Practical Pulse Oximetry

Nocturnal Pulse Oximetry Studies in Patients with COPD
Part II: Treatment of nocturnal hypoxemia and practical case examples

Ari Chaouat, MD Service de Pneumologie Hôpital de Hautepierre Strasbourg Cedex France

The article also available in PDF: 195KB

Treatment of nocturnal hypoxemia in COPD

One of the prime elements in the treatment of advanced chronic obstructive pulmonary disease (COPD) accompanied with respiratory failure is to correct hypoxemia. While the indications for standard oxygen therapy are well defined [28], the same cannot be said of isolated nocturnal oxygen therapy. There is still controversy as to the importance of treating such COPD patients who are not severely hypoxemic in daytime, but who experience marked nighttime desaturation during sleep.

Standard long-term oxygen therapy is indicated for COPD patients with marked, persistent hypoxemia, a daytime PaO2 below 55-60 mmHg. This is the important group of patients who demonstrate the most profound nocturnal hypoxemia. To be effective, long-term oxygen therapy should be applied for at least 16 hours out of 24 hours, and the sleep period must be totally covered [28].

The usual rate of oxygen administration is 1.5 to 3 L/min. One may ask are these rates sufficient to correct episodes of potentially severe desaturation during sleep? In a landmark study, an oxygen flow rate of 2 L/min was seen to be effective, as the mean SpO2 was improved from 53 ±29 % to 90 ±9% [29]. Episodes of desaturation still persisted, but there were less of them and they were not that severe.

The efficacy of standard oxygen therapy at a normal rate has been confirmed by other studies, as well [6,21,30], However, nocturnal oximetry is useful in checking that the selected oxygen flow will ensure nighttime SpO2 of over 90%. In general, nocturnal oxygen therapy has a favorable effect on pulmonary hypertensive jolts [21] and on cardiac rhythm disorders [23].

In oxygen therapy, one might fear of a progressive rise in PaCO2 during sleep, as hypoxic stimulus is suppressed, and there may be a diminished ventilatory response to CO2. Several studies have demonstrated that the risk is minimal, at least in the case of stable patients with COPD [29,30]. However, obstructive sleep apnea syndrome (OSAS) is worth noting here, as well a subgroup of patients with COPD but without OSAS. They may develop a progressive increase in PaCO2, and often experience acute exacerbation of the disease under oxygen therapy. They may benefit from long-term ventilatory support.

It is good to bear in mind that patients with COPD and OSAS may show a greater rise in PaCO2, which emphasizes importance of making correct diagnosis at an early stage.

Oxygen therapy only during sleep: Some COPD patients whose condition does not indicate standard, long-term oxygen therapy may still suffer severe nighttime hypoxemia. A study with 40 COPD patients having daytime PaO2 of 60 to 65 mmHg showed that 18 of 40 spent over 30% of their sleep time with a SpO2 below 90% [8].

Nocturnal oxygen therapy might be indicated, but there is not enough proof regarding the effect of sleep time oxygen therapy for patients with COPD [31]. More studies are needed on the effects of isolated nocturnal hypoxemia, as well.

Practicalities of nocturnal SpO2 monitoring

Pulse oximeters are invaluable, non-invasive tools for the assessment of nocturnal hypoxemia in patients with COPD. The two most common events that interfere with accurate measurement of SpO2, motion and low perfusion, are generally not encountered in sleep studies for patients with COPD. Indeed, SpO2 monitoring of is performed during a stable state of the disease, and patients who are agitated or in a state of shock are excluded.

Provided that the patient is cooperative, continuous nocturnal SpO2monitoring is usually accurate. However, due to the high proportion of smokers in the COPD population, it could be beneficial to check the amount of carbon monoxide with a whole-blood oximeter just before starting the sleep study. Benefits and cautions regarding nocturnal pulse oximetry in patients with COPD are summarized in Table 1.

Table 1: Practical aspects related to nocturnal pulse oximetry in patients with COPD.

Clinical cases

Case 1, diagnosis of sleep-related hypoxemia in COPD.
Traditionally, sleep studies in COPD patients have mostly been recommended only in two scenarios:

• Hypoxemia or right heart failure develops in the presence of relatively mild airflow limitation
• The patient has symptoms suggesting the presence of sleep apnea

Despite that rather narrow definition, this author feels that nighttime monitoring of SpO2 is indicated in all patients with a resting daytime PaO2 of below 65 mmHg.

Figure 2 included in this part II of the article, shows examples of continuous measurements of SpO2 in two patients with COPD. Both patients had daytime PaO2 of 64 mmHg. Please note the lower trend tracing, as it is representative of a typical nocturnal "desaturator" patient. The patient spent 155 minutes of the recording with a SpO2 below 90 %.

Figure 2. Two patient examples (A and B) with different over night pulse oximetry trends. Both patients had daytime PaO2 of 64 mmHg: Trend tracing in A is characteristic to a "non-desaturator", whereas curve B is a typical example of a "desaturator".

Case 2, Diagnosis of associated OSAS.
When obstructive sleep apnea syndrome is suspected, a continuous nighttime monitoring of SpO2 should be performed. Such a recording may show profound hypoxemia (Figure 3), particularly during REM sleep. In addition, there may be a characteristic swinging SpO2 pattern seen outside REM sleep. This phenomenon is often related to respiratory obstructive events. The suspected diagnosis of OSAS must then be confirmed with a polysomnography.

Figure 3. Over night oximetry of a patient having an association of COPD and OSAS. The above (red) tracing shows profound hypoxemia, particularly during REM sleep. There are the characteristic swinging saturation patterns even outside REM sleep. This is related to obstructive apnea and obstructive hypopnea.

Case 3: Control of the level of SpO2 under long-term oxygen therapy or long-term ventilatory support.
The primary goal of oxygen therapy and ventilatory support is to increase the baseline PaO2 to over 60 mmHg (8.0 kPa), or to produce a SpO2 of over 90 %: Hence, monitoring SpO2 during sleep would be advisable.

A 62 year-old male with severe COPD was a candidate for long-term oxygen therapy. This patient’s typical pulmonary physiologic values are shown in table 2.

Table 2: Characteristics of the patient with severe COPD.

• Male, 62 year-old, ex-smoker (50 pack-year)
• Severe dyspnea on exertion
• FEV1 (23 % of the predicted value) 0.67 L
• FVC (38 % of the predicted value) 1.41 L
• FEV1/FVC -ratio 47 %
• Arterial oxygen tension (PaO2) 4 8 mm Hg
• Arterial carbon dioxide tension (PaCO2) 58 mm Hg
  - FEV1 = Forced expiratory volume in 1 sec.
  - FVC = Forced vital capacity

Initially, therapy was initiated with oxygen flow of 3 L/min, allowing a satisfactory improvement of hypoxemia at rest, but only in daytime. Despite, the nocturnal oximetry recording showed constant low mean nighttime SpO2 values of 83 %.

Due to frequent exacerbations of COPD, an elevated PaCO2 and persistent sleep time desaturation during oxygen therapy, long-term ventilatory support was started in addition to the oxygen therapy. Thereafter, nighttime recordings of SpO2 showed improvement to a mean SpO2 of 92 %. Notably, the patient spent only 2 % of the monitored time with SpO2 values below 90%.

Figure 4. Oximetry during sleep in a patient with very severe COPD, graph illustrate three different treatment periods. Periods A shows SpO2 with ambient air, whereas B was during oxygen therapy (3 L/min), and C when patient received both ventilatory support and oxygen therapy. As the current recording shows, SpO2 was satisfactory (> 90 %) only during period C.

The recordings in figure 4 were performed during the same night, 24 hours before patient’s discharge. Three weeks had elapsed after admission for acute exacerbation of COPD.

There were three, 30 minute sleep periods: under ambient air, under oxygen therapy, and under ventilatory support plus oxygen therapy. The recordings demonstrate a gradual increase in SpO2 while new modalities of therapy were initiated. Such a SpO2 recording is very practical in controlling the therapeutic oxygen flow rate, as well as for adjusting the patient’s ventilator pressure and volume settings.

This case demonstrates that nocturnal SpO2 monitoring was effective in facilitating the choice of care in chronic respiratory failure, and allowed a suitable correction of nocturnal hypoxemia (Figure 4).

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Last updated: 8 June 2005Created
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