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A 32 s breathing pause in a sleep apnea patient
A 32 s breathing pause in a sleep apnea patient
Apnea, apnoea, or apnœa (Greek: ἄπνοια, from ἀ-, privative, πνέειν, to breathe) is a term for suspension of external breathing. During apnea, there is no movement of the muscles of respiration and the volume of the lungs initially remains unchanged. Depending on the patency of the airways, there may or may not be a flow of gas between the lungs and the environment; gas exchange within the lungs and cellular respiration are not affected.
Apnea can be voluntarily achieved, drug-induced (such as opiate toxicity or tryptamine toxicity), mechanically induced (for example, by strangulation or choking), or it can occur as a consequence of neurological disease or trauma. During sleep in patients who are suffering from sleep apnea, these events will occur up to 20-30 times per hour, every night.
Under normal conditions, humans cannot store much oxygen in the body. Prolonged apnea leads to severe lack of oxygen in the blood circulation. 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 consequences.
Untrained humans cannot sustain voluntary apnea for more than one or two minutes. 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. 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.
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. 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 and for more than four minutes. Apneists, in this context, are people who can hold their breath for a long time.
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. 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. Lowering the CO2 concentration increases the pH of the blood, thus increasing the time before 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. One using this method can suddenly lose consciousness—a shallow water blackout—as a result. If a person loses consciousness underwater, especially in fresh water, there is a considerable danger that they will drown. An alert diving partner would be in the best position to rescue such a person.
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. This phenomenon (apneic oxygenation) is explained as follows:
With the onset of apnea, an underpressure 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. However, if the airways are patent (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. 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.
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, 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 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. 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 and for short procedures.
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.
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: coma, absence of brainstem reflexes, and apnea (defined as the inability of the patient to breathe unaided, that is, with no life support systems). The apnea test follows a delineated protocol.
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