The movements of breathing are innervated from a nervous centre situated in the medulla oblongata, in the grey substance of the floor of the fourth ventricle a little above the point of the calamus scriptorius. The part above this may be sliced away without stopping the respiratory movements, but they completely cease when the part indicated is destroyed.


The movements continue after all afferent nervous paths or connections with higher centres have been severed, and they are undoubtedly dependent in the main on the condition of the blood passing through the centre.

The key to the main conditions governing the movements of breathing has been furnished by examination of the air from the lung alveoli in man.* A sample of alveolar air is easily obtained by suddenly expiring deeply through a piece of wide-bored rubber tubing about 4 feet long. At the end of the expiration the sample is taken from the end of the tube nearest the mouth, and consists of pure alveolar air unmixed with the more or less pure air with which the respiratory passages are filled at the beginning of an expiration. By examining the alveolar air during normal breathing it is found that the breathing is so regulated as to keep the percentage of carbon dioxide practically constant for each individual, provided the barometric pressure is constant. For different men the normal percentage varies from about 4' 7 to 6*4 per cent. average about 5*6 per cent. while in women and children the average is about O5 per cent, lower.* If air containing, say, 2 or 3 per cent, of carbon dioxide is breathed, the breathing immediately becomes deeper, so that the percentage in the alveolar air is only very slightly increased. An increase of as little as 0'25 per cent, in the alveolar air corresponds to an increase of as much as 100 per cent, in the depth of breathing. This shows how extraordinarily delicate is the reaction of the respiratory centre to the stimulus of carbon dioxide. A rise of 1 per cent, of carbon dioxide in the alveolar air causes marked air-hunger and great hyperpnoea. From numerous experiments, there can be no doubt that the stimulus is conveyed to the centre by the blood. The nerve cells of the centre, or perhaps more probably specific end organs belonging to these cells, possibly at synapses, seem to possess a specific sensibility for the slightest increase or diminution of carbon dioxide, just as the end organs of the retina have a specific sensibility for light-waves.

Experiments made at different barometric pressures show that it is the partial pressure, and not the mere percentage, of carbon dioxide in the alveolar air which is the determining factor. If the barometric pressure is increased, the percentage falls in exact inverse proportion. All subsequent investigation has completely confirmed the conclusion originally reached by Paul Bert,f that the physiological effects of a gas vary with its partial pressure.

By forced breathing the proportion of carbon dioxide in the alveolar air, and consequently also in the arterial blood, may be reduced greatly. When this is so, the rhythmic activity of the respiratory centre is entirely suspended, so that a condition of apncea is produced. Apncea was formerly attributed to excess of oxygen in the arterial blood, and more recently to a summation of inhibitory stimuli conveyed by the vagus nerve. Neither of these causes has any influence in producing apncea. Excess of oxygen in the air breathed has no influence at all on breathing under normal conditions, but if the rate or frequency of breathing oxygen is voluntarily or artificially increased, complete or partial apnoea of course follows from the accompanying removal of carbon dioxide. Vagus influence is excluded by the fact that excessive ventilation of the lungs does not produce apncea if the percentage of the C02 in the alveolar air is prevented from falling ; and from the teleological standpoint the inherent improbability of the existence of such a thing as vagus apnoea is very evident. Apneea can be promptly produced in the ordinary way after the vagus nerves are cut, or in an animal whose respiratory centre is supplied with arterial blood from another animal in which the breathing is excessive.

In some persons and animals forced breathing causes no apnosa.This is probably due to the fact that the deficiency of carbon dioxide in the blood causes a compensatory constriction of the arterioles supplying the respiratory centre, the consequence being that the pressure of carbon dioxide in the centre is still sufficient, when deficiency of oxygen is superadded, to maintain rhythmic excitation.

Any variations in the production of carbon dioxide within the body are met by corresponding variations in the ventilation of the lung alveoli, so that the partial pressure of carbon dioxide in the alveolar air, and consequently in the arterial blood, remains nearly constant. During muscular work, for instance, both production of carbon dioxide and alveolar ventilation may be increased to about ten times the normal. As absorption of oxygen by the lungs nearly always runs closely parallel with discharge of carbon dioxide, it is evident that this regulation of breathing insures a proper supply of oxygen as well as a proper discharge of carbon dioxide.

Within pretty wide limits, variations in the lung ventilation are usually brought about by varying the depth rather than the frequency of breathing. Frequency of breathing is thus no measure of the amount of air breathed, and varies greatly in different individuals during rest in a normal condition. Owing to the existence of the "dead space" of the respiratory air-passages, only about two-thirds of the pure air of an ordinary breath reach the lung alveoli. It is clear, therefore, that increased depth is more efficient than increased frequency of breathing. Indeed, very frequent, but at the same time shallow, breathing might coincide with quite insufficient ventilation of the alveoli.

It was discovered by Hering and Breuer that distension of the lungs inhibits inspiration, while collapse of the lungs stimulates inspiration, and that the effects are due to afferent impulses passing up the vagus nerve, and are absent if the vagi are severed. These observations have led to some erroneous theories as to the regulation of respiration. Their true interpretation is, that just as muscular movements are guided by afferent impulses, which inform us as to the completion or otherwise of the movements willed, so the action of the respiratory centre is guided by impulses which coordinate its action according to the degree of distension or collapse of the lungs. Waste of time and muscular effort is thus saved in breathing, through the existence of the vagus impulses, but the  stimulus which determines rhythmic respiratory activity under normal conditions is carbon dioxide alone.

Under abnormal or unusual conditions, other causes besides excess of carbon dioxide may help to excite the respiratory centre. When, for instance, air containing a very low percentage of oxygen is breathed, great hyperpncea is usually produced. This is accompanied by marked cyanosis, indicating that the arterial blood is very imperfectly saturated with oxygen. In man the effect of want of oxygen is scarcely noticeable, as a rule, until the oxygen percentage of the inspired air falls below 14 per cent. ; and the hyperpncea only becomes very marked with a much lower percentage. The effect varies, however, according to circumstances, and varies very distinctly in different individuals under the same circumstances. Some persons, indeed, seem to lose consciousness without any preceding noticeable hyperpncea, when breathing air in which the oxygen is rapidly diminishing ; while others react with great hyperpncea. The hyperpnoea is far more marked if the diminution in the oxygen is pretty rapid. With a slow diminution there seems to be very little hyperpncea none that would be readily noticed before consciousness is lost.

Experiment shows that the effect of want of oxygen on the breathing depends very closely on the percentage (or rather partial pressure) of carbon dioxide in the alveolar air.* When the deficiency of oxygen occurs pretty rapidly, the percentage of carbon dioxide in the alveolar air remains fairly high, owing to the fact that it takes some time to diminish appreciably the large store of preformed carbon dioxide in the blood and tissues. If, on the other hand, the deficiency of oxygen occurs less rapidly, there is time for the slightly increased breathing to wash out the preformed carbon dioxide quietly, so that no marked hyperpncea occurs. Cyanosis and loss of consciousness thus occur without any preceding struggle for breath. If a large amount of carbon dioxide has been first removed by voluntary forced breathing, or artificial breathing, extreme cyanosis, and even death in the case of animals subjected to prolonged and excessive artificial breathing,")" occurs before any return of natural breathing. It is quite clear, therefore, that want of oxygen by itself does not excite the respiratory centre. It only lowers the threshold at which carbon dioxide excites the centre. Very considerable cyanosis may thus coexist with breathing which is only slightly deeper than usual. This increased depth of breathing may not be at all noticeable, and can only be demonstrated by analyzing the alveolar air and finding the partial pressure of carbon dioxide abnormally low. Such a condition exists in persons who are at considerable altitudes, and are thus suffering from anoxhsemia, and in various pathological conditions, as will be seen below.

It is known that not only carbonic acid, but also other acids, have the power of exciting the respiratory centre. The deep breathing seen in cases of acid-poisoning or in diabetic coma, where the blood is charged with oxybutyric acid, is similar to the breathing produced by excess of carbonic acid. It is also known that want of oxygen in any form leads to the production in the living tissues of lactic acid, which passes into the blood, and may be abundantly present in the urine. All the respiratory phenomena produced by want of oxygen are consistent with the theory that it may not be want of oxygen itself, but the presence of diminished alkalinity of the blood or tissues of the respiratory centre, or of abnormal metabolic products, which accounts for the effect of want of oxygen in lowering the threshold at which carbonic acid excites the respiratory centre.* After fairly prolonged shortage of oxygen the threshold for carbon dioxide remains low for a considerable time after the oxygen want has been completely removed. The blood seems to take some time to regain its normal alkalinity.

The presence of lactic acid also explains a phenomenon which is observed after any severe muscular exertion, such as running a race or running quickly up several stairs. For about an hour after the exertion the alveolar carbon dioxide percentage remains quite distinctly low. During the severe exertion the oxygen-supply brought to the muscles by the circulation cannot keep pace with the consumption of oxygen, and consequently lactic acid is produced, and has been found in the blood and urine. f The alkalinity of the blood has also been found to be diminished, and the increase of lactic acid and diminished alkalinity last about the same time as the diminished alveolar carbon dioxide. The rapid diminution of the blood alkalinity during excessive exertion greatly increases the hyperpncsa, as a large amount of preformed carbon dioxide has to be washed out from the blood and tissues in order to compensate for the lowered exciting threshold of carbon dioxide partial pressure. For the same reason the respiratory quotient i.e., the relation of the volume of carbon dioxide given of! to that of the oxygen absorbed by the body is abnormally high. On settling down to continued hard work, the alkalinity of the blood ceases to diminish, unless the work is very excessive, and the excessive hyperpncea passes off. This probably explains in part the well-known phenomenon of " second wind," and the desirability of taking hard work easily at first, Feldman and Hillf have found that when oxygen is breathed instead of air, the formation of lactic acid during muscular exertion is greatly diminished, as the supply of oxygen to the muscles is increased.

Short exposure to want of oxygen acts as a rule so promptly on the respiratory centre, and the hyperpnoea disappears again so promptly when sufficient oxygen is supplied, that it seerrs almost certain that if it is lactic or other acid which acts on the centre it is formed, and perhaps again destroyed or assimilated, in situ. The facts relating to the effects of carbon dioxide, and of acids and alkalies, on the respiratory centre suggest that it is to the hydrogen ion concentration that the centre really responds ; but this supposition has not yet been experimentally verified.

In animals, such as dogs, which regulate their discharge of heat by increasing the frequency of breathing, rise of temperature excites the respiratory centre to very frequent and shallow respirations (polypnoea). In man the discharge of heat is regulated in other ways, and this type of breathing does not occur normally. With rise of body temperature produced artificially, however, there occurs a marked lowering of the threshold of alveolar carbon dioxide pressure in addition to an increase in the respiratory exchange. There is thus some hyperpncea, which is markedly increased on any exertion. Whether this effect is directly caused by rise of temperature in the respiratory centre is not yet known.

In connection with pathological irregularities of breathing, it is a matter of considerable interest to understand why normal breathing follows so smoothly and easily the requirements of the body. At first sight it is not at all evident why the breathing is not irregular, the respiratory movements now overshooting the mark, and now entirely ceasing, as actually occurs in Cheyne-Stokes breathing. As we have just seen, the respiratory centre is sensitive to the minutest changes in the partial pressure of carbon dioxide in the blood. We might therefore expect it to start into violent activity on any sudden increase of production of carbon dioxide, as in muscular activity, and to be pulled up again rapidly and completely by the great fall in the carbon dioxide content of the arterial blood caused by the greatly increased pulmonary ventilation. The breathing would thus resemble the action of a steam-engine with a very sensitive governor and no flywheel. Breathing of this type is actually met with in disease and in healthy persons living at high altitudes, but under normal conditions it does not occur. For instance, the hyperpnoea accompanying muscular exertion comes on and passes off quite smoothly and regularly.

There is more than one reason for this. In the first place, the lungs contain a considerable amount of air (the so-called " reserve " and " residual " air), equivalent in volume to about six ordinary breaths. It thus takes some little time for this air to be greatly changed in composition, either by changes in the venosity of the venous blood or by changes in the rate of the pulmonary ventilation. Were it not for this considerable volume of air in the lungs, there would be risk of sudden fainting from lack of oxygen. In a

Comments (0)

There are no comments posted here yet

Leave your comments

  1. Posting comment as a guest. Sign up or login to your account.
Attachments (0 / 3)
Share Your Location

This website puts documents at your disposal only and solely for information purposes. They can not in any way replace the consultation of a physician or the care provided by a qualified practitioner and should therefore never be interpreted as being able to do so.