The World Health Organization and the National Institutes of Health define a person to be overweight when he or she has a body mass index (BMI) between 25 and 29.9 kg per m², and a person to be obese when BMI is ≥30 kg per m². Morbid obesity is variably defined as a BMI >35 or 40 kg per m². The National Health and Nutrition Examination Survey for 2003 to 2004 estimates that 66.2% of the adults in the United States between the age of 20 and 74 years are either overweight or obese (33.4% overweight, 32.9% obese) and early data from 2005 to 2006 show no significant change in the prevalence of obesity; however, the 2008 Behavioral Risk Factor Surveillance System, a state-based cross-sectional random survey of the adult population of United States, showed considerable differences in the prevalence of obesity across states.

As for all patients, managing the airway of obese patients requires a structured, methodical assessment to identify the specific predictors of difficult bag-mask ventilation (BMV), cricothyrotomy, extraglottic device (EGD) placement, and tracheal intubation. It is controversial whether obesity, per se, is a predictor of difficult laryngoscopy, or whether obese patients tend to have a higher incidence of other markers of difficult intubation. Patient attributes differ, and some obese patients may have multiple anatomical risk factors for difficult airway in addition to obesity, whereas others may not. Nevertheless, morbidly obese patients develop both physiologic and anatomic changes that can make airway management particularly challenging as morbidly obese patients not only have excess adipose tissue on the breast, neck, thoracic wall, and abdomen but also internally in the mouth and pharynx. When compared with lean patients, this excess tissue makes accessing the airway (intubation and tracheostomy) and maintaining patency (during sedation or mask ventilation) of the upper airway more difficult.

The degree of pathologic, physiologic, and anatomical changes correlate with the degree and extent of obesity and many comorbidities common with obese patients. The physiologic and anatomical changes associated with morbid obesity are listed in Box 39-1. The main effects of obesity on airway management are (1) rapid arterial desaturation, secondary to a decreased functional residual capacity (FRC) and increased oxygen consumption; (2) difficult airway management, specifically difficult BMV, resulting from increased risk of obstruction from excess pharyngeal adipose tissue and increased resistance resulting from the weight of the chest wall and the mass of abdominal contents limiting diaphragmatic excursion; and (3) difficult laryngoscopy, intubation, and cricothyrotomy.

Obesity affects almost every aspect of normal physiology, most notably the respiratory and cardiovascular systems. Obese patients often have baseline hypoxemia with a widened alveolar-arterial oxygen gradient, which is primarily because of ventilation-perfusion (V/Q) mismatching. Lung volumes develop a restrictive pattern with multiple disturbances, the most important of which is decreased FRC. Notably, these indices change exponentially with the degree of obesity. The decline in FRC has been ascribed to “mass loading” of the abdomen and splinting of the diaphragm. FRC may be reduced to the extent that it falls within the range of closing capacity, thus leading to small airway closure and V/Q mismatch. The FRC declines further when the individual assumes the supine position, resulting in worsening of the V/Q mismatch, right-to-left shunt, and arterial hypoxemia. Although the vital capacity, total lung capacity (TLC), and FRC may be maintained in mild obesity, they can be reduced by up to 30% in morbidly obese patients and up to 50% in severely obese patients. The decreased FRC causes rapid oxyhemoglobin desaturation during the apneic phase of rapid sequence intubation (RSI), even in the setting of adequate preoxygenation (see Chapter 19).

The work of breathing (WOB) is increased 30% to 400% in morbidly obese patients because of decreased chest wall compliance, increased airway resistance, and an abnormal diaphragmatic position. These changes limit the maximum ventilatory capacity (MVC). The obese patient has elevated oxygen consumption and carbon dioxide (CO₂) production because of the metabolic activity of the excess body mass.

Cardiovascular changes in obesity include increased extracellular volume, cardiac output, left ventricular end diastolic pressure, and left ventricular hypertrophy (LVH). The absolute total blood volume (BV) is increased, but it is relatively less on a volume/weight basis when compared with lean patients (50 vs. 75 ml per kg). Cardiac morbidity, including hypertension (HTN), ischemic heart disease, and cardiomyopathy, all correlate with progressive obesity.

Other changes include an increase in renal blood flow (RBF) and glomerular filtration rate (GFR), fatty infiltration of the liver, and a propensity for diabetes mellitus and obstructive sleep apnea (Box 39-1).

Increased chest wall weight, increased facial girth, and redundant pharyngeal tissue all contribute to defining obesity as an independent risk factor for difficult BMV (see Chapter 2). Obese patients tend to have a smaller pharyngeal space because of deposition of adipose tissue into the tongue, tonsillar pillars, and aryepiglottic folds. Patients with obesity have an increased risk of having obstructive sleep apnea and facial hair (in men), which are also independent risk factors for difficult BMV. Difficult BMV should be anticipated in the obese patient, often requiring a two-person technique with both oral and nasopharyngeal airways in place. In severe or superobese patients, BMV may simply be impossible as the mask seal pressure required to overcome the increased weight and resistance may be far in excess of that possible with a bag and mask. In addition, challenging BMV is associated with difficult intubation in 30% of the cases. Intubation difficulty is also associated with increased neck circumference and high Mallampati scores. Cricothyrotomy is more difficult because of the increase in neck circumference, the thickness of the subcutaneous tissues, anatomical distortions, and adipose tissue obscuring landmarks, often requiring deeper and longer incisions. EGDs may not be able to overcome the high resistance of the weighted chest wall and restricted diaphragms.