1 Define chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a spectrum of diseases that includes emphysema, chronic bronchitis, and asthmatic bronchitis. It is characterized by progressive increased resistance to breathing. Airflow limitation may be caused by loss of elastic recoil or obstruction of small or large (or both) conducting airways. The increased resistance may have some degree of reversibility. Cardinal symptoms are cough, dyspnea, and wheezing.

2 What are the features of asthma and asthmatic bronchitis?

Asthma

This heterogeneous disorder is characterized by reversible airway obstruction.

Precipitating factors include exercise, dander, pollen, and intubation.

Symptoms improve with bronchodilator and immunosuppressive therapy.

Asthmatic bronchitis

It consists of airway obstruction, chronic productive cough, and episodic bronchospasm.

It can result from progression of asthma or chronic bronchitis.

There is less improvement with bronchodilator therapy; some degree of airway obstruction at all times.

3 Describe chronic bronchitis and emphysema

Chronic bronchitis: Characterized by cough, sputum production, recurrent infection, and airway obstruction for many months to several years. Patients with chronic bronchitis have mucous gland hyperplasia, mucus plugging, inflammation and edema, peribronchiolar fibrosis, airway narrowing, and bronchoconstriction. Decreased airway lumina caused by mucus and inflammation increase resistance to flow of gases.

Emphysema: Characterized by progressive dyspnea and variable cough. Destruction of the elastic and collagen network of alveolar walls without resultant fibrosis leads to abnormal enlargement of air spaces. In addition, the loss of airway support leads to airway narrowing and collapse during expiration (air trapping).

4 List contributory factors associated with the development of chronic obstructive pulmonary disease

Smoking: Smoking impairs ciliary function, depresses alveolar macrophages; leads to increased mucous gland proliferation and mucus production; increases the inflammatory response in the lung; leading to increased proteolytic enzyme release; reduces surfactant integrity; and causes increased airway reactivity.

Occupational and environmental exposure: Animal dander, toluene and other chemicals, various grains, cotton, and sulfur dioxide and nitrogen dioxide in air pollution.

Recurrent infection: Bacterial, atypical organisms (mycoplasma), and viral (including human immunodeficiency virus, which can produce an emphysema-like picture).

Familial and genetic factors: A predisposition to COPD exists and is more common in men than women. α₁-antitrypsin deficiency is a genetic disorder resulting in autodigestion of pulmonary tissue by proteases and should be suspected in younger patients with basilar bullae on chest x-ray film. Smoking accelerates its presentation and progression.

5 What historical information should be obtained before surgery?

Smoking history: number of packs per day and duration in years

Dyspnea, wheezing, productive cough, and exercise tolerance

Hospitalizations for COPD, including the need for intubation and mechanical ventilation

Medications, including home oxygen therapy and steroid use, either systemic or inhaled

Recent pulmonary infections, exacerbations, or change in character of sputum

Weight loss that may be caused by end-stage pulmonary disease or lung cancer

Symptoms of right-sided heart failure, including peripheral edema, hepatomegaly, jaundice, and anorexia secondary to liver and splanchnic congestion

6 What features distinguish pink puffers from blue bloaters?

7 List abnormal physical findings in patients with chronic obstructive pulmonary disease

Tachypnea and use of accessory muscles

Distant or focally diminished breath sounds, wheezing, or rhonchi

Jugular venous distention, hepatojugular reflux, and peripheral edema suggest right heart failure

Palpation of peripheral pulses is an indirect measure of stroke volume

8 What laboratory examinations are useful?

White cell count and hematocrit: Elevation suggests infection and chronic hypoxemia, respectively.

Electrolytes: Bicarbonate levels are elevated to buffer a chronic respiratory acidosis if the patient retains carbon dioxide. Hypokalemia can occur with repeated use of β-adrenergic agonists.

Chest x-ray film: Look for lung hyperinflation, bullae or blebs, flattened diaphragm, increased retrosternal air space, atelectasis, cardiac enlargement, infiltrate, effusion, masses, or pneumothorax.

Electrocardiogram: Look for decreased amplitude, signs of right atrial (peaked P waves in leads II and V₁) or ventricular enlargement (right axis deviation, R/S ratio in V₆ ≤1, increased R wave in V₁ and V₂, right bundle-branch block), and arrhythmias. Atrial arrhythmias are common, especially multifocal atrial tachycardia and atrial fibrillation.

Arterial blood gas: Hypoxemia, hypercarbia, and acid-base status, including compensation, can be evaluated.

Spirometry is discussed in Chapter 9.

9 How does a chronically elevated arterial carbon dioxide partial pressure affect the respiratory drive in a person with chronic obstructive pulmonary disease?

Persons with COPD have a reduced ventilatory drive in response to levels of carbon dioxide (CO₂). Chronically elevated arterial carbon dioxide partial pressure (PaCO₂) produces increased cerebrospinal fluid bicarbonate concentrations. The respiratory chemoreceptors at the medulla become “reset” to a higher concentration of CO₂. Thus diminished ventilatory drive secondary to CO₂ exists. In these patients ventilatory drive may be more dependent on PO₂.

10 What are the deleterious effects of oxygen administration in these patients?

Inhalation of 100% oxygen may increase ventilation-perfusion mismatch by inhibiting hypoxic pulmonary vasoconstriction (HPV). HPV is an autoregulatory mechanism in the pulmonary vasculature that decreases blood flow to poorly ventilated areas of the lung, ensuring that more blood flow is available for gas exchange in better ventilated areas of the lung. Inhibition of HPV results in increased perfusion of poorly ventilated areas of lung, contributing to hypoxemia and/or hypercarbia. It is prudent to always administer the minimum oxygen necessary to achieve the desired goal, perhaps a pulse oximetry value between 90% and 95%.

11 How do general anesthesia and surgery affect pulmonary mechanics?

Vital capacity is reduced by 25% to 50%, and residual volume increases by 13% following many general anesthetics and surgical procedures. Upper abdominal incisions and thoracotomy affect pulmonary mechanics the greatest, followed by lower abdominal incisions and sternotomy. Expiratory reserve volume decreases by 25% after lower abdominal surgery and 60% after upper abdominal and thoracic surgery. Tidal volume decreases 20%, and pulmonary compliance and functional residual capacity decrease 33%. Atelectasis, hypoventilation, hypoxemia, and pulmonary infection may result. Many of these changes require a minimum of 1 to 2 weeks to resolve.

12 What factors are associated with an increased perioperative morbidity or mortality?

Increased morbidity results from hypoxemia, hypoventilation resulting in acute hypercarbia, pulmonary infection, prolonged intubation, and mechanical ventilation. Intensive care days and overall hospitalization are prolonged, and mortality is increased.

Patients presenting for lobectomy or pneumonectomy must have pulmonary function and arterial blood gas values that are superior to the values in Table 40-1. If any of the aforementioned criteria are not satisfied, further preoperative testing is indicated to determine the risk-benefit ratio for lung resection. Further tests include split-lung function, regional perfusion, regional ventilation, regional bronchial balloon occlusion, and pulmonary artery balloon occlusion studies. A forced expiratory volume in 1 second (FEV₁) less than 800 ml in a 70-kg person is probably incompatible with life and is an absolute contraindication to lung resection because of the high incidence for extended mechanical ventilation.

13 List the common pharmacologic agents used to treat COPD and their mechanisms of action

See Table 40-2.

TABLE 40-2 Agents used to Treat Chronic Obstructive Pulmonary Disease

cAMP, Cyclic adenosine monophosphate; cGMP, cyclic guanosine monophosphate.

14 What therapies are available to reduce perioperative pulmonary risk?

Stop smoking.

Cessation for 48 hours before surgery decreases carboxyhemoglobin levels. The oxyhemoglobin dissociation curve shifts to the right, allowing increased tissue oxygen availability.

Cessation for 4 to 6 weeks before surgery has been shown to decrease the incidence of postoperative pulmonary complications.

Cessation for 2 to 3 months before surgery results in all of the previous benefits plus improved ciliary function, improved pulmonary mechanics, and reduced sputum production.

Optimize pharmacologic therapy. Continue medications even on the day of surgery.

Recognize and treat underlying pulmonary infection.

Maximize nutritional support, hydration, and chest physiotherapy.

Institute effective postoperative analgesia, allowing the patient to cough effectively, take large tidal volumes, and ambulate early after surgery.

15 Do advantages exist with regional anesthesia techniques in patients with chronic obstructive pulmonary disease?

Regional anesthesia, including extremity and neuraxial blockade, avoids endotracheal intubation. However, spinal or epidural blockade above the T10 dermatome may reduce effective coughing secondary to abdominal muscle dysfunction, leading to decreased sputum clearance and atelectasis. Concerning brachial plexus anesthesia, pneumothorax or blockade of the phrenic nerve, causing hemidiaphragmatic paralysis, is a risk. Sedation administered during or after these procedures may depress respiratory drive and should be titrated to effect.

Local anesthetics infused through catheters placed into the brachial plexus sheath or the lumbar and thoracic epidural space provide superior postoperative analgesia. Neuraxial techniques improve pulmonary mechanics and opioids can be administered at much lower doses and with less sedation when compared to other parenteral routes.

16 What agents can be used for induction and maintenance of general anesthesia?

The standard induction agents can all be used safely. Ketamine produces bronchodilation secondary to its sympathomimetic effects by direct antagonism of bronchoconstricting mediators, but secretions increase remarkably. Anecdotal evidence exists of bronchodilating properties from propofol. Intravenous lidocaine given before intubation can help blunt airway reflexes.

All volatile anesthetics produce bronchodilation. Desflurane is an airway irritant, although once the patient is intubated this is rarely a problem; it has the advantage of rapid clearance once discontinued.

Nitrous oxide increases the volume and pressure of blebs or bullae, thereby increasing the risk of barotrauma and pneumothorax. In addition, it may increase pulmonary vascular resistance and pulmonary artery pressures. This would be especially deleterious in patients with coexisting pulmonary hypertension or cor pulmonale. Therefore nitrous oxide should be avoided in patients with COPD.

17 Discuss the particular concerns regarding muscle relaxation (and reversal) in patients with chronic obstructive pulmonary disease

Atracurium and d-tubocurarine produce histamine release and might best be avoided. Succinylcholine also produces histamine release, and the benefits and risks of rapid paralysis and endotracheal intubation must be evaluated when considering its use.

Anticholinesterases (neostigmine and edrophonium) reverse the effects of nondepolarizing relaxants. Theoretically they may precipitate bronchospasm and bronchorrhea secondary to stimulation of postganglionic muscarinic receptors. However, clinically bronchospasm is rarely seen after administration of these agents, possibly because anticholinergic agents (atropine or glycopyrrolate) are concurrently administered.

18 Discuss the choice of opioids in these patients

Opioids blunt airway reflexes and deepen anesthesia. Morphine produces histamine release and should be used with caution. Hydromorphone, fentanyl, sufentanil, and remifentanil do not cause histamine release. Always consider the residual respiratory depressant affects of opioids at the end of surgery.

19 Define auto-PEEP

Air trapping is known as auto-PEEP (positive end-expiratory pressure) and results from “stacking” of breaths when full exhalation is not allowed to occur. Auto-PEEP results in impairment of oxygenation and ventilation aand hemodynamic compromise by decreasing preload and increasing pulmonary vascular resistance. Increasing expiratory time reduces the likelihood of auto-PEEP. This can be accomplished by increasing the expiratory phase of ventilation and decreasing the respiratory rate.

20 Form a differential diagnosis for intraoperative wheezing

Bronchoconstriction (but remember: all that wheezes is not asthma)

Mechanical obstruction of the endotracheal tube by secretions or kinking

Aspiration of gastric contents or of a foreign body (i.e., a dislodged tooth)

Endobronchial intubation (most commonly right mainstem intubation)

Inadequate anesthesia

Pulmonary edema (cardiogenic and noncardiogenic)

Pneumothorax

Pulmonary embolus

21 How would you treat intraoperative bronchospasm?

Administer 100% oxygen and manually ventilate, allowing sufficient expiratory time. Identify and correct the underlying condition as discussed in Question 20.

Administer therapy:

Relieve mechanical obstructions.

Increase the volatile anesthetic agents and/or administer intravenous lidocaine, ketamine, or propofol.

Administer β-adrenergic agonists: aerosolized via the endotracheal tube (e.g., albuterol), subcutaneously (e.g., terbutaline), or intravenously (e.g., epinephrine or terbutaline).

Administer anitcholinergic bronchodilators: aerosolized via the endotracheal tube (e.g., ipratropium) or intravenously (e.g., atropine or glycopyrrolate).

Intravenous aminophylline and corticosteroids are also suggested therapies.

Although controversial, extubation may be beneficial because the endotracheal tube may be a stimulus for bronchoconstriction.

22 What factors may determine the need for postoperative mechanical ventilation?

Patients who exhibit a resting PaCO₂ >45 to 50, FEV₁ <1 L, forced vital capacity (FVC) <50% to 70% of predicted, or FEV₁/FVC <50% may require postoperative ventilation, especially for upper abdominal and thoracic surgeries. Consider how well the patient was prepared before surgery, the respiratory rate and work of breathing, the tidal volume and negative inspiratory force generated by the patient, arterial blood gas parameters, and body temperature. Is there residual neuromuscular blockade or effects of anesthetic agents? Is analgesia satisfactory?

23 Should H₂-receptor antagonists be avoided in patients with chronic obstructive pulmonary disease?

H₁-receptor stimulation results in bronchoconstriction and H₂-receptor stimulation results in bronchodilation. Theoretically H₂-receptor antagonists would result in unopposed H₁-receptor stimulation, causing bronchoconstriction. Many patients with COPD take corticosteroids, have symptoms of gastritis or peptic ulcers, and receive H₂ antagonists. Use of H₂-receptor antagonists should be individualized, and the patients observed for adverse side effects.

24 At the conclusion of surgery, should a patient with chronic obstructive pulmonary disease be extubated deep or awake?

Perhaps the better question is: can the surgical procedure be performed under regional anesthesia, avoiding endotracheal anesthesia altogether? If general anesthesia is required, perhaps a mask anesthetic or use of the laryngeal mask airway would limit the stimulation inherent in endotracheal intubation.

In an intubated patient with reactive airway disease, airway reflexes may be blunted through use of lidocaine (intravenous or intratracheal) and aerosolized β-adrenergic agonists. Selected patients may be candidates for deep extubation. Patients at risk for aspiration and those with difficult airways are not candidates for deep extubation. Typically deep extubation is accomplished with the patient breathing spontaneously, deeply anesthetized with a volatile agent, with airway reflexes suppressed. Deep extubation is not a 100% guarantee against bronchospasm as the patient awakens further.