The sudden onset of dyspnea is typically accompanied by physical signs of distress (Fig. 4-1). For example, patients in distress appear anxious, with eyes wide open, the forehead furrowed, and the nostrils flared. These patients may be diaphoretic and flushed. They also may try to sit upright or, if seated, lean forward with their elbows resting on a bedside table or their knees. If they are in respiratory or cardiac distress, they may be ashen, pale, or cyanotic and using their accessory muscles of respiration (e.g., the sternocleidomastoid, scalene, and trapezius muscles). In severe respiratory distress, the intercostal spaces and the supraclavicular notch may appear indented (retracted) during active inspiration. The patient may complain of not getting enough air. Paradoxical or abnormal movement of the thorax and abdomen may be noted, and abnormal breath sounds may be heard on auscultation. Tachycardia, arrhythmias, and hypotension also are common findings.⁵ Pulse oximetry is a quick and cost-effective method of assessing arterial oxygen saturation and pulse rate (see Chapter 10). (NOTE: Anemia and reduced cardiac output can compromise oxygen delivery to the tissues. In such cases, reduced pulse pressures and blood flow may prevent the pulse oximeter from accurately estimating the patient’s actual arterial oxygen saturation and heart rate.)

In acute respiratory failure (ARF), respiratory activity is absent or is insufficient to maintain adequate oxygen uptake and carbon dioxide clearance. Clinically, ARF may be defined as the inability to maintain Pao₂, Paco₂, and pH at acceptable levels. These levels generally are considered to be (1) a PaO₂ below the predicted normal range for the patient’s age under ambient (atmospheric) conditions, (2) a Paco₂ greater than 50 mm Hg and rising, and (3) a falling pH of 7.25 and lower.1–3

Two forms of ARF have been described: hypoxemic respiratory failure and hypercapnic respiratory failure.⁶ Hypoxemic respiratory failure is a result of severe ventilation/perfusion () mismatching. It can also occur with diffusion defects, right-to-left shunting, alveolar hypoventilation, aging, and inadequate inspired oxygen. A good working definition of acute hypoxemic respiratory failure is acute life-threatening or vital organ–threatening tissue hypoxia.³ Hypoxemic respiratory failure can be treated with oxygen or in combination with positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) (see Chapter 13). Mechanical ventilation may also be necessary if hypoxemic respiratory failure occurs along with acute hypercapnic respiratory failure and an increased work of breathing.

Acute hypercapnic respiratory failure, or acute ventilatory failure, occurs when a person cannot achieve adequate ventilation to maintain a normal Paco₂. The ventilatory pump consists of the respiratory muscles, thoracic cage, and nerves that are controlled by respiratory centers in the brainstem. Three types of disorders can lead to pump failure (Box 4-2):

As shown in Table 4-1, the clinical signs of hypoxemia and hypercapnia closely resemble the signs seen in patients with respiratory distress (see Fig. 4-1 and Key Point 4-1). Tachycardia and tachypnea are early indicators of hypoxia. In some cases of hypoxemic respiratory failure, the patient’s condition can be treated successfully by administering enriched oxygen mixtures. However, some hypoxemic conditions, such as severe shunting, are refractory to oxygen therapy (i.e., administering enriched oxygen mixtures does not significantly reduce the level of hypoxemia).

In patients with hypercapnic respiratory failure, PaCO₂ levels are elevated with accompanying hypoxemia unless the patient is receiving oxygen therapy. Elevation of PaCO₂ leads to an increase in cerebral blood flow as a result of dilation of cerebral blood vessels. Severe hypercapnia eventually leads to CO₂ narcosis, cerebral depression, coma, and death.

Untreated hypoxemia, hypercapnia, and acidosis can lead to cardiac dysrhythmias, ventricular fibrillation, and even cardiac arrest.⁷ The potential for these consequences underscores the importance of recognizing that a patient is in acute or impending respiratory failure and the need to initiate therapy in a timely manner. The elements required to achieve a successful outcome are (1) use of supplemental oxygen therapy, (2) maintenance of a patent airway, and (3) continuous monitoring of oxygenation and ventilatory status with pulse oximetry and arterial blood gas (ABG) analysis.

Other CNS disorders associated with tumors, stroke, or head trauma can alter the normal pattern of breathing. For example, a head injury might result in cerebral hemorrhage and increased intracranial pressure (ICP). If significant bleeding occurs with these types of injuries, abnormal breathing patterns such as Cheyne-Stokes respirations or Biot respirations may occur. In many cases, cerebral abnormalities can also affect normal reflex responses, such as swallowing. In these cases endotracheal intubation may be required to protect the airway from aspiration or from obstruction by the tongue (Case Study 4-1).

There is considerable debate about whether controlled hyperventilation should be used as a ventilatory technique in patients with a closed head injury. Controlled hyperventilation lowers the PaCO₂ and increases the pH, resulting in reduced cerebral perfusion and reduced ICP. It is important to understand that this effect is temporary, lasting only about 24 hours, because the body eventually adapts to the change through renal compensatory mechanisms.⁸ Although controlled hyperventilation is still used by some clinicians to lower sudden increases in ICP, clinicians must keep in mind that the desire to use this technique for patients with traumatic brain injury is not by itself an indication for intubation and mechanical ventilation.³ Furthermore, patients with traumatic brain injury have a better long-range outcome (3-6 months) when controlled hyperventilation is not used.⁸

Neuromuscular disorders that can lead to respiratory failure usually are the result of one of the following:

The onset of respiratory failure can vary considerably depending on the cause of the neuromuscular dysfunction. Drug-induced neuromuscular failure usually has a rapid onset (Case Study 4-2), whereas the onset of respiratory failure in disease states like myasthenia gravis may not occur for days or years, or it might not happen at all. Regardless of the cause, intubation and mechanical ventilation are indicated if respiratory fatigue occurs rapidly in a patient with a neuromuscular disorder and ARF is imminent.⁹

The maximum inspiratory pressure (MIP) and vital capacity (VC) can be used to assess respiratory muscle strength of patients with neuromuscular disorders. These measurements are noninvasive, relatively easy to obtain, and inexpensive. Respiratory therapists can measure MIP and VC every 2 to 4 hours to monitor changes in respiratory status. Commonly cited threshold values are an MIP of −20 to −30 cm H₂O or less (i.e., 0 to −20 cm H₂O) and a VC lower than 10 to 15 mL/kg. Note that although these measures are often used, their effectiveness in improving outcomes has not been established (Table 4-2).³ (Techniques for measuring MIP and VC are discussed later in this chapter.)

Determination of baseline ABG values, along with periodic measurement of oxygen saturation by pulse oximetry (Spo₂) is also appropriate when caring for patients with neuromuscular problems. Repeating the ABG analysis may be indicated if the patient’s clinical status changes significantly. Furthermore, if the patient’s condition progressively worsens, the practitioner should not wait until an acute situation develops to intervene (Case Study 4-3). Clinicians generally agree that invasive positive-pressure ventilation should be initiated before acute respiratory acidosis develops.³

An increase in the WOB can lead to respiratory failure secondary to respiratory muscle fatigue. WOB normally accounts for 1% to 4% of total oxygen consumption at rest.10 In patients experiencing respiratory distress, the WOB can increase to as much as 35% to 40% of total oxygen consumption.^11,12 Increased WOB usually is associated with an increased rate or depth of breathing (or both). More work is required to move the same V_T when the patient has obstructed airways, a restrictive lung disorder, or both (Case Study 4-4). A patient’s tolerance to maintain the increased WOB is limited by the eventual fatigue of respiratory muscles. Increased WOB can induce hypoventilation, respiratory insufficiency, and eventually respiratory failure.

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