Limits...
Long-term oxygen therapy: are we prescribing appropriately?

Güell Rous R - Int J Chron Obstruct Pulmon Dis (2008)

Bottom Line: It also appears to reduce the number of hospitalizations, increase effort capacity, and improve health-related quality of life.The benefits of LTOT depend on correction of hypoxemia.During sleep, continuous monitoring of SaO2 and PaCO2 should be performed to confirm correction of SaO2 overnight.

View Article: PubMed Central - PubMed

Affiliation: Departament de Pneumologia, Hospital de la Santa Creu I de Sant Pau, Barcelona, Spain. mguellr@santpau.es

ABSTRACT
Long-term oxygen therapy (LTOT) is the treatment proven to improve survival in chronic obstructive pulmonary disease (COPD) patients with chronic respiratory failure. It also appears to reduce the number of hospitalizations, increase effort capacity, and improve health-related quality of life. Standard LTOT criteria are related to COPD patients who have PaO2 < 60 mmHg, are in a clinical stable situation, and are receiving optimal pharmacological treatment. According to LTOT guidelines, oxygen should be prescribed for at least 18 hours per day although some authors consider 24 hours would be more beneficial. The benefits of LTOT depend on correction of hypoxemia. Arterial blood gases should be measured at rest. During exercise, an effort test should be done to assure adequate SaO2. During sleep, continuous monitoring of SaO2 and PaCO2 should be performed to confirm correction of SaO2 overnight. An arterial blood gas sample should be taken at awakening to assess PaCO, in order to prevent hypoventilation from the oxygen therapy. Several issues that need to be addressed are the use of LTOT in COPD patients with moderate hypoxemia, the efficacy of LTOT in patients who desaturate during exercise or during sleep, the optimal dosage of oxygen supplementation, LTOT compliance, and the LTOT prescription in diseases other than COPD.

Show MeSH

Related in: MedlinePlus

Evolution of pH▪: oxygen flow titrated at daytime,▴: 1 litre increase in oxygen flow.Note: p < 0.05 Samolski et al in press.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2629963&req=5

f3-copd-3-231: Evolution of pH▪: oxygen flow titrated at daytime,▴: 1 litre increase in oxygen flow.Note: p < 0.05 Samolski et al in press.

Mentions: Oxygen therapy can generate several potentially detrimental effects. The most relevant of these is hypercapnia, which is mediated by mechanisms such as hypoventilation, ventilation-perfusion redistribution, or the Haldane effect. Moreover, sleep itself generates ventilatory alterations that include a decrease in baseline metabolism, an increase in airway resistance, hypotonia of the respiratory pump, and decreased sensitivity of respiratory centers. In healthy individuals, these alterations generate only small changes in PaO2 or PaCO2 during the night, but in COPD patients they may cause severe hypoxemia and hypercapnia. In this population, physiopathologic phenomena such as greater hypoventilation due to a reduction in tidal volume, greater alterations in ventilation-perfusion distribution, associated OSAS and reduction of mucociliar clearance may also be key to increased hypercapnia and development of sleep hypoventilation (SH). O’Donoghue and colleagues (2003) and Tárrega and colleagues (2002) observed SH in a high percentage of COPD patients, 43% and 59%, respectively, and suggested the finding was likely due to the oxygen therapy. Increasing the resting flow rate by 1 or 2 l min−1 may therefore exacerbate hypoventilation. Our group recently conducted a study to evaluate changes in gas exchange. We increased the nocturnal flow rate by 1 liter and observed that this induced SH and respiratory acidosis in a significant number of patients who did not have SH when they received the same oxygen titration as during the day (34.2% vs. 23.7% of patients) (Figures 2 and 3) (Samolski et al in press). This finding further supports the hypothesis that oxygen can induce hypoventilation. Plant and colleagues (2000) had previously shown that a high oxygen flow rate in acute respiratory failure in COPD patients was the most frequent cause of hypercapnia and led to the need for noninvasive ventilation. Such results reinforce the need to evaluate and titrate the nocturnal oxygen flow individually, at least in hypercapnic COPD patients.


Long-term oxygen therapy: are we prescribing appropriately?

Güell Rous R - Int J Chron Obstruct Pulmon Dis (2008)

Evolution of pH▪: oxygen flow titrated at daytime,▴: 1 litre increase in oxygen flow.Note: p < 0.05 Samolski et al in press.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2629963&req=5

f3-copd-3-231: Evolution of pH▪: oxygen flow titrated at daytime,▴: 1 litre increase in oxygen flow.Note: p < 0.05 Samolski et al in press.
Mentions: Oxygen therapy can generate several potentially detrimental effects. The most relevant of these is hypercapnia, which is mediated by mechanisms such as hypoventilation, ventilation-perfusion redistribution, or the Haldane effect. Moreover, sleep itself generates ventilatory alterations that include a decrease in baseline metabolism, an increase in airway resistance, hypotonia of the respiratory pump, and decreased sensitivity of respiratory centers. In healthy individuals, these alterations generate only small changes in PaO2 or PaCO2 during the night, but in COPD patients they may cause severe hypoxemia and hypercapnia. In this population, physiopathologic phenomena such as greater hypoventilation due to a reduction in tidal volume, greater alterations in ventilation-perfusion distribution, associated OSAS and reduction of mucociliar clearance may also be key to increased hypercapnia and development of sleep hypoventilation (SH). O’Donoghue and colleagues (2003) and Tárrega and colleagues (2002) observed SH in a high percentage of COPD patients, 43% and 59%, respectively, and suggested the finding was likely due to the oxygen therapy. Increasing the resting flow rate by 1 or 2 l min−1 may therefore exacerbate hypoventilation. Our group recently conducted a study to evaluate changes in gas exchange. We increased the nocturnal flow rate by 1 liter and observed that this induced SH and respiratory acidosis in a significant number of patients who did not have SH when they received the same oxygen titration as during the day (34.2% vs. 23.7% of patients) (Figures 2 and 3) (Samolski et al in press). This finding further supports the hypothesis that oxygen can induce hypoventilation. Plant and colleagues (2000) had previously shown that a high oxygen flow rate in acute respiratory failure in COPD patients was the most frequent cause of hypercapnia and led to the need for noninvasive ventilation. Such results reinforce the need to evaluate and titrate the nocturnal oxygen flow individually, at least in hypercapnic COPD patients.

Bottom Line: It also appears to reduce the number of hospitalizations, increase effort capacity, and improve health-related quality of life.The benefits of LTOT depend on correction of hypoxemia.During sleep, continuous monitoring of SaO2 and PaCO2 should be performed to confirm correction of SaO2 overnight.

View Article: PubMed Central - PubMed

Affiliation: Departament de Pneumologia, Hospital de la Santa Creu I de Sant Pau, Barcelona, Spain. mguellr@santpau.es

ABSTRACT
Long-term oxygen therapy (LTOT) is the treatment proven to improve survival in chronic obstructive pulmonary disease (COPD) patients with chronic respiratory failure. It also appears to reduce the number of hospitalizations, increase effort capacity, and improve health-related quality of life. Standard LTOT criteria are related to COPD patients who have PaO2 < 60 mmHg, are in a clinical stable situation, and are receiving optimal pharmacological treatment. According to LTOT guidelines, oxygen should be prescribed for at least 18 hours per day although some authors consider 24 hours would be more beneficial. The benefits of LTOT depend on correction of hypoxemia. Arterial blood gases should be measured at rest. During exercise, an effort test should be done to assure adequate SaO2. During sleep, continuous monitoring of SaO2 and PaCO2 should be performed to confirm correction of SaO2 overnight. An arterial blood gas sample should be taken at awakening to assess PaCO, in order to prevent hypoventilation from the oxygen therapy. Several issues that need to be addressed are the use of LTOT in COPD patients with moderate hypoxemia, the efficacy of LTOT in patients who desaturate during exercise or during sleep, the optimal dosage of oxygen supplementation, LTOT compliance, and the LTOT prescription in diseases other than COPD.

Show MeSH
Related in: MedlinePlus