Ventilatory Mechanics in the Patient With Obesity

Luigi Grassi, M.D.; Robert Kacmarek, Ph.D.; Lorenzo Berra, M.D.


Anesthesiology. 2020;132(5):1246-1256. 

In This Article

Mechanics During Spontaneous Breathing

In humans, the majority of the adipose tissue is distributed in the subcutaneous space, particularly in the abdomen; as the body mass index increases, both the subcutaneous and the visceral adipose components show a tendency to increase.[14] Abdominal fat can be thought of as a liquid mass influencing the pressures in the ventral coelom cavity. The interplay between the increased abdominal pressure and the elastic structures in the thoracic space, such as the lungs, has been extensively studied. In obesity, the cephalic displacement of the diaphragm by the abdominal fat affects the lung volumes, producing a restrictive pattern whose hallmark is the reduction in the functional residual capacity (FRC) and in the expiratory reserve volume[15–17] (Figure 1). The more significant decreases in FRC and expiratory reserve volumes are observed for mild increments of body mass index (between 25 and 35 of body mass index, corresponding to overweight and class I obesity[15]), and are accompanied by a reduction in total lung capacity and vital capacity, but not in inspiratory capacity and residual volume.[17] In most of the cases, the ratio between the forced expiratory volume during the first second and the forced vital capacity (forced expiratory volume during the first second/forced vital capacity) is preserved.[15,17] However, the behavior of the respiratory system changes when a subject with obesity transitions from sitting to the supine position. In the flat situation, there is no further reduction in FRC and expiratory reserve volume, contrary to what is observed in the lean person, indicating that, when standing, people with obesity are already breathing near their residual volume. Instead, there is a significant increase in airway resistance, with consequent limitation in the expiratory flow and the development of intrinsic positive end-expiratory pressure (PEEP).[16] Intrinsic PEEP results in an increase in the work of breathing.[18] Hence, in a subject with obesity lying supine, expiratory flow limitation and consequent air trapping at low FRC become the main feature, with the respiratory pattern converting from simple restrictive to mixed restrictive-obstructive. This phenomenon has not been fully elucidated. The person with obesity breathes at very low lung volumes, and low lung volumes are known to be associated with expiratory flow limitation since elastic recoil is a determinant of the airway's caliber.[19] On the other hand, in the upright position, the increased elastance observed in the obese lung is able to compensate for the reduction in FRC and the increased airway resistance, preserving expiratory flows until the expiratory reserve volume is obliterated.[20] It is possible that once supine, this labile compensation is altered by other factors that further contribute to airway closure, such as an increased intrathoracic blood volume or the occlusion of the upper airways by fat loading, with the resulting flow limitation and air trapping.[16] Some of the changes observed in the supine position are illustrated in Figure 2.

Figure 2.

Changes induced by central obesity in supine position during spontaneous breathing, sedation and paralysis, and mechanical ventilation. (A) The patient is actively breathing. Displacement of the diaphragm by a high abdominal load (horizontal red arrows) leads to high pleural pressure and lung volumes reduction with consequent narrowing of the small airways (red arrows in subpanel a, representing a partially collapsed airway-alveolar unit). Airway collapse at low lung volume is partially counteracted by the contraction of the inspiratory muscles (green arrows), which lowers pleural pressure, at the cost of a high work of breathing produced by the patient (work of breathing [WOB] patient). (B) The patient is sedated and paralyzed, with suboptimal manual intermittent positive pressure ventilation (IPPV). Paralysis prevents inspiratory muscular contraction (red crosses on the green arrows) and pronounced total collapse of the small airways predominates (subpanel b). Concomitant administration of a high fraction of inspired oxygen (FIO2) results in reabsorption atelectasis in underventilated alveolar units (subpanel c), with further reductions in expiratory lung volumes, deterioration of compliance, and shunting leading to hypoxemia. (C) Mechanical ventilation with a titrated level of positive end-expiratory pressure (PEEP) counteracts small airways collapse (subpanel d), restoring lung volumes and, consequently, lung mechanics and oxygenation.