ORIGINAL ARTICLES

EFFECT OF OXYGEN ON EXERCISE ABILITY IN CHRONIC RESPIRATORY INSUFFICIENCY☆

This chapter reviews the known effects of chronic oxygen therapy, its indications, and the various delivery systems now available. Oxygen therapy has become very important in the treatment of severe chronic obstructive pulmonary disease (COPD). Long-term oxygen improves survival in hypoxemic COPD. Other benefits of oxygen include better exercise tolerance, decreased dyspnea, and improvements in neuropsychological performance. In addition, there appear to be beneficial effects on pulmonary hemodynamics, sleep quality, reduced minute ventilation, and WOB. Hypoxemia is defined as an abnormally low arterial oxygen tension P_aO₂. The physiologic causes of hypoxemia include a low inspired partial pressure of oxygen, abnormal ventilation–perfusion relationship, decreased diffusion capacity, alveolar hypoventilation, and right to left shunt. Oxygen therapy increases the F_iO₂ and is the primary treatment for hypoxemia resulting from the first three causes. The hypoxemia of alveolar hypoventilation is best treated by increased ventilation while a true shunt is by definition unresponsive to hyperoxia. Although the reason for increased survival with oxygen is not clear, there is evidence that O₂ can improve pulmonary hemodynamics and leads to reduced cardiac work and greater oxygen delivery. The consequences of exercise induced and nocturnal desaturation are not absolutely known. Clinicians should be aware of air travel-induced hypoxemia in COPD and be able to identify those who need oxygen in flight. Once a patient meets the criteria for oxygen prescription, the physician must complete the certificate of Medical Necessity Form specifying the indication for oxygen, type of system and liter flow at rest, exercise and sleep.

This chapter reviews the known effects of chronic oxygen therapy, its indications, and the various delivery systems now available. Oxygen therapy has become very important in the treatment of severe chronic obstructive pulmonary disease (COPD). Long-term oxygen improves survival in hypoxemic COPD. Other benefits of oxygen include better exercise tolerance, decreased dyspnea, and improvements in neuropsychological performance. In addition, there appear to be beneficial effects on pulmonary hemodynamics, sleep quality, reduced minute ventilation, and WOB. Hypoxemia is defined as an abnormally low arterial oxygen tension P_aO₂. The physiologic causes of hypoxemia include a low inspired partial pressure of oxygen, abnormal ventilation–perfusion relationship, decreased diffusion capacity, alveolar hypoventilation, and right to left shunt. Oxygen therapy increases the F_iO₂ and is the primary treatment for hypoxemia resulting from the first three causes. The hypoxemia of alveolar hypoventilation is best treated by increased ventilation while a true shunt is by definition unresponsive to hyperoxia. Although the reason for increased survival with oxygen is not clear, there is evidence that O₂ can improve pulmonary hemodynamics and leads to reduced cardiac work and greater oxygen delivery. The consequences of exercise induced and nocturnal desaturation are not absolutely known. Clinicians should be aware of air travel-induced hypoxemia in COPD and be able to identify those who need oxygen in flight. Once a patient meets the criteria for oxygen prescription, the physician must complete the certificate of Medical Necessity Form specifying the indication for oxygen, type of system and liter flow at rest, exercise and sleep.

Differences in oxygen delivery between portable oxygen concentrators (POC) and liquid oxygen (LO) portable units, pose a question if POCs are equally effective as LOs in reducing exercise-induced hypoxaemia.

Randomized, single-blind clinical trial.

Thirteen COPD patients (means: age 66±11 year, FEV₁ 35.2±13.7% predicted) and respiratory failure (means: PaO₂ 52±5 mmHg, PaCO₂ 51.3±7.5 mmHg).

All patients underwent a series of 6-min walk tests (6 MWT) carried out in random order among one of the three devices: POC, LO cylinder and cylinder with compressed air (CA). Oxygen supplementation was 3 lpm for LO and an equivalent to 3 lpm in a pulse flow system for POC.

The mean SpO₂ was equally improved at rest: 92.9±2.8% with POC and 91.7±2.0% with LO compared to CA—87.8±2.7% (POC and LO vs. CA p<0.05). POC and LO significantly improved oxygenation during 6 MWT (mean SpO₂ was 84.3±5% and 83.8±4.2%, respectively) compared to breathing CA—77.6±7.4%, p<0.05. Mean 6 MWT distance increased with LO (350±83 m) and POC (342±96 m) when compared to CA (317±84 m), however, these differences were not statistically significant. Dyspnoea score assessed at the end of the exercise (Borg scale) was significantly lower when breathing oxygen (4.2±1.2 with POC and 4.1±1.7 with LO vs. 5.4±1.9 with CA, p<0.05).

Effectiveness of oxygen supplementation from a POC did not differ from the LO source during 6 MWT in COPD patients with respiratory failure. Oxygen at 3 lpm flow was not sufficient to prevent hypoxaemia during strenuous exercise.

This essay summarizes 16 reports, published since 1956, that describe the effects of hyperoxia on exercise endurance in persons with COPD who have severe airflow obstruction (ie, FEV₁ < 1.0 L or < 39% of predicted) and mild hypoxemia at rest (ie, Pao₂ > 62 mm Hg or arterial oxygen saturation [Sao₂] measured by pulse oximetry of > 91%). The term hyperoxia is used because, in a proportion of study participants, oxygen administration increased exercise endurance in a dose-dependent fashion, up to a fraction of inspired oxygen of 0.5 or a flow of 100% O₂ of 6 L/min. The process appears to be dependent on an increase in Pao₂ rather than on the restoration of Sao₂ to normal levels. The results of pulmonary function tests were not predictive of response. Increased exercise performance was associated with a decrease in dyspnea, respiratory frequency, and minute ventilation. The slowing of respiratory frequency and the decrease in pulmonary air trapping likely accounted for the decrease in dyspnea. Slowing of the respiratory rate, which occurred at the expense of the retention of CO₂, is most likely due to a hyperoxia-induced decrease in chemoreceptor ventilatory drive from the aortic and carotid bodies. Research is called for to determine the following: (1) the prevalence of COPD patients who have severe airflow limitation accompanied by mild hypoxemia; (2) the proportion of these patients who show improvements in exercise performance during a test of hyperoxic exercise; and (3) whether enhanced exercise performance during a brief test translates into a meaningful increase in the ability to perform the activities of daily living.