What Is Cheyne-Stokes Respiration? Causes & Treatment

Cheyne-Stokes respiration is a breathing disorder in which breathing repeatedly cycles between periods of no breathing at all and periods of deep, fast breathing. The pattern is distinctive: breaths gradually get deeper and faster, peak in intensity, then gradually become shallower until breathing stops completely for several seconds. Then the cycle starts again. Each full cycle typically lasts 45 to 90 seconds, and the pattern can repeat for hours, most often during sleep.

What the Breathing Pattern Looks Like

If you watched someone with Cheyne-Stokes respiration while they slept, you’d see their chest movements slowly ramp up from nothing to large, deep breaths, then gradually taper back down until their chest goes completely still. After a pause of several seconds (the apnea phase), the whole sequence restarts. Doctors describe this as a “crescendo-decrescendo” pattern, meaning the breath volume rises and falls like a wave.

This is different from ordinary snoring or obstructive sleep apnea, where breathing stops because the airway physically collapses. In Cheyne-Stokes respiration, the airway is open. The problem is that the brain temporarily stops sending the signal to breathe. That makes it a form of central sleep apnea, meaning the interruption originates in the brain’s breathing control centers rather than in the throat or chest.

To formally diagnose the pattern, the American Academy of Sleep Medicine requires at least three consecutive cycles of apnea or reduced breathing separated by the characteristic crescendo-decrescendo wave, with each cycle lasting at least 40 seconds. It occurs primarily during lighter stages of sleep but can also appear when a person is awake.

Why It Happens: The Feedback Loop Problem

Your brain constantly monitors carbon dioxide levels in your blood. When CO2 rises, the brain tells you to breathe faster to blow it off. When CO2 drops, the brain dials breathing back. In a healthy person, this feedback loop works smoothly and keeps breathing steady.

Cheyne-Stokes respiration develops when that feedback loop becomes unstable. Two things typically go wrong at once. First, the brain’s CO2 sensors become overly sensitive, so they overreact to small changes. Second, there’s a delay in how quickly the brain receives updated information about blood gas levels. In heart failure, for example, sluggish circulation means it takes longer for blood leaving the lungs to reach the sensors in the brain. By the time the brain registers that CO2 has dropped, it has already driven breathing too hard for too long. So it overcorrects by shutting breathing down. CO2 then builds up during the pause, the sensors eventually detect the rise, and they overcorrect again in the other direction. The result is that constant oscillation between too much breathing and none at all.

Conditions That Cause It

Heart failure is the most common condition linked to Cheyne-Stokes respiration. When the heart pumps weakly, blood circulates more slowly, which lengthens that feedback delay between the lungs and brain. The weaker the heart, the longer the delay, and the more pronounced the breathing cycles tend to be.

Stroke and other brain injuries are the second major cause. Research on patients with brainstem strokes found that Cheyne-Stokes respiration appeared specifically in those with extensive bilateral damage to the pons, a structure deep in the brainstem that helps regulate breathing rhythm. Other neurological conditions, including brain tumors, traumatic brain injuries, and advanced dementia, can produce the same pattern when they affect the brain’s respiratory control areas.

Kidney failure and certain medications that suppress the central nervous system (particularly opioids) can also trigger the pattern. And notably, it happens in perfectly healthy people at high altitude. Above about 3,000 meters (roughly 9,800 feet), nearly all healthy individuals develop periodic breathing during sleep. The thin air makes CO2 sensors hypersensitive, creating the same unstable feedback loop that heart failure or brain damage produces at sea level. In healthy climbers, the pattern resolves once they descend or acclimatize.

How It Affects Sleep and Daily Life

Because the pattern clusters in lighter sleep stages, it fragments sleep badly. The repeated drops in oxygen and the brief arousals that follow each apnea phase prevent the brain from settling into deep, restorative sleep. People with Cheyne-Stokes respiration often wake feeling unrefreshed, experience excessive daytime sleepiness, and may notice morning headaches. Bed partners are frequently the first to notice, describing long pauses in breathing that can be alarming to witness.

In people with heart failure, poor sleep quality from Cheyne-Stokes respiration creates a vicious cycle. Sleep disruption raises stress hormones and blood pressure, which puts additional strain on an already weakened heart. This is one reason the pattern is considered a marker of more advanced disease rather than a harmless quirk of breathing.

How It’s Diagnosed

A sleep study, called polysomnography, is the standard way to confirm Cheyne-Stokes respiration. During the study, sensors track airflow, chest and abdominal movement, blood oxygen levels, brain waves, and heart rhythm. The crescendo-decrescendo wave pattern in airflow and chest excursion is visually distinctive on the recording, making it relatively straightforward for a sleep specialist to identify. The key distinction from other types of central sleep apnea is that characteristic waxing and waning wave shape. Other forms of central apnea involve sudden stops and starts without the gradual ramp-up and taper.

What the Prognosis Looks Like

Whether Cheyne-Stokes respiration itself worsens outcomes, or simply reflects the severity of an underlying condition, is a question researchers have wrestled with for years. One study that followed 57 heart failure patients on modern treatments over an average of 38 months found that mortality didn’t differ significantly between those with and without the breathing pattern. In patients without cardiac pacing devices, about 35% of those with Cheyne-Stokes respiration died during follow-up compared to 40% without it. These numbers were not statistically meaningful, suggesting the pattern may be more of a marker for disease severity than an independent killer.

That said, the presence of Cheyne-Stokes respiration in someone with heart failure signals that the heart is pumping poorly enough to create significant circulatory delays. It tends to appear in more advanced stages of the disease and is generally taken as a sign that treatment needs to be optimized.

Treatment Options and Limitations

The first priority is treating whatever underlying condition is driving the abnormal breathing. In heart failure, optimizing cardiac medications and managing fluid overload can sometimes reduce or eliminate the pattern. When kidney failure is the trigger, dialysis may improve it. For altitude-related periodic breathing, descent or supplemental oxygen resolves the issue.

For persistent cases, supplemental oxygen during sleep can dampen the oscillations by keeping blood oxygen levels more stable, which reduces the exaggerated response from CO2 sensors. This is generally considered a safe option.

A more advanced device called adaptive servo-ventilation (ASV) was developed specifically for this type of breathing disorder. It delivers varying amounts of air pressure through a mask, automatically increasing support during apnea phases and backing off during the hyperventilation phases to smooth out the cycle. ASV is effective at normalizing the breathing pattern on a sleep study. However, a major trial published in the New England Journal of Medicine found a serious problem: in 1,325 heart failure patients with reduced heart function, those randomly assigned to use ASV had significantly higher rates of death from any cause (28% increased risk) and cardiovascular death (34% increased risk) compared to those who received standard medical care alone. As a result, ASV is now considered unsafe for heart failure patients whose hearts pump weakly, and its use in that population has largely been abandoned.

For people with Cheyne-Stokes respiration from neurological causes or other conditions, treatment decisions are more individualized, and the evidence base is thinner. The focus remains on managing the underlying disease while monitoring sleep quality and oxygen levels.