4: How does Rebreathing Occur

Chapter 4: How can Depleted Rebreathing occur?

In what follows three issues will be considered:

· does the system that controls breathing work fully,

· are there physical qualities of early infants that make depleted rebreathing more likely,

· does an early infant have the capacity to move or act to improve their situation (can they roll over even if they want to)?

Breathing Regulatory System

It is reasonable to conclude that if there is a system in place that regulates breathing properly, then depleted rebreathing should never take place, as it does in the case of SIDS. The breathing control system should increase or decrease breathing as necessary. If a child’s breathing were restricted, as it might be by bedding, then it could be expected that the child would move to alleviate the distress caused by the accumulation of carbon dioxide in the lungs, breathe quicker or deeper, or cry to gain attention to their situation. However, in a few cases for early infants, this doesn’t take place and a SIDS death occurs. We need to understand what is the different between early infants (pre one year olds for the most part) and that of older infants and adults. It is in understanding those differences that will give us the insight into how to reduce the incidence of SIDS and other disorders.

One of the ways we practice breathing is not precisely regulated breaths, but many short breaths interjected with one deep breath to clear our lungs. Is the lack of this deep breath the difference with early infants? Perhaps noticing that an infant is taking these deep cleansing breaths is a good indicator that there is less danger of suffering the results of depleted rebreathing, SIDS or learning disabilities. This is worth investigating.

Is the system that controls breathing working effectively, if at all? A key suspect considered in the regulation of breathing is the arcuate nucleus, part of the medulla oblongata. A recent study by Hannah Kinney, (Kinney HC, Filiano JJ. Brain research in the sudden infant death syndrome. In: Kraus HF, Byard RW, editors. Sudden infant death syndrome: a diagnostic approach. London: Chapman and Hal; 2001) has found that the arcuate nucleus (considered as that part of the brain responsible for breathing), positioned on the underside of the brain stem, is underdeveloped or missing in some (but not all) SIDS babies. If this breathing control is missing or under developed, then abnormal levels of oxygen and carbon dioxide could be expected to accumulate in the lungs causing harm to a child. The child would not be aroused and not adjust to the discomfort. The lowered levels of oxygen reaching the brain over a period of time would harm brain cells to the point that death occurs. Could this be implicated in SIDS? Certainly, but the question begs, how can SIDS take place for those who have a fully developed arcuate nucleus. The answer could be that there is a sequence of events as a child’s brain develops (as a brain emerges to full maturity). Perhaps first the arcuate nucleus must develop fully, and only after that does it take over control of breathing. Therefore, some SIDS deaths may appear to have a fully developed arcuate nucleus but at a point that it has not yet taken full control of the lungs. Therefore there may be a period of time that breathing is not controlled automatically, despite the appearance of the arcuate nucleus. For some infants this development period may be a short time, while for others this development may emerge more slowly. It is possible that every child at some time has endured some danger of suffering a SIDS death through depleted rebreathing, but for those that emerge more slowly, that period of time leaves them at risk of suffering a SIDS death for a longer period of time. However, it is possible that for some births this part of the brain has fully developed by the time of birth, such that there is no danger ever of suffering a SIDS death.

We could infer that a premature birth is more likely to have a longer period of time during which they are in danger, as they are more likely to be using their lungs (as opposed to gaining their oxygen through the placenta) during a time that the arcuate nucleus has not yet developed. If that be the case then it would be expected that premature babies suffer a higher incidence of SIDS deaths, which statistically they significantly do ( and I may add that they also suffer a higher incidence of learning disabilities).

If the development of the breathing control system is involved (as I believe it usually is), then isn’t a faulty breathing regulatory system the cause of SIDS? Not necessarily. The lack or underdevelopment of a breathing control system does not cause death. It only opens the possibility of improper levels of oxygen and carbon dioxide in the lungs (and therefore in the blood), as a result of depleted rebreathing. It is only through depleted rebreathing that SIDS deaths occur. Again, it is quite possible that all infants endure a period of danger while the breathing control system comes on stream, but for most early infants they pass through this stage with sufficient oxygen in their lungs at all times such that they suffer no harm. In other words, the variance of acceptable oxygen to carbon dioxide ratios is never exceeded for an unacceptable period of time. Practices such as the Back to Sleep program enable this to happen.

Another avenue of research has shown that some SIDS babies have elevated levels of fetal hemoglobin (Perry, G W, Vargas-Cuba, Ruben, Vertes, Robert P: Fetal hemoglobin levels in SIDS. College of American Pathologists, Oct 1997). Coincidental with the time that a child is in danger of suffering a SIDS death is that period of time where a child experiences reducing levels of fetal hemoglobin and increasing levels of adult hemoglobin. As a child moves from complete dependence in the womb without the use of lungs to eventual full independence with completely functioning lungs, there may be a window of vulnerability as breathing processes come on stream including that of adult hemoglobin. How or whether levels of fetal hemoglobin impact or work with the automatic breathing system is not fully understood.

Fetal hemoglobin may impact breathing in either of two ways. Perhaps the breathing regulatory system is less aroused by or sensitive to carbon dioxide while there are higher levels of fetal hemoglobin as compared to adult hemoglobin. Or perhaps fetal hemoglobin is slow or reluctant to release carbon dioxide into the lungs (and weak at taking in oxygen).

If fetal hemoglobin reduces the sensitivity of the lungs to improper levels of oxygen and carbon dioxide, then there is the possibility that high levels of fetal hemoglobin may reduce the distress caused by carbon dioxide, resulting in insufficient correction to breathing, and increase the possibility of harm to the infant. I’m suggesting here that fetal hemoglobin works most effectively transferring oxygen and carbon dioxide via the placenta before birth. When blood passes through the lungs of the unborn fetus, it does not trigger any discomfort in the lungs. As such fetal hemoglobin is poor at signalling to the lungs and infant that an improper level of oxygen and carbon dioxide exists, and as such the infant will not react sufficiently to low levels of oxygen when placed in a situation where their breathing is restricted in any way.

If fetal hemoglobin were reluctant to release carbon dioxide into the lungs (and weak at taking on oxygen), then we could expect the lungs to respond by more frequent, quicker or deeper breathing (assuming that the control system was fully functional). If the control system is fully functional, then in this case the level of fetal hemoglobin should not matter as breathing would adjust appropriately to protect the child. However, if other stressors are in place, such as breathing into bedding, the infant may not be able to react sufficiently, the result being insufficient uptake of oxygen. The fact that research has shown increased levels of fetal hemoglobin in SIDS cases, should cause us to imply that there is some measure of involvement. High levels of fetal hemoglobin may not directly cause SIDS, but may increase the chance that SIDS could occur, because it increases the danger that rebreathing is harmful. High levels of fetal hemoglobin may have a reduced ability to transfer oxygen and carbon dioxide through the lung membrane into the air in the lungs (considering that fetal hemoglobin is designed to work effectively with the placenta, not the lungs), and with this weakness the lungs need an improved balance of oxygen and carbon dioxide in the lungs for harm not to occur. Perhaps normally a child can withstand healthily a balance or proportion between oxygen and carbon dioxide down to a 30/70 split (I uses the numbers here only to explain my point). If it becomes reduced to a 30/70 split (only 30 oxygen/70 carbon dioxide), then the child may begin experiencing harm. Perhaps in the case of high fetal hemoglobin levels, the child can only sustain health down to a 40/60 split of oxygen vs. carbon dioxide, due to its reduced ability to absorb oxygen from the lungs effectively. In other words these infants are less tolerant of poor oxygen levels in the lungs. If this is the case, then they may be more susceptible to suffering SIDS, than would be a normal child when depleted rebreathing occurs.

Another interesting fact is that the risk of SIDS is highest between babies’ second week to sixth month. Why is a baby at lower risk for the first few week of their life? I believe that this may be due to fetal hemoglobin. Fetal hemoglobin may have a reserve of oxygen, such that depleted rebreathing has little impact for the first few weeks. Think of it this way. The threat of depleted rebreathing decreases over time, for most completely by the sixth month, as the babies lungs firm up, and the baby is able to lift themselves to protect themselves. Fetal hemoglobin protects the baby decreasingly over time, for most to about the second week. Wedged between is a period from about the second week until about the sixth or eighth month, when depleted rebreathing, if it takes place, is more likely to cause harm to the early infant.

Again, does the automatic regulation process for breathing or this process along with high levels of fetal hemoglobin have a role in SIDS deaths? I believe so in most SIDS cases. However, please consider that without depleted rebreathing, SIDS deaths still would not occur. It is the occurrence or event of depleted rebreathing that results in the damage to an infant’s brain such that death or disabilities occur. A poorly operating breathing regulatory system doesn’t, on its own, cause SIDS. Neither do high levels of fetal hemoglobin cause SIDS. These only open up the possibility that depleted rebreathing might take place. As long as parents and caregivers ensure that any early infant has unobstructed access to fresh air, the child will do fine. Let’s now look at what are the other conditions of an early infant that may lead to rebreathing being harmful.

Developing Lungs:

What are the physical limitations or conditions of an early infant under which rebreathing would be a threat to newborns as opposed to everyone else? One is that the lungs of early infants are simply underdeveloped at this point in their lives, but will gain in efficiency over time. Lungs work like a bellows, which have a stiff outer rib cage as a frame and a flexible diaphragm, which is the source of energy to move the frame so that it opens and shuts. The problem for newborns may exist that their skeletal frame, their ribs, are still too flexible to support the drawing of air into the lungs efficiently. They work, but not as well as they will in their future when their ribs are stiffer. The efficiency of the lungs will improve as the bones in their rib cage stiffen. However, the first few months remain as a vulnerable time when the lungs don’t work as effectively as they will in the future. When a newborn tries to open their lungs, their rib cage can tend to flex rather than stay rigid which is necessary for the inhalation of oxygen. Likewise on exhaling the ribcage can flex rather than be stiff which would be needed for the expiration of air. This condition, underdeveloped lung capacity, is one of the physical limitations that I believe may lead to rebreathing and harm to an early infant. Because of this early condition, any pressure on the ribcage may severely reduce an early infant’s ability to draw in sufficient air.

There are instances where a child can be bound excessively, either through tight swaddling, tight covers (sometimes tucked in tightly to prevent the child from turning over onto their tummy), or tight bound straps as used in car seats and some strollers. These bindings reduce the ability of the lungs to breathe deeply and therefore increase the chance that the child may suffer harm due to rebreathing. These will be the times that the child does not have their mouth or nose pressed into bedding or soft toys and still suffers a SIDS tragedy. Sadly at times these practices may have been undertaken by parents in order to protect their child.

Usually in these tragic cases the breathing regulatory system is probably underdeveloped such that the early infant makes no effort to correct their short breaths (due to their restricted lungs). However, even if this regulatory system is working, they may not be able to breathe fast enough or deep enough to prevent depleted rebreathing due to the tightness of their bindings.

Consider a child that may be in a deep sleep (often driving and movement can do this), and the arousal signals are not strong enough to wake them. They may pass from sleep directly into unconsciousness. Therefore there may be times that a child’s breathing regulatory system is fully developed, is sitting up, does not have their mouth or nose obstructed, yet they still suffer a SIDS death due to their lungs being bound too tightly. I believe these are rare but do happen.

Relative size of passageways to that of lungs:

Another physical limitation of a newborn is that a newborn’s head is disproportionately large as compared to the rest of their body. Therefore, their throat and mouth passageways are somewhat disproportionately large as compared to the developing lungs. As a result it is very difficult for newborns, considering the development of their lungs and the large air passageways, to exhale enough spent air, and draw in sufficient fresh air to keep the balance of oxygen and carbon dioxide safe in the lungs. As they grow this inefficiency diminishes and is eliminated. While they are early infants they can breathe sufficiently, but it is tenuous at best. Any situation or event (such as, breathing into bedding or tight swaddling) may impact on this tenuous condition and could result in depleted rebreathing.

Considering this size limitation of newborns and how it may impact on rebreathing, is there a difference between breathing through the mouth as opposed to breathing through the nose? I believe that breathing through the nose is more effective and should be encouraged in light of this early weakness of breathing. The nose passageways are narrower than that of the mouth and as a result there is less redrawn air and more new air drawn in with each breath. Also the passageways being narrower result in an increased velocity of air flow. The narrower passageways will blow spent air further away from the face, thereby ensuring that the following air draw in is new fresh air, and not the air that has just been exhaled. The nose acts somewhat like a venturi effect, for when air is exhaled through the nose, the fast flowing jet of air pulls in fresh air from the top and sides of the nose to the front of the nose, after which it is drawn in as new fresh air. The velocity of air movement while breathing through the mouth is much slower than through the nose due to the larger size of the mouth. Air that has just been exhaled through the mouth may remain just in front of the mouth when there is poor ventilation. As a result much of that spent air will be redrawn into the lungs. Therefore the potential for depleted rebreathing is greater when using the mouth to breath as opposed to breathing through the nose. Therefore anything that promotes breathing through the nose will reduce the risk of SIDS and other disorders. It is not surprising that the incidence of SIDS is significantly lower for those infants who practice thumb sucking and the use of a pacifier (Joanna Briggs Institute. Early childhood pacifier use in relation to breastfeeding, SIDS, infection and dental malocclusion, Best Practice. 2005) as thumb sucking and pacifiers force the child to breath through the nose avoiding or reducing depleted rebreathing.

Only recently have I come across some research that suggests that there is a higher risk for a SIDS death when the early infant is predominantly using their mouth to breathe (M. P. L'Hoir, A. C. Engelberts, G. T. J. van Well, P. H. Damsté, N. K. Idema, P. Westers, G. J. Mellenbergh, W. H. G. Wolters, J. Huber; Dummy use, thumb sucking, mouth breathing and cot death, European Journal of Pediatrics, October 1999). Hopefully what I have suggested regarding early development and relative sizes helps to explain why.

An infant's lungs at birth are functional but not fully efficient. It takes a number of months for the lungs to go from inoperative before birth to fully functioning at about one year of age. During these months, the child is at risk. It is important for parents to know about the risks during those months, and what they can do to minimize any potential tragedy.

There is a significant additional risk of suffering a SIDS death for small babies, especially premature babies. Why is this? I believe that there are a number of reasons. This is partly due to the weak pliable nature of their ribcage, the relative size of the babies’ head as compared to that of the lungs, and the fact that their breathing regulatory system may yet be fully developed. These conspire to result in an increased risk of suffering a depleted rebreathing event. Because of this it is not surprising that premature and relatively smaller babies suffer a higher incidence of SIDS and learning disabilities.

Ability to react:

Lastly, is the child able to react? If a child’s mouth or nose is imbedded in bedding, do they have the physical strength and ability to move to improve their situation. We can assume that they do, but that is a huge assumption. While in their mother’s womb, their body was supported. But right after birth, are their neck muscles strong enough to lift their head away from an obstruction? Are their arms strong enough to lift themselves even a bit or turn themselves over? Have they learned yet how to control their movements? If they are always bound or left on their backs, how can their arm and neck muscles develop and strengthen to the point that they can protect themselves? Are they tucked into a position such that they are unable to react? Are they bound either through swaddling or straps of a car seat or stroller in such a way that they are physically unable to help themselves not to mention fully breathe, even if they wish? Are they at a stage of development such that they have control of their arm and body movements so that they can protect themselves? The comments I am making here is that there are physical limitations and circumstances present for an early infant such that they have not developed to the point that they have the physical means or strength to address their breathing needs. Swaddling not only prevents babies from developing the strength that they will need, but also delays the natural learning process for muscle control and movement.


I just want to mention here that I believe that many stillborn babies are actually SIDS deaths, caused by a complication of the flow of blood and oxygen to the baby. The causes of this are many, but often due to complications of the placenta.

Summing up

What is important to point out here is that it does not matter what the cause, be it the breathing control system, the physical limitations of their lungs, or the strength or stage of development of the early infant; it is always depleted rebreathing that harms the child. Perhaps in some instances all conspire together to cause harm to the child, while in other instances they work on their own; but no matter which it is, it is always depleted rebreathing that results in the harm to the child. Without depleted rebreathing there should be no harm to the child.

At some point we may know all of the strengths and limitations in the growth process of newborns and be able to make accommodations to any or all deficiencies. But at this point we don’t. However, keep in mind that if the child is getting an adequate supply of oxygen due to our practices, then there are few fears. Knowing that a particular early infant is more at risk than others to harm due to depleted rebreathing would be very helpful, but at this time mostly unnecessary. We should just assume that all newborns are at risk of depleted rebreathing up to about the age of about one year old. If we take measures to assure that a child’s breathing is never impaired, there should be little danger. How we attend to the child is what will make the difference.

Understanding that an early infant has a vulnerability to depleted rebreathing is important, but also is the understanding of those situations or events that could lead to it. Knowing those potentially depleted situations or events will lead to preventative practices that reduce the potential for harm. But before I address those situations I wish to discuss a few other issues about SIDS and depleted rebreathing.

Barry Stanley