cm (40 inches) for men and greater than 88 cm (35 inches) for women.
A new proposed definition of obesity would include a BMI ≥ 25 kg/m² and a waist-to-height ratio ≥ 0.5 with medical, functional, or psychological impairments. Obesity can be further stratified into three different categories.^3,4

Figure 1. Classification of obesity in adults 18 years or older. Source: Centers for Disease Control and Prevention.³https://www.cdc.gov/bmi/adult-calculator/bmi-categories.html
Abbreviation: BMI, body mass index

Patients with obesity have an increased risk for chronic diseases, such as type 2 diabetes mellitus, hypertension, cardiovascular disease, and cancer.²
Similarly, the impact of obesity on pulmonary function is multifactorial, stemming primarily from mechanical effects and the risk of progression to a chronic inflammatory condition.

Dynamic Lung Volumes

The mechanical effects of adiposity accumulation and increased blood volume affect pulmonary function by reducing lung volumes and capacity and by restricting lung expansion (reducing lung compliance).
- Excess central or abdominal adiposity, relative to peripheral adiposity, has a greater impact on functional (dynamic) lung volumes.⁵
As central adiposity increases, the diaphragm elevates and exhibits reduced downward excursion during inhalation, while chest wall and mediastinal adiposity further restrict respiratory system and lung expansion.^5,6
Lung compliance is also related to premature peripheral airway closures, as the external and pleural pressure is greater than internal airway pressure (reduced closing volume).
ERV, the additional air that can be forcibly exhaled beyond normal exhalation, is the lung volume that decreases the most with increasing obesity.⁶
FRC, the volume remaining in the lung at the end of a normal exhalation (the equilibrium point between the elastic recoil of the lung and the chest wall), is progressively reduced with increasing obesity.⁶
The reduction in TLC and residual volume is present with increasing obesity, but less affected than ERV and FRC.⁵
Due to alterations in lung volumes, increased resistance, and decreased compliance, obesity increases patients’ work of breathing.⁶

Figure 2. Normal dynamic lung volumes. Source: Wikimedia Commons.⁷ https://commons.wikimedia.org/wiki/File:LungVolume.jpg

Pulmonary Function Tests (PFTs)

Although lung volumes are compromised in proportion to obesity severity, the pattern of lung pathophysiology has been reported to shift from obstructive to restrictive with increasing patient age.⁸
In children and young adults with obesity, PFTs resemble an obstructive pattern with a lower forced expiratory volume (FEV)₁/force vital capacity (FVC) ratio similar to asthma, likely due to the disproportionate growth between lung parenchyma and airways during development (dysanapsis).^8,9
- Airway dysanapsis in obese children is associated with the development of lung disease with reduced response to inhaled corticosteroids and increased morbidity.⁹
In older adults with obesity, spirometric patterns are typically restrictive, characterized by reduced FEV_₁ and FVC, with a preserved or increased FEV_₁/FVC ratio.⁸
- The shift of pulmonary pattern occurs after approximately 35 years of age in men and 40 years of age in women.

Figure 3. Changes in PFTs that resemble either obstructive or restrictive physiology. Source: Biology for Majors.¹⁰https://courses.lumenlearning.com/wm-biology2/chapter/the-work-of-breathing/#:~:text=The%20ratio%20of%20FEV1%20(the%20amount%20of,person%20has%20restrictive%20or%20obstructive%20lung%20disease.
Abbreviations: FEV, forced expiratory volume; FRC, force vital capacity; PFTs, pulmonary function tests

Arterial Blood Gases

As central adiposity and overall BMI increase, ventilation and oxygenation become impaired.
Alveolar hypoventilation is present in approximately 1-10% of patients with obesity.¹¹
Ventilation-perfusion mismatch increases the risk and frequency of hypoxemia events.¹¹
- Obesity leads to premature peripheral airway closure and regions of atelectasis that may exacerbate or prolong the episodes of hypoxemia.^11,12
Hypoxemia events worsen while supine, thereby increasing the risk of nocturnal hypoxemia and ultimately resulting in obstructive sleep apnea.¹¹
Patients are at risk of developing OHS, which is defined as sleep-disordered breathing and chronic daytime hypercapnia (arterial partial pressure of carbon dioxide, PaCO₂, ≥ 45 mmHg).¹²
- The proposed mechanism of hypercapnia encompasses alveolar hypoventilation, reduced lung volumes, and impaired compensatory mechanisms, including limited ventilatory drive and impaired lung muscle function.^11,12
- A serum HCO₃− concentration less than 27 mmol/L rules out chronic hypercapnia.¹¹
Management of obese patients with underlying ventilatory disorders should focus on noninvasive ventilation (NIV) in the acute setting to prevent further respiratory failure and on continuous positive airway pressure (CPAP) for long-term management in a stable state.^1,5,11
Treatment with CPAP and/or NIV has shown a significant decrease in mortality in patients with OHS.¹²
Weight-loss strategies, both surgical and nonsurgical, are the only treatment to attenuate the effects of obesity on pulmonary function.

Figure 4. Flowchart for management of acute and chronic hypercapnia in a patient with obesity. Source: Rabec C et al. Eur Respir Rev. 2025;34(176):240190.¹¹ CC BY NC 4.0. https://pmc.ncbi.nlm.nih.gov/articles/PMC12076159/
Abbreviations: NIV, noninvasive ventilation; OSA, obstructive sleep apnea; CPAP, continuous positive airway pressure

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