Postoperative pulmonary complications (POPCs) such as exacerbation of preexisting lung disease, pneumonia, and/or respiratory failure are as prevalent as cardiac complications and contribute to morbidity, mortality, and increased length of hospital stay. Although more research is needed, currently the risk factors for POPCs can be broadly classified into patient related and procedure related. POPCs can be reduced in all types of procedures by identifying patients at risk, optimizing their medical therapy preoperatively, performing vigilant intraoperative care, and by delivering aggressive postoperative care emphasizing analgesia and lung expansion.

A. Evidence from a meta-analysis supports risk reduction for specific patients (see section III.A.1)

B. Procedure-related risk factors include

1. General anesthesia

2. Emergency surgery

3. Surgery lasting more than 3 hours

4. Surgical site (abdominal, thoracic, head and neck, vascular, and neurosurgery)

C. Recommended postoperative interventions for those at risk include using lung expansion maneuvers and using nasogastric tubes selectively (see section VIII)

A. Obstructive airway diseases are characterized by abnormal expiratory gas flow rates. The airflow limitation can be structural or functional. The mechanism of hypoxemia in obstructive disease is primarily through regional mismatching of ventilation and perfusion ([V with dot above]/[Q with dot above] mismatch). Dyspnea, a major symptom, is multifactorial in origin but is in large part related to loading of the respiratory muscles.

1. Chronic obstructive pulmonary disease (COPD) is a slowly progressive obstructive lung disease involving the airways and/or pulmonary parenchyma, resulting in a gradual loss of lung function. COPD doubles the risk of POPCs and is associated with increased postoperative cardiac and renal complications. It is generally classified as being attributable to either emphysema (“pink puffer”) or chronic bronchitis (“blue bloater”). Although these often coexist, below they are considered as separate entities.

a. Emphysema is due to abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destructive changes of the alveolar wall. This leads to loss of the normal elastic recoil of the lung with subsequent premature airway closure at higher than normal lung volumes during exhalation.

b. Chronic bronchitis is defined as the presence of productive cough for at least 3 months in each of 2 successive years in a person in
whom the excessive secretions are not due to other diseases. The most common precipitant is cigarette smoking.

2. Asthma is a complex and heterogeneous syndrome characterized by variable airflow obstruction, airway inflammation, and increased airway responsiveness to a variety of stimuli that include exercise, cooling, drying and/or instrumentation of the airways, infection, medications, and occupational exposure.

3. Cystic fibrosis (CF) involves the secretion of highly viscous mucus. This results in airway obstruction, fibrosis, chronic pulmonary infection, and cachexia. Late changes include pneumothorax and bronchiectasis with hemoptysis, hypoxemia, carbon dioxide retention, and respiratory failure.

B. Restrictive pulmonary disease is characterized by a decrease in lung compliance and may be intrinsic or extrinsic. Airway resistance is usually normal, whereas lung volumes and diffusing capacity are reduced. As in obstructive disease, the primary cause of hypoxemia in restrictive states is [V with dot above]/[Q with dot above] mismatch. Often patients have multiple reasons for pulmonary dysfunction as well as mixed obstructive and restrictive defects. Proper diagnosis requires a careful history and physical examination. Pulmonary function testing may be required to differentiate obstructive from restrictive defects and can be used to assess a patient’s response to therapy.

1. Intrinsic

a. Pulmonary edema occurs when fluid accumulates in the interstitium and alveoli by hydrostatic, cardiogenic (e.g., congestive heart failure [CHF]), or “noncardiogenic” (e.g., acute respiratory distress syndrome [ARDS]) mechanisms.

b. Pulmonary interstitial disease causes inflammation/fibrosis of interstitium, alveoli, or vascular beds. The latter may lead to pulmonary hypertension and cor pulmonale. Examples include sarcoidosis, chronic hypersensitivity pneumonitis, and radiation fibrosis.

2. Extrinsic

a. Pleural disease, either fibrosis or effusion.

b. Chest wall deformity, such as kyphoscoliosis, ankylosing spondylitis, pectus excavatum, trauma, or burns.

c. Diaphragmatic compression by obesity, ascites, pregnancy, or from retraction during abdominal surgery.

C. Pulmonary hypertension is characterized by a mean pulmonary artery pressure of more than 25 mm Hg at rest (or >30 mm Hg with exercise), with a normal pulmonary artery occlusion (capillary wedge) pressure. It can result in right atrial and right ventricular dilatation, hypertrophy and failure, and likely increases POPCs. It is classified as follows:

1. Primary pulmonary arterial hypertension occurs due to idiopathic fibrin deposition in the pulmonary capillaries and arterioles accompanied by increased thrombogenesis. The total cross-sectional area of the pulmonary vasculature may be markedly decreased

2. Pulmonary hypertension due to left heart failure

3. Pulmonary hypertension due to lung diseases and/or hypoxia

4. Chronic thromboembolic pulmonary hypertension

5. Pulmonary hypertension with unclear and/or multifactorial mechanisms (e.g., sarcoidosis and vasculitis)

1. Patient-related information to be obtained, per meta-analysis, includes advanced age (>60), preexisting lung disease (e.g., COPD), and nonpulmonary information related to overall physical fitness and conditions
(ASA-PS 2 or greater, poor functional status, malnutrition, and CHF). Other risk factors may include hypoxemia, anemia, obstructive sleep apnea (OSA), recent respiratory infection, and current sepsis. Among laboratory predictors, good evidence exists only for low serum albumin levels (<30 g/L) in predicting POPCs.

2. Symptoms of respiratory disease such as cough, expectoration, hemoptysis, wheezing, dyspnea, and chest pain should be elicited. Occupational exposures, medications, recent changes in clinical status as well as symptoms of OSA should be defined.

3. Chronic cough may suggest bronchitis or asthma. If cough is productive, sputum should be examined for evidence of infection and, if appropriate, sent for Gram stain, culture, or cytology.

4. Smoking history should be quantified in pack years (number of packs smoked per day multiplied by the number of years smoked). The risks of malignancy, COPD, and POPCs are directly proportional to the smoking history.

5. Dyspnea is an uncomfortable sensation of breathing. The activity level should be defined; severe dyspnea (occurring at minimal activity or at rest) may be a predictor of both poor ventilatory reserve and the need for postoperative ventilatory support.

1. Body habitus and general appearance.

a. Obesity, pregnancy, and kyphoscoliosis reduce lung volumes and capacities (functional residual capacity [FRC] and total lung capacity [TLC]) and pulmonary compliance and predispose to atelectasis and hypoxemia.

b. Cachectic malnourished patients have blunted respiratory drive and decreased muscle strength and are predisposed to pneumonia.

c. Cyanosis requires a minimum reduced hemoglobin concentration of 5 g/dL. The appearance of cyanosis depends on many factors, including cardiac output, oxygen uptake by the tissue, and hemoglobin concentration. Cyanosis suggests hypoxemia but can be unreliable.

2. Respiratory signs. Respiratory rate and pattern, diaphragmatic coordination, and the use of accessory muscles should be assessed.

a. Tachypnea, a respiratory rate greater than 25 breaths/minute, is usually the earliest sign of respiratory distress.

b. Respiratory pattern

1. Pursed-lip breathing, tripoding, and visible expiratory effort may indicate airway obstruction.

2. Accessory muscle use increases with load and dysfunction of the diaphragm and intercostal muscles.

3. Asymmetry of chest wall expansion may result from unilateral bronchial obstruction, trauma, pneumothorax, pleural effusion, lung consolidation, or unilateral phrenic nerve injury (causing an elevated hemidiaphragm).

4. Tracheal deviation may suggest pneumothorax or mediastinal disease with tracheal compression. Severe cases may cause difficulty during intubation or airway obstruction during induction of general anesthesia.

5. Inspiratory paradox. Normally, the abdominal wall should move outward with the chest wall during inspiration. Inspiratory paradox occurs when the abdomen collapses as the chest wall expands during inspiration and suggests paralysis or severe dysfunction of the diaphragm.

c. Auscultation

1. Diminished breath sounds may indicate local consolidation, pneumothorax, or pleural effusion.

2. Rales, usually in dependent portions, may indicate atelectasis or CHF.

3. Wheezing may indicate obstructive airway disease.

4. Stridor may indicate upper airway narrowing.

3. Cardiovascular signs

a. Pulsus paradoxus can be seen in patients with asthma and is defined as a fall in systolic blood pressure of greater than 10 mm Hg during inspiration. It is probably due to selective impairment of left ventricular filling and ejection secondary to the negative pleural pressure generated during spontaneous ventilation. Pulsus paradoxus can also be seen with pericardial tamponade and superior vena cava obstruction, but the physiologic mechanism is different than it is with asthma.

b. Pulmonary hypertension occurs as a result of elevated pulmonary vascular resistance.

c. Physical signs may include splitting of the second heart sound with an accentuated pulmonic component, jugular venous distention, hepatomegaly, hepatojugular reflux, and peripheral edema.

d. Factors that may acutely increase pulmonary vascular resistance include hypoxia, hypercarbia, acidosis, pulmonary embolism, ARDS, and the application of high levels of positive end-expiratory pressure (PEEP).

1. Chest radiograph

a. Hyperinflation and decreased vascular markings are characteristic of COPD and asthma.

b. Pleural effusion, pulmonary fibrosis, and skeletal abnormalities (kyphoscoliosis and rib fractures) may predict restrictive disease states.

c. Air space disease, including CHF, consolidation, atelectasis, lobar collapse (bronchial obstruction), and pneumothorax, is an important predictor of [V with dot above]/[Q with dot above] mismatch and hypoxemia.