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(Chest. 2003;123:59-66.)
© 2003 American College of Chest Physicians

Effects of Nasal Continuous Positive Airway Pressure on Oxygen Body Stores in Patients With Cheyne-Stokes Respiration and Congestive Heart Failure*

Samuel L. Krachman, DO, FCCP; Joseph Crocetti, DO; Thomas J. Berger, BA, RPSGT, PA-C; Wissam Chatila, MD, FCCP; Howard J. Eisen, MD and Gilbert E. D’Alonzo, DO, FCCP

* From the Sleep Disorders Center (Dr. Krachman and Mr. Berger), Division of Pulmonary and Critical Care (Drs. Crocetti, Chatila, and D’Alonzo), and Division of Cardiology (Dr. Eisen), Temple University School of Medicine, Philadelphia, PA.

Correspondence to: Samuel L. Krachman, DO, FCCP, Temple University School of Medicine, Division of Pulmonary and Critical Care, 767 Parkinson Pavilion, Broad and Tioga Sts, Philadelphia, PA 19140


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: The mechanism(s) by which nasal continuous positive airway pressure (CPAP) is effective in the treatment of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure (CHF) remains uncertain, and may involve an increase in total oxygen body stores (dampening), changes in central and peripheral controller gain, and/or improvement in cardiac function. The purpose of this study was to evaluate the effects of nasal CPAP on total oxygen stores, as measured by the rate of fall of arterial oxyhemoglobin saturation (dSaO2/dt), to determine if dampening may play a role in the attenuation of CSR in patients with CHF.

Design: Prospective controlled trial.

Setting: University hospital.

Patients: Nine male patients (mean ± SD age, 59 ± 8 years) with CHF and a mean left ventricular ejection fraction (LVEF) of 16 ± 4%.

Interventions and measurements: All patients had known CSR, as identified on a baseline polysomnographic study. Patients then underwent repeat polysomnography while receiving nasal CPAP (9 ± 0.3 cm H2O). The polysomnography consisted of recording of breathing pattern, pulse oximetry, and EEG. dSaO2/dt was measured as the slope of a line drawn adjacent to the falling linear portion of the arterial oxygen saturation (SaO2) curve associated with a central apnea. All patients underwent echocardiography and right-heart catheterization within 1 month of the study to measure LVEF and cardiac hemodynamics, respectively.

Results: There was a significant decrease in the apnea-hypopnea index (AHI) with nasal CPAP, from 44 ± 27 events per hour at baseline to 15 ± 24 events per hour with nasal CPAP (p = 0.004). When compared to baseline, dSaO2/dt significantly decreased with nasal CPAP from 0.42 ± 0.15% to 0.20 ± 0.07%/s (p < 0.001). The postapneic SaO2, when compared to baseline, significantly increased with nasal CPAP, from 87 ± 5% to 91 ± 4% (p < 0.05). The preapneic SaO2 did not significantly change, from a baseline of 96 ± 2% to 96 ± 3% with nasal CPAP (p = 0.8). When compared to baseline, the apnea duration and heart rate did not change with nasal CPAP. While there was a significant correlation noted between baseline postapneic SaO2 and dSaO2/dt (r = 0.8, p = 0.02), no correlation was seen between baseline preapneic SaO2 and dSaO2/dt (r = 0.1, p = 0.7). A significant correlation was noted between baseline dSaO2/dt and the AHI (r = 0.7, p = 0.02). With CPAP, there was a significant correlation noted between dSaO2/dt and the AHI (R = 0.7, p = 0.04), but no correlation was noted between dSaO2/dt and postapneic SaO2 (R = 0.1, p = 0.8).

Conclusion: Nasal CPAP significantly decreases dSaO2/dt and thus increases total body oxygen stores in patients with CSR and CHF. By increasing oxygen body stores, dampening may be one of the mechanisms responsible for the attenuation of CSR seen with nasal CPAP.

Key Words: Cheyne-Stokes respiration • congestive heart failure • dampening • nasal continuous positive airway pressure


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Approximately 45 to 56% of patients with congestive heart failure (CHF) and a left ventricular ejection fraction (LVEF) of < 45% have Cheyne-Stokes respiration (CSR) during sleep.1 2 3 4 Characterized by a crescendo-decrescendo alteration in tidal volume separated by periods of apnea or hypopnea, CSR has been associated with an increased mortality in patients with CHF.2 5 6 We have demonstrated that nasal continuous positive airway pressure (CPAP) and oxygen therapy were equally effective at decreasing the apnea-hypopnea index (AHI) in patients with CSR and CHF.4 Yet, the mechanism(s) by which these treatment modalities improve CSR is uncertain and may involve increasing total body oxygen stores (dampening), changes in central and peripheral controller gain, and/or improvement in cardiac function. In particular, it has been suggested that nasal CPAP is effective by decreasing interstitial edema and pulmonary vagal afferent stimulation, resulting in a decrease in central and peripheral controller gain.7 8 9 But an increased controller gain does not appear to be the sole mechanism responsible, as not all patients with CHF and CSR demonstrate an increased sensitivity to CO2.10 11

Dampening refers to the ability of the body to stabilize PaO2 and PaCO2 during changes in ventilation. In patients with CHF, interstitial edema causes a decrease in functional residual capacity (FRC),12 leading to a decrease in total body oxygen and CO2 stores. As a result, the respiratory system becomes unstable (underdampened), with exaggerated changes in PaO2 and PaCO2 during transient changes in ventilation. CSR can develop as a result of these changes in blood gas tensions.

The rate of fall of arterial oxyhemoglobin saturation (dSaO2/dt) has been shown to correlate with total body oxygen stores and is dependent on thoracic volume, resting total body oxygen consumption (O2), preapneic arterial oxygen saturation (SaO2), and mixed venous oxygen saturation (SvO2).13 14 15 16 17 18 19 We prospectively studied a group of patients with severe CHF (LVEF < 40%) and CSR to evaluate the effects of nasal CPAP on total body oxygen stores, as measured by dSaO2/dt, to determine if dampening may play a role in the attenuation of CSR; and to determine which factors correlate with dSaO2/dt in patients with CSR and CHF.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patient Selection
Nine male patients with severe CHF (New York Heart Association class IV) were studied in a nonblinded manner. Patients were all in medically stable condition for at least 1 month prior to the start of the study, with no change in their treatment regimens during the study period. The patients were all known to have CSR, as identified during a baseline polysomnographic study as part of a previous study.4 Patients were excluded from the study for the following: (1) if there was an episode of acute pulmonary edema within 1 month prior to the study, (2) if there was a history of a cerebral vascular accident, or (3) if patients refused to complete all the required polysomnographic studies. Our institutional review board approved the protocol, and informed consent was obtained from all patients prior to the study.

Patients were admitted to a special inpatient heart failure unit where they were evaluated and listed for heart transplantation, as previously described.4 The patients’ treatment regimens were optimized, and all patients were ambulatory and participating in physical conditioning classes at the time of the study.

Cardiac Hemodynamics and Echocardiography
All patients underwent right-heart catheterization within 1 month of the study. Parameters that were obtained included measurement of right atrial pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure. In addition, cardiac output was measured as the mean of three recordings using thermodilution technique. An echocardiogram was also obtained on each patient to determine LVEF.

Therapeutic Interventions
All patients were acclimated to nasal CPAP (REMstar; Respironics; Murrysville, PA) during the daytime prior to their study night, as previously described.4 In brief, patients received nasal CPAP bid for 1- to 2-h periods while awake at an initial pressure of 5 cm H2O. During a 5- to 7-day period, nasal CPAP was increased 2 cm H2O/d toward a goal of 10 to 12 cm H2O, as tolerated. Nasal CPAP was administered during the study night at the maximal determined pressure (9 ± 0.3 cm H2O).

Sleep Studies
Polysomnography consisted of recordings of abdominal and rib cage motion (Resp-EZ; EPM Systems; Midlothian, CA), finger pulse oximetry (model N-100; Nellcor Puritan Bennett; Pleasanton, CA), oral and nasal thermistors, ECG, electro-oculogram, digastric electromyogram, and EEG. The pulse oximeter used a signaling average of 5 to 7 s, similar to previous studies measuring dSaO2/dt.20 All variables were recorded continuously and stored on a computerized system (Alice 3; Healthdyne Information Enterprises; Marietta, GA). Sleep stage was classified by the standard criteria of Rechtschaffen and Kales.21 Total sleep time (TST), and sleep efficiency (defined as TST divided by time in bed) were also determined. Arousals were defined as the appearance of {alpha} activity for 3 to 15 s.22 Central apneas were defined by the lack of airflow for > 10 s, associated with the absence of rib cage and abdominal movement. Central hypopneas were defined by a 50% decrease in airflow for > 10 s, associated with a decrease in rib cage and abdominal excursion and a lack of abdominal-rib cage paradox. The central AHI was expressed as the number of apneas and hypopneas per hour of sleep. CSR was determined to be present when the central AHI was >= 10 events per hour,7 with events associated with a crescendo-decrescendo alteration in breathing pattern characteristic of CSR. dSaO2/dt was measured as the slope of a line drawn adjacent to the falling linear portion of the SaO2 curve associated with a central apnea (Fig 1 ).17 18 The SaO2 prior to the linear fall in SaO2 is referred to as the preapneic SaO2 (Fig 1) , and the postapneic SaO2 refers to the SaO2 at the flattened portion of the curve, following the linear descent (Fig 1) . For each study, the dSaO2/dt, preapneic SaO2, and postapneic SaO2 were determined by calculating the mean of 10 consecutive measurements obtained during an episode of CSR. The 10 consecutive apneas were chosen during the second sustained episode of CSR, during the first half of the night, while the patient was in stable stage 2 sleep. There were no awakenings or movement times during the sequence of CSR that was utilized for the measurements.



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  		Figure 1. Example of measuring dSaO2/dt associated with a central apnea in a patient with CHF and CSR. C3A2 represents an EEG tracing demonstrating stage 2 sleep. Central apneas are noted on monitoring nasal airflow (NAF), along with thoracic (THO) and abdominal (ABD) motion. dSaO2/dt is measured as the slope of the line drawn adjacent to the falling linear portion of the SaO2 curve (a represents the preapneic SaO2, and b is the postapneic SaO2). REOG = right electro-oculogram; LEOG = left electro-oculogram; Chin = chin electromyogram; sec = second.

 
Protocol
All patients underwent baseline polysomnography that identified the presence of CSR. Repeat polysomnography while administering nasal CPAP at the maximized tolerated pressure was then performed 12 ± 6 days after the baseline study. All patients were in stable condition with no change in their medical regimens between the two studies.

Statistical Analysis
Data are represented as mean ± SD. Paired t tests were used to compare baseline variables to those obtained with nasal CPAP. The relationship between dSaO2/dt and the preapneic SaO2, postapneic SaO2, and AHI were assessed by Pearson correlation coefficients.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Patient Characteristics
Nine male patients (mean age, 59 ± 8 years; body mass index [BMI], 28 ± 6) were studied (Table 1 ). The mean LVEF was 16 ± 4% on a maximized treatment regimen, which included a continuous infusion of an inotropic agent. Baseline cardiac hemodynamics demonstrated a cardiac index of 2.5 ± 0.6 L/min/m2, mean pulmonary artery pressure of 31 ± 11 mm Hg, pulmonary capillary wedge pressure of 20 ± 8 mm Hg, and a heart rate of 78 ± 21 beats/min. The baseline AHI was 44 ± 27 events per hour, with a TST of 324 ± 59 min, sleep efficiency of 82 ± 8%, and an arousal index of 14 ± 13 arousals per hour (Table 1) .


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  		Table 1. Patient Characteristics (n = 9)*

 
Effects of Nasal CPAP
Nasal CPAP resulted in a significant decrease in the AHI, from 44 ± 27 events per hour at baseline, to 15 ± 24 events per hour with nasal CPAP (p = 0.004). The apnea index significantly decreased with nasal CPAP, from 34 ± 31 to 14 ± 32 events per hour (p = 0.006), with no significant change in the hypopnea index, from 11 ± 21 to 1 ± 1 events per hour (p = 0.2). When compared to baseline, nasal CPAP significantly decreased the dSaO2/dt, from 0.42 ± 0.15% to 0.20 ± 0.07%/s (p < 0.001; Fig 2 ). The postapneic SaO2, when compared to baseline, significantly increased with nasal CPAP from 87 ± 5% to 91 ± 4% (p < 0.05; Fig 3 ). There was no significant change in the preapneic SaO2, from a baseline of 96 ± 2% to 96 ± 3% with nasal CPAP (p = 0.8; Fig 4 ). When compared to baseline, there was no significant change in apnea duration with nasal CPAP, from 21 ± 3 to 21 ± 6 s (p = 0.9). Heart rate, when compared to baseline, did not significantly change with nasal CPAP, from 78 ± 21 to 73 ± 16 beats/min, respectively (p = 0.3).



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  		Figure 2. Effects of nasal CPAP on dSaO2/dt. Compared with baseline measurements, nasal CPAP resulted in a significant decrease in dSaO2/dt (*p < 0.001).

 


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  		Figure 3. Effects of nasal CPAP on postapneic SaO2. When compared to baseline measurements, nasal CPAP significantly increased the postapneic SaO2 (*p < 0.05). See Figure 1 legend for expansion of abbreviation.

 


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  		Figure 4. Effects of nasal CPAP on preapneic SaO2. Compared to baseline measurements, there was no significant change in the preapneic SaO2 with nasal CPAP (p = 0.8). See Figure 1 legend for expansion of abbreviations.

 
At baseline, there was a significant correlation between postapneic SaO2 and dSaO2/dt (r = - 0.8, p = 0.02; Fig 5 , top, A). There was no correlation noted between baseline preapneic SaO2 and dSaO2/dt (r = - 0.1, p = 0.7; Fig 5 , bottom, B). Additionally, a significant correlation was noted between baseline dSaO2/dt and the AHI (r = 0.7, p = 0.02; Fig 6 ). With CPAP, there was a significant correlation noted between dSaO2/dt and the AHI (R = 0.7, p = 0.04), but no correlation noted between dSaO2/dt and postapneic SaO2 (R = - 0.1, p = 0.8).



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  		Figure 5. Correlation of baseline dSaO2/dt with preapneic and postapneic SaO2. Top, A: At baseline, there was a significant correlation between postapneic SaO2 and dSaO2/dt (r = - 0.8, p = 0.02). Bottom, B: At baseline, there was not a significant correlation noted between preapneic SaO2 and dSaO2/dt (r = - 0.1, p = 0.7). See Figure 1 legend for expansion of abbreviation.

 


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  		Figure 6. At baseline, a significant correlation was noted between the AHI and dSaO2/dt (r = 0.7, p = 0.02). hr = hour; see Figure 1 legend for expansion of abbreviation.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
An increase in total body oxygen stores, resulting in a dampening effect on the respiratory control system, is thought to be responsible for the effectiveness of oxygen in the treatment of CSR in patients with CHF.23 The effects of nasal CPAP on total oxygen body stores, and thus dampening, in these patients has not previously been investigated. There are three major findings in this study: (1) nasal CPAP significantly reduced dSaO2/dt in patients with CSR and CHF; (2) in patients with CHF and CSR, the baseline postapneic but not the preapneic SaO2 correlated with dSaO2/dt; and (3) there was a significant correlation between dSaO2/dt and the AHI.

The endogenous stores of oxygen of the body are rather limited (approximately 2 L), as compared to that of CO2 (120 L), due to differences in tissue-binding affinities.24 25 Approximately 25% of the total oxygen stores of the body are contained in the lung and 15% in the tissues, with the majority (60%) contained in the blood due to the binding affinity for hemoglobin.25 During breath-holding, as well as with central and obstructive apneas, dSaO2/dt, as a reflection of total oxygen body stores, has been shown to correlate with a number of factors, including thoracic volume, O2, preapneic SaO2, and SvO2.13 14 15 16 17 18 19

The volume of oxygen stored in the lungs is equal to lung volume times the alveolar fractional concentration of oxygen.24 Findley et al13 examined the impact of lung volume on the fall in SaO2 during voluntary breath-holding in seven normal males. Initial lung volume was found to be the most important determinant for both the fall in SaO2 as well as the minimal SaO2. The most severe decreases in SaO2 were noted at lower initial lung volumes (< 2 to 3 L), more specifically at lung volumes below closing capacity where dependent airways are more susceptible to closure. Similarly, Hurewitz and Sampson14 demonstrated that lung volume (measured at FRC) was an important determinant for the rate of fall in alveolar oxygen tension during breath-holding. The decrease in alveolar oxygen tension was found to be responsible for the associated decrease in SaO2.

Patients with CHF have a restrictive ventilatory pattern with a reduction in lung volumes.12 By recruiting alveoli and redistributing lung water, positive end-expiratory pressure may increase total oxygen body stores by increasing end-expiratory lung volume.26 27 CPAP has been shown to increase lung volumes, including FRC, at levels of 5 to 11 cm H2O,28 29 30 31 which is similar to the mean CPAP level of 9 cm H2O used in our patients. Although lung volumes were not directly measured in our study, an increase in FRC could be responsible for the observed decrease in dSaO2/dt and thus the increase in total oxygen body stores seen with nasal CPAP.

The preapneic SaO2 has been shown to be an important determinant for dSaO2/dt during breath-holding as well as during central and obstructive apneas.15 17 Yet, other studies have not demonstrated as strong a correlation between the two variables,18 and a component of the relationship was attributed to a decrease in lung oxygen stores created by having the subjects breath hypoxic gas mixtures.15 In the present study, there was no correlation noted between baseline dSaO2/dt and preapneic SaO2. In addition, there was no significant change in preapneic SaO2 with nasal CPAP. One possible explanation may involve the fact that the preapneic SaO2 was 96% at baseline, with a further increase in SaO2 expected to be marginal with nasal CPAP.

Another important determinant of dSaO2/dt is the preapneic SvO2.17 18 Since the majority of the oxygen stores of the body are contained in the blood, and 70% of the total blood volume is venous, it is understandable that a change in SvO2 could effect dSaO2/dt, especially in the presence of underlying lung disease. In our study, we did not directly measure SvO2 but we did measure postapneic SaO2, which at baseline was found to inversely correlate with dSaO2/dt (Fig 5 , top, A). Postapneic SaO2 may influence SvO2, especially in patients with CHF where there is an increase in both the circulation time and oxygen extraction.7 The use of nasal CPAP resulted in a significant increase in postapneic SaO2, with a possible corresponding increase in SvO2. Although apnea duration may affect postapneic SaO2 values, nasal CPAP was noted to have no effect on apnea duration in our patients.

With nasal CPAP, an inverse correlation was no longer noted between dSaO2/dt and postapneic SaO2. Yet, it should be noted that with nasal CPAP, the postapneic SaO2 had increased from 87 ± 5 to 91 ± 4 mm Hg. With an increase in the postapneic SaO2 to > 90%, its effect on SvO2 may be less significant, with other factors, such as lung volume, becoming more important in determining total body oxygen stores.

A decrease in O2 could also account for the change in dSaO2/dt seen with nasal CPAP, but this seems less likely. Differences in body weight are responsible for the correlation between the rate of fall of alveolar oxygen tension and O2 noted during breath-holding.14 Obese subjects have higher preapneic O2 measurements and thus a greater rate of fall of alveolar oxygen tensions. In the present study, our patients were not morbidly obese (BMI, 28 ± 6), and thus would not be expected to have an elevated baseline O2. Furthermore, the mechanism(s) by which nasal CPAP would decrease O2 is uncertain. Nasal CPAP may increase cardiac output in patient with CHF,32 33 with a corresponding increase in oxygen delivery resulting in either no change34 or an increase35 in O2.

Other mechanisms may be responsible for the decrease in dSaO2/dt seen with nasal CPAP. As noted, nasal CPAP can have significant effects on cardiac function in patients with CHF.32 33 An increase in cardiac output may result in a significant increase in SvO2, with a corresponding increase in total oxygen body stores. Others have suggested that a reduction in cardiac output could result in a decrease in dSaO2/dt, by its effect on the lung to chemoreceptor circulation time.20 Yet, it has previously been demonstrated that nasal CPAP, at levels similar to those used in the present study, have no effect on circulation time in patients with CSR and CHF.4

Mechanisms other than underdampening appear to be important in the development of CSR in CHF. An increase in central and peripheral controller gain is thought to be responsible for the hyperventilation-induced resting hypocapnia seen in these patients.7 8 9 10 11 With an arousal induced hyperpnea, PaCO2 decreases below the sleeping apneic threshold, resulting in a central apnea. In the presence of an increased central and peripheral controller gain, the ventilatory response to the increase in PaCO2 at the end of an apnea is exaggerated, resulting in the development of CSR. Javaheri11 demonstrated that the ventilatory response to CO2 was significantly elevated in those patients with, as compared to those without CSR, despite a similar degree of heart failure. More recently, Solin et al10 reported that both central and peripheral CO2 ventilatory responses are increased in patients with CSR as compared to those without CSR, as well as normal control subjects. Yet, in both studies, there was a considerable amount of overlap in the ventilatory response to CO2 noted between the groups, emphasizing the importance of other mechanisms in the development of CSR. In addition, our study demonstrated a significant correlation between the baseline dSaO2/dt and the AHI (r = 0.7, p = 0.02; Fig 6 ), suggesting that other mechanisms, such as underdampening, may be important in the development of CSR.

Nasal CPAP has been shown to be effective in the treatment of CSR in CHF when used over a variable amount of time.4 9 33 36 One mechanism that appears to be responsible is the ability of nasal CPAP to increase PaCO2, so that it remains well above the apneic threshold. Naughton et al9 demonstrated that 1 month of nasal CPAP resulted in an increase in nocturnal transcutaneous PCO2, secondary to a decrease in tidal volume. The authors postulated that an improvement in left ventricular function with nasal CPAP reduced interstitial edema and pulmonary vagal afferent stimulation, resulting in a decrease in central controller gain. Yet, the effects of nasal CPAP on central or peripheral controller gain have not been evaluated. In addition, although there was a decrease in tidal volume, other lung volumes, including FRC, will increase with nasal CPAP, resulting in an increase in the volume of oxygen stored in the lungs. Finally, it is important to note that although both the AHI and dSaO2/dt decreased with nasal CPAP in our study, the correlation between the two indexes remained significant (R = 0.7, p = 0.04). Therefore, other mechanisms, including a dampening effect, may play a role in the effectiveness of nasal CPAP on CSR in patients with CHF.

There are a number of limitations with our study that need to be discussed. First, none of the variables that determine total oxygen body stores, and thus dSaO2/dt, including measurement of lung volumes, were evaluated in the present study. Thus, it is uncertain which variables were affected by nasal CPAP that led to the significant attenuation in dSaO2/dt. Second, the present study evaluated the acute effects of nasal CPAP on dSaO2/dt. Whether more prolonged therapy will have a similar and sustained effect has yet to be determined. Third, the studies were performed in a nonblinded manner. We believe this did not effect the measurement of dSaO2/dt, as it was performed in a standardized manner in a sleeping patient. Finally, in addition to apnea duration, the repetitive nature of the apneas may effect dSaO2/dt, mostly by its effects on preapnea SaO2 and SvO2.17 The dSaO2/dt was calculated by taking the mean of 10 consecutive apneas at baseline and while administering nasal CPAP. We found no correlation between the 10 sequential baseline central apneas and their corresponding dSaO2/dt, for all nine patients individually (data not shown), as well as for the group as a whole (r = - 0.2, p = 0.6). Therefore, the repetitive nature of the central apneas did not effect total oxygen body stores, and the decrease in dSaO2/dt observed with nasal CPAP is independent of its effects at decreasing the number of central apneas during the night.

In conclusion, nasal CPAP is effective at decreasing dSaO2/dt and thus increasing total body oxygen stores in patients with CSR and CHF. By increasing total body oxygen stores, dampening may be one of the mechanisms partially responsible for the attenuation of CSR seen with nasal CPAP. In patients with CSR and CHF, baseline AHI and postapneic but not preapneic SaO2 correlate with total oxygen body stores, as reflected in the measurement of dSaO2/dt. Which physiologic variables are affected by nasal CPAP and are responsible for the decrease in dSaO2/dt, and whether similar findings are seen after more prolonged use, awaits further investigation.


   Footnotes
 
Abbreviations: AHI = apnea-hypopnea index; BMI = body mass index; CHF = congestive heart failure; CPAP = continuous positive airway pressure; CSR = Cheyne-Stokes respiration; dSaO2/dt = rate of fall of arterial oxyhemoglobin saturation; FRC = functional residual volume; LVEF = left ventricular ejection fraction; SaO2 = arterial oxygen saturation; SvO2 = mixed venous oxygen saturation; TST = total sleep time; O2 = oxygen consumption

Received for publication September 21, 2001. Accepted for publication July 10, 2002.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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SPO2 slope and instability
Lawrence A Lynn DO FCCP
Chest Online, 6 Feb 2003 [Full text]
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