What Is the Difference Between Apnea and Hypopnea?

An apnea is a pause in breathing during sleep where airflow stops almost entirely for at least ten seconds, while a hypopnea is a partial reduction in airflow, typically a drop of at least 30%, lasting the same minimum duration. Both events disrupt normal sleep and reduce oxygen levels, but hypopneas are subtler and harder to define, which has made them surprisingly controversial in sleep medicine. How hypopnea is scored has changed several times over the past two decades, and the definition a sleep lab uses can shift a person’s diagnosis from normal to abnormal.

What Happens During Each Event

During an apnea, the airway either collapses completely (obstructive apnea) or the brain temporarily stops sending the signal to breathe (central apnea). Either way, air movement drops to near zero. The sleeper’s oxygen level falls, carbon dioxide builds up, and the brain eventually triggers a brief arousal, often so short the person doesn’t remember it, to restart breathing. This cycle can repeat dozens or even hundreds of times per night.

A hypopnea follows a similar pattern but in a milder form. The airway narrows rather than closing, so airflow decreases but doesn’t stop. The oxygen dip is usually smaller, the arousal briefer or sometimes absent. Because the reduction is partial, hypopneas can be harder to spot on a sleep study tracing, and whether a given dip in airflow “counts” as a hypopnea depends heavily on which scoring rule the technician is using.

There is also a related event called a respiratory effort-related arousal, or RERA, which is an even subtler breathing disturbance. A RERA involves at least ten seconds of increasing effort to breathe that ends in an arousal but doesn’t meet the threshold for a hypopnea. RERAs are combined with apneas and hypopneas into a broader measure called the respiratory disturbance index.

Why the Definition of Hypopnea Keeps Changing

Apnea has a fairly stable definition: airflow drops by 90% or more for at least ten seconds. Hypopnea, by contrast, has been redefined multiple times. The disagreement centers on two questions: how much does airflow have to drop, and what counts as evidence that the drop actually harmed the sleeper?

In 1999, the American Academy of Sleep Medicine defined a hypopnea as a 50% or greater decrease in airflow, or a smaller decrease accompanied by either a blood oxygen drop of at least 3% or a brain arousal. In 2007, the threshold was tightened: airflow had to fall by at least 30%, and it only counted if blood oxygen dropped by at least 4%. Then in 2012, the rule was loosened again, requiring a 30% airflow reduction but allowing either a 3% oxygen desaturation or an arousal to qualify.

These differences sound technical, but they have real consequences. The 2012 definition captures substantially more events than the 2007 one, because a 3% oxygen drop happens more easily than a 4% drop, and because arousals are common even with mild airway narrowing. One comparison found that the 2012 criteria produced average scores roughly two and a half times higher than the stricter 2007 criteria in the same patients.

³ A systematic review confirmed the pattern: the 2012 scoring criteria consistently resulted in greater apparent prevalence and severity of sleep-disordered breathing compared to the 2007 criteria.

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In practical terms, switching from the stricter to the more sensitive hypopnea definition captured roughly an additional 12% of obstructive sleep apnea diagnoses in one large study. That means thousands of people whose breathing disturbances would have been classified as normal under the old rule are now told they have a sleep disorder.

⁵ Whether those additional diagnoses actually lead to better outcomes is still being worked out, which is part of why the definition remains a live debate rather than a settled question.

The Combined Score That Drives Your Diagnosis

In clinical practice, apneas and hypopneas are rarely discussed separately. Instead, they are lumped together into the apnea-hypopnea index, or AHI, which is the total number of apneas plus hypopneas per hour of sleep. This single number is the main tool used to diagnose obstructive sleep apnea and decide how severe it is.

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The standard severity thresholds are widely used across sleep labs. An AHI below 5 events per hour is considered normal. An AHI from 5 to just under 15 is mild, from 15 to 30 is moderate, and above 30 is severe.

⁷ These cutoffs were established decades ago, and while they remain the standard, they’ve drawn criticism for being somewhat arbitrary. The index treats a ten-second apnea with a large oxygen drop the same as a brief hypopnea with a tiny desaturation, and it doesn’t account for how long each event lasts or how much oxygen is lost during it.

Because hypopneas are typically more common than apneas in most people with obstructive sleep apnea, your AHI is often driven more by hypopneas than by complete breathing pauses. A high percentage of hypopneas relative to apneas tends to indicate that the airway is only partially collapsible rather than fully closing, which can have implications for which treatments work best.

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Obstructive Versus Central Origins

Most people hear “sleep apnea” and picture an obstructive event, where throat muscles relax and the airway physically collapses. But both apneas and hypopneas can also be central in origin, meaning the brain temporarily reduces or stops its breathing signal without any physical obstruction. This distinction matters for treatment: obstructive events respond well to CPAP, which splints the airway open, while central events may not improve or can even worsen with standard CPAP.

Distinguishing obstructive from central apneas during a sleep study is relatively straightforward. In an obstructive apnea, the person’s chest and abdomen keep trying to move against the closed airway. In a central apnea, there’s no breathing effort at all. Researchers have found good agreement between diaphragm activity measurements and esophageal pressure readings when classifying central apneas, though roughly a third of central events identified by standard external sensors couldn’t be confirmed by more precise measures of breathing effort.

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Hypopneas are harder to classify as obstructive or central because the airflow doesn’t stop completely, making it tricky to tell whether the reduction comes from a narrowing airway or a weakened breathing drive. It has been suggested that a hypopnea is likely obstructive when it’s accompanied by snoring, flattening of the airflow signal, or the chest and abdomen moving in opposite directions, a sign of the body straining against a partially blocked airway.

¹⁰ In standard clinical practice, most labs don’t routinely classify hypopneas as obstructive or central, which can leave some ambiguity in the diagnosis.

What Both Events Do to the Body

Whether breathing stops completely or just drops, the downstream effects on the body follow a similar path. The repeated drops in oxygen, spikes in carbon dioxide, and micro-arousals from sleep trigger a stress response through the sympathetic nervous system, the same “fight or flight” wiring that activates when you’re startled or anxious.

Studies in which volunteers experienced repeated hypoxic apneas (their oxygen saturation dropping to around 83%) showed that sympathetic nerve activity increased significantly and stayed elevated, while blood pressure also rose transiently.

¹¹ When the same experiment was done with apneas in room air (so oxygen levels stayed normal), neither sympathetic activity nor blood pressure changed, confirming that the oxygen drop, not the act of pausing breathing itself, drives the harmful response.

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In people with heart failure who also have sleep apnea, both obstructive and central apneas boost sympathetic nerve activity through the same mechanisms of recurring oxygen drops, carbon dioxide buildup, and arousal.

¹³ Over months and years, this nightly sympathetic overdrive is thought to contribute to high blood pressure, heart rhythm problems, and cardiovascular disease. The total burden of events, apneas and hypopneas combined, matters more than whether each individual event is a full stop or a partial reduction.

Why REM Sleep Makes Things Worse

Most people with obstructive sleep apnea notice that their breathing events cluster during REM sleep, the stage associated with vivid dreaming. During REM, the muscles that hold the upper airway open lose much of their tone, making collapse more likely. Research measuring airway compliance across sleep stages found that the upper airway was most collapsible during REM sleep, with compliance significantly lower than during non-REM stages.

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Some people have sleep apnea that occurs predominantly or exclusively during REM sleep, sometimes called REM-predominant OSA. This can be misleading diagnostically. One study found that people with REM-predominant obstructive sleep apnea had an overall AHI roughly half that of people whose events were spread across all sleep stages, yet their daytime sleepiness scores were similar.

¹⁵ In other words, the AHI underestimated how impaired these patients actually felt during the day. REM-predominant OSA is more common in women and younger adults, populations that may be more likely to have their sleep apnea overlooked because their overall numbers don’t look alarming.

How These Events Are Detected

The gold standard for measuring apneas and hypopneas is in-lab polysomnography, where a technician monitors brain waves, eye movements, muscle activity, airflow, chest and abdominal movement, and blood oxygen simultaneously. Different sensors pick up different events with varying accuracy. A comparison of four airflow sensors found substantial differences: the nasal pressure transducer detected about 30% more apneas than the standard thermal sensor, while respiratory belt signals missed about 30% of events.

¹⁶ The sensor choice alone can meaningfully change a person’s AHI, which is another layer of variability on top of the scoring-rule differences discussed earlier.

Home sleep tests have become increasingly common as a more convenient and cheaper alternative. These portable devices typically measure fewer signals, often just airflow, oxygen, and chest movement, without brain-wave monitoring. One comparison found that home testing had about 95% sensitivity for detecting any sleep apnea (AHI of 5 or more) but was less accurate for grading moderate-to-severe disease, with sensitivity around 80% at that threshold.

¹⁷ The gap between the home test score and the lab score also widened as sleep apnea got more severe, suggesting home devices tend to undercount events in people with the worst disease.

Wearable Technology and Simpler Screening

Researchers are working to estimate the AHI from even simpler signals, like those available from a smartwatch or a single chest sensor. A deep-learning model using just two sensors, abdominal movement and pulse oximetry, correctly classified about 72% of patients into the right severity category, with over 99% placed within one category of the correct one.

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Another approach uses only the photoplethysmography signal from a wrist-worn device, the same light-based pulse sensor found in commercial smartwatches. Testing on nearly 200 clinical recordings found moderate agreement with polysomnography and reasonable ability to screen for OSA across severity levels.

¹⁹ Interestingly, machine-learning models trained on this same type of signal can also distinguish apneas from hypopneas based on differences in how blood flow patterns change during each event type, achieving reasonable accuracy especially when the person is sleeping on their back.

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None of these wearable approaches are ready to replace polysomnography for formal diagnosis, but they point toward a future where long-term monitoring at home could catch breathing problems that a single-night lab study might miss. A person whose apnea is position-dependent or occurs mainly during REM could have a perfectly normal-looking study on the one night they happen to sleep differently.

How Treatment Handles the Two Event Types

Continuous positive airway pressure, CPAP, remains the first-line treatment and works by blowing a steady stream of air to keep the airway from narrowing or collapsing. It reduces both apneas and hypopneas, though modern auto-adjusting CPAP machines don’t track these events with the same precision as a sleep lab. One study comparing an auto-CPAP device’s built-in event counts against simultaneous polysomnography found poor agreement for both obstructive apneas and hypopneas individually, even though the total AHI was roughly captured.

²¹ The device was better at detecting central apneas than obstructive ones, which is worth knowing if your doctor is using your CPAP’s data downloads to judge how well treatment is working.

For people with milder disease, especially when hypopneas predominate over apneas, oral appliances that advance the lower jaw offer an alternative. One randomized crossover trial found that a mandibular advancement device reduced the average AHI from about 15 to about 12 events per hour, and about 46% of patients achieved at least a 50% reduction in their AHI.

²² These devices tend to work best when the problem is partial airway narrowing (hypopneas) rather than complete collapse (apneas), because the jaw advancement may be enough to keep a partially narrowing airway open but insufficient to prevent full obstruction.

The ratio of hypopneas to apneas can actually help predict which patients will respond to treatments other than CPAP. A high proportion of hypopneas suggests the airway isn’t fully collapsing, which means factors like arousal threshold and breathing control instability may play a bigger role than anatomy alone. Research into these non-anatomical drivers of sleep apnea is growing, and clinical trials are increasingly using a high hypopnea percentage as a way to select patients for newer therapies targeting these mechanisms.

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Scoring Differences in Children and Adolescents

Pediatric sleep medicine uses different rules for scoring respiratory events. In children, an apnea can be as short as two missed breaths (rather than the adult ten-second minimum), and hypopneas may be scored with a lower airflow-reduction threshold. When adolescents’ sleep studies were scored using both adult and pediatric criteria, the results diverged considerably. One study found that the median AHI scored by pediatric rules was 1.7 events per hour, while the same recordings scored under the stricter adult rule (requiring a 4% oxygen drop) yielded a median of just 0.4 events per hour.

²³ Switching to the more sensitive adult rule (3% desaturation or arousal) brought the median closer to the pediatric result at 1.4 per hour, but the gap between the strictest and most generous adult scoring systems was still striking. For teenagers in particular, which scoring system is applied can determine whether they receive a diagnosis or are told their breathing is fine.

This scoring gap is especially relevant because untreated sleep-disordered breathing in adolescents has been linked to problems with attention, school performance, and growth. A teen whose study is scored using the stricter adult hypopnea rule might fall below the diagnostic threshold, while the same data scored by pediatric standards would flag a problem worth treating. If your child or teenager is evaluated for sleep apnea, it’s worth asking which scoring criteria were applied and whether both adult and pediatric rules were considered.