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Roberts: Clinical Procedures in Emergency Medicine, 5th ed.
Copyright © 2009 Saunders, An Imprint of Elsevier
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OXYGEN THERAPY
Adequate O2 delivery depends upon the inspired partial pressure of O2, alveolar ventilation, pulmonary gas exchange, oxygen-carrying capacity of the blood, andcardiac output. The easiest factor to manipulate is the partial pressure of inspired O2, accomplished by simply increasing the fraction of inspired oxygen    with supplemental O2.
Indications and Contraindications
Resuscitate all patients in cardiac arrest or respiratory arrest with 100% O2. The most certain indication for supplemental O2 is the presence of arterial hypoxemia, defined by a PaO2<60 mm Hg or arterial oxygen saturation (SaO2) less than 90%.[39] Normal subjects will begin to experience memory loss at an arterial oxygen partial pressure (Pao2) of 45 mm Hg and loss of consciousness occurs at a Pao2 of 30 mm Hg. [40] [41] [42] Chronically hypoxemic patients can adapt and function quite well with a Pao2 of 50 mm Hg or lower.[43]
When tissue hypoxia is present or suspected, giveO2 therapy. [39] [44] Shock states resulting from hemorrhage, vasodilatory states, low cardiac output, and obstructive lesions can all lead to tissue hypoxia and should benefit from supplemental O2. Whatever the cause of the shock state, the administration of O2 is indicated until the situation can be thoroughly evaluated and cause-specific therapy is instituted.
Respiratory distress withoutdocumented arterial hypoxemia is a common indication for O2 administration, although no evidence exists to support this practice.[45] O2 therapy for acute myocardial infarction is often recommended, but there is no difference in outcomes between patients receiving O2 or those receiving room air after myocardial infarction. The AHA gives a class I recommendation for O2 only in patients with hypoxemia,cyanosis, or respiratory distress. [39] [44] [46] [47] [48] Although O2 is routinely administered to acute stroke patients, no convincing evidence exists that this practice is beneficial without documented hypoxia; it is not recommended by current guidelines. [49] [50] [51] It is reasonable to administer O2 to hypotensive patients and those with severe trauma until tissue hypoxia can bedefinitively excluded.[45]
Administer O2 to patients with carbon monoxide poisoning. The half-life of carboxyhemoglobin is 4 to 5 hours in a subject breathing room air but can be decreased to approximately 1 hour by the administration of 100% O2 by non-rebreather face mask at atmospheric pressure.[52]
There are no contraindications to O2 therapy when a definite indication exists. The risks of hypoxemiaare grave and undeniable. O2 therapy should never be withheld from a hypoxemic patient for fear of complications or clinical deterioration. CO2 retention is not a contraindication to O2 therapy. Rather, it demands that the clinician administer O2 carefully and recognize the potential for respiratory acidosis and clinical deterioration. Although the mechanism of respiratory acidosis developing inCOPD patients administered O2 is debated, its occurrence is not. [53] [54] Caution should be used when administering supplemental O2 to patients with an arterial carbon dioxide pressure    over 40 mm Hg, but it should not be withheld.
Oxygen Delivery Devices
High-flow delivery systems provide an    that is relatively constant despite changes in the patient's respiratory pattern. The Venturi maskis the high-flow delivery device that is widely available ( Fig. 3–4A and inset). Room air is entrained into the system through entrainment ports and mixes with the O2 provided from the O2 source. The proportion of entrained air, and therefore the    , is constant and is determined by the velocity of the O2 jet and size of the entrainment ports. Because the total gas flow (O2 plus air through...