Obstructive and restrictive diseases are the two most common abnormal patterns as determined by PFTs. The former are by far the more common. Obstructive diseases include asthma, emphysema, chronic bronchitis, cystic fibrosis, bronchiectasis, and bronchiolitis. The primary characteristic of these disorders is resistance to airflow. An MMEF of less than 70% (forced expiratory flow [FEF25–75%]) is often the only abnormality early in the course of these disorders. Values for FEF25–75% in adult males and females are normally greater than 2.0 L/s and 1.6 L/s, respectively. As the disease progresses, both forced expiratory volume in the first second of exhalation (FEV1) and the FEV1/FVC (forced vital capacity) ratio are less than 70% of the predicted values.
Elevated airway resistance and air trapping increase the work of breathing; respiratory gas exchange is impaired because of ventilation/perfusion (V̇/Q̇) imbalance. The predominance of expiratory airflow resistance results in air trapping; residual volume and total lung capacity (TLC) increase. Wheezing is a common finding and represents turbulent airflow. It is often absent with mild obstruction that may be manifested initially only by prolonged exhalation. Progressive obstruction typically results first in expiratory wheezing only, and then in both inspiratory and expiratory wheezing. With marked obstruction, wheezing may be absent when airflow has nearly ceased.
Asthma is a common disorder, affecting 5% to 7% of the population. Its primary characteristic is airway (bronchiolar) inflammation and hyperreactivity in response to a variety of stimuli. Clinically, asthma is manifested by episodic attacks of dyspnea, cough, and wheezing. Airway obstruction, which is generally reversible, is the result of bronchial smooth muscle constriction, edema, and increased secretions. Classically, the obstruction is precipitated by a variety of airborne substances, including pollens, animal dander, dusts, pollutants, and various chemicals. Some patients also develop bronchospasm following ingestion of aspirin, nonsteroidal antiinflammatory agents, sulfites, or other compounds. Exercise, cold air, emotional excitement, and viral infections also precipitate bronchospasm in many patients. Asthma is classified as acute or chronic. Chronic asthma is further classified as intermittent (mild) and mild, moderate, and severe persistent disease.
The terms extrinsic (allergic) asthma (attacks related to environmental exposures) and intrinsic (idiosyncratic) asthma (attacks usually occurring without provocation) were used in the past, but these classifications were imperfect; many patients show features of both forms. Moreover, overlap with chronic bronchitis (see later discussion) is common.
The pathophysiology of asthma involves the local release of various chemical mediators in the airway, and, possibly, overactivity of the parasympathetic nervous system. Inhaled substances can initiate bronchospasm through both specific and nonspecific immune mechanisms by degranulating bronchial mast cells. In classic allergic asthma, antigen binding to immunoglobulin E (IgE) on the surface of mast cells causes degranulation. Bronchoconstriction is the result of the subsequent release of histamine; bradykinin; leukotrienes C, D, and E; platelet-activating factor; prostaglandins (PG) E2, F2α, and D2; and neutrophil and eosinophil chemotactic factors. The parasympathetic nervous system plays a major role in maintaining normal bronchial tone; a normal diurnal variation in tone is recognized in most individuals, with peak airway resistance occurring early in the morning (at about 6:00 AM). Vagal afferents in the bronchi are sensitive to histamine and multiple noxious stimuli, including cold air, inhaled irritants, and instrumentation (eg, tracheal intubation). Reflex vagal activation results in bronchoconstriction, which is mediated by an increase in intracellular cyclic guanosine monophosphate (cGMP).
During an asthma attack, bronchoconstriction, mucosal edema, and secretions increase resistance to gas flow at all levels of the lower airways. As an attack resolves, airway resistance normalizes first in the larger airways (mainstem, lobar, segmental, and subsegmental bronchi), and then in more peripheral airways. Consequently, expiratory flow rates are initially decreased throughout an entire forced exhalation, but during resolution of the attack, the expiratory flow rate is reduced only at low lung volumes. TLC, residual volume (RV), and FRC are all increased. In acutely ill patients, RV and FRC are often increased by more than 400% and 100%, respectively. Prolonged or severe attacks markedly increase the work of breathing and can fatigue respiratory muscles. The number of alveolar units with low (V̇/Q̇) ratios increases, resulting in hypoxemia. Tachypnea is likely and typically produces hypocapnia. A normal or high PaCO2 indicates that the patient can no longer maintain the work of breathing and is often a sign of impending respiratory failure. A pulsus paradoxus and electrocardiographic signs of right ventricular strain (ST-segment changes, right axis deviation, and right bundle-branch block) are also indicative of severe airway obstruction.
Drugs used to treat asthma include β-adrenergic agonists, methylxanthines, glucocorticoids, anticholinergics, leukotriene modifiers, and mast-cell–stabilizing agents. Although devoid of any bronchodilating properties, cromolyn sodium and nedocromil are effective in preventing bronchospasm by blocking the degranulation of mast cells.
Sympathomimetic agents (eg, albuterol) are the most commonly used for acute exacerbations. They produce bronchodilation via β2-agonist activity. Activation of β2-adrenergic receptors on bronchiolar smooth muscle stimulates the activity of adenylate cyclase, which results in the formation of intracellular cyclic adenosine monophosphate (cAMP). These agents are usually administered via a metered-dose inhaler or by aerosol. Use of more selective β2-agonists, such as terbutaline or albuterol, may decrease the incidence of undesirable β1 cardiac effects, but are often not particularly selective in high doses.
Traditionally, methylxanthines are thought to produce bronchodilation by inhibiting phosphodiesterase, the enzyme responsible for the breakdown of cAMP. Their pulmonary effects seem much more complex and include catecholamine release, blockade of histamine release, and diaphragmatic stimulation. Unfortunately, theophylline has a narrow therapeutic range; therapeutic blood levels are considered to be 10 to 20 mcg/mL. Lower levels, however, may be effective. Aminophylline is the only available intravenous theophylline preparation.
Glucocorticoids are used for both acute treatment and maintenance therapy of patients with asthma because of their antiinflammatory and membrane-stabilizing effects. Beclomethasone, triamcinolone, fluticasone, and budesonide are synthetic steroids commonly used in metered-dose inhalers for maintenance therapy. Although they are associated with a low incidence of undesirable systemic effects, inhaled administration does not necessarily prevent adrenal suppression. Intravenous hydrocortisone or methylprednisolone is used acutely for severe attacks, followed by tapering doses of oral prednisone. Glucocorticoids usually require several hours to become effective.
Anticholinergic agents produce bronchodilation through their antimuscarinic action and may block reflex bronchoconstriction. Ipratropium, a congener of atropine that can be given by a metered-dose inhaler or aerosol, is a moderately effective bronchodilator without appreciable systemic anticholinergic effects.
A. Preoperative Management
The emphasis in evaluating patients with asthma should be on determining the severity and recent course of the disease, as well as on ascertaining whether the patient is in optimal condition. Patients with poorly controlled asthma or wheezing at the time of anesthesia induction have a greater risk of perioperative complications. Conversely, well-controlled asthma has not been shown to be a risk factor for intraoperative or postoperative complications. A thorough history and physical examination are of critical importance. The patient should have no or minimal dyspnea, wheezing, or cough. Complete resolution of recent exacerbations should be confirmed by chest auscultation. Patients with frequent or chronic bronchospasm should be placed on an optimal bronchodilating regimen. A chest radiograph identifies air trapping; hyperinflation results in a flattened diaphragm, a small-appearing heart, and hyperlucent lung fields. PFTs—particularly expiratory airflow measurements such as FEV1, FEV1/FVC, FEF25-75%, and peak expiratory flow rate—help in assessing the severity of airway obstruction and reversibility after bronchodilator treatment. Comparisons with previous measurements are invaluable.
Asthmatic patients with active bronchospasm presenting for emergency surgery should be treated aggressively. Supplemental oxygen, aerosolized β2-agonists, and intravenous glucocorticoids can dramatically improve lung function in a few hours. Arterial blood gases may be useful in evaluating severity and adequacy of treatment. Hypoxemia and hypercapnia are typical of moderate or severe disease; even slight hypercapnia is indicative of severe air trapping and may be a sign of impending respiratory failure.
Anticholinergic agents are not customarily given unless very copious secretions are present or if ketamine is to be used for induction of anesthesia. In typical intramuscular doses, anticholinergics are not effective in preventing reflex bronchospasm following intubation. The use of an H2-blocking agent (such as cimetidine, ranitidine, or famotidine) is theoretically detrimental, since H2-receptor activation normally produces bronchodilation; in the event of histamine release, unopposed H1 activation with H2 blockade may accentuate bronchoconstriction.
Bronchodilators should be continued up to the time of surgery; these include β-agonists, inhaled glucocorticoids, leukotriene modifiers, mast-cell stabilizers, theophyllines, and anticholinergics. Patients who receive chronic glucocorticoid therapy with more than 5 mg/d of prednisone (or its equivalent) should receive a graduated supplementation schedule based on the severity of the illness and complexity of the surgical procedure. Supplemental doses should be tapered to baseline within 1 to 2 days.
B. Intraoperative Management
The most critical time for asthmatic patients undergoing anesthesia is during instrumentation of the airway. General anesthesia with noninvasive ventilation or regional anesthesia will circumvent this problem, but neither eliminates the possibility of bronchospasm. In fact, some clinicians believe that high spinal or epidural anesthesia may aggravate bronchoconstriction by blocking sympathetic tone to the lower airways (T1–T4) and allowing unopposed parasympathetic activity. Pain, emotional stress, or stimulation during light general anesthesia can precipitate bronchospasm. Drugs often associated with histamine release (eg, atracurium, morphine, and meperidine) should be avoided or given very slowly when used.
The choice of induction agent is less important if adequate depth of anesthesia is achieved before intubation or surgical stimulation. Thiopental may occasionally induce bronchospasm as a result of exaggerated histamine release. Propofol and etomidate are suitable induction agents; propofol may also produce bronchodilation. Ketamine has bronchodilating properties and is a good choice for patients with asthma who are also hemodynamically unstable. Ketamine should probably not be used in patients with high theophylline levels, as the combined actions of the two drugs might precipitate seizure activity. Sevoflurane usually provides the smoothest inhalation induction with bronchodilation in asthmatics. Isoflurane and desflurane are more pungent and may result in cough, laryngospasm, and bronchospasm during inhalation induction.
Reflex bronchospasm can be blunted before intubation by an additional dose of the induction agent, ventilating the patient with a 2 to 3 minimum alveolar concentration (MAC) of a volatile agent for 5 min, or administering intravenous or intratracheal lidocaine (1–2 mg/kg). Note that intratracheal lidocaine itself can initiate bronchospasm if an inadequate dose of induction agent has been used. Administration of an anticholinergic agent may block reflex bronchospasm, but causes excessive tachycardia. Although succinylcholine may on occasion induce marked histamine release, it can generally be safely used in asthmatic patients. In the absence of capnography, confirmation of correct tracheal placement by chest auscultation can be difficult in the presence of marked bronchospasm.
Volatile anesthetics are most often used for maintenance of anesthesia to take advantage of their potent bronchodilating properties. Ventilation should incorporate warmed humidified gases whenever possible. Airflow obstruction during expiration is apparent on capnography as a delayed rise of the end-tidal CO2 value (Figure 24–2); the severity of obstruction is generally inversely related to the rate of rise in end-tidal CO2. Severe bronchospasm is manifested by rising peak inspiratory pressures and incomplete exhalation. Tidal volumes of 6 mL/kg, with prolongation of the expiratory time, may allow more uniform distribution of gas flow to both lungs and may help avoid air trapping. The PaCO2 may increase, which is acceptable if there is no contraindication from a cardiovascular or neurologic perspective.
Capnograph of a patient with expiratory airway obstruction.
Intraoperative bronchospasm is usually manifested as wheezing, increasing peak airway pressures (plateau pressure may remain unchanged), decreasing exhaled tidal volumes, or a slowly rising waveform on the capnograph. Other causes can simulate bronchospasm: These include obstruction of the tracheal tube from kinking, secretions, or an overinflated balloon; bronchial intubation; active expiratory efforts (straining); pulmonary edema or embolism; and pneumothorax. Bronchospasm should be treated by increasing the concentration of the volatile agent and administering an aerosolized bronchodilator. Infusion of low-dose epinephrine may be needed if bronchospasm is refractory to other interventions.
Intravenous hydrocortisone can be given, particularly in patients with a history of responding to glucocorticoid therapy. At the completion of surgery, the patient should ideally be free of wheezing. Reversal of nondepolarizing neuromuscular blocking agents with anticholinesterase agents generally does not precipitate bronchoconstriction if preceded by the appropriate dose of an anticholinergic agent. Sugammadex avoids the issue of increasing acetylcholine concentration; however, cases of allergic reaction to sugammadex have been reported. Deep extubation (before the return of airway reflexes) reduces the risk of bronchospasm on emergence. Lidocaine as a bolus (1.5–2 mg/kg) may help to obtund airway reflexes upon emergence.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
COPD is the most common pulmonary disorder encountered in anesthetic practice, and its prevalence increases with age. The disorder is strongly associated with cigarette smoking and has a male predominance. COPD is currently defined as a disease state characterized by airflow limitation that is not fully reversible. The chronic airflow limitation of this disease is due to a mixture of small and large airway disease (chronic bronchitis/bronchiolitis) and parenchymal destruction (emphysema), with representation of these two components varying from patient to patient.
Most patients with COPD are asymptomatic or only mildly symptomatic, but show expiratory airflow obstruction upon PFTs. In many patients, the obstruction has an element of reversibility, presumably from bronchospasm (as shown by improvement in response to administration of a bronchodilator). With advancing disease, maldistribution of both ventilation and pulmonary blood flow results in areas of low (V̇/Q̇) ratios (intrapulmonary shunt), as well as areas of high (V̇/Q̇) ratios (dead space).
The clinical diagnosis of chronic bronchitis is defined by the presence of a productive cough on most days of 3 consecutive months for at least 2 consecutive years. In addition to cigarette smoking, exposure to air pollutants, occupational exposure to dusts, recurrent pulmonary infections, and familial factors may be responsible. Secretions from hypertrophied bronchial mucous glands and mucosal edema from inflammation of the airways produce airflow obstruction. Recurrent pulmonary infections (viral and bacterial) are common and often associated with bronchospasm. RV is increased, but TLC is often normal. Intrapulmonary shunting and hypoxemia are common.
In patients with COPD, chronic hypoxemia leads to erythrocytosis, pulmonary hypertension, and eventually right ventricular failure (cor pulmonale); this combination of findings is often referred to as the “blue bloater” syndrome, but less than 5% of patients with COPD fit this description (Table 24–2). In the course of disease progression, patients gradually develop chronic CO2 retention; the normal ventilatory drive becomes less sensitive to arterial CO2 tension and may be depressed by oxygen administration (see below).
TABLE 24–2Signs and symptoms of chronic obstructive pulmonary disease. ||Download (.pdf) TABLE 24–2 Signs and symptoms of chronic obstructive pulmonary disease.
|Feature ||Chronic Bronchitis ||Emphysema |
|Cough ||Frequent ||With exertion |
|Sputum ||Copious ||Scant |
|Hematocrit ||Elevated ||Normal |
|PaCO2 (mm Hg) ||Often elevated (>40) ||Usually normal or <40 |
|Chest radiograph ||Increased lung markings ||Hyperinflation |
|Elastic recoil ||Normal ||Decreased |
|Airway resistance ||Increased ||Normal to slightly increased |
|Cor pulmonale ||Early ||Late |
Emphysema is a pathological disorder characterized by irreversible enlargement of the airways distal to terminal bronchioles and destruction of alveolar septa. The diagnosis can be reliably made with computed tomography (CT) of the chest. Mild apical emphysematous changes are a normal, clinically insignificant consequence of aging. Significant emphysema is more frequently related to cigarette smoking. Less commonly, emphysema occurs at an early age and is associated with a homozygous deficiency of α1-antitrypsin. This is a protease inhibitor that prevents excessive activity of proteolytic enzymes (mainly elastase) in the lungs; these enzymes are produced by pulmonary neutrophils and macrophages in response to infection and pollutants. Emphysema associated with smoking may similarly be due to a relative imbalance between protease and antiprotease activities in susceptible individuals.
Emphysema may exist in a centrilobular or panlobular form. The centrilobular (or centriacinar) form results from dilation or destruction of the respiratory bronchioles, is more closely associated with tobacco smoking, and has predominantly an upper lobe distribution. The panlobular (or panacinar) form results in a more even dilation and destruction of the entire acinus, is associated with α1-antitrypsin deficiency, and has predominantly a lower lobe distribution.
Loss of the elastic recoil that normally supports small airways by radial traction allows premature collapse during exhalation, leading to expiratory flow limitation with air trapping and hyperinflation (see Table 24–2). Patients characteristically have increases in RV, FRC, TLC, and the RV/TLC ratio.
Disruption of the alveolar–capillary structure and loss of the acinar structure lead to decreased diffusion lung capacity, (V̇/Q̇) mismatch, and impairment of gas exchange. Also, normal parenchyma may become compressed by the hyperinflated portions of the lung, resulting in a further increase in the (V̇/Q̇) mismatch. Due to the higher diffusibility of CO2, its elimination is well preserved until (V̇/Q̇) abnormalities become severe. Chronic CO2 retention occurs slowly and generally results in a compensated respiratory acidosis on blood gas analysis. Arterial oxygen tension is usually normal or slightly reduced. Acute CO2 retention is a sign of impending respiratory failure.
Destruction of pulmonary capillaries in the alveolar septa leads to the development of mild to moderate pulmonary hypertension. When dyspneic, patients with emphysema often purse their lips to delay closure of the small airways, which accounts for the term “pink puffers” that is often used. However, as mentioned above, most patients diagnosed with COPD have a combination of bronchitis and emphysema.
Treatment for COPD is primarily supportive. Cessation of smoking is the long-term intervention that has been shown to reduce the rate of decline in lung function. Various guidelines have been suggested to aid in the primary medical management of patients with COPD. In general, spirometry is employed to assess the severity of airflow reduction characteristic of obstruction, and whether there is a response to bronchodilators. For bronchodilator-responsive patients, short-acting bronchodilators are recommended when FEV1 is greater than 80% of predicted and longer-acting bronchodilators and inhaled corticosteroids are suggested as FEV1 and patient symptoms worsen. Inhaled β2-adrenergic agonists, glucocorticoids, and ipratropium are routinely employed. Hypoxemia is treated with supplemental oxygen. Patients with chronic hypoxemia (PaO2 <55 mm Hg) and pulmonary hypertension require low-flow oxygen therapy (1–2 L/min). CO2 retention may be exacerbated in patients with reduced hypoxic ventilatory drive. Consequently, oxygen therapy is targeted to a hemoglobin oxygen saturation of 90%.
Pulmonary rehabilitation may improve the functional status of the patient by improving physical symptoms and exercise capacity.
A. Preoperative Management
Patients with COPD should be prepared prior to elective surgical procedures in the same way as patients with asthma (see earlier discussion). They should be questioned about recent changes in dyspnea, sputum, and wheezing. Patients with an FEV1 less than 50% of predicted (1.2–1.5 L) usually have dyspnea on exertion, whereas those with an FEV1 less than 25% (<1 L in men) typically have dyspnea with minimal activity. The latter finding, in patients with predominantly chronic bronchitis, is also often associated with CO2 retention and pulmonary hypertension. PFTs, chest radiographs, and arterial blood gas measurements, if available, should be reviewed carefully. The presence of bullous changes on the radiograph should be noted. Many patients have concomitant cardiac disease and should also receive a careful cardiovascular evaluation.
In contrast to asthma, only limited improvement in respiratory function may be seen after a short period of intensive preoperative preparation. Nonetheless, preoperative interventions in patients with COPD aimed at correcting hypoxemia, relieving bronchospasm, mobilizing and reducing secretions, and treating infections may decrease the incidence of postoperative pulmonary complications. Patients at greatest risk of complications are those with preoperative pulmonary function measurements less than 50% of predicted. The possibility that postoperative ventilation may be necessary in high-risk patients should be discussed with both the patient and the surgeon.
Smoking should be discontinued for at least 6 to 8 weeks before the operation to decrease secretions and to reduce pulmonary complications. Cigarette smoking increases mucus production and decreases clearance. Both gaseous and particulate phases of cigarette smoke can deplete glutathione and vitamin C and may promote oxidative injury to tissues. Cessation of smoking for as little as 24 h has theoretical beneficial effects on the oxygen-carrying capacity of hemoglobin; acute inhalation of cigarette smoke releases carbon monoxide, which increases carboxyhemoglobin levels, as well as nitric oxide, and nitrogen dioxide, which can lead to formation of methemoglobin.
Long-acting bronchodilators and mucolytics should be continued, including on the day of surgery. COPD exacerbations should be treated aggressively.
Preoperative chest physiotherapy and lung expansion interventions with incentive spirometry, deep breathing exercises, cough, chest percussion, and postural drainage may be beneficial in decreasing postoperative pulmonary complications.
B. Intraoperative Management
Although regional anesthesia is often considered preferable to general anesthesia, high spinal or epidural anesthesia can decrease lung volumes, restrict the use of accessory respiratory muscles, and produce an ineffective cough, leading to dyspnea and retention of secretions. Loss of proprioception from the chest and positions such as lithotomy or lateral decubitus may accentuate dyspnea in awake patients. Concerns about hemidiaphragmatic paralysis may make interscalene blocks a less attractive option in the lung disease patient.
Preoxygenation prior to induction of general anesthesia prevents the rapid oxygen desaturation often seen in these patients. The selection of anesthetic agents and general intraoperative management must be tailored to the specific needs and goals of every patient. Unfortunately, the use of bronchodilating anesthetics improves only the reversible component of airflow obstruction; significant expiratory obstruction may still present, even under deep anesthesia. Expiratory airflow limitation, especially under positive pressure ventilation, may lead to air trapping, dynamic hyperinflation, and elevated intrinsic positive end-expiratory pressure (iPEEP). Dynamic hyperinflation may result in volutrauma to the lungs, hemodynamic instability, hypercapnia, and acidosis. Interventions to mitigate air trapping include: (1) allowing more time to exhale by decreasing both the respiratory rate and inspiratory/expiratory (I:E) ratio; (2) allowing permissive hypercapnia; (3) applying low levels of extrinsic PEEP; and (4) aggressively treating bronchospasm.
Intraoperative causes of hypotension in these patients include (in addition to the usual “suspects”) pneumothorax and right heart failure due to hypercapnia and acidosis. A pneumothorax may manifest as hypoxemia, increased peak airway pressures, decreasing tidal volumes, and abrupt cardiovascular collapse unresponsive to fluid and vasopressor administration.
Nitrous oxide should be avoided in patients with bullae and pulmonary hypertension. Inhibition of hypoxic pulmonary vasoconstriction by inhalation anesthetics is usually not clinically apparent at usual doses. However, due to increased dead space, patients with severe COPD have unpredictable uptake and distribution of inhalational agents, and the end-tidal volatile anesthetic concentration is inaccurate.
Although pulse oximetry accurately detects significant arterial desaturation, direct measurement of arterial oxygen tensions may be necessary to detect more subtle changes in intrapulmonary shunting. Moreover, arterial CO2 measurements can guide ventilation because increased dead space widens the normal arterial-to-end-tidal CO2 gradient. Moderate hypercapnia with a PaCO2 of up to 70 mm Hg may be well tolerated in the short term, assuming a reasonable cardiovascular reserve. Hemodynamic support with inotropic agents may be required in more compromised patients. Hemodynamic monitoring should be dictated by any underlying cardiac dysfunction, as well as the extent of the surgery and the established enhanced recovery protocols in your unit. Successful extubation at the end of the procedure depends on multiple factors: adequate pain control, reversal of neuromuscular blockade, absence of significant bronchospasm and secretions, absence of significant hypercapnia and acidosis, and absence of respiratory depression due to residual anesthetic agents. Patients with an FEV1 below 50% may require a period of postoperative ventilation, particularly following upper abdominal and thoracic operations.