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Apnea
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Apnea
Other namesApnoea
A 32 second breathing pause in a sleep apnea patient
SpecialtyPulmonology, pediatrics

Apnea (also spelled apnoea in British English)[1] is the temporary cessation of breathing. During apnea, there is no movement of the muscles of inhalation,[citation needed] and the volume of the lungs initially remains unchanged. Depending on how blocked the airways are (patency), there may or may not be a flow of gas between the lungs and the environment. If there is sufficient flow, gas exchange within the lungs and cellular respiration would not be severely affected. Voluntarily doing this is called holding one's breath. Apnea may first be diagnosed in childhood, and it is recommended to consult an ENT specialist, allergist or sleep physician to discuss symptoms when noticed; malformation and/or malfunctioning of the upper airways may be observed by an orthodontist.[2]

Cause

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Apnea can be involuntary—for example, drug-induced (such as by opiate toxicity), mechanically / physiologically induced (for example, by strangulation or choking), or a consequence of neurological disease or trauma. During sleep, people with severe sleep apnea can have over thirty episodes of intermittent apnea per hour every night.[3]

Apnea can also be observed during periods of heightened emotion, such as during crying or accompanied by the Valsalva maneuver when a person laughs. Apnea is a common feature of sobbing while crying, characterized by slow but deep and erratic breathing followed by brief periods of breath holding.

Another example of apnea are breath-holding spells; these are sometimes emotional in cause and are usually observed in children as a result of frustration, emotional stress and other psychological extremes.

Voluntary apnea can be achieved by closing the vocal cords, simultaneously keeping the mouth closed and blocking the nasal vestibule, or constantly activating expiratory muscles, not allowing any inspiration.

Complications

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Under normal conditions, humans cannot store much oxygen in the body. Prolonged apnea leads to severe lack of oxygen in the blood circulation, leading to dysfunction of organ systems. Permanent brain damage can occur after as little as three minutes and death will inevitably ensue after a few more minutes unless ventilation is restored. However, under special circumstances such as hypothermia, hyperbaric oxygenation, apneic oxygenation (see below), or extracorporeal membrane oxygenation, much longer periods of apnea may be tolerated without severe detrimental consequences.

Untrained humans usually cannot sustain voluntary apnea for more than one or two minutes, since the urge to breathe becomes unbearable.[citation needed] The reason for the time limit of voluntary apnea is that the rate of breathing and the volume of each breath are tightly regulated to maintain constant values of CO2 tension and pH of the blood more than oxygen levels. In apnea, CO2 is not removed through the lungs and accumulates in the blood. The consequent rise in CO2 tension and drop in pH result in stimulation of the respiratory centre in the brain which eventually cannot be overcome voluntarily. The accumulation of carbon dioxide in the lungs will eventually irritate and trigger impulses from the respiratory center part of the brain and the phrenic nerve. Rising levels of carbon dioxide signal the body to breathe and resume unconscious respiration forcibly. The lungs start to feel as if they are burning, and the signals the body receives from the brain when CO2 levels are too high include strong, painful, and involuntary contractions or spasms of the diaphragm and the muscles in between the ribs. At some point, the spasms become so frequent, intense and unbearable that continued holding of the breath is nearly impossible.[citation needed]

When a person is immersed in water, physiological changes due to the mammalian diving reflex enable somewhat longer tolerance of apnea even in untrained persons as breathing is not possible underwater. Tolerance can in addition be trained. The ancient technique of free-diving requires breath-holding, and world-class free-divers can hold their breath underwater up to depths of 214 metres (702 ft) and for more than four minutes.[4] Apneists, in this context, are people who can hold their breath for a long time.

Hyperventilation

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Voluntary hyperventilation before beginning voluntary apnea is commonly believed to allow the person involved to safely hold their breath for a longer period. In reality, it will give the impression that one does not need to breathe, while the body is actually experiencing a blood-oxygen level that would normally, and indirectly, invoke a strong dyspnea and eventually involuntary breathing. Some have incorrectly attributed the effect of hyperventilation to increased oxygen in the blood, not realizing that it is actually due to a decrease in CO2 in the blood and lungs. Blood leaving the lungs is normally fully saturated with oxygen, so hyperventilation of normal air cannot increase the amount of oxygen available, as oxygen in blood is the direct factor. Lowering the CO2 concentration increases the pH of the blood, thus increasing the time before blood becomes acidic enough so the respiratory center becomes stimulated, as described above. While hyperventilation will yield slightly longer breath-holding times, any small time increase is at the expense of possible hypoxia, though it might not be felt as easily.[5] One using this method can suddenly lose consciousness unnoticed—a shallow water blackout—as a result. If a person loses consciousness underwater, there is considerable danger that they will drown. An alert diving partner or nearby lifeguard would be in the best position to rescue such a person. Static apnea blackout occurs at the surface when a motionless diver holds their breath long enough for the circulating oxygen in blood to fall below that required for the brain to maintain consciousness. It involves no pressure changes in the body and is usually performed to enhance breath-hold time. It should never be practiced alone, but under strict safety protocols with a safety guard or equipment beside the diver.

Apneic oxygenation

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Because the exchange of gases between the blood and airspace of the lungs is independent of the movement of gas to and from the lungs, enough oxygen can be delivered to the circulation even if a person is apneic, and even if the diaphragm does not move. With the onset of apnea, low pressure develops in the airspace of the lungs because more oxygen is absorbed than CO2 is released. With the airways closed or obstructed, this will lead to a gradual collapse of the lungs and suffocation. However, if the airways are open, any gas supplied to the upper airways will follow the pressure gradient and flow into the lungs to replace the oxygen consumed. If pure oxygen is supplied, this process will serve to replenish the oxygen stored in the lungs and resume sufficient ventilation. The uptake of oxygen into the blood will then remain at the usual level, and the normal functioning of the organs will not be affected. A consequence of this hyperoxygenation is the occurrence of "nitrogen washout", which can lead to atelectasis.[6]

However, no CO2 is removed during apnea. The partial pressure of CO2 in the airspace of the lungs will quickly equilibrate with that of the blood. As the blood is loaded with CO2 from the metabolism without a way to remove it, more and more CO2 will accumulate and eventually displace oxygen and other gases from the airspace. CO2 will also accumulate in the tissues of the body, resulting in respiratory acidosis.

Under ideal conditions (i.e., if pure oxygen is breathed before onset of apnea to remove all nitrogen from the lungs, and pure supplemental oxygen is insufflated), apneic oxygenation could theoretically be sufficient to provide enough oxygen for survival of more than one hour's duration in a healthy adult.[citation needed] However, accumulation of carbon dioxide (described above) would remain the limiting factor.

Apneic oxygenation is more than a physiologic curiosity. It can be employed to provide a sufficient amount of oxygen in thoracic surgery when apnea cannot be avoided, and during manipulations of the airways such as bronchoscopy, intubation, and surgery of the upper airways. However, because of the limitations described above, apneic oxygenation is inferior to extracorporal circulation using a heart-lung machine and is therefore used only in emergencies, short procedures, or where extracorporal circulation cannot be accessed. Use of PEEP valves is also an accepted alternative (5 cm H2O in average weight patients and 10 cm H2O significantly improved lung and chest wall compliance in morbidly obese patients).[7]

In 1959, Frumin described the use of apneic oxygenation during anesthesia and surgery. Of the eight test subjects in this landmark study, the highest recorded PaCO2 was 250 millimeters of mercury, and the lowest arterial pH was 6.72 after 53 minutes of apnea.[8]

Apnea scientific studies

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Studies found spleen volume is slightly reduced during short breath-hold apnea in healthy adults.[9]

Apnea test in determining brain death

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A recommended practice for the clinical diagnosis of brain death formulated by the American Academy of Neurology hinges on the conjunction of three diagnostic criteria: a coma, absence of brainstem reflexes, and apnea (defined as the inability of the patient to breathe unaided: that is, with no life support systems like ventilators). The apnea test follows a delineated protocol.[10] Apnea testing is not suitable in patients who are hemodynamically unstable with increasing vasopressor needs, metabolic acidosis, or require high levels of ventilatory support. Apnea testing carries the risk of arrhythmias, worsening hemodynamic instability, or metabolic acidosis beyond the level of recovery and can potentially make the patient unsuitable for organ donation (see above). In this situation a confirmatory test is warranted as it is unsafe to perform the apnea test to the patient.[9]

Etymology and pronunciation

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The word apnea (or apnoea) uses combining forms of a- + -pnea, from Greek: ἄπνοια, from ἀ-, privative, πνέειν, to breathe. See pronunciation information at dyspnea.

See also

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References

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Sources

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Apnea

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from Grokipedia
Apnea is the temporary cessation of , marked by the absence of through the and due to either a lack of respiratory effort or an obstruction in the airway. Medically, it is defined as a pause in lasting at least 10 seconds in adults or 20 seconds in infants (or shorter durations if accompanied by , , or oxygen desaturation). This condition can occur voluntarily, as in breath-holding, but is more commonly involuntary and serves as a critical symptom of underlying physiological disruptions. Apnea manifests in various forms depending on its cause and , with key types including obstructive apnea, where is blocked despite persistent respiratory muscle activity (often due to anatomical narrowing of the upper airway); central apnea, characterized by absent respiratory effort stemming from impaired signaling; and mixed apnea, a combination of the two mechanisms. These types are prevalent in specific populations, such as apnea of prematurity in neonates (affecting approximately 85% of infants born at ≤34 weeks' due to immature respiratory control), and in adults during sleep, where (OSA) is the most common variant, involving repeated upper airway collapse. , by contrast, arises from failures in the central nervous system's regulation of ventilation, often linked to heart failure or use. The condition's implications are profound, as even brief episodes can result in (low blood oxygen), (elevated ), and , potentially progressing to respiratory or if untreated. In clinical settings, apnea monitoring is essential for at-risk groups, including premature infants and patients with chronic respiratory or neurological disorders, where interventions like (CPAP) or pharmacological agents (e.g., for neonates) can mitigate risks. OSA, in particular, affects an estimated 10-30% of adults globally and is associated with heightened cardiovascular morbidity, including and , underscoring the need for diagnosis via .

Overview and Types

Definition

Apnea is defined as the temporary cessation of , characterized by the complete absence of airflow at the and for at least 10 seconds in adults and 20 seconds in infants (or shorter durations if accompanied by , , or oxygen desaturation). This condition arises from either a lack of respiratory effort or an obstruction preventing air entry, distinguishing it from voluntary breath-holding or normal pauses in respiration. Unlike , which involves a partial reduction in (typically by at least 30%) accompanied by oxygen desaturation or , apnea represents a total halt in ventilation. It also differs from dyspnea, defined as labored or difficult breathing due to increased effort, and from , a prolonged and potentially fatal stoppage of breathing that requires immediate intervention if the heart continues to function. Physiologically, breathing is regulated by respiratory centers in the , including the dorsal and ventral respiratory groups in the medulla oblongata and the pneumotaxic center in the , which generate rhythmic signals to the diaphragm and . During an apneic episode, the interruption in ventilation leads to (decreased blood oxygen levels) and (elevated levels), triggering compensatory mechanisms like increased respiratory drive upon resumption, though repeated events can strain cardiovascular and neurological systems. Epidemiologically, apnea, particularly in the form of , affects an estimated 936 million adults aged 30–69 years worldwide, with prevalence rising significantly in the elderly (up to 50–60% experiencing related sleep disorders) and in vulnerable populations such as premature newborns, where apnea of prematurity affects up to 50% of very low birth-weight infants and is nearly universal in those born before 28 weeks gestation. Various types of apnea exist, including and central forms, which are detailed in the classification section.

Classification of Apnea

Apnea is classified based on its underlying mechanisms and the physiological or environmental context in which it occurs, distinguishing between types that involve physical airway obstruction, neurological failure of respiratory drive, or combinations thereof. (OSA) is characterized by recurrent episodes of upper airway collapse during sleep, leading to complete cessation of airflow (obstructive apnea) or partial reduction () despite ongoing respiratory effort. This type arises from anatomical blockage rather than dysfunction. Central sleep apnea (CSA) involves pauses in breathing due to a lack of neural signals from the to the respiratory muscles, with no detectable effort during the apneic event. Subtypes include primary CSA (idiopathic) and secondary forms linked to specific conditions, but all share the absence of brainstem-initiated breathing commands. Mixed apnea combines central and obstructive elements within the same episode, typically beginning with absent respiratory effort (central phase) followed by airway obstruction despite resumed effort (obstructive phase). This hybrid form is common in sleep-disordered breathing and reflects overlapping pathophysiological processes. Other specialized forms of apnea include neonatal apnea, prevalent in premature infants and classified similarly as central (no effort), obstructive (effort against blockage), or mixed (combination), with mixed events comprising about half of cases. Diving apnea, or breath-hold apnea, denotes voluntary suspension of breathing while submerged in water, ranging from recreational to competitive . Drug-induced apnea primarily presents as a central type, triggered by medications such as opioids that suppress respiratory centers. Apnea can also be contextualized as sleep-related, encompassing syndromes like OSA, , and mixed apnea that disrupt nocturnal breathing patterns, or non-sleep-related, occurring in settings such as general , high-altitude exposure, or acute neurological events where breathing pauses arise independently of sleep.

Causes and Pathophysiology

Etiological Factors

Apnea encompasses several types, including (OSA) and (CSA), each with distinct etiological factors that precipitate episodes of breathing cessation. In OSA, anatomical abnormalities play a primary role by obstructing the upper airway during . Obesity contributes significantly through fat deposition around the upper airway, leading to its narrowing and collapse under negative inspiratory pressure. Enlarged tonsils or adenoids similarly impede airflow, particularly in children and some adults, by physically blocking the pharyngeal space. For CSA, neurological etiologies predominate, disrupting the brainstem's respiratory control centers. Brainstem lesions, such as those from strokes or infections, impair the automatic regulation of breathing, resulting in absent respiratory effort during apneic events. Congenital disorders like Ondine's curse, or congenital central hypoventilation syndrome (CCHS), arise from mutations in the PHOX2B gene, which affect neural crest development and lead to inadequate ventilatory drive, especially during sleep. Environmental and iatrogenic factors can trigger apnea across both types. High-altitude hypoxia induces periodic breathing patterns characteristic of CSA by altering sensitivity to oxygen levels. suppresses central respiratory drive, often causing CSA through mu-opioid receptor activation in the . complications, including residual effects of sedatives and neuromuscular blockers, increase upper airway collapsibility and respiratory depression, heightening apnea risk postoperatively, particularly in susceptible individuals. Genetic predispositions contribute to familial forms of syndromes. In OSA, familial aggregation shows estimates of 30-40%, linked to polygenic traits influencing craniofacial structure and ventilatory control, though no single dominates. For CSA-related syndromes like CCHS, specific expansions in the polyalanine tract of the PHOX2B gene are identified in over 90% of cases, confirming a monogenic .

Underlying Mechanisms

The respiratory maintains through a network of central and peripheral chemoreceptors that monitor blood gas levels and pH to regulate ventilation. Central chemoreceptors, located in the , primarily detect changes in pH influenced by arterial CO₂ levels, responding to by increasing and depth to restore . Peripheral chemoreceptors, situated in the carotid bodies and , sense both hypoxia and , with a more pronounced sensitivity to low O₂ partial pressure (PaO₂ below 60 mmHg), triggering rapid ventilatory adjustments via afferent signals to the respiratory centers. These feedback loops operate continuously but are modulated during sleep, where sensitivity to CO₂ decreases, potentially leading to and apneic episodes if thresholds are exceeded. In obstructive and central apnea, the apnea-hypopnea cycle arises from disruptions in this control, culminating in recurrent from driven by accumulating hypoxia and . During an apneic event, cessation of airflow (in obstructive cases) or ventilatory effort (in central cases) causes PaO₂ to fall and PaCO₂ to rise progressively, stimulating chemoreceptors beyond thresholds, typically after 10-30 seconds. This chemical drive provokes a brief cortical , restoring upper airway patency or respiratory drive momentarily, which normalizes gas levels but fragments . The cycle repeats as resumes, with each event exacerbating instability in the ventilatory control loop, particularly in non-REM where thresholds are higher. At the cellular level, central apnea involves impaired brainstem signaling, where neurotransmitters like serotonin (5-HT) play a key modulatory role in stabilizing respiratory rhythm. Serotoninergic neurons in the raphe nuclei enhance the drive to breathe by facilitating excitatory inputs to phrenic motor neurons; depletion or dysfunction of these pathways, as seen in conditions like congenital central hypoventilation syndrome, increases apneic frequency by reducing ventilatory response to hypercapnia. In contrast, obstructive apnea stems from phasic and tonic collapse of upper airway dilator muscles, such as the genioglossus, due to diminished neural activation during sleep. Loss of wakefulness-related excitatory inputs leads to hypotonia, allowing negative intraluminal pressure during inspiration to overcome structural support, resulting in airway occlusion. These mechanisms culminate in gas exchange failure, quantifiable through the alveolar gas equation, which highlights how apnea disrupts O₂ delivery: PAO2=PIO2−PACO2RPA_{O_2} = PI_{O_2} - \frac{PACO_2}{R}, where PAO2PA_{O_2} is alveolar O₂ , PIO2PI_{O_2} is inspired O₂ , PACO2PACO_2 approximates arterial CO₂, and RR is the respiratory exchange ratio (typically 0.8). During apnea, absent ventilation causes PACO2PACO_2 to rise rapidly while PAO2PA_{O_2} plummets, widening the alveolar-arterial O₂ gradient and inducing systemic until arousal restores airflow. This equation underscores the biochemical basis of hypoxic drive in prolonging apneic cycles if feedback is blunted.

Clinical Presentation and Diagnosis

Symptoms and Signs

Apnea, particularly in the context of sleep-related disorders, manifests through a range of subjective symptoms and observable signs that disrupt normal breathing patterns during sleep. Common symptoms include loud , , and morning headaches, which often arise from repeated interruptions in airflow leading to fragmented sleep. Patients may also report awakening with a dry mouth, , or sudden awakenings accompanied by gasping for air, reflecting the body's response to oxygen desaturation. These experiences contribute to overall fatigue and reduced . Observable signs of apnea are frequently reported by bed partners or caregivers and include witnessed episodes of breathing cessation lasting 10 seconds or longer in adults, irregular breathing patterns such as pauses followed by abrupt resumption, and in severe cases, indicated by bluish discoloration of the skin due to hypoxia. These signs highlight the physiological strain of apneic events, where stops despite ongoing respiratory effort in obstructive forms or without effort in central forms. In neonatal contexts, such as apnea of prematurity, presentation differs and includes pauses in breathing lasting 20 seconds or longer, or shorter pauses accompanied by (heart rate <100 bpm), oxygen desaturation (<80-85% for premies), cyanosis, pallor, or hypotonia. These events often occur without warning and are linked to immature respiratory control in preterm infants. Symptoms and signs vary by type of apnea. In obstructive sleep apnea (OSA), the most prevalent form caused by upper airway blockage, patients typically exhibit prominent snoring, choking or gasping sounds upon resumption of breathing, and restless sleep due to repeated arousal attempts to reopen the airway. In contrast, central sleep apnea (CSA), resulting from lapses in brainstem signaling, often presents with more silent pauses in breathing without snoring, shortness of breath upon awakening, and occasional arousals from prolonged central apneic events accompanied by shortness of breath, though daytime fatigue remains a shared feature. Severity of apnea's impact, especially on daytime functioning, is commonly assessed using the Epworth Sleepiness Scale (ESS), a validated self-report questionnaire that rates the likelihood of dozing in eight everyday situations, with scores ranging from 0 to 24; scores above 10 indicate excessive daytime sleepiness linked to apneic burden. This tool helps quantify the subjective burden of symptoms like fatigue and concentration difficulties, guiding clinical evaluation of apnea's effects across severities.

Diagnostic Approaches

The diagnosis of apnea, particularly in the context of sleep-disordered breathing, relies on objective assessments to confirm the presence, type, and severity of apneic events, often prompted by clinical symptoms such as excessive daytime sleepiness or snoring. These approaches distinguish between obstructive sleep apnea (OSA), central sleep apnea (CSA), and other forms by quantifying respiratory pauses and associated physiological changes. Polysomnography (PSG) serves as the gold standard for diagnosing sleep apnea, conducted in a sleep laboratory to monitor multiple physiological parameters overnight. It records electroencephalography (EEG) for sleep staging, nasal and oral airflow via thermistors or pressure transducers, respiratory effort through thoracoabdominal bands, oxygen saturation using pulse oximetry, and additional metrics like electrocardiography, electromyography, and sometimes transcutaneous carbon dioxide levels. This comprehensive evaluation allows for the identification of apneas—defined as complete cessations of airflow for at least 10 seconds in adults—and hypopneas, which involve partial airflow reductions of 30-50% with associated desaturation or arousal. PSG is particularly valuable for complex cases, including mixed or central apneas, and facilitates simultaneous titration of therapies like continuous positive airway pressure. The severity of sleep apnea is quantified using the Apnea-Hypopnea Index (AHI), calculated as the total number of apneic and hypopneic events divided by the hours of sleep:
AHI=total apneas + hypopneashours of sleep\text{AHI} = \frac{\text{total apneas + hypopneas}}{\text{hours of sleep}}
Thresholds classify OSA as mild (AHI 5-15 events per hour), moderate (15-30 events per hour), or severe (>30 events per hour), guiding clinical management decisions. These criteria, established by organizations like the , emphasize arousals or oxygen desaturations of at least 3-4% for hypopnea scoring to ensure diagnostic accuracy. For screening obstructive sleep apnea in uncomplicated adults, home sleep apnea testing (HSAT) offers a convenient alternative using portable, unattended devices classified as Type III monitors with 4-7 channels. These devices typically measure airflow (via nasal pressure cannulae), respiratory effort (with inductance plethysmography belts), , and , providing an estimated AHI without full staging. HSAT is recommended for high pretest probability cases but requires follow-up PSG if results are inconclusive or for non-OSA diagnoses. In non-sleep-related apnea, such as acute respiratory events or syndromes, simpler tests like and arterial blood gas (ABG) analysis assess oxygenation and ventilation status. For neonatal apnea, typically occurs in the via continuous cardiorespiratory monitoring, including impedance pneumography for respiratory effort, for , and to detect desaturations and associated with apneic episodes. noninvasively monitors peripheral oxygen saturation to detect desaturations suggestive of apneic episodes, though it lacks specificity for event typing and is not diagnostic alone. ABG sampling measures arterial of (PaCO₂ >45 mmHg indicating ) and oxygen levels, aiding in the evaluation of central or hypercapnic apneas beyond sleep contexts.

Treatment and Management

Therapeutic Interventions

(PAP) therapy serves as the first-line treatment for moderate to severe (OSA), delivering pressurized air through a to maintain airway patency during sleep. (CPAP), the most common form, applies a constant (typically 4-20 cm H₂O) throughout the respiratory cycle to prevent upper airway collapse by increasing intraluminal and reducing . Settings are adjusted via in-laboratory or home auto-adjusting PAP (APAP) devices, which dynamically vary based on detected limitations before potentially switching to fixed levels after initial use. PAP is indicated for adults with OSA across all severities, particularly those with , , or cardiovascular comorbidities, where it reduces the apnea-hypopnea index (AHI) by approximately 86% (from a mean of 32.7 to 4.1 events/hour) and improves scores by 2.4 points. Bilevel PAP (BPAP) is preferred for CPAP-intolerant patients requiring higher s, offering inspiratory and expiratory differentials without differing significantly in AHI reduction from CPAP. Surgical interventions target anatomical obstructions in OSA when PAP fails or is declined. Uvulopalatopharyngoplasty (UPPP) involves excision of the uvula, posterior soft palate, and tonsils (if present) to widen the oropharyngeal airway, indicated for patients with polysomnography-confirmed OSA and favorable anatomy such as lower body mass index (BMI) or milder disease severity. Efficacy varies by outcome definition, with 24% of patients achieving postoperative AHI ≤5 events/hour, 33% reaching ≤10 events/hour, and 51% experiencing ≥50% AHI reduction or final AHI ≤20 events/hour; long-term success (beyond 6 months) diminishes due to potential cicatricial narrowing, with mean AHI reduction of 54.4% at 6 months. In severe, refractory OSA cases where noninvasive options are ineffective, tracheostomy bypasses the upper airway obstruction by creating a direct tracheal opening, indicated for patients with life-threatening complications or CPAP intolerance. This procedure markedly improves outcomes, reducing AHI from a mean of 92.0 to 17.3 events/hour, apnea index from 73.0 to 0.2 events/hour, and oxygen desaturation index from 78.2 to 20.8 events/hour, while decreasing daytime sleepiness and mortality risk. For apnea of prematurity (AOP) in neonates, is the first-line pharmacological treatment, administered intravenously or orally at an initial of 20 mg/kg followed by doses of 5-10 mg/kg daily, to stimulate immature respiratory centers and reduce apneic episodes by up to 50-70%. (nCPAP) at 4-8 cm H₂O is a primary to stabilize the airway and improve ventilation, often combined with caffeine for severe cases affecting up to 50% of very low-birth-weight infants; alternatives include high-flow or nasal intermittent positive pressure ventilation if nCPAP is intolerable. As of May 2025, these approaches remain standard, with monitoring for resolution typically by 36-40 weeks postmenstrual age. Pharmacological approaches are limited but targeted for specific apnea subtypes. , a , is used for (CSA), including high-altitude cases where it induces to stimulate ventilation. Administered at 250 mg daily, it decreases AHI by 13-35 events/hour and time by 38.6%, with nocturnal increasing by 1.85-4.75%. Per the 2025 (AASM) guideline, acetazolamide receives a conditional recommendation for primary CSA, CSA due to , and opioid-induced CSA (all etiologies). Other CSA treatments include adaptive servo-ventilation (ASV) for most etiologies (conditional, with caution in heart failure with reduced <45% due to cardiovascular risks), bilevel PAP with backup rate, low-flow oxygen (1-3 L/min), and transvenous phrenic nerve stimulation for moderate-to-severe primary CSA or CSA due to heart failure in PAP-intolerant patients (FDA-approved 2017, conditional recommendation). For both OSA and CSA, avoidance of sedatives such as alcohol, tranquilizers, and sleeping pills is recommended, as they relax pharyngeal muscles and exacerbate airway collapse. Emerging therapies include hypoglossal nerve stimulation (HGNS), an implantable device that electrically stimulates the hypoglossal nerve to protrude the tongue and prevent airway collapse during sleep. Indicated as a second-line option for moderate to severe OSA (AHI 15-65 events/hour) in CPAP-nonadherent patients with BMI <35 kg/m² and no concentric palatal collapse (confirmed by drug-induced sleep endoscopy), HGNS achieves ≥50% AHI reduction to <10 events/hour in about 58% of cases, lowering mean AHI from 30.7 to 8.5 events/hour. Patient selection incorporating endotypic traits like higher arousal threshold enhances response rates.

Preventive Strategies

Preventive strategies for apnea, particularly obstructive sleep apnea (OSA), focus on modifiable lifestyle and behavioral factors that can reduce the risk of onset or mitigate severity in susceptible individuals. These approaches emphasize proactive measures to address anatomical and physiological vulnerabilities in the upper airway, such as excess tissue or muscle tone relaxation, without relying on medical interventions. By targeting these factors, individuals can potentially lower the apnea-hypopnea index (AHI) and improve overall sleep quality, especially in cases of mild to moderate OSA. Weight management plays a central role in preventing and alleviating OSA, as excess body weight contributes to fat deposition around the upper airway, narrowing the pharyngeal space and increasing collapsibility during sleep. Achieving and maintaining a healthy body mass index (BMI) through balanced diet and regular physical activity can significantly reduce OSA severity; for instance, a weight loss of at least 10% of body weight has been shown to decrease AHI by up to 26% in overweight individuals. Even modest reductions, such as 5-10% of initial body weight, improve airway patency and daytime symptoms like excessive sleepiness. Guidelines recommend combining caloric restriction with aerobic exercise for sustainable results, as obesity is a primary modifiable risk factor affecting up to 70% of OSA cases. Positional therapy offers a simple, non-invasive method to prevent apneic events by discouraging supine (back) sleeping, which exacerbates airway collapse due to gravitational forces on the tongue and soft tissues. Sleeping on the side or stomach maintains better upper airway alignment, reducing the frequency of obstructive events in positional OSA, where symptoms predominantly occur in the supine position—a pattern seen in approximately 25-50% of patients. Techniques include using a backpack-like device with a tennis ball sewn into the back of pajamas to prompt side sleeping or wearable vibratory devices that alert users to roll over when supine. Studies demonstrate that consistent positional therapy can lower overall AHI by 50-60% in responsive individuals, making it particularly effective for mild cases or as an adjunct to other measures. Avoiding substances that relax upper airway muscles is crucial for prevention, as they heighten the risk of airway obstruction during sleep. Alcohol consumption, even in moderate amounts, increases OSA risk by 25% by depressing neural drive to pharyngeal dilator muscles and prolonging apneic episodes; abstaining from alcohol 4-6 hours before bedtime is advised to minimize this effect. Similarly, smoking promotes chronic inflammation and edema in the upper airway, contributing to narrowing and elevating OSA prevalence by up to 2-4 times in habitual smokers; cessation programs can reverse these changes over time, reducing symptom severity. These behavioral adjustments are foundational, as they directly counteract relaxant effects that worsen collapsibility in vulnerable individuals. Screening protocols are essential for high-risk occupational groups, such as commercial truck drivers and pilots, where untreated OSA impairs alertness and elevates crash risk. In truck drivers, OSA prevalence reaches 28-77%, prompting the Federal Motor Carrier Safety Administration (FMCSA) to recommend routine screening using tools like the Berlin Questionnaire or BMI thresholds (>30 kg/m²) followed by for positives, with mandatory evaluation for those showing symptoms like witnessed apneas. For pilots, the (FAA) mandates assessment during medical certification, requiring sleep studies for BMI ≥40 or suggestive symptoms to ensure ; early detection allows preventive lifestyle interventions before certification issues arise. These targeted protocols, often employer-mandated, facilitate timely risk reduction in safety-critical professions.

Complications and Prognosis

Acute Complications

Apnea episodes, whether occurring during sleep or medical procedures, can rapidly lead to severe physiological disruptions, primarily through (low blood oxygen levels) and (elevated levels). These conditions arise from interrupted , causing significant oxygen desaturation (e.g., below 90%, and in severe cases below 80%) and CO₂ retention, which stimulate intense chemoreflex responses and activation. In (OSA), such intermittent events increase myocardial oxygen demand and provoke , heightening immediate cardiovascular strain. Hypoxemia and hypercapnia directly contribute to acute cardiac arrhythmias, including bradyarrhythmias like and ventricular ectopy, with OSA patients facing a 2- to 4-fold elevated risk of nocturnal complex arrhythmias such as (odds ratio 4.02) and (odds ratio 3.40). Additionally, can lower seizure thresholds by inducing and neuronal damage in brain regions like the hippocampus, potentially triggering in susceptible individuals, particularly those with , where apneic desaturations exacerbate cortical excitability. In procedural contexts, such as , undiagnosed or unmanaged apnea elevates risks of immediate postoperative , with OSA patients experiencing complications at a rate of 48.9% compared to 31.4% in non-OSA individuals, including oxygen desaturation, , and severe pulmonary events like . sensitivity in these patients further heightens the likelihood of ventilatory depression and in the post- care unit. Neonatal apnea, common in preterm infants, presents emergency risks through immature respiratory control. Preterm infants with apnea of prematurity face heightened risk due to immature respiratory control and shared neural vulnerabilities like serotonergic deficiencies impairing responses, but apnea and are distinct; environmental factors such as prone sleeping compound this risk. Untreated OSA carries significant immediate mortality risks from fatal apneic events, with 46% of sudden cardiac deaths occurring between midnight and 6 a.m.—a of 2.57 compared to daytime hours—driven by nocturnal and arrhythmias in severe cases (apnea-hypopnea index ≥40). Over longer observation, severe untreated OSA yields a 19% versus 4% in those without apnea, with a of 3.2 for all-cause death.

Chronic Effects and Outcomes

Chronic obstructive sleep apnea (OSA) is associated with a substantially elevated risk of cardiovascular diseases due to repeated episodes of hypoxia and sympathetic activation, leading to and . Untreated OSA increases the incidence of by up to twofold, as intermittent promotes vascular stiffness and sodium retention. Furthermore, individuals with severe OSA face a 2- to 3-fold higher risk of compared to those without, independent of other risk factors such as age and , with odds ratios ranging from 2.24 to 3.84 in prospective studies. Heart failure risk is also amplified, with OSA contributing to left ventricular strain and , resulting in a prevalence of OSA as high as 40-80% among patients. Metabolically, persistent OSA exacerbates through mechanisms including and disrupted glucose , independent of . This association heightens the risk of by 50-80%, with epidemiological data showing a dose-dependent relationship where severe OSA correlates with poorer glycemic control and higher incidence. Longitudinal studies confirm that OSA promotes glucose intolerance and beta-cell dysfunction, further compounding components like . Neurocognitive consequences of chronic OSA include deficits in and executive function, stemming from fragmentation and cerebral that impair hippocampal integrity and activity. Patients often exhibit moderate impairments in verbal and visual recall, with effect sizes indicating a 0.5-1 standard deviation decline compared to non-apneic controls. Additionally, OSA is an independent risk factor for depression, with prevalence rates up to 40% higher in affected individuals, linked to altered serotonin pathways and chronic . These impacts can persist even after treatment initiation, underscoring the need for early intervention. Prognostically, untreated moderate-to-severe OSA is linked to reduced long-term , with 5-year mortality rates reaching 74% in non-treated groups versus 29% in those adherent to (CPAP) therapy, as evidenced by survival curve analyses in cohort studies. As of 2024, recent studies reaffirm these risks, with effective CPAP reducing all-cause mortality by approximately 37% and cardiovascular mortality by up to 55%, based on hazard ratios from large-scale observational data following patients over multiple years. Overall, effective management improves , particularly in older adults, by addressing the cumulative burden of comorbidities.

Specialized Applications and Research

Apneic Oxygenation

Apneic oxygenation is a clinical technique that maintains in patients during periods of apnea by delivering supplemental oxygen, typically through a , without active ventilation. This method leverages the body's ongoing oxygen consumption to facilitate passive , thereby delaying in controlled procedural settings. The physiological mechanism relies on apneic diffusion, where oxygen continuously flows into the alveoli due to a subatmospheric created by the absorption of oxygen into the bloodstream during apnea. Administered via low-flow or high-flow nasal oxygen at rates of 15-60 L/min, this passive diffusion prevents significant desaturation by replenishing alveolar oxygen, even as accumulates. The process, often preceded by preoxygenation with 100% oxygen to denitrogenate the lungs, exploits the cardiogenic oscillations—small pressure changes from cardiac activity—that promote gas mixing without bulk . Historically, apneic oxygenation was first systematically described in the literature during the , with a landmark 1959 study by Frumin et al. demonstrating its feasibility in humans. In that experiment, eight healthy patients undergoing tolerated apnea for 18 to 55 minutes while maintaining oxygen saturations above 98% after preoxygenation, highlighting the technique's potential to extend safe apnea duration significantly beyond typical limits of a few minutes. In clinical practice, apneic oxygenation is primarily applied during procedures requiring transient apnea, such as endotracheal and rigid , where it can extend the safe apnea time to 30-60 minutes in select patients. For instance, in emergency , it reduces the incidence of during , with studies showing improved maintenance in obese individuals and those at risk of rapid desaturation. In , variants like transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) have enabled procedures lasting a of 14 minutes (range 5-65 minutes) by combining high-flow nasal oxygen with passive oxygenation. A key limitation is the absence of carbon dioxide clearance in passive apneic oxygenation, resulting in progressive and potential , which can limit the technique's duration to 20-30 minutes in many cases before ventilatory support is required. In passive apneic oxygenation, this buildup occurs at a rate of approximately 3-6 mmHg per minute. However, high-flow techniques like THRIVE can reduce this rate to about 1-2 mmHg per minute through dead space flushing. This may necessitate monitoring of end-tidal CO2 or gases in prolonged applications. Additionally, depends on adequate preoxygenation; residual in the lungs can shorten safe apnea time, and the technique is less reliable in patients with low , such as the morbidly obese or those with lung pathology.

Apnea Test in Brain Death Determination

The apnea test serves as a critical confirmatory procedure in the determination of , also known as death by neurologic criteria (DNC), by assessing the absence of brainstem-mediated respiratory drive. It involves temporarily disconnecting the patient from to observe for any spontaneous efforts while monitoring physiological parameters, thereby confirming irreversible loss of brainstem function. This test is typically performed after prerequisite clinical evaluations, including and absence of brainstem reflexes, and is recommended as part of standardized protocols for adults. The protocol begins with ensuring prerequisites are met to avoid confounding factors: the patient must have a core body temperature of at least 36°C, systolic of at least 100 mm Hg (or mean arterial pressure of at least 75 mm Hg), absence of central nervous system depressants or neuromuscular blocking agents, and correction of any , acid-base, or endocrine disturbances. Normal baseline arterial blood gas values are required, with PaCO₂ between 35–45 mm Hg and pH between 7.35–7.45, unless chronic is present. Pre-oxygenation follows, administering 100% oxygen for at least 10 minutes to achieve a PaO₂ greater than 200 mm Hg. The is then disconnected, and oxygen is supplied via a at 4–6 L/min or through (CPAP) to minimize desaturation risks. Throughout the test, continuous monitoring of , , , and end-tidal CO₂ occurs, with observation for any chest or abdominal movements indicative of respiratory effort. gas (ABG) analysis is performed after 8–10 minutes or when PaCO₂ is estimated to reach the target. The test is considered positive, confirming , if no spontaneous respirations are observed after 8–10 minutes, with a PaCO₂ of at least 60 mm Hg (or 20 mm Hg above the baseline if higher) and a less than 7.30 on ABG. If the initial test is inconclusive or aborted, it may be repeated after resolving issues, or ancillary tests such as or nuclear can be used as alternatives. In pediatric cases, similar principles apply but with two apnea tests required, one after each clinical examination. Contraindications include severe cardiopulmonary disease, such as significant injury or hemodynamic instability, where the test could precipitate ; in such scenarios, ancillary testing is mandated. The test must be aborted immediately if spontaneous breathing occurs, falls below 85%, or hemodynamic instability develops (e.g., systolic below 90–100 mm Hg despite vasoppressor support), to protect the patient's stability and potential organ viability. Ethically, the apnea test underscores the principle of determining death based on irreversible cessation of all brain functions, independent of considerations, to avoid any perception of . Clinicians are obligated to prioritize the patient's , inform families about the evaluation process, and offer opportunities for , though is not required for the determination itself. Its confirmation of is pivotal for legal declaration of death, enabling under the dead donor rule, which prohibits retrieval causing death, thereby facilitating transplantation while respecting through family communication and grief support.

Key Scientific Studies

The Sleep Heart Health Study (SHHS), initiated in the mid-1990s as a multicenter prospective cohort involving over 6,000 participants aged 40 and older, provided foundational evidence linking obstructive sleep apnea (OSA) to cardiovascular disease through polysomnographic assessments and longitudinal follow-up. Early cross-sectional analyses from the study demonstrated that moderate to severe OSA, defined by an apnea-hypopnea index (AHI) of 15 or higher events per hour, was associated with a 2- to 3-fold increased prevalence of self-reported coronary heart disease, heart failure, and stroke, independent of confounding factors like age, sex, and body mass index. Subsequent prospective findings confirmed these associations, showing that untreated OSA predicted incident cardiovascular events, including a 68% higher risk of coronary heart disease in women with severe OSA over four years of follow-up. The study's cohort design and standardized home polysomnography enabled robust adjustments for comorbidities, establishing OSA as an independent risk factor for cardiovascular morbidity. The Wisconsin Sleep Cohort Study (WSCS), a community-based longitudinal investigation started in 1989 with over 1,500 middle-aged adults, further elucidated the relationship between OSA severity and through repeated and monitoring. Baseline data revealed a dose-response association, where individuals with an AHI of 15 or greater had an odds ratio of 2.89 for prevalent compared to those with AHI below 5, after controlling for age, , and . Longitudinal analyses over four years indicated that severe OSA at baseline independently predicted new-onset , with a relative risk of 2.89 for AHI ≥15 versus <5, highlighting the progressive impact of sleep-disordered breathing on regulation. These findings underscored the role of nocturnal and sympathetic activation in OSA-related hypertensive , influencing clinical guidelines for screening high-risk populations. In the , genome-wide association studies (GWAS) have advanced the understanding of OSA's genetic underpinnings, identifying multiple loci associated with disease risk and related traits like and duration. Building on earlier work, a 2023 GWAS in the Million Program cohort of 568,576 participants (meta-analysis total of 916,696 individuals), predominantly of European descent but including diverse subgroups, discovered 32 new genomic loci linked to OSA, with lead signals in pathways regulating and neural signaling; these loci collectively accounted for 7-10% of phenotypic variance. Such studies have shifted focus toward polygenic risk scores for OSA prediction, though replication in non-European populations remains limited. More recently, a 2025 genome-wide analysis in over 1.6 million participants identified 147 independent loci associated with OSA, estimating SNP-based at 16%. Despite these advances, significant research gaps persist in OSA studies, including the underrepresentation of non-Western populations, which may obscure ethnic-specific profiles and estimates. For instance, most large-scale cohorts like SHHS and WSCS draw primarily from North American and European groups, potentially underestimating OSA burden in Asian and African ancestries where craniofacial anatomy and environmental factors differ. Additionally, pediatric OSA research is notably underrepresented, with fewer than 10% of major studies focusing on children despite distinct etiologies like adenotonsillar and long-term neurodevelopmental risks. Addressing these gaps through diverse, age-stratified cohorts could enhance personalized interventions and global applicability.

Historical and Linguistic Aspects

Etymology and Pronunciation

The term "apnea" derives from the ancient Greek word ápnoia (ἄπνοια), meaning "absence of breath" or "without breathing," composed of the privative prefix a- (ἀ-, "without") and pnoḗ (πνοή, "breathing" or "breath," from the verb pneîn, "to breathe"). This etymological root reflects the condition's core characteristic of suspended respiration, and the word entered English via New Latin apnoea around 1719. In English, "apnea" is pronounced /ˈæp.ni.ə/, with stress on the first , though variations such as /əpˈniː.ə/ occur in some medical and British contexts, emphasizing the long "e" sound. The term evolved from texts, including the (circa 5th–4th century BCE), where apnoia described pathological breathlessness, often linked to conditions like suffocation or uterine disorders in early gynecological discussions. Related terms include "apneic" (pertaining to apnea, first used in 1883) and compounds like "," which retain structure a- + -pnea. In non-English languages, equivalents preserve similar roots, such as French apnée (meaning cessation of , especially in diving or medical contexts) and German Apnoe.

Historical Developments

The recognition of apnea, particularly in the context of sleep-related cessation, traces back to ancient medical observations. In the from the 5th century BCE, descriptions of nocturnal "strangling" sensations, noisy , and sudden deaths hint at early encounters with symptoms akin to , often linked to or chest obstructions. Similarly, Aristotle's 4th-century BCE On Breath examined the of respiration, including the vital role of air intake and the pathological implications of its interruption, such as suffocation in non-respiring creatures and the cooling function of breath in humans. By the , more specific portrayals emerged in and . ' 1837 novel The Posthumous Papers of the Pickwick Club depicted "the fat boy" Joe with profound daytime somnolence, loud snoring, and obesity—symptoms retrospectively identified as classic , inspiring the eponymous "Pickwickian syndrome." This literary reference was medically formalized in 1877 when William Henry Broadbent described similar cases of obesity-related respiratory pauses during sleep, shifting focus toward clinical observation. The brought systematic study and . In the , polygraphic monitoring first documented apneic episodes in non- patients, challenging prior assumptions of as the sole cause. Christian Guilleminault's seminal 1976 paper coined " syndrome," delineating it as recurrent upper airway collapse during , distinct from central apnea, based on studies of 25 adult males using nocturnal . This work, conducted at Stanford's inaugural clinic established in 1970 by William Dement, catalyzed the field's growth. In the , the proliferation of dedicated sleep laboratories enabled widespread diagnosis, with over 300 centers operational by decade's end. The (AASM), founded in 1975 as the Association of Sleep Disorders Centers, issued its first diagnostic classification in 1979 and accreditation standards for sleep labs in 1987, standardizing protocols and elevating apnea recognition as a major concern. Subsequent decades saw further advancements in treatment and recognition. In 1981, Australian physician Colin Sullivan invented (CPAP), a non-invasive that became the gold standard for managing by maintaining airway patency during sleep. was formally recognized as a by the American Board of Medical Specialties in 2007, following the establishment of board certification. As of 2024, the AASM updated its clinical practice guideline for the treatment of in adults, incorporating evidence on emerging therapies like stimulation alongside CPAP.

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