The Pre-brief
Over the span of decades, the worldwide prevalence of obesity has increased in such a magnitude that has allowed it to gain recognition as a global epidemic. By definition, obesity refers to the excess distribution of adipose tissue and has various methods for which it can be quantified. Clinically, body mass index (BMI) has gained wide acceptance and is commonly utilized to quantify the extent of obesity in many medical institutions. Systemically, obesity is a disease that alters normal physiological function across a wide range of organ systems. In the ICU, morbidly obese patients often exhibit drastically altered respiratory mechanics that impose management dilemmas in their care.
Obesity: Central vs Peripheral
There are primarily two clinically recognized patterns of fat distribution. Central obesity is characterized by the accumulation of adipose tissue in the abdominal and thoracic cavities, along with the visceral organs. Peripheral obesity is characterized by the accumulation of adipose tissue in extremities such as upper/lower limbs, hips, and subcutaneous tissue. Of the two patterns of obesity, it is the central pattern which is more likely to be causative of deranged respiratory mechanics that are often observed in obesity.
Obesity and Lung Volumes
Static and dynamic lung volumes in the obese patient are primarily altered by excess deposition of adipose tissue in the upper airways, chest wall and abdominal cavity. As BMI increases, the accumulation of excess adipose tissue in the abdominal cavity causes cephalic displacement of the diaphragm with reductions in almost all static lung volumes, particularly total lung capacity (TLC), functional residual capacity (FRC) and expiratory reserve volume (ERV). These effects are more pronounced in the supine position where gravity exerts less influence on the distribution of ventilation to dependent regions of the lung, and as BMI increases. Dynamic changes are also observed as the severity of obesity increases with reductions in forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC); however, the FEV1:FVC ratio is typically preserved in the normal range indicating a restrictive deficit.
Obesity and Respiratory Mechanics
Hallmark findings in obesity include alterations of the mechanical properties of the lungs and chest wall. Excess adipose tissue in the chest wall reduces chest wall compliance and restricts outward displacement during respiration. Excess adipose tissue in the abdominal cavity causes upward displacement of the diaphragm while the accompanying increase in intra-abdominal pressure restricts downward displacement during respiration, reducing lung compliance.
Because of these changes, the total volume of the lungs at FRC is lower, with lung alveoli now best represented at a lower, flatter, and less compliant portion of the pressure-volume curve. The net effect is an overall reduction in the total compliance of the respiratory system. Â
The small airways and alveoli in the dependent regions of the lung consist of volumes that are significantly lower than they are at the apex. As lung volume falls towards residual volume (RV) after a normal tidal breath, they approach a point below which further decreases in lung volume would result in closure and collapse of small airways and alveoli in those dependent regions. This volume represents the closing capacity (CC) and is typically much less than FRC even in mild-moderate obesity. As the severity of obesity progresses, however, FRC may eventually reach and subsequently fall below CC resulting in airway collapse, increased airway resistance and expiratory flow limitation. In these patients it is possible to observe a reduced FEV1:FVC ratio indicating the development of a mixed restrictive/obstructive deficit.Â
Airway Narrowing and Hyperresponsiveness
There are several potential mechanisms which may lead to airway narrowing severe obesity. Deposition of adipose tissue surrounding the upper airways may result in structural changes and reduced airway patency. Another plausible theory is that with an abundance of adipose tissue, the secretion of large amounts of adipocyte-derived factors into the upper airways introduces a chronic inflammatory state that eventually leads to structural remodeling of the upper airways with airway narrowing. With airway narrowing and flow limitation, this can lead to gas trapping and an elevation in the RV/TLC ratio which is usually normal in obesity. Chronic inflammation of the upper airways may also shed some light on a possible link between obesity and airway hyperresponsiveness as demonstrated by exaggerated responses to methacholine challenge tests in several studies. Â
Obesity and Ventilation/Perfusion Mismatch
Obesity introduces alterations to the normal distribution pattern of ventilation throughout the lungs resulting in mismatches between ventilation and perfusion. As FVC approaches RV, airway closure and atelectasis become a concern, particularly in the dependent regions of the lung as they receive most of the pulmonary blood flow by the effects of gravity. This creates significant areas of intrapulmonary shunting that may ultimately cause widening of the alveolar-arterial (A-a) gradient and hypoxemia.
The Debrief
- Central obesity is associated with altered respiratory mechanics that complicate the management of critically ill patients.
- Increased intrapleural pressure and reduced diaphragmatic expansion leads to reduced TLC, ERV and FRC. The FEV1/FVC ratio is, however, normally preserved 🡪 Restrictive Lung Defect
- Increased airway resistance results when FRC drops below CC causing small airway collapse.
- Those patients may show expiratory flow limitation and reduced FEV1 🡪 Mixed/Obstructive Lung Defect
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