Research ArticleOriginal Research

Nocturnal Oximetry and Transcutaneous Carbon Dioxide in Home-Ventilated Neuromuscular Patients

Julie Nardi, Hélène Prigent, Annie Adala, Mikaëlle Bohic, François Lebargy, Maria-Antonia Quera-Salva, David Orlikowski and Frédéric Lofaso
Respiratory Care September 2012, 57 (9) 1425-1430; DOI: https://doi.org/10.4187/respcare.01658

Abstract

BACKGROUND: Pulse oximetry alone has been suggested to determine which patients on home mechanical ventilation (MV) require further investigation of nocturnal gas exchange. In patients with neuromuscular diseases, alveolar hypoventilation (AH) is rarely accompanied with ventilation-perfusion ratio heterogeneity, and, therefore, oximetry may be less sensitive for detecting AH than in patients with lung disease.

OBJECTIVE: To determine whether pulse oximetry (SpO2) and transcutaneous carbon dioxide (PtcCO2) during the same night were interchangeable or complementary for assessing home MV efficiency in patients with neuromuscular diseases.

METHODS: Data were collected retrospectively from the charts of 58 patients with chronic neuromuscular respiratory failure receiving follow-up at a home MV unit. SpO2 and PtcCO2 were recorded during a 1-night hospital stay as part of standard patient care. We compared AH detection rates by PtcCO2, SpO2, and both.

RESULTS: AH was detected based on PtcCO2 alone in 24 (41%) patients, and based on SpO2 alone with 3 different cutoffs in 3 (5%), 8 (14%), and 13 (22%) patients, respectively. Using both PtcCO2 and SpO2 showed AH in 25 (43%) patients.

CONCLUSIONS: Pulse oximetry alone is not sufficient to exclude AH when assessing home MV efficiency in patients with neuromuscular diseases. Both PtcCO2 and SpO2 should be recorded overnight as the first-line investigation in this population.

Introduction

Home mechanical ventilation (MV) is used to diminish alveolar hypoventilation (AH), and is generally applied initially at night.1 Studies have shown that simultaneous recording of transcutaneous carbon dioxide partial pressure (PtcCO2) and pulse oximetry (SpO2) is the best method for assessing the efficiency of nocturnal home MV in improving blood gas values1–5 and detecting prolonged AH and short periods of sleep-related breathing disorders (leaks, asynchrony, and glottis closure). However, to save time and diminish costs, screening with nocturnal pulse oximetry alone, which is easier than recording PtcCO2, especially at home, has been suggested as a means of identifying those patients who require further nocturnal investigations.6–8 The criteria used to define AH differ according to the cause of respiratory failure and are more sensitive for restrictive than obstructive diseases.1 In addition, restrictive defects due to neuromuscular diseases (NMDs) are usually characterized by higher baseline PaO2 values than are obstructive defects.9 Therefore, AH detection using SpO2 alone may lack sensitivity in patients with NMDs.

The objective of the present study was to compare SpO2 and PtcCO2 values recorded during the same night in patients with NMDs, to determine whether these 2 parameters are interchangeable or complementary for assessing the efficiency of MV.

QUICK LOOK

Current knowledge

Nocturnal ventilation in patients with neuromuscular disease is often indicated for reversal of alveolar hypoventilation. These patients are often monitored with oximetry for detection of gas exchange abnormalities.

What this paper contributes to our knowledge

Pulse oximetry alone cannot exclude alveolar hypoventilation when assessing home mechanical ventilation efficiency in patients with neuromuscular diseases. Both transcutaneously measured partial pressure of carbon dioxide (PtcCO2) and SpO2 should be recorded overnight as the first-line investigation.

Methods

The study protocol was approved by the French Data Protection Authority (Commission Informatique et Libertés), in accordance with French legislation.

Study Patients

Data were collected retrospectively from the charts of patients with NMDs receiving follow-up at the home MV unit of the Raymond Poincaré Teaching Hospital, Garches, France. The patients had chronic restrictive respiratory failure and underwent a routine evaluation of the invasive or noninvasive MV protocol they used at home. This evaluation was done during a 1-night hospital stay, as part of standard patient care, between June 2009 and July 2011. Both SpO2 and PtcCO2 were recorded overnight. We did not include patients on oxygen therapy or having daytime PaO2 values < 60 mm Hg.

Data Collection

The following were collected: anthropometric parameters; type of NMD; symptoms of sleep-disordered breathing or nocturnal hypoventilation (numerous awakenings, nocturnal agitation, diurnal asthenia, sleepiness); lung function test results (vital capacity, maximal inspiratory and expiratory static mouth pressures); time since MV initiation; time on MV per 24-hour cycle; ventilatory parameters; and interface.

PtcCO2 and SpO2 Measurements

Overnight continuous noninvasive PtcCO2 and SpO2 monitoring was achieved using a monitor (Digital Monitoring System, SenTec, Therwil, Switzerland) equipped with a noninvasive combined PtcCO2 (Severinghaus-type electrode), SpO2, and heart rate sensor (V-Sign, SenTec, Therwil, Switzerland). Recording was started at the patient's usual bedtime and lasted 8 hours, which was the maximal possible recording duration with this device.

As recommended by the manufacturer, the electrode was calibrated in a docking station before each measurement, using a service gas (mixture of 8% CO2, 12% O2, and 80% N2) (SenTec, Therwil, Switzerland), which took approximately 4–11 min. The sensor membrane was changed every 14 days. The skin was cleansed thoroughly with isopropanol 70%, then dried. A small drop of sensor gel (SenTec, Therwil, Switzerland) was applied to the center of the sensor membrane surface, which was then secured to the ear lobe with a low-pressure ear clip and a tape in front of the ear. The electrode temperature was set at 42°C to increase blood flow, thereby improving skin permeability to gases and arterializing the capillaries in order to record PtcCO2 values and subsequently to estimate PaCO2. PtcCO2 monitoring began after 5–8 min (required for warming of the measurement site, complete local arterialization, and equilibration of CO2 concentrations between the skin and sensor) and lasted 8 hours. In the event of PtcCO2 signal interruption due to patient movements or passive body mobilization, the electrode was recalibrated and the sensor secured again to the earlobe. According to the manufacturer, measurement resolution was typically 0.8 mm Hg, with an in vitro drift estimated at < 1%/hour and a response time shorter than 80 s.

Overnight SpO2 was recorded in the first patients using both pulse oximetry with a finger sensor (BlueNight, SleepInnov Technology, Moirans, France) and the pulse oximetry sensor incorporated in the combined PtcCO2, SpO2, and heart rate sensor described above. No significant differences were found between the values supplied by the 2 SpO2 sensors, and, consequently, only the combined sensor was used in the remaining patients.

Daytime Blood Gas Measurement

According to routine clinical practice in the unit, daytime blood gas values were obtained in all patients receiving invasive MV, on the morning after the overnight recording. The blood sample was drawn at rest, in the sitting position. In addition, in patients on noninvasive MV, daytime blood gas values were measured in the afternoon on room air.

Data Analysis

Normal blood gas values were defined based on the normal values for our laboratory: pH 7.38–7.42, PaO2 90–100 mm Hg, bicarbonate 24–28 mmol/L, and base excess 0 ± 2 mmol/L. Daytime hypercapnia was defined as PaCO2 > 45 mm Hg.1

Specifically designed software (V-Stats 3.00, SenTec, Therwil, Switzerland) was used to transfer and analyze stored nocturnal SpO2 and PtcCO2 data. Graphs and tables were established, and times spent above or below predefined PtcCO2 or SpO2 cutoffs were determined. We visually examined the graphs for each entire recording night to identify artifact-free periods. We then determined the artifact-free recording times; the maximal, minimal, and mean nocturnal PtcCO2 and SpO2 values; and the times spent with PtcCO2 ≥ 49 mm Hg and with SpO2 < 90%.

Nocturnal AH was defined as abnormal PtcCO2 or SpO2 values. PtcCO2 was considered abnormal when the maximal value was ≥ 49 mm Hg.10 Three different criteria were used to define abnormal SpO2, in separate analyses: a value ≤ 88% for at least 5 consecutive minutes (criterion 1),1 mean nocturnal SpO2 < 90% or SpO2 < 90% during ≥ 10% of the total recording time (criterion 2),6,11 and mean nocturnal SpO2 < 92% or SpO2 < 92% during ≥ 10% of the total recording time (criterion 3).5

Statistics

The data are described as median and IQR. We used the chi-square test to compare AH detection by SpO2 alone and PtcCO2 alone, to compare clinical characteritics between patients with and without nocturnal elevated PtcCO2 values and to correlate presence of symptoms with nocturnal gas exchange abnormalities. The Mann-Whitney test was used to compare continuous variables between patients with and without nocturnal hypercapnia.

P values < .05 were considered significant. All analyses were performed using statistics software (Prism 5, GraphPad Software, San Diego, California).

Results

Population Characteristics

We identified 169 patients with nocturnal PtcCO2 recordings performed at our home MV unit during the study period. Among them, 58 (34%) were home MV users. None of these 58 patients was on oxygen therapy. Table 1 shows the main characteristics of the study population.

View this table:
Table 1.

Characteristics of the Study Population (n = 58)

Of the 58 study patients, 33 (57%) had severe respiratory muscle disease, with vital capacity values < 20% of predicted, and maximal inspiratory and expiratory static mouth pressure values < 30% of predicted in 41 (71%) patients and 43 (74%) patients, respectively. Forty-one (71%) patients used volume controlled ventilators. Body mass index was ≥ 30 kg/m2 in 3 patients (one each with kyphoscoliosis, Steinert myotony, and facioscapulohumeral muscular dystrophy). No patient had obstructive lung disease. The symptoms questionnaire was retrieved in 29 medical records among the 58 patients included: 18 patients showed symptoms of sleep-disordered breathing or nocturnal hypoventilation, and 11 patients were completely asymptomatic.

Nocturnal SpO2 and PtcCO2 Monitoring

Abnormal peak PtcCO2 values indicated AH in 24 (41%) of the 58 patients, and abnormal SpO2 values in 3 (5%), 8 (14%), and 13 (22%) patients, with criteria 1, 2, and 3, respectively. The chi-square test comparing PtcCO2 and SpO2 showed highly significant differences using both SpO2 criteria (P < .001 for criteria 1 and 2, and P = .03 for criterion 3).

Table 2 shows the results of combining PtcCO2 and SpO2 values for diagnosing AH. Among the 34 patients with normal PtcCO2 values, 33 (97%, 57% of the overall study population) had normal SpO2 values and one (3%, 2% of the overall study population) had abnormal SpO2 values, according to criteria 1 or 2; this latter number increased to 4 (12%, 7% of the overall study population) patients with normal PtcCO2 and abnormal SpO2 considering criterion 3. Among the 24 patients with abnormal PtcCO2 values, only 2 (8%) had abnormal SpO2 values according to criterion 1, 7 (29%) according to criterion 2, and 15 (38%) according to criterion 3. Thus, the prevalence of high PtcCO2 values among patients without hypoxemia was 40% (22/55) when criterion 1 was used, 34% (17/50) when criterion 2 was used, and 33% (15/45) when criterion 3 was used.

View this table:
Table 2.

Cross-Tabulation of PtcCO2 and SpO2 Monitoring (n = 58)

As reported in Table 3, using both PtcCO2 and SpO2 (criterion 2) showed AH in 25 (43%) patients. The 2 tests combined increased the AH diagnosis rate by 29.3%, compared with SpO2 alone (criterion 2), and by 1.7% compared with PtcCO2 alone.

View this table:
Table 3.

Combination of SpO2 and PtcCO2 Results

No correlation was found between symptoms of sleep-disordered breathing or nocturnal hypoventilation (18/29) and abnormalities of PtcCO2 or SpO2 with criteria 1, 2, or 3 (P = .81, P = .43, P = .36, and P = .14, respectively).

The 5 myotonic dystrophy patients were all ventilated using noninvasive MV. Four of them presented elevated nocturnal PtcCO2, but none of them presented oxygen desaturation according to criterion 1, whereas 3 of them presented oxygen desaturation according to criterion 2. The myotonic dystrophy patient without abnormal PtcCO2 presented oxygen desaturation according to criterion 3 (SpO2 < 92%).

Nocturnal PtcCO2 Versus Morning Blood Gas Values

Among the 24 patients with nocturnal hypercapnia, 8 (33%) had high PaCO2 values the next morning during objective wakefulness, whereas the remaining 16 patients (67%) had normal PaCO2 values (P < .001). Moreover, patients with nocturnal hypercapnia had significantly higher values for the morning bicarbonate concentration (27.2 mmol/L [24.9–28.5 mmol/L] vs 22.4 mmol/L [20.1–25.4 mmol/L], P < .001) and base excess (1.8 mmol/L [0.6–3.6 mmol/L] vs −1.6 mmol/L [-3–1.4 mmol/L], P = .001), compared to patients with normal nocturnal PtcCO2 values. We did not find any other significant difference between the 2 groups of patients with and without nocturnal elevated PtcCO2 values, respectively, when comparing anthropometric parameters, respiratory functional test values, and MV characteristics.

Discussion

In our study of patients with NMDs, nocturnal pulse oximetry used to assess the efficiency of MV was not sufficient to exclude AH. About one third of the patients had AH manifesting as high PtcCO2 values without substantial oxygen desaturation according to the usual SpO2 criteria.1,6 On the other hand, oxygen desaturation without nocturnal hypercapnia was rare.

The usual criteria used to determine whether home MV is needed1 were challenged recently by a study in which nocturnal hypercapnia predicted diurnal hypercapnia in patients with NMDs, and correcting nocturnal hypercapnia by MV prevented acute hypercapnia crises.10 The cutoff used to define hypercapnia in this study was 49 mm Hg.10 We also used this cutoff in our study, as no consensus exists about the best nocturnal PCO2 criterion for assessing MV efficiency. Like Ward et al,10 we did not use a minimal duration of PtcCO2 ≥ 49 mm Hg. In fact, 2 patients had a hypercapnia duration of < 5 min. Transferring these 2 patients in the non-hypercapnic group would not have changed the statistics significance and therefore the interpretation of the study. The cutoff used to define daytime hypercapnia is 45 mm Hg,1 which takes into account the normal PCO2 increase during sleep in adults.12

For oxygen saturation we used the recommended cutoff for determining when MV is indicated,1 considering that SpO2 should not be ≤ 88% for ≥ 5 consecutive minutes when MV is efficient (SpO2 criterion 1). According to a study of MV in patients with kyphoscoliosis, a reasonable goal is a mean nocturnal SpO2 ≥ 90%, with < 10% of the total recording time at SpO2 < 90% after the correction of leaks.6,11 We used this possibly more sensitive cutoff for a separate analysis in our study (SpO2 criterion 2). Finally, we also studied a third criterion for SpO2 analysis (mean nocturnal SpO2 ≥ 92%, with < 10% of the total recording time at SpO2 < 92%),5 considering that the value of 90% may be too severe. With this latter criterion we increased detection of SpO2 abnormalities, including patients with normal PtcCO2 (see Table 2), suggesting another mechanism than AH for explaining oxygen desaturation.

With both SpO2 cutoffs, PtcCO2 was more sensitive than oximetry for detecting AH. Our criteria were similar to those used by Paiva et al, who compared SpO2 and PtcCO2 in a pediatric population with a variety of causes of respiratory failure.5 This study provided the first evidence that hypercapnia was common during MV in patients without oxygen desaturation. Moreover, we did not find significant correlation between the clinical examination and nocturnal gas exchange abnormalities.

The sensitivity of SpO2 for detecting AH is probably higher in patients with COPD. First, the diurnal hypercapnia cutoff used to determine when MV is required is higher in patients with COPD than in those with restrictive lung diseases.1 Second, when COPD is so severe as to require MV, there is usually substantial heterogeneity in the ventilation-perfusion ratio.9,13,14 Therefore, independently from AH severity, hypoxemia is common, and PaO2 values may fall to levels at the steep portion of the oxyhemoglobin dissociation curve, where small PaO2 decreases induced by worsening AH are associated with large drops in SpO2.13,15–17 For instance, a PaCO2 increase of 5 mm Hg diminishes PaO2 by about 6 mm Hg, which is largely sufficient to markedly decrease SpO2 when PaO2 is initially low. Thus, in patients with COPD, pulse oximetry alone may be accurate for detecting nocturnal respiratory anomalies, including AH.6

An advantage of SpO2 monitoring is the ability to detect brief decreases in MV efficiency, possibly explained by residual obstructive events, decreases in the central ventilatory command, or unintentional leaks.6 Theoretically, these brief anomalies are not associated with PaCO2 increases. In our population, however, nocturnal oxygen desaturation without hypercapnia was rare. Nevertheless, in practice, and given that currently available PtcCO2 devices can accurately measure instantaneous SpO2, the issue is not choosing between SpO2 and PtcCO2, but adding PtcCO2 to SpO2.

The limitations of transcutaneous CO2 monitors have been largely overcome in recent years. First, although electrode calibration before each recording remains necessary, membrane changes can be performed less frequently. Second, the lag time has decreased from 5 min on average4 to approximately 2 min,18 and the issue of sensor drift over the night has been solved by introducing a compensation that allows continuous recording for 8 hours without substantial signal drift19 and without requiring 2 PaCO2 determinations at the beginning and end of monitoring.18 Third, several studies have shown good agreement between arterial and transcutaneous values, even during MV.18,19 Finally, PtcCO2-SpO2 measurement devices are now sufficiently easy to use that they are suitable for home monitoring.5

Conclusions

In conclusion, given the design and performance improvements in transcutaneous CO2 monitors, together with their ability to simultaneously monitor SpO2 recording, and our results showing that PtcCO2 is considerably more sensitive than SpO2 for detecting MV inefficiency in patients with NMDs, we recommend the first-line use of nocturnal PtcCO2 and SpO2 monitoring rather than pulse oximetry alone for evaluating MV efficiency. If CO2 monitoring is not available, a criterion usable in clinical practice for determining oximetry abnormalities should be adjusted individually with the knowledge of diurnal PaO2 in order to appreciate the facility of SpO2 decreasing during hypoventilation. In addition, morning blood gas determination should be preferred to evening blood gas determination for appreciating nocturnal MV effectiveness, as morning bicarbonate and base excess levels may accurately reflect nocturnal respiratory acidosis.

Footnotes

  • Correspondence: Julie Nardi MD, Services des Maladies Respiratoires, Hôpital Maison Blanche, Centre Hospitalier Universitaire, 45, Rue de Cognacq Jay, 51092 Reims, France. E-mail: jnardi{at}chu-reims.fr.

  • The authors have disclosed no conflicts of interest.

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