Apnea (also spelledapnoea inBritish English)[1] is the temporary cessation ofbreathing, which may be voluntary or involuntary. During apnea, there is no movement of themuscles ofinhalation,[citation needed] and the volume of thelungs initially remains unchanged. Depending on how blocked theairways are (patency), there may or may not be a flow ofgas between the lungs and the environment. If there is sufficient flow,gas exchange within the lungs andcellular 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 ear-nose-throat 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]
Apnea can be involuntary—for example,drug-induced (such as byopiate toxicity), mechanically / physiologically induced (for example, bystrangulation orchoking), or a consequence of neurological disease ortrauma. During sleep, people with severesleep apnea can have over thirty episodes of intermittent apnea per hour every night.[3]
Apnea can also be observed during periods of heightenedemotion, such as duringcrying or accompanied by theValsalva maneuver when a personlaughs. 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 arebreath-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 thevocal cords, simultaneously keeping the mouth closed and blocking thenasal vestibule, or constantly activating expiratory muscles, not allowing any inspiration.
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 ofCO2 tension andpH of theblood 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 thephrenic 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 mammaliandiving 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 offree-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.
Voluntaryhyperventilation 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 strongdyspnea 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 possiblehypoxia, though it might not be felt as easily.[5] One using this method can suddenly lose consciousness unnoticed—ashallow water blackout—as a result. If a person loses consciousness underwater, there is considerable danger that they willdrown. 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.
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 thediaphragm 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 toatelectasis.[6]
However, no CO2 is removed during apnea. Thepartial 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 inrespiratory acidosis.
Under ideal conditions (i.e., if pure oxygen is breathed before onset of apnea to remove allnitrogen from the lungs, and pure supplemental oxygen isinsufflated), 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 inthoracic surgery when apnea cannot be avoided, and during manipulations of the airways such asbronchoscopy,intubation, and surgery of the upper airways. However, because of the limitations described above, apneic oxygenation is inferior to extracorporal circulation using aheart-lung machine and is therefore used only in emergencies, short procedures, or where extracorporal circulation cannot be accessed. Use ofPEEP 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 recordedPaCO2 was 250millimeters of mercury, and the lowest arterialpH was 6.72 after 53 minutes of apnea.[8]
A recommended practice for the clinical diagnosis ofbrain death formulated by theAmerican Academy of Neurology hinges on the conjunction of three diagnostic criteria: acoma, absence ofbrainstem reflexes, and apnea (defined as the inability of the patient tobreathe unaided: that is, with nolife support systems likeventilators). 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]
^"Where is it". Archived fromthe original on 27 September 2008. Retrieved2 March 2008. for 214-metre diving record
^Given, Mac F. (1 April 1997). "The Effect of Hyperventilation on the Ability to Hold One's Breath: Testing the Influence of Beliefs versus Physiology".The American Biology Teacher.59 (4):229–231.doi:10.2307/4450291.JSTOR4450291.