Cheyne-Stokes Respiration and Congestive Heart Failure: Are Oxygen Stores the Critical Factor?

Abstract

Cheyne-Stokes respiration (CSR) is a pattern of increasing, followed by decreasing, ventilation leading to a period of apnea. CSR is associated with several conditions, including CNS dysfunction, ascent to high-altitude and, as investigated in this issue of CHEST (see page 59) congestive heart failure.1Cherniack NS Longobardo GS Cheyne-Stokes breathing.N Engl J Med. 1973; 288: 952-957Crossref PubMed Scopus (155) Google Scholar Typically, CSR is most obvious during non-rapid eye movement sleep when metabolic control of breathing predominates.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar The initiation of CSR may depend on a narrow difference between the resting end-tidal CO2 (Petco2) and the apneic threshold for CO2.3Xie A Skatrud JB Puleo DS et al.Apnea-hypopnea threshold for CO2 in patients with congestive heart failure.Am J Respir Crit Care Med. 2002; 165: 1245-1250Crossref PubMed Scopus (189) Google Scholar This enhances the likelihood that apnea will occur under conditions that favor a decrease in CO2 and an increase in the apneic threshold such as a transient arousal followed by the onset of sleep. As reviewed,1Cherniack NS Longobardo GS Cheyne-Stokes breathing.N Engl J Med. 1973; 288: 952-957Crossref PubMed Scopus (155) Google Scholar2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar once initiated, CSR is maintained, in part, by the interactive effect of fluctuations in CO2 and O2 on central and peripheral chemoreceptors. The increasing ventilation results from progressive elevation of CO2 levels above the apneic threshold plus a progressive decrease in O2. The decreasing ventilation results from a progressive decline of CO2 and increase in O2 due to hyperpnea from chemoreceptor stimulation. As discussed, apnea is then the result of a CO2 level below the apneic threshold possibly combined with little or no hypoxic stimulation. Several factors may make CSR more likely to be present. These include a delayed circulation time from the heart to the respiratory chemoreceptors (eg, from congestive heart failure), chemoreceptors that are overly sensitive to CO2, frequent arousals, various reflexes, upper airway instability, and the interactive effect of an increase in CO2 with a decrease in O2 that is known to produce greater than additive respiratory chemostimulation.4Kellogg RH Central chemical regulation of respiration.in: Fenn WO Rahn H Handbook of physiology. Williams & Wilkens, Baltimore, MD1964: 507-534Google ScholarCSR is common in patients with heart failure and appears to occur in approximately 40% of patients with an ejection fraction < 45%.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar For reasons that are not fully defined, patients with CSR associated with congestive heart failure appear to have a higher mortality than those without CSR.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar5Sin DD Logan AG Fitzgerald FS et al.Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation. 2000; 102: 61-66Crossref PubMed Scopus (554) Google Scholar In addition, CSR disrupts sleep and can lead to symptoms such as insomnia and daytime sleepiness.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar6Guilleminault C Cler A Labanowski M et al.Cardiac function and benzodiazepines.Sleep. 1993; 16: 524-528PubMed Google ScholarAlthough the pattern of CSR is well established, it is unclear if there are at least two subsets of CSR, one which involves the CNS without any upper airway instability (ie, without potential partial or complete obstruction) and one which is combined with at least the potential for partial or complete upper airway obstruction.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar This confusion stems, in part, from several observations including the positive response to continuous positive airway pressure (CPAP), the presence of obstructive apneas and hypopneas in most patients with otherwise classic CSR,2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar7Javaheri S Parker TJ Wexler L et al.Occult sleep-disordered breathing in stable congestive heart failure.Ann Intern Med. 1995; 122: 487-492Crossref PubMed Scopus (276) Google Scholar and the observation that many patients with CSR also snore.8Ancoli-Israel S Engler RL Friedman PJ et al.Comparison of patients with central sleep apnea: with and without Cheyne-Stokes respiration.Chest. 1994; 106: 780-786Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar To distinguish between these two subsets is difficult since even intrathoracic pressure measurements to determine respiratory effort may not be able to determine coexistent upper airway instability if there is no respiratory effort during the apnea.The authors have examined the hypothesis that CSR is improved by increasing body stores of O2. The hypothesis depends, in part, on the concept that by reducing the degree of hypoxia, the interactive effect of CO2 and hypoxia will be diminished, leading to reduced stimulation of the respiratory chemoreceptors. The authors and others have previously demonstrated that addition of supplemental oxygen in CSR associated with congestive heart failure reduces the number of CSR episodes.9Krachman SL D'Alonzo GE Berger TJ et al.Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure.Chest. 1999; 116: 1550-1557Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar10Franklin KA Eriksson P Sahlin C et al.Reversal of central sleep apnea with oxygen.Chest. 1997; 111: 163-169Abstract Full Text Full Text PDF PubMed Scopus (157) Google Scholar The current study pursues this hypothesis by attempting to increase O2 stores in the lung with CPAP by presumably increasing functional residual capacity. The hypothesis is supported by the finding that CPAP of an average of 9 cm H2O of pressure reduces not only the number of episodes of CSR but also the slope of decline in arterial oxygen saturation during each episode. The authors have made attempts to exclude occult obstructive sleep apnea as a contributor to the reduction in number of CSR events, but the evidence is indirect since no direct measure was made of respiratory effort. Of note, several previous studies have measured respiratory effort by measuring intrathoracic pressure. These studies have documented that there is no obvious respiratory effort during CSR, indicating that the CSR cannot be explained readily by obstructive events. In addition, CSR typically is lessened or ablated during rapid eye movement sleep, a time when obstructive sleep apnea is typically worsened.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google ScholarAlthough the authors' data support the hypothesis, alternative explanations are possible. As acknowledged by the authors, these include an improvement in cardiac function from CPAP with a decrease in circulation time and/or an increase in CO2 from CPAP2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar so that the CO2 remains above the apneic threshold. In addition, reversal of occult obstructive sleep apnea may contribute. It is also possible that the pressure of CPAP on the upper airway activates or inhibits a reflex that interacts with the CNS to reduce CSR.Although improvement in CSR with CPAP has been reported in a number of studies,2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar9Krachman SL D'Alonzo GE Berger TJ et al.Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure.Chest. 1999; 116: 1550-1557Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar this response is not universal.6Guilleminault C Cler A Labanowski M et al.Cardiac function and benzodiazepines.Sleep. 1993; 16: 524-528PubMed Google Scholar11Davies RJ Harrington KJ Ormerod OJ et al.Nasal continuous positive airway pressure in chronic heart failure with sleep-disordered breathing.Am Rev Respir Dis. 1993; 147: 630-634Crossref PubMed Scopus (119) Google Scholar12Buckle P Millar T Kryger M The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure.Chest. 1992; 102: 31-35Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar The explanation for this discrepancy is unclear. Explanations may include insufficient time of treatment, insufficient CPAP pressure, and selection of cardiac nonresponders to CPAP,13Baratz DM Westbrook PR Shah PK et al.Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure.Chest. 1992; 102: 1397-1440Abstract Full Text Full Text PDF PubMed Scopus (132) Google Scholar such as perhaps those with a low left ventricular end-diastolic pressure2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar14Philip-Joet FF Paganelli FF Dutau HL et al.Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure.Respiration. 1999; 66: 136-143Crossref PubMed Scopus (61) Google Scholar or those without any upper airway instability.As mentioned, CSR is associated with an increase in mortality in patients with congestive heart failure.5Sin DD Logan AG Fitzgerald FS et al.Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation. 2000; 102: 61-66Crossref PubMed Scopus (554) Google Scholar One hypothesis is that there is a contribution to reduced cardiac function from the repetitive hypoxemic episodes.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar If correct, it is possible that prevention of hypoxia will decrease mortality. An expansion of this hypothesis is that treatment of congestive heart failure with CPAP will decrease mortality from a sequence of events that includes afterload reduction on the left ventricle as well as from the favorable effects of reducing hypoxemia. If reduction in CSR alone is the goal, then improving O2 stores with supplemental oxygen may be sufficient. There is a note of caution in that it appears that the reduction in CSR events may be less compared to CPAP or other forms of positive pressure treatment.15Teschler H Dohring J Wang Y-M et al.Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure.Am J Respir Crit Care Med. 2001; 164: 614-619Crossref PubMed Scopus (564) Google Scholar16Lorenzi-Filho G Rankin F Bies I et al.Effects of inhaled carbon dioxide and oxygen on Cheyne-Stokes respiration in patients with heart failure.Am J Respir Crit Care Med. 1999; 159: 1490-1498Crossref PubMed Scopus (199) Google Scholar17Javaheri S Ahmed M Parker TJ et al.Effects of nasal O2 on sleep-related disordered breathing in ambulatory patients with stable heart failure.Sleep. 1999; 22: 1101-1106Crossref PubMed Scopus (138) Google Scholar If CPAP improvement in heart function is part of the goal, then CPAP will be necessary. It should be pointed out that the effects of O2 and CPAP are not mutually exclusive. Both may work to increase CO2, which may increase the difference between Petco2 and the apneic threshold. In addition, oxygen may potentially improve cardiac function by improving oxygen delivery to the heart.The CPAP hypothesis of treatment is currently being tested in a multicenter trial in Canada.18Bradley RD Logan AG Floras JS Rationale and design of the Canadian Continuous Positive Airway Pressure trial for congestive heart failure patients with central sleep apnea: CANPAP. The CANPAP Investigators.Can J Cardiol. 2001; 17: 677-684PubMed Google Scholar The hypothesis being tested includes improvement of cardiac function from CPAP independent of the effect on CSR, and there are two limbs to the trial, CPAP and no CPAP.The current study supports but does not answer the question posed in the title of this editorial. To explore the question further, it would be necessary to determine if reversal of hypoxia by increasing oxygen stores would improve outcome including mortality and health status in CSR associated with congestive heart failure. To date, this hypothesis has not been tested. In order to better understand the role of O2 stores in the production of CSR and possible mortality in congestive heart failure, a proper prospective randomized trial of supplemental oxygen vs no oxygen vs CPAP should be undertaken. It is also possible that a combination of CPAP and supplemental O2 may be needed to realize the full benefits of therapy. Cheyne-Stokes respiration (CSR) is a pattern of increasing, followed by decreasing, ventilation leading to a period of apnea. CSR is associated with several conditions, including CNS dysfunction, ascent to high-altitude and, as investigated in this issue of CHEST (see page 59) congestive heart failure.1Cherniack NS Longobardo GS Cheyne-Stokes breathing.N Engl J Med. 1973; 288: 952-957Crossref PubMed Scopus (155) Google Scholar Typically, CSR is most obvious during non-rapid eye movement sleep when metabolic control of breathing predominates.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar The initiation of CSR may depend on a narrow difference between the resting end-tidal CO2 (Petco2) and the apneic threshold for CO2.3Xie A Skatrud JB Puleo DS et al.Apnea-hypopnea threshold for CO2 in patients with congestive heart failure.Am J Respir Crit Care Med. 2002; 165: 1245-1250Crossref PubMed Scopus (189) Google Scholar This enhances the likelihood that apnea will occur under conditions that favor a decrease in CO2 and an increase in the apneic threshold such as a transient arousal followed by the onset of sleep. As reviewed,1Cherniack NS Longobardo GS Cheyne-Stokes breathing.N Engl J Med. 1973; 288: 952-957Crossref PubMed Scopus (155) Google Scholar2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar once initiated, CSR is maintained, in part, by the interactive effect of fluctuations in CO2 and O2 on central and peripheral chemoreceptors. The increasing ventilation results from progressive elevation of CO2 levels above the apneic threshold plus a progressive decrease in O2. The decreasing ventilation results from a progressive decline of CO2 and increase in O2 due to hyperpnea from chemoreceptor stimulation. As discussed, apnea is then the result of a CO2 level below the apneic threshold possibly combined with little or no hypoxic stimulation. Several factors may make CSR more likely to be present. These include a delayed circulation time from the heart to the respiratory chemoreceptors (eg, from congestive heart failure), chemoreceptors that are overly sensitive to CO2, frequent arousals, various reflexes, upper airway instability, and the interactive effect of an increase in CO2 with a decrease in O2 that is known to produce greater than additive respiratory chemostimulation.4Kellogg RH Central chemical regulation of respiration.in: Fenn WO Rahn H Handbook of physiology. Williams & Wilkens, Baltimore, MD1964: 507-534Google Scholar CSR is common in patients with heart failure and appears to occur in approximately 40% of patients with an ejection fraction < 45%.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar For reasons that are not fully defined, patients with CSR associated with congestive heart failure appear to have a higher mortality than those without CSR.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar5Sin DD Logan AG Fitzgerald FS et al.Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation. 2000; 102: 61-66Crossref PubMed Scopus (554) Google Scholar In addition, CSR disrupts sleep and can lead to symptoms such as insomnia and daytime sleepiness.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar6Guilleminault C Cler A Labanowski M et al.Cardiac function and benzodiazepines.Sleep. 1993; 16: 524-528PubMed Google Scholar Although the pattern of CSR is well established, it is unclear if there are at least two subsets of CSR, one which involves the CNS without any upper airway instability (ie, without potential partial or complete obstruction) and one which is combined with at least the potential for partial or complete upper airway obstruction.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar This confusion stems, in part, from several observations including the positive response to continuous positive airway pressure (CPAP), the presence of obstructive apneas and hypopneas in most patients with otherwise classic CSR,2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar7Javaheri S Parker TJ Wexler L et al.Occult sleep-disordered breathing in stable congestive heart failure.Ann Intern Med. 1995; 122: 487-492Crossref PubMed Scopus (276) Google Scholar and the observation that many patients with CSR also snore.8Ancoli-Israel S Engler RL Friedman PJ et al.Comparison of patients with central sleep apnea: with and without Cheyne-Stokes respiration.Chest. 1994; 106: 780-786Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar To distinguish between these two subsets is difficult since even intrathoracic pressure measurements to determine respiratory effort may not be able to determine coexistent upper airway instability if there is no respiratory effort during the apnea. The authors have examined the hypothesis that CSR is improved by increasing body stores of O2. The hypothesis depends, in part, on the concept that by reducing the degree of hypoxia, the interactive effect of CO2 and hypoxia will be diminished, leading to reduced stimulation of the respiratory chemoreceptors. The authors and others have previously demonstrated that addition of supplemental oxygen in CSR associated with congestive heart failure reduces the number of CSR episodes.9Krachman SL D'Alonzo GE Berger TJ et al.Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure.Chest. 1999; 116: 1550-1557Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar10Franklin KA Eriksson P Sahlin C et al.Reversal of central sleep apnea with oxygen.Chest. 1997; 111: 163-169Abstract Full Text Full Text PDF PubMed Scopus (157) Google Scholar The current study pursues this hypothesis by attempting to increase O2 stores in the lung with CPAP by presumably increasing functional residual capacity. The hypothesis is supported by the finding that CPAP of an average of 9 cm H2O of pressure reduces not only the number of episodes of CSR but also the slope of decline in arterial oxygen saturation during each episode. The authors have made attempts to exclude occult obstructive sleep apnea as a contributor to the reduction in number of CSR events, but the evidence is indirect since no direct measure was made of respiratory effort. Of note, several previous studies have measured respiratory effort by measuring intrathoracic pressure. These studies have documented that there is no obvious respiratory effort during CSR, indicating that the CSR cannot be explained readily by obstructive events. In addition, CSR typically is lessened or ablated during rapid eye movement sleep, a time when obstructive sleep apnea is typically worsened.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar Although the authors' data support the hypothesis, alternative explanations are possible. As acknowledged by the authors, these include an improvement in cardiac function from CPAP with a decrease in circulation time and/or an increase in CO2 from CPAP2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar so that the CO2 remains above the apneic threshold. In addition, reversal of occult obstructive sleep apnea may contribute. It is also possible that the pressure of CPAP on the upper airway activates or inhibits a reflex that interacts with the CNS to reduce CSR. Although improvement in CSR with CPAP has been reported in a number of studies,2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar9Krachman SL D'Alonzo GE Berger TJ et al.Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure.Chest. 1999; 116: 1550-1557Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar this response is not universal.6Guilleminault C Cler A Labanowski M et al.Cardiac function and benzodiazepines.Sleep. 1993; 16: 524-528PubMed Google Scholar11Davies RJ Harrington KJ Ormerod OJ et al.Nasal continuous positive airway pressure in chronic heart failure with sleep-disordered breathing.Am Rev Respir Dis. 1993; 147: 630-634Crossref PubMed Scopus (119) Google Scholar12Buckle P Millar T Kryger M The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure.Chest. 1992; 102: 31-35Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar The explanation for this discrepancy is unclear. Explanations may include insufficient time of treatment, insufficient CPAP pressure, and selection of cardiac nonresponders to CPAP,13Baratz DM Westbrook PR Shah PK et al.Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure.Chest. 1992; 102: 1397-1440Abstract Full Text Full Text PDF PubMed Scopus (132) Google Scholar such as perhaps those with a low left ventricular end-diastolic pressure2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar14Philip-Joet FF Paganelli FF Dutau HL et al.Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure.Respiration. 1999; 66: 136-143Crossref PubMed Scopus (61) Google Scholar or those without any upper airway instability. As mentioned, CSR is associated with an increase in mortality in patients with congestive heart failure.5Sin DD Logan AG Fitzgerald FS et al.Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation. 2000; 102: 61-66Crossref PubMed Scopus (554) Google Scholar One hypothesis is that there is a contribution to reduced cardiac function from the repetitive hypoxemic episodes.2Leung RST Bradley TD Sleep apnea and cardiovascular disease.Am J Respir Crit Care Med. 2001; 164: 2147-2165Crossref PubMed Scopus (544) Google Scholar If correct, it is possible that prevention of hypoxia will decrease mortality. An expansion of this hypothesis is that treatment of congestive heart failure with CPAP will decrease mortality from a sequence of events that includes afterload reduction on the left ventricle as well as from the favorable effects of reducing hypoxemia. If reduction in CSR alone is the goal, then improving O2 stores with supplemental oxygen may be sufficient. There is a note of caution in that it appears that the reduction in CSR events may be less compared to CPAP or other forms of positive pressure treatment.15Teschler H Dohring J Wang Y-M et al.Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure.Am J Respir Crit Care Med. 2001; 164: 614-619Crossref PubMed Scopus (564) Google Scholar16Lorenzi-Filho G Rankin F Bies I et al.Effects of inhaled carbon dioxide and oxygen on Cheyne-Stokes respiration in patients with heart failure.Am J Respir Crit Care Med. 1999; 159: 1490-1498Crossref PubMed Scopus (199) Google Scholar17Javaheri S Ahmed M Parker TJ et al.Effects of nasal O2 on sleep-related disordered breathing in ambulatory patients with stable heart failure.Sleep. 1999; 22: 1101-1106Crossref PubMed Scopus (138) Google Scholar If CPAP improvement in heart function is part of the goal, then CPAP will be necessary. It should be pointed out that the effects of O2 and CPAP are not mutually exclusive. Both may work to increase CO2, which may increase the difference between Petco2 and the apneic threshold. In addition, oxygen may potentially improve cardiac function by improving oxygen delivery to the heart. The CPAP hypothesis of treatment is currently being tested in a multicenter trial in Canada.18Bradley RD Logan AG Floras JS Rationale and design of the Canadian Continuous Positive Airway Pressure trial for congestive heart failure patients with central sleep apnea: CANPAP. The CANPAP Investigators.Can J Cardiol. 2001; 17: 677-684PubMed Google Scholar The hypothesis being tested includes improvement of cardiac function from CPAP independent of the effect on CSR, and there are two limbs to the trial, CPAP and no CPAP. The current study supports but does not answer the question posed in the title of this editorial. To explore the question further, it would be necessary to determine if reversal of hypoxia by increasing oxygen stores would improve outcome including mortality and health status in CSR associated with congestive heart failure. To date, this hypothesis has not been tested. In order to better understand the role of O2 stores in the production of CSR and possible mortality in congestive heart failure, a proper prospective randomized trial of supplemental oxygen vs no oxygen vs CPAP should be undertaken. It is also possible that a combination of CPAP and supplemental O2 may be needed to realize the full benefits of therapy.