Bolante, Rhanne S.

CON IV- A01

Hazards of Oxygen

Oxygen therapy may be associated with such adverse effects as absorptive atelectasis and reduction of hypoxic vasoconstriction that might extend ventilation/perfusion (V'/Q') mismatch. In general, oxygen therapy is safe and effective. The net effect of oxygen therapy is to reverse hypoxemia and the benefits far outweigh any risks. Hazards the clinician must recognise include oxygen toxicity, CO2 retention and physical hazards during the storage and handling of oxygen. Absorption atelectasis The atmosphere is composed of 78% nitrogen and 21% oxygen. Since oxygen is exchanged at the alveolicapillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse. Absorption atelectasis refers to the condition where the reduction of nitrogen concentration in the lungs causes a collapse. Under normal circumstances, the air you breathe contains nearly 78% of nitrogen. It is this nitrogen that helps keep the alveoli or air sacs in the lungs open and functioning properly. Nitrogen provides a certain amount of surface tension that prevents the collapse of the alveoli. This decreases the nitrogen concentration in the air and leads to absorption atelectasis. Oxygen Toxicity Patients exposed to inspiratory oxygen fraction (Fi,O2) >50% may experience oxygen toxicity, particularly if the exposure is prolonged. Oxygen toxicity is related to free radicals. The major end product of normal oxygen metabolism is water. Some oxygen molecules, however, are converted into highly reactive species called radicals, which include superoxide anions, perhydroxy radicals and hydroxyl radicals, and are toxic to alveolar and tracheobronchial cells. Pathophysiological changes include decreased lung compliance, reduced inspiratory airflow, decreased diffusing capacity and small airway dysfunction. While these changes are well recognised in the acute care setting of mechanically ventilated patients receiving FI,O2 >50%, little is known about the long-term effect of low flow (24-28%) oxygen. It is widely accepted that the increased survival and quality-of-life benefits of long-term oxygen therapy outweigh the possible risks. Carbon Dioxide Retention There has been an overemphasis that administration of oxygen may lead to respiratory drive depression, hypercapnia with resulting respiratory acidosis. This has caused some clinicians to be overly

timid about prescribing oxygen. Oxygen-induced hypercapnia does rarely occur, but it is even rarer that this leads to respiratory acidosis. The mechanism is that alveolar hypoxia leads to pulmonary artery vasoconstriction, which causes increased blood perfusion to under-ventilated alveoli. As better-ventilated lung units receive less perfusion, the V/Q mismatch becomes greater. In most cases, titrating oxygen flow so as to maintain Pa,O2 at 8-8.6 kPa (60-65 mmHg) can minimize the likelihood of hypercapnia and respiratory acidosis. When hypercapnia is present, initial oxygen delivery settings should be titrated using serial ABG assessments rather than relying solely on oximetry. CO2 retention is tolerable for patients with an intact renal system, since they are capable of reabsorbing enough bicarbonate and maintain acid-base balance. The ability of patients to tolerate CO2 retention (permissive hypercapnia) is thought to be an adaptive mechanism that lessens the work of breathing. Accordingly, there is a significant population of COPD patients who are chronic CO2 retainers while maintaining their pH in a normal range. In all cases, correction of hypoxemia takes precedence over concerns about CO2 retention. Depression of Ventilation Anxiolytic and antidyspneic affects of oxygen therapy can promote sleep which then results in loss of voluntary drive to breathe. Respiration is then sustained only by metabolic control mechansims which then can contribute to increasing hypercarbia. Hypoventilation resulting from the above mechanisms then decreases inspiratory flow demand reducing the amount of entrained air, especially with low flow oxygen systems, which then may increase the FiO2 delivered to the patient when then can exacerbate the above mechanisms further. Physical Hazards The major physical hazards of oxygen therapy are fires or explosions. Most fires are caused by patients lighting cigarettes as oxygen is flowing into their noses [30]. While the cannula is constructed of fireretardant plastic, both the cannula and the patients nose will burn in the presence of a flame and oxygen in high concentrations. Patients, family and other care-givers must be warned not to smoke near oxygen. In general, major accidents associated with oxygen therapy are rare and can be avoided by good patient and family training along with common sense. Gas Oxygen Compressed gas oxygen containers should not be stored near water heaters, furnaces or other sources of heat or flame. A compressed oxygen cylinder can be accidentally knocked over, causing explosive disconnection of the regulator and rendering the cylinder a dangerous missile. Liquid Oxygen Serious freeze burns can occur if the patient does not take proper precautions while transfilling liquid oxygen. Bacterial Infections Associated with Humidifiers Contamination of oxygen humidifiers occurs more commonly on long term oxygen devices such as home concentrators. Common Bacterial species found included Klebsiella aerogenes Pseudomonas species, Streptococcus viridans, Streptococcus epidermidis. Pathologic infections are rare in spite of this finding. Hospital based disposable humidifiers do not appear to pose a significant threat even up to 12 weeks as

long as they are maintained properly with appropriate changes of tubing and use of reservoir bags in patient lines.