Chapter 24 Chronic Pulmonary Disease
Obstructive pulmonary disease
1. What are some examples of obstructive pulmonary disease?
2. What is obstructive pulmonary disease?
3. Why does arterial hypoxemia occur in patients with obstructive pulmonary disease?
4. Why does carbon dioxide retention occur in patients with obstructive pulmonary disease?
5. What are common physical, radiographic, and functional findings in patients with obstructive pulmonary disease?
Asthma
7. How is the diagnosis of asthma made?
8. What are some of the physical examination findings noted in patients with asthma during periods of normal pulmonary function? What are some of the physical examination findings noted in patients with bronchial asthma during periods of exacerbation of their asthma?
9. What are some findings found in the pulmonary function studies and flow-volume loops during asthma exacerbations?
10. What agents are commonly used for the chronic treatment of asthma?
11. How can an acute asthmatic attack be treated?
12. How should the patient with asthma be assessed preoperatively?
13. How should a patient with asthma be assessed before a thoracic or abdominal procedure?
14. Is regional anesthesia the preferred anesthetic choice in patients with bronchial asthma scheduled to undergo surgery on the extremities?
15. What is the goal of the anesthetic management of patients with asthma?
16. What agents may be used for the induction of general anesthesia in patients with asthma? What is an advantage and a disadvantage of ketamine for these patients?
17. Which neuromuscular blocking drugs are associated with histamine release? What is the concern regarding the use of these neuromuscular blocking drugs in patients with asthma?
18. What is the benefit of using a slow respiratory rate when mechanically ventilating the lungs of a patient with asthma?
19. What is a benefit of maintaining adequate hydration intraoperatively in patients with asthma and chronic obstructive pulmonary disease (COPD)?
20. What are the options for extubation of the trachea that will minimize the degree of airway hyperreactivity in response to manipulation of the endotracheal tube?
21. How can the reversal of neuromuscular blocking drugs with anticholinesterases cause bronchospasm?
22. Name five potential causes of intraoperative bronchospasm.
Chronic obstructive pulmonary disease
24. What characterizes pulmonary emphysema physiologically?
25. What characterizes chronic bronchitis physiologically?
26. How do emphysema and chronic bronchitis differ clinically?
27. Why is the work of breathing increased in patients with pulmonary emphysema?
28. For patients with COPD scheduled to undergo a surgical procedure, what should the preoperative evaluation include? When might preoperative pulmonary function tests be necessary?
29. What are some pulmonary function test and arterial blood gas measurement results that indicate that the patient is at an increased risk of postoperative respiratory failure? What are some treatment interventions that may be warranted by the preoperative evaluation of the patient’s pulmonary function?
30. What are the main considerations for the anesthetic management of patients with COPD?
31. What are some potential disadvantages of using nitrous oxide as part of a general anesthetic in patients with COPD?
32. What are two methods by which anesthesiologists may minimize the drying of secretions in the airways of patients with COPD in the intraoperative period?
33. What ventilatory settings are appropriate for intraoperative mechanical ventilation of the lungs of patients with COPD?
34. What characterizes chronic bronchitis physiologically? What is the major predisposing factor to the development of chronic bronchitis?
35. What is the impact of COPD on the postoperative course?
36. What is the clinical significance of an exacerbation of COPD, and what is its implication on an upcoming surgical procedure?
Pulmonary hypertension
37. How is pulmonary hypertension defined? What is the most common form of pulmonary hypertension?
38. What are the physiologic effects of pulmonary hypertension?
39. How can pulmonary hypertension affect the performance of the left ventricle?
40. What are the main anesthetic considerations for patients with pulmonary hypertension?
Anesthesia for lung resection
Preoperative Evaluation and Preparation
44. What are some preoperative considerations for the patient scheduled to undergo thoracic surgery?
45. What are some specific preoperative history and physical examination findings that are indicative of an increased risk of postoperative pulmonary complications after thoracic surgery?
46. What are some preoperative prophylactic measures that may be taken in an attempt to minimize postoperative pulmonary complications?
47. How does cigarette smoking affect the lungs physiologically?
48. What is the benefit of the preoperative cessation of cigarette smoking? After what duration of time after the cessation of smoking are these benefits noted to occur?
49. For which patients are preoperative pulmonary function tests indicated?
50. What values derived from pulmonary function tests are indicative of an increased risk of postoperative pulmonary morbidity after a pneumonectomy?
51. What are PPO − FEV1 (predicted postoperative FEV1) and PPO – DLCO (predicted postoperative DLCO)?
Management of Anesthesia
52. What are some benefits of the administration of volatile anesthetics for patients undergoing thoracic surgery?
53. What is a disadvantage of the administration of nitrous oxide for patients undergoing thoracic surgery?
54. What is a benefit of the administration of nondepolarizing neuromuscular blocking drugs for patients undergoing thoracic surgery?
Isolation of the lungs
55. What are some absolute indications for one-lung ventilation during surgery and anesthesia? What are some relative indications for one-lung ventilation during surgery and anesthesia?
56. What is the most frequently used double-lumen endotracheal tube used for the isolation of the right or left lung or for one-lung ventilation during thoracic surgery?
57. What is the potential problem with an endobronchial tube placed in the right bronchus for isolation of the right lung? How can this problem be avoided?
58. What size double-lumen endotracheal tube is usually appropriate for adult patients? What depth in centimeters typically places the endobronchial tube in approximately the correct position in most adult patients of average height?
59. What is the technique for placement of a left-sided double-lumen endotracheal tube? How is the proper placement of a double-lumen endotracheal tube best confirmed?
60. What is the single-lumen Univent tube? What is its potential advantage for ventilation?
61. What is a Arndt endobronchial blocker?
62. What is a Cohen tip deflecting endobronchial blocker?
63. How does a bronchial blocker compare to a double-lumen endotracheal tube?
Gas exchange during one lung ventilation
64. How does the lateral decubitus position during mechanical ventilation of the lungs affect the ventilation-to-perfusion ratio in the lungs?
65. What are four factors that influence the amount of perfusion that goes to the nondependent, unventilated lung during ventilation of a patient in the lateral decubitus position with a double-lumen endotracheal tube?
66. What are the interventions that can be made when arterial hypoxemia is noted in a patient during ventilation for thoracic surgery?
Answers*
Obstructive pulmonary disease
1. Examples of obstructive pulmonary disease include asthma, emphysema, chronic bronchitis, and cystic fibrosis. Emphysema and chronic bronchitis are overlapping clinical manifestations of the same disease – COPD. Obstructive pulmonary disease is characterized by the progressive, persistent obstruction to air flow, particularly expiratory flow. Asthma is an acute form of obstructive disease, which is treatable and at least partially reversible even when established. If asthma persists over time, either because it is untreated or because it is particularly severe, it may develop irreversible air flow obstruction and become a chronic disease not significantly different from emphysema and chronic bronchitis. (431)
2. Obstructive pulmonary disease is chiefly characterized by expiratory flow limitation due to increased airway resistance coupled with the loss of elastic lung recoil. These factors lead to lung hyperinflation, increased work of breathing, and impaired gas exchange. Obstructive pulmonary disease is the most frequent cause of chronic pulmonary disease. (431)
3. Arterial hypoxemia occurs in patients with obstructive pulmonary disease because of ventilation-perfusion mismatch. Decreased ventilation (which preferentially leads to hypoxemia) occurs because of the progressive destruction of functional alveoli. (433)
4. Carbon dioxide retention occurs in patients with obstructive pulmonary disease because of ventilation-perfusion mismatch. Both decreased ventilation and decreased perfusion (dead space) lead to hypercarbia. Initially, this is compensated by hyperventilation. As patients become older and weaker, such compensation fails, leading to chronic carbon dioxide retention. (433)
5. Patients with obstructive pulmonary disease often appear dyspneic, with a hyperinflated, “barreled” chest. Upon careful examination, you will notice a prolonged expiratory phase often terminated by obvious expiratory muscle activity – an attempt to exhale the whole tidal volume. On chest auscultation, lung sounds are distant (because of the hyperinflation), sometimes with associated wheezing. On the chest radiogram the lungs appear very “tall” and the diaphragm flattened. The lung fields may appear hyperlucent, and the vasculature may be difficult to discern. Pulmonary function studies in patients with obstructive pulmonary disease will reveal a decreased volume of the gas that can be forcefully exhaled in 1 second (FEV1). The vital capacity may also be decreased, but not to as great an extent as the FEV1, resulting in a decreased FEV1/FVC ratio. (431)
Asthma
6. Asthma is characterized by reversible expiratory flow obstruction, airway hyperreactivity, and chronic inflammation leading to airway edema, secretions, and progressive thickening. (431)
7. The diagnosis of asthma is made primarily on the clinical history of increasing coughing and wheezing spells with or without the identification of a supposed trigger. Common triggers include pollens, medications, cold air temperature, and exercise. Spirometry shows an obstructive defect (low FEV1) that is partially reversible (12% to 15%) with inhaled bronchodilators. The sputum taken from patients with asthma often contains eosinophils, in contrast to the neutrophils most commonly found in the sputum of patients with bronchitis. (341, Figure 27-1)
8. Patients with asthma during periods of normal pulmonary function are typically devoid of any signs of pulmonary disease, although scattered expiratory wheezing can still be heard. During periods of exacerbation, typical signs and symptoms include breathlessness, coughing fits, and chest tightness, associated with the objective finding of a prolonged expiratory phase and wheezing, sometimes audible without the aid of a stethoscope.
9. Pulmonary function studies during asthma exacerbations reveal a decrease in the FEV1 and FEV1/FVC. The FEV1 may be used as a measure of the degree of obstruction and the effectiveness of interventions. A flow-volume loop during an asthma exacerbation reveals a downward scooping of the expiratory phase, with a normal shape of the inspiratory phase. A significant response to a bronchodilator may normalize the aspect of the loop that is characteristic of bronchial asthma and increase the FEV1. An increase of 12% is judged clinically significant, and is used to separate asthma from COPD by functional criteria. (431-433, Figure 27-1; Table 27-1)
10. Chronic treatment of asthma includes antiinflammatory agents and bronchodilators. Inhaled corticosteroids (beclometasone and fluticasone) have potent antiinflammatory effects and are considered a mainstay of chronic asthma treatment. Long-acting β2-adrenergic agonists (salmeterol and formoterol) and anticholinergics (tiotropium) are effective bronchodilators used to treat moderate to severe asthma. Their advantage in respect to the traditional counterparts (see later discussion) is their longer duration of action that allows single daily administration. With that, they are also not indicated in the treatment of an acute exacerbation. Other antiinflammatory agents effective in the chronic (and not in the acute) setting are the leukotriene antagonists and synthesis inhibitors (montelukast, zafirlukast, and zileuton). Methylxanthines (aminophylline, theophylline) are no longer recommended in the treatment of asthma. (431-432)
11. An acute asthmatic attack should be treated with the administration of oxygen, nebulized β2-agonists and anticholinergics, and intravenous glucocorticoids. Subcutaneous epinephrine is also rapidly effective, but the side effects need to be balanced with its need in each patient. Occasionally standard therapy will not be sufficient, as evidenced by persistent respiratory distress, worsening hypercapnea, hypoxemia, and mental status changes. In these cases, non-invasive ventilation may be very effective, as it will support ventilation and avoid fatigue while the pharmacologic treatment takes its effect. Tracheal intubation has become a rare occurrence in the acute treatment of asthma, and is reserved for the most severe and persistent cases and status asthmaticus. In unusual and extreme circumstances, inhalational anesthetic agents have been successfully administered through an intubated airway. All halogenated agents (isoflurane, sevoflurane, and desflurane) have direct bronchodilator properties, independent of catecholaminergic and cholinergic receptors, thus working as an addition to the ongoing therapy. (432-433)
12. The preoperative assessment of patients with asthma should include a detailed history, including any recent exacerbation, the occurrence of emergency room visits and/or hospitalizations, and mechanical ventilation for asthma. Physical examination may reveal tachypnea, dyspnea, and, on auscultation, expiratory wheezing. Patients with a benign history and physical examination do not require any special intervention other than continuing their current medications. If on inhaled bronchodilators on an “as needed” basis, they should be instructed to use the bronchodilator on the morning of surgery and to bring it to the operating room. Patients who are symptomatic or who have suffered a recent exacerbation may benefit from postponement of elective surgery until their medical status can be optimized. (432, 434)
13. Open abdominal and thoracic surgery is associated with the highest incidence of respiratory complications because of a combination of the effects of postoperative pain, as well as respiratory muscle dysfunction. Hence, additional preoperative testing may be warranted if the clinical suspicion of severe or untreated respiratory disease arises. This assessment should be carried out by a pulmonologist familiar with the perioperative challenges of obstructive pulmonary disease, and may include the performance of pulmonary function studies. Of particular utility to the anesthesiologist is to know whether the possible expiratory flow limitation (i.e., a low FEV1) is reversible with bronchodilators. (432, 434)
14. Regional anesthesia may be preferred over general anesthesia in patients with asthma scheduled for surgery on the extremities. It avoids manipulation of the airway and the risk of bronchospasm. However, modern medications and anesthetic techniques are safe in patients with less than severe, symptomatic asthma. Ventilation through a laryngeal mask airway is less stimulating than through an endotracheal tube; many anesthetic drugs are also bronchodilators, such as halogenated inhalational agents and propofol. (432)
15. The goal of the anesthetic management of patients with asthma is to avoid precipitating bronchoconstriction. While regional or neuraxial anesthesia may be preferable, a well-conducted general anesthetic also has advantages, including the ability to deliver bronchodilators (volatile anesthetic agents) and to provide pulmonary toilet by deep tracheal suction and/or bronchoscopy. A sufficient depth of anesthesia before intubation of the trachea minimizes the risk of acute bronchospasm at the time of the induction of anesthesia. This can be accomplished both with intravenous agents and volatile anesthetics. The latter can be used as the sole induction agent (rarely used in adults because of the length of time needed for establishing adequate intubating conditions) or by mixing them during an intravenous induction. (432)
16. Currently available induction agents such as propofol and ketamine have bronchodilating effects. Propofol is a more manageable agent devoid of potential psychogenic side effects. On the other hand, ketamine has a substantial analgesic effect that may turn out to be helpful in particular circumstances where opiate agents may not be desired. (432)
17. Neuromuscular blocking drugs associated with histamine release include succinylcholine, atracurium, and mivacurium. Histamine release may precipitate/aggravate bronchospasm, although this is a rare occurrence. Regardless, the availability of nonhistamine releasing neuromuscular blocking drugs such as vecuronium, rocuronium, and cisatracurium allows the anesthesiologist to safely choose the preferred agent based on individual priorities. (432)
18. A slow respiratory rate during mechanical ventilation of the lungs of a patient with asthma allows time for maximal exhalation of gases from obstructed airways. (432)
19. Adequate intraoperative hydration of patients with asthma may facilitate the removal of secretions from the airways by making the secretions less viscous. (432, 434)
20. Extubation of the trachea in the asthmatic patient may be challenging. The presence of an endotracheal tube in the airway of a sufficiently awake patient may trigger irritation and bronchospasm. Two different approaches may be used. The first is to extubate the trachea while the patient is still deeply anesthetized. This requires that (1) no contraindication to having an unprotected airway, such as gastroesophageal reflux, upper gastrointestinal surgery, etc., and (2) spontaneous breathing with no or only partial ventilatory support, to avoid inflation of the stomach with positive pressure ventilation. Care should be paid to suction the airway above the tracheal tube cuff before deflating it. Alternatively, the patient can be allowed to be fully awake before the endotracheal tube is removed. This approach, however, may trigger bronchospasm, which can be minimized by administering additional inhaled bronchodilator prior to awakening.
21. The reversal of neuromuscular blocking drugs with an anticholinesterase such as neostigmine has the potential to cause bronchospasm from cholinergic stimulation. However, the anticholinesterase is administered in association with an anticholinergic agent that selectively blocks the muscarinic effects of acetylcholine (bronchospasm, hyperperistalsis, tachycardia), leaving the nicotinic effects (neuromuscular junction) intact. Atropine and glycopyrrolate are prototype agents in this group. (432)
22. Potential causes of intraoperative bronchospasm include acute bronchial asthma, inadequate depth of anesthesia, endobronchial intubation, aspiration of gastric contents, pneumothorax, and foreign body in the airways. (432)
23. Intraoperative bronchospasm is rarely due to an acute asthma exacerbation, except for patients who were already symptomatic preoperatively. Once mechanical causes are ruled out and treated (e.g., pneumothorax, foreign body in the airways), intraoperative treatment of bronchospasm does not differ significantly to its treatment outside the operating room, except for the additional measure of deepening the level of anesthesia when possible. The first-line drugs are the inhaled bronchodilators (β2-agonists and anticholinergics), preferably administered with a spacer that allows collection of the drug and subsequent delivery during inspiration. Corticosteroids can also be used, although their onset of action is not immediate. If central venous access is available, a low dose of epinephrine (less than 1 μg/min) can be very effective and mostly devoid of side effects. Alternatively, epinephrine can be administered subcutaneously. (432-433)
Chronic obstructive pulmonary disease
24. Pulmonary emphysema is characterized by the loss of elastic recoil of the lungs due to the progressive destruction of lung parenchyma. The loss of elastic recoil leads to collapse of relatively small airways during exhalation, and in turn an increase in airway resistance. This results in hyperinflation of the alveoli, and the destruction of interalveolar septa with the creation of bullae, and an increase work of breathing. All these phenomena accelerate the progression of the disease toward severe COPD. Gas exchange in patients with COPD is characterized by ventilation to perfusion mismatch leading to hypoxemia, which in turns leads to polycythemia, pulmonary hypertension, and in severe cases supplemental oxygen requirements. (433)
25. Chronic bronchitis is characterized by an increased airway resistance due to excessive mucous secretion in the tracheobronchial tree. Long-standing increased airways resistance results in increased work of breathing, dynamic hyperinflation and auto-PEEP, and the predisposition to pulmonary infections such as acute tracheobronchitis and pneumonia. All these phenomena accelerate the progression of the disease toward severe COPD. (433)
26. Emphysema and chronic bronchitis constitute two somewhat different ways to arrive at the same pathologic endpoint: COPD. Emphysema occurs more on the basis of progressive destruction of the lung parenchyma, particularly elastic fibers, and loss of expiratory recoil of the lung. Chronic bronchitis occurs more on the basis of chronic respiratory infection. Hence, the distinction between emphysema and chronic bronchitis is more academic than clinical and it has faded away in the recent literature, which considers them variants of the same disease: COPD, with similar etiologic factors (cigarette smoking), evolution, and complications. (433)
27. The loss of elastic recoil may prevent the lungs to reach functional residual capacity (FRC) at end expiration as they normally would. Ending expiration at a lung volume above FRC exerts a pressure in the alveoli higher than atmospheric (which by convention we call 0 mm Hg). This pressure is often called “intrinsic positive expiratory pressure” (intrinsic PEEP) or “auto-PEEP” and just like PEEP it is related to an increased FRC. Unlike externally applied PEEP, however, intrinsic PEEP needs to be fully overcome before gas flow in the airways becomes negative and inspiration starts. This occurs at every breath and it may be taxing depending upon the magnitude of auto-PEEP and the conditions of the patient. (433)
28. The preoperative evaluation of patients with pulmonary emphysema should include an assessment of the patient’s current symptoms of dyspnea, cough, and sputum production. Exercise tolerance should also be assessed. Based on the clinical history, physical examination findings, and the surgical procedure, preoperative pulmonary function tests and arterial blood gas measurements may be indicated. These studies may help to determine the extent of disease, whether there are any reversible components of the disease such as bronchospasm or infection, and the risk of postoperative respiratory failure. (432-444)
29. The major concern for patients with pulmonary emphysema scheduled to undergo surgical procedures is the risk of postoperative respiratory failure and the need for prolonged intubation of the trachea. Pulmonary function test results that indicate that the patient is at an increased risk for postoperative respiratory failure include an FEV1 less than 2 L and or less than 50% of predicted, or the presence of arterial hypoxemia or hypercarbia. A PaCO2 measurement of 50 mm Hg or higher is an indication that the patient is at an increased risk of postoperative respiratory failure. Arterial hypoxemia warrants treatment with supplemental oxygen in an attempt to improve peripheral oxygen availability, as well as decrease pulmonary vascular resistance and possibly the pressure load of the right ventricle. (434)
30. Intraoperative management of patients with COPD implies similar consideration as those for asthma patients, except that airway irritability is generally less severe. Nonetheless, it is advisable to minimize airway stimulation, to use regional anesthesia if the procedure allows it, to consider extubating the trachea during deep anesthesia, and to always deliver generous bronchodilation. The latter can be accomplished by administering inhaled β2-agonists, anticholinergic agents, and halogenated inhalational agents. When possible, management of the airway by mask or LMA is preferable to endotracheal intubation. When intubated, the airways can be thoroughly suctioned with the aid of a bronchoscope to facilitate secretion clearance in the immediate postoperative period. (433)
31. Disadvantages of using nitrous oxide as part of a general anesthetic in patients with pulmonary emphysema include the potential for nitrous oxide to diffuse into bullae and cause its expansion or even rupture, leading to a tension pneumothorax. In addition, using nitrous oxide obviously limits the inspired fraction of oxygen that can be administered concurrently. (434)
32. Two methods by which anesthesiologists may minimize the drying of secretions in the airways of patients with pulmonary emphysema in the intraoperative period is through the humidification of inspired gases and the maintenance of adequate hydration. (432, 433)
33. Mechanical ventilation of the lungs of patients with COPD may be complicated by the presence of significant expiratory flow limitation, which is present in different degrees at baseline and may be aggravated by intraoperative bronchospasm. Expiratory flow limitation tends to impede the elimination of CO2, and ultimately causes hypercapnia and acute respiratory acidosis. Allowing a long expiratory phase facilitates expiratory emptying of the lungs and CO2 clearance. However, this strategy may be limited by the necessity to deliver a minute ventilation sufficient to maintain adequate CO2 clearance. Increasing tidal volume over respiratory rate may accomplish the goal to a degree, but this also is limited by the potential for alveolar overdistention and barotrauma. Hence, there is no specific formula for success, and various combinations of the above may be tried and may work differently in each individual patient. It is important also to remember the reason for the expiratory flow limitation (high expiratory resistance, bronchospasm) and treat it with generous administration of bronchodilators. (432, 433)
34. Chronic bronchitis is a state of chronic inflammation of the airways with excessive secretions of mucus that causes a progressive increase in airway resistance to air flow. Predisposition to frequent bronchial infection aggravates the clinical picture by adding a purulent component to the tracheobronchial secretions and the general debilitating effects of recurrent infections. The major predisposing factor to the development of chronic bronchitis, as with pulmonary emphysema, is cigarette smoking. (433)
35. COPD affects multiple aspects of lung physiology, principally gas exchange and respiratory mechanics. Hence, they have a much narrower margin of reserve and are at high risk to develop postoperative respiratory complications including pneumonia, and the need for prolonged mechanical ventilation. Interventions that may limit respiratory complications include: (1) preoperative optimization of symptoms like bronchospasm and excessive secretions; (2) careful intraoperative management including either a regional anesthetic or a general anesthetic with generous administration of bronchodilators, retrieval of secretions by deep tracheal suctioning or bronchoscopy, and sufficient hydration; (3) effective postoperative pain control, possibly including regional techniques such as epidural analgesia or continuous peripheral blocks through an indwelling catheter; and (4) a careful evaluation and control of comorbidities such as ischemic heart disease, arrhythmia, and gastroesophageal reflux, which may coexist and contribute to the development of acute respiratory failure. (433)
36. Acute exacerbations of COPD are characterized by acute worsening of dyspnea, sputum production, and sputum purulence. They generally imply a new or renewed respiratory infection, and, in the general outlook of the disease, further decline of respiratory function. When occurring in proximity to a scheduled operation, they constitute an increased risk factor for postoperative respiratory complications. If at all possible, surgery should be postponed and the patient treated with established protocols for COPD exacerbation, including antibiotics, bronchodilators, and often a corticosteroid taper. (433-434)
Pulmonary hypertension
37. Pulmonary hypertension is defined as a mean pulmonary artery pressure greater than 30 mm Hg. Pulmonary hypertension is most commonly secondary to cardiac (congestive heart failure, mitral valve disease) and pulmonary (COPD) disease. Primary pulmonary hypertension is rarer and also more severe. (434)
38. Pulmonary hypertension physiologically leads to an increased pressure in the pulmonary vascular bed constituting an increased pressure load to the right ventricle, which initially compensates with dilation and hypertrophy that allow for the preservation of myocardial stroke volume. As the load to the right ventricle persists or increases, the right ventricle eventually fails and stroke volume and cardiac output fall, leading to chronic right-side congestive heart failure or cor pulmonale. Clinical signs of right ventricular failure include peripheral edema, hepatomegaly, jugular vein distention, and eventually hypoxemia and dyspnea. (434, 435)
39. Pulmonary hypertension may affect the performance of the left ventricle via the development of right ventricular pressure and then volume overload. As the right ventricle responds to the increased pressure afterload, it first hypertrophies and then dilates. As this occurs, the right ventricle assumes a spherical shape and pushes the interventricular septum into the left ventricular cavity. As a result, the volume of the left ventricle decreases, and diastolic filling is compromised, which in turn results in a smaller stroke volume and lower cardiac output. (434)
40. Patients with significant pulmonary hypertension are at risk of developing acute right-side congestive heart failure during anesthesia. Attention must be paid to minimize stimuli that may further increase pulmonary artery pressure, such as hypoxemia, hypercarbia, acidemia, and high catecholamine discharge, as it may occur from acute stress due to light anesthesia. It is important to preserve the preload to the right ventricle by careful maintenance of circulating volume during large open procedures or significant blood loss. On the other hand, excessive volume overload will eventually result in failure of the right ventricle similarly to what happens with the left ventricle. It is then easy to see how such delicate equilibrium may need to be monitored closely (with, for example, a pulmonary artery catheter or a transesophageal echography). Treatment of acute on chronic RV failure is often disappointing, as few selective pulmonary vasodilators are available and are not always effective. These include phosphodiesterase inhibitors (milrinone), inhaled prostacyclin (Flolan), and inhaled nitric oxide. (434, 435)
Obstructive sleep apnea
41. Obstructive sleep apnea is very common, particularly in the male gender, since it may affect as many as 25% of men in the United States. Obesity is by far the most significant risk factor, but obstructive sleep apnea can also occur independently of airway anatomy (central sleep apnea). (435)
42. Obstructive sleep apnea is generally associated with obesity; hence, all the cardiorespiratory and metabolic consequences of obesity are often present in patients with obstructive sleep apnea. When untreated, obstructive sleep apnea causes frequent periods of severe hypoxemia, with the consequent development of pulmonary hypertension over time. Most relevant for anesthesia, physiologic abnormalities of obstructive sleep apnea include a high Mallampati score, low lung volumes, a decreased functional residual capacity, chronic hypoxemia and hypercarbia, atherosclerotic and hypertensive cardiovascular disease, congestive heart failure, gastroesophageal reflux, and metabolic disease, in particular type 2 diabetes mellitus. (435)
43. There are several anesthetic considerations for the patient with obstructive sleep apnea. These patients may have a more challenging airway due to the large amount of redundant tissue that may make ventilation and intubation of the trachea difficult. For this reason it may be preferable to induce general anesthesia in a rapid sequence, avoiding attempts at ventilation all together, after a prolonged preoxygenation, possibly in a slight reversed Trendelenburg position, and prepared with alternative tracheal intubation techniques. Intraoperatively, attention has to be paid to avoid major alveolar collapse by administering positive end-expiratory pressure and occasional large breaths. Extubation should be carried out with the patient wide awake and ready to collaborate with deep breathing. Pharmacologic management of the patient with obstructive sleep apnea should be aimed toward the maintenance of a patent airway. Preoperative benzodiazepines may relax the airway tissues such that pharyngeal space becomes reduced and hypoventilation ensues. Medications that depress the central nervous system may augment this effect and lead to hypopnea, arterial hypoxemia, and hypercapnia both prior to the induction of anesthesia and upon awakening. Opioids can decrease the respiratory drive and further contribute to these complications. If the patient used CPAP at home, it should be available in the postoperative period and used if necessary. (435-436)
Anesthesia for lung resection
Preoperative Evaluation and Preparation
44. Preoperative considerations for the patient scheduled to undergo thoracic surgery include the medical management of the pulmonary disease, the evaluation of coexisting disease and its management, the evaluation of pulmonary function with pulmonary function tests, the selection of intraoperative anesthetics and monitors, the effect of ventilation and/or the lateral decubitus position that may be required intraoperatively, the plan for postoperative pain control, and the potential need for continued mechanical ventilation of the lungs in the postoperative period. Perhaps the main purpose of the preoperative evaluation of patients scheduled to undergo thoracic surgery is to institute perioperative therapy in an effort to minimize postoperative complications. (436)
45. Preoperative history and physical examination findings that are indicative of an increased risk of postoperative pulmonary complications after thoracic surgery include dyspnea, cough, sputum production, wheezing, a history of cigarette smoking, obesity, and advanced age. Another risk factor for postoperative pulmonary complications after thoracic surgery is an inexperienced surgeon. (432, 436)
46. Preoperative prophylactic measures that may be taken in an attempt to minimize postoperative complications include the discontinuation of smoking cigarettes, treatment of any pulmonary infections, treatment of any reversible component of increased airway resistance, mobilization of any secretions, and teaching the patient deep breathing exercises and coughing exercises. These prophylactic measures should be instituted at least 48 to 72 hours before surgery. (436)
47. Cigarette smoking increases the irritability of the small airways, causes mucus hypersecretion, and decreases mucociliary transport. Carbon monoxide may also have negative inotropic effects. The net effect of this for patients scheduled to undergo thoracic surgery is an increase in the incidence of complications in the postoperative period. (433, 436)
48. There are many benefits of the preoperative cessation of cigarette smoking. Twelve to twenty-four hours after the cessation of cigarette smoking, there are significant decreases in the carboxyhemoglobin level and a decrease in nicotine-induced tachycardia. The oxyhemoglobin dissociation curve shifts to the right, making more oxygen available at the tissues. One to two weeks after the cessation of cigarette smoking, there begins to be a decrease in the amount of mucus secretions in the airways; 8 to 12 weeks after the cessation of cigarette smoking, there is marked improvement in mucociliary transport, small airway reactivity, and secretions in the small airways. This is evidenced by the decrease in postoperative respiratory complications in patients who have quit smoking cigarettes for at least 8 weeks before surgery. (436)
49. Preoperative pulmonary function tests predict which patients may be at an increased risk for postoperative pulmonary complications after thoracic surgery. Patients with a history of chronic pulmonary disease or with severe, limiting pulmonary symptoms in the presence of abnormal findings on the physical examination or chest radiograph are candidates for preoperative pulmonary function studies. (436)
50. The following values from a pulmonary function test are indicative of increased risk of postoperative pulmonary morbidity after a pneumonectomy: FEV1 less than 2 L or FEV1 predicted less than 80%. Similarly DLCO less than 80% predicted is also associated with increased morbidity. A decrease in oxygen consumption, less than 10 mL/kg/min as measured by exercise testing, predicts a postoperative mortality rate of 25% to 50% and should prompt discussion of alternatives to surgical resection. (436-37, Figure 27-2)
51. The lung has 42 segments (22 segments on the right and 20 segments on the left). Depending on the number of segments of the lung that will be resected, an estimate of the postoperative FEV1 can be obtained. Predicted postoperative FEV1 (PPO FEV1) = Preoperative FEV1 − (1 − % functional lung tissue removed/100). A PPO FEV1 of less than 40% is associated with poor outcomes. Similar to FEV1, the DLCO estimate, based on the number of lung segments to be resected, is the predicted postoperative DLCO (PPO DLCO). A PPO DLCO of less than 40% carries an increased risk of postoperative complications. (436, Figures 27-2 and 27-3)
Management of Anesthesia
52. The benefits of the administration of volatile anesthetics for patients undergoing thoracic surgery include the effect of decreasing airway reflexes, the lack of influence on regional hypoxic pulmonary vasoconstriction, a high inspired concentration of oxygen that may be delivered concurrently, and the ability to be eliminated postoperatively. (436)
53. Disadvantages of the administration of nitrous oxide for patients undergoing thoracic surgery include:
54. The benefits of the administration of nondepolarizing neuromuscular blocking drugs for patients undergoing thoracic surgery include improved conditions for endotracheal intubation, improved surgical exposure through rib separation. and the facilitation of controlled ventilation of the lungs. (436)
Isolation of the lungs
55. Absolute indications for one-lung ventilation during surgery and anesthesia include the need to isolate the lungs from each other to avoid contamination from one lung to the other of infected material or blood, the presence of a bronchopleural fistula, surgical opening of a major airway, a giant unilateral lung cyst or bullae, tracheobronchial tree disruption, life-threatening hypoxemia due to unilateral lung disease, and unilateral lung lavage of pulmonary alveolar proteinosis. Relative indications for one-lung ventilation during surgery and anesthesia include improving operating conditions during a lobectomy, pneumonectomy, resection of a thoracic aneurysm, or operations on the esophagus.
56. The Robertshaw endobronchial tube is the most frequently used double-lumen endotracheal tube for the isolation of the right or left lung for one-lung ventilation during thoracic surgery. The left-sided tube has a longer bronchial tube than the right-sided tube. Several manufacturers produce clear disposable polyvinyl chloride tubes. (438, Figure 27-5)
57. An endobronchial tube placed in the right bronchus for isolation of the right lung could potentially obstruct the lumen of the right upper lobe bronchus. This occurs secondary to the short distance between the carina and the takeoff to the right upper lobe bronchus. The right-sided double lumen tubes are designed to incorporate a separate opening in the bronchial lumen to allow ventilation of the right upper lobe. Proper positioning of a right-sided DLT must include fiberoptic guidance. (439, Figure 27-9)
58. For most adult women, a size 37 French double-lumen tube is appropriate, and for most men a 39 French tube is the appropriate size. Endobronchial tube placement is in the correct position at an average depth of insertion referenced to the corner of the mouth of 29 cm for patients 170 cm tall. For each 10-cm increase or decrease in the patient’s height, the average depth of endobronchial tube placement correspondingly changes by 1 cm. (438)
59. The technique for placement of a left-sided double-lumen endotracheal tube begins with holding the tube with the distal curve facing anteriorly. Once the bronchial cuff is inserted past the vocal cords, the stylet is removed, the tube is rotated 90 degrees to the left, and the tube advanced until moderate resistance is encountered. The proper placement of a double-lumen endotracheal tube is best confirmed with fiberoptic visualization through the tracheal portion of the double-lumen tube. The desired position of the tube corresponds to visualization of the superior portion of the bronchial cuff, when inflated, just past the bifurcation of the carina. The bronchial side can be confirmed by its orientation to the tracheal rings, which are complete anteriorly. Confirmation of endobronchial tube placement by auscultation alone leads to error in up to 48% of placements. (439, Figure 27-7)
60. The Univent tube has two compartments: a main lumen for conventional air passage and a small lumen embedded in the anterior wall of the endotracheal tube that permits passage of the movable bronchial blocker. The bronchial blocker is a relatively stiff catheter that has an internal channel measuring 2 mm through which oxygen may be insufflated. After tracheal intubation with the bronchial blocker retracted, initial positioning is accomplished by rotating the tube to the right or left position, so that the BB is advanced into the corresponding mainstem bronchus. Fiberoptic visualization should be used to confirm appropriate mainstem intubation and to guide the depth of insertion. The advantage of the Univent tube is that it then converts to a single-lumen endotracheal tube with the withdrawal of the bronchial blocker when isolation of the lungs is no longer needed. An example in which this may be advantageous is when postoperative ventilation of the lungs is anticipated and changing a double-lumen tube to a single-lumen tube at the conclusion of the surgical procedure could be dangerous or difficult. (441-442, Figures 27-10 and 27-11)
61. The Arndt endobronchial blocker is a wire-guided catheter. The bronchial blocker is coupled to the bronchoscope through the guide loop after they are passed through a multiairway adapter. The bronchoscope is advanced to the desired mainstem bronchus. Since the bronchial blocker is coupled to the bronchoscope, it is in turn positioned in the desired bronchus. (442, Figure 27-12)
62. The Cohen tip deflecting endobronchial blocker is introduced into a single-lumen endotracheal tube. The flexible tip of the bronchial blocker is directed into the desired bronchus by using the control wheel on the proximal end of the blocker. (442, Figure 27-13)
63. Bronchial blockers provide equivalent surgical exposure (lung collapse) when compared with a left-sided double-lumen tube, during left-sided open or video assisted thoracoscopic surgery. But bronchial blockers require a longer time to position and need more frequent intraoperative manipulation. (442)
Gas Exchange during One-Lung Ventilation
64. A patient in the lateral decubitus position undergoing mechanical ventilation of the lungs has an increase in pulmonary ventilation-to-perfusion mismatch. The effects on pulmonary blood flow are primarily due to gravity, lung volume, and regional vascular resistance. The dependent lung receives proportionally more blood flow than the nondependent lung. The dependent lung is ventilated relatively less secondary to the loss of lung volume from compression by the mediastinum, abdominal contents, and positioning support structures. These factors together create an increase in pulmonary ventilation-to-perfusion mismatching. The ventilation-to-perfusion ratio can be improved with the application of PEEP to the dependent lung. (442-444)
65. Four factors that influence the amount of perfusion that goes to the nondependent, unventilated lung during ventilation of a patient in the lateral decubitus position with a double-lumen endotracheal tube include gravity, hypoxic pulmonary vasoconstriction, direct surgical compression of blood flow, and presence of pulmonary artery hypertension. (444)
66. Arterial hypoxemia when noted during ventilation for thoracic surgery calls for confirming proper placement of a double-lumen endotracheal tube using a fiberoptic bronchoscope. Next, the administration of a low level (5 to 10 cm H2O) of PEEP to the nondependent lung helps. Sometimes this may interfere with the surgical dissection. A slow inflation of 2 L/min of oxygen into the nonventilated lung for 2 seconds and repeated every 10 seconds for 5 minutes until the saturation rises has been shown to improve oxygenation during ventilation. Sustained lung inflation of 30 to 40 cm H2O to the dependent lung along with application of PEEP helps in recruitment of collapsed lung. Although this may improve arterial oxygenation, it may also cause an increase in the pulmonary vascular resistance in the ventilated, dependent lung and in turn worsen the hypoxia. (445, Table 27-2)
Conclusion of surgery
67. Chest tubes are placed after thoracic surgery to ensure continued expansion of the lung by evacuating fluid and air that may leak from alveoli that have been incised. Kinking of a chest tube after thoracic surgery places the patient at risk for a tension pneumothorax. (446)
68. Extubation of the trachea after thoracic surgery should take place at the conclusion of the surgery to minimize the complications associated with mechanical ventilation (barotrauma, ventilator-associated pneumonia). (446)
Postoperative pulmonary complications
69. The most common postoperative pulmonary complication after thoracic surgery is atelectasis. Other common postoperative pulmonary complications include hypoventilation and arterial hypoxemia. These problems may be related to intraoperative problems (aspiration, trauma) or problems during the postoperative period due to the inability to mobilize secretions and effectively expand the operative lung. Early mobilization after surgery reestablishes physiologic lung volumes and gas exchange, and seems to be the most effective way to prevent postoperative pulmonary complications. (446)
70. Adequate analgesia after thoracic surgery is important. Thoracic epidural analgesia (TEA) provides effective postoperative pain relief, improved pulmonary function, and prompt mobility. TEA is associated with a lower mortality rate and fewer respiratory complications. (446)
Mediastinoscopy
71. The most frequent reason for the performance of a mediastinoscopy is to determine the diagnosis and/or resectability of lung cancer. (446)
72. The most common complications that can occur after the performance of a mediastinoscopy include hemorrhage and a pneumothorax. Other potential complications include a recurrent laryngeal nerve injury, infection, air embolism, and phrenic nerve injury. (446)
