Sleep-disordered breathing (SDB) is a broad medical term encompassing a range of conditions that involve abnormal breathing patterns during sleep. These disturbances can vary widely, from increased resistance to airflow to the complete cessation of breath. This abnormal breathing leads to repeated drops in blood oxygen levels and causes frequent, brief awakenings, which fragment sleep architecture.
The prevalence of SDB is significant, and its impact extends far beyond simple fatigue or snoring. Untreated SDB is associated with an elevated risk for serious health issues, including hypertension, stroke, heart disease, and type 2 diabetes. The chronic lack of restorative sleep can also impair cognitive function, decrease productivity, and increase the likelihood of accidents, underscoring why recognizing and managing this condition is a major public health concern.
The Spectrum of Sleep-Disordered Breathing
SDB exists on a continuum, with different classifications based on the underlying cause of the breathing disruption. The most common form is Obstructive Sleep Apnea (OSA), which involves a physical blockage of the upper airway during sleep. In OSA, the muscles supporting the soft palate, tongue, and throat relax, causing the airway to narrow or fully collapse, which prevents air from reaching the lungs despite the body’s effort to breathe. These obstructive events, known as apneas or hypopneas, typically last 10 seconds or longer and are often characterized by loud snoring, gasping, or choking sounds.
Central Sleep Apnea (CSA) represents a different physiological problem, where the airway remains open, but the brain fails to send the proper signals to the muscles controlling breathing. Unlike OSA, which is a mechanical issue, CSA is a neurological one, resulting in a temporary lack of respiratory effort. This type is often linked to underlying medical conditions like heart failure or stroke, or it may be caused by certain medications.
A less severe form of SDB is Upper Airway Resistance Syndrome (UARS), which falls between simple snoring and full-blown OSA. In UARS, the upper airway narrows enough to increase the effort needed to breathe, but it does not cause a complete apnea or significant drop in oxygen saturation. This increased effort leads to frequent, subtle brain wave changes, called respiratory effort-related arousals, which interrupt sleep continuity without the person fully waking up. A mixed sleep apnea diagnosis is also possible, involving both obstructive and central events.
Identifying the Underlying Causes
The development of SDB is often multifactorial, stemming from a combination of anatomical, physiological, and lifestyle elements. A major anatomical contributor to OSA is the physical structure of the upper airway, with a small jaw, a large neck circumference, or enlarged tonsils and adenoids predisposing individuals to airway collapse.
Obesity is a major risk factor, as excess tissue deposition in the neck and around the pharynx mechanically narrows the airway. The incidence of OSA increases substantially with weight gain, showing a correlation between body mass index and disorder severity. Advancing age also contributes to risk, as muscle tone naturally decreases and the control of breathing becomes less stable.
Specific underlying conditions are more likely to cause CSA, particularly congestive heart failure and other cardiovascular diseases which can disrupt the stability of the body’s respiratory control system. Genetics play a role as well, with SDB often running in families due to shared craniofacial features or inherited differences in ventilatory control. The use of alcohol or sedatives before sleep can further compound the issue by relaxing the throat muscles and interfering with the brain’s ability to maintain stable breathing.
Diagnostic Processes
The process of confirming an SDB diagnosis relies on monitoring physiological functions during sleep, with the gold standard being a laboratory-based test called Polysomnography (PSG). This comprehensive sleep study involves spending a night at a specialized center where various sensors track multiple bodily activities. The PSG measures brain waves (electroencephalogram), eye movements, muscle activity, and heart rhythm to determine sleep stages and identify sleep fragmentation.
The study monitors breathing through sensors that detect airflow, measure respiratory effort, and track blood oxygen saturation. The collected data allows clinicians to calculate the Apnea-Hypopnea Index (AHI), which represents the average number of apneas and hypopneas per hour of sleep. This index is used to determine the presence and severity of SDB, with a higher AHI indicating more frequent and severe breathing disturbances.
For many patients, a physician may recommend an at-home sleep apnea test, which is a simplified version of the PSG. These portable monitors typically measure airflow, respiratory effort, and oxygen saturation, which is sufficient for diagnosing moderate to severe OSA in appropriate candidates. While home testing offers convenience, a full PSG may still be necessary if the initial home test is inconclusive or if the patient is suspected of having a less common form of SDB, such as CSA.
Therapeutic Approaches
The treatment for SDB is tailored to the specific diagnosis and the severity of the condition. For most cases of moderate to severe OSA, the first-line therapy is Continuous Positive Airway Pressure (CPAP). A CPAP machine delivers a stream of pressurized air through a mask worn over the nose or mouth, which acts as a pneumatic splint to keep the upper airway open during sleep. This restores normal blood oxygen levels and sleep continuity.
Other forms of positive airway pressure are also used, such as Bi-level Positive Airway Pressure (BiPAP), which provides different pressures for inhalation and exhalation, or Auto-PAP (APAP), which automatically adjusts the pressure based on the patient’s breathing needs. For patients with mild to moderate OSA or those who cannot tolerate CPAP, an oral appliance may be an effective alternative. These custom-fitted devices, resembling a mouthguard, work by repositioning the lower jaw and tongue forward to enlarge the airway space.
Lifestyle modifications are recommended for all patients, regardless of severity, with weight loss being particularly impactful for those who are overweight or obese. Even a modest reduction in body weight can significantly decrease SDB severity by reducing tissue mass around the throat. Positional therapy, which involves avoiding sleeping on the back, is also helpful since gravity exacerbates airway collapse. For patients with specific anatomical issues, surgical interventions may be considered to remove obstructive tissue or advance the jaw structure.