Nocturnal SaO2 Research Articles

Sleep and Nocturnal Mouthpiece IPPV Efficiency in Postpoliomyelitis Ventilator Users

Intermittent positive pressure ventilation (IPPV) can be delivered via various oral, nasal, or oronasal interfaces as an alternative to tracheostomy for up to 24 h of ventilatory support. Nocturnal nasal IPPV is often associated with frequent transient but at times severe oxyhemoglobin desaturations (dSaO2s) and sleep fragmentation. The purpose of this study was to determine if nocturnal mouthpiece IPPV is also associated with dSaO2s and sleep disruption. Twenty-seven postpolio ventilator-assisted individuals (VAIs) using mouthpiece IPPV with little or no ventilator-free breathing time (VFBT) underwent nocturnal oxyhemoglobin saturation (SaO2) monitoring. In addition, 15 underwent nocturnal capnography and 13 underwent polysomnography. Mean nocturnal SaO2 was normal in 22 of 27 and maximum end-tidal PCO2 was normal in 12 of 15 VAIs. Use of lipseal retention for nocturnal mouthpiece IPPV significantly improved blood gas values during sleep. The polysomnography results demonstrated relatively normal sleep efficiency. Nocturnal mouthpiece IPPV is most effective with lipseal retention. It can provide normal alveolar ventilation and SaO2 during sleep for VAIs with little or no measurable vital capacity or VFBT. Because transient dSaO2s can be eliminated with lipseal retention, it may disrupt sleep less than nasal IPPV.

Hematocrit Levels in Sleep Apnea

This study addresses the hypothesis that patients with obstructive sleep apnea, who exhibit recurrent episodes of oxygen desaturation at night, have higher hematocrit levels than nonapneic control subjects. We prospectively studied 624 patients referred to the sleep disorders center at St. Michael's Hospital because of suspicion of sleep apnea. All patients had nocturnal polysomnography and measurements of hematocrit level, hemoglobin value, WBC count, and platelet count. Smoking history and awake oxygen saturation (SaO2) was recorded in all of them. Nocturnal oxygenation was assessed using three indices: lowest nocturnal SaO2 (LoSaO2), mean nocturnal SaO2 (MnSaO2) and percent of total sleep time spent at SaO2 lower than 85 percent (TST85%). Patients with TST85% in the lowest quartile (TST85% = 0) had minimally lower hematocrit levels than patients with TST85% in the highest quartile (8 < or = TST85% < or = 90): 0.41 +/- 0.03 vs 0.40 +/- 0.02 in female subjects and 0.45 +/- 0.05 vs 0.43 +/- 0.05 in male subjects, respectively (p < 0.05). Multiple linear regression analysis revealed that MnSaO2, age, and pack-years of smoking were significant predictors of hematocrit level, but they accounted for only 9 percent of the variability in hematocrit level (multiple R2 = 0.087; p < 0.05). We conclude that intermittent nocturnal hypoxemia during episodes of apnea does not lead to clinical polycythemia, but is associated with minor elevations in hematocrit value. These small elevations are unlikely to be useful as markers of hypoxic stress associated with sleep apnea.

Role of Hyperventilation in the Pathogenesis of Central Sleep Apneas in Patients with Congestive Heart Failure

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.

Nocturnal Oxygen Saturation and Sleep Quality in Long-Term Survivors of Thoracoplasty

The extent and the predictors of nocturnal hypoxemia were studied in 9 men and 11 women treated for pulmonary tuberculosis by thoracoplasty 30-54 years previously. The patients had a scoliotic (Cobb) angle of 4-53 degrees. Median values for pulmonary function were: forced expiratory volume in 1 s 1.2 liters (49% of the predicted value), vital capacity 1.9 liters (54%), total lung capacity 3.6 liters (62%), and supine waking partial pressure for arterial oxygen 9.7 kPa. Four patients were hypercapnic. The patients' mean nocturnal SaO2 ranged from 83 to 94% (median 91.8%), and the SaO2 level below which the patients spent 10% of the total nocturnal recording time ranged from 78 to 92% (median 89.4%). A multiple stepwise linear regression analysis identified supine waking SaO2 as a significant predictor of nocturnal O2 desaturation, accounting for about 80% of the variability in nocturnal SaO2 levels; lung function values and Cobb angle were not significant independent predictors. The sleep quality, assessed by EEG, was good. It is concluded that in thoracoplasty patients with mild hypoxemia during wakefulness, the degree of sleep-related oxygen desaturation was modest and closely related to the waking level of SaO2.

Nocturnal oxygen saturation in advanced chronic obstructive pulmonary disease after a moderate dose of ethanol

The effect of a moderate oral dose of ethanol/(0.5 g.kg-1 body weight) on nocturnal arterial oxygen saturation (SaO2) was evaluated in nine male patients with advanced chronic obstructive pulmonary disease (COPD), (median forced expiratory volume in one second (FEV1) 0.9 l, arterial oxygen tension (PaO2) 9.3 kPa, arterial carbon dioxide tension (PaCO2) 5.3 kPa). During the four study nights (two after alcohol and two after placebo intake), the patients were monitored by whole-night computerized recordings of SaO2 (Biox-oximeter), airflow (thermistors) and respiratory as well as body movements (static charge sensitive bed). After alcohol intake, the mean blood ethanol concentration (SEM) in the evening was 42(2.3) mg.100 ml-1. Alcohol intake was associated with a marginal deterioration of nocturnal oxygenation; the mean (SEM) nocturnal SaO2 was 88.4(2.0) % after alcohol ingestion and 89.1(1.6) % after placebo ingestion, respectively. Only during the first 2 h in bed was there a statistically significant difference in SaO2 in favour of placebo (p less than 0.05). It is concluded that moderate alcohol intake in the evening, corresponding to "social" drinking, did not substantially aggravate nocturnal oxygenation in our patients with advanced COPD and mild to moderate daytime hypoxaemia.

Analysis of nocturnal disturbed breathing in the elderly using desaturation index

This study was conducted to examine the nocturnal ventilatory parameters and gas exchange in the elderly with nocturnal disturbed breathing. In order to facilitate analysis of ventilatory parameters with minimum manpower, we developed an unattended continuous nocturnal monitoring system for ventilation and arterial oxygen saturation. Using this system, nocturnal ventilatory parameters and gas exchange were investigated in our geriatric ward. We investigated 30 elderly subjects aged between 65 and 94 (mean age 77.8 +/- 6.5 years, male; female = 15:15). The subjects were free of severe cardiovascular and cerebrovascular disorders, and underwent 10 hours of continuous monitoring of ventilation and arterial oxygen saturation (SaO2). Number of significant desaturation (SDS; desaturation greater than 4% in SaO2 from the baseline value) and desaturation index (DI; sigma SDS(%) x duration (hour)) were calculated using the same system. The number of apnea episodes significantly correlated with DI and the number of SDS. DI also significantly correlated with lowest SaO2, while the number of SDS and the number of apneas were not found to be correlated with lowest SaO2. The number of SDS and the number of apnea episodes did not correlated with lowest SaO2. From the view point of gas exchange during the night, newly introduced DI is more comprehensive parameter when compared with the number of apneas or SDS. Subjects with a DI of over 0.5 were assigned to the group A (n = 8, mean age = 77.8) and the remaining subjects were assigned to group B (n = 22, mean age = 77.8). We compared the group A with the group B regarding nocturnal ventilatory parameters and SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Evolution of Nocturnal Oxyhemoglobin Desaturation in Patients with Chronic Obstructive Pulmonary Disease and a Daytime PaO2above 60 mm Hg

We studied 31 clinically stable chronic obstructive pulmonary disease (COPD) patients with a PaO2 greater than or equal to 60 mm Hg using polysomnographic sleep study at baseline (between 1983 and 1986) and at a mean follow-up time of 42.5 months to examine the evolution of rapid-eye-movement (REM) sleep nocturnal oxyhemoglobin desaturation (NOD). Arterial blood gases and spirometry measured at baseline and follow-up were compared with mean nocturnal SaO2 and to other REM sleep SaO2 parameters. We postulated that the onset of NOD would be seen most frequently in those patients with marked derangements of lung mechanics and greater longitudinal deterioration in arterial blood gases. Eight of the subjects developed REM-NOD on follow-up polysomnography. The appearance of REM-NOD was not related, or only minimally so, to initial PaO2, PaCO2, or mean nocturnal SaO2. Upon follow-up, however, the onset of NOD was always associated with deterioration of daytime PaO2 and PaCO2, mainly in those patients with the most severe baseline derangement of spirometry (lung mechanics). On the other hand, one group showed equivalent deterioration in daytime PaO2 and a stable PaCO2 but had less severely deranged baseline mechanics and demonstrated a fall in mean nocturnal SaO2 only. The findings in this latter group indicate that the development of NOD is not purely a result of decreasing daytime PaO2. We conclude that the onset of REM-NOD is mainly related to a severe derangement of lung mechanics with deterioration of resting awake gas exchange (progressive hypoxemia, hypercarbia, and worsening airflow).(ABSTRACT TRUNCATED AT 250 WORDS)

Value of nocturnal oxygen saturation as a screening test for sleep apnoea.

The sensitivity and specificity of overnight recording of arterial oxygen saturation (SaO2) in routine clinical practice was evaluated in 41 subjects who were being investigated for possible sleep apnoea-hypopnoea syndrome. SaO2 was measured with an ear probe oximeter (Biox IIa) and chart recorder during an "acclimatisation" night immediately before a detailed polysomnographic study. The recordings were classified by two observers as positive, negative, or uninterpretable. Twelve of the 41 patients had the obstructive sleep apnoea syndrome when defined in terms of an apnoea-hypopnoea index greater than 15 events an hour on the second night. The sensitivity of nocturnal SaO2 on the acclimatisation night when the diagnostic criterion was an apnoea-hypopnoea index of greater than 5, greater than 15, and greater than 25/h was 60%, 75%, and 100% respectively. Corresponding values for specificity were 95%, 86%, and 80%. Oximetry alone therefore allowed recognition of a moderate or severe sleep apnoea syndrome. In routine practice an appreciable number of equivocal results is likely and repeat oximetry or more detailed polysomnography will then be required if clinical suspicion is high.

Existe-t-il des facteurs prédictifs du syndrome d'apnées du sommeil chez les obèses ?

This study characterizes patients with sleep apnea syndrome (SAS) among 83 obese subjects investigated with polysomnography. Thirty five patients (22 males, 13 females) had a SAS. Age, BMI, blood pressure, functional complaints, pulmonary function tests were identical in the SAS and in the non SAS groups. Fifteen SAS patients were treated with continuous positive airway pressure wich normalized nocturnal SaO2.

Intermittent Abdominal Pressure Ventilator in a Regimen of Noninvasive Ventilatory Support*

The purpose of this work is to present 640 patient-years of experience using the intermittent abdominal pressure ventilator (IAPV) in a regimen of noninvasive ventilatory support for patients with paralytic/restrictive respiratory insufficiency. Fifty-two of the 54 patients who used the IAPV used 24-hour noninvasive ventilatory support. Thirty-eight of the 52 patients could tolerate less than 15 minutes of free time off their ventilators except by the successful use of glossopharyngeal breathing (GPB). No patient, however, retained an indwelling tracheostomy and none required or used supplemental oxygen therapy. Forty-eight of the 54 patients used the IAPV for daytime support for a mean of 12.9 +/- 11.5 years (3 months to 39 years) while using other forms of noninvasive support overnight. All 48 patients maintained normal minute ventilation and end-tidal PCO2 on the IAPV. One patient used the IAPV only for nocturnal ventilatory support for six months. Five patients relied on the IAPV as their sole method of ventilatory support 24 hours a day for a mean of 13.4 +/- 11.2 years (range, 2 to 31 years). Three of these five patients had no free time and were studied by nocturnal SaO2 monitoring that demonstrated a mean SaO2 of 95 percent or greater and a minimum SaO2 of 86 percent. The maximum end-tidal PCO2 was 49 mm Hg during sleep on the IAPV. The 48 patients receiving daytime IAPV support reported few difficulties. However, two of the five patients using the IAPV 24 hours a day had development of sacral decubiti. The IAPV became ineffective for 12 patients after 12.3 +/- 9.5 years of use. These patients then switched to daytime mouth IPPV. We conclude that the IAPV is a safe and effective method of long-term daytime ventilatory support for patients with paralytic/restrictive respiratory insufficiency. Its use is optimized when employed in combination with other noninvasive methods of ventilatory support, thus eliminating the need for tracheostomy, and optimizing the use of GPB. Regular follow-up is important because the IAPV can become less effective with time.

Daytime Hypercapnia in the Development of Nocturnal Hypoxemia in COPD

Arterial oxyhemoglobin saturation (SaO2) falls to a variable extent during sleep in patients with COPD. These nocturnal falls in SaO2 may contribute to the development of pulmonary hypertension, nocturnal cardiac arrhythmias, and death during sleep. In order to determine which physiologic factors measured during wakefulness might contribute to the development of nocturnal hypoxemia, we performed multiple stepwise linear regression analyses in 48 patients with stable COPD with mean and lowest nocturnal SaO2 as dependent variables. It was concluded that the two chief variables, measured while awake, which are associated with alterations in nocturnal oxygenation in patients with COPD are baseline awake SaO2 and PaCO2. Hypercapnia appears to be a risk factor for the development of nocturnal hypoxemia in patients who are normoxic while awake.

Effect of nasal continuous positive airway pressure on sleep apnea in congestive heart failure.

We studied five patients with chronic stable congestive heart failure (CHF), all of whom demonstrated recurrent apneas in association with Cheyne-Stokes respiration (CSR) during sleep. All five patients had symptoms consistent with a sleep apnea syndrome. Nasal continuous positive airway pressure (NCPAP) was administered at 8 to 12.5 cm H2O to all patients during sleep. The number of apneas fell from (mean +/- SE) 60 +/- 12/h of sleep on the control night to 9 +/- 7/h of sleep (p less than 0.01) on the NCPAP night, whereas mean nocturnal SaO2 rose from 88 +/- 2% on the control night to 92 +/- 2% (p less than 0.025) while on NCPAP. This was associated with resolution of symptoms of sleep apnea. In addition, resting left ventricular ejection fraction (LVEF) as measured by radionuclide angiography (RNA) rose from 31 +/- 8% while off NCPAP to 38 +/- 10% (p less than 0.05) while on NCPAP. Furthermore, all five patients experienced marked improvement in symptoms of heart failure from functional classes III and IV (New York Heart Association Classification) prior to NCPAP therapy to class II after NCPAP therapy was instituted. We conclude that, in certain patients, CSR during sleep associated with chronic CHF constitutes a sleep apnea syndrome, which can be alleviated by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function.

Do sleep studies contribute to the management of patients with severe chronic obstructive pulmonary disease?

To determine whether studies of breathing and oxygenation during sleep are clinically useful, we have assessed whether the detection of excess nocturnal hypoxemia in patients with chronic obstructive pulmonary disease (COPD) is of prognostic importance. Ninety-seven patients with COPD were followed for 32 to 108 (median, 70) months after studies of overnight oxygenation. Significant relationships (p less than 0.001) were obtained between mean oxygen saturation (SaO2) asleep and awake. There was similarly a significant relationship between lowest SaO2 asleep and awake, but this relationship was improved by the inclusion of awake arterial carbon dioxide tension (PaCO2). The patients who were more hypoxic at night than predicted from these regression relationships had similar survivals to the patients who were less hypoxic at night than predicted, whether excess nocturnal hypoxia was defined in terms of mean or lowest SaO2 during sleep. In the 66 patients who did not subsequently receive long-term oxygen therapy, none of the indices of nocturnal oxygenation was related to survival, the only significant predictor of survival being daytime arterial oxygen tension (PaO2). For all 97 patients, both mean nocturnal SaO2 and lowest SaO2 during sleep were related to survival (p less than 0.05), and percent predicted vital capacity was also related to survival (p less than 0.05). Neither of the oxygen saturations during sleep significantly added to the more readily and cheaply measured percent predicted vital capacity in determining survival in these patients. Thus, in patients with COPD, excess nocturnal hypoxemia is not associated with an impaired prognosis, and so studies of oxygenation during sleep cannot be recommended in the routine clinical management of these patients.

Inspiratory muscle training in patients with chronic obstructive pulmonary disease: Chen H, Dukes R, Martin BJ. Am Rev Respir Dis 131:251, 1985

We analyze the effect of inspiratory muscle training (IMT) in patients with chronic obstructive pulmonary disease (COPD), with special emphasis on its effects on inspiratory muscle function and clinical outcomes. We reviewed only randomized, controlled studies that have either controlled both the load and the breathing pattern when using resistive training or have employed a threshold trainer in which the load is independent of the pattern of breathing, since methodological aspects may explain inconsistent results in the literature. In these circumstances, most of the studies demonstrated positive effects on inspiratory muscle function. Clinical effects were seldom evaluated; limited available data showed a reduction in dyspnea that was related to an increase in maximal inspiratory pressures (PIMax). When exercise capacity was evaluated through the distance the patients were able to walk in 6 or 12 minutes, most studies demonstrated a significant increase. Other reported positive effects were improvement in nocturnal SaO2, inspiratory muscle power output and maximal inspiratory flow rate. Based in this review, a recommended training regime appears to be an intermediate load (30-40% PIMax) using a threshold device for 30 minutes daily for at least 5 weeks. Although in the literature the criteria for selecting patients are not always well defined, we consider IMT as a helpful procedure for pulmonar rehabilitation in those patients with a moderately severe inspiratory muscle dysfunction presenting dyspnea during daily living activities despite optimal therapy.

Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea.

Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.