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W1991388479 abstract "Providing perioperative care to infants and children undergoing thoracic surgery presents many challenges to the pediatric surgeon, anesthesiologist, pulmonologist, and intensivist. This review will focus on the intraoperative anesthetic care of infants and children undergoing noncardiac thoracic surgery. Surgical disorders of infants and children are reviewed, with an emphasis on features affecting anesthetic management. Techniques for performing single-lung ventilation (SLV) in pediatric patients are summarized. Anesthetic management, including regional anesthetic techniques, is described. Surgical Lesions of the Chest Neonates and Infants A variety of congenital intrathoracic lesions for which surgery is required may present in the newborn period or within the first year of life. These include lesions of the trachea and bronchi, lung parenchyma, and diaphragm. Tracheal stenosis may be acquired or congenital. Tracheal stenosis occurs most often because of prolonged tracheal intubation, often in neonates with infant respiratory distress syndrome associated with prematurity. Ischemic injury of the tracheal mucosa may occur because of a tight-fitting endotracheal tube (ETT) at the level of the cricoid cartilage, which becomes scarred and constricted. Subglottic stenosis may develop, resulting in stridor after tracheal extubation. Reintubation may be required because of oxygen desaturation and hypercarbia. Fiberoptic bronchoscopy is used to evaluate the severity of the stenosis and exclude other causes of stridor (e.g., vocal cord paralysis or laryngomalacia). When general anesthesia is required, inhaled anesthesia may be administered via a face mask, with the fiberoptic bronchoscope inserted through an adaptor in the mask and into the nasopharynx. This is usually performed with the patient breathing spontaneously (1). Alternatively, a laryngeal mask may be used as a conduit (2). Local anesthesia is applied to the vocal cords and trachea through the bronchoscope. Attention must be directed to the dose of local anesthetic used, as systemic absorption may lead to local anesthetic toxicity (3). A cricoid split procedure may be performed for infants with acquired subglottic stenosis. After diagnostic bronchoscopy, either the patient is intubated with an ETT or a rigid bronchoscope is left in place during the operation. During rigid bronchoscopy, positive pressure ventilation is performed by connecting the anesthesia breathing circuit to the side arm of the bronchoscope. Anesthesia may be maintained with inhaled anesthetics or an IV anesthetic technique, such as propofol and remifentanil (4). A horizontal incision is made over the cricoid cartilage, after which a vertical incision is made through the inferior portion of the thyroid cartilage, the cricoid cartilage, and the first tracheal ring. Typically, an ETT a half size larger than the original tube is placed after the repair. Congenital tracheal stenosis may be segmental, occurring in the region of the cricoid cartilage, the midtrachea, or just above the carina. In some cases, the stenotic segment is long, including multiple small tracheal cartilages. Infants present with suprasternal, intercostal, and subcostal retractions, which worsen during agitation and with intercurrent respiratory infections. For patients with severe tracheal stenosis, a laryngotracheoplasty may be performed. This procedure involves the placement of a costal, auricular, or laryngeal cartilage graft into the anterior trachea, the posterior trachea, or both (5). In some cases, a stent may be positioned within the trachea. A previously indwelling tracheostomy tube may be exchanged for an anode tube during the procedure, and this may be either removed or replaced at the end of the operation, depending on whether or not additional staged operations are planned. Rarely, repair of distal tracheal and bronchial stenosis may require cardiopulmonary bypass. Patients may remain intubated and ventilated for a variable period of time after surgery. In these cases, sedation, analgesia, and neuromuscular blockade are maintained after surgery. Pulmonary sequestrations result from disordered embryogenesis producing a nonfunctional mass of lung tissue supplied by anomalous systemic arteries. Intralobar sequestrations are usually found in the left posterior segments. Arterial supply arises from the aorta, above or below the diaphragm, whereas venous drainage is usually through the pulmonary veins. They are usually isolated anomalies and may not present until late in childhood or adulthood. Extralobar sequestrations occur just above or below the diaphragm and are also usually left-sided. Their arterial supply is from small, anomalous pulmonary or systemic arterial branches, and venous drainage is systemic (e.g., portal or azygous vein). Communication with the foregut and associated anomalies are common, including bronchial agenesis, duplication of the colon, vertebral anomalies, and diaphragmatic defects. Presenting signs include cough, pneumonia, and failure to thrive and often present during the neonatal period, usually before the age of 2 yr. Diagnostic studies include arteriography and computerized tomography (CT) scans of the chest and abdomen. Magnetic resonance imaging may provide high-resolution images, including definition of vascular supply. This may obviate the need for angiography (6). Surgical resection is performed after diagnosis. Pulmonary sequestrations do not generally become hyperinflated during positive-pressure ventilation. Nitrous oxide administration may result in expansion of these masses, however, and should be avoided. Pulmonary hypoplasia may be caused by a variety of intrauterine problems, including those that compress the developing lungs (congenital diaphragmatic hernia, tumor, pleural effusion), oligohydramnios (fetal renal failure with oliguria), and absent or poor fetal breathing movements (Werdnig-Hoffman disease, congenital myotonic dystrophy, anencephaly, agenesis of phrenic nerves). Space occupying intrathoracic lesions may cause unilateral lung hypoplasia, whereas the latter conditions usually result in bilateral hypoplasia that is not often amenable to surgery. The scimitar syndrome presents with hypoplasia of the right lung and anomalous pulmonary venous drainage to the inferior vena cava. Chest radiography may reveal a crescent-shaped shadow along the right heart border that resembles a Turkish sword or scimitar. Unilateral lung hypoplasia may be associated with recurrent pneumonia, hypoxemia, or both caused by ventilation/perfusion (V/Q) mismatching and may therefore require surgical resection. Excessive positive-pressure ventilation may result in barotrauma and pneumothorax, pneumomediastinum, or interstitial emphysema on the affected or contralateral side (see discussion below). Congenital cystic lesions in the thorax may be classified into three categories (7). Bronchogenic cysts result from abnormal budding or branching of the tracheobronchial tree. They may cause respiratory distress, recurrent pneumonia, or atelectasis caused by lung compression. Bronchogenic cysts may be paratracheal, hilar, carinal, or paraesophageal and usually do not communicate with the airways. These cysts are most often unilocular and are filled with mucoid material. Bronchogenic cysts associated with clinical signs are generally treated with surgical excision (8). Rarely, these lesions do communicate with the airway; rupture with spillage of fluid into the tracheobronchial tree during anesthesia has been reported (9). Dermoid cysts are clinically similar to bronchogenic cysts but differ histologically, because they are lined with keratinized, squamous epithelium rather than respiratory (ciliated columnar) epithelium. They usually present later in childhood or adulthood. Cystic adenomatoid malformations (CAM) are structurally similar to bronchioles but lack associated alveoli, bronchial glands, and cartilage (10). Because these lesions communicate with the airway, they may become overdistended because of gas trapping, leading to respiratory distress in the first few days of life. When they are multiple and air filled, CAM may resemble congenital diaphragmatic hernia (CDH) radiographically. Treatment is surgical resection of the affected lobe. As with CDH, prognosis depends on the amount of remaining lung tissue, which may be hypoplastic because of compression in utero(11). Congenital lobar emphysema often presents with respiratory distress shortly after birth (12). This lesion may be caused by ball-valve bronchial obstruction in utero, causing progressive distal overdistension with fetal lung fluid. The resultant emphysematous lobe may compress the lung bilaterally, resulting in a variable degree of hypoplasia. Congenital cardiac deformities are present in about 15% of patients (13). Radiographic signs of hyperinflation may be misinterpreted as tension pneumothorax or atelectasis on the contralateral side (Fig. 1). Surgical resection is usually performed when the Pao2 is <50 mm Hg despite supplemental oxygen administration (14). Positive-pressure ventilation may exacerbate lung hyperinflation. Nitrous oxide is contraindicated, and isolation of the lungs during anesthesia is desirable.Figure 1: Congenital lobar emphysema. The radiographic appearance may be confused with tension pneumothorax or decreased lung volume (e.g., atelectasis) on the contralateral side.CDH is a life-threatening condition occurring in approximately 1 in 2000 live births. Failure of a portion of the fetal diaphragm to develop allows abdominal contents to enter the thorax, interfering with normal lung growth. Most often (70%–80% of diaphragmatic defects), a portion of the left posterior diaphragm fails to close, forming a triangular defect known as the foramen of Bochdalek. Hernias through the foramen of Bochdalek occurring early in fetal life usually cause respiratory failure immediately after birth because of pulmonary hypoplasia. Distension of the gut postnatally, as with bag-and-mask ventilation, exacerbates the ventilatory compromise by further compressing the lungs. The diagnosis is often made before birth, and fetal surgical repair has been described (15). Neonates present with tachypnea, a scaphoid abdomen, and absent breath sounds over the affected side. Chest radiography (CXR) typically shows bowel in the left hemithorax, with deviation of the heart and mediastinum to the right and compression of the right lung (Fig. 2A). Right-sided hernias (Fig. 2B) may occur late and present with milder signs. In the presence of significant respiratory distress, bag-and-mask ventilation should be avoided and immediate tracheal intubation performed.Figure 2: Congenital diaphragmatic hernia. This lesion occurs more often on the left side (A) but may also occur on the right (B).Because pulmonary hypertension with right-to-left shunting contributes to severe hypoxemia in neonates with CDH, a variety of vasodilators have been used. These include tolazoline, prostacyclin, dipyridamole, and nitric oxide (16–20). High-frequency oscillatory ventilation has been used in conjunction with pulmonary vasodilator therapy to improve oxygenation before surgery (21). In cases of severe lung hypoplasia and pulmonary hypertension refractory to these therapies (e.g., Pao2 <50 mm Hg with a fraction of inspired oxygen of 1.0), extracorporeal membrane oxygenation (ECMO) should be initiated early to avoid progressive lung injury. Improved outcomes have been associated with early use of ECMO followed by delayed surgical repair (22). A particularly poor prognosis is predicted if CDH is associated with cardiac deformities, a preoperative alveolar-to-arterial oxygen gradient >500 mm Hg, or severe hypercarbia despite vigorous ventilation (23,24). Prognosis has also been correlated with pulmonary compliance and radiographic findings (25–27). Surgical correction via a subcostal incision with ipsilateral chest tube placement may be performed before or during ECMO (28,29). In patients undergoing surgical repair off ECMO, pulmonary hypertension is the major cause of morbidity and mortality. Hyperventilation to induce a respiratory alkalosis and 100% oxygen should be administered to decrease pulmonary vascular resistance. The anesthetic should be designed to minimize sympathetic discharge that may exacerbate pulmonary hypertension (e.g., a large-dose opioid technique). Infants should be ventilated with small tidal volumes and low inflating pressures to avoid pneumothorax on the contralateral (usually right) side. Both nitric oxide and high-frequency oscillatory ventilation have been used during surgical repair (30,31). A high index of suspicion of right-sided pneumothorax should be maintained, and a thoracostomy tube should be placed in the event of acute deterioration of respiratory or circulatory function. It is also imperative that normal body temperature, intravascular volume, and acid-base status be maintained. Mechanical ventilation is continued after surgery in nearly all cases. Failure of the central and lateral portions of the diaphragm to fuse results in a retrosternal defect, the foramen of Morgagni. This usually presents with signs of bowel obstruction rather than respiratory distress. Repair is usually performed via an abdominal incision. Tracheoesophageal fistula (TEF), esophageal atresia, or both occur in approximately 1 in 4000 live births. In 80%–85% of infants, this lesion includes esophageal atresia with a distal esophageal pouch and a tracheal fistulous connection (32,33). The fistula is usually located 1 or 2 tracheal rings above the carina. Afflicted neonates present with spillover of pooled oral secretions from the pouch and may develop progressive gastric distension and tracheal aspiration of acidic gastric contents via the fistula. A common association is the VACTERL complex, consisting of vertebral, anorectal, cardiac, tracheoesophageal, renal, or limb defects (34). Esophageal atresia is confirmed when an orogastric tube passed through the mouth cannot be advanced more than about 7 cm (Fig. 3). The tube should be secured and placed on continuous suction, after which a chest radiograph is diagnostic.Figure 3: Tracheoesophageal fistula. The most common variant of this lesion includes esophageal atresia and a distal fistula.Mask ventilation and tracheal intubation are avoided before surgery if possible, because they may exacerbate gastric distension and respiratory compromise. When the trachea is intubated, an attempt is made to occlude the tracheal orifice of the fistula with the tracheal tube. The tip of the tracheal tube is positioned just above the carina by auscultation of diminished breath sounds over the left axilla as the tube is advanced into the right mainstem bronchus, after which the tube is retracted until breath sounds are increased (Fig. 4A). A small fiberoptic bronchoscope may be passed through the tracheal tube to confirm appropriate placement. Occasionally, emergency gastrostomy is performed because of massive gastric distension. Placement of a balloon-tipped catheter in the fistula via the gastrostomy may be performed under guidance with a fiberoptic bronchoscope to prevent further gastric distension and enable effective positive-pressure ventilation in cases of significant lung disease (Fig. 4B) (35). Antegrade occlusion of a TEF has also been reported with a balloon-tipped catheter advanced through the trachea into the fistula (Fig. 4C) (36). Preoperative evaluation should be performed to diagnose associated anomalies, particularly cardiac, musculoskeletal, and gastrointestinal defects, which occur in 30%–50% of patients (37). A poorer prognosis in infants with TEF and esophageal atresia is correlated with prematurity and underlying lung disease, as well as the coexistence of other congenital anomalies (33).Figure 4: Methods for minimizing gastric insufflation in infants with a tracheoesophageal fistula. The tip of the endotracheal tube may be placed distal to the fistula in many cases (A). Alternatively, a balloon-tipped catheter may be placed in the fistula via a gastrostomy (B) or the trachea (C).Surgical repair usually involves a right thoracotomy and extrapleural dissection of the posterior mediastinum. In most cases, the fistula is ligated, and primary esophageal anastomosis is performed (short gap atresia). In cases in which the esophageal gap is long, the proximal segment is preserved for subsequent staged anastomosis with or without intestinal interposition (33).The trachea may be intubated with the patient breathing spontaneously or during gentle positive-pressure ventilation with small tidal volumes to avoid gastric distension. If a gastrostomy tube is in place, occlusion of the fistula may be confirmed by cessation of bubbling via an underwater tubing connected to the gastrostomy or appearance of CO2 by gas analysis (38). Alternatively, the tracheal tube may be positioned in the mainstem bronchus opposite the side of the thoracotomy incision until the fistula is ligated. Esophageal atresia without connection to the trachea occurs much less often. These lesions are generally diagnosed by radiography after inability to pass an orogastric tube, at which time an absence of gas in the abdomen may be noted (Fig. 5). So-called H-type TEF without esophageal atresia is relatively rare. Patients with H-type lesions may present later in childhood or adulthood with recurrent pneumonias or gastric distension during positive-pressure ventilation (39).Figure 5: Esophageal atresia without a tracheoesophageal fistula.Patent ductus arteriosus (PDA) and coarctation of the thoracic aorta (COTA) are relatively common vascular lesions with a wide range of presentations. PDA occurs in approximately 1 in 2500 live full-term births and accounts for approximately 10% of congenital heart defects (40). Forty percent of premature infants weighing <1750 g and 80% of those <1200 g have a PDA (41). The PDA in these infants is typically quite large and often results in congestive heart failure because of left-to-right shunting of blood, with pulmonary edema and decreased systemic perfusion. Small PDAs may close spontaneously or in response to the administration of indomethacin. Alternatively, small lesions may present with a heart murmur in asymptomatic children. Surgical repair via a left thoracotomy (or right thoracotomy in infants with a right-sided aortic arch) may be performed in the neonatal intensive care unit in premature infants. In this setting, an IV anesthetic with fentanyl for analgesia, a benzodiazepine for amnesia and hypnosis, and a neuromuscular blocking drug may be most pragmatic. Many of these patients have congestive heart failure and are mechanically ventilated both before and after surgery. Larger infants may be well suited for regional anesthesia plus inhaled or short-acting IV anesthesia and planned tracheal extubation in the operating room. COTA is a localized narrowing of the aorta occurring close to the insertion of the ductus arteriosus into the aorta. COTA occurs in 1 in 1200–2000 live births (42,43). COTA may present in the newborn as a critical aortic obstruction in which the PDA supplies most of the perfusion to the lower body. These patients are frequently critically ill, with a metabolic acidosis and cyanosis of the lower body. Prostaglandin E1 is infused before surgery to maintain ductal patency until surgical correction can be performed. COTA more typically presents later in childhood with arterial hypertension in the upper extremities and low blood pressure in the lower extremities, with poor or absent femoral pulses. Turner’s syndrome and bicuspid aortic valve or other congenital cardiac defects may be associated with COTA. Cardiomegaly, systemic hypertension, and congestive heart failure may be present. The surgical treatment of COTA is usually accomplished via a left thoracotomy and may consist of resection of the coarcted segment of aorta with end-to-end anastomosis, subclavian flap repair, or the use of synthetic graft material. Arterial blood pressure should be monitored above and below the coarctation, e.g., with a radial arterial catheter and a blood pressure cuff on a lower extremity. The distal arterial pressure should generally be maintained >45 mm Hg to maintain renal perfusion (44). The patient’s body temperature is often cooled to 35°C to minimize ischemic spinal cord injury during aortic occlusion. Despite this, the incidence of paraplegia after COTA repair is approximately 1 in 250 (44). Proposed mechanisms for paraplegia include inadequate distal perfusion pressure during aortic occlusion, interruption of the blood supply via the anterior spinal artery, and increased cerebrospinal fluid pressure. Hypertension after surgery may be treated with β-blockers (e.g., esmolol) or a variety of other drugs (45). Untreated systemic hypertension may be accompanied by abdominal pain and even bowel perforation secondary to mesenteric insufficiency, thought to be caused by arteritis associated with an acute increase in arterial perfusion. These findings may be accompanied by fever, leukocytosis, melena, and abdominal distension and are referred to as postcoarctectomy syndrome. As an alternative to coarctectomy, balloon angioplasty may be performed for both native and recurrent coarctations (46). Vascular rings are anomalies of the aortic arch, right subclavian artery, or pulmonary arteries that compress the trachea and esophagus. These abnormalities are generally produced by the failure of portions of the fourth or sixth embryonic aortic arches to regress or develop normally. The most common varieties of vascular rings are composed of a double aortic arch, a right-sided arch with a left ductus (or ligamentum) arteriosus, anomalous right subclavian or innominate artery, or a pulmonary artery sling. Most children with vascular rings are asymptomatic or mildly symptomatic during infancy and outgrow their respiratory signs (e.g., stridor) as the trachea becomes more cartilaginous. In cases of severely compromised airways caused by vascular rings, infants present during the first month of life with stridor, recurrent respiratory infections, or dysphagia (47). CXR and barium esophagrams are diagnostic. Surgical repair is generally performed through a left lateral thoracotomy. Patients with tracheomalacia caused by extrinsic compression may have airway obstruction because of tracheal collapse during the induction of anesthesia and after tracheal extubation. Vascular rings may cause tracheal compression similar to anterior mediastinal masses. Inhaled induction has been recommended, followed by administration of assisted or controlled ventilation before the administration of muscle relaxants (48). A rigid bronchoscope should be at hand, because it may be lifesaving in the event of tracheal collapse. Airway compression may be exacerbated during lateral decubitus positioning, in which case immediate repositioning should be performed. Because of the risk of hemorrhage during surgery, appropriate vascular access should be secured before skin incision, and blood must be available for transfusion. Childhood Many of the lesions described above may not be diagnosed until childhood. These include pulmonary sequestration, arteriovenous abnormalities, cystic lesions, lobar emphysema, PDA, COTA, and vascular rings. Other disorders for which thoracic surgery is performed in children, either for definitive treatment or diagnostic purposes, include tumors, infectious diseases, and musculoskeletal deformities. Tumors of the lung, mediastinum, and pleura may be primary or metastatic (49). Primary tumors of the chest are uncommon in children. Perhaps the most common are lymphoblastic lymphoma, a form of non-Hodgkin’s lymphoma, and Hodgkin’s disease. These neoplasms usually present as an anterior mediastinal (thymic) mass with pleural effusion, dyspnea caused by airways obstruction, pain, or superior vena cava syndrome (swelling of the upper arms, face, and neck) (Fig. 6) (50,51). The induction of anesthesia in patients with anterior mediastinal masses may be associated with severe airway and circulatory collapse (52,53). Accordingly, institutions should have an algorithm in place for the evaluation of these patients, including preoperative CT scanning, echocardiography, and flow-volume studies, as well as their treatment (Fig. 7). Careful consideration should be given to performing a biopsy under local anesthesia or initiating chemotherapy or limited radiation therapy before subjecting the child to general anesthesia to effect a decrease in tumor mass and life-threatening airway or vascular occlusion.Figure 6: Anterior mediastinal mass caused by lymphoma with associated pleural effusion before (A) and after (B) treatment with corticosteroids.Figure 7: An algorithm for evaluation and treatment of children with an anterior mediastinal mass. PICU = pediatric intensive care unit; CBC = complete blood count; CT = computerized tomography; CXR = chest radiography; SVC = single-lung ventilation; LP = lumbar puncture.Neuroblastoma, the most common solid extracranial solid tumor of childhood, often arises in the posterior thoracic sympathetic chain. Signs and symptoms of intrathoracic neuroblastoma include Horner’s syndrome (lesions of the cervical and upper thoracic sympathetic chain), spinal cord compression, and bone pain. Uncommonly, hypertension, tachycardia, and flushing may occur spontaneously or during surgical manipulation because of tumor catecholamine secretion. Ganglioneuroblastomas and ganglioneuromas are variants of neuroblastoma that are also derived from neural crest cells and are histologically benign. Osteogenic sarcoma (osteosarcoma) and Ewing’s sarcoma arise in long bones but often metastasize to the lung. Other tumors of childhood, including rhabdomyosarcoma and germ cell tumors, may also metastasize to the lung. Empyema is a complication of bacterial pneumonia most often caused by Staphylococcus aureus and Streptococcus pneumoniae. Haemophilus influenzae type b is much less common because of the use of the Haemophilus influenzae type b vaccine in young children (54). Empyema is diagnosed by CXR or CT scan, or both, and is associated with prolonged fever and leukocytosis. Despite therapy with antibiotics and chest tube drainage, with or without pleural streptokinase or urokinase instillation, surgical treatment is often necessary (55). Rarely, lung abscesses that persist despite antibiotics and percutaneous drainage may also require surgical treatment. Surgical lung biopsy may be performed for diagnostic purposes in cases of interstitial lung disease, which may be infectious (Pneumocystis, respiratory syncytial virus, cytomegalovirus) or noninfectious (e.g., nonspecific or allergic). Pulmonary arteriovenous fistulas and malformations occur most often along with widespread vascular abnormalities, as in patients with Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasis) (56). These lesions may present during infancy or childhood with hypoxemia because of right-to-left shunting of blood, or with congestive heart failure. Acquired arteriovenous fistulas may develop in children with liver disease, increased pulmonary artery pressure (e.g., pulmonary hypoplasia, mitral stenosis, cystic fibrosis), after cavopulmonary shunting, or after chest trauma (57,58). Surgical intervention is warranted when these lesions are focal and severe. Many of these fistulas can be completely or partially coil occluded in the catheterization laboratory. Persistent lesions may require surgical resection. Pectus excavatum results from excessive growth of the costochondral cartilages, with resultant inward depression of the sternum. Pectus excavatum may be associated with Marfan’s syndrome or chronic airway obstruction with large negative intrathoracic pressure during inspiration. Children with severe deformities may have circulatory impairment caused by distortion of the heart and great vessels, or respiratory compromise caused by lung compression. If possible, surgical repair is deferred until late childhood or adolescence, when the ribs and sternum are more fully calcified. A variety of surgical repairs have been described, ranging from complete resection of the sternum to minimally invasive surgery with placement of a retrosternal strut through small incisions in the lateral chest. Of note, complications of the latter technique include perforation of the lungs and heart (59). Preoperative pulmonary function abnormalities may not be significantly improved after surgery (60,61). Kyphoscoliosis is a curvature of the spine measuring 10° or more in the frontal plane. This disorder may present as infantile (<3 yr old), juvenile (3–10 yr old), or adolescent (>10 yr old) forms. Kyphoscoliosis may be associated with congenital malformations of the vertebra, neuromuscular disease (e.g., muscular dystrophy), or neoplastic diseases (e.g., neurofibromatosis), or it may be idiopathic. Surgical correction is delayed until the teenage years unless the deformity is severe, and it consists of posterior spinal fusion with instrumentation with or without anterior spinal fusion. The latter may be performed thoracoscopically (62,63). Ventilation/Perfusion During Thoracic Surgery Ventilation is normally distributed preferentially to dependent regions of the lung, so that there is a gradient of increasing ventilation from the most nondependent to the most dependent lung segments. Because of gravitational effects, perfusion normally follows a similar distribution, with increased blood flow to dependent lung segments. Therefore, ventilation and perfusion are normally well matched. During thoracic surgery, several factors act to increase V/Q mismatch. General anesthesia, neuromuscular blockade, and mechanical ventilation cause a decrease in functional residua" @default.
W1991388479 created "2016-06-24" @default.
W1991388479 creator A5010826355 @default.
W1991388479 date "2001-06-01" @default.
W1991388479 modified "2023-09-25" @default.
W1991388479 title "Pediatric Thoracic Anesthesia" @default.
W1991388479 cites W1014987334 @default.
W1991388479 cites W1483385029 @default.
W1991388479 cites W1514589238 @default.
W1991388479 cites W1529813525 @default.
W1991388479 cites W1599109036 @default.
W1991388479 cites W160585132 @default.
W1991388479 cites W176402751 @default.
W1991388479 cites W188477534 @default.
W1991388479 cites W1964740662 @default.
W1991388479 cites W1967185592 @default.
W1991388479 cites W1967558092 @default.
W1991388479 cites W1969780253 @default.
W1991388479 cites W1969894203 @default.
W1991388479 cites W1969971840 @default.
W1991388479 cites W1971263120 @default.
W1991388479 cites W1972506380 @default.
W1991388479 cites W1973053414 @default.
W1991388479 cites W1973183503 @default.
W1991388479 cites W1974354968 @default.
W1991388479 cites W1975302048 @default.
W1991388479 cites W1980359091 @default.
W1991388479 cites W1982891177 @default.
W1991388479 cites W1983338305 @default.
W1991388479 cites W1985205847 @default.
W1991388479 cites W1985856887 @default.
W1991388479 cites W1986606267 @default.
W1991388479 cites W1989352413 @default.
W1991388479 cites W1989382477 @default.
W1991388479 cites W1990721978 @default.
W1991388479 cites W1991407726 @default.
W1991388479 cites W1992885405 @default.
W1991388479 cites W1993232348 @default.
W1991388479 cites W1994856189 @default.
W1991388479 cites W1994856308 @default.
W1991388479 cites W1996342040 @default.
W1991388479 cites W1996760529 @default.
W1991388479 cites W1997351760 @default.
W1991388479 cites W2002790364 @default.
W1991388479 cites W2002908453 @default.
W1991388479 cites W2004567491 @default.
W1991388479 cites W2004829978 @default.
W1991388479 cites W2005578016 @default.
W1991388479 cites W2008144671 @default.
W1991388479 cites W2009192187 @default.
W1991388479 cites W2009662177 @default.
W1991388479 cites W2010436538 @default.
W1991388479 cites W2010465125 @default.
W1991388479 cites W2011240347 @default.
W1991388479 cites W2012127316 @default.
W1991388479 cites W2012237380 @default.
W1991388479 cites W2012709422 @default.
W1991388479 cites W2012981731 @default.
W1991388479 cites W2013134312 @default.
W1991388479 cites W2013325190 @default.
W1991388479 cites W2013948834 @default.
W1991388479 cites W2014621985 @default.
W1991388479 cites W2015008620 @default.
W1991388479 cites W2017119389 @default.
W1991388479 cites W2017902648 @default.
W1991388479 cites W2018948052 @default.
W1991388479 cites W2020062515 @default.
W1991388479 cites W2021725133 @default.
W1991388479 cites W2023774400 @default.
W1991388479 cites W2023833111 @default.
W1991388479 cites W2027197227 @default.
W1991388479 cites W2027601043 @default.
W1991388479 cites W2029597442 @default.
W1991388479 cites W2030031590 @default.
W1991388479 cites W2030895845 @default.
W1991388479 cites W2036307 @default.
W1991388479 cites W2036862004 @default.
W1991388479 cites W2045047240 @default.
W1991388479 cites W2046229512 @default.
W1991388479 cites W2047925069 @default.
W1991388479 cites W2049708332 @default.
W1991388479 cites W2051990511 @default.
W1991388479 cites W2053388256 @default.
W1991388479 cites W2054344739 @default.
W1991388479 cites W2057371139 @default.
W1991388479 cites W2057919084 @default.
W1991388479 cites W2058107046 @default.
W1991388479 cites W2058919411 @default.
W1991388479 cites W2060252135 @default.
W1991388479 cites W2060855606 @default.
W1991388479 cites W2063631985 @default.
W1991388479 cites W2063719818 @default.
W1991388479 cites W2063786713 @default.
W1991388479 cites W2067110984 @default.
W1991388479 cites W2067543264 @default.
W1991388479 cites W2068150173 @default.
W1991388479 cites W2068879614 @default.
W1991388479 cites W2069063448 @default.