Alveolar hypoventilation occurs when the amount of oxygen being brought into the alveoli is insufficient to meet the metabolic needs of the body.6 This can be the result of increasing metabolic oxygen needs or decreasing ventilation.⁵ Hypoxemia caused by alveolar hypoventilation is associated with hypercapnia and commonly results from extrapulmonary disorders.^1,7

Ventilation/perfusion (V/Q) mismatching occurs when ventilation and blood flow are mismatched in various regions of the lung in excess of what is normal. Blood passes through alveoli that are underventilated for the given amount of perfusion, leaving these areas with a lower-than-normal amount of oxygen. V/Q mismatching is the most common cause of hypoxemia and is usually the result of alveoli that are partially collapsed or partially filled with fluid.1,7

The extreme form of V/Q mismatching, intrapulmonary shunting, occurs when blood reaches the arterial system without participating in gas exchange. The mixing of unoxygenated (shunted) blood and oxygenated blood lowers the average level of oxygen present in the blood. Intrapulmonary shunting occurs when blood passes through a portion of a lung that is not ventilated. This may be the result of (1) alveolar collapse secondary to atelectasis or (2) alveolar flooding with pus, blood, or fluid.1,7

If allowed to progress, hypoxemia can result in a deficit of oxygen at the cellular level. As the tissue demands for oxygen continue and the supply diminishes, an oxygen supply/demand imbalance occurs and tissue hypoxia develops. Decreased oxygen to the cells contributes to impaired tissue perfusion and the development of lactic acidosis and multiple organ dysfunction syndrome.⁸

Actions to improve oxygenation include supplemental oxygen administration and the use of positive airway pressure.8 The purpose of oxygen therapy is to correct hypoxemia, and although the absolute level of hypoxemia varies in each patient, most treatment approaches aim to keep the arterial hemoglobin oxygen saturation greater than 90%.⁹ The goal is to keep the tissues’ needs satisfied but not produce hypercapnia or oxygen toxicity.⁹ Supplemental oxygen administration is effective in treating hypoxemia related to alveolar hypoventilation and V/Q mismatching. When intrapulmonary shunting exists, supplemental oxygen alone is ineffective.¹¹ In this situation, positive pressure is necessary to open collapsed alveoli and facilitate their participation in gas exchange. Positive pressure is delivered via invasive and noninvasive mechanical ventilation. To avoid intubation, positive pressure is usually administered initially noninvasively via a mask.^12,13 For further information on noninvasive ventilation, see Chapter 16.

Interventions to improve ventilation include the use of noninvasive and invasive mechanical ventilation. Depending on the underlying cause and the severity of the ARF, the patient may be initially treated with noninvasive ventilation.12 However, one study found that those patients with a pH of less than 7.25 at initial presentation had an increased likelihood of the need for invasive mechanical ventilation.¹⁴ The selection of ventilatory mode and settings depends on the patient’s underlying condition, severity of respiratory failure, and body size. Initially the patient is started on volume ventilation in the assist/control mode. In the patient with chronic hypercapnia, the settings should be adjusted to keep the arterial blood gas values within the parameters expected to be maintained by the patient after extubation.¹⁵ For further information on mechanical ventilation see Chapter 16.

Medications to facilitate dilation of the airways may also be of benefit in the treatment of the patient with ARF. Bronchodilators, such as beta₂-agonists and anticholinergic agents, aid in smooth muscle relaxation and are of particular benefit to patients with airflow limitations. Methylxanthines, such as aminophylline, are no longer recommended because of their negative side effects. Steroids also are often administered to decrease airway inflammation and enhance the effects of the beta₂-agonists. Mucolytics and expectorants are also no longer used since they have been found to be of no benefit in this patient population.16

Sedation is necessary in many patients to assist with maintaining adequate ventilation. It can be used to comfort the patient and decrease the work of breathing, particularly if the patient is fighting the ventilator. Analgesics should be administered for pain control.^17,18 In some patients, sedation does not decrease spontaneous respiratory efforts enough to allow adequate ventilation. Neuromuscular paralysis may be necessary to facilitate optimal ventilation. Paralysis also may be necessary to decrease oxygen consumption in the severely compromised patient.¹⁸

Acidosis may occur in the patient for a number of reasons. Hypoxemia causes impaired tissue perfusion, which leads to the production of lactic acid and the development of metabolic acidosis. Impaired ventilation leads to the accumulation of carbon dioxide and the development of respiratory acidosis. Once the patient is adequately oxygenated and ventilated, the acidosis should correct itself. The use of sodium bicarbonate to correct the acidosis has been shown to be of minimal benefit to the patient and thus is no longer recommended as first-line treatment. Bicarbonate therapy shifts the oxygen-hemoglobin dissociation curve to the left and can worsen tissue hypoxia. Sodium bicarbonate may be used if the acidosis is severe (pH <7.1), refractory to therapy, and causing dysrhythmias or hemodynamic instability.19

The initiation of nutrition support is of utmost importance in the management of the patient with ARF. The goals of nutrition support are to meet the overall nutritional needs of the patient while avoiding overfeeding, to prevent nutrition delivery-related complications, and to improve patient outcomes.20 Failure to provide the patient with adequate nutrition support results in the development of malnutrition. Both malnutrition and overfeeding can interfere with the performance of the pulmonary system, further perpetuating ARF. Malnutrition decreases the patient’s ventilatory drive and muscle strength, whereas overfeeding increases carbon dioxide production, which then increases the patient’s ventilatory demand, resulting in respiratory muscle fatigue.²¹

The enteral route is the preferred method of nutrition administration. If the patient cannot tolerate enteral feedings or cannot receive enough nutrients enterally, he or she will be started on parenteral nutrition. Because the parenteral route is associated with a higher rate of complications, the goal is to switch to enteral feedings as soon as the patient can tolerate them.^20,21 Nutrition support should be initiated before the third day of mechanical ventilation for the well-nourished patient and within 24 hours for the malnourished patient.^20,21

The patient with acute respiratory failure may experience a number of complications including ischemic-anoxic encephalopathy,22 cardiac dysrhythmias,²³ venous thromboembolism,²⁴ and gastrointestinal bleeding.²⁵ Ischemic-anoxic encephalopathy results from hypoxemia, hypercapnia, and acidosis.²² Dysrhythmias are precipitated by hypoxemia, acidosis, electrolyte imbalances, and the administration of beta₂-agonists.²³ Maintaining oxygenation, normalizing electrolytes, and monitoring drug levels will facilitate the prevention and treatment of encephalopathy and dysrhythmias.^22,23 Venous thromboembolism is precipitated by venous stasis resulting from immobility and can be prevented through the use of graduated compression stockings or pneumatic compression devices and low-dose unfractionated heparin or low-molecular-weight heparin.²⁴ Gastrointestinal bleeding can be prevented through the use of histamine₂-antagonists, cytoprotective agents, or proton pump inhibitors.²⁵ In addition, the patient is at risk for the complications associated with an artificial airway, mechanical ventilation, enteral and parenteral nutrition, and peripheral arterial cannulation.

Early in the patient’s hospital stay, the patient and family should be taught about acute respiratory failure, its etiologies, and its treatment. As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the reoccurrence of the precipitating disorder (Patient Education box on Acute Respiratory Failure). If the patient smokes, he or she should be encouraged to stop smoking and be referred to a smoking cessation program (Evidence-Based Collaborative Practice box on Smoking Cessation Guidelines). In addition, the importance of participating in a pulmonary rehabilitation program should be stressed. Additional information for the patient can be found at the American Lung Association website (www.lungusa.org).

Within the first 72 hours after the initial insult, the exudative phase or acute phase ensues. Once released, the mediators cause injury to the pulmonary capillaries, resulting in increased capillary membrane permeability leading to the leakage of fluid filled with protein, blood cells, fibrin, and activated cellular and humoral mediators into the pulmonary interstitium. Damage to the pulmonary capillaries also causes the development of microthrombi and elevation of pulmonary artery pressures. As fluid enters the pulmonary interstitium, the lymphatics are overwhelmed and unable to drain all the accumulating fluid, resulting in the development of interstitial edema. Fluid is then forced from the interstitial space into the alveoli, resulting in alveolar edema. Pulmonary interstitial edema also causes compression of the alveoli and small airways. Alveolar edema causes swelling of the type I alveolar epithelial cells and flooding of the alveoli. Protein and fibrin in the edema fluid precipitate the formation of hyaline membranes over the alveoli. Eventually, the type II alveolar epithelial cells are also damaged, leading to impaired surfactant production. Injury to the alveolar epithelial cells and the loss of surfactant lead to further alveolar collapse.38,39

Hypoxemia occurs as a result of intrapulmonary shunting and V/Q mismatching secondary to compression, collapse, and flooding of the alveoli and small airways. Increased work of breathing occurs as a result of increased airway resistance, decreased functional residual capacity (FRC), and decreased lung compliance secondary to atelectasis and compression of the small airways. Hypoxemia and the increased work of breathing lead to patient fatigue and the development of alveolar hypoventilation. Pulmonary hypertension occurs as a result of damage to the pulmonary capillaries, microthrombi, and hypoxic vasoconstriction leading to the development of increased alveolar dead space and right ventricular afterload. Hypoxemia worsens as a result of alveolar hypoventilation and increased alveolar dead space. Right ventricular afterload increases and leads to right ventricular dysfunction and a decrease in cardiac output.³⁸

This phase begins as disordered healing and starts in the lungs. Cellular granulation and collagen deposition occur within the alveolar-capillary membrane. The alveoli become enlarged and irregularly shaped (fibrotic) and the pulmonary capillaries become scarred and obliterated. This leads to further stiffening of the lungs, increasing pulmonary hypertension, and continued hypoxemia.38,39

Recovery occurs over several weeks as structural and vascular remodeling take place to reestablish the alveolar-capillary membrane. The hyaline membranes are cleared and intraalveolar fluid is transported out of the alveolus into the interstitium. The type II alveolar epithelial cells multiply, some of which differentiate to type I alveolar epithelial cells, facilitating the restoration of the alveolus. Alveolar macrophages remove cellular debris.38,39

Traditionally the patient with ALI was ventilated with a mode of volume ventilation, such as assist/control ventilation (A/CV) or synchronized intermittent mandatory ventilation (SIMV), with tidal volumes adjusted to deliver 10 to 15 ml/kg. Current research now indicates that this approach may have actually led to further lung injury. It is now known that repeated opening and closing of the alveoli cause injury to the lung units (atelectrauma), resulting in inhibited surfactant production, and increased inflammation (biotrauma), resulting in the release of mediators and an increase in pulmonary capillary membrane permeability. In addition, excessive pressure in the alveoli (barotrauma) or excessive volume in the alveoli (volutrauma) leads to excessive alveolar wall stress and damage to the alveolar-capillary membrane, resulting in air escaping into the surrounding spaces.42 Thus several different approaches have been developed to facilitate the mechanical ventilation of the patient with ALI.

Oxygen is administered at the lowest level possible to support tissue oxygenation. Continued exposure to high levels of oxygen can lead to oxygen toxicity, which perpetuates the entire process. The goal of oxygen therapy is to maintain an arterial hemoglobin oxygen saturation of 90% or greater using the lowest level of oxygen—preferably less than 0.50.35

Adequate tissue perfusion depends on an adequate supply of oxygen being transported to the tissues. An adequate CO and hemoglobin level is critical to oxygen transport. CO depends on heart rate, preload, afterload, and contractility. A variety of fluids and medications are used to manipulate this parameter. Newer approaches to fluid management include maintaining a very low intravascular volume (pulmonary artery occlusion pressure of 5 to 8 mm Hg) with fluid restriction and diuretics, while supporting the CO with vasoactive and inotropic medications. The goal is to decrease the amount of fluid leakage into the lungs.46