The hallmark of COPD is the evidence of a productive cough and a progressive decrease in the patient’s exercise tolerance. Three major diseases are part of COPD: asthma, emphysema, and chronic bronchitis.² All are characterized by airway obstruction. These diseases may have medically reversible components, such as bronchospasm, or they may have irreversible components, such as alveolar septal destruction. Some of the reversible components of asthma, such as retained secretions, bronchospasms, and infections, can be corrected with the interaction of the physician, nurse, physical therapist, and respiratory therapist. The treatment of asthma can include oxygen therapy, bronchodilators, chest physiotherapy, and proper hydration.

Chronic bronchitis is associated with chronic cigarette smoking. The nurse can contribute greatly to the patient’s future health with strong influences to refrain from smoking.³ Other therapy for the reversible components can include the use of bronchodilators, chest physiotherapy, and oxygen.

The patient with emphysema usually has airway destruction that is irreversible. As the alveolar septa are destroyed, insufficient alveolar ventilation ensues and eventually leads to hypercarbia. As the disease progresses, carbon dioxide cannot be expelled from the lungs and is retained there. The patient usually increases minute ventilation to try to compensate for the hypercarbia. Respiratory acidosis develops slowly as the various acid-base buffer systems try to neutralize the accumulated acid. In this compensated state, the patient usually has a near-normal pH, high plasma bicarbonate, low chloride concentration, and high total carbon dioxide levels. The PaCO₂ usually is low because some inspired oxygen is unable to cross into the blood from the lungs because of the decreased respiratory diffusion membrane surface area in the lungs. Pulmonary hypertension usually appears as the disease progresses. Cor pulmonale may develop, and because of the pulmonary venous engorgement, the right heart may begin to fail. The patient with emphysema who has irreversible destruction can be treated with chest physiotherapy, bronchodilators, and steroids.

Cigarette smoking as A precursor to the development of COPD

Cigarette smoking has been well established as one of the major precursors to chronic bronchitis and emphysema—two of the three disease components of COPD. Cigarette smoking affects the manner in which a patient recovers from an anesthetic.⁴^,⁵ The perianesthesia nurse should be aware of the diverse reactions that smoking can have on the patient who is emerging from an inhalation anesthetic. Studies on the relationship between smoking and its effects on anesthesia indicate an increase in the risk factor in the patient who smokes. Although the incidence rate of smoking is decreasing slowly, it continues to rise in the teenage population.

Respiratory effects of smoking

A growing body of convincing scientific literature suggests that almost all pulmonary disease is related in some way to the inhalation of infectious or irritant particulate material. Cigarette smoke in its gaseous phase contains nitrogen, oxygen, carbon dioxide, carbon monoxide, hydrogen, argon, methane, hydrogen cyanide, ammonia, nitrogen dioxide, and acetone. In the particulate phase, cigarette smoke contains nicotine, tar, acids, alcohol, phenols, and hydrocarbons. The bottom line is that cigarette smoke contains oxidants, and the oxidants can damage cells and the extracellular matrix components of the lung, leading to significant damage to the tissue in the lungs. Smokers who inhale nicotine from a cigarette into the lungs actually receive 25% to 30% of the nicotine contained in the cigarette. Thirty percent is destroyed with combustion, and 40% is lost in the side stream. Therefore, if a person inhales the smoke from a cigarette that contains 2.5 mg of nicotine, 1 mg of nicotine is actually absorbed by the lungs. In addition, filters are known to make little difference in this absorption. Contrary to some opinions, the smoking of cigars and pipes also presents a risk for pulmonary disease.⁶ Carbon monoxide combines with the hemoglobin molecule at the same point as oxygen does. It has an affinity for this receptor point that is 210-fold greater than that of oxygen⁷; therefore the oxygen-carrying capacity of hemoglobin is reduced, and the end result is that less oxygen is relinquished to the tissues by the hemoglobin. When carbon monoxide combines with hemoglobin, a compound called carboxyhemoglobin is formed. The amount of carboxyhemoglobin in the blood is especially important in the patient who has a diseased myocardium, because myocardial oxygenation is limited by the flow of the blood through the coronary arteries. During stress, such as in surgery and anesthesia, the amount of carboxyhemoglobin saturation could lead to severe myocardial hypoxia in patients who smoke heavily and have coronary artery disease because the diseased coronary arteries cannot increase the flow significantly. The only means of prevention of hypoxia is an increase in the extraction of oxygen from the hemoglobin. Small amounts of carboxyhemoglobin can hinder the uncoupling of the oxygen and thus result in yet more oxygen retention at any given tension. This effect clearly is greater when the oxygen tension is further reduced by local ischemia and any additional vasoconstriction associated with smoking.

Smoking is an important causative factor in chronic pulmonary disease, especially the obstructive type.⁸ The characteristic pulmonary function alterations in smokers usually include a reduction in vital capacity, an increase in residual volume to total lung capacity, an uneven distribution of inspired gas, a decrease in dynamic compliance, and an increase in nonelastic resistance. Most critically, chronic cigarette smoking ultimately causes the forced expiratory volume in the first second (FEV₁) to be less that 80% of normal, a critical sign of COPD.

Chronic bronchitis is the disease most often associated with smoking and is seen often by the perianesthesia nurse. Hypertrophy of bronchial mucous glands with production of excessive mucus is the hallmark of this disease. A vicious cycle develops as this failure to remove the mucus leads to retention of pathogenic organisms and irritants. The resulting distorted alveolar septa and the increased pressure on the alveoli from chronic bronchitis can lead to emphysema.

Cigarette smoke can cause a progression from hyperplasia to metaplasia to neoplasia in the lungs. Eaton-Lambert syndrome is sometimes associated with bronchial carcinoma and is often called the myasthenic syndrome because its symptoms resemble those of myasthenia gravis (MG). This syndrome in some way affects neuromuscular transmission, and patients have the classic symptoms of muscle weakness. These patients are especially sensitive to the skeletal neuromuscular blocking agents used in clinical anesthesia. If the anesthetist is unaware of this syndrome and administers the normal dose of skeletal muscle relaxants, the patient will probably be unable to breathe spontaneously on emergence from anesthesia, even when pharmacologic reversal of the muscle relaxant is attempted. In this situation, postoperative mechanical ventilation is necessary.

Cardiovascular effects of smoking

The correlation between vascular disease and smoking is strong. Smoking can influence thrombosis, and because thrombi and platelets contribute to the development of arteriosclerosis, smoking can contribute to arteriosclerosis and its complications.

Inhalation of nicotine produces a release of catecholamines, activates the carotid and aortic chemoreceptor bodies, and directly stimulates the muscles of the vessel walls. As a result, the immediate effects of smoking even a small number of cigarettes can be fairly marked, with production of increases in heart rate, peripheral resistance, cardiac workload, and blood pressure. Each of these actions causes a greater myocardial oxygen demand. Furthermore, because the smoker’s hemoglobin can provide less oxygen to the myocardium, smoking can cause cardiac arrhythmias, either through myocardial anoxia or epinephrine release.

Surgical considerations

The incidence rate of pulmonary complications in patients who have undergone abdominal or thoracic surgery is high. Changes occur in the pulmonary status of the patient who undergoes anesthesia and surgery. In the postoperative phase, these changes are characterized by gradual or abrupt alveolar collapse. The patient with COPD, when subjected to surgery, then represents an even higher risk for postoperative complications. These patients must be given meticulous preoperative care so that they are in the best possible health when they enter surgery. This preoperative medical treatment usually includes hydration, nutrition, chest physiotherapy, bronchodilators, and prophylactic antibiotics if an infection is present. Serial pulmonary function tests and arterial blood gas determinations are used to monitor the progression of the preoperative treatment.⁷

When the patient’s pulmonary function reaches a peak before surgery (i.e., when the pulmonary function test and arterial blood gas test results no longer show continued improvement), surgery is considered because the patient has reached optimal pulmonary status.

Care of the COPD patient

Perianesthesia care focuses on prevention of complications. The modified stir-up regimen should include frequent cascade coughing, sustained maximal inspirations (SMIs), and repositioning of the patient (see Chapters 12 and 28). An appropriately implemented modified stir-up regimen is of great importance, especially in patients who are recovering from upper abdominal or thoracic operations. Surgery at these sites can cause decreased ventilatory effort and a complete absence of sighs by the patient. Given that the patient already has compromised respiratory function, the possibility of retained secretions and atelectasis is magnified. As a result, these patients represent a significant challenge to the perianesthesia nurse (Box 48-1).

BOX 48-1 Risk Reduction Strategies to Decrease the Incidence of Postoperative Complications in Patients with COPD

Preoperative

• Encourage cessation of smoking for at least 8 weeks.

• Treat evidence of expiratory airflow obstruction (e.g., bronchodilator therapy).

• Treat respiratory infection with appropriate antibiotics.

• Initiate patient education regarding lung volume expansion maneuvers.

Intraoperative

• Use minimally invasive surgical (laparoscopic) techniques when possible.

• Consider using regional anesthesia.

• Avoid the use of long-acting neuromuscular blocking drugs.

• Avoid surgical procedures longer than 3 hours.

Postoperative

• Continue tracheal intubation and mechanical ventilation (likely after abdominal or intrathoracic surgery and a preoperative PaCO₂ > 50 mm Hg and FEV₁/FVC < 0.5; maintain PaO₂ at 60 to 100 mm Hg and PaCO₂ in a range that maintains the pH at 7.35 to 7.45).

• Institute lung-volume expansion maneuvers (voluntary deep breathing, incentive spirometry, continuous positive airway pressure).

• Use chest physiotherapy.

• Maximize analgesia (neuraxial opioids, intercostals nerve blocks, patient-controlled analgesia).

FEV₁, Forced expiratory volume in the first second; FVC, forced vital capacity.

From Stoelting RK, Dierdoff SF: Handbook for anesthesia and co-existing disease, ed 2, New York, 2002, Churchill Livingstone; Data from Smetana GW: Preoperative pulmonary evalution, N Engl J Med 340:93−944, 1999.

When the patient is completely reactive from anesthesia, the use of the incentive spirometer may be helpful in reducing the incidence of atelectasis. Consequently, the perianesthesia nurse who is responsible for supportive measures should assist and encourage the patient in using the SMI with or without the incentive spirometer. On the basis of subjective research findings, if the perianesthesia nurse explains the rationale of the SMI maneuver and properly instructs the patient in the use of the technique before surgery, the patient is more likely to correctly use the SMI maneuver after surgery with or without coaching. The performance of the SMI maneuver, with or without mechanical devices, should be monitored by the nurse to ensure proper production of a sustained inspiration with a 3-second inspiratory hold. The perianesthesia nurse should also encourage and monitor the patient’s performance of the cascade cough to facilitate early secretion clearance.

Patients with COPD have some component of reactive airways disease. Consequently, the airway becomes compliant and can become compressed during a forced expiratory maneuver. This dynamic compression of the airways is a function of the equal pressure point theory, as discussed in Chapter 12. To reduce the amount of dynamic compression of the airway during exhalation, the patient should be encouraged to use pursed-lip breathing. Breathing through pursed lips during exhalation can be the same as adding 5 to 10 cm H₂O of positive end-expiratory pressure. Increasing the pressure inside the airway during exhalation reduces the amount of dynamic compression of the airways and decreases the amount of air trapping that commonly occurs in patients with COPD.

Audible wheezing will require the use of a fast-acting bronchodilator such as albuterol. Arterial blood gases may be ordered, and capnography may be used to monitor end-tidal CO₂.⁹

The cardiac status should be monitored meticulously because of the frequent involvement of the heart in the pathologic disorders of these patients. Kidney function should also be monitored because it may be altered, especially in patients with fluid retention and edema of the extremities.

The patient with severe COPD who has marked hypercarbia can present difficulties in the PACU. Patients who have severe emphysema usually fit into this category. Ventilatory effort in these patients is stimulated by the hypoxic drive, in which lack of oxygen stimulates ventilation. Hypoxia indirectly stimulates the respiratory center by means of chemoreceptors in the carotid bodies located at the bifurcation of the carotid artery. When the patient receives 100% oxygen to breathe in the PACU, oxygen tensions rise in the inspired gas; the carotid and aortic chemoreceptors cease to function; and the patient quickly becomes apneic. The patient’s respiratory status should be assessed carefully and the physician consulted before 100% oxygen is administered. Mist therapy after surgery aids in liquefying the secretions and helps in the all-important maintenance of a patent tracheobronchial tree. If excessive bronchial drainage is not removed, it provides a convenient avenue for bacteria and might also obstruct the airways, thus leading to insufficient alveolar ventilation and hypoxia.

The patient with COPD should be under constant surveillance for signs of cardiopulmonary decompensation, including shallow rapid gasping respirations, severe dyspnea, substernal retraction, and disorientation. Blood pressure may be elevated or low, but the patient usually has tachycardia, fever, and muscle rigidity. Cyanosis may be present.

Patients who are cigarette smokers have significant postanesthesia risks.⁶ Cigarette smokers who have smoked for a long period of time and have an FEV₁ less than 80% usually have an increased risk of pulmonary complications in comparison with nonsmokers. Patients who smoke more than two packs of cigarettes per day are especially prone to perianesthetic complications. In addition, patients who have had a long history of smoking (>20 pack years) and are presently in a nonsmoking situation still can have pulmonary complications. Many of these complications develop when cigarette smokers have a preexisting chronic respiratory disease, usually bronchitis. The major postoperative complications associated with smoking are infection, atelectasis, pleural effusion, pulmonary infarction, and bronchitis.

Complications associated with chronic cigarette smoking revolve around the inability of the patient to clear secretions. The goal of nursing care in the PACU centers on clearing the tracheobronchial tree, which necessitates frequent suctioning, cascade coughing, and the SMI maneuver. If rales and rhonchi are heard on auscultation, percussion and postural drainage should be initiated.

Because cardiovascular disease is associated with a long history of cigarette smoking, the patient should have continuous electrocardiographic monitoring. Arrhythmias, such as premature ventricular contractions, should be addressed because they may be the first signs of decreased myocardial oxygenation in the cigarette smoker.

Respiratory depressant drugs, such as opioids, should be given in low doses, or they should be avoided completely if the COPD is severe. Repositioning of the patient and splinting of the incision site, in addition to reducing the anxiety usually seen in these patients, reduces the need for opioids. Some form of regional analgesia may be beneficial for these patients.⁸