ICU (and other) patients without respiratory disorders may develop hypoxia (O₂ saturation < 90%) during a hospital stay. Hypoxia in patients with known respiratory conditions is discussed under those disorders.

Etiology

Numerous disorders cause hypoxia (eg, dyspnea, respiratory failure; see Table 6: Approach to the Critically Ill Patient: Some Causes of Oxygen Desaturation); however, acute hypoxia developing in a patient hospitalized with a nonrespiratory illness usually has a more limited set of causes. These causes can be divided into

• Disorders of ventilation
• Disorders of oxygenation

Table 6
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Some Causes of Oxygen Desaturation Mechanism Examples Disorders of ventilation Decreased ventilatory drive Decreased mental status (eg, caused by head injury, oversedation, sepsis, shock, or stroke) Obstructed ventilation Bronchospasm Dislodgement of endotracheal tube Mucus plugging of the airways or endotracheal tube Severe pain in the chest, abdomen, or both Rib fractures Thoracic or abdominal surgery Disorders of oxygenation Pulmonary causes Acute respiratory distress syndrome Atelectasis, pneumonia, pneumothorax, pulmonary embolus, pulmonary contusion, aspiration pneumonitis Nonpulmonary causes Iatrogenic fluid overload Heart failure (eg, due to exacerbation of underlying disease or to acute MI)

Evaluation

Total fluid volume given during the hospital stay and, in particular, the previous 24 h should be ascertained to identify volume overload. Drugs should be reviewed for sedative administration and dosage. In significant hypoxia (O₂ saturation < 85%), treatment begins simultaneously with evaluation.

History

Very sudden onset dyspnea and hypoxia suggest pulmonary embolus (PE) or pneumothorax (mainly in a patient on positive pressure ventilation). Fever, chills, and productive cough (or increased secretions) suggest pneumonia. A history of cardiopulmonary disease (eg, asthma, COPD, heart failure) may indicate an exacerbation of the disease. Unilateral extremity pain suggests deep venous thrombosis (DVT) and hence possible PE. Preceding major trauma or sepsis requiring significant resuscitation suggests acute respiratory distress syndrome. Preceding chest trauma suggests pulmonary contusion.

Physical examination

Patency of the airway and strength and adequacy of respirations should be assessed immediately. For patients on mechanical ventilation, it is important to determine that the endotracheal tube is not obstructed or dislodged. Unilateral decreased breath sounds with clear lung fields suggest pneumothorax or right mainstem bronchus intubation; with crackles and fever, pneumonia is more likely. Distended neck veins with bilateral lung crackles suggest volume overload; distention with clear lungs and tracheal deviation suggests tension pneumothorax. Bilateral lower-extremity edema suggests heart failure, but unilateral edema suggests DVT and hence possible PE. Wheezing represents bronchospasm (typically asthma or allergic reaction, but it occurs rarely with PE or heart failure). Decreased mental status suggests hypoventilation.

Testing

Hypoxia is generally recognized initially by pulse oximetry. Patients should have a chest x-ray, ECG, and ABGs (to confirm hypoxia and evaluate adequacy of ventilation). If diagnosis remains unclear after these tests, testing for PE (see Pulmonary Embolism: Diagnosis) should be considered. Bronchoscopy may be done in intubated patients to rule out (and remove) a tracheobronchial plug. Pulmonary artery catheterization may be needed to rule out heart failure if volume status is unclear.

Treatment

Identified causes are treated as discussed elsewhere in The Manual. If hypoventilation persists, mechanical ventilation via noninvasive positive pressure ventilation or endotracheal intubation is necessary (see Respiratory Failure and Mechanical Ventilation). Persistent hypoxia requires supplemental O₂.

O₂ therapy

The amount of O₂ given is guided by ABG or pulse oximetry to maintain Pao₂ between 60 and 80 mm Hg (ie, 92 to 100% saturation) without causing O₂ toxicity. This level provides satisfactory tissue O₂ delivery; because the oxyhemoglobin dissociation curve is sigmoidal, increasing Pao₂ to > 80 mm Hg increases O₂ delivery very little and is not necessary. The lowest fractional inspired O₂ (Fio₂) that provides an acceptable Pao₂ should be provided. O₂ toxicity is both concentration- and time-dependent. Sustained elevations in Fio₂ > 60% result in inflammatory changes, alveolar infiltration, and, eventually, pulmonary fibrosis. An Fio₂ > 60% should be avoided unless necessary for survival. An Fio₂ < 60% is well tolerated for long periods.

An Fio₂ < 40% can be given via nasal cannula or simple face mask. A nasal cannula uses an O₂ flow of 1 to 6 L/min. Because 6 L/min is sufficient to fill the nasopharynx, higher flow rates are of no benefit. Simple face masks and nasal cannulas do not deliver a precise Fio₂ because of inconsistent admixture of O₂ with room air from leakage and mouth breathing. However, Venturi-type masks can deliver very accurate O₂ concentrations.

An Fio₂ > 40% requires use of an O₂ mask with a reservoir that is inflated by O₂ from the supply. In the typical nonrebreather mask, the patient inhales 100% O₂ from the reservoir, but during exhalation, a rubber flap valve diverts exhaled breath to the environment, preventing admixture of CO₂ and water vapor with the inspired O₂. Nonetheless, because of leakage, such masks deliver an Fio₂ of at most 80 to 90%.

Key Points

• Hypoxia can be caused by disorders of ventilation and/or oxygenation and is usually first recognized by pulse oximetry.
• Patients should have a chest x-ray, ECG, and ABGs (to confirm hypoxia and evaluate adequacy of ventilation); if diagnosis remains unclear, consider testing for pulmonary embolus.
• Give O₂ as needed to maintain Pao₂ between 60 and 80 mm Hg (ie, 92 to 100% saturation) and treat the cause.

Last full review/revision October 2012 by Soumitra R. Eachempati, MD