Resph'atory Medicine (1990) 84, 199-201

Nocturnal oxygen desaturation in patients using long-term oxygen therapy for chronic airflow limitation

N. CARROLL, M. J. WALSHAW, C. C. EVANS AND C. R. K. HIND

Department of Medicine, Royal Liverpool Hospital, University of Liverpool, Liverpool L7 8ZP, U.K.

Nocturnal oxygen desaturation in patients receiving long-term oxygen therapy is described despite adequate daytime oxygenation (Pao 2 > 8 kPa). Domiciliary oximetry overnight was performed on ten patients receiving long-term oxygen treatment for chronic airflow limitation: six patients were well saturated throughout the night with a fall in Sao 2 to below 90% for only 1% of the monitoring time; four showed significant desaturation with a fall in Sao2 to below 90% for periods of 15--47% of the monitoring time.

Introduction

Tile life expectancy of patients with respiratory failure as a complication of severe chronic airflow limitation (CAL) is increased by the use of oxygen for 15 h or more each day (1,2). The DHSS guidelines for the prescription of such long-term oxygen therapy (LTOT) suggest that a flow rate sufficient to increase the daytime arterial oxygen tension (Pao2) to over 8 kPa should be used. However, although a daytime Pao 2 of 8 kPa may provide satisfactory daytime oxy- genation, some patients with CAL hypoventilate dur- ing periods of rapid eye movement sleep (3) and/or demonstrate obstructive sleep apnoea (4), which may result in nocturnal oxygen desaturation despite the use of LTOT. Furthermore, in a recent study by Fletcher et al. of patients with CAL and a daytime Pao 2 of > 8 kPa while breathing air, significant oxygen de- saturation was seen in 27% of cases when monitored during sleep (5).

Hitherto, no assessment of nocturnal oxygenation has been thought necessary in the evaluation of patients receiving LTOT using an oxygen concentrator. There- fore, to determine whether nocturnal desaturation does occur in LTOT patients despite adequate daytime oxygenation (Pao 2 > 8 kPa), we performed domicili- ary oximetry overnight in ten consecutive patients receiving LTOT for severe CAL.

Methods

We studied ten patients (5 male: 5 female; mean age 67 years, range 57-75) with CAL, who had been receiv- ing LTOT delivered by an oxygen concentrator for at least 6 months (mean 12 months, range 6-36). All had severe chronic airflow limitation (mean FEV 1 530 ml,

Received 26 June 1989 and accepted 8 December 1989.

range 300-800) and had been clinically stable for at least 6 weeks preceding this study.

Recordings were made in the patient's home using an Ohmeda Biox 3700 pulse oximeter and a pen recorder. The probe was attached to the patient's ear at their usual bedtime, whilst they were using their oxy- gen concentrator, and was left undisturbed overnight. Arterial blood was then sampled and transported on ice for analysis within 30 rain. The following morning the equipment was collected and the traces analysed. A second night of oximetry was subsequently performed in the two patients with the most marked oxygen de- saturation following an increase in oxygen flow rate.

Results

All ten patients studied had an awake Pao 2 > 8 kPa whilst using their oxygen concentrator (mean 11.4 kPa, range 8.1-14.8) with an oxygen saturation (Sao2) of 90 % or more. Sleep quality was reported by all patients as representative of a usual night's sleep, There was no evidence of ear compression artefact or poor quality signal on any of the oximetric traces.

We found that six patients were well oxygenated throughout the night with a fall in saturation to below 90% for less than 1% of the monitoring time. The other four patients demonstrated significant oxygen desaturation with between 15 and 47% of the monitor- ing time spent with an Sao 2 of less than 90% (Patient 1, 60rain; Patient 2, 100min; Patient 3, 180min; and Patient 4, 240 min). The minimum Sao 2 overnight for each patient was 80%, 81%, 72% and 72% respect- ively. Patient 4 was restudied following an increase in oxygen flow rate to 31 min -I which corrected the nocturnal desaturation (Fig. 1). However, increase in oxygen flow rate in Patient 1, who had a Paco 2 of 9.5 kPa whilst using 21 min -I oxygen, produced

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Nocturnal oxygen desaturation 201

symptomatic hypercapnia and was therefore not con- tinued. Patients 2 and 3 had oximetric traces suggestive o fcoexisting upper airway obstruction, and repeat oxi- metry in Patient 3 following an increase in oxygen flow rate did not demonstrate improved oxygenation. Review of the daytime Sao 2 in all 10 patients showed that all six 'non-desaturators' had an awake Sao 2 of >94%, whilst in three of the four nocturnal 'desaturators' this was < 93%.

Discussion

Despite adequate daytime oxygenation whilst using LTOT, significant nocturnal desaturation was found in four of the ten consecutive patients studied, due to hypoventilation (two cases) or coexisting hypoventi- lation and upper airway obstruction (two cases). Confirmation of these findings requires formal poly- somnography though many patients sleep badly in the laboratory setting. Domiciliary oximetry allows a more usual night's sleep to be monitored and was readily accepted by the patients studied here. All patients in this study fulfilled the DHSS criteria for the provision of LTOT. Although three of the four nocturnal 'desaturators' had a lower awake oxygen saturation (Sao2) than the 6 'non-desaturators', in all cases awake Sao 2 was acceptable (90% or more).

The original studies (1,2) of domiciliary oxygen therapy in patients with hypoxaemic CAL made no assessment of the effects of nocturnal hypoxaemia. The relevance of nocturnal hypoxaemia in such patients is not known, but in patients with restrictive chest wall disease, the correction of sleep-related hypoxaemia is associated with resolution of daytime respiratory failure (6). We would therefore speculate that the presence of significant nocturnal desauration despite LTOT may explain why LTOT is only of

benefit in a proportion of patients (1,2). Domiciliary oximetry may identify this subgroup of LTOT patients who may not derive maximal benefit because of de- saturation at night, which is when a large proportion of their daily oxygen use takes place. These patients may gain greater benefit from alternative methods of treatment (e.g. nasal ventilation) (7), or from an alter- ation in overnight oxygen flow rate. We therefore suggest that domiciliary oximetry, which is a simple screening test, may identify this subgroup and should be considered in all patients currently using LTOT.

References

1. Medical Research Council Working Party. Long term domiciliary oxygen therapy in chronic hypoxic cot pul- monale complicating chronic bronchitis and emphysema. Lancet 1981; I: 681-685.

2. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxaemic chronic obstruc- tive lung disease: a clinical trial. Atilt httern Med 1980; 93: 391-398.

3. Catterall JR, Douglas N J, Calverley PMA, Shapiro CM, Brezinova V, Brash HM, Flenley DC. Transient hypox- ae,nia during sleep in chronic obstructive pulmonary dis- ease is not a sleep apnoea syndrome. Am Rev Respir Dis 1983; 128: 24--29.

4. Goldstein RS, Ramcharan V, Bowes G, McNicholas WT, Bradley D, Phillipson EA. Effect of supplemental noc- turnal oxygen on gas exchange in patients with severe obstructive lung disease. N Engl J Med 1984; 310: 425-429.

5. Fletcher EC, Miller J, Divine GW, Fletcher JG, Miller T. Nocturnal oxyhaemoglobin desaturation in COPD patients with arterial oxygen tensions above 60 mmHg. Chest 1987; 92: 604-608.

6. Sawicka EH, Loh L, Branthwaite MA. Domiciliary venti- latory support: an analysis of outcome. Thorax 1988; 43: 31-35.

7. Carroll N, Branthwaite MA. Control of nocturnal b.ypo- ventilation by nasal intermittent positive pressure venti- lation. Thorax 1988; 43: 349-353.