Central Sleep Apnea: When the Heart Drives the Breathing Pattern

Central Sleep Apnea: When the Heart Drives the Breathing Pattern

Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Information is based on current medical literature and clinical guidelines but may not apply to your specific situation. Individual responses vary based on personal medical history and concurrent conditions. Always consult qualified healthcare providers for medical decisions. Never delay seeking medical care based on content you’ve read. If experiencing a medical emergency, seek immediate medical attention.

These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not replace medical care.

In Brief: Central sleep apnea is not an airway problem — the throat stays open, but the brain briefly stops sending the signal to breathe. In heart failure it usually appears as Cheyne-Stokes respiration, a rhythmic waxing and waning of breathing that reflects an unstable control loop in a failing circulation rather than a disease of the lungs or throat. It is common in heart failure, easily missed because its symptoms overlap with heart failure itself, and linked to worse outcomes — though whether it drives that risk or only marks a sicker heart is debated. The first treatment is to treat the heart failure itself; when central apnea persists, options include oxygen, CPAP, and phrenic-nerve stimulation, each with limits. The central lesson is a cautionary one: a large trial found that one device therapy controlled the apneas yet increased cardiovascular death in reduced-ejection-fraction heart failure, so reducing apneas is not the same as improving survival.

A Different Kind of Apnea

Article 3 described obstructive sleep apnea, where the airway collapses and the body fights to breathe against a closed throat. Central sleep apnea is its mirror image. The airway stays open. What stops is the signal.

The contrast is worth making concrete. In an obstructive event, the brain is still issuing the command to breathe, and the chest and diaphragm keep straining — like pushing against a door that has slammed shut. In a central event, the door is open, but no one is pushing: for several seconds the brain simply stops sending the drive to breathe, and the chest goes still.(1, 2) Both end in the same place — airflow stops, oxygen falls, the brain rouses — but they begin at opposite ends of the breathing system, and that difference shapes everything about how central apnea is understood and treated.

Central sleep apnea is less a disease in its own right than a sign that the system controlling breathing has become unstable.(2) The most important cause in cardiology is heart failure, where the failing heart itself sets the breathing rhythm askew — which is why this article treats central apnea and heart failure together.(1, 16)

The Several Forms of Central Sleep Apnea

Central apnea is a final common pathway reached by several different routes, and the route matters for treatment.(2)

The form most relevant here is heart-failure-associated central apnea, which usually shows up as Cheyne-Stokes respiration — the rhythmic crescendo-and-decrescendo pattern described below.(1, 16) A second form is opioid-induced central apnea, in which narcotics suppress the brainstem’s respiratory drive directly; its pattern and management differ, and it is a growing clinical problem. A third is treatment-emergent central apnea: central events that appear when a person with obstructive apnea is first started on CPAP. The mechanism is different from heart-failure apnea, and in most people it settles over weeks to months as therapy continues, though a minority have a more persistent course.(25) Central apnea also occurs at high altitude and, less commonly, on its own without an identifiable cause.

These forms share the same surface appearance on a sleep study — effort stops, airflow stops — but arise from different disturbances, so lumping them together obscures more than it reveals. The rest of this article concerns the heart-failure form.

Why a Failing Heart Disrupts Breathing

To see how a failing heart unsettles breathing, it helps to start with how breathing is normally kept steady.

Breathing runs on a feedback system. Sensors in the brainstem and in the carotid arteries track carbon dioxide and, to a lesser extent, oxygen. When carbon dioxide rises, they call for more breathing; when it falls, they call for less.(2, 3) During wakefulness the system tolerates a fair amount of noise. During sleep it becomes far less forgiving, because below a certain carbon dioxide level — the apneic threshold — the drive to breathe switches off entirely until carbon dioxide climbs back.(3) In healthy sleep, the normal carbon dioxide level sits comfortably above that threshold, so ordinary breath-to-breath variation never crosses it.

Heart failure narrows that safety margin in several reinforcing ways. Congestion and high filling pressures in the lungs stimulate receptors that drive a person to breathe a little faster and deeper, lowering carbon dioxide and pushing the resting level down toward the apneic threshold.(7, 8, 9) Many patients also develop heightened chemosensitivity — the sensors overreact, so a small rise in carbon dioxide produces an outsized burst of breathing, which then overshoots and drops carbon dioxide below the threshold.(5) And a weak heart pumps blood slowly, so it takes longer than normal for a change in the lungs to reach the sensors in the brain.

That last delay is the key to the oscillation, and an everyday analogy makes it intuitive. Picture a shower fed by a long pipe, so there is a lag between turning the valve and feeling the change. You nudge it toward hot, feel nothing, nudge further — then a wave of scalding water arrives, so you yank it toward cold, and a few seconds later an icy wave comes back. The water never settles; it swings between extremes because the feedback arrives too late to fine-tune. The failing circulation does the same thing to breathing. Oversensitive sensors (a heavy hand on the valve) plus delayed information (the long pipe) turn smooth, steady breathing into a repeating cycle of too much and then none at all.(2, 3)

This is why heart-failure central apnea is best understood not as a lung disease or a throat disease, but as a control problem produced by the heart itself.

Cheyne-Stokes Respiration

The visible result of that unstable loop is Cheyne-Stokes respiration, named for the two nineteenth-century physicians who described it. Breathing grows steadily deeper and faster, peaks, then fades steadily away to a pause of several seconds with no breathing at all — after which the crescendo begins again.(16) On a sleep tracing it looks like a series of smooth, symmetrical spindles separated by flat gaps. A full cycle commonly runs roughly 45 to 90 seconds, and — fittingly for a problem of circulatory delay — the cycle tends to lengthen as the heart weakens and blood moves more slowly.

What the person experiences, if anything, is usually vague: restless or fragmented sleep, brief awakenings, sometimes a sense of breathlessness on waking. A bed partner is often the better witness, describing breathing that “stops and starts” or “speeds up and trails off” through the night. Because the pattern waxes and wanes rather than ending in the dramatic gasp typical of obstructive apnea, it is easy to overlook.

Whether Cheyne-Stokes respiration is purely harmful, partly protective, or simply a marker of how sick the heart has become has been debated for years.(4) That uncertainty is not academic hand-wringing; as the treatment section shows, it turned out to matter a great deal.

How Common It Is in Heart Failure

Sleep-disordered breathing is strikingly common in heart failure, and a substantial share of it is central rather than obstructive. In a contemporary study of 700 patients with symptomatic heart failure and reduced ejection fraction, the majority had sleep-disordered breathing, with central and obstructive forms each accounting for a large fraction.(10) Even among patients with milder, well-treated heart failure, the prevalence is high.(11)

The exact numbers vary widely between studies, and for good reasons rather than sloppy ones. Prevalence depends on both the population and the method. It varies with how sick the patients are, whether ejection fraction is reduced or preserved, whether they are stable or recently decompensated, how central events were scored, and whether testing used full polysomnography or a home device.(10, 11) The breathing pattern can even shift within a single night and from night to night, with the same patient showing more obstructive events early and more central events later as fluid redistributes. The honest summary: central sleep apnea is common in heart failure — common enough to look for. But any single prevalence figure is an estimate tied to a particular population and method, not a fixed rate.

Recognizing It Is Hard

Central sleep apnea in heart failure is easy to miss, and the reason is built into the disease. Its daytime consequences — fatigue, poor sleep quality, reduced exercise tolerance, low mood — are the same complaints heart failure itself produces, so they get attributed to the heart and never prompt a question about breathing during sleep.(1, 16)

The classic alerting symptom of obstructive apnea, severe daytime sleepiness, is also less reliable here. Many heart-failure patients with central apnea are not especially sleepy, in part because the heightened sympathetic activity that accompanies their disease tends to keep them aroused.(14) The absence of sleepiness can therefore falsely reassure both patient and clinician. As with obstructive apnea, the most useful observations often come from a bed partner who has watched the breathing pause and restart — but many patients sleep alone, and the pattern goes unwitnessed. The practical consequence is that central apnea is frequently found only when someone specifically looks for it.

What It Means for the Heart

Central sleep apnea travels with worse outcomes in heart failure. In several cohorts, patients with central apnea and Cheyne-Stokes respiration have had higher mortality than comparable patients without it, and the severity of nocturnal breathing disturbance has tracked with prognosis.(12, 13) Nocturnal hypoxemia — time spent with low oxygen overnight — has likewise been associated with increased mortality in stable heart failure.(15) The biological case for harm is coherent: each cycle brings a dip in oxygen, a surge of sympathetic activity, and added strain on an already failing heart, repeated through the night.(14)

But coherence is not proof, and here the distinction between a cause and a marker is decisive. Central apnea becomes more frequent and more severe as the heart deteriorates, which means it could be largely a thermometer for heart-failure severity rather than an independent driver of harm — the smoke rather than the fire.(4) If that is true, then removing the apnea without improving the heart might do little, and an aggressive attempt to suppress it could even backfire. This is not a hypothetical worry. As the next sections show, it is exactly what a major trial encountered: a treatment that abolished the apneas did not extend life and, in one group, shortened it. The association between central apnea and poor outcomes is firmly established; the claim that the apnea itself is the thing to attack is not.

Treatment: Treat the Heart First

Because heart-failure central apnea is driven by the heart, the foundation of treatment is optimizing the heart failure itself. Guideline-directed medical therapy, relief of congestion, and device therapy where indicated can all reduce the frequency of central events, sometimes substantially, by stabilizing the circulation that destabilized breathing in the first place.(5) Cardiac resynchronization therapy, used in appropriately selected patients with conduction delay, has been shown to reduce central apnea and Cheyne-Stokes respiration alongside its effects on cardiac function.(23) Reducing fluid overload matters too, in part because overnight fluid redistribution contributes to both obstructive and central events.(24) In short, the best “sleep apnea treatment” in this setting is often better heart-failure treatment.

When central apnea persists despite optimized heart-failure care, several options exist, each with real limits.

Nocturnal oxygen can lessen central events and has improved sleep-related quality-of-life measures in heart-failure patients with central apnea, though it has not been shown to prolong life.(21) CPAP was tested directly in this population in the CANPAP trial, which randomized 258 patients with heart failure and central apnea. CPAP reduced the apnea-hypopnea index, raised nighttime oxygen, lowered sympathetic markers, and modestly improved ejection fraction and walking distance — but it did not improve survival free of heart transplantation.(18) Phrenic-nerve stimulation uses an implanted device that paces the diaphragm to produce a more natural breathing rhythm. It reduced central events in a randomized trial and is an option in selected patients, though its long-term outcome data are still developing.(22) The most important entry in the table, adaptive servo-ventilation, requires its own section.

The SERVE-HF Trial and the ASV Safety Lesson

Adaptive servo-ventilation is a sophisticated form of positive-airway-pressure therapy. It monitors breathing breath by breath and delivers just enough pressure support to smooth out the crescendo-decrescendo pattern — in effect, steadying the unstable loop. On the metric it was designed to fix, it works well: it controls central apnea and Cheyne-Stokes respiration more effectively than the other options. For a time it was used with enthusiasm in heart-failure patients, on the reasonable assumption that abolishing the apnea would help the heart.

The SERVE-HF trial tested that assumption and overturned it.(19) It randomized 1,325 patients with symptomatic heart failure, reduced ejection fraction (45% or below), and predominantly central sleep apnea. They received either adaptive servo-ventilation plus guideline-based care or guideline-based care alone, with a median follow-up of about 31 months. The therapy did what it was supposed to do to the breathing. It did not improve the main outcome — a composite of death and cardiovascular events was no better than control (54.1% versus 50.8%; hazard ratio 1.13, 95% CI 0.97–1.31). And on the outcomes that matter most, it did harm. All-cause mortality was higher with the device (hazard ratio 1.28, 95% CI 1.06–1.55). Cardiovascular death was higher still: it occurred in about 30% of the ASV group versus 24% of the control group, a relative increase of roughly a third (hazard ratio 1.34, 95% CI 1.09–1.65).(19)

The lesson is best stated plainly: reducing the apneas did not help, and appears to have hurt. The device silenced the warning sign without fixing what it was warning about — and silencing it carried a price. Exactly why remains uncertain; the trial was not designed to prove a mechanism, and the harm may relate to how the pressure therapy interacts with an already compromised circulation. What the trial established is narrow and firm: in chronic heart failure with reduced ejection fraction and predominantly central sleep apnea, adaptive servo-ventilation increases the risk of death and should not be used.(19, 20) On that basis it is now contraindicated in this group. What the trial did not establish is broader. It did not show that central apnea is harmless, that no treatment helps, or that ASV is unsafe in other groups. In patients with preserved ejection fraction or predominantly obstructive apnea, the question remains open.

This is the clearest illustration in the series of a principle stated earlier — that a treatment changing a number on a test is not the same as a treatment improving a life. Central apnea looked like a target. Hitting it cleanly did not help and, in this group, did harm.

Diagnosis

When sleep-disordered breathing is suspected in heart failure, the distinction between central and obstructive disease is not a technicality — it points to entirely different treatment paths, and as SERVE-HF showed, getting it wrong can carry consequences. For that reason, in-laboratory polysomnography is generally preferred over a simple home test in this setting. Full polysomnography measures respiratory effort directly, which is what separates a central event (no effort) from an obstructive one (effort against a closed airway), and it can characterize Cheyne-Stokes respiration, which many home devices are not designed to identify.(1, 17) Many heart-failure patients also have a mix of central and obstructive events, sometimes shifting through the night, and quantifying that mix requires the fuller study.(6, 17)

A useful sleep-study report in a heart-failure patient should do more than print a single apnea-hypopnea index. It should state the proportion of central versus obstructive events, note whether Cheyne-Stokes respiration was present, and describe the oxygen picture — the lowest saturation reached and the time spent below 90% — since nocturnal hypoxemia carries its own prognostic weight.(15) It should also record the arousal index and specify whether the study was an attended in-laboratory test or a home recording. These details are what let a clinician choose a path rather than guess at one.

Living With It: Practical Considerations

A few everyday factors influence nighttime breathing in this setting, and they are worth knowing without turning them into a self-treatment program. Fluid status matters: when fluid that pooled in the legs during the day redistributes toward the chest and neck at night, it can worsen both obstructive and central events, which is one reason good control of congestion helps.(24) Alcohol and sedatives can suppress and destabilize breathing and are generally best minimized. Opioids deserve particular mention, because they can cause or worsen central apnea directly; anyone on long-term opioids who has heart failure or known sleep-disordered breathing should make sure their clinicians know about both.(2, 25)

If you have heart failure and think central apnea may be part of your picture, a handful of questions can make a clinic visit more productive: What is my most recent ejection fraction, and is it reduced or preserved? If a sleep study is done, were my events predominantly central or obstructive, and was Cheyne-Stokes respiration present? How much of the night did I spend with low oxygen? Given those answers, what is the role — if any — of treating the breathing versus intensifying heart-failure therapy?

One caution applies with unusual force here. Because the right approach depends on ejection fraction and on the central-versus-obstructive mix, and because one effective-looking therapy is outright contraindicated in part of this population, no one should start, stop, or change positive-airway-pressure therapy based on an article. These are decisions for a clinician who knows your heart.

Common Assumptions Measured Against the Physiology

The Bottom Line

Central sleep apnea is a disorder of the control of breathing, not of the airway: the throat stays open while the brain briefly stops sending the drive to breathe. Where obstructive apnea is a problem the body imposes on the heart, central apnea in heart failure reverses the arrow: the failing heart imposes the problem on breathing. Slow circulation and oversensitive carbon-dioxide feedback push breathing into the self-sustaining oscillation seen as Cheyne-Stokes respiration. It is common in heart failure, often missed because its daytime symptoms blend into heart failure itself, and associated with worse outcomes — though how much reflects cause versus a marker of cardiac severity remains unsettled. Treatment begins with optimizing the heart failure, since better cardiac care is often the most effective way to steady the breathing; when central apnea persists, oxygen, CPAP, and phrenic-nerve stimulation are options, each without proven survival benefit. The defining caution is SERVE-HF: adaptive servo-ventilation controlled the apneas but raised cardiovascular death in reduced-ejection-fraction heart failure, and it is now contraindicated there. It is the field’s clearest reminder that suppressing an abnormal sign is not the same as improving a life — that the honest measure of a therapy is what it does to people, not to a tracing. Distinguish central from obstructive disease, ideally with in-laboratory polysomnography, before any treatment — and no one should change airway-pressure therapy on their own.

What Comes Next

Article 5 turns from breathing to wakefulness, taking up insomnia and the cost of hyperarousal. Where central apnea is the heart disturbing sleep, insomnia is often a nervous system that will not power down. It is a state of physiological overactivation with its own measurable consequences for blood pressure and cardiovascular risk — and its own evidence-based first-line treatment.

Key Terms

Central sleep apnea (CSA): Repeated pauses in breathing during sleep caused by a temporary absence of the brain’s drive to breathe, so respiratory effort stops while the airway remains open.

Cheyne-Stokes respiration: A pattern of central sleep apnea common in heart failure, in which breathing rises and falls in a smooth crescendo-decrescendo cycle separated by central pauses; cycle length tends to lengthen as the heart weakens.

Apneic threshold: The level of carbon dioxide below which the drive to breathe switches off during sleep. Central apnea occurs when breathing drops carbon dioxide below this point.

Ejection fraction (EF): The percentage of blood the left ventricle pumps out with each beat. A normal value is roughly 55–70%.

Heart failure with reduced ejection fraction (HFrEF): Heart failure in which the ejection fraction is reduced (commonly defined as 40% or below). The SERVE-HF contraindication to adaptive servo-ventilation applies to this group.

Heart failure with preserved ejection fraction (HFpEF): Heart failure in which the ejection fraction is normal or near-normal but the heart fills poorly. The role and safety of various sleep-apnea therapies are less defined here.

Adaptive servo-ventilation (ASV): A positive-airway-pressure therapy that adjusts breath by breath to smooth out central apnea. It is contraindicated in symptomatic HFrEF with predominantly central sleep apnea.

Predominantly central: A sleep study in which the majority of apneas and hypopneas are central rather than obstructive — the pattern that defines the population in which ASV proved harmful.

Treatment-emergent central sleep apnea: Central events that appear after starting CPAP for obstructive sleep apnea; a distinct mechanism that usually resolves over weeks to months but occasionally persists.

References

1. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol. 2017;69(7):841-858. doi:10.1016/j.jacc.2016.11.069. PMID: 28209226.
2. Eckert DJ, Jordan AS, Merchia P, Malhotra A. Central sleep apnea: pathophysiology and treatment. Chest. 2007;131(2):595-607. doi:10.1378/chest.06.2287.
3. Dempsey JA. Crossing the apnoeic threshold: causes and consequences. Exp Physiol. 2005;90(1):13-24. doi:10.1113/expphysiol.2004.028985. PMID: 15572458.
4. Naughton MT. Cheyne-Stokes respiration: friend or foe? Thorax. 2012;67(4):357-360. doi:10.1136/thoraxjnl-2011-200927. PMID: 22318163.
5. Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med. 1999;341(13):949-954. doi:10.1056/NEJM199909233411304. PMID: 10498490.
6. Bradley TD, Floras JS. Sleep apnea and heart failure: Part I: obstructive sleep apnea. Circulation. 2003;107(12):1671-1678. doi:10.1161/01.CIR.0000061757.12581.15. PMID: 12668504.
7. Solin P, Bergin P, Richardson M, Kaye DM, Walters EH, Naughton MT. Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation. 1999;99(12):1574-1579. doi:10.1161/01.CIR.99.12.1574. PMID: 10096933.
8. Lorenzi-Filho G, Azevedo ER, Parker JD, Bradley TD. Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure. Eur Respir J. 2002;19(1):37-40. PMID: 11843325.
9. Naughton M, Benard D, Tam A, Rutherford R, Bradley TD. Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. Am Rev Respir Dis. 1993;148(2):330-338. doi:10.1164/ajrccm/148.2.330. PMID: 8342895.
10. Oldenburg O, Lamp B, Faber L, Teschler H, Horstkotte D, Töpfer V. Sleep-disordered breathing in patients with symptomatic heart failure: a contemporary study of prevalence in and characteristics of 700 patients. Eur J Heart Fail. 2007;9(3):251-257. doi:10.1016/j.ejheart.2006.08.003. PMID: 17027333.
11. Vazir A, Hastings PC, Dayer M, et al. A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction. Eur J Heart Fail. 2007;9(3):243-250. doi:10.1016/j.ejheart.2006.08.001. PMID: 17030014.
12. Lanfranchi PA, Braghiroli A, Bosimini E, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation. 1999;99(11):1435-1440. doi:10.1161/01.CIR.99.11.1435. PMID: 10086966.
13. Javaheri S, Shukla R, Zeigler H, Wexler L. Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure. J Am Coll Cardiol. 2007;49(20):2028-2034. doi:10.1016/j.jacc.2007.01.084.
14. Spaak J, Egri ZJ, Kubo T, et al. Muscle sympathetic nerve activity during wakefulness in heart failure patients with and without sleep apnea. Hypertension. 2005;46(6):1327-1332. PMID: 16286569.
15. Oldenburg O, Wellmann B, Buchholz A, et al. Nocturnal hypoxaemia is associated with increased mortality in stable heart failure patients. Eur Heart J. 2016;37(21):1695-1703. doi:10.1093/eurheartj/ehv624. PMID: 26612581.
16. Bradley TD, Floras JS. Sleep apnea and heart failure: Part II: central sleep apnea. Circulation. 2003;107(13):1822-1826. doi:10.1161/01.CIR.0000061758.05044.64. PMID: 12682029.
17. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(3):479-504. doi:10.5664/jcsm.6506. PMID: 28162150.
18. Bradley TD, Logan AG, Kimoff RJ, et al; CANPAP Investigators. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med. 2005;353(19):2025-2033. doi:10.1056/NEJMoa051001. PMID: 16282177.
19. Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive servo-ventilation for central sleep apnea in systolic heart failure. N Engl J Med. 2015;373(12):1095-1105. doi:10.1056/NEJMoa1506459. PMID: 26323938.
20. Aurora RN, Bista SR, Casey KR, et al. Updated adaptive servo-ventilation recommendations for the 2012 AASM guideline: “The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses.” J Clin Sleep Med. 2016;12(5):757-761. doi:10.5664/jcsm.5812. PMID: 27092695.
21. Sasayama S, Izumi T, Matsuzaki M, et al; CHF-HOT Study Group. Improvement of quality of life with nocturnal oxygen therapy in heart failure patients with central sleep apnea. Circ J. 2009;73(7):1255-1262. doi:10.1253/circj.CJ-08-1210. PMID: 19448327.
22. Costanzo MR, Ponikowski P, Javaheri S, et al; remedé System Pivotal Trial Study Group. Transvenous neurostimulation for central sleep apnoea: a randomised controlled trial. Lancet. 2016;388(10048):974-982. doi:10.1016/S0140-6736(16)30961-8. PMID: 27598679.
23. Sinha AM, Skobel EC, Breithardt OA, et al. Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure. J Am Coll Cardiol. 2004;44(1):68-71. doi:10.1016/j.jacc.2004.03.040. PMID: 15234409.
24. Yumino D, Redolfi S, Ruttanaumpawan P, et al. Nocturnal rostral fluid shift: a unifying concept for the pathogenesis of obstructive and central sleep apnea in men with heart failure. Circulation. 2010;121(14):1598-1605. doi:10.1161/CIRCULATIONAHA.109.902452. PMID: 20351237.
25. Nigam G, Riaz M, Chang ET, Camacho M. Natural history of treatment-emergent central sleep apnea on positive airway pressure: a systematic review. Ann Thorac Med. 2018;13(2):86-91. doi:10.4103/atm.ATM_321_17. PMID: 29675059.

HeartBuddi • Your heart. Own it.