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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.
Numerous disorders cause hypoxia (eg, dyspnea, respiratory failure—see Table: 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
Some Causes of Oxygen Desaturation
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.
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. Symptoms and signs of MI may indicate acute valvular insufficiency, pulmonary edema, or cardiogenic shock. 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.
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. Findings are suggestive as follows:
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 with pulmonary edema, cardiogenic shock, pericardial tamponade (often without crackles), or acute valvular insufficiency.
Distended neck veins with clear lungs or unilateral decrease in breath sounds and tracheal deviation suggest 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.
Hypoxia is generally recognized initially by pulse oximetry. Patients should have the following:
Bedside intensivist-performed echocardiography (see page Monitoring and Testing the Critical Care Patient : Hand-held echocardiography) may be used to assess for hemodynamically significant pericardial effusion or reduced global left ventricular function until formal echocardiography can be done. Elevated serum levels of brain (B-type) natriuretic peptide (BNP) may help differentiate heart failure from other causes of hypoxia. If diagnosis remains unclear after these tests, testing for PE (see page Pulmonary Embolism (PE) : Diagnosis) should be considered. Bronchoscopy may be done in intubated patients to rule out (and remove) a tracheobronchial plug.
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 page Respiratory Failure and Mechanical Ventilation). Persistent hypoxia requires supplemental O2.
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%.
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.
* This is the Professional Version. *