The etiologies of ARF may be classified as extrapulmonary or intrapulmonary, depending on the component of the respiratory system that is affected. Extrapulmonary causes include disorders that affect the brain, the spinal cord, the neuromuscular system, the thorax, the pleura, and the upper airways. Intrapulmonary causes include disorders that affect the lower airways and alveoli, the pulmonary circulation, and the alveolar-capillary membrane.6 Table 15-1 lists the different etiologies of ARF and their associated disorders.

Hypoxemia is the result of impaired gas exchange and is the hallmark of acute respiratory failure. Hypercapnia may be present, depending on the underlying cause of the problem. The main causes of hypoxemia are alveolar hypoventilation, ventilation/perfusion (V/Q) mismatching, and intrapulmonary shunting.1,7 Type I respiratory failure usually results from V/Q mismatching and intrapulmonary shunting, whereas type II respiratory failure usually results from alveolar hypoventilation, which may or may not be accompanied by V/Q mismatching and intrapulmonary shunting.¹

The patient with ARF may experience a variety of clinical manifestations, depending on the underlying cause and the extent of tissue hypoxia. The clinical manifestations commonly seen in the patient with ARF are usually related to the development of hypoxemia, hypercapnia, and acidosis.9 Because the clinical symptoms are so varied, they are not considered reliable in predicting the degree of hypoxemia or hypercapnia¹ or the severity of ARF.³

Diagnosing and following the course of respiratory failure is best accomplished by ABG analysis. ABG analysis confirms the level of PaCO₂, PaO₂, and blood pH. ARF is generally accepted as being present when the PaO₂ is less than 60 mm Hg. If the patient is also experiencing hypercapnia, the PaCO₂ will be greater than 45 mm Hg. In patients with chronically elevated PaCO₂ levels, these criteria must be broadened to include a pH less than 7.35.⁹

A variety of additional tests are performed depending on the patient’s underlying condition. These include bronchoscopy for airway surveillance or specimen retrieval, chest radiography, thoracic ultrasound, thoracic computed tomography, and selected lung function studies.¹⁰

A wide variety of clinical conditions is associated with the development of ALI. These are categorized as direct or indirect, depending on the primary site of injury (Box 15-1).^35,38 Direct injuries are those in which the lung epithelium sustains a direct insult. Indirect injuries are those in which the insult occurs elsewhere in the body and mediators are transmitted via the blood stream to the lungs. Sepsis, aspiration of gastric contents, diffuse pneumonia, and trauma were found to be major risk factors for the development of ALI.³⁷

The mortality rate for ARDS is estimated to be 34% to 58%.³⁷

The progression of ALI can be described in three phases: exudative, fibroproliferative, and resolution. ALI is initiated with stimulation of the inflammatory-immune system as a result of a direct or indirect injury (Figure 15-1). Inflammatory mediators are released from the site of injury, resulting in the activation and accumulation of the neutrophils, macrophages, and platelets in the pulmonary capillaries. These cellular mediators initiate the release of humoral mediators that cause damage to the alveolar-capillary membrane.³⁸

Initially the patient with ALI may be seen with a variety of clinical manifestations, depending on the precipitating event. As the disorder progresses, the patient’s signs and symptoms can be associated with the phase of ALI that he or she is experiencing (Table 15-2). During the exudative phase, the patient presents with tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use. During the fibroproliferative phase, the patient’s signs and symptoms progress to agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure develops.^40,41

Arterial blood-gas analysis reveals a low PaO₂, despite increases in supplemental oxygen administration (refractory hypoxemia).⁴⁰ Initially the PaCO₂ is low as a result of hyperventilation, but eventually the PaCO₂ increases as the patient fatigues. The pH is high initially but decreases as respiratory acidosis develops.^40,41

Initially the chest x-ray film may be normal, because changes in the lungs do not become evident for up to 24 hours. As the pulmonary edema becomes apparent, diffuse, patchy interstitial and alveolar infiltrates appear. This progresses to multifocal consolidation of the lungs, which appears as a “whiteout” on the chest x-ray film.⁴⁰

Medical management of the patient with ALI involves a multifaceted approach. This strategy includes treating the underlying cause, promoting gas exchange, supporting tissue oxygenation, and preventing complications. Given the severity of hypoxemia, the patient is intubated and mechanically ventilated to facilitate adequate gas exchange.42

Development of acute pneumonia implies a defect in host defenses, a particularly virulent organism, or an overwhelming inoculation event. Bacterial invasion of the lower respiratory tract can occur by inhalation of aerosolized infectious particles, aspiration of organisms colonizing the oropharynx, migration of organisms from adjacent sites of colonization, direct inoculation of organisms into the lower airway, spread of infection to the lungs from adjacent structures, spread of infection to the lung through the blood, and reactivation of latent infection (usually in the setting of immunosuppression). The most common mechanism appears to be aspiration of oropharyngeal organisms.52 Table 15-3 lists the precipitating conditions that can facilitate the development of pneumonia.

Figure 15-2 depicts the pathophysiology of HAP. Colonization of the patient’s oropharynx with infectious organisms is a major contributor to the development of HAP. Normally the oropharynx has a stable population of resident flora that may be anaerobic or aerobic. When stress occurs, such as with illness, surgery, or infection, pathogenic organisms replace normal resident flora. Previous antibiotic therapy also affects the resident flora population, making replacement by pathological organisms more likely. The pathogens are then able to invade the sterile lower respiratory tract.³⁰

Disruption of the gag and cough reflexes, altered consciousness, abnormal swallowing, and artificial airways all predispose the patient to aspiration and colonization of the lungs and subsequent infection. Histamine₂ agonists, antacids, and enteral feedings also contribute to this problem because they raise the pH of the stomach and promote bacterial overgrowth. The nasogastric tube then acts as a wick, facilitating the movement of bacteria from the stomach to the pharynx, where the bacteria can be aspirated.⁴⁸

Infection results in pulmonary inflammation with or without significant exudates. Increased capillary permeability occurs, leading to increased interstitial and alveolar fluid. V/Q mismatching and intrapulmonary shunting occurs, resulting in hypoxemia as lung consolidation progresses. Untreated pneumonia can result in ARF and initiation of the inflammatory-immune response. In addition, the patient may develop a pleural effusion. This is the result of the vascular response to inflammation, whereby capillary permeability is increased and fluid from the pulmonary capillaries diffuses into the pleural space.^48,53

Prevention of VAP is discussed under the mechanical ventilation section of Chapter 16.

The clinical manifestations of pneumonia will vary with the offending pathogen. The patient may first be seen with a variety of signs and symptoms including dyspnea, fever, and cough (productive or nonproductive). Coarse crackles on auscultation and dullness to percussion may also be present.53 Patients with severe CAP may manifest confusion and disorientation, tachypnea, hypoxemia, uremia, leukopenia, thrombocytopenia, hypothermia, and hypotension.⁵²

Chest radiography is used to evaluate the patient with suspected pneumonia. The diagnosis is established by the presence of a new pulmonary infiltrate. The radiographic pattern of the infiltrates will vary with the organism.⁵⁴ A sputum Gram stain and culture are done to facilitate the identification of the infectious pathogen. In 50% of cases, though, a causative agent is not identified.⁴⁸ A diagnostic bronchoscopy may be needed, particularly if the diagnosis is unclear or current therapy is not working.⁴⁹ In addition, a complete blood count with differential, chemistry panel, blood cultures, and arterial blood gases is obtained.⁵¹

Medical management of the patient with pneumonia should include antibiotic therapy, oxygen therapy for hypoxemia, mechanical ventilation if acute respiratory failure develops, fluid management for hydration, nutritional support, and treatment of associated medical problems and complications. For patients having difficulty mobilizing secretions, a therapeutic bronchoscopy may be necessary.53,54

A number of factors have been identified that place the patient at risk for aspiration (Table 15-4). Gastric contents and oropharyngeal bacteria (see Pneumonia earlier in this chapter) are the most common aspirates of the critically ill patient.^57,58 The effects of gastric contents on the lungs will vary based on the pH of the liquid. If the pH is less than 2.5, the patient will develop a severe chemical pneumonitis resulting in hypoxemia. If the pH is greater than 2.5, the immediate damage to the lungs will be lessened but the elevated pH may have promoted bacterial overgrowth of the stomach.^57,58 Once the bacteria-laden gastric contents are aspirated into the lungs, overwhelming bacterial pneumonia can develop.⁵⁸

Clinically, the patient presents with signs of acute respiratory distress, and gastric contents may be present in the oropharynx. The patient will have shortness of breath, coughing, wheezing, cyanosis, and signs of hypoxemia. Tachypnea, tachycardia, hypotension, fever, and crackles also are present. Copious amounts of sputum are produced as alveolar edema develops.57,58

ABGs reflect severe hypoxemia. Chest x-ray film changes appear 12 to 24 hours after the initial aspiration, with no one pattern being diagnostic of the event. Infiltrates will appear in a variety of distribution patterns depending on the position of the patient during aspiration and the volume of the aspirate. If bacterial infection becomes established, leukocytosis and positive sputum cultures occur.⁵⁸

Management of the patient with aspiration lung disorder includes both emergency and follow-up treatment. When aspiration is witnessed, emergency treatment should be instituted to secure the airway and minimize pulmonary damage. The upper airway should be suctioned immediately to remove the gastric contents.57,58 Direct visualization by bronchoscopy is indicated to remove large particulate aspirate⁶¹ or to confirm an unwitnessed aspiration event.⁵⁹ Bronchoalveolar lavage is not recommended because this practice disseminates the aspirate in lungs and increases damage. Prophylactic antibiotics are not recommended either.⁵⁹

After airway clearance, attention should be given to supporting oxygenation and hemodynamics. Hypoxemia should be corrected with supplemental oxygen or mechanical ventilation with PEEP, if necessary.^57–59 Hemodynamic changes result from fluid shifts into the lungs that can occur after massive aspirations. Monitoring intravascular volume is essential, and judicious amounts of replacement fluids should be instituted to maintain adequate urinary output and vital signs.⁵⁹

Initially antibiotic therapy is not indicated. If symptoms fail to resolve within 48 hours, empiric antibiotic therapy should be initiated. Corticosteroids have not demonstrated to be of any benefit in the treatment of aspiration pneumonitis and thus are not recommended either.⁵⁸

A pulmonary embolism (PE) occurs when a clot (thrombotic embolus) or other matter (nonthrombotic embolus) lodges in the pulmonary arterial system, disrupting the blood flow to a region of the lungs (Figure 15-3). The majority of thrombotic emboli arise from the deep leg veins, particularly the iliac, femoral, and popliteal veins.⁶¹ Other sources include the right ventricle, the upper extremities, and the pelvic veins. Nonthrombotic emboli arise from fat, tumors, amniotic fluid, air, and foreign bodies. This section of the chapter focuses on thrombotic emboli.

A number of predisposing factors and precipitating conditions put a patient at risk for developing a PE (Box 15-3). Of the three predisposing factors (i.e., hypercoagulability, injury to vascular endothelium, and venous stasis [Virchow’s triad]), endothelial injury appears to be the most significant.⁶¹

A massive PE occurs with the blockage of a lobar or larger artery, resulting in occlusion of more than 40% of the pulmonary vascular bed. Blockage of the pulmonary arterial system has both pulmonary and hemodynamic consequences.62 The effects on the pulmonary system are increased alveolar dead space, bronchoconstriction, and compensatory shunting.⁶⁷ The hemodynamic effects include an increase in pulmonary vascular resistance and right ventricular workload.^62,63

The patient with a pulmonary embolism may have any number of presenting signs and symptoms, with the most common being tachycardia and tachypnea. Additional signs and symptoms that may be present include dyspnea, apprehension, increased pulmonic component of the second heart sound (P₁)_, fever, crackles, pleuritic chest pain, cough, evidence of a deep vein thrombosis, and hemoptysis.61 Syncope and hemodynamic instability can occur as a result of right ventricular failure.⁶⁴

Initial laboratory studies and diagnostic procedures that may be done are ABG analysis, D-dimer, electrocardiogram (ECG), chest radiography, and echocardiography (ECHO). ABGs may show a low PaO₂, indicating hypoxemia; a low PaCO₂, indicating hypocarbia; and a high pH, indicating a respiratory alkalosis. The hypocarbia with resulting respiratory alkalosis is caused by tachypnea.⁶³ An elevated D-dimer will occur with a PE and a number of other disorders. A normal D-dimer will not occur with a PE and thus can be used to rule out a PE as the diagnosis.⁶² The most frequent ECG finding seen in the patient with a PE is sinus tachycardia.⁶¹ The classic ECG pattern associated with a PE—S wave in lead I, and Q wave with inverted T wave in lead III—is seen in fewer than 20% of patients.⁶⁴ Other ECG findings associated with a PE include right bundle branch block, new-onset atrial fibrillation, T-wave inversion in the anterior or inferior leads⁶⁵, and ST-segment changes.⁶⁵ Chest x-ray findings vary from normal to abnormal and are of little value in confirming the presence of a PE. Abnormal findings include cardiomegaly, pleural effusion, elevated hemidiaphragm, enlargement of the right descending pulmonary artery (Palla’s sign), a wedge-shaped density above the diaphragm (Hampton’s hump), and the presence of atelectasis.⁶³ An ECHO, either transthoracic or transesophageal, is also useful in the identification of a PE, because it can provide visualization of any emboli in the central pulmonary arteries. In addition, it can be used for assessing the hemodynamic consequences of the PE on the right side of the heart.⁶²

Differentiating a PE from other illnesses can be difficult because many of its clinical manifestations are found in a variety of other disorders.⁶¹ Thus a variety of other tests may be necessary, including a V/Q scintigraphy, pulmonary angiogram, and deep vein thrombosis (DVT) studies.^61–63 Given the advent of more sophisticated computed tomography (CT) scanners, the spiral CT is also being used to diagnose a PE.^63,64 A definitive diagnosis of a PE requires confirmation by a high-probability V/Q scan, an abnormal pulmonary angiogram or CT, or strong clinical suspicion coupled with abnormal findings on lower extremity DVT studies.⁶³

Medical management of the patient with a pulmonary embolism involves both prevention and treatment strategies. Prevention strategies include the use of prophylactic anticoagulation with low-dose or adjusted-dose heparin, low-molecular-weight heparin, or oral anticoagulants (Table 15-5). The use of graduated compression stockings and pneumatic compression have also been demonstrated as effective methods of prophylaxis in low-risk patients.⁶⁵

Treatment strategies include preventing the recurrence of a PE, facilitating clot dissolution, reversing the effects of pulmonary hypertension, promoting gas exchange, and preventing complications. Medical interventions to promote gas exchange include supplemental oxygen administration, intubation, and mechanical ventilation.⁶²

Prevention of pulmonary embolism should be a major nursing focus, because the majority of critically ill patients are at risk for this disorder. Nursing actions are aimed at preventing the development of DVT, which is a major complication of immobility and a leading cause of PE. These measures include the use of graduated compression stockings or pneumatic compression devices, active/passive range-of-motion exercises involving foot extension, adequate hydration, and progressive ambulation.24

Nursing management of the patient with a PE incorporates a variety of nursing diagnoses (Nursing Diagnosis Priorities box on Pulmonary Embolus). Nursing priorities are directed toward (1) optimizing oxygenation and ventilation, (2) monitoring for bleeding, (3) providing comfort and emotional support, (4) maintaining surveillance for complications, and (5) educating the patient and family.

The precipitating cause of the attack is usually an upper respiratory infection, allergen exposure, or a decrease in antiinflammatory medications. Other factors that have been implicated include overreliance on bronchodilators, environmental pollutants, lack of access to health care, failure to identify worsening airflow obstruction, and noncompliance with the health care regimen.69

An asthma attack is initiated when exposure to an irritant or trigger occurs, resulting in the initiation of the inflammatory-immune response in the airways. Bronchospasm occurs along with increased vascular permeability and increased mucus production. Mucosal edema and thick, tenacious mucus further increase airway responsiveness. The combination of bronchospasm, airway inflammation, and hyperresponsiveness results in narrowing of the airways and airflow obstruction. These changes have significant effects on the pulmonary and cardiovascular systems.69

Initially the patient may present with a cough, wheezing, and dyspnea. As the attack continues, the patient develops tachypnea, tachycardia, diaphoresis, increased accessory muscle use, and pulsus paradoxus greater than 25 mm Hg. Decreased level of consciousness, inability to speak, significantly diminished or absent breath sounds, and inability to lie supine herald the onset of acute respiratory failure.70–73

Initial ABGs indicate hypocapnia and respiratory alkalosis caused by hyperventilation. As the attack continues and the patient starts to fatigue, hypoxemia and hypercapnia develop.⁷⁰ Lactic acidosis also may occur as a result of lactate overproduction by the respiratory muscles. The end result is the development of respiratory and metabolic acidosis.⁷¹

Deterioration of pulmonary function tests despite aggressive bronchodilator therapy is diagnostic of status asthmaticus and indicates the potential need for intubation. A peak expiratory flow rate (PEFR) less than 40% of predicted or an FEV₁ (maximum volume of gas that the patient can exhale in 1 second [forced expiratory volume in 1 second]) less than 20% of predicted indicates severe airflow obstruction, and the need for intubation with mechanical ventilation may be imminent.⁷²

Medical management of the patient with status asthmaticus is directed toward supporting oxygenation and ventilation. Bronchodilators, corticosteroids, oxygen therapy, and intubation and mechanical ventilation are the mainstays of therapy.70

A wide variety of physiological and psychological factors contribute to the development of LTMVD. Physiological factors include those conditions that result in decreased gas exchange, increased ventilatory workload, increased ventilatory demand, decreased ventilatory drive, and increased respiratory muscle fatigue (Box 15-4).⁷⁵ Psychological factors include those conditions that result in loss of breathing pattern control, lack of motivation and confidence, and delirium (Box 15-5).⁷⁶ The development of LTMVD also is affected by the severity and duration of the patient’s current illness and any underlying chronic health problems.⁷⁷

The goal of medical and nursing management of the patient with LTMVD is successful weaning. The Third National Study Group on Weaning from Mechanical Ventilation, sponsored by the American Association of Critical-Care Nurses, proposed the Weaning Continuum Model that divides weaning into three stages: preweaning, weaning process, and weaning outcome.78 It is within this framework that the management of the long-term ventilator-dependent patient is described. In addition, the common nursing diagnoses for this patient population are listed in the Nursing Diagnosis Priorities box on Long-Term Mechanical Ventilation.