Key words
bronchial blocker, Chronic pulmonary disease, double-lumen endobronchial tube, lung isolation, mediastinal masses, one-lung ventilation, preoperative assessment
The editors and publisher would like to thank Drs. Luca M. Bigatello and Venkatesh Srinivasa for contributing to this chapter in the previous edition of this work. It has served as the foundation for the current chapter.
Introduction
Chronic respiratory problems include obstructive and restrictive lung diseases, obstructive sleep apnea (OSA), and pulmonary hypertension. Obstructive lung diseases are commonly divided into reactive airway disorders (asthma) and chronic obstructive pulmonary disease (COPD). However, many patients have more than one type of lung disease. Avoiding general anesthesia, if possible, with regional or local anesthesia is usually preferable for patients with chronic respiratory diseases.
History
Common symptoms elicited in all patients include cough, wheezing, shortness of breath, chest tightness, sputum production, and reduced exercise tolerance. Important components of the history are recent exacerbations, current and previous therapies including hospital admissions, emergency room visits, and tobacco use.
Physical Examination
Signs of chronic respiratory disease include tachypnea, cyanosis, use of accessory muscles of respiration, and clubbing of the fingers. Of prime importance are the presence of unequal breath sounds, wheezing, and rales during auscultative examination.
Laboratory Examination
Chest Imaging
A recent preoperative chest x-ray examination is not required for all patients but should be considered in any patient with a chronic respiratory disease or a patient with a recent change in respiratory symptoms or signs.
Spirometry
Simple spirometry (expired volume or flow vs. time), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV 1 ) ( Fig. 27.1 ) are not required in all stable patients but should be ordered if there is any doubt about the severity of disease, such as a recent change in symptoms, if the patient is unable to give a clear history, or if any patient with chronic lung disease is having lung surgery. Full pulmonary function tests (plethysmography) ( Fig. 27.2 ) including measurement of residual volume (RV), functional residual capacity (FRC), and measurement of the lung diffusing capacity for carbon monoxide (D lco ) are only indicated if the diagnosis or severity of the lung disease is unclear from the simple spirometry procedure.
Gas Exchange
Oxygen saturation (pulse oximetry, Sp o 2 %) should be documented preoperatively in every patient with a chronic respiratory disease. Arterial blood gases are required preoperatively in patients with moderate or severe chronic respiratory disease who are at risk of requiring postoperative mechanical ventilation (major abdominal, thoracic, cardiac, spine, or neurosurgery) or if symptoms have become more intense.
Asthma
Clinical Presentation
Asthma is a common form of episodic recurrent lower airway obstruction that affects 3% to 5% of the population. Sixty-five percent of people with asthma become symptomatic before age 5 years. Patients with childhood asthma often become quiescent with time but can have recurrences. Inflammation of the airways is a hallmark of asthma. Steroids (inhaled, oral, or both) are the most effective medications in controlling this inflammation. The inflamed airway is hyperresponsive to irritant stimuli with subsequent bronchospasm and mucous secretions. Bronchospastic stimuli can include allergens, dust, cold air, instrumentation of the airways, and medications (aspirin or histamine-releasing drugs). Asthmatics are at risk for life-threatening bronchospasm during anesthesia if improperly managed, particularly during or recently after a respiratory tract infection. Elective surgery should therefore be delayed at least 6 weeks after a respiratory infection in these patients.
The severity of asthma is defined by the amount of treatment required to control symptoms ( Box 27.1 ). Most patients will be conducting steps 1 or 2 of this treatment protocol. After step 3, when anesthetizing patients extra caution is required. A history of severe or life-threatening exacerbations, or being a patient in intensive care or with endotracheal intubation, is indicative of patients at increased risk of major pulmonary complications. Peak expiratory flow (PEF) rate is a very simple and useful measurement of the severity of asthma. Many patients measure their own PEF to guide their therapy. PEF rates less than 50% of the predicted value (corrected for age/gender/height) indicate severe asthma. A PEF increase of more than 15% after bronchodilator administration suggests inadequate treatment of asthma.
- 1.
Inhaled short-acting β 2 -agonists (e.g., salbutamol 100-200 μg prn)
- 2.
Inhaled short-acting β 2 -agonists and inhaled steroids at up to 400 μg/day
- 3.
Step 2 and additional long-acting β 2 -agonist (LABA)
- 4.
Inhaled steroids up to 800 μg/day and LABA/leukotriene receptor antagonist
- 5.
Oral steroids/additional therapy as required reducing steroid use
prn, As needed.
Suppression of the hypothalamic-pituitary-adrenal (HPA) axis may occur with corticosteroid therapy. Adrenal crisis may be precipitated by the stress of surgery. Short courses of oral prednisone used to treat asthma exacerbations can affect HPA function for up to 10 days, but dysfunction is unlikely to be prolonged. Large doses, prolonged therapy (>3 weeks), evening dosing, and continuous (as opposed to alternate day) dosing all increase suppression of the HPA axis and may take up to a year before returning to normal. Inhaled steroids are less likely to cause suppression of HPA axis.
Management of Anesthesia
The adequacy of asthma control needs to be assessed during preoperative evaluation, and symptoms uncharacteristic of asthma need to be excluded ( Table 27.1 ) (also see Chapter 13 ). Principles of perioperative management of patients with asthma are outlined in Box 27.2 . Volatile anesthetics, particularly sevoflurane, reduce bronchomotor tone and produce a degree of bronchodilation (except desflurane) that may be helpful in patients with obstructive lung disease or bronchoconstriction.
| History Suggestive of Inadequate Asthma Control | |
|---|---|
Frequency of symptoms
|
| Features Uncharacteristic of Asthma | Differential Diagnosis |
|---|---|
| Unremitting wheeze/stridor | Suggestive of fixed airway obstruction |
| Persisting wet cough/productive cough | Suggestive of suppurative lung disease |
| Wheeze present from birth (rare with asthma) | Tracheomalacia/bronchomalacia |
| A monophonic wheeze loudest over the glottis | Vocal cord dysfunction |
- •
Usual inhalers per normal on day of surgery. Inhaled β 2 -agonists prior to anesthesia.
- •
Avoid lower airway manipulation (e.g., endotracheal intubation) if possible. Use regional anesthesia, or an LMA/mask for general anesthesia if possible.
- •
Avoid medications that release histamine (e.g., thiopental, morphine, atracurium).
- •
Use anesthetic drugs that promote bronchodilation (propofol, ketamine, sevoflurane).
- •
If instrumentation of the lower airway is necessary, it should be performed after attaining a deep level of general anesthesia to decrease airway reflexes.
LMA, Laryngeal mask airway.
Chronic Obstructive Pulmonary Disease
Clinical Presentation
COPD incorporates three disorders: emphysema, peripheral airways disease, and chronic bronchitis. The FEV 1 /FVC ratio will be less than 70%, and RV will be increased. The severity of COPD is assessed by the percent of FEV 1 : stage I, more than 50% predicted (this category includes both mild and moderate COPD); stage II, 35% to 50%; and stage III, less than 35%. Stage I patients should not have significant dyspnea, hypoxemia, or hypercarbia. Specific complications of COPD to be considered preoperatively are described next.
Carbon Dioxide Retention (Baseline Pa co 2 > 45 mm Hg)
Many stage II or III COPD patients have an elevated Pa co 2 at rest. CO 2 retainers cannot be differentiated from nonretainers on the basis of history, physical examination, or spirometry. When these patients are given supplemental oxygen, their Pa co 2 values increase because increased inspired oxygen concentrations cause an increase in alveolar dead space owing to a decrease in regional hypoxic pulmonary vasoconstriction and the Haldane effect. However, supplemental oxygen must be administered to these patients to prevent the hypoxemia associated with the postoperative decrease in FRC. Increased CO 2 concentrations above baseline lead to respiratory acidosis, which causes cardiovascular changes (tachycardia, hypotension, and pulmonary vasoconstriction). Pa co 2 levels more than 80 mm Hg can cause a decreased level of consciousness. The increase in Pa co 2 in these patients postoperatively should be anticipated and monitored. To identify these patients preoperatively, patients with stage II or III COPD should have an analysis of arterial blood gas performed.
Right Ventricular Dysfunction
Right ventricular dysfunction occurs in up to 50% of patients with severe COPD. Chronic recurrent hypoxemia is the cause of right ventricular dysfunction and subsequent progression to cor pulmonale. Cor pulmonale occurs in 70% of adult COPD patients with an FEV 1 less than 0.6 L. Mortality risk in these patients is primarily related to chronic hypoxemia. Administration of oxygen is the only therapy that improves long-term survival and decreases right-sided heart strain associated with COPD. Patients who have a resting Pa o 2 less than 55 mm Hg should receive supplemental oxygen to maintain Pa o 2 at 60 to 65 mm Hg at home.
Bullae
Many patients with moderate or severe COPD develop cystic air spaces in the lung parenchyma known as bullae. These bullae will often be asymptomatic unless they occupy more than 50% of the hemithorax, in which case the patient will present with findings of restrictive respiratory disease in addition to their obstructive disease. A bulla is actually a localized loss of structural support tissue in the lung with elastic recoil of surrounding parenchyma. The pressure in a bulla is the mean pressure in the surrounding alveoli averaged over the respiratory cycle. Whenever positive-pressure ventilation is used, the pressure in a bulla will become positive in relation to the adjacent lung tissue and the bulla will expand with the attendant risk of rupture, tension pneumothorax, and bronchopleural fistula. Positive-pressure ventilation can be used safely in patients with bullae, provided the airway pressures are low and adequate expertise and equipment is immediately available to insert a chest drain and obtain lung isolation if necessary. Nitrous oxide will diffuse into a bulla more quickly than the less soluble nitrogen can diffuse out and may lead to rupture of the bulla. The presence of bullae should be ascertained by examination of chest imaging of any patient with COPD preoperatively.
Flow Limitation
Severe COPD patients are often flow limited, even during normal breathing. Flow limitation occurs when any increase in expiratory effort will not produce an increase in flow at that given lung volume. Flow limitation is present in normal patients only during a forced expiratory maneuver and in patients with COPD as a result of the loss of lung elastic recoil. During positive-pressure ventilation this can lead to the development of an intrinsic positive end-expiratory pressure (auto-PEEP). Severely flow-limited patients are at risk of hemodynamic collapse during positive-pressure ventilation owing to dynamic hyperinflation of the lungs leading to obstruction of pulmonary blood flow.
Perioperative Management
Four treatable complications of COPD must be actively sought and managed at the time of preoperative assessment: atelectasis, bronchospasm, respiratory tract infections, and congestive heart failure. Atelectasis impairs local lung lymphocyte and macrophage function predisposing to infection. Wheezing may be a symptom both of airways obstruction and congestive heart failure. All patients with COPD should receive bronchodilator therapy as guided by their symptoms. If sympathomimetic and anticholinergic bronchodilators provide inadequate therapy, a trial of corticosteroid therapy should be instituted.
COPD patients have fewer postoperative pulmonary complications when intensive chest physiotherapy is initiated preoperatively. Even in patients with severe COPD, exercise tolerance can be improved with physiotherapy at least 1 month or more. Among COPD patients, those with excessive sputum benefit the most from chest physiotherapy. A comprehensive program of pulmonary rehabilitation involving physiotherapy, exercise, nutrition, and education has been shown consistently to improve functional capacity for patients with severe COPD. These programs typically have a duration of several months and are generally not an option in resections for malignancy.
Interstitial Lung Disease
Interstitial lung disease (ILD) is a chronic restrictive pulmonary disease (i.e., FEV 1 < 70% predicted, FEV 1 /FVC ratio normal or increased, and RV decreased). Approximately 35% of ILD is attributable to an identifiable cause, such as exposure to inorganic dust, organic antigen, drugs, or radiation. The inciting agent in the remaining 65% of patients is unknown. In many of these patients, the lung is part of an autoimmune disorder.
Elastic recoil of the lungs increases as a consequence of inflammation and fibrosis of the alveolar walls, which results in decreased lung volumes. Early in the disease, patients adapt to smaller tidal volumes by increasing their respiratory rate. As the disease progresses, increased respiratory effort and energy are required to maintain sufficient tidal volumes to prevent alveolar hypoventilation. Uneven disease distribution throughout the lung can cause significant ventilation/perfusion mismatch and is the primary cause of hypoxemia in patients with ILD.
Controlled ventilation via an endotracheal tube is often the most reliable and safest approach to optimizing oxygenation and ventilation in patients with ILD when a general anesthetic is required. The goal of mechanical ventilation in patients with ILD is to maintain adequate ventilation and oxygenation while minimizing the risks of barotrauma and acute lung injury. Potential strategies to minimize airway pressures include the use of long durations of inspiration compared to the duration of expiration ratios (e.g., ratios of 1:1 to 1:1.5), small tidal volumes, and rapid respiratory rates. In contrast to obstructive lung disease, PEEP can be used safely in ILD.
Cystic Fibrosis
Cystic fibrosis is an autosomal recessive disorder that results in impaired transport of sodium, chloride, and water across epithelial tissue. This leads to exocrine gland malfunction with abnormally viscous secretions, which can cause obstruction of the respiratory tracts, pancreas, biliary system, intestines, and sweat glands. It presents as a mixed obstructive and restrictive lung disease. Inability to clear the thick purulent secretions enhances bacterial growth and, as the disease advances, leads to bronchiectasis. The early mortality of cystic fibrosis is primarily the result of pulmonary complications, including air-trapping, pneumothorax, massive hemoptysis, and respiratory failure. Effective sputum elimination is a key goal in the long-term management of cystic fibrosis. To optimize patients with cystic fibrosis for anesthesia, chest physiotherapy should be performed immediately prior to surgery. Endotracheal intubation with a large endotracheal tube is preferred as it facilitates endobronchial toileting with a suction catheter, bronchoscopy, or both.
Obstructive Sleep Apnea
Clinical Presentation
OSA affects approximately 4% of middle-aged men and 2% of middle-aged women (also see Chapter 50 ). Obesity is the most important physical characteristic associated with OSA, though OSA may be present in patients with a normal body mass index (BMI) and absent in the obese (also see Chapter 29 ).
Patients with risk factors (male gender, middle age, BMI > 28 kg/m 2 , alcohol and sedative use) presenting for surgery should be screened for signs and symptoms of OSA ( Box 27.3 ).
- 1.
Predisposing clinical characteristics:
- •
Body mass index (BMI) ≥ 35 kg/m 2 (or 95th percentile for age and gender)
- •
Neck circumference of ≥17 inches (men) or ≥16 inches (women)
- •
Craniofacial abnormalities affecting the airway
- •
Anatomic nasal obstruction
- •
Tonsils touching or nearly touching in the midline
- •
- 2.
History of apparent airway obstruction during sleep (two or more of the following are present):
- •
Frequent snoring
- •
Observed pauses in breathing during sleep
- •
Awakens from sleep with choking sensation
- •
Frequent arousals from sleep
- •
- 3.
Somnolence:
- •
Frequent somnolence or fatigue despite adequate “sleep”
- •
Falls asleep easily in a nonstimulating environment despite “adequate sleep”
- •
If a patient has signs or symptoms in two or more of the previous categories, there is a significant probability that he or she has obstructive sleep apnea (OSA). The severity of OSA can be determined using a sleep study. In the absence of a sleep study, patients should be treated as though they have moderate sleep apnea unless one of the previous signs or symptoms is severely abnormal (i.e., marked increased BMI) in which case they are classified as having severe sleep apnea.
The pathophysiology of airflow obstruction is related primarily to upper airway pharyngeal collapse. Upper airway patency depends on the action of dilator muscles (i.e., tensor palatine, genioglossus muscle, and hyoid muscles). During sleep, laryngeal muscle tone is decreased and apnea occurs when the upper airway collapses. Nonobese patients may develop OSA as a result of adenotonsillar hypertrophy or craniofacial abnormalities (retrognathia). Recurrent episodes of apnea or hypopnea lead to hypoxia, hypercapnia, increased sympathetic stimulation, and arousal from sleep. Patients may develop cardiopulmonary dysfunction manifesting as systemic or pulmonary hypertension and cor pulmonale. Nonrestoration of sleep can lead to cognitive dysfunction manifesting as intellectual impairment and hypersomnolence.
The diagnosis of OSA can be based on clinical impression or a formal sleep study. OSA should be suspected when a patient with predisposing clinical risk factors reports heavy snoring and excessive daytime sleepiness, which are the cardinal features of OSA. OSA is characterized by frequent episodes of apnea or hypopnea during sleep. Apnea is defined as complete cessation of breathing for 10 seconds or more. Hypopnea is defined as more than 50% decrease in ventilation or oxygen desaturation of more than 3% to 4% for 10 seconds or more. It is definitively diagnosed by polysomnography in a sleep laboratory. The severity of OSA is measured by using the apnea-hypopnea index (AHI), which is the number of apneic or hypopneic episodes occurring per hour of sleep ( Table 27.2 ).
| Adult AHI | Pediatric AHI | OSA Severity | OSA Severity Score |
|---|---|---|---|
| 6-20 | 1-5 | Mild | 1 |
| 21-40 | 6-10 | Moderate | 2 |
| >40 | >10 | Severe | 3 |
Treatment of Obstructive Sleep Apnea
Treatment should include correction of reversible exacerbating factors by means of weight reduction, avoidance of alcohol and sedatives, and nasal decongestants, if needed. Patients with mild OSA can achieve clinical improvement through lifestyle modification. For severe OSA, the three main therapeutic options are continuous positive airway pressure (CPAP), dental appliances, and upper airway surgery.
Preoperative Evaluation of Patients With Obstructive Sleep Apnea
The goals of the preoperative assessment are to identify anticipated difficulties in airway management (difficult ventilation via a face mask, endotracheal intubation, or both) and coexisting cardiovascular disease. Associated medical conditions should be treated, in as much as possible, prior to elective surgery.
- 1.
Airway: Anticipated difficulties with airway management include difficult ventilation via a mask and tracheal intubation.
- 2.
Respiratory system: Patients with obesity will have evidence of restrictive lung disease on pulmonary function testing secondary to decreased chest wall compliance.
- 3.
Cardiovascular system: Preoperative evaluation should be directed toward the detection of end-organ dysfunction resulting from chronic hypoxemia, hypercarbia, and polycythemia. Systemic hypertension, pulmonary hypertension, and signs of biventricular dysfunction (cor pulmonale and congestive heart failure) should be sought.
- 4.
Endocrine and gastrointestinal systems: Fasting blood glucose levels should be sought to screen for type II diabetes. Symptoms of esophageal reflux should lead to aspiration prophylaxis prior to induction of anesthesia. Liver function tests may indicate fatty liver infiltration causing hepatic dysfunction in severe cases.
Perioperative Management
Patients with OSA are exquisitely sensitive to the respiratory depressant and sedative effects of benzodiazepines and opioids, which can cause upper airway obstruction or apnea. These medications should be withheld preoperatively or used with caution in a monitored environment.
Intraoperative anesthetic concerns in patients with OSA relate to (1) airway management; (2) choice of anesthetic technique; (3) patient positioning; (4) monitoring—inaccurate noninvasive blood pressure measurements and significant underlying cardiorespiratory disease warrant insertion of an arterial line for analysis of arterial blood gas monitoring and beat-to-beat blood pressure measurements; and (5) vascular access—difficult intravenous (IV) access secondary to excess adipose tissue may necessitate central line placement.
Upper airway abnormalities or increased airway adiposity in patients with OSA predisposes them as difficult to adequately ventilate with a bag and mask apparatus following induction of anesthesia. Oral and nasopharyngeal airways should be readily available. Excessive pharyngeal adipose tissue can make exposure of the glottic opening difficult during direct laryngoscopy and endotracheal intubation.
Use of short-acting inhaled (sevoflurane and desflurane) and injected (propofol, remifentanil) drugs are recommended for intraoperative use to minimize postoperative respiratory depression. Nitrous oxide is best avoided in patients with coexisting pulmonary hypertension (also see Chapter 7 ). Short- to intermediate-acting neuromuscular blocking drugs (also see Chapter 11 ) can be used for muscle relaxation if required.
The anesthesia provider should consider tracheal extubation with the patient in a semiupright position with an oral or nasopharyngeal airway in place to facilitate spontaneous ventilation. A two-person bag and mask ventilation may be required and possible reintubation of the trachea will be required should acute airway obstruction develop. Administration of supplemental oxygen via a face mask should be provided during transfer of the patient to the postanesthesia care unit (PACU) (also see Chapter 39 ). CPAP must be available for postoperative use in patients on CPAP or bilevel positive airway pressure (BiPAP) preoperatively.
Postoperative Management
Multimodal analgesia with nonsteroidal antiinflammatory drugs (NSAIDs), acetaminophen, and regional analgesia aims to minimize opiate analgesia and resultant respiratory depression. CPAP should be reinstituted postoperatively. Surveillance in a high-dependency unit such as the PACU, step-down unit, or intensive care unit (ICU) is prudent for patients with severe OSA (also see Chapter 39 ).
Postoperative disposition of OSA is influenced by three factors:
- 1.
Severity of the OSA (either by historical information or objective findings of a sleep study) (see Table 27.2 )
- 2.
Invasiveness of the surgical procedure and anesthesia ( Table 27.3 )
Table 27.3
Scoring Invasiveness of Surgery and Anesthesia
Surgery
Anesthesia
Invasive Score
Superficial or peripheral
Local infiltration or peripheral nerve block with no sedation
0
Moderate sedation
Spinal or epidural
1
General anesthetic
2
Major or airway
General anesthetic
3
- 3.
Predicted postoperative opioid use ( Table 27.4 )
Table 27.4
Scoring of Opioid Requirement
Opioid Requirement
Score
None
0
Low-dose oral
1
High-dose oral
2
Parenteral or spinal/epidural
3
A patient with increased perioperative risk of airway obstruction and resultant hypoxemia (perioperative OSA risk score greater than 4) should receive continuous oxygen saturation monitoring in either the ICU, a step-down unit, or telemetry unit ( Box 27.4 ) (also see Chapter 41 ).
OSA Severity Score (1-3)
+
Invasiveness of anesthesia or surgery (1-3)
OR
Postoperative opioid requirement (1-3) (whichever is greater)
If risk score = 4 →increased perioperative risk
If risk score ≥ 5 →significantly increased perioperative risk
OSA, Obstructive sleep apnea.
Obesity Hypoventilation Syndrome
Obesity hypoventilation syndrome (OHS) is defined by chronic daytime hypoxemia (Pa o 2 < 65 mm Hg) and hypoventilation (Pa co 2 > 45 mm Hg) in an obese patient without coexisting COPD. It is a long-term consequence of OSA. Patients exhibit signs of central sleep apnea (apnea without respiratory efforts). This may culminate in the pickwickian syndrome characterized by obesity, daytime hypersomnolence, hypoxemia, and hypercarbia.
Preoperatively, obese patients should be screened for OHS with pulse oximetry. Patients with oxygen saturation less than 96% warrant analysis of arterial blood gases to assess carbon dioxide retention.
Ultimately, the information obtained from preoperative investigations allows the anesthesia provider to optimize the patient’s clinical status prior to elective surgery and plan perioperative care, including arrangements for appropriate postoperative monitoring (i.e., step-down bed, ICU). Interventions may include treatment of coexisting conditions (systemic hypertension, cardiac dysrhythmias, congestive heart failure) and initiation of CPAP. A 2-week period of CPAP therapy is usually quite effective in correcting the abnormal ventilatory drive of patients with OHS.
Pulmonary Hypertension
Pathophysiology
Patients with pulmonary hypertension (mean pulmonary artery pressure > 25 mm Hg by catheterization or systolic pulmonary artery pressure > 50 mm Hg on echocardiography) may present for a variety of noncardiac surgical procedures. Patients with pulmonary hypertension are at increased risk of respiratory complications and prolonged intubation after noncardiac surgery.
Preoperative Evaluation
There are two commonly encountered types of pulmonary hypertension: pulmonary hypertension from left-sided heart disease and pulmonary hypertension from lung disease. Patients who present for noncardiac surgery are more likely to have pulmonary hypertension because of lung disease. Much of what has been learned about anesthesia for patients with pulmonary hypertension owing to lung disease has come from clinical experience in pulmonary endarterectomies and lung transplantation. Avoiding hypotension is the key to managing these patients ( Box 27.5 ).
- •
Avoid hypotensive and vasodilating anesthetic drugs whenever possible
- •
Ketamine does not exacerbate pulmonary hypertension
- •
Support mean blood pressure with vasopressors: norepinephrine, phenylephrine, vasopressin
- •
Use inhaled pulmonary vasodilators (nitric oxide, prostacyclin) in preference to intravenous vasodilators as needed
- •
Use thoracic epidural local anesthetics cautiously and with inotropes as needed
- •
Monitor cardiac output if possible
Management of Anesthesia
The increased right ventricular transmural and intracavitary pressures associated with pulmonary hypertension may restrict perfusion of the right coronary artery during systole, especially as pulmonary artery pressures approach systemic levels. The impact of pulmonary hypertension on right ventricular dysfunction has several anesthetic implications. The hemodynamic goals are similar to other conditions in which cardiac output is relatively fixed. Care should be taken to avoid physiologic states that will worsen pulmonary hypertension, such as hypoxemia, hypercarbia, acidosis, and hypothermia. Conditions that impair right ventricular filling, such as tachycardia and arrhythmias, are not well tolerated. Ideally, under anesthesia, right ventricular contractility and systemic vascular resistance are maintained or increased while pulmonary vascular resistance is decreased. Ketamine is a useful anesthetic in pulmonary hypertension due to lung disease. Inotropes and inodilators, such as dobutamine and milrinone, may improve hemodynamics in patients with pulmonary hypertension due to left-sided heart disease; however, they decrease systemic vascular tone and tachycardia and can lead to a deterioration in the hemodynamics of patients with pulmonary hypertension due to lung disease. Vasopressors such as phenylephrine, norepinephrine, and vasopressin are commonly used to maintain a systemic blood pressure greater than pulmonary pressures. Vasopressin can increase systemic blood pressure significantly without affecting pulmonary artery pressure in patients with pulmonary hypertension. In patients with severe pulmonary hypertension, selective inhaled pulmonary vasodilators, including nitric oxide (10 to 40 ppm) or nebulized prostaglandins (prostacyclin 50 ng/kg/min), should be considered.
Lumbar epidural analgesia and anesthesia have been used in obstetric patients with pulmonary hypertension, and occasionally thoracic epidural analgesia is used in patients with pulmonary hypertension (also see Chapter 23 ). Patients with pulmonary hypertension due to lung disease seem to be extremely dependent on tonic cardiac sympathetic innervation for normal hemodynamic stability. These patients will often require a low-dose infusion of inotropes or vasopressors during thoracic epidural local analgesia.
Anesthesia for Lung Resection
Thoracic surgery is a relatively young specialty that has been significantly aided by the development of positive-pressure ventilation in the early 1950s, and advanced by the use of double-lumen endobronchial tubes (DLTs) and flexible bronchoscopes. These developments now enable a thoracic anesthesiologist to employ reliable lung isolation allowing surgical access to the thorax and managing anesthesia during one-lung ventilation (OLV).
Preoperative Assessment for Pulmonary Resection
Preoperative assessment prior to pulmonary resection aims to identify patients at increased risk of perioperative morbidity and mortality in order to focus resources and improve their outcome. Postoperative preservation of respiratory function is proportional to the amount of lung parenchyma preserved. The major causes of perioperative morbidity and mortality risks in the thoracic surgical population are respiratory complications. Major respiratory complications, such as atelectasis, pneumonia, and respiratory failure, occur in 15% to 20% of patients and account for much of the 3% to 4% mortality rate. Objective measures of pulmonary function are required to guide anesthetic management and to transmit information easily between members of the health care team.
Objective Assessment of Pulmonary Function
No test of respiratory function is adequate as a sole preoperative assessment. Before surgery, respiratory function should be assessed in three related but independent areas: respiratory mechanics, gas exchange, and cardiorespiratory interaction ( Fig. 27.3 ). This “three-legged stool” approach can be used to plan intraoperative and postoperative management.
Respiratory Mechanics
Of all objective measures obtained via spirometry (e.g., FVC, FEV 1 , ratio of FEV 1 :FVC), the FEV 1 is most helpful. Spirometry measurements should be expressed as a percent of predicted volume corrected for age, sex, and height (e.g., an FEV 1 of 74%). The predicted postoperative FEV 1 (ppoFEV 1 %) is the most effective test for prediction of postthoracotomy respiratory complications. It is calculated as follows:
ppoFEV1%=preoperativeFEV1%×(100−%offunctionaltissueremoved/100)
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