Acute Respiratory Failure

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Chapter 27 Acute Respiratory Failure

Acute respiratory failure is the inability to maintain adequate gas exchange. It is defined by abnormalities of arterial oxygen (Pao2) and carbon dioxide (Paco2) tensions. Hypoxemia may occur with a normal or low Paco2 (type 1 respiratory failure) or with an elevated Paco2 (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 SVO2 (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.

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.

Examination

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

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 (Sao2), Pao2, and Paco2, useful information is obtained from (1) calculation of the alveolar-arterial (A-a) Po2 gradient, (2) measurement of Svo2, and (3) assessment of metabolic parameters (pH, bicarbonate, base excess, and lactate; see Chapters 1 and Chapter 31).

Svo2 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 (SSVCo2). The normal value for Svo2 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 PAo2 and Pao2, where PAo2 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 FIo2. 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 FIo2. 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 Pao2 and the fractional inspired oxygen (Pao2/FIo2) 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 Pao2/FIo2 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, SVo2, 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.

Treatment

Treatment of acute respiratory failure is both supportive and specific to the underlying condition. Specific treatments are discussed in specific causes of respiratory failure. Supportive treatments are listed subsequently. The treatment goals are outlined in Table 27-2.

Table 27-2 Therapeutic Aims for Managing Acute Respiratory Failure

SaO2 ≥ 90% (approximately 7 kPa or 55 mmHg)
pH >7.25
Respiratory rate <30 to 35/min*
Ability to speak in short sentences
Hemodynamic stability
Ability to protect airway

* Higher respiratory rates cannot usually be sustained indefinitely; exhaustion and respiratory arrest are likely to supervene.

Respiratory failure severe enough to cause a fall in the level of consciousness such that the patient cannot obey commands mandates endotracheal intubation to protect against pulmonary aspiration.

Positive Pressure Ventilation

Positive pressure ventilation is used to improve gas exchange and reduce the work of breathing. It may be invasive (see Chapter 29) or noninvasive (see Chapter 28).

The need for ventilatory support depends on the severity of the respiratory failure, the rate of deterioration, the underlying disease process, and the need to protect the airway. When respiratory failure develops rapidly or occurs in the context of multiple organ dysfunction syndrome, early institution of invasive ventilation is indicated. However, if respiratory failure develops slowly and is not associated with severe metabolic derangement or other organ failure, urgent intubation may not be required, and other targeted therapy (e.g., antibiotics, physical therapy, diuretics) may be tried first. The signs of severe respiratory failure that, if not rapidly corrected, indicate the need for urgent intubation and ventilation are listed in Table 27-3.

Table 27-3 Features of Severe Respiratory Failure That Indicate the Need for Urgent Endotracheal Intubation

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Respiratory System
SaO2 ≤ 85% (approximately 6.5 kPa or 50 mmHg) with high-flow face-mask oxygen or an FIO2 ≥ 0.6 with noninvasive ventilation
Rising PaCo2* with respiratory acidemia (pH < 7.1)
Respiratory distress: respiratory rate >40/min, intercostal in-drawing, use of accessory muscles, the inability to speak more than one or two words between breaths
Cardiovascular System
Heart rate >120 beats/min
Falling blood pressure or cardiac output or escalating inotrope requirements
Increasing lactic acidosis
Central Nervous System
Confusion and agitation