Brian K. Parker, MD, MS; Sara Manning, MD; Michael E. Winters, MD, MBA


Western J Emerg Med. 2019;20(2):323-330. 

In This Article

Alterations in Respiratory Physiology

The respiratory system of the obese patient undergoes several anatomic and physiologic alterations that affect emergent airway management and initiation of mechanical ventilation. Anatomically, obese patients have an increased neck circumference due to excess cervical adipose tissue. Increased neck circumference is strongly associated with the upper airway collapse observed in obstructive sleep apnea.[4] Additionally, increased soft tissue deposition in the relatively closed space of the oropharyngeal cavity leads to pharyngeal airway narrowing.[5] As observed in sleep, loss of neuronal compensation in the setting of sedation with or without paralytic can lead to upper airway collapse. Increased neck circumference as well as dorsocervical fat deposition can limit neck extension. While it remains unclear if obesity is an independent risk factor for a difficult airway, obesity and its associated conditions are considered in several commonly used scoring systems to assess for potentially difficult intubations, including the Wilson scoring system, LEMON (Look-Evaluate-Mallampati-Obstruction-Neck mobility), and the HEAVEN (Hypoxemia, Extremes of size, Anatomic challenges, Vomit/blood/fluid, Exsanguination/anemia, Neck mobility issues) criteria.[6–8] Rapid access to a surgical airway can be limited when landmarks are obscured in a short, obese neck. Some recommend initial sharp dissection followed by palpation within the incision to facilitate landmark identification.[9] Overall, obesity and its associated anatomic changes should alert the EP to the possibility of a difficult airway and prompt appropriate planning and back-up.

Physiologically, obese patients have markedly decreased lung volumes. In fact, for each unit increase in BMI, functional residual capacity (FRC), expiratory reserve volume, vital capacity, total lung capacity, and residual capacity decrease 0.5% to 5%.[10] Of these changes in lung volumes, the reduction in FRC is perhaps the most important, as further decreases lead to the closure of small airways and an increase in airway resistance.[1] Reduction in FRC is an important contributor to the marked limitation in safe apnea time in the obese. Increased airway resistance results in under-ventilated areas of lung, atelectasis, and intrapulmonary shunting.[1] Decreased lung volumes also reduce lung compliance in the obese patient. In addition to decreased lung volumes, decreased lung compliance, increased airway resistance, and intrapulmonary shunting, obese patients also develop ventilation-perfusion (V/Q) mismatch due to the fact that their upper lung zones are aerated preferentially, whereas lower lung zones are perfused preferentially.[1] Finally, chest wall compliance is reduced due to the increase in adipose tissue in the thoracic cage. All of these alterations in respiratory physiology can be worsened when the obese patient is placed in the supine position.

As a result of these physiologic changes, it is not surprising that oxygen consumption and the work of breathing (WOB) are significantly increased in the obese patient.[11] Oxygen consumption is approximately 1.5 times higher in the obese patient than in the non-obese patient.[11] Due to the increase in oxygen consumption and WOB, obese patients produce more carbon dioxide than non-obese patients.[12] To compensate, the obese patient adopts a rapid, shallow breathing pattern. In fact, normal spontaneous respiratory rates in the morbidly obese patient range from 15–21 breaths per minute compared with 10-12 breaths per minute in non-obese patients.[13,14]

Overall, these anatomic and physiologic alterations in respiratory physiology lead to a marked decrease in pulmonary reserve.[1] Decreased pulmonary reserve predisposes the patient to the rapid onset of hypoxemia during rapid sequence intubation (RSI), which can result in peri-intubation cardiac arrest.