Chapter 27 Acute Respiratory Failure

Acute respiratory failure is the inability to maintain adequate gas exchange. It is defined by abnormalities of arterial oxygen (P_ao₂) and carbon dioxide (P_aco₂) tensions. Hypoxemia may occur with a normal or low P_aco₂ (type 1 respiratory failure) or with an elevated P_aco₂ (type 2 respiratory failure). Respiratory failure is commonly associated with respiratory distress, which manifests as tachypnea, dyspnea, and the use of the accessory muscles of breathing.

Respiratory failure is relatively common in cardiac surgery patients and has a wide variety of causes (Table 27-1). The need for prolonged ventilatory support (>72 hours) occurs in approximately 6% of patients undergoing coronary artery bypass graft surgery,¹ and reintubation is required in approximately 3% of patients.²

Table 27-1 Common Causes of Postoperative Respiratory Failure Hypoxemia in Patients After Cardiac Surgery

On Arrival in the ICU and During Mechanical Ventilation

Pulmonary edema

Atelectasis/lobar collapse

Endobronchial intubation

Pneumothorax

Hemothorax

Ventilator dysynchrony

Bronchospasm

Low S_VO₂ (low cardiac output,^* anemia)

Immediately Following Extubation

Residual sedative or opioid drugs

Residual neuromuscular blockade

Atelectasis

Upper airway obstruction/edema

Late Deterioration in Respiratory Function

Cardiac tamponade (following removal of pacing wires)

Pneumothorax (following removal of chest drains)

Left ventricular dysfunction

Arrhythmias (particularly atrial fibrillation)

Atelectasis and lobar collapse

Sepsis (pneumonia, mediastinitis)

Pulmonary embolus

Pulmonary edema

ICU, intensive care unit.

* Causes of low cardiac output in the early period after cardiac surgery include all conditions listed in Table 20-4 with the exception of low systemic vascular resistance.

This chapter is divided into three sections: (1) mechanisms of respiratory failure; (2) diagnosis and treatment of respiratory failure; (3) specific causes of respiratory failure. Only an overview of respiratory failure is provided here. The physiological mechanisms of respiratory failure are explored in greater detail in Chapter 1, and the ventilatory treatment is described in Chapters 28 and Chapter 29.

MECHANISMS OF RESPIRATORY FAILURE

Acute respiratory failure arises because of problems with: (1) the lungs and chest wall; (2) the heart; or (3) the central nervous system (CNS) and neuromuscular system. There are also a number of factors that, although not direct causes, exacerbate respiratory failure.

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.)

APPROACH TO PATIENTS WITH ACUTE RESPIRATORY DISTRESS

As with all acute problems in the intensive care unit, diagnosis and treatment must proceed simultaneously.

Diagnosis

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

Clinical Context

A cardiac cause for respiratory failure must always be considered in patients with histories of left ventricular dysfunction and in those who have recently undergone cardiac surgery. Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for pneumothorax, pneumonia, and arrhythmias. Postoperative patients, particularly those who are obese or have limited mobility, are at increased risk for atelectasis, pneumonia, and pulmonary embolism. Right ventricular dysfunction predisposes to right-to-left shunting across a patent foramen ovale (PFO). Certain patients are at increased risk for developing acute lung injury (ALI) and acute respiratory distress syndrome (ARDS; see subsequent material). Patients with reduced levels of consciousness are at increased risk for hypoventilation and pulmonary aspiration.

Examination

Examination of the respiratory and cardiovascular systems is important, but it must be rapid and targeted. The following physical findings should be sought:

• The absence of respiratory distress. This is uncommon and suggests a CNS or neuromuscular problem.

• Reduced respiratory excursion or reduced breath sounds in one hemithorax. These signs are consistent with endobronchial intubation, pneumothorax, lobar collapse, or hemothorax. Dullness to percussion is suggestive of lobar collapse, consolidation, or hemo-thorax/pleural effusion. Hyperresonance to percussion is suggestive of pneumothorax.

• Bronchial breathing. This is suggestive of lobar collapse or pneumonia.

• Crackles on chest auscultation. These are nonspecific but are suggestive of pulmonary edema.

• Inspiratory stridor. This is indicative of extrathoracic airway obstruction, typically laryngeal edema after extubation.

• Expiratory wheeze. This is suggestive of intrathoracic airway obstruction (bronchospasm, retained secretions, blood clot) or pulmonary edema. Pulmonary edema, not bronchospasm, is the most common cause of wheezing in cardiac surgery patients.

• A hot swollen leg. This suggests the possibility of deep venous thrombosis and pulmonary embolus.

• An unstable sternal wound and systemic sepsis. These suggest mediastinitis.

If appropriate, a targeted neurologic assessment should be performed, focusing on level of consciousness (Glasgow coma scale), cough, gag reflex, and focal neurologic deficit (see Chapter 37).

Investigations

Blood Gas Analysis and Oximetry.

In addition to measurement of arterial oxygen saturation (S_ao₂), P_ao₂, and P_aco₂, useful information is obtained from (1) calculation of the alveolar-arterial (A-a) Po₂ gradient, (2) measurement of S_vo₂, and (3) assessment of metabolic parameters (pH, bicarbonate, base excess, and lactate; see Chapters 1 and Chapter 31).

S_vo₂ is obtained from blood drawn from the distal port of a pulmonary artery catheter, but a reasonable approximation is obtained from blood drawn from the proximal port of a central venous catheter (S_SVCo₂). The normal value for S_vo₂ is 75%. A low value (<60%) suggests that oxygen delivery is inadequate for the patient’s needs and, in the presence of intrapulmonary shunting, will exacerbate hypoxemia.

The A-a gradient is the difference between P_Ao₂ and P_ao₂, where P_Ao₂ is calculated from the alveolar air equation (see Equation 1-18). With healthy lungs breathing air, the A-a gradient is very low, less than 1 κPa (<7.5 mmHg). However, the A-a gradient is influenced by age and F_Io₂. At age 40, the upper limit of normal is about 3 κPa (23 mmHg), increasing to 5 κPa (38 mmHg) at age 80 (when breathing room air). To this must be added 0.75 to 1 κPa (6 to 7.6 mmHg) for every 10% increase in F_Io₂. Within these limitations, the A-a gradient can be used to differentiate hypoventilation (normal A-a gradient) from intrapulmonary shunting (elevated A-a gradient).

The ratio between P_ao₂ and the fractional inspired oxygen (P_ao₂/F_Io₂) is a widely used measure of the degree of impairment of oxygenation, and it has the advantage of being largely independent of oxygen therapy. A P_ao₂/F_Io₂ ratio of 25 κPa (188 mmHg) corresponds to a shunt fraction of about 20% and constitutes severely impaired oxygenation.

Chest Radiography.

The chest radiograph (see Chapter 6) is essential in the assessment of respiratory failure. If possible, the film should be obtained while the patient is erect because this position improves the diagnostic yield, particularly in terms of pleural collections and pneumothoraces. In a patient with respiratory failure, a normal chest radiograph is consistent with the diagnoses of hypoventilation, microatelectasis, low SVo2, and shunting across a PFO.

Hemodynamic Monitoring and Echocardiography.

Hemodynamic evaluation (see Chapter 8) is an integral part of the assessment of respiratory failure. A PAC allows for quantification of cardiac output, S_Vo₂, and pulmonary artery wedge pressure (PAWP). PAWP helps to determine the cause of pulmonary edema (see subsequent material). Echocardiography (see Chapter 7) reliably identifies the cause of low cardiac output (see Chapter 20) and can be used to identify a PFO.