A Short Guide to Maximizing Long-term O2 Therapy

Q:Which patients with chronic obstructive pulmonary disease (COPD)benefit most from long-term oxygen therapy?

A:Long-term oxygen therapy (LTOT) improves both the length and qualityof life of hypoxemic patients with COPD.^1,2 It is the only therapy thatclearly increases survival for selected patients with advanced stable COPD.¹

LTOT is prescribed both for patients with exacerbations of COPD and forthose with advanced disease.

Exacerbations of COPD. LTOT may be prescribed for hypoxemicpatients at discharge from the hospital following an acute exacerbation.Hypoxemia is defined as a resting arterial oxygen saturation (SaO₂) of 88% orless, which corresponds to a partial pressure of arterial oxygen (PaO₂) of55 mm Hg or less. Many hypoxemic patients recover sufficient lung functionso as not to need oxygen for physiologic indications. After about 60 to 90 daysof LTOT, retest these patients once they have not received oxygen for 20 minutesto determine if significant hypoxemia is still present. In many patients,LTOT can be discontinued if normoxia is found with pulse oximetry or, betteryet, arterial blood gas analysis.

Advanced disease. The second group of candidates for LTOT are thosewith stable advanced COPD characterized by compelling symptoms, such asdyspnea on exertion, evidence of right-sided heart failure, or morning headache.^3,4 These patients are typically being treated with a maintenance regimenof inhaled bronchodilators (anticholinergics, β-agonists, or both); theophyllinewhen appropriate; and, often, inhaled corticosteroids.

Patients with an SaO₂ of 88% or less and a PaO₂ of 55 mm Hg or lessqualify for third-party reimbursement (Table). Reimbursement is also allowedfor an SaO₂ as high as 89% if a patient has secondary polycythemia with a hematocritof 55% or more or clinical signs of cor pulmonale (verified on chestradiography and ECG).

Once a patient with chronic stable COPD requires oxygen, he or shewill need it for life. There is no need to retest for hypoxemia after LTOT hasbeen administered for months. Because oxygen is a potent bronchodilatorand vasodilator, it has a restorative effect in some patients. Thus, if LTOTimproves ventilation/perfusion matching, room-air PaO₂ may rise. It is as inappropriateto withhold oxygen from patients with this successful outcomeas it would be to withhold insulin from a patient with diabetes after blood glucoseis controlled or to withhold systemic antihypertensives after serioushypertension is controlled.

JUDGING THE NEED FOR LTOT
Should all patients with a PaO₂ of 55 mm Hg or less or an SaO2 of 88% orless be treated with LTOT? Absolutely not! If this were the norm, virtually theentire population of Leadville, Colo (at an altitude of 10,000 ft), for example,would qualify. Persons with normal cardiovascular and respiratory function can compensate for moderate and even severe hypoxemia-witness those whoclimb the Himalayas. Patients with compromised respiratory or cardiovascularfunctions often cannot compensate.

Many patients and their physicians believe that the purpose of LTOTis to reduce dyspnea on exertion. Although dyspnea may diminish following aperiod of pulmonary rehabilitation during which oxygen may be used, oxygenalone has little effect on dyspnea. This is because dyspnea is associated withaltered pulmonary mechanics and the increased work of breathing, not thehypoxemic state.

The best way to judge the need for LTOT is to interpret the physiologicabnormalities in the context of the patient's symptoms, quality of life, andevidence of end-organ dysfunction. My view is that the criteria for LTOT aretoo restrictive, but I have never been able to convince third-party payers ofthis.

In ambulatory patients, continuous oxygen from a portable liquid systemhas been associated with lower mortality than oxygen used for shorter periods(such as nocturnally) from a stationary system.¹

References:

REFERENCES:1. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronicobstructive lung disease: a clinical trial. Ann Intern Med. 1980;93:391-398.
2. Petty TL. Home oxygen: a revolution in the care of advanced COPD. Med Clin North Am. 1990;74:715-729.
3. The Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonaryfunction in chronic obstructive pulmonary disease. N Engl J Med. 2000;343:1902-1909.
4. Pauwels RA, Buist AS, Calverley PM, et al. Global strategy for the diagnosis, management, and preventionof chronic obstructive pulmonary disease: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease(GOLD) Workshop summary. Am J Respir Crit Care Med. 2001;163:1256-1276.
5. Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy. Whitehouse Station, NJ; 1999:579.