Acute Respiratory Failure

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9 Acute Respiratory Failure

Acute respiratory failure is one of the leading causes of admission to an intensive care unit (ICU). Behrendt et al. reported that the incidence of acute respiratory failure requiring hospitalization was 137 per 100,000 population in the United States, and the median age of the patients was 69 years.¹ More recently, Ray et al. reported that 29% of patients presenting to an emergency department (ED) with acute respiratory failure require admission to an ICU.²

Acute respiratory failure can be secondary to either a failure of oxygenation (hypoxic respiratory failure), a failure of elimination of carbon dioxide (hypercarbic respiratory [ventilatory] failure), or both problems simultaneously. Chronic obstructive pulmonary disease (COPD) with acute exacerbation is the most common cause of ventilatory failure requiring ICU admission.

Pathophysiology

The primary gas exchange functions of the lung are the transport of oxygen from inspired air (or some other gas mixture) to hemoglobin (Hb) in the bloodstream and elimination of carbon dioxide. Dysfunction of either function results in acute respiratory failure (or at least acute respiratory dysfunction).

Causes of Hypoxic Respiratory Failure

Hypoventilation

The partial pressure of carbon dioxide in arterial blood (PaCO₂) increases when minute ventilation decreases. An increase in PaCO₂ decreases alveolar partial pressure of oxygen (PAO₂) because the carbon dioxide displaces oxygen in the alveoli. The relationship between PAO₂ and PaCO₂ is described by the alveolar gas equation:

The causes of hypoventilation are discussed below.

Ventilation/Perfusion Mismatch

Gas exchange is optimal when ventilation and perfusion in the lung are matched. A decrease in perfusion relative to ventilation (i.e., an increase in physiologic dead space) or a decrease in ventilation relative to perfusion (shunt) results in ventilation-perfusion () mismatching. Hypoxia occurs as a result of mismatching because of admixture of venous with arterial blood at the capillary level. mismatching is the most common cause of hypoxia in hospitalized patients. In contrast to hypoxemia caused by an anatomic shunt, hypoxemia caused by mismatching can be improved by administration of supplemental oxygen.

Shunt

Right-to-left shunting refers to the process whereby deoxygenated venous blood bypasses functioning alveolar-pulmonary capillary units and then mixes with oxygenated arterial blood. Right-to-left shunts can be caused by anatomic derangements, such as certain congenital cardiac malformations (e.g., atrial septal defect), but they can also occur when mismatching is so severe that a portion of pulmonary arterial blood flows through lung regions with essentially no ventilation. Potential causes of this sort of physiologic shunting include pneumonia, lung contusion, or severe congestive heart failure. Oxygenation cannot be improved with supplemental oxygen in patients with a true right-to-left shunt, irrespective of whether the shunt is caused by an anatomic or a functional derangement.

Diffusion Impairment

Thickening of the alveolar endothelial/epithelial barrier or a decrease in transit time in the pulmonary capillary bed (due to very high cardiac output) can impair diffusion of oxygen from the alveoli into the blood.

High Altitude

Barometric pressure decreases with increasing altitude; as a result, the partial pressure of oxygen in the ambient atmosphere decreases as well. Consequently, unless supplemental oxygen is provided, hypoxia is an inevitable consequence of respiration at high altitude.

Impaired Tissue Perfusion

When tissue perfusion is impaired, the cells attempt to maintain normal oxygen consumption by extracting more oxygen from the available blood supply. As a consequence, venous oxygen tension decreases. Unless the fractional pulmonary shunt flow is zero, the decrease in mixed venous oxygen tension inevitably leads to a decrease in arterial oxygen tension. Although low cardiac output or impaired blood flow to tissues can cause hypoxia, hypoperfusion per se is rarely a primary cause of clinically significant hypoxia. Nevertheless, hypoperfusion is a common factor that exacerbates the degree of hypoxia caused by other problems.

If the circulating concentration of carboxyhemoglobin or methemoglobin increases, the oxygen-carrying capacity of the blood decreases. Although arterial oxygen tension may be normal, arterial oxygen saturation is abnormally low because of the presence of Hb derivatives that are incapable of transporting oxygen.

Hypercarbic Respiratory Failure

PaCO₂ is inversely proportional to alveolar ventilation; thus, PaCO₂ increases when the elimination of carbon dioxide is decreased because of a decrease in minute ventilation. PaCO₂ also increases if minute ventilation remains constant but carbon dioxide production increases. Primary pulmonary diseases are the most common cause of hypercarbia, although nonpulmonary causes contribute to hypoventilation, increased PaCO₂, and the need for mechanical ventilatory support.

Minute ventilation can be decreased owing to pulmonary or nonpulmonary factors. Pulmonary causes of impaired minute ventilation include large airway obstruction (e.g., due to the presence of a foreign body or laryngeal spasm), small airway obstruction (e.g., bronchospasm), and destruction of lung parenchyma (e.g., emphysema). Extrapulmonary causes of hypercarbia include neurologic and muscular problems. Neurologic problems include depression of central respiratory drive due to the pharmacologic effects of narcotics or sedatives; depression of respiratory drive as a consequence of stroke, intracranial hemorrhage, or head trauma (i.e., central alveolar hypoventilation); and impaired neuromuscular transmission due to phrenic nerve injury or spinal cord injury (C5 or higher), Guillain-Barré syndrome, myasthenia gravis, or the polyneuropathy of critical illness. Muscular weakness or skeletal abnormalities can cause a decrease in tidal volume and minute ventilation. Causes of hypoventilation secondary to musculoskeletal abnormalities are prolonged use of neuromuscular blocking agents, malnutrition, hypomagnesemia, hypokalemia, hypophosphatemia, kyphoscoliosis, rib fractures, and flail chest, to name several.

In rare cases, hypercarbia can be secondary to increased carbon dioxide production and relative hypoventilation due to overfeeding, since fat synthesis increases the rate of carbon dioxide production relative to the rate of oxygen consumption (respiratory quotient >1.0). Hypermetabolism, such as occurs with high fever or thyrotoxicosis, also is associated with increased carbon dioxide production and (in the setting of already impaired minute ventilation) can exacerbate hypercarbia.

Clinical Presentation

Dyspnea is the most common symptom associated with acute respiratory failure. Dyspnea is usually associated with rapid shallow breathing and the use of accessory respiratory muscles. Active use of the accessory muscles of respiration during expiration is indicative of impaired airflow during exhalation, a common problem in patients with COPD.

The investigations to evaluate the causes of respiratory failure depend on the suspected mechanism of acute respiratory failure and the primary disease process. Pulse oximetry is a useful monitoring tool and should be carried out in all cases. Other worthwhile diagnostic studies include:

• Analysis of arterial blood gases – will permit diagnosis of a widened alveolar-arterial PO₂ gradient and/or hypercarbia.

• Examination of the chest radiograph – useful in almost all cases. If the chest film is clear, the differential diagnosis should include pulmonary embolism, anatomic right-to-left shunt, pneumothorax, cirrhosis, and COPD. If the chest radiograph shows unilateral infiltrates or effusion, the differential diagnosis should include pleural effusion, aspiration, lobar pneumonia, atelectasis, and infarction. If bilateral infiltrates are present, the differential diagnosis should include pulmonary edema (cardiac and noncardiac causes), pneumonia, and pulmonary hemorrhage.³

Other more specialized tests (e.g., computed tomography, cultures) are needed based on the differential diagnosis for the suspected primary disease.

Management

The goal is to maintain adequate oxygenation and ventilation and treat the primary cause of respiratory failure. For hypoxic respiratory failure, the primary goal is to improve arterial oxygenation. In most cases, a reasonable goal is to maintain PaO₂ above 65 to 70 mm Hg and arterial blood oxygen saturation (SaO₂) above 90%. In very severe cases of hypoxi respiratory failure, efforts to achieve these indices of arterial oxygenation will require interventions, namely very high airway pressures during mechanical ventilation and delivery of 100% oxygen in the inspired gas—interventions that can further damage the lung. Accordingly, in rare instances, it may be prudent to tolerate lower SaO₂ values rather than using ventilator settings that could exacerbate lung damage.

Administration of supplemental oxygen will improve oxygenation in most clinical situations except in the presence of a true shunt. Low-flow oxygen can be delivered using a nasal canula or a face mask. The maximum FIO₂ that can be delivered using these approaches is about 0.4. This level of oxygen supplementation is inadequate when the alveolar-arterial (A-a) PO₂ gradient is very wide. The FIO₂ in the inspired gas delivered using a nasal canula or face mask is a function of minute ventilation. When minute ventilation is high, the FIO₂ in the inspired gas delivered using a nasal canula or face mask is lower than when minute ventilation is lower. Accordingly, low-flow methods of providing supplemental oxygen should be used cautiously in patients who are dependent on hypoxic drive or have very high minute ventilation. A higher FIO₂ can be provided if a face mask is combined with a reservoir bag, because contamination of the inspired gas mixture with room air is minimized.

Noninvasive positive pressure ventilation (NIPPV) and mechanical ventilation via an endotracheal tube are two approaches for providing supplemental oxygen and, at the same time, providing partial or total support for minute ventilation (i.e., decreasing the work of breathing). In hemodynamically stable patients with mild or moderate respiratory failure, NIPPV may decrease the need for intubation and mechanical ventilation and decrease the patient’s length of stay in the ICU.^4,⁵ NIPPV should not be used in patients with altered mental status, who are unable to protect the airway, or for patients who are unable to clear secretions adequately. For some patients, tolerance for NIPPV can be improved by using a nasal mask and starting at a lower level of inspiratory pressure (5 cm H₂O).

In cases of hypercarbic respiratory failure, the primary goal of treatment is to maintain arterial pH above 7.32 with a PaCO₂ appropriate for the pH.⁶ In the absence of marked acidemia or hypoxemia, hypercarbia is well tolerated. Accordingly, it may be preferable under some circumstances to accept PaCO₂ values that are abnormally high (e.g., >45 mm Hg) rather than risk damaging (or further damaging) the lungs with ventilator settings that promote excessive shear stress within the pulmonary parenchyma.

Bronchodilators can be delivered as metered dose inhalers or nebulizers. Patients with tachypnea and respiratory distress may not be able to use metered dose inhalers. The bronchodilating effects of β-adrenergic agonists and anticholinergic drugs are synergistic. Long-acting β-adrenergic agonists should not be used to treat acute exacerbations of chronic bronchospasm. Corticosteroids are often used to treat acute exacerbations of diseases associated with airway inflammation and bronchospasm (e.g., asthma, COPD). Intravenous methylprednisolone (40 mg IV every 12 hours to 125 mg IV every 6 hours) is often employed if the response is inadequate to initial efforts using bronchodilator treatments with β-adrenergic agonists and anticholinergic agents. Aerosolized steroids may not improve bronchospasm during the acute episode but are useful for maintenance treatment. Patients who experience changes in the nature of the sputum and signs of infection may benefit from a short course (7–10 days) of antibiotic therapy.

The use of NIPPV in hemodynamically stable patients with mild to moderate ventilatory failure may decrease the need for mechanical ventilatory support and length of stay. The precautions while using NIPPV are the same as listed previously.