Although patients with severe OSA seem to be at higher risk of perioperative complications [39], careful observation and early intervention should be recommended for patients with all grades of severity of sleep-disordered breathing [31, 40]. Various strategies can be employed to reduce the risks and avoid adverse outcomes. Preoperatively, the use of anxiolytic premedication is not recommended [41]. There is evidence that regional anesthesia (RA) is preferable over general anesthesia (GA) whenever possible [42]. Regional anesthesia minimally affects respiratory drive, it avoids the side effect of anesthetic agents, particularly on the arousal responses during apneic episodes. Regional anesthesia may also avoid or reduce the need for sedative drugs and opioids during the entire perioperative period. It has been well established that the presence of OSA may lead to difficulties in airway management both in terms of difficult mask ventilation and tracheal intubation [43–46]. Although these findings do not imply that awake intubation is necessary in all patients with OSA, prudence dictates that clinicians should have immediate access to alternative techniques to secure the airway and ventilate the patient. There is evidence that many anesthetic agents cause exaggerated responses in patients with sleep apnea. Drugs such as thiopentone, propofol, opioids, benzodiazepines, and nitrous oxide may blunt the tone of the pharyngeal musculature that acts to maintain airway patency. The choice of induction and maintenance agents is probably not important, although it would seem reasonable to avoid large doses of long-acting drugs. This is true with both neuromuscular blocking agents and benzodiazepines. As a matter of fact, anesthesia techniques using short half-life agents should be advised to avoid any residual drugs in the respiratory system [47, 48]. Whenever the patient is extubated, whether early in the operating room or later in the recovery room or in the ICU, the patient should be fully awake [49]. Full recovery from neuromuscular blockade should be proven by a neuromuscular blockade monitor. In the case of difficult airways, guidelines for safe extubation should be followed [50].

The postoperative disposition of the OSA patient will depend on three main components: invasiveness of the surgery, severity (known or predicted) of OSA, and requirement for postoperative opioids. The American Society of Anesthesiologists (ASA) guidelines suggest that all patients with known or suspected OSA who have received general anesthesia should be monitored in the PACU (post-anesthesia care unit). However, there are currently no evidence-based guidelines addressing the optimal length of monitoring required in the PACU and the ASA recommendations are difficult to adhere to, especially in the context of a community hospital [50].

Unlike NPPV, during CPAP the pressure applied to the respiratory system is only generated by the patient’s respiratory muscles (P _app = P _Musc). In this case, transpulmonary pressure, which is generated by the respiratory muscles, has to overcome the upper airway resistances, which means that in patients with OSA CPAP is effective on the lower airways only if it opens the upper airways [68, 69]. CPAP maintains a constant pressure in the upper airways during inspiration and expiration that acts as a pneumatic splint, allowing patency of the upper airway throughout the respiratory cycle [70–72]. Beyond this, CPAP is aimed at improving arterial blood gases and at decreasing work of breathing by:

CPAP is aimed at improving oxygenation through an amelioration of ventilation-perfusion mismatch by promoting alveolar recruitment [73] and by maintaining the alveoli open and by counteracting PEEPi alone in association with NPPV [74–76].

Although “genuine” CPAP is commonly used for mild hypoxemic ARF without clear signs of respiratory muscle fatigue, the level of evidence of CPAP effectiveness as a single mode of ventilation support in manifested ARF without cardiopulmonary edema (CPE) is still low [77]. CPAP is also aimed at improving left ventricular performance in chronic heart failure and is considered as a first-line therapy in CPE [78–81. To understand the mechanism of CPAP in patients with OSA it is necessary to focus on the complex mechanisms of heart-lung interaction (Fig. 63.3). With each obstructive event and the associated hypoxemia and hypercapnia, there is a generation of a deep subatmospheric intrathoracic pressure (ITP) due to the occluded airway with associated left ventricular afterload, increased pulmonary artery pressures, decreased left ventricular compliance, and increased myocardial oxygen demand [68]. The heart and lungs share a common intrathoracic compartment. The heart feels as a “container” the modification of ITP generated during changes of transpulmonary pressure during tidal breathing and accordingly modifies both venous return to the heart and left ventricular (LV) ejection pressure [82]. ITP decreases with inspiratory efforts and reducing right atrial pressure will augment venous return and its pressure gradient. In turn, the increase in right ventricular (RV) filling increases RV output, but dilating the right ventricle may theoretically cause the shift of intraventricular septum into the left ventricle, decreasing its diastolic compliance and arterial pulse pressure (pulsus paradoxus) [82]. With sustained decreases in ITP, as may occur with inspiration against an occluded airway (Mueller maneuver), this transient increase in venous return declines with the increased blood flow to the left ventricle and the intraventricular septum returns to its neutral position [83]. However, the decreasing ITP also increases LV afterload because LV ejection occurs into an arterial circuit in which the surrounding pressure is atmospheric pressure, not ITP [82]. LV afterload reflects the maximal wall stress on the left ventricle during ejection. According to the Laplace theorem, LV wall stress is a function of the product of the transmural pressure and the radius of curvature of the left ventricle [82]. This increased afterload explains the development of acute pulmonary edema in patients with severe airways obstruction or with OSA with repetitive negative swings during deep sleep. The increasing wall stress causes subendocardial ischemia and impairs LV systolic performance for a while, even after the strain phase of the increases ITP is over.

The oxygen desaturation leads to an increase in pulmonary vascular resistance due to hypoxic pulmonary vasoconstriction. In OSA patients, CPAP improves cardiovascular performance and decreases heart failure by reducing the incidence of both negative swings in ITP and arterial desaturation [84]. Interestingly, patients with chronic heart failure (CHF) have a prolonged depression in LV performance following ITP, even in the absence of hypoxemia [85]. Patients with CHF have increased circulating blood volume. Thus, negative swings in ITP will induce a greater increase in venous return than in healthy volunteers, suggesting that RV dilation is the primary cause of depressed LV performance [82]. Theoretically, measures aimed at reducing circulating blood volume, but also aimed to decrease LV afterload, would limit LV depression during OSA events [82].

Interestingly, Kaw et al. [86], in a study reporting the perioperative outcomes in a large cohort of patients undergoing cardiac surgery, comparing those with and without pulmonary hypertension (PH), found that 27 patients encountered significant postoperative complications. Patient characteristics significantly associated with postoperative mortality and morbidity on univariate analysis were affected by diabetes mellitus (DM), OSA, and chronic renal insufficiency (CRI). CPAP, by reducing the obstructive events, should also reduce the risk of increasing LV afterload.

CPAP is usually provided by a flow generator that delivers constant positive pressure or by ventilators [53, 87–90]. Although the intrathoracic pressure delivered by high-flow CPAP used in intensive care units cannot be compared to the unpredictable levels obtained with the devices commonly used for home treatment of OSA, they are all able to maintain the upper airways open, preventing the occurrence of obstructive events.

When CPAP is delivered by a bi-level turbine-driven ventilator, equal levels of inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP)/positive end-expiratory pressure (PEEP) generate CPAP.