2.2. Obstructive Sleep Apnea
OSA is diagnosed in 5% of the obese population and is characterized by 10-second episodes of apnea (breathing cessation despite respiratory efforts against a closed glottis). The resulting chronic hypoxemia causes secondary polycythemia, hypercapnia, pulmonary, and systemic vasoconstriction and leads to an increased risk of cardiac and cerebral ischemia and intrapulmonary shunting [
8,
9]. Patients with OSA show impaired pulmonary gas exchange both at rest and with exercise, and some studies have suggested an effect of male gender and adipose tissue distribution on the severity of this impairment [
2]. Patients with OSA show larger decreases in lung volumes and compliance when anesthetized, and they are more prone to atelectasis and increased closing volumes and oxygen requirement [
10]. This in turn contributes to rapid desaturation during induction of general anesthesia, especially in the absence of adequate preoxygenation or during difficult mask ventilation or intubation. A subgroup of patients with OSA can have
obesity hypoventilation syndrome (OHS). OHS is defined as chronic hypoventilation (PaCO
2 > 45

mmHg) in the absence of lung, chest wall, and neurological disease [
11]. Hypoventilation and apnea are central, and probably due to progressive desensitization to hypercapnia, which leads to an increased dependence on the hypoxic drive to maintain respiration. It affects 8–10% of patients with BMI > 30–34

kg/m
2 and 18–25% of patients with BMI > 40

kg/m
2 [
11]. The presence of OSA or OHS should be screened in the preoperative evaluation, to optimize perioperative care. Several scoring systems have been developed for this purpose. The most commonly used system is the
STOP (Snoring, day time Tiredness, Observed apnea, high blood Pressure)-
BANG (BMI > 35, Age > 50; Neck circumference > 40

cm, Gender = male) questionnaire [
12]. If patients answer yes to three or more questions, they are considered at high risk for OSA, and a sleep study should be obtained [
12]. The use of continuous positive airway pressure (CPAP) at night can decrease apnea spells and reduce subsequent cardiac structural changes [
13]. However, it is unclear how much time is necessary before a clinical improvement is seen. Patients using CPAP at home should continue to use it in the postoperative period as well, and arrangements should be made for continuous monitoring when discharged from the postoperative anesthesia care unit (PACU) to the floor. The presence of OSA should prompt customization of the anesthetic plan, by minimizing the use of long acting sedative medications, intravenous narcotics, and muscle relaxants. Regional techniques for postoperative analgesia should be favored if amenable.