Pulmonary Dysfunction

A wide variety of acute and chronic pulmonary diseases can cause respiratory failure, but in virtually all cases, the primary physiologic mechanism is impaired ventilation-perfusion (V/Q) matching within the lung. Regions of low V/Q ratio constitute relative intrapulmonary shunt and cause hypoxemia, whereas regions of high V/Q ratio constitute relative dead-space ventilation and exacerbate hypercarbia. Respiratory distress occurs due to either hypoxemia—which is a potent respiratory stimulant—or to increased work of breathing. Increased work of breathing is caused by reduced respiratory compliance, increased airways resistance, or the need for increased minute ventilation secondary to increased oxygen consumption or carbon dioxide production. Pulmonary disease can be broadly divided into conditions in which the compliance of the lungs or chest wall is reduced (restrictive lung disease) and conditions in which airways resistance is increased (obstructive lung disease). V/Q mismatch occurs in both.

Cardiac Dysfunction

Cardiac dysfunction is both a direct and an indirect cause of respiratory failure. The direct mechanism is cardiogenic pulmonary edema due to left heart disease. The indirect mechanism occurs because of the effects of reduced cardiac output on mixed venous oxygen saturation (S_Vo₂; see Exacerbating Factors in subsequent material). Because positive pressure ventilation reduces left ventricular afterload, impaired left heart function is an important cause of failure to wean from ventilatory support.

Central Nervous System and Neuromuscular Dysfunction

Dysfunction of the CNS or neuromuscular system can lead to hypoventilation, loss of protective airway reflexes, and impaired swallowing. Hypoventilation causes hypercarbia and, if severe, hypoxemia. Impaired swallowing and loss of protective airway reflexes predispose a patient to pulmonary aspiration.

Exacerbating Factors

With normal lung function, the main determinant of P_ao₂ is alveolar oxygen tension (P_Ao₂). However, with intrapulmonary shunting, systemic venous blood passes through the lungs without being oxygenated, and S_Vo₂ becomes an important determinant of P_ao₂. Low S_Vo₂ can arise from anemia, low cardiac output, and high metabolic rate. This is illustrated in Figure 27-1, which shows the relationship between cardiac output and arterial oxygenation at various levels of intrapulmonary shunting.

Figure 27.1 The relationship between cardiac output and the alveolar-arterial Po₂ gradient in the presence of various levels of intrapulmonary shunting. As shunt fraction increases, the effect of low cardiac output on the alveolar-arterial gradient becomes more important.

(From Nunn JF: Applied Respiratory Physiology, ed 3. Philadelphia, Butterworth, 1987, with permission.)

Diagnosis

Important diagnostic information is obtained from the clinical context, physical examination, and simple bedside tests.

Treatment

Treatment of acute respiratory failure is both supportive and specific to the underlying condition. Specific treatments are discussed in specific causes of respiratory failure. Supportive treatments are listed subsequently. The treatment goals are outlined in Table 27-2.

Table 27-2 Therapeutic Aims for Managing Acute Respiratory Failure

* Higher respiratory rates cannot usually be sustained indefinitely; exhaustion and respiratory arrest are likely to supervene.

† Respiratory failure severe enough to cause a fall in the level of consciousness such that the patient cannot obey commands mandates endotracheal intubation to protect against pulmonary aspiration.

Atelectasis

In atelectasis, regions of collapsed, airless alveoli are present. These occur for two main reasons. First, microatelectasis occurs because of the closure of small airways due to the encroachment of closing capacity on the functional residual capacity (see Chapter 1). Once these small airways become obstructed, gas within distal alveoli is absorbed (absorption atelectasis), and alveolar collapse occurs. Microatelectasis is common in patients who are obese, elderly, anesthetized, in a supine position or who have reduced lung compliance. It tends to develop in dependent regions of the lung. Also, atelectasis occurs when mucus plugs medium-sized and large airways because of excessive secretions, impaired bronchial mucociliary function, and poor cough. Mucus plugging results in lobar, segmental, or sub segmental collapse. Collapse of an entire lung is usually caused by endobronchial intubation.

Atelectasis occurs in all patients after major surgery and in anyone who is mechanically ventilated for longer than a few hours, but patients undergoing cardiac or thoracic surgery are at particular risk. Periods without ventilation of the lungs while on cardiopulmonary bypass encourage atelectasis, particularly if the lung collapses to below the functional residual capacity—as happens if the pleura is opened. Patients receiving a high F_Io₂ are at increased risk for absorption atelectasis because oxygen is more readily absorbed (by adjacent red blood cells) than is nitrogen. After extubation, pain from the sternotomy and chest drains, which contributes to chest wall splinting and poor cough, also predisposes to atelectasis. Left lower lobe collapse is extremely common after cardiac surgery.

Atelectasis causes impaired gas exchange and reduced lung compliance. Microatelectasis and lobar collapse may be the primary cause of respiratory failure or may coexist with and exacerbate other causes of respiratory failure.

On examination, there may be dullness to percussion and reduced breath sounds over atelectatic lung, most commonly at the lung bases. Microatelectasis may not be apparent on a chest radiograph but is clearly seen on a computed tomography scan of the chest (Fig. 27-2). Lobar collapse is readily apparent on a chest radiograph (see Chapter 6).

Figure 27.2 Computed tomography scan showing atelectasis in a patient with acute respiratory distress syndrome. Areas of dependent atelectasis (A) and pleural fluid (F) can be seen. The anterior portions of the lungs are relatively spared.

Treatment is directed toward reexpanding the collapsed alveoli. In spontaneously breathing patients treatment includes incentive spirometry, huffing and coughing exercises, saline nebulizers to aid sputum expectoration, and adequate analgesia. Ventilatory strategies include continuous positive airway pressure (CPAP; noninvasive ventilation) and positive end-expiratory pressure (PEEP; invasive ventilation). In invasively ventilated patients, mucus plugging in large airways may be ameliorated by tracheal suctioning and low-volume (10 ml) saline lavage. However, if the primary problem is microatelectasis or pulmonary edema, aggressive tracheal toilet may worsen gas exchange because of the repetitive loss of PEEP.

Pulmonary Edema

Pulmonary edema is an increase in extravascular lung water and may be cardiogenic or noncardiogenic, depending on whether pulmonary capillary hydrostatic pressure is elevated or normal. Cardiogenic pulmonary edema is defined as pulmonary edema in association with a PAWP greater than 18 mmHg. The causes of noncardiogenic pulmonary edema are listed in Table 27-4.

Table 27-4 Causes of Noncardiogenic Pulmonary Edema That May Be Encountered in the Cardiothoracic ICU

ICU, intensive care unit; TRALI, transfusion related acute lung injury; CPB, cardiopulmonary bypass

In most circumstances, pulmonary edema can be differentiated from other causes of acute respiratory failure, and cardiogenic and noncardiogenic edema can be distinguished, on the basis of the history, the examination, and simple bedside tests (troponin, B-type natriuretic peptide, electrocardiogram, chest radiograph, and echocardiogram; see Chapter 19). Only very rarely is pulmonary artery catheterization required for diagnosis, but it may be useful to guide therapy.

Irrespective of the cause, pulmonary edema results in a clinical syndrome of hypoxemia and respiratory distress. Crackles and wheezes may be heard on auscultation of the chest. If expiratory wheeze is marked, it may easily be mistaken for bronchospasm. The chest radiograph typically demonstrates interstitial or alveolar shadowing (see Chapter 6). Certain radiographic features may help to distinguish cardiogenic from noncardiogenic pulmonary edema; these features are listed in Table 27-5 (see Figs. 6-8 and 6-17).

Table 27-5 Radiographic Features That May Distinguish Cardiogenic From Noncardiogenic Pulmonary Edema

Modified from Ware LB, Matthay MA: Clinical practice: acute pulmonary edema. N Engl J Med 353:2788-2796, 2005, with permission.

Aspiration

Pulmonary aspiration usually occurs in patients who have one or more risk factors, such as an enteral feeding tube, gastroesophageal reflux, vomiting, reduced level of consciousness, or impaired swallowing. Impaired swallowing may be caused by a stroke, muscle weakness, or a tracheotomy tube. The presence of a cuffed endotracheal or tracheotomy tube does not reliably prevent aspiration, but may limit its severity. Pulmonary aspiration occurs in up to 20% of patients who undergo emergency endotracheal intubation.⁴

The clinical features of aspiration vary from a subclinical event detectable only by sensitive assays (e.g., the presence of pepsin in the tracheal secretions) to a symptomatic episode with choking, coughing, and recovery of fluid or particulate material from the trachea. Aspiration, particularly of gastric contents, can result in severe chemical pneumonitis, characterized by alveolar edema, bronchospasm, V/Q mismatch, and atelectasis. Severe hypoxemia and respiratory distress can develop very rapidly. Crackles and wheezes may be heard on chest auscultation. Fever and leukocytosis are common. The chest radiograph may show patchy infiltrates in dependent regions which, when the patient is in the supine position, are the posterior segments of the upper lobes and the superior segments of the lower lobes (Fig. 27-3). Secondary bacterial pneumonia or ARDS can supervene.

Figure 27.3 Chest radiograph showing pulmonary aspiration. Diffuse alveolar shadowing is seen in the right-middle zone, consistent with aspiration of blood (in the supine position) into the apical segment of the lower lobe and the posterior segments of the upper lobe. To a lesser extent, alveolar shadowing is present on the left also. A central venous catheter, endotracheal tube, and nasogastric tube (tip behind the apex of the left ventricle) are also seen.

Guidelines for the treatment of major pulmonary aspiration in a critically unwell patient have been developed.⁵ In the first instance, the patient should be positioned on his or her side and the oropharynx should be suctioned. If particulate material is aspirated or the patient is in significant respiratory distress, endotracheal intubation followed by tracheal toilet is recommended. Removal of particulate matter may be aided by bronchoscopy. Bronchospasm should be treated by nebulized bronchodilators. Prophylactic antimicrobials are not recommended, but if pulmonary infiltrates do not clear or worsen, antimicrobial therapy like that used for ventilator-associated pneumonia (see Chapter 35) is indicated. Corticosteroids are not recommended.

Chronic Obstructive Pulmonary Disease

COPD incorporates three clinical entities: asthma, emphysema, and chronic bronchitis. Asthma is characterized by bronchiolar smooth muscle hypertrophy, bronchospasm, and increased airway secretions. Emphysema is characterized by loss of pulmonary elastic tissue, destruction of alveolar capillary units, and airway collapse. The main pathologic processes in chronic bronchitis are airway inflammation and excess secretions. In an individual patient, characteristics of all three conditions may coexist, but one usually predominates. Increased airflow resistance is common to all patients with COPD.

Mild to moderate COPD does not substantially increase the risk of death in patients undergoing cardiac surgery.^6,7 However, the risk of adverse events, such as prolonged intubation, repeat intubation, and arrhythmias, is increased.^8,9 Elderly patients (>75 years) with COPD who are being treated with corticosteroids have a very high perioperative risk.⁷

Pathophysiology

Increased airways resistance is spontaneously breathing patients results in increased work of breathing. Initially this occurs during inspiration but as airways resistance increases, expiration also becomes an active, energy-requiring process. (Expiration is normally passive; see Chapter 1 and Fig. 29-5F) When airway resistance is high, alveolar pressure may not fall to zero by the time expiration has finished, which leads to air trapping (auto-PEEP). There are two main effects of auto-PEEP. First, tidal ventilation occurs at higher lung volumes, which positions the lung on a less favorable part of the compliance curve (see Fig. 1-15). Second, the respiratory muscles must expend additional effort during inspiration to reduce alveolar pressure to zero before gas flow occurs. This effort is termed the inspiratory threshold load, and it is explained in Figure 27-4.

Figure 27.4 The effect of continuous positive airway pressure (CPAP) on inspiratory threshold load in a patient with automatic positive end-expiratory pressure (PEEP) due to increased resistance in the airway. A, B, C, and D, phases of the respiratory cycle with 10 cm H₂O of intrinsic (auto-) PEEP present. E, F, G, and H, the same situation but with 10 cm H₂O CPAP. A shows the start of passive expiration, with pleural pressure of 0 cm H₂O and alveolar pressure at +20 cm H₂O. In B, the patient has reached end expiration and, because of high airway resistance, the alveolar pressure has fallen only to +10 cm H₂O (auto-PEEP is present). During the start of inspiration, because of this auto-PEEP, some respiratory muscle work must be done to expand the thoracic cavity and drop the alveolar pressure to 0 cm H₂O. This muscle work is termed the inspiratory threshold load, and is depicted in C. Further thoracic cavity expansion allows gas to flow into the lungs when the alveolar pressure falls below atmospheric pressure (D). In the same patient, breathing with CPAP applied via a tightly fitting face mask, expiration occurs normally (it is not impeded by the CPAP when airways resistance is high) and ceases at end-expiration when the alveolar pressure equals the airway pressure (E and F). At the beginning of inspiration, chest excursion immediately drops the alveolar pressure below airway pressure (+10 cm H₂O), and gas flow commences (G). Additional chest expansion decreases alveolar pressure to a subatmospheric level and further gas flow occurs. Note that with CPAP, the inspiratory threshold load is reduced and the intrapleural pressure that must be achieved to expand the chest is reduced (compare D and H). Other forms of spontaneous positive pressure ventilation (e.g., bilevel positive airways pressure and pressure support with PEEP) have similar beneficial effects on the work of breathing in patients with auto-PEEP.

Besides increasing work of breathing, COPD also causes V/Q mismatch, which can lead to hypoxemia and hypercarbia. COPD patients with hypercarbic respiratory failure can experience worsening of their carbon dioxide retention when given supplemental oxygen. This has long been ascribed to inhibition of hypoxic ventilatory drive, and to a degree this is true. However, the majority of the increase in P_aco₂ is due to inhibition of hypoxic pulmonary vasoconstriction, which results in increased blood flow to poorly ventilated lung units and reduced flow to well-ventilated lung units. This redistribution of blood flow increases alveolar dead space, which leads to hypercarbia (see Chapter 1). Although real, the problem of oxygen-induced hypercarbia has been overstated. Severe respiratory compromise is rare and, as long as patients are carefully monitored, supplemental oxygen may be safely administered to patients with COPD.

Assessment and Treatment

Patients with COPD commonly have a barrel-shaped chest. The lungs are hyperresonant to percussion, and on auscultation breath sounds are reduced and expiratory wheezes and crackles may be heard. The chest radiograph typically shows lung hyperinflation with a reduced cardiothoracic ratio, flattened diaphragms, and sometimes bullae (Fig. 27-5). With severe COPD, there may be a compensated respiratory acidosis, indicative of chronically elevated P_aco₂, and an elevated hematocrit, indicative of chronic hypoxemia.

Figure 27.5 Erect chest radiograph demonstrating bullous emphysema. The diaphragms are flattened and the cardiothoracic ratio is low. Large bullae can be seen bilaterally at both bases.

In patients with COPD, respiratory function should be optimized prior to cardiac or thoracic surgery. This involves smoking cessation, nutritional support, and treatment of bronchospasm or infection. However, despite these measures postoperative decompensation can occur.

Treatment of postoperative decompensation involves: (1) general supportive measures, such as supplemental oxygen, physical therapy, effective analgesia, and ventilatory support; and (2) correction of precipitating causes, such as bronchospasm, pneumonia, and pneumothorax. Treatment of bronchospasm involves inhaled bronchodilators (see Chapter 28), intravenous corticosteroids and, occasionally, intravenous infusions of albuterol, aminophylline, or epinephrine. If there is evidence of pneumonia (see Chapter 35), intravenous antimicrobial therapy is appropriate. However, routine use of antibiotics for all exacerbations of COPD is not appropriate.¹⁰ Prior to commencing antibiotics, a sputum specimen should be sent for microscopy, culture, and sensitivity. Commonly encountered pathologic organisms include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and, occasionally, Pseudomonas aeruginosa and Klebsiella pneumoniae. Empiric antibiotic therapy should be guided by local prevalence and resistance patterns but is typically similar to that for ventilatorassociated pneumonia (see Chapter 35).

Ventilatory strategies for COPD are outlined in Chapters 28 and Chapter 29. Noninvasive ventilation can be very effective in treating acute hypercarbic respiratory failure secondary to COPD. In Figure 27-4 it can be seen that CPAP (and PEEP) reduce the inspiratory threshold load and therefore reduce the work of breathing in patients with auto-PEEP. If invasive ventilation is required, appropriate ventilator settings must be used to avoid causing barotrauma and dynamic lung hyperinflation, which can cause profound cardiovascular compromise.

Extrathoracic Airway Obstruction

Extrathoracic airway obstruction occurs most commonly at the level of the pharynx or laryngeal inlet. The cardinal feature of extrathoracic obstruction is inspiratory stridor.

Pneumothorax

Pneumothoraces occur postoperatively for a variety of reasons, including (1) lung injury at the time of surgery or during invasive procedures—particularly the placement of subclavian central venous catheters; (2) entrainment of air during chest drain removal; (3) ventilator-induced barotrauma, particularly in patients with COPD or ARDS. Pneumothorax may also occur spontaneously or as the result of chest trauma.

Because of the elastic recoil of the lung, once the pleura (either parietal or visceral) is breached, air enters the chest cavity and the lung collapses, resulting in a “simple” pneumothorax (see Fig. 25-3). If the source of air entry is self-limited (e.g., during removal of chest drains), a small pneumothorax typically develops. Clinically, there may be signs of reduced chest movement and diminished air entry on the affected side. The diagnosis is easily missed, particularly in patients with COPD, who normally have quiet breath sounds.

If the site of air entry into the pleura functions as a one-way valve, a tension pneumothorax will develop (see Fig. 25-3). A tension pneumothorax may develop very rapidly in patients receiving positive pressure ventilation. Tension pneumothorax results in hyperinflation of the affected pleural space and compression of the mediastinal structures, resulting in obstruction of the venous return and, potentially, cardiorespiratory collapse. Immediate needle thoracocentesis may be lifesaving (see Chapter 40).

If there is clinical suspicion of a pneumothorax, a chest radiograph—ideally taken with the patient erect—must be obtained. In general, in a spontaneously breathing patient, pneumothoraces involving more than 25% of the lung field should be drained. In patients who are receiving positive pressure ventilation, all pneumothoraces should be drained.¹¹ Following drainage, atelectasis or air leak may cause ongoing impairment of gas exchange.

Hemothorax and Pleural Effusion

Most hemothoraces that occur following cardiac surgery are a result of mediastinal or sternal bleeding that gravitates to an opened pleural cavity. Pleural effusions commonly develop a few days following surgery in patients with elevated systemic venous pressure. Large hemothoraces and pleural effusions are usually apparent on chest radiograph, particularly on erect films (see Fig. 6-18). Smaller collections are best diagnosed by ultrasound imaging of the pleural spaces. Ultrasound scanning allows for accurate localization of the collection and the diaphragm and may be used to guide drain placement. Fluid collections that are less than about 400 ml generally do not warrant draining except as a diagnostic procedure. As with pneumothoraces, significant atelectasis may coexist with pleural collections.

Pulmonary Hemorrhage

Bleeding within the parenchyma of the lung may occur due to surgical retraction or handling of the lung (e.g., during procedures on the descending thoracic aorta; see Chapter 11); thoracic trauma (e.g., pulmonary contusion; see Chapter 25); and a wide variety of medical conditions (see Chapter 26). Merely a few hundred milliliters of blood within the alveolar space can cause acute respiratory failure. Radiographically, pulmonary hemorrhage appears as alveolar shadowing, which may be localized to a specific lobe or lung.

Phrenic Nerve Injury

Phrenic nerve dysfunction is common following cardiac surgery; it can occur in up to 70% of cases (see Chapter 37). However, complete paresis of a hemidiaphragm occurs in less than 10% of patients.^12,13 Phrenic nerve dysfunction is identified by the development of a raised hemidiaphragm on the chest radiograph following extubation (see Fig. 6-25). Phrenic nerve injury can cause, and also can be mistaken for, lower lobe atelectasis. In isolation, unilateral phrenic nerve palsy does not usually cause respiratory embarrassment, but if it is bilateral (very rare) or if it occurs in association with other pulmonary disease, it can contribute to severe respiratory compromise. The diagnosis is confirmed by identifying paradoxic motion of the diaphragm with ultrasound imaging. Treatment is supportive but occasionally, diaphragmatic plication may be performed.

Hypoventilation

Hypoventilation may be due to reduced level of consciousness, weakness, or exhaustion secondary to increased work of breathing. The most common cause of reduced level of consciousness following extubation is residual effects of sedative-hypnotic or opioid drugs, particularly in elderly patients.

Patients who are over sedated or whose airways are not protected should be intubated and ventilated. Naloxone (see Chapter 4) can be used to reverse the effects of opioids but can precipitate pain, agitation, hypertension, and myocardial ischemia. Flumazenil (see Chapter 4) may be used to reverse benzodiazepine-induced sedation. Although less problematic than naloxone, flumazenil can cause agitation, arrhythmias, and hypertension. If residual neuromuscular blockade is suspected, neuromuscular function should be assessed with a nerve stimulator (see Chapter 4), and if it is present, it may be reversed by administering neostigmine (see Chapter 4). Weakness that occurs in the setting of prolonged critical illness has a number of causes and is discussed in Chapter 37.

Intracardiac Shunting

Hypoxemia due to right-to-left intracardiac shunting occurs with certain congenital cardiac abnormalities (see Chapter 15). These conditions are usually well documented in a patient’s medical records. However, right-to-left shunting can also occur across a PFO in a patient who is not suspected of having a congenital cardiac defect. A PFO is present in about 25% of patients,¹⁴ and right-to-left shunting occurs when right atrial pressure exceeds left atrial pressure. Right ventricular dysfunction and patient-ventilator dysynchrony predispose to right-to-left shunting across a PFO. Hypoxemia may develop and resolve over a few seconds. Central venous pressure is usually high but there may be little else to suggest the diagnosis. A PFO may be identified by transesophageal echocardiography (see Chapter 7). The diagnosis and treatment of right ventricular dysfunction and patient ventilator dysynchrony are described in Chapters 20, 24 and 29.