Postoperative Tracheal Extubation

Abstract

Although tracheal intubation receives much attention, especially with regard to management of the difficult airway, tracheal extubation has received relatively little emphasis. The scope and significance of problems occurring after tracheal extubation are real. Adverse outcomes involving the respiratory system comprise the single largest class of injury reported in the ASA Closed Claims Study [1]. Obvious adverse events related to tracheal extubation accounted for 35 of the 522 or 7% of the respiratory-related claims. Certainly additional morbidity related to extubation could be accounted for in other categories of adverse respiratory events, such as inadequate ventilation, airway obstruction, bronchospasm, and aspiration. Others have documented a 4%-9% incidence of serious adverse respiratory events in the immediate postextubation period [2,3] and preventable anesthesia-related etiologies were noted as important by Ruth et al. [2]. Mathew et al. [4], in a retrospective review of more than 13,000 anesthetics, noted that emergency tracheal reintubations occurred in only 0.19% of patients, and that the majority of tracheal reintubations were due to preventable anesthesia-related factors. Perhaps a greater percentage of patients experience postextubation difficulties but do not require reintubation of the trachea. Reasons for tracheal reintubation in the intensive care setting may differ, but the reported incidence in that arena is similarly 4% [5]. Anesthesiologists recognize the immediate postextubation period as one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur and frequently result in hypoxemia. Such hypoxemia is most often corrected within minutes. Less frequently, postextubation hypoxemia can rapidly result in serious morbidity. In this report we will review the known physiologic and pathophysiologic changes associated with anesthesia and surgery that can influence respiratory function after tracheal extubation, the physiologic impact of extubation itself, criteria used for predicting successful extubation, and different techniques and interventions used for tracheal extubation. It is not our intent to review the complications of laryngoscopy and tracheal intubation. However, common complications of tracheal intubation, with special emphasis on the airway, will be discussed in detail as they frequently affect respiratory function after tracheal extubation. More uncommon and miscellaneous complications, such as problems related to the endotracheal tube cuff, recently have been reviewed [6]. Effects of Anesthesia and Surgery on Respiratory Function After Extubation After the "ideal" extubation, patients would exhibit adequate ventilatory drive, a normal breathing pattern, a patent airway with intact protective reflexes, normal pulmonary function, and the absence of any mechanical perturbations such as coughing. Unfortunately, all of these conditions are rarely, if ever, achieved in patients extubated after anesthesia. Understanding the potential interactions between anesthesia, surgery, and extubation on respiratory function helps define many of the complications that occur at this crucial juncture in anesthesia care. This section will include a discussion of the effects of anesthesia and surgery on the respiratory system which are common during extubation, with major emphasis on the airway and lung. Airway Changes Any form of airway dysfunction, such as obstruction after tracheal extubation, is an immediate threat to patient safety. Significant airway compromise leads to diminished minute ventilatory volumes and hypoxemia ensues in a variable, but often rapid fashion. A differential diagnosis of acute postoperative obstruction of the upper airway after extubation includes: laryngospasm, relaxed airway muscles, soft tissue edema, cervical hematoma, vocal-cord paralysis, and vocal-cord dysfunction Table 1. Airway obstruction from foreign body aspiration (e.g., temperature probe condoms) will not be reviewed but deserves mention.Table 1: Differential Diagnosis of Postoperative Airway ObstructionLaryngospasm Laryngospasm, defined by Keating [7] as a protective reflex, can be life-threatening when it occurs after extubation. Historically, a patient in Stage II anesthesia has been thought to be particularly vulnerable to laryngospasm [8]. Stimulation of a variety of sites from the nasal mucosa to the diaphragm can evoke laryngospasm [9]. Most commonly, laryngospasm is a reaction to a foreign body or substance near the glottis. Blood or saliva, even in small amounts, can elicit laryngospasm. It has been suggested that laryngospasm can be prevented by extubating a patient under deep anesthesia, while the laryngeal reflexes are depressed [8]. However, substantial proof of this tenet is lacking. Suzuki and Sasaki [10] contend that laryngospasm is solely attributable to prolonged adduction of the vocal cords mediated via the superior laryngeal nerve and cricothyroid muscle. Ikari and Sasaki [11] have demonstrated that the firing threshold of the laryngeal adductor neurons involved in laryngospasm varies in a sinusoidal manner during spontaneous ventilation. Interestingly, reflex laryngeal closure occurs more readily during expiration than inspiration Figure 1. Others believe that laryngospasm also involves closure of the glottis in addition to adduction of the vocal cords. Closure of the glottis results from contraction of the lateral cricoarytenoid and thyroarytenoid muscles, which are innervated by the recurrent laryngeal nerve [9]. Clinical recognition and treatment of laryngospasm must be expedient (see below), if complications such as hypoxemia or pulmonary edema are to be avoided [12].Figure 1: Mean threshold in volts for reflex glottic closure (laryngospasm) plotted with respect to respiratory phase. Note the increased threshold during inspiration. (Adapted with permission from: Ikari T, Saski CT. Glottic closure reflex control mechanisms. Ann Otol 1980;89:220-4.)Airway Relaxation Airway obstruction related to relaxation of airway soft tissue is frequently associated with residual effects of anesthesia. Such obstruction is purported to be most commonly due to relaxation of the airway (pharyngolaryngeal) muscles. Physiologic maintenance of upper airway patency occurs by a complex mechanism that involves the muscles inserted into the hyoid bone and thyroid cartilage [13]. During normal inspiration, an increase in tonic activity of these strap muscles precedes contraction of the diaphragm and prevents apposition of the tongue and soft palate against the posterior pharyngeal wall [14]. Drummond [15], administered sodium thiopental to 14 patients which resulted in a decrease in electromyographic activity of the strap muscles that was associated with airway obstruction. Airway collapse has been prevented by stimulation of the strap muscles in rabbits [16]. The mechanisms of airway obstruction in sleep disorders also involves a decrease in the tonic activity of these upper airway muscles. The actual tissue producing obstruction is a point of debate, but likely sites include the tongue, soft palate, and/or epiglottis. Evidence implicating the tongue as responsible for upper airway obstruction after extubation is derived from several sources including descriptions of the mechanism of obstruction in unconscious patients, other sleep apnea studies, and several anesthesia reports [17-21]. Safar et al. [17], after evaluating lateral radiographs in anesthetized patients concluded that obstruction is secondary to posterior prolapse of the tongue. Sleep apnea patients also experience obstruction from relaxation of the tongue secondary to decreased airway muscle tone that occurs during rapid eye movement sleep [18,19]. Studies using electromyograms in obstructive sleep apnea patients have recorded decreased activity of the genioglossus muscle concurrent with airway obstruction [19]. Nishino et al. [20], reported decreases in hypoglossal nerve activity which correlated inversely with increasing halothane concentrations in cats; however, there were no observations concerning airway obstruction. In addition, reports of intraoperative airway obstruction during bilateral carotid endarterectomy under cervical plexus block suggest bilateral hypoglossal nerve dysfunction as a contributing factor [21]. Using fluoroscopy and lateral radiography, others have demonstrated that obstruction occurs at the level of the soft palate in sleep apnea patients [22]. Nandi et al. [23] demonstrated obstruction at the soft palate in 17 of 18 patients, the epiglottis in 4 of 18 patients, and the tongue in 0 of 18 patients Figure 2 and Figure 3. Boiden [24], using bronchoscopy, had similar findings, and proposed that the relative position of the hyoid bone to the thyroid cartilage determines the degree of airway patency [24]. Thus, the head tilt and jaw thrust recommended by Morikawa et al. [25] results in ventral movement of the hyoid bone relative to the thyroid cartilage, and is effective in opening the airway. The soft palate appears to be the most likely site of airway obstruction. Nevertheless, prolapse of the tongue, especially when it is large, can probably also impair airway patency.Figure 2: Radiographic evidence before (left) and after (right) induction of anesthesia, demonstrating soft palate obstruction of the airway during anesthesia. Arrows indicate airway opening and narrowing. (Adapted with permission from Nandi PR. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)Figure 3: Diagrammatic representation of the pharyngeal outline based on radiograph Figure 2 measurements before (solid line) and after (dotted line) induction of anesthesia. 1, soft palate; 2, base of tongue; 3, hyoid bone; 4, epiglottis. (Adapted with permission from Nunn JF. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)Pharyngolaryngeal Edema Uvular and/or soft palate edema is a potential cause of postextubation airway obstruction [26]. The pathophysiology of uvular edema is undetermined, but suggested possibilities include mechanical trauma and/or impeded venous drainage from airway devices including endotracheal tubes [27], oral airways [28], nasal airways [29], laryngeal mask airways [30], and vigorous suctioning of the airway [31]. Pregnant patients, and especially those with toxemia, may experience significant uvular and/or pharyngolaryngeal edema and related airway obstruction [32]. Surgery involving the anterior neck, including dissections or cervical spine operations, may also result in pharyngolaryngeal edema and airway obstruction. Avoiding bilateral neck dissections in an attempt to prevent serious edema has been recommended [33], but, significant edema and supraglottic obstruction can occur even after delayed contralateral second stage procedures [34]. One proposed mechanism of edema after neck surgery is the physical disruption of lymphatic drainage. Emery et al. [35] presented a review of seven cases of postoperative upper airway obstruction after anterior cervical spine surgery. Five of the seven patients had evidence of pharyngolaryngeal edema, while none of the seven cases had evidence of cervical hematoma. Cervical Hematoma Cervical hematoma after anterior neck surgery can also cause airway obstruction. Such hematomas can develop postoperatively, and cause delayed airway obstruction after extubation. The purported mechanism of airway obstruction associated with cervical hematoma is the obstruction of venous and lymphatic systems by the expanding mass, resulting in pharyngolaryngeal edema [36]. Edematous mucosal folds can eventually obliterate the glottis [36]. Compression of adjacent airway structures, such as the trachea, by a hematoma is not commonly found [37]. O'Sullivan et al. [36], described the postoperative course of six carotid endarterectomy patients who formed cervical hematomas. Stridor and respiratory compromise, which required immediate surgical intervention, developed in four of six patients. After induction of general anesthesia, three of these patients were impossible to manually ventilate and two could not be intubated. The two patients without evidence of stridor also returned to the operating room. One of these two could not be manually ventilated and both were difficult to intubate. Another reported case of cervical hematoma involved a 57-yr-old patient who developed airway obstruction 12 h after thyroidectomy. A significant hematoma developed, but its evacuation did not relieve airway obstruction. The persistent airway obstruction was thought to be secondary to pharyngolaryngeal edema [38]. The incidence of cervical wound hematoma after carotid endarterectomy is cited as 1.9%, with an unknown percentage of these patients developing airway obstruction [39]. When these patients return to the operating room for reexploration, the absence of stridor or respiratory distress does not predict freedom from "difficult airway" problems. Hematoma, as well as pharyngolaryngeal edema, may render manual ventilation by mask and/or visualization of the vocal cords and tracheal intubation difficult or impossible. In addition, evacuation of the hematoma may not ameliorate existing airway compromise. Such patients should be extubated cautiously and when there is evidence that pharyngolaryngeal edema has diminished. Lingual Edema Oral surgery can produce edema of the tongue and compromise postoperative airway function, especially after palatoplasty or pharyngeal flap surgery [40]. Prolonged placement of a mouth gag, commonly used in cleft palate repair, can result in lingual edema as described by Schettler [41]. Periodic relief of pressure from mouth gag devices should help reduce associated lingual edema [42]. Head position during neurosurgery has also been reported to contribute to lingual edema. Patients undergoing a craniotomy in the sitting position may have their head in such extreme flexion that obstruction of venous drainage of the tongue results in lingual edema, macroglossia, and airway obstruction [43]. During such head flexion the presence of an oral airway may exacerbate compression of the tongue and further compromise lingual circulation. An allergic reaction to glutaraldehyde solution, used to sterilize laryngoscope blades, is another unique cause of lingual edema. Edema can be so severe as to lead to reintubation during recovery [44]. Severe allergic reactions in general may involve part or all of several airway structures and can also result in edema and airway compromise. Vocal Cord Paralysis Unilateral vocal cord paralysis may cause persistent hoarseness after extubation [45]. Bilateral vocal cord paralysis may produce upper airway obstruction [46,47]. Vocal cord paralysis is usually secondary to injury of the recurrent laryngeal nerve resulting in unopposed superior laryngeal nerve mediated adduction of the vocal cords. Such an injury can occur with neck surgery (especially thyroidectomy) [48], thoracic surgery [49,50], internal jugular line placement [51], and endotracheal intubation [52-55]. Endotracheal tubes are frequently cited as a cause of vocal cord paralysis, and suggested mechanisms include endotracheal tube cuff compression of the recurrent laryngeal nerve against the lamina of the thyroid cartilage. Positioning of the endotracheal tube cuff just below or adjacent to the vocal cords may increase the incidence of this problem. Excessive cuff inflation and/or high cuff pressures resulting from diffusion of nitrous oxide can also contribute to vocal cord damage, especially in cuffs that are positioned just below the cords. Vocal Cord Dysfunction Vocal cord dysfunction (VCD) is an uncommon clinical cause of airway obstruction. VCD was first described in 1902 by Osler [56]. It has since been described by various synonyms, including paroxysmal vocal cord motion [57], factitious asthma [58], emotional laryngeal wheezing [59], and Munchausen's stridor [60]. All of the above entities are similar in their clinical presentation. The patient population, from the few reported cases [61,62], appears to consist predominantly of young females with a recent history of an upper respiratory tract infection and emotional stress [59,61,63]. VCD presents with laryngeal stridor or upper airway wheezing similar to asthma [59,64], but the wheezing is unresponsive to bronchodilator therapy [58,63,65]. Patients complain of inspiratory difficulties that result from paradoxical adduction of the vocal cords during inspiration [59]. Obstruction can be severe and require the institution of an artificial or surgical airway [61,66]. Flow volume loops will reveal variable extrathoracic obstruction with a marked decrease in inspiratory flow compared to expiratory flow [61], but visualization of the vocal cords during a symptomatic episode is necessary for a definitive diagnosis [67]. Recommendations for successful extubation of these patients include avoiding an awake extubation or, if possible, providing adequate sedation at the time of extubation. Sedation alleviates the dynamic inspiratory obstruction by reducing inspiratory effort and flow. Treatment of a VCD episode includes verbal reassurance, asking the patient to focus on the expiratory phase of breathing [62], and sedation if the diagnosis of VCD as the cause of respiratory distress is certain [58]. Laryngeal Incompetence Several investigations have demonstrated that laryngeal incompetence occurs after extubation whether or not residual anesthetic effects are present. Tomlin et al. [68] evaluated 56 patients undergoing simple surface surgery under "light" balanced anesthesia; 12 patients developed postoperative atelectasis, 6 of whom aspirated when asked to swallow 10 mL of contrast medium 2 or more hours after surgery. The majority of these patients (4 of 6) demonstrating this finding had been intubated. Gardner [69] demonstrated aspiration in 10 of 94 patients 2 to 4 days after extubation, and Siedlecki et al. [70] found that 27% of responsive patients aspirated radiopaque dye immediately after extubation. Cardiac surgery patients also have a high risk (33%) of aspiration when extubated early (less than 8 h) after surgery, even if awake. This risk significantly decreases to 5% when extubation is performed later [71]. Residual anesthetic effects may contribute to this high incidence of aspiration in the early postoperative period. In summary, laryngeal incompetence is common and the risk of aspiration after extubation is not eliminated by the presence of consciousness. Swallowing Swallowing, another airway protection reflex, can also be impaired by a host of factors after surgery and anesthesia. As recently reviewed [72], topical anesthetics, tracheostomy, tracheal intubation, neurologic or airway structure injury, conscious intravenous sedation, inhalation of 50% nitrous oxide, and even sleep can depress swallowing and permit pulmonary aspiration. Pavlin et al. [73] and Isono et al. [74] have also demonstrated that partial paralysis with neuromuscular blockers depresses swallowing, too. Control of Breathing While it is not the purpose of this review to completely describe the impact of anesthesia on the control of breathing, it is necessary to highlight the major factors affecting ventilatory drive during tracheal extubation. Airway function is also linked to the central neural control of breathing and, like spontaneous ventilation, is depressed by anesthesia. Inhalation drugs, opioids, sedative-hypnotics, and muscle relaxants are the common anesthetics that can depress the ventilatory response to carbon dioxide and/or hypoxia. Significant residual drug effects are often present at the time of tracheal extubation. Inhalation drugs alter the regulation of CO2 partial pressures, as evidenced by the correlation between increasing alveolar concentrations of various potent inhaled anesthetics, and increases in resting CO2 tensions and declines in ventilatory responses to CO2[75-77]. Low concentrations of the potent inhalation drugs (less than 0.5 minimum alveolar anesthetic concentration (MAC)) should not, in and of themselves, produce clinically troublesome blunting of ventilatory response to CO2 during extubation and recovery from surgery [78]. However, low concentrations of potent inhalation drugs may blunt the hypoxic ventilatory response and such an effect can pose a significant risk. Halothane, enflurane, and isoflurane, at 1 MAC in dogs, produce significant depression of hypoxic ventilatory drive. Enflurane has been reported to be the greatest depressant of hypoxic ventilatory drive and isoflurane the least [79]. Knill et al. [78,80,81] performed several investigations of hypoxic ventilatory drives in humans and demonstrated that even low concentrations (0.1 MAC) of halothane and enflurane greatly decrease the ventilatory response to isocapnic hypoxia. A more recent report suggests that hypoxic ventilatory drive may not be depressed by low concentrations of isoflurane [82]. Decreases in hypoxic, but not hypercapnic, ventilatory drive occur with nitrous oxide as well [83]. All mu receptor opioid agonists, including morphine, fentanyl, sufentanil, and alfentanil, produce dose-dependent depression of ventilation, primarily through a direct action on the medullary respiratory center [84]. The responsiveness of the respiratory center to CO2 is significantly reduced by opioids. The slope of the ventilatory response to CO2 is decreased, and minute ventilatory responses to increases in PaCO2 are shifted to the right. The apneic threshold and resting arterial PCO2 are also increased by opioids. Thus, the primary mechanism whereby the body regulates minute ventilation and protects itself from significant increases in CO2 and respiratory acidosis is significantly impaired by opioids. Opioids also decrease hypoxic ventilatory drive [85,86], and blunt the increase in respiratory drive normally associated with increased loads, such as increased airway resistance [85]. Delayed or recurrent respiratory depression can occur in patients recovering from general anesthesia who have received fentanyl [87], morphine [88], meperidine [89], alfentanil [90], and sufentanil [91]. Explanations for this phenomenon include a lack of stimulation or pain, administration of supplemental analgesics and other medications, renarcotization after naloxone administration, motor activity causing release of opioids stored in skeletal muscle, hypothermia, hypovolemia, and hypotension. Investigators have noted second peaks in plasma fentanyl levels during the drug's elimination phase [92]. Secondary peaks in fentanyl plasma levels produce parallel decreases in CO2 sensitivity and breathing [93]. Benzodiazepines have also been shown to decrease the acute ventilatory response to hypercarbia and hypoxia [94]. This action is not as profound as that observed after opioid agonists. Antagonism of significant residual benzodiazepine effects with flumazenil can be followed by resedation because of the shorter duration of action of the latter drug. Vecuronium and d-tubocurarine can also decrease hypoxic ventilatory drive, supposedly by blocking nicotinic cholinergic receptors in the carotid body [95,96]. Acetylcholine is one of the carotid body neurotransmitters involved in facilitating hypoxic ventilatory drive [96]. Recurrence of troublesome ventilatory depression can occur after extubation without obvious cause. Tracheal extubation, patient transport, and initial recovery room nursing assessment can result in significant patient stimulation. Once these events have passed, overall stimulation can subside, and possibly result in an apparent "renarcotization" with inadequate and/or obstructed ventilation. Sleep, too, especially in association with the actions of opioid analgesics, results in significant depression of ventilatory drive [97]. Pulmonary Function The lung routinely undergoes significant physiologic and, at times, pathophysiologic changes during general anesthesia that can persist after tracheal extubation. These changes frequently include decreased lung volumes, abnormalities in gas exchange, augmented work of breathing, and depressed mucociliary function. These changes are rarely, if ever, of benefit. They can be detrimental and, at times, may result in significant patient morbidity. Thus, the impact of anesthesia and surgery on lung function can significantly influence results after tracheal extubation. Lung Volumes The most apparent and easily explained lung volume change after extubation is an increase in dead space, which occurs as a result of substituting the endotracheal tube volume with the upper airway volume. Significant changes in functional residual capacity (FRC) also occur perioperatively. FRC usually decreases by approximately 18% of total lung capacity or approximately 500-1000 mL with induction of general anesthesia [98,99]. Postoperative decreases in FRC are associated with surgery of the abdomen or thorax [100,101]. It is unclear whether FRC is decreased immediately after tracheal extubation. Ali et al. [100] and Colgan and Whang [101] demonstrated that, although FRC is not decreased immediately after extubation, it is decreased several hours later. Strandberg et al. [102] demonstrated a decrease in FRC in 90% of patients 1 h after surgery. The decrease in FRC seen after induction of anesthesia and after extubation may be caused by different mechanisms [103]. The decrease in FRC seen immediately after induction was well illustrated by Brismar et al. [99]. In that study computed tomography revealed areas of compression atelectasis Figure 4. The mechanism for this decrease in FRC after induction of anesthesia has been attributed to a cephalad shift of the diaphragm [104], rib cage instability [105,106], and increased intrathoracic blood volume [105]. Interestingly, neuromuscular block (NMB) after induction of general anesthesia does not result in a further decrease in FRC [105]. The mechanism underlying postoperative decreases in FRC is usually related to diaphragmatic dysfunction [102,107,108]. Simonneau et al. [107] reported that diaphragmatic dysfunction after abdominal surgery could last up to 1 wk and resulted in a greater reliance on rib cage movement for breathing. Diaphragmatic dysfunction is though to be secondary to surgical irritation, inadequate pain control, and/or abdominal distention. In addition to diaphragmatic dysfunction, another cause of postoperative decreases in FRC is guarded breathing (splinting). Relief of pain can partially restore FRC [108] and vital capacity [109], and improve oxygenation [110].Figure 4: Transverse computed tomography scans of the thorax before (upper) and after (lower) induction of anesthesia, demonstrating areas of compression atelectasis (arrows) in the dependent regions of both lungs. (Adapted with permission from Brismar B, et al. Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis. Anesthesiology 1985;62:422-8.)While the clinical consequences of decreases in FRC are often not problematic, decreases in FRC are often large enough to cause atelectasis Figure 4 and ventilation-perfusion abnormalities that impair gas exchange and decrease oxygen stores. Such lung volume changes, if present at the time of extubation, can compromise a patient's ability to tolerate airway difficulties by decreasing the time available for intervention and prevention of hypoxemia. Hypoxemia The incidence of hypoxemia, most frequently defined as an oxyhemoglobin saturation less than 90%, after extubation and recovery from general anesthesia is high. As many as 24% of children [111] and 32% of adults after a general anesthetic will be hypoxemic upon arrival at a postanesthesia care unit if no supplemental oxygen is provided during transport [112]. Marshall and Wyche [113], in a review of hypoxemia during and after anesthesia, categorized postoperative hypoxia into early and late causes. Besides inadequate minute ventilation or airway obstruction, other causes of early hypoxemia include increased ventilation/perfusion mismatch [114], increased alveolar-to-arterial gradient [115], diffusion hypoxia [116], obligatory posthyperventilation hypoventilation [117,118], shivering [119], inhibition of hypoxic pulmonary vasoconstriction [120], and a decrease in cardiac output [121]. Late causes include increased ventilation/perfusion mismatch [122,123] preexisting pulmonary disease [124], old age [124], gender (with males experiencing hypoxemia more frequently than females) [125], and obesity [126]. Although the intraoperative administration of opioids occasionally has been reported to increase postoperative hypoxemia [127], the vast majority of studies have not demonstrated that the use of opioids in anesthesia is associated with an increased incidence of postoperative hypoxemia [128]. Diffusion hypoxia, another cause of hypoxemia in patients emerging from anesthesia was first reported by Fink [116], who thought the outward diffusion of N2 O could dilute alveolar oxygen. With the continuous application of supplemental oxygen during emergence and recovery from anesthesia the incidence of clinically significant diffusion hypoxia is rare but not unheard of [129,130]. Mucociliary dysfunction associated with anesthesia and surgery can also contribute to postoperative hypoxemia. Bronchial epithelial cell cilia normally clear mucous from the respiratory tract [131]. Patients with atelectasis have been shown to have delayed mucociliary clearance [132]. Anesthesia, tracheal intubation and surgery result in mucociliary dysfunction and abnormal or retrograde mucous flow. Mucous pooling in dependent areas can contribute to impaired gas exchange. Work of Breathing Tracheal extubation of a spontaneously breathing patient can decre