Anesthesia for patients with interstitial lung disease or other restrictive disorders

INTRODUCTION — Restrictive respiratory diseases are a heterogeneous group of disorders characterized by reduction in total lung capacity and decreased compliance on pulmonary function testing, but with preservation of expiratory flow. Conditions that may cause such restriction include:

●Intrinsic disorders such as interstitial lung diseases (ILDs; also called diffuse parenchymal lung diseases) that cause diffuse inflammation or scarring of the lung tissue

●Extrinsic disorders such as abnormalities of the chest wall (eg, pectus excavatum, kyphoscoliosis), pleura (eg, effusion, trapped lung), or abdomen (eg, ascites, obesity, masses) that mechanically compress the lungs or limit their expansion

●Neuromuscular diseases affecting chest wall nerves and muscles to decrease the ability of the respiratory muscles to inflate and deflate the lungs, resulting in chronically-reduced lung volumes and restrictive physiology

Patients with restrictive respiratory disorders are at high risk for perioperative morbidity and mortality. It is not uncommon for patients with chronic restrictive respiratory disorders to present for a surgical procedure [1,2]. In one study, the prevalence of a restrictive spirometric pattern on pulmonary function testing was approximately 7 to 11 percent, similar to the prevalence of a spirometric pattern indicating chronic obstructive pulmonary disease (COPD) [1].

This topic addresses anesthetic and perioperative management of patients with restrictive physiology due to intrinsic or extrinsic disorders. Management of patients with restrictive physiology due to neuromuscular disease is discussed separately. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation" and "Respiratory muscle weakness due to neuromuscular disease: Management" and "Perioperative care of the surgical patient with neurologic disease".)

Anesthetic and perioperative management of patients with COPD are addressed in separate topics. (See "Anesthesia for patients with chronic obstructive pulmonary disease" and "Evaluation of perioperative pulmonary risk".)

PERIOPERATIVE CONSIDERATIONS FOR SPECIFIC LUNG DISORDERS — Patients with an underlying disease that causes restrictive physiology have increased intrapulmonary or chest wall resistance that impedes lung expansion. Such resistance can initially be overcome by increased work of breathing in a spontaneously-breathing patient or by increasing driving pressure into the lungs in a mechanically-ventilated patient. However, inefficiency of gas exchange eventually leads to respiratory failure if the underlying lung disease process is worsening. Any impairment of tissue oxygenation in the awake patient is typically exacerbated in the anesthetized patient [3].

Intrinsic restrictive lung disorders (interstitial lung disease) — Various chronic intrinsic parenchymal lung disorders that cause inflammation or scarring of the lung tissue share several common clinical, radiographic, and pathophysiologic features (algorithm 1). Examples of causes of diffuse parenchymal lung diseases include idiopathic pulmonary fibrosis (IPF), rheumatic disease, granulomatous lung disorders (eg, sarcoidosis), or environmental exposures. These disorders are known as ILDs. Extensive alterations of alveolar and airway architecture are present in addition to interstitial processes. Medical management of patients with restrictive lung disorders due to ILD is discussed separately. (See "Approach to the adult with interstitial lung disease: Clinical evaluation" and "Approach to the adult with interstitial lung disease: Diagnostic testing".)

Idiopathic interstitial pneumonias — IPF is the most common type of idiopathic interstitial pneumonia (IIP). Clinical features of IPF include nonproductive cough, dyspnea on exertion, a restrictive pattern on pulmonary function tests (PFTs), with impaired gas transfer, and bibasilar reticular opacities, traction bronchiectasis, and often subpleural honeycomb cysts on high resolution computed tomography (HRCT) (image 1 and image 2 and image 3). (See "Clinical manifestations and diagnosis of idiopathic pulmonary fibrosis".)

Patients with IPF are often older adults and may have one or more comorbid conditions that further increase perioperative risk. Approximate prevalence of these conditions varies [4,5]:

●Pulmonary hypertension (PH)

●Obstructive sleep apnea (OSA)

●Chronic obstructive pulmonary disease (COPD)

●Lung cancer

●Ischemic heart disease

●Gastroesophageal reflux disease

Patients with IPF experience progressive fibrosis, and are at risk for acute exacerbations of IPF characterized by worsening dyspnea over days to weeks that is not fully explained by heart failure or fluid overload. HRCT typically reveals new bilateral ground glass opacification and/or consolidation superimposed on a background of findings consistent with chronic interstitial pneumonia. Elective or semi-elective surgery is delayed if an acute exacerbation is suspected to enable evaluation and treatment of the patient and to prevent worsening after a surgical procedure. Lung infection, malignancy, and thromboembolic disease must be excluded. Typically, bronchoscopy with bronchoalveolar lavage is performed to evaluate for lung infection. Broad-spectrum antibiotics are initiated, as well as empiric treatment with systemic glucocorticoids. Acute exacerbations of IPF carry a poor prognosis. Details regarding evaluation and management are discussed in other topics. (See "Acute exacerbations of idiopathic pulmonary fibrosis".)

Other IIPs include nonspecific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonia, cryptogenic organizing pneumonia, and acute interstitial pneumonia (algorithm 1). Furthermore, interstitial lung disease may develop or worsen after severe pulmonary involvement (eg, acute respiratory distress syndrome [ARDS]) due to COVID-19 or other acute viral illness. (See "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")", section on 'Cardiopulmonary symptoms'.)

While all the IIPs are typically associated with restrictive changes on PFTs, the radiographic patterns, degree of inflammation, and likelihood of progression differ. IPF is characterized by progressive fibrosis; the other IIPs may have more inflammation and respond to systemic glucocorticoids; and patients with RB-ILD may respond to smoking cessation. (See "Idiopathic interstitial pneumonias: Classification and pathology".)

Interstitial lung disease due to systemic disorders — ILD may be associated with underlying connective tissue diseases, such as rheumatoid arthritis [6], polymyositis/dermatomyositis [7], Sjögren syndrome [8], systemic lupus erythematous [9], or systemic sclerosis [10], and is a common feature of sarcoidosis [11]. Although many of the clinical and histologic manifestations are similar to those exhibited by patients with IPF, disease progression is often limited and may not require treatment [12]. Moreover, response to immunosuppressive treatment and prognosis are generally better than in patients with IPF [8]. (See "Causes, clinical manifestations, evaluation, and diagnosis of nonspecific interstitial pneumonia", section on 'Connective tissue disease' and "Causes, clinical manifestations, evaluation, and diagnosis of nonspecific interstitial pneumonia", section on 'Interstitial pneumonia with autoimmune features'.)

Environmental causes of lung damage — A variety of occupational and environmental exposures are associated with ILD (table 1 and table 2). (See "Approach to the adult with interstitial lung disease: Clinical evaluation", section on 'Occupational and environmental exposures'.)

Chronic lung fibrosis may also be caused by irradiation of the thorax (eg, for mediastinal lymphoma, lung cancer, breast cancer). In addition, certain medications may result in ILD (table 3). (See "Approach to the adult with interstitial lung disease: Clinical evaluation", section on 'Prior medication use and irradiation'.)

Extrinsic restrictive disorders — Several conditions extrinsic to the lung parenchyma result in chronically-reduced lung volumes (eg, total lung capacity [TLC] and vital capacity [VC]) due to mechanical compression or other limitations on lung expansion. For most of these processes, the restrictive pattern on PFTs (low TLC and VC) is not accompanied by abnormal gas transfer.

Increased chest wall impedance — Abnormalities of the chest wall or pleura that increase chest wall impedance include (see "Chest wall diseases and restrictive physiology"):

●Space-occupying pathological conditions – Space-occupying conditions that involve the intrathoracic space (or chest wall) can prevent adequate lung expansion with consequent pulmonary restriction. Examples of such conditions include pleural effusion, pneumothorax, pleural scarring due to hemothorax, and primary or metastatic tumors.

●Ankylosing spondylitis, kyphosis, scoliosis – Ankylosing spondylitis causes fixation of the chest wall through fusion of the costovertebral joints, and kyphosis (ie, anteroposterior angulation of the spine) may also be present. Patients with vertebral compression fractures due to osteoporosis can also develop kyphosis. Idiopathic scoliosis with lateral displacement or curvature of the spine typically presents in adolescents, but can affect adult lung function if untreated. Severe kyphosis and moderate to severe scoliosis can impair pulmonary compliance causing low lung volumes and a restrictive pattern on PFTs. (See "Chest wall diseases and restrictive physiology", section on 'Ankylosing spondylitis' and "Chest wall diseases and restrictive physiology", section on 'Kyphosis and scoliosis'.)

●Congenital abnormalities of the chest wall – Pectus excavatum, pectus carinatum, and other congenital abnormalities of the chest wall can impair chest wall function, as explained in detail in a separate topic. (See "Chest wall diseases and restrictive physiology", section on 'Congenital and childhood abnormalities'.)

●Traumatic and iatrogenic abnormalities of the chest wall – Prior thoracoplasty with rib resection or flail chest due to multiple rib and/or sternal fractures may result in a restrictive ventilatory defect with decreased forced vital capacity (FVC) and TLC; residual volume (RV) is typically preserved (figure 1). (See "Chest wall diseases and restrictive physiology", section on 'Traumatic and iatrogenic processes'.)

Increased intraabdominal pressure — Processes that increase intraabdominal pressure impede diaphragmatic excursion and affect respiratory system compliance typically resulting in reduced lung volumes and lung atelectasis. (See "Chest wall diseases and restrictive physiology", section on 'Abdominal processes'.)

●Patients with central obesity – Patients with central obesity (body mass index [BMI] >30 kg/m²) and an increased waist-to-hip ratio and/or abdominal girth may have restrictive physiology due to increased weight of the chest wall and decreased diaphragmatic excursion due to increased abdominal adipose tissue. Modest weight loss may improve pulmonary function and exercise tolerance. (See "Chest wall diseases and restrictive physiology", section on 'Obesity'.)

Anesthetic implications of the respiratory effects of obesity, including hypoventilation with carbon dioxide retention and OSA, are discussed separately. (See "Anesthesia for the patient with obesity" and "Intraoperative management of adults with obstructive sleep apnea".)

●Ascites – Ascites is an accumulation of extravascular fluid within the peritoneum that may occur due to processes such as hypoalbuminemia, heart failure, cirrhosis, and malignancy. Mild to moderate reductions in FRC, TLC, FVC, and expiratory reserve volume typically occur. Diuretics are standard components of treatment in ascites. For patients with tense ascites, large volume paracentesis may have a beneficial effect upon lung function by decreasing the inspiratory load. (See "Chest wall diseases and restrictive physiology", section on 'Ascites'.)

●Pregnancy – There are several changes in respiratory mechanics that occur in pregnancy, although restrictive physiology is relatively rare [13] (see "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes"). However, pregnant patients with preexisting severe restrictive lung disease (eg, sarcoidosis, lymphangioleiomyomatosis) are particularly vulnerable to hypoxic or hypercapnic respiratory failure during anesthesia [14].

PREANESTHESIA CONSULTATION — Goals of the preanesthetic consultation for patients with chronic restrictive respiratory disease are similar to those for patients with chronic obstructive pulmonary disease (COPD). These include assessing the severity of lung disease and working with the patient's pulmonary specialist to optimize preoperative condition. Comorbid conditions that can significantly impact overall perioperative risk are common in patients with chronic restrictive respiratory disease; thus, treatable issues should be identified and managed [15]. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Preanesthesia consultation'.)

History and physical examination — Patients with chronic restrictive respiratory disease should be evaluated for signs and symptoms due to hypoxemia, hypercapnia, increased work of breathing, or difficulty clearing pulmonary sections.

●History – The patient's current functional capacity and issues related to the cause and treatment of restrictive respiratory disease are assessed. Specific issues include (see "Approach to the adult with interstitial lung disease: Clinical evaluation", section on 'History'):

•Current cardiopulmonary symptoms, including respiratory symptoms such as dyspnea, cough, wheezing, or hemoptysis. Note activities or positions that worsen symptoms. For example, positional dyspnea may worsen when lying supine in a patient with diaphragm dysfunction, or when lying in right decubitus position in those with significant right-sided pleural disease.

•Need for oxygen therapy, including current or past oxygen requirements and the frequency and flow rate required for symptom relief. Ask about symptoms of hypoxemia (eg, dyspnea, morning headaches) and symptoms of hypercapnia (eg, muscle twitching, lethargy, confusion, headache).

•Presence of associated cardiorespiratory conditions. In patients with pulmonary fibrosis, progressive loss and remodeling of pulmonary blood vessels can occur over time with increases in pulmonary vascular resistance leading to pulmonary hypertension (PH; pulmonary artery systolic pressure ≥20 mmHg at rest) and right heart failure [16,17]. Significant cardiomyopathy may be present in patients with sarcoidosis. Anesthetic management of patients with right and/or left heart failure is discussed separately. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure" and "Intraoperative management for noncardiac surgery in patients with heart failure".)

•Presence of other comorbid conditions that may increase perioperative risk of morbidity and mortality. Symptoms due to extrapulmonary rheumatic disease include musculoskeletal pain, weakness, fatigue, fever, pleuritis, joint pain or swelling, or dry eyes. Patients with significant orthopnea, peripheral edema, skeletal muscle weakness, pleuritis, or fever should undergo further evaluation for myocardial or pericardial disease, respiratory muscle weakness, or an intercurrent flare of the rheumatic disease. However, pulmonary manifestations may develop before other systemic manifestations in some patients, particularly those with rheumatoid arthritis, systemic lupus erythematosus, or polymyositis-dermatomyositis.

•History of tobacco use (eg, pack years, past or anticipated quit date) and efforts directed toward smoking cessation.

Also, other relevant exposures that may contribute to the development or progression of ILD should be identified, including irradiation to chest or lung, or medications associated with lung injury (eg, amiodarone, nitrofurantoin, antineoplastic agents).

•Records of prior hospitalizations, particularly any prior episodes of respiratory failure requiring endotracheal intubation.

●Physical examination – Aspects of the physical examination of particular interest to the anesthesiologist include (see "Approach to the adult with interstitial lung disease: Clinical evaluation", section on 'Physical examination'):

•Body mass index (BMI).

•Pulse oximetry both at rest and with exertion.

•External visual inspection including any external deformities of the chest wall.

•Lung auscultation and percussion to determine whether crackles are present at baseline and whether pleural disease may be contributory.

•Cardiac examination, including evidence of right heart failure. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'History and physical examination'.)

•Evidence of systemic comorbidities such as muscle weakness or multi-organ dysfunction.

Pulmonary function testing — The main roles of pulmonary function tests (PFTs) are to clarify the type and severity of respiratory impairment, which may help guide ventilation during surgery, assess likelihood for prolonged ventilator dependence, and identify patients with such severe respiratory impairment that elective surgery should be reconsidered. A comprehensive preoperative pulmonary evaluation that includes spirometry screening should be considered in patients with:

●Hypoxemia on room air (or for patients who need home oxygen therapy) if the cause is uncertain

●Serum bicarbonate level >33 mEq/L or arterial carbon dioxide tension (PaCO₂) >50 mmHg in a patient whose pulmonary status has not been previously evaluated

●History of respiratory failure resulting from a problem that has persisted

●Severe dyspnea, particularly if attributed to a current respiratory disease

●Difficulty assessing pulmonary function by clinical examination

●Suspected PH

●The need to distinguish among potential causes of significant respiratory compromise

●The need to determine the response to bronchodilators

●The need to predict lung function after planned lung resection

In most patients with chronic restrictive respiratory disease, PFTs will have been previously obtained by the patient's primary physician or specialist. Available PFTs are examined to determine the severity and pattern of chronic restrictive respiratory disease. PFTs are typically repeated before major surgery if the patient exhibits dyspnea at rest or with minimal exertion, or if imaging studies show new abnormalities (see 'Other tests' below). Measurements typically include upright spirometry, lung volumes, and diffusing capacity for carbon monoxide (DLCO).

●Spirometry – The hallmark of restrictive physiology on spirometry is the presence of matched reductions in the total exhaled volume (known as the forced vital capacity [FVC]) and the volume exhaled in the first second (known as the forced expiratory volume in one second [FEV₁]), with absence of airflow obstruction (algorithm 2) [18]. Thus, the ratio of these values (FEV₁/FVC) is preserved. (See "Overview of pulmonary function testing in adults", section on 'Restrictive ventilatory defect'.)

●Measurement of absolute lung volumes – While restrictive impairment is suspected based on spirometry values, measurement of lung volumes is necessary to confirm restriction and exclude air trapping since this causes similar changes on spirometry. Measurement of total lung capacity (TLC) is used to classify the severity of chronic restrictive disease:

•Mild – TLC 65 to 80 percent of predicted value

•Moderate – TLC 50 to 65 percent of predicted value

•Severe – TLC <50 percent of predicted value

●Assessment of gas transfer – DLCO measurements aid in diagnosis of the underlying process. The DLCO helps to distinguish between ILD in which DLCO is usually reduced versus other causes of restriction in which DLCO is usually normal (algorithm 2). Specifically, impaired DLCO suggests a process involving the pulmonary parenchyma (ie, ILD) or pulmonary vasculature (eg, PH), whereas a normal DLCO is typically seen in conditions that cause increased chest wall impedance or respiratory muscle weakness [18]. Changes in DLCO over time are employed to identify disease progression and monitor response to treatments [19]. (See "Diffusing capacity for carbon monoxide", section on 'Interpretation'.)

An abnormal resting peripheral arterial oxygen saturation (SpO₂) may indicate abnormal gas transfer, although patients with ILD may have near-normal oxygen saturation at rest, but desaturation on exertion.

Other tests — Other preoperative tests may be obtained in selected patients (see "Evaluation of perioperative pulmonary risk", section on 'Preoperative risk assessment'):

●Arterial blood gases – Indicators that arterial blood gas (ABG) measurements might be useful include a resting SpO₂ <93 percent or an abnormal serum bicarbonate. (See "Evaluation of perioperative pulmonary risk", section on 'Assessment of oxygenation and hypercapnia'.)

●Imaging studies – In selected patients, chest radiographs and high resolution computed tomography (HRCT) scan may be ordered by the pulmonary specialist, particularly if these studies have not been done in the past year, or if there is a recent increase in symptoms or decrease in exercise tolerance.

●Assessment of exercise capacity – Exercise capacity can be assessed with a six-minute walk test (6MWT) or, less commonly, a cardiopulmonary exercise test. The 6MWT assesses the distance walked in six minutes and the pulse oxygen saturation during the test and compares the results with age- and sex-based normal values. Since exertional desaturation is typically present in patients with ILD or PH, the 6MWT is often used to assess disease progression. (See "Overview of pulmonary function testing in adults", section on 'Six-minute walk test'.)

Exercise performance testing (eg, a cardiopulmonary exercise test), if available, may provide useful prognostic information for perioperative risk stratification for patients undergoing high risk intra-abdominal surgery [20]. (See "Cardiopulmonary exercise testing in cardiovascular disease".)

Interventions to optimize pulmonary function — Interventions to optimize pulmonary function and risk factor modification may include (see "Strategies to reduce postoperative pulmonary complications in adults"):

●Counseling regarding preoperative smoking cessation is important to reduce the risk of postoperative pulmonary complications, particularly in patients with markedly reduced baseline functional capacity [21]. Although optimal timing is at least eight weeks prior to surgery, even cessation for as little as two days may have some benefit (eg, decreased carboxyhemoglobin levels, elimination of nicotine effects, and improved mucociliary clearance). More detailed discussions are available in other topics. (See "Evaluation of perioperative pulmonary risk", section on 'Smoking' and "Strategies to reduce postoperative pulmonary complications in adults", section on 'Smoking cessation'.)

●For obese patients, weight reduction prior to elective surgery may improve respiratory mechanics, minimize risk for sleep apnea, although formal study is lacking. (See "Obesity in adults: Overview of management", section on 'Importance of weight loss'.)

●Oxygen therapy is the cornerstone of treatment for alleviation of symptoms in many patients with ILD. Ensuring optimal use of chronic oxygen administration requires consultation with a pulmonary specialist. In selected patients, pulmonary rehabilitation may be employed to alleviate dyspnea and improve exercise capacity and quality of life [15]. (See "Pulmonary rehabilitation".)

●Elective surgery is postponed in patients with active upper respiratory infection. (See "Anesthesia for adults with upper respiratory infection".)

Other interventions

●Other preexisting comorbid medical conditions should be optimally treated.

●Educational and emotional support is necessary for patients with severe restrictive respiratory impairment. (See "Palliative care for adults with nonmalignant chronic lung disease".)

INTRAOPERATIVE MANAGEMENT — Intraoperative anesthetic management of the patient with chronic restrictive respiratory disease requires an understanding of the patient's disease (eg, etiology of disease, severity, functional status), as well the planned surgical approach including patient positioning. Consultation with the surgeon and the pulmonary specialist is useful to plan anesthetic care.

Monitored anesthesia care — For appropriately-selected patients and surgical procedures, monitored anesthesia care (MAC) with minimal sedation may be advantageous if the patient remains conscious. This technique allows a faster recovery time and reduced risk of pulmonary complications compared with general anesthesia.

However, unintentional over-sedation can result in a sleep-like state characterized by a reduction in cortical and lung mechanical responsiveness to hypercapnia and hypoxemia, as well as decreased tidal volume. The consequences of these effects are exacerbated by underlying restrictive respiratory impairment [22]. Thus, over-sedation should be avoided by using sedative and/or analgesic agents that are short-acting or have minimal or rapidly reversible respiratory depressant effects. The patient's respiratory pattern, end-tidal carbon dioxide (ETCO₂), and peripheral oxygen saturation (SpO₂) are closely monitored for signs of respiratory decompensation, and the anesthesiologist should be prepared to provide urgent airway management and ventilatory support if necessary. (See "Monitored anesthesia care in adults", section on 'Monitoring depth of sedation and analgesia' and "Monitored anesthesia care in adults", section on 'Drugs used for sedation and analgesia for monitored anesthesia care'.)

Infusion of the alpha₂ agonist dexmedetomidine may have advantages compared with other agents used during MAC; spontaneous respiration and airway patency are typically preserved, and a normal ventilatory response to hypercapnia is maintained. (See "Monitored anesthesia care in adults", section on 'Dexmedetomidine'.)

Neuraxial anesthesia — Compared with general anesthesia, neuraxial anesthesia (ie, spinal or epidural anesthesia) of the lower body may be advantageous for surgical anesthesia and postoperative analgesia because pulmonary gas exchange is only mildly impaired; thus, arterial oxygenation and carbon dioxide elimination are well maintained [23,24]. In one retrospective study of patients with ILD undergoing thoracoscopic lung biopsy, 29 patients received general anesthesia while 15 received thoracic epidural anesthesia (TEA) [24]. Eight patients in the general anesthesia group experienced acute worsening ILD including one perioperative death, while no patients in the TEA group experienced worsened lung function. In addition, operative and recovery times were shorter in the TEA group, and no patients with TEA required conversion to general anesthesia.

However, effects of neuraxial anesthesia on respiratory mechanics depend on the extent of motor blockade. Although diaphragmatic function is often spared even when a sensory block reaches the cervical segments, high neuraxial techniques that include all thoracic and lumbar segments reduce inspiratory capacity and expiratory reserve volume approaches zero [25].

Peripheral nerve blocks — Compared with either general or neuraxial anesthesia, peripheral nerve blocks may have advantages for surgical anesthesia and postoperative analgesia in selected cases. (See "Overview of peripheral nerve blocks".)

For surgical procedures that involve the upper extremities, the brachial plexus can be blocked at several levels. Since many of these approaches are associated with an inherent risk of respiratory complications, they should be used cautiously in any patient with limited respiratory reserve [26]. Also, immediate recognition and treatment of respiratory decompensation is critically important. Examples of upper extremity nerve blocks that should be avoided or used with caution include (see "Upper extremity nerve blocks: Techniques"):

●Interscalene block – Interscalene blocks are associated with a 100 percent incidence of phrenic nerve block that results in hemidiaphragmatic paralysis and a 25 to 30 percent reduction in forced expiratory volume in one second (FEV₁) as well as forced vital capacity (FVC). There is also a risk of causing a pneumothorax, although less than for supraclavicular blocks. (See "Upper extremity nerve blocks: Techniques", section on 'Interscalene block'.)

●Supraclavicular block – Supraclavicular blocks are associated with a relatively high (up to 6 percent) incidence of pneumothorax, which can present with immediate or delayed symptoms. (See "Upper extremity nerve blocks: Techniques", section on 'Supraclavicular block'.)

●Infraclavicular block – Infraclavicular blocks are associated with rare risk of pneumothorax, but risk is minimized with appropriate procedural technique. (See "Upper extremity nerve blocks: Techniques", section on 'Infraclavicular block'.)

Other regional blocks that are used in the upper extremities include axillary blocks, wrist blocks, intercostobrachial blocks; these blocks do not increase risk for respiratory complications. (See "Upper extremity nerve blocks: Techniques".)

General anesthesia — Arterial oxygenation is impaired in patients with healthy lungs during general anesthesia and even more so in those with chronic restrictive respiratory disease. Hypoxemia may be worse in patients with additional comorbidities that impair gas exchange (eg, tobacco use, abdominal obesity, pulmonary hypertension [PH]) [27,28].

Airway management — Induction of general anesthesia in the head-up position (eg, reverse Trendelenburg or semi-recumbent position) is preferred to the supine position for optimal maintenance of functional residual capacity (FRC). Extended periods of apnea are poorly tolerated due to reduced FRC; thus, the airway is rapidly secured immediately after induction. Administration of intravenous (IV) lidocaine 1 to 1.5 mg/kg one to three minutes before tracheal intubation may decrease airway irritability during laryngoscopy and insertion of an endotracheal tube or laryngeal mask airway. (See "Induction of general anesthesia: Overview", section on 'Intravenous anesthetic induction'.)

An inhalation anesthetic induction with sevoflurane can be used in patients without significant risk factors for pulmonary aspiration. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)

An awake intubation may be employed in selected patients with severe restrictive respiratory disease if even a brief period of apnea is anticipated, particularly if mask ventilation may be difficult. Preparation for awake intubation typically includes administration of a drying agent (eg, glycopyrrolate 0.2 mg IV) to decrease airway secretions. Detailed discussion of difficult airway management is available in a separate topics. (See "Management of the difficult airway for general anesthesia in adults", section on 'Securing the airway' and "Management of the difficult airway for general anesthesia in adults", section on 'Awake intubation'.)

Selection of anesthetic agents — Generally, anesthetic agents are selected based on individual procedure-related considerations, although agents with prolonged respiratory depressant effects are avoided. In patients with chronic restrictive respiratory disease, specific agent-related considerations include the following:

●Propofol – Propofol is typically employed for rapid induction and/or ongoing maintenance of general anesthesia in hemodynamically stable patients because it has bronchodilatory properties associated with decreases in airway resistance. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

●Ketamine – Ketamine is often employed for induction in hemodynamically unstable patients because it increases sympathetic tone and also has bronchodilatory properties. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

●Opioids – Opioids may be used to suppress the cough reflex and deepen anesthesia. Short-acting opioids such as remifentanil are preferred to minimize the risk of opioid-induced respiratory depression in the postoperative period (table 4). (See "Maintenance of general anesthesia: Overview", section on 'Analgesic component: Opioid agents' and "Perioperative uses of intravenous opioids: Specific agents", section on 'Remifentanil'.)

●Dexmedetomidine – Dexmedetomidine is often selected as an adjunct agent during general anesthesia to reduce doses of inhalation or other IV anesthetic agents and to reduce opioid requirements. (See 'Monitored anesthesia care' above and "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine'.)

●Volatile anesthetics – Most potent volatile inhalation anesthetic agents (eg, sevoflurane, isoflurane, halothane) are bronchodilators that decrease airway responsiveness and attenuate bronchospasm. Sevoflurane has the most pronounced bronchodilatory properties of the available inhalation anesthetics (see "Inhalation anesthetic agents: Clinical effects and uses", section on 'Respiratory effects'). Desflurane is typically avoided in patients with any type of chronic lung disease since high concentrations cause bronchial irritation and may increase airway resistance. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Disadvantages and adverse effects'.)

At higher doses, all volatile inhalation agents progressively reverse hypoxic pulmonary vasoconstriction by promoting perfusion of poorly ventilated lung and thereby increasing ventilation-perfusion (V/Q) mismatch. These effects may worsen intrapulmonary shunting with resultant hypoxemia, necessitating an increase in the fraction of inspired oxygen concentration (FiO₂) and/or small increases in positive end-expiratory pressure (PEEP). (See 'Mechanical ventilation' below.)

All volatile inhalation anesthetics are rapidly eliminated via the lungs. However, the presence of a large V/Q mismatch slows the speed of uptake and elimination, particularly with the more soluble inhalation anesthetic agents (eg, isoflurane) [29]. (See "Inhalation anesthetic agents: Properties and delivery", section on 'Respiratory factors'.)

●Nitrous oxide – Nitrous oxide (N₂O) is typically avoided in patients with PH due to potential increases in pulmonary vascular resistance (PVR). Also, N₂O should be used with caution in patients with honeycomb cysts due to ILD since this gas diffuses into any air-filled cavity to displace nitrogen, which may result in enlargement or rupture of a cyst and development of tension pneumothorax. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Disadvantages and adverse effects'.)

Positioning — Surgical positioning during general anesthesia and mechanical ventilation has significant physiologic effects on ventilation, pulmonary perfusion, and intrathoracic pressure. In the patient with severe restrictive respiratory disease, these physiologic effects may cause inadequate tissue perfusion such that alternative positioning approaches may be necessary. (See "Patient positioning for surgery and anesthesia in adults", section on 'General considerations'.)

Specific position-related concerns include the following (see "Patient positioning for surgery and anesthesia in adults"):

●Supine position – The supine position is associated with a marked reduction in FRC that is further reduced during general anesthesia [30,31]. Lung compliance may be reduced with resultant airway closure, atelectasis, and V/Q mismatch. Although changing position from supine to semi-recumbent (30 degrees head-up) increases lung volumes, oxygenation may not improve [30]. (See "Patient positioning for surgery and anesthesia in adults", section on 'Physiologic effects of supine position'.)

●Lateral decubitus position – Due to gravitational forces, the lateral decubitus position results in V/Q mismatch, particularly during general anesthesia. Perfusion increases while ventilation decreases in the dependent lung, and FRC and compliance are reduced [32,33]. Concurrent decreases in perfusion and increases in ventilation occur in the nondependent lung. In a patient with restrictive respiratory disease, the resultant V/Q mismatch can cause severe impairments in oxygenation during anesthesia in the lateral decubitus position, necessitating an increase in FiO₂. Application of PEEP may improve oxygenation by reducing atelectasis in the dependent lung areas; however, high levels of PEEP should be avoided [34,35] (see 'Mechanical ventilation' below). It is also important to avoid administration of large volumes of fluid that may accumulate in the dependent lung because this increases peak airway pressures and eventually leads to inadequate ventilation. (See "Patient positioning for surgery and anesthesia in adults", section on 'Physiologic effects of lateral decubitus positioning'.)

●Prone position – Compared with the supine position, the prone position may reduce pulmonary compliance resulting in higher peak airway pressures. Also, venous return to the heart is decreased, while systemic and pulmonary vascular resistances are increased, particularly if the abdomen is compressed [36]. However, if abdominal compression is avoided, the prone position often has beneficial effects on pulmonary function, with increased FRC, improved V/Q matching, and improved oxygenation (figure 2 and table 5) [37]. (See "Patient positioning for surgery and anesthesia in adults", section on 'Physiologic effects of prone positioning' and "Prone ventilation for adult patients with acute respiratory distress syndrome", section on 'Physiologic effects on oxygenation'.)

●Sitting position – Intrathoracic pressure is lowest when a patient is placed in the sitting position, resulting in optimal respiratory mechanics during mechanical ventilation. Compared with supine, lateral, and prone positions, FRC and lung compliance increase in the sitting position because the abdominal contents fall away from the diaphragm [37]. However, the ultimate effect on oxygenation depends on cardiac output, which tends to fall in the sitting position [38]. (See "Patient positioning for surgery and anesthesia in adults", section on 'Physiologic effects of sitting position'.)

●Trendelenburg position – Compared with the supine position, the Trendelenburg position is associated with increased venous return, central blood volume, and mean arterial pressure. Cephalic movement of the abdominal viscera against the diaphragm decreases FRC and pulmonary compliance, which can lead to atelectasis.

●Reverse Trendelenburg position – The head-up tilt, or reverse Trendelenburg position, causes pooling of blood in the lower extremities and abdominal vasculature. The reduction in central blood volume and venous return leads to decreases in stroke volume and cardiac output. However, the reverse Trendelenburg position relieves the pressure from the abdominal contents on the diaphragm and chest wall, resulting in increases in FRC and pulmonary compliance.

●Lithotomy position – The lithotomy position is often associated with minor transient increases in venous return. Cephalic displacement of the diaphragm might result in decreases in FRC and pulmonary compliance.

Mechanical ventilation — Goals of intraoperative mechanical ventilation include facilitation of optimal oxygenation and ventilation. Equally important is the need to recognize and minimize the inherent risk of ventilator-induced lung injury since patients with restrictive respiratory disease are particularly vulnerable to this complication. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia'.)

●Tidal volume – We use low tidal volumes (approximately 6 mL/kg) and increase the inspiratory time of the respiratory cycle to an inspiratory to expiratory [I:E] ratio of 1:1 to 2:1 to minimize the risk of high intrathoracic pressures. Patients with restrictive respiratory disease and poor respiratory system compliance are at risk for development of high intrathoracic pressures, which can cause a significant decrease in venous return and cardiac output, resulting in systemic hypotension. Other adverse effects of high intrathoracic pressures include barotrauma and volutrauma leading to the development of acute lung injury or acute respiratory distress syndrome. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults" and "Ventilator-induced lung injury".)

Respiratory acidosis is a known consequence of low tidal volume ventilation. However, this may be offset by a small increase in respiratory rate that does not induce auto-PEEP, as well as measures to reduce dead space such as shortening the ventilator tubing. (See "Ventilator management strategies for adults with acute respiratory distress syndrome".)

Skeletal muscle paralysis and adequate sedation typically facilitate coordination with ventilator-delivered breaths and minimize airway pressures. Administration of inhaled bronchodilators in patients who have some component of reversible bronchoconstriction may further improve oxygenation and ventilation. (See "Mechanical ventilation during anesthesia in adults", section on 'Tidal volume' and "Mechanical ventilation during anesthesia in adults", section on 'Inspiratory to expiratory ratio'.)

●Fraction of inspired oxygen – The fraction of inspired oxygen (FiO₂) and ventilator settings should be adjusted to maintain arterial oxygen tension (PaO₂) >60 mmHg and/or SpO₂ >90 percent. (See "Mechanical ventilation during anesthesia in adults", section on 'Fraction of inspired oxygen'.)

●Respiratory rate – In general, the respiratory rate should be adjusted to maintain arterial carbon dioxide tension (PaCO₂) in a range that results in arterial pH between 7.35 and 7.45. Patients with chronic respiratory acidosis due to severe restrictive respiratory disease, should be maintained close to their baseline PaCO₂. (See "Mechanical ventilation during anesthesia in adults", section on 'Respiratory rate'.)

●Positive end-expiratory pressure – We employ initial positive end-expiratory pressure (PEEP) of 5 cm H₂O in patients with restrictive respiratory disease, and subsequently increase the level of PEEP cautiously, as needed to achieve adequate oxygenation, realizing that higher PEEP (eg, >10 cm H₂O) is more likely to cause hypotension. (See "Positive end-expiratory pressure (PEEP)".)

Beneficial effects of PEEP include prevention of alveolar collapse and maintenance of adequate FRC and end-expiratory lung volume recruited during inspiration [39]. Additionally, PEEP can partially re-expand atelectatic lung regions, thereby increasing alveolar ventilation and decreasing the degree of intrapulmonary shunt and V/Q mismatch [40]. However, application of PEEP does not typically result in a proportional increase in arterial oxygenation.

Potential adverse effects of PEEP include significant increases in the intrathoracic plateau pressures particularly if PEEP pressures are >10 cm H₂O. As noted above, high intrathoracic pressures impair venous return and decrease cardiac output resulting in systemic hypotension and end-organ hypoperfusion. Moreover, application of PEEP can redistribute blood flow away from aerated lung toward atelectatic areas, worsening V/Q mismatch and hypoxemia [41]. (See "Mechanical ventilation during anesthesia in adults", section on 'Positive end-expiratory pressure'.)

Other measures employed during mechanical ventilation include humidification of inspired gases (or use of low inspiratory gas flows) to keep the airways moist, thereby preventing desiccation of respiratory secretions and consequent atelectasis [42]. (See "The ventilator circuit", section on 'Heaters and humidifiers'.)

Emergence and extubation — Emergence from general anesthesia and tracheal extubation can be associated with serious complications in patients with chronic restrictive respiratory disease, even when preceded by an uneventful procedure. (See "Emergence from general anesthesia".)

Preparations for emergence and the process itself are similar for patients with restrictive respiratory disease compared with other patients. If possible, these patients should be extubated in the reverse Trendelenburg position. It is particularly important to avoid residual effects of neuromuscular blocking agents (NMBAs) or anesthetic agents, since these would contribute to poor respiratory effort in the postoperative period. Thus, long-acting opioids and benzodiazepines should be avoided, and reversal agents for NMBAs should be administered when appropriate. (See "Maintenance of general anesthesia: Overview", section on 'Transition to the emergence phase' and "Extubation following anesthesia".)

Tracheal extubation should be considered only when the patient is alert and cooperative and able to demonstrate adequate ventilatory effort without excessive tachypnea, tachycardia, hypoxemia, hypercapnia, or other signs of respiratory distress (eg, diaphoresis). Similar to patients without restrictive lung disease, general guidelines indicating a high probability of successful extubation include the following:

●Vital capacity (VC) >15 mL/kg; however, patients with severe restrictive respiratory diseases may have a lower baseline VC

●PaO₂ >60 mmHg with an FiO₂ <0.5

●Negative inspiratory pressure >-20 cm H₂O

●Normal arterial pH (7.35 to 7.45)

●Respiratory rate <20 breaths/minute

Atelectasis is an important cause of hypoxemia in the early postoperative period, and this can be worsened if pain-associated splinting and inhibition of cough occur. Thus, adequate analgesia is particularly important. Provision of continuous positive airway pressure is more effective than increasing FiO₂ to achieve optimal oxygenation in patients with atelectasis, and might prevent the need for reintubation [43]. Also, early mobilization is important for optimal pulmonary function [44].

MANAGEMENT OF INTRAOPERATIVE COMPLICATIONS

Hypoxemia — Regardless of anesthetic technique, intraoperative hypoxemia is common in patients with chronic restrictive respiratory disease. Prompt identification and treatment of underlying causes of hypoxemia are essential to maintain adequate tissue oxygenation and minimize perioperative morbidity. In rare cases, tension pneumothorax or pulmonary embolism may result in sudden hypoxemia accompanied by severe hypotension in a mechanically ventilated patient; this requires emergency treatment as described in a separate topic. (See "Intraoperative management of shock in adults", section on 'Tension pneumothorax or hemothorax' and "Intraoperative management of shock in adults", section on 'Pulmonary embolism'.)

V/Q mismatch — The most common cause of hypoxemia during general anesthesia is ventilation-perfusion (V/Q) mismatch. Sudden hypoxemia due to V/Q mismatch is usually due to atelectasis, which might not respond to an increase in the fraction of inspired oxygen content (FiO₂). In such cases, we employ 5 to 10 cm H₂O of positive end-expiratory pressure (PEEP). Other causes of V/Q mismatch are sought and treated (eg, mucus plugging or migration of the endotracheal tube into the right or left main-stem bronchus).

Impaired diffusion — In conditions of impaired diffusion, the entire length of the capillary may be required before the capillary blood has been fully oxygenated, even in resting conditions. If the perfusion time and distance is not sufficient to facilitate oxygen equilibrium between the alveolus and capillary, the arterial oxygen content can drop. Increases in heart rate decrease the perfusion time, and can result in rapid decreases in PaO₂, especially in patients with ILD such as idiopathic pulmonary fibrosis (IPF) [45].

Decreased mixed venous oxygen content — The mixed venous blood oxygen content (CvO₂) is the amount of oxygen bound to hemoglobin plus the amount of oxygen dissolved in mixed venous blood, while SvO₂ is the mixed venous oxyhemoglobin saturation and PvO₂ is the mixed venous oxygen tension. A decrease in SvO₂ with concurrent reduction in arterial oxygen tension (PaO₂) may be due to decreased oxygen content in delivered arterial blood (eg, severe anemia), decreased oxygen delivery due to decreased cardiac output (eg, hypovolemia), or increased oxygen consumption. (See "Oxygen delivery and consumption".)

Arterial hypoxemia is especially likely in patients with restrictive lung disease and significant V/Q mismatching and shunting. In such patients at baseline, PaO₂ may be 80 mmHg when mixed venous oxygen tension is 50 mmHg. However, if PvO₂ is suddenly decreased to 20 mmHg due to a decrease in cardiac output, the PaO₂ would decrease to 40 mmHg without any change in the degree of V/Q mismatch or shunt. Therefore, decreases in cardiac output state should be carefully avoided and/or immediately treated since rapid development of hypoxemia can occur.

Arrhythmias — Patients with severe chronic restrictive respiratory disease are particularly vulnerable to atrial and ventricular arrhythmias due to hypoxemia and/or hypercapnia, acid-base disturbances, increased sympathetic nervous system activity, medication effects (eg, beta₂-agonists), and the frequent presence of comorbid conditions such as ischemic heart disease or pulmonary hypertension (PH) with cor pulmonale [16]. Prompt diagnosis of the arrhythmia and correction of the underlying cause are necessary, as well as antiarrhythmic agents if indicated. (See "Arrhythmias during anesthesia".)

Exacerbation of pulmonary hypertension — In patients with chronic PH and cor pulmonale, factors that increase pulmonary vascular resistance (PVR) should be avoided, including hypoxemia, hypercapnia, acidosis, hyperthermia, nitrous oxide, and hyperinflation of the lungs (ie high PEEP or large tidal volumes) [16]. If acute worsening of PH is suspected, treatment may be initiated [16]. Since the underlying cause for exacerbation is typically hypoxemia, measures to increase oxygenation are critical. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Treatment and prognosis".)

Patients with severe ILD often require increases in PEEP to maintain adequate oxygenation, but treatment can be particularly challenging if concomitant right heart failure is present [16]. For example, a patient with IPF and secondary PH who is ventilated with low lung volumes might require relatively higher PEEP to achieve adequate tissue oxygenation. However, the resultant increase in intrathoracic pressures can increase PVR and right ventricular strain, and may also decrease venous return to the right heart, thereby decreasing preload and further worsening right ventricular failure. These effects can result in significant systemic hypotension requiring vasopressor and inotropic support. In such cases, a pulmonary artery catheter may be inserted to guide therapy. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Vasopressors and inotropes'.)

MANAGEMENT IN THE POST-ANESTHESIA CARE UNIT — Patients with chronic restrictive respiratory disease should be monitored closely in the immediate postoperative period for any signs of respiratory decompensation. Provision of adequate analgesia is essential to facilitate the patient's ability to cough and take a deep breath, thereby minimizing development of atelectasis.

Early mobilization and incentive spirometry may decrease pulmonary complications by promoting deeper breathing, lung expansion, and cough. If necessary, a trial of noninvasive ventilation or high-flow O₂ delivered via nasal cannulae may be employed in the post-anesthesia care unit to decrease work of breathing, reduce respiratory rate, and decrease risk of requiring reintubation. Rarely, postoperative mechanical ventilation may be necessary in a patient with severe pulmonary dysfunction. (See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Postoperative strategies' and "Respiratory problems in the post-anesthesia care unit (PACU)", section on 'Supplemental oxygen' and "Respiratory problems in the post-anesthesia care unit (PACU)", section on 'Ventilatory support'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pulmonary function testing" and "Society guideline links: Interstitial lung disease" and "Society guideline links: Pulmonary hypertension in adults" and "Society guideline links: Idiopathic scoliosis in adolescents".)

SUMMARY AND RECOMMENDATIONS

●Restrictive respiratory diseases are a heterogeneous group of conditions characterized by a restrictive pattern on pulmonary function testing (ie, reduced total lung capacity [TLC] and vital capacity [VC]), decreased respiratory system compliance, and preservation of expiratory airflow. (See 'Perioperative considerations for specific lung disorders' above.)

●The cause of the restrictive changes can be intrinsic or extrinsic to the lung parenchyma. The various interstitial lung diseases (ILDs; eg, idiopathic pulmonary fibrosis [IPF], rheumatoid lung, sarcoidosis) are examples of intrinsic restrictive disorders. Diseases of the chest wall (eg, scoliosis, pectus carinatum), pleura (eg, mesothelioma), and abdomen (eg, obesity, ascites) that decrease respiratory system compliance are examples of extrinsic restrictive respiratory processes. (See 'Perioperative considerations for specific lung disorders' above.)

●Preoperative evaluation in patients with restrictive respiratory disease includes a comprehensive risk assessment with a thorough history and physical examination and review of pulmonary function tests (PFTs) and imaging. The goal is to clarify the type and severity of respiratory impairment, which may help guide ventilation during surgery, assess likelihood for prolonged ventilator dependence, and identify patients with such severe respiratory impairment that elective surgery should be reconsidered. (See 'Preanesthesia consultation' above.)

●Perioperative risk factor modification, including smoking cessation, optimal use of oxygen therapy and pulmonary rehabilitation, weight loss for obese patients, optimization of all preexisting comorbid conditions, and educational and emotional support, is recommended prior to elective surgery. (See 'Interventions to optimize pulmonary function' above.)

●Choice of anesthetic technique (eg, monitored anesthesia care [MAC], neuraxial anesthesia, peripheral nerve block, or general anesthesia) should be made on an individual basis depending on severity of the patients restrictive respiratory disease and comorbidities and requirements for the planned surgical procedure.

•MAC with minimal sedation may be advantageous if the patient remains conscious because of a faster recovery time and reduced risk of pulmonary complications compared with general anesthesia. However, unintentional over-sedation should be avoided as this may lead to reduced responsiveness to hypercapnia and hypoxemia and reduced tidal volumes. Consequences of these effects may be exacerbated by underlying restrictive respiratory impairment. (See 'Monitored anesthesia care' above.)

•Neuraxial anesthesia (ie, spinal or epidural anesthesia) of the lower body with minimal sedation may be advantageous compared with general anesthesia because pulmonary gas exchange is only mildly impaired. However, high neuraxial techniques that include all thoracic and lumbar segments reduce inspiratory capacity and expiratory reserve volume. (See 'Neuraxial anesthesia' above.)

•Compared with either general or neuraxial anesthesia, peripheral nerve blocks with minimal sedation may have advantages for surgical anesthesia and postoperative analgesia in selected cases. However, upper extremity blocks of the brachial plexus are associated with an inherent risk of respiratory complications and should be used cautiously. (See 'Peripheral nerve blocks' above.)

•During general anesthesia, arterial oxygenation is impaired in patients with healthy lungs, and even more so in those with chronic restrictive respiratory disease, particularly if additional comorbidities that impair gas exchange are present (eg, tobacco use, abdominal obesity, pulmonary hypertension [PH]). (See 'General anesthesia' above.)

-Anesthetic agents are selected based on individual procedure-related considerations, although agents with prolonged respiratory depressant effects are avoided. (See 'Selection of anesthetic agents' above.)

-Induction of general anesthesia in the head-up position (eg, reverse Trendelenburg or semi-recumbent position) is preferred to the supine position to optimally maintain FRC. Extended periods of apnea are poorly tolerated due to reduced functional residual capacity (FRC); thus, the airway is rapidly secured immediately after induction of anesthesia. (See 'Airway management' above.)

-Surgical positioning during general anesthesia and mechanical ventilation has significant physiologic effects on ventilation, pulmonary perfusion, and intrathoracic pressure. In some cases, alternative positioning approaches may be necessary. (See 'Positioning' above.)

●Settings for mechanical ventilation during general anesthesia include (see 'Mechanical ventilation' above):

•Low tidal volume (approximately 6 mL/kg) with inspiratory to expiratory [I:E] ratio 1:1 to 2:1 to minimize intrathoracic pressures

•Fraction of inspired oxygen (FiO₂) adjusted to maintain arterial oxygen tension (PaO₂) >60 mmHg and/or peripheral arterial oxygen saturation SpO₂ >90 percent

•Respiratory rate adjusted to maintain an arterial carbon dioxide tension (PaCO₂) that results in arterial pH between 7.35 and 7.45 (or close to baseline PaCO₂ in patients with chronic respiratory acidosis)

•Initial positive end-expiratory pressure (PEEP) of 5 cm H₂O, with avoidance of PEEP >10 cm H₂O

●Tracheal extubation can be considered when the patient is alert and cooperative with the following parameters (see 'Emergence and extubation' above):

•VC >15 mL/kg; however, patients with severe restrictive respiratory diseases may have a lower baseline VC

•PaO₂ >60 mmHg with an FiO₂ <0.5

•Negative inspiratory pressure >-20 cm H₂O

•Normal arterial pH (7.35 to 7.45)

•Respiratory rate <20 breaths/minute

●Intraoperative complications require rapid identification and treatment; these include hypoxemia (eg, due to ventilation/perfusion mismatch, impaired diffusion, or decreased mixed venous oxygen content), arrhythmias, or exacerbation of PH. (See 'Management of intraoperative complications' above.)

●Postoperative management includes provision of adequate analgesia to facilitate ability to cough and take a deep breath, thereby minimizing development of atelectasis, as well as early mobilization and incentive spirometry. If necessary, a trial of noninvasive ventilation may be employed to decrease work of breathing, reduce respiratory rate, and decrease risk of requiring reintubation. (See 'Management in the post-anesthesia care unit' above.)