Low-Flow Systems. Low-flow systems, in which the oxygen flow is lower than the inspiratory flow rate, have a limited ability to raise the FIO2 because they depend on entrained room air to make up the balance of the inspired gas. The FIO2 of these systems is extremely sensitive to small changes in the ventilatory pattern. Nasal cannulae—small, flexible prongs that sit just inside each naris—deliver oxygen at 1-6 L/min. The nasopharynx acts as a reservoir for storing the oxygen, and patients may breathe through either the mouth or nose as long as the nasal passages remain patent. These devices typically deliver 24-28% FIO2 at 2-3 L/min. Up to 40% FIO2 is possible at higher flow rates, although this is poorly tolerated for more than brief periods because of mucosal drying. The simple face mask, a clear plastic mask with side holes for clearance of expiratory gas and inspiratory air entrainment, is used when higher concentrations of oxygen delivered without tight control are desired. The maximum FIO2 of a face mask can be increased from around 60% at 6-15 L/min to > 85% by adding a 600- to 1000-mL reservoir bag. With this partial rebreathing mask, most of the inspired volume is drawn from the reservoir, avoiding dilution by entrainment of room air.
High-Flow Systems. The most commonly used high-flow oxygen delivery device is the Venturi-style mask, which uses a specially designed mask insert to entrain room air reliably in a fixed ratio and thus provides a relatively constant FIO2 at relatively high flow rates. Typically, each insert is designed to operate at a specific oxygen flow rate, and different inserts are required to change the FIO2. Lower delivered FIO2 values use greater entrainment ratios, resulting in higher total (oxygen plus entrained air) flows to the patient, ranging from 80 L/min for 24% FIO2 to 40 L/min at 50% FIO2. While these flow rates are much higher than those obtained with low-flow devices, they still may be lower than the peak inspiratory flows for patients in respiratory distress, and thus the actual delivered O2 concentration may be lower than the nominal value. Oxygen nebulizers, another type of Venturi-style device, provide patients with humidified oxygen at 35-100% FIO2 at high flow rates. Finally, oxygen blenders provide high inspired oxygen concentrations at very high flow rates. These devices mix high-pressure compressed air and oxygen to achieve any concentration of O2 from 21-100% at flow rates of up to 100 L/min. These same blenders are used to provide control of FIO2 for ventilators, CPAP/BiPAP machines, oxygenators, and other devices with similar requirements. Again, despite the high flows, the delivery of high FIO2 to an individual patient also depends on maintaining a tight-fitting seal to the airway and/or the use of reservoirs to minimize entrainment of diluting room air.
Monitoring of Oxygenation. Monitoring and titration are required to meet the therapeutic goal of oxygen therapy and to avoid complications and side effects. Although cyanosis is a physical finding of substantial clinical importance, it is not an early, sensitive, or reliable index of oxygenation. Cyanosis appears when ~5 g/dL of deoxyhemoglobin is present in arterial blood, representing an oxygen saturation of ~67% when a normal amount of hemoglobin (15 g/dL) is present. However, when anemia lowers the hemoglobin to 10 g/dL, then cyanosis does not appear until the arterial blood saturation has decreased to 50%. Invasive approaches for monitoring oxygenation include intermittent laboratory analysis of arterial or mixed venous blood gases and placement of intravascular cannulae capable of continuous measurement of oxygen tension. The latter method, which relies on fiber-optic oximetry, is used frequently for the continuous measurement of mixed venous hemoglobin saturation as an index of tissue extraction of oxygen, usually in critically ill patients.
Noninvasive monitoring of arterial oxygen saturation can be achieved using transcutaneous pulse oximetry, in which oxygen saturation is measured from the differential absorption of light by oxyhemoglobin and deoxyhemoglobin and the arterial saturation determined from the pulsatile component of this signal. Application is simple, and calibration is not required. Pulse oximetry measures hemoglobin saturation and not PO2. It is not sensitive to increases in PO2 that exceed levels required to saturate the blood fully. Pulse oximetry is very useful for monitoring the adequacy of oxygenation during procedures requiring sedation or anesthesia, rapid evaluation and monitoring of potentially compromised patients, and titrating oxygen therapy in situations where toxicity from oxygen or side effects of excess oxygen are of concern. Near infrared spectroscopy (NIRS) is a noninvasive technique being used to monitor oxygen content in the cerebral cortex. Unlike pulse oximetry NIRS measures all reflected light in both pulsatile arterial blood and nonpulsatile venous blood, the primary compartment in the cerebral vascular bed. NIRS is useful to monitor cerebral oxygenation in surgical procedures involving cardiopulmonary bypass and circulatory arrest (Guarracino, 2008).
Complications of Oxygen Therapy. Administration of supplemental oxygen is not without potential complications. In addition to the potential to promote absorption atelectasis and depress ventilation (discussed earlier), high flows of dry oxygen can dry out and irritate mucosal surfaces of the airway and the eyes, as well as decrease mucociliary transport and clearance of secretions. Humidified oxygen thus should be used when prolonged therapy (>1 hour) is required. Finally, any oxygen-enriched atmosphere constitutes a fire hazard, and appropriate precautions must be taken both in the operating room and for patients on oxygen at home.
It is important to realize that hypoxemia still can occur despite the administration of supplemental oxygen. Furthermore, when supplemental oxygen is administered, desaturation occurs at a later time after airway obstruction or hypoventilation, potentially delaying the detection of these critical events. Therefore, whether or not oxygen is administered to a patient at risk for these problems, it is essential that both O2 saturation and adequacy of ventilation be assessed frequently.
Therapeutic Uses of Oxygen
Correction of Hypoxia. The primary therapeutic use of oxygen is to correct hypoxia. Hypoxia is most commonly a manifestation of an underlying disease, and administration of oxygen thus should be viewed as temporizing therapy. Efforts must be directed at correcting the cause of the hypoxia. For example, airway obstruction is unlikely to respond to an increase in inspired oxygen tension without relief of the obstruction. More important, while hypoxemia owing to hypoventilation after a narcotic overdose can be improved with supplemental oxygen administration, the patient remains at risk for respiratory failure if ventilation is not increased through stimulation, narcotic reversal, or mechanical ventilation. Hypoxia resulting from most pulmonary diseases can be alleviated at least partially by administration of oxygen, allowing time for definitive therapy to reverse the primary process. Thus, administration of oxygen is basic and important treatment for all forms of hypoxia.
Reduction of Partial Pressure of an Inert Gas. Since nitrogen constitutes some 79% of ambient air, it also is the predominant gas in most gas-filled spaces in the body. In situations such as bowel distension from obstruction or ileus, intravascular air embolism, or pneumothorax, it is desirable to reduce the volume of air-filled spaces. Since nitrogen is relatively insoluble, inhalation of high concentrations of oxygen (and thus low concentrations of nitrogen) rapidly lowers the total-body partial pressure of nitrogen and provides a substantial gradient for the removal of nitrogen from gas spaces. Administration of oxygen for air embolism is additionally beneficial because it helps to relieve localized hypoxia distal to the vascular obstruction. In the case of decompression sickness, or bends, lowering the inert gas tension in blood and tissues by oxygen inhalation prior to or during a barometric decompression reduces the supersaturation that occurs after decompression so that bubbles do not form. If bubbles do form in either tissues or the vasculature, administration of oxygen is based on the same rationale as that described for gas embolism.
Hyperbaric Oxygen Therapy. Oxygen can be administered at greater than atmospheric pressure in hyerbaric chambers (Thom, 2009). Clinical uses of hyperbaric oxygen therapy include the treatment of trauma, burns, radiation damage, infections, non-healing ulcers, skin grafts, spasticity, and other neurological conditions. Hyperbaric chambers can withstand pressures that range from 200 to 600 kPa (2-6 atm), although inhaled oxygen tension that exceeds 300 kPa (3 atm) rarely is used. Chambers range from single-person units to multiroom establishments housing complex medical equipment.
Hyperbaric oxygen therapy has two components: increased hydrostatic pressure and increased O2 pressure. Both factors are necessary for the treatment of decompression sickness and air embolism. The hydrostatic pressure reduces bubble volume, and the absence of inspired nitrogen increases the gradient for elimination of nitrogen and reduces hypoxia in downstream tissues. Increased oxygen pressure at the tissue is the primary therapeutic goal for other indications for hyperbaric O2. A small increase in PO2 in ischemic areas enhances the bactericidal activity of leukocytes and increases angiogenesis. Repetitive brief exposures to hyperbaric oxygen may enhance therapy for chronic refractory osteomyelitis, osteoradionecrosis, crush injury, or the recovery of compromised skin and tissue grafts. Increased O2 tension can be bacteriostatic and useful in the treatment for the spread of infection with Clostridium perfringens and clostridial myonecrosis (gas gangrene).
Hyperbaric oxygen may be useful in generalized hypoxia. In CO poisoning, hemoglobin (Hb) and myoglobin become unavailable for O2 binding because of the high affinity of these proteins for CO. Affinity for CO is ~250 times greater than the affinity for O2; thus, an alveolar concentration of CO = 0.4 mm Hg (1/250th that of alveolar O2, which is ~100 mm Hg), will compete equally with O2 for binding sites on Hb. High Po2 facilitates competition of O2 for Hb binding sites as CO is exchanged in the alveoli. In addition, hyperbaric O2 increases the availability of dissolved O2 in the blood (Table 19–4). In a randomized clinical trial (Weaver et al., 2002), hyperbaric O2 decreased the incidence of long- and short-term neurological sequelae after CO intoxication. The occasional use of hyperbaric oxygen in cyanide poisoning has a similar rationale. Hyperbaric oxygen may be useful in severe short-term anemia since sufficient oxygen can be dissolved in the plasma at 3 atm to meet metabolic demand. Such treatment must be limited because oxygen toxicity depends on increased Po2, not on the oxygen content of the blood.
Adverse effects of hyperbaric oxygen therapy include middle ear barotrauma, CNS toxicity, seizures, lung toxicity, and aspiration pneumonia. Contraindications to hyperbaric oxygen therapy include pneumothorax and concurrent doxorubicin, bleomycin, or disulfiram therapy. Relative contraindications include respiratory tract infections, severe obstructive lung disease, fever, seizure disorders, optic neuritis, pregnancy, concurrent steroid use, and claustrophobia.