1911 Encyclopædia Britannica/Respiratory System

by Edmund Owen

RESPIRATORY SYSTEM. (1). Anatomy—The respiratory tract consists of the nasal cavities, the pharynx, the larynx, the trachea, the bronchi and the lungs, but of these the two first parts have been treated in separate articles (see Olfactory System and Pharanyx).

The larynx is the upper part of the air tube which is specially modified for the production of notes of varying pitch, though it is not responsible for the whole of the voice. Its framework is made up of several cartilages which are moved on one another by muscles, and it is lined internally by mucous membrane which is continuous above with that of the pharynx and below with that of the trachea or windpipe. The larynx is situated in the front of the neck and corresponds to the fourth, fifth and sixth cervical vertebrae. For its superficial anatomy see Anatomy, Superficial and Artistic.

The thyroid cartilage (see fig. 1) is the largest, and consists of two plates or alae which are joined in the mid-ventral line. At the upper part of their junction is the thyroid notch and just below that is a forward projection, the pomum Adami, best marked in adult males. From the upper part of the posterior border of each aia the superior cornu rises up to be joined to the tip of the great cornu of the hyoid bone by the lateral thyro-hyoid ligament, while from the lower part of the same border the inferior cornu passes down to be fastened to the cricoid cartilage by the crico-thyroid capsule. From the upper border of each ala the thyro-hyoid membrane runs up to the hyoid bone, while near the back of the outer surface of each the oblique line of the thyroid cartilage runs downward and forward.

The cricoid cartilage (see figs. 1 and 2) is something like a signet ring with the seal behind; its lower border, however, is horizontal. To the mid-ventral part of its upper border is attached the mesial part of the crico - thyroid membrane, which attaches it to the lower border of the thyroid cartilage though the lateral parts of this membrane pass up internally to the thyroid cartilage and their upper free edges form the

After D. J. Cunningham, from Cunningham’s Text-Book of Anatomy.

Fig. 1.—Profile View of the Cartilages and Ligaments of the Larynx.

true vocal cords. On the summit of the signet part of the cricoid are placed the two arytenoid cartilages (see fig. 2), each of which

After D. J. Cunningham, from Cunningham’s Text-book of Anatomy.

Fig. 2.—Cartilages and Ligaments of Larynx, as seen from behind.

forms a pyramid with its apex upward and with an anterior posterior and internal or mesial surface. The base articulates with the cricoid by a concave facet, surrounded by the crico-arytenoid capsule, and the two arytenoids are able to glide toward or away from one another, in addition to which each can rotate round a vertical axis. From the front of the base a delicate process projects which, as it is attached to the true vocal cord, is called the vocal process, while from the outer part of the base another stouter process attaches the two crico-arytenoid muscles and so is known as the muscular process. Above each arytenoid are two smaller cartilages known as the cornicula laryngis or cartilages of Santorini and the cuneiform cartilages, but they are not of any practical importance.

The epiglottis (see fig. 3), on the other hand, is a very important structure, since it forms a lid to the larynx in swallowing: only the box moves up to the lid instead of the lid moving down to the box. It is leaf-shaped, the stalk (thyro-epiglottis ligament) being attached to the junction of the thyroid cartilages inside the larynx, while the anterior surface of the leaf is closely attached to the root of the tongue and body of the hyoid bone. The posterior or laryngeal surface is pitted for glands, and near the point where the stalk joins the leaf is a convexity which is known as the cushion of the epiglottis. All the cartilages of the larynx are of the hyaline variety except the epiglottis, the cornicula laryngis and the cuneiform cartilages, which are yellow elastic. The result is that all except these three tend to ossify as middle age is approached.

After D. J. Cunningham from Cunningham’s Text-Book of Anatomy.

Fig. 3.—Mesial Section through Larynx to show the outer wall of the right half.

The muscles of the larynx are: (1) the crico-thyroids, which are attached to the lower border of the thyroid and the anterior part of the cricoid, by pulling up which they make the upper part of the signet, with the arytenoids attached to it, move back and so tighten the vocal cords. (2) The thyro-arytenoids (see fig. 4), which run back from the junction of the thyroid alae to the front of the arytenoids and side of the epiglottis; they pull the arytenoids toward the thyroid and so relax the cords. (3) The single arytenoideus muscle, which runs from the back of one arytenoid to the other and approximates these cartilages. (4) The lateral crico-arytenoids (see fig. 4) which draw the muscular processes of the arytenoids forward toward the ring of the cricoid and, by so doing, twist the, vocal processes, with the cords attached, inward toward one another; and (5) the posterior crico-arytenoids (see fig. 4) which run from the back of the signet part of the cricoid to the back of the muscular processes of the arytenoid and, by pulling these backward, twist the vocal processes outward and so separate the vocal cords. All these muscles are supplied by the recurrent laryngeal nerve, except the crico-thyroid which is innervated by the external branch of the superior laryngeal (see Nerves, Cranial).

The mucous membrane of the larynx is continuous with that of the pharynx at the aryteno-epiglottidean folds which run from the sides of the epiglottis to the top of the arytenoid cartilages (see (fig. 3). To the outer side of each fold is the sinus pyriformis (see Pharynx). From the middle of the junction of the alae of the thyroid cartilage to the vocal processes of the arytenoids the mucous membrane is reflected over, and closely bound to, the true vocal cords which contain elastic tissue and, as has been mentioned, are the upper free edges of the lateral parts of the crico-thyroid membrane. The chink between the two

After D. J. Cunningham, from Cunningham’s Text-Book of Anatomy.
Fig. 4.—Dissection of the Muscles in the Lateral Wall of the Larynx. The right ala of the thyroid cartilage has been removed.

true vocal cords is the glottis or rima glottidis. Just above the true vocal cords is the opening into a recess on each side which runs upward and backward and is known as the laryngeal saccule; its opening is the laryngeal sinus. The upper lip of this slit-like opening is called the false vocal cord.

The mucous membrane is closely bound down to the epiglottis and to the true vocal cords, elsewhere there is plenty of sub mucous tissue in which the products of inflammation may collect and cause “oedema laryngis,” a condition which is mechanically prevented from passing the true vocal cords. In the upper part of the front and sides of the larynx and over the true vocal cords the mucous membrane is lined by squamous epithelium, but elsewhere the epithelium is of the columnar ciliated variety: it is supplied by the superior laryngeal branch of the vagus nerve and above the glottis is peculiarly sensitive.

The Trachea or windpipe (see fig. 5) is the tube which carries the air between the larynx and the bronchi; it is from four to four and a half inches long and lies partly in the neck and partly in the thorax; It begins where the larynx ends at the lower border of the sixth cervical, and divides into its two bronchi opposite the fifth thoracic vertebra. The tube is kept always open by rings of cartilage, which, however, are wanting behind, and, as it passes down, it comes to lie farther and farther from the ventral surface of the body, following the concavity of the thoracic region of the spinal column. In the whole of its downward course it has the oesophagus close behind it, while in front are the isthmus of the thyroid, the left innominate vein, the innominate artery and the arch of the aorta. On each side of it and touching it is the vagus nerve.

The cervical part of the tube is not much more than an inch in length, but it can be lengthened by throwing back the head. This, of course, is the region in which tracheotomy is performed, and it should be remembered that in children, and sometimes in adults, the great left innominate vein lies above the level of the top of the sternum.

In transverse section the trachea is rather wider from side to side than from before backward. In life the former measurement is said to be about 12·5 mm. and the latter 11 mm. It is made up of an external fibro-elastic membrane in which the cartilaginous rings lie, while behind, where these rings are wanting, is a layer of unstriped muscle which, when it contracts, draws the hind ends of the rings together and so diminishes the calibre of the tube. Inside these is plentiful submucous tissue

After D. J. Cunningham, from Cunningham's Text-Book of Anatomy.

Fig. 5.—The Trachea and Bronchi. The thyroid body is indicated by a dotted line.

containing mucous glands and quantities of lymphoid tissue, while the whole is lined internally by columnar ciliated epithelium. The Bronchi (see fig. 5) are the two tubes into which the trachea divides, but, since the branches, which these tubes give off later, are also called bronchi, it may be clearer to speak of primary, secondary and tertiary bronchi. Each primary bronchus runs downward and outward, but the right one is more in a line with the direction of the trachea than the left. The right primary bronchus has also a greater calibre than the left because the right lung is the larger, and for these two reasons when a foreign body enters the trachea it usually enters the right bronchus.

The first secondary bronchus comes off about an inch from the bifurcation of the trachea on the right side and, as it lies above the level of the pulmonary artery, it is known as the eparterial bronchus. On the left side the first branch is about two inches from the bifurcation and, like all the remaining secondary bronchi, is hyparterial: the left primary bronchus is therefore twice as long as the right. After the eparterial secondary bronchus is given off the direction of the right primary bronchus is carried on by the hyparterial secondary bronchus, and this, just before reaching the hilum of the lung, divides into upper and lower tertiary bronchi, while the left lower secondary hyparterial bronchus does not divide before reaching the hilum of its lung. Into the hilum or root of the right lung, therefore, three bronchial tubes enter, while on the left side there are only two. The firmly rooted habit of associating the term bronchi with those parts of the main tubes which lie between the bifurcation of the trachea and the point where the first branch comes off makes it very difficult to suggest a nomenclature which calls up any picture of the actual state of things to the mind. Certainly the classification into primary, secondary and tertiary bronchi only goes a very little way toward this, and it should be realized that, call them what we may, there are two long tapering tubes which run from the bifurcation of the trachea to the lower and back part of each lung, and give off a series of large ventral and small dorsal branches. The upper part of each of these long tubes or stem bronchi is outside the lung and in the middle mediastinum of the thorax, the lower part embedded in the substance of the lung. The structure of the bronchi is practically identical with that of the trachea. (See G. S. Huntington's " Eparterial Bronchial System of the Mammalia, " Am. Journ. Med. Sci. (Phila. 1898). See also Quain's Anatomy, London, last edition.)

The Lungs are two pyramidal, spongy, slate-coloured, very vascular organs in which the blood is oxygenated. Each lies in its own side of the thorax and is surrounded by its own pleural cavity (see COELOM and Smiocs MEMBRANES), and has an apex which projects into the side of the root of the neck, a base which is hollowed for the convexity of the diaphragm, an outer surface which is convex and lies against the ribs, an inner surface concave for the heart, pericardium and great vessels, a sharp anterior border which overlaps the pericardium and a broad, rounded posterior border which lies at the side of the spinal column. Each lung is nearly divided into two by a primary fissure which runs obliquely downward and forward, while the right lung has a secondary Jissure which runs horizontally forward from near the middle of the primary fissure. The left lung has therefore an upper and lower or basal lobe, while the right has upper, middle and lower lobes. On the inner surface of each lung is the root or hilum at which alone its vessels, nerves and ducts (bronchi) can enter and leave it. The structures contained in the root of each lung arerthe branches and tributaries of (1) the pulmonary artery, (2) the pulmonary veins, (3) the bronchi, (4) the bronchial arteries, (5) the bronchial veins, (6) the bronchial lymphatic vessels and glands, (7) the pulmonary plexuses of nerves. Of these the first three are the largest and, in dividing the root from in front, the veins are first cut, then the arteries and last the bronchi. As has been pointed out already, the eparterial bronchus on the right side is above the level of the artery, but all the others -(hyparterial) are on a lower level.

The bronchial arteries supply the substance of the lung; there are usually two on each side, and they lie behind the bronchi. The blood which they carry is chiefly returned by the pulmonary veins bringing oxidized blood back to the heart, so that here there is a normal and harmless mixture of arterial and venous blood. If there are any bronchial veins (their presence is doubted by some, and the writer has himself carefully but unsuccessfully searched for them several times), they open into the azygos veins of their own side. The bronchial lymphatic vessels lie behind the pulmonary vessels and open into several large glands which are black from straining off the carbon left in the lungs from the atmosphere.

There is an anterior and posterior pulmonary plexus of nerves on each side, the fibres of which are derived from the vagus and the upper thoracic ganglia of the sympathetic. Structure of the Lungs.—As the bronchi become smaller and smaller by repeated division, the cartilage completely surrounds them and tends to form irregular plates instead of rings -they are therefore cylindrical, but when the terminal branches (lobular bronchi) are reached, the cartilage disappears and hemispherical bulgings called alveoli occur (fig. 6 A). At the very end of each lobular bronchus is an irregular chamber, the atrium (fig. 6 At), and from this a number of thin-walled sacs, about 1 mm. in diameter, open out. These are called the infundibula (fig. 6 I), and their walls are pouched by hemispherical air-cells or alveoli like those in the lobular bronchi. Each lobular bronchus with its atrium and infundibula forms what is known as a lobule of the lung, and these lobules are separated by connective tissue, and their outlines are evident on the surface of the lung.

Fig. 6.—Diagram of Two Lobules of the Lung. B. Bronchus. A. Alveolus. I. Infundibulum. L.B. Lobular bronchus. At. Atrium. Lob. Lobule.

The muscular tissue, which in the larger tubes was confined to the dorsal part, forms a complete layer in the smaller; but when the lobular bronchi are reached, it stops and the mucous membrane is surrounded by the elastic layer. In the lobular bronchi, too, the lining epithelium gradually changes from the ciliated to the stratified or pavement variety, and this is the only kind which is found in the infundibula and alveoli. Surrounding each alveolus is a plexus of capillary vessels so rich that the spaces between the capillaries are no wider than the capillaries themselves, and it is here that the exchange of gases takes place between the air and the blood.

Embryology.—The respiratory system is developed from the ventral surface of the foregut as a long gutter-like pouch which reaches from just behind the rudiment of the tongue to the stomach. Limiting the anterior or cephalic end of this is a fl-shaped elevation in the ventral wall of the pharynx which separates the ventral ends of the third and fourth visceral bars and is known as the furcula; it is from this that the epiglottis, aryteno-epiglottidean folds and arytenoid cartilages are developed. Later on the respiratory tube is separated from the digestive by two ridges, one on each side, which, uniting, form a transverse partition. In the region of the furcula, however, the partition stops and here the two tubes communicate. The caudal end of the respiratory tube buds out into the two primary bronchi, and the right one of these, later on, bears three buds, while the left has only two; these are the secondary bronchi, which keep on dividing into two, one branch keeping the line of the parent stem to form the stem bronchus, while the other goes off at an angle. By the repeated divisions of these tubes the complex " bronchial tree " is formed and from the terminal shoots the infundibula bud out. The alveoli only develop in the last three months of foetal life. The thyroid cartilage is probably formed from the fourth and fifth bronchial bars, while the cricoid seems to be the enlarged first ring of the trachea. Before birth the lungs are solid and much less vascular than after breathing is established. Their slaty colour is gradually gained from the deposit of carbon from the atmosphere. (For further details see Quain's Anatomy, vol. i., Lond. 1908.) Comparative Anatomy.-It has been shown (see PHARYNX) that in the lower vertebrates respiration is brought about by the blood vessels surrounding the gill clefts. In the higher fishes (Ganoids and Teleosteans) the " swim bladder " appears as a diverticulum from the dorsal Wall of the alimentary canal, and its duct (d. pneumatic us) sometimes remains open and at others becomes a solid cord. In the former case it is probable that the blood is to some extent oxidized in the vascular wall of this bladder. In the Dipnoi (mud-fish) the opening of the swim bladder shifts to the ventral side of the pharynx and the bladder walls become sacculated and very vascular, so that, when the rivers are dried up, the fish can breathe altogether by means of it. In the S. American and African species of mud-fish the bladder or lung, as it may now be called, is divided by a longitudinal septum in its posterior (caudal) part into right and left halves. In this sub-class of Dipnoi, therefore, a general agreement is seen with the embryology or ontogeny of Man's lungs. In the Amphibia the two lungs are quite separate though they are mere sacculated bags without bronchi. A trachea, however, appears in some species (e.g. Siren) and a definite larynx with arytenoid cartilages, vocal cords and complicated muscles is established in the Anura (frogs and toads). In most of the Reptilia the bag-like lungs are elaborated into spongy organs with arborizing bronchi in their interior. From the crocodiles upward a main or stem bronchus passes to the caudal end of the lung, and from this the branches or lateral bronchi come off. The larynx shows little advance on that of the Anura. The respiratory organs of birds are highly specialized. The larynx is rudimentary, and sound is produced by the syrinx, a. secondary larynx at the bifurcation of the trachea; this may be tracheal, bronchial or, most often, tracheo-bronchial. The lungs are small and closely connected with the ribs, while from them numerous large air sacs extend among the viscera, muscles and into many of the bones, which, by being filled with hot air, help to maintain the high temperature and lessen the specific gravity of the body. This pneumaticity of the bones is to a certain extent reproduced by the air sinuses of the skull in crocodiles and mammals, and it must be pointed out that the amount of air in the bones does not necessarily correspond with the power of iiight, for the Ratitae (ostriches and emeus) have very pneumatic bones, while in the sea-gulls they are hardly pneumatic at all.

In mammals the thyroid cartilage becomes an important element in the larynx, and in the Echidna the upper and lower parts of it, derived respectively from the fourth and fifth bronchial bars, are separate (R. H. Burne, fourn. Anat. and Phys. xxxviii. p. xxvii.). The whole larynx is much nearer the head than in Man, and in young animals the epiglottis is intra-narial, i.e. projects up behind the soft palate. This prevents the milk trickling into the larynx during suckling, and is especially well seen in the Marsupials and Cetacea, though evidences of it are present in the human embryo. In the lower mammals an inter-arytenoid cartilage is very frequent (see J. Symington, " The Marsupial Larynx, " J. Anat. and Phys. xxxiii. 31, also " The Monotreme Larynx, " ib. xxxiv. 90). The lungs show a good deal of variation in their lobulation; among the porcupines as many as forty lobes have been counted in the right lung, while in other mammals no lobulation at all could be made out. The azygous lobe of the right lung is a fairly constant structure and is situated between the post-caval vein and the oesophagus. It is supplied by the terminal branch of the right stem bronchus and, although it is usually absent in Man, the bronchus which should have supplied it is always to be found. (F. G. P.)

I

(2) PHYSIOLOGY

So far as is known, the intake'of oxygen, either free or combined, and the output of carbon dioxide, are an essential part of the life of all organisms. The two processes are so closely associated with one another that they are always included together under the designation of respiration, which may thus be defined as the physiological process which is concerned in the intake of oxygen and output of carbon dioxide. According to the evidence at present available, it is only within living cells that the respiratory oxygen is consumed and the carbon dioxide formed. The mere conveying of oxygen from the surrounding air or Water to these cells, and of carbon dioxide from them to the air or Water, is, however, in itself a complex process in the higher animals; and accordingly an account of animal respiration naturally falls into two divisions, the first of which (L) is concerned with the manner in which oxygen and carbon dioxide are conveyed to and from the living tissues, and the second (II.) with the consumption of oxygen and formation of carbon dioxide by the living tissues themselves.

I. In all the more highly organized animals there are special respiratory organs: the lungs in the higher vertebrates; the gills in fishes; the tracheae in insects; and various rudimentary forms of lungs or gills in other higher invertebrates. In the present article attention will be specially confined to the case of the higher vertebrates, and in particular to man.

Air is brought into the lungs by the movements of breathing (see above, Movements of Respiration). Oxygen from this air passes through the delicate lining membrane of the air-cells of the lungs into the blood, where it enters into loose chemical combination with the haemoglobin of the red corpuscles (see Blood). In this form it is conveyed onwards to the heart, and thence through the arteries to the capillaries, where it again parts from the haemoglobin, and passes through the capillary walls to the tissues, where it is consumed. Carbon dioxide passes out from the tissues into the blood in a corresponding manner, , enters into loose combination as bicarbonate, and possibly in other ways, in the blood, and is conveyed by the veins to the lungs, whence it passes out in the expired air. Pure atmospheric air contains 20·93% of oxygen, ·03% of carbon dioxide and 79·04% of nitrogen (with which is mixed about 0·9% of argon). The dried expired air in man contains about 3·5% of carbon dioxide and 17% of oxygen, so that roughly speaking the carbon dioxide is increased by about 3·5% and the oxygen diminished by 4%. Expired air as it leaves the body contains about 6%, of moisture, compared with usually about 1% in the inspired air. The added moisture and higher temperature of expired air make it decidedly lighter than pure air.

Owing to the unpleasant effects often produced in badly ventilated rooms it was for long supposed that some poisonous volatile “organic matter” is also given off in the breath. Careful investigation has shown that this is not the case. The unpleasant effects are partly due to heat and moisture, and partly to odours which are usually not of respiratory origin. The carbon dioxide present in the air of even very badly ventilated rooms is present in far too small proportions to have any sensible effect.

The average volume of air inspired per minute by healthy adult men during rest is about 7 litres or ·25 cub. ft. In different individuals the frequency of breathing varies considerably—from about 7 to 25 per minute, the depth of each breath varying about inversely as the frequency. During muscular work the volume of air breathed may be six or eight times as much as during rest. The volume of carbon dioxide given off varies from about half a cubic foot per hour during complete rest to 5 cub. ft. during severe exertion, but averages about 0·9 cub. ft. per hour, and will reach or exceed 1 cub. ft. per hour during even very light exertion. The volume of oxygen consumed is about a seventh greater than that of the carbon dioxide given off.

The breathing is regulated from a nervous centre situated in the medulla oblongata, which is the lowest part of the brain. If this centre is destroyed or injured the breathing stops and death rapidly results. From the respiratory centre rhythmic efferent impulses proceed down the motor nerves supplying the diaphragm, intercostals and other respiratory muscles. Afferent impulses through various nerves may temporarily affect the rhythm of the respiratory centre. Of these afferent impulses by far the most important are those which proceed up the vagus nerve from the lungs themselves. On distention of the lungs with air the inspiratory impulses from the respiratory centre are suddenly arrested or “inhibited”; on the other hand, collapse of the lung strongly excites to inspiratory effort. On section of the vagus nerve these effects disappear, and the breathing becomes less frequent and much more laboured. The vagus nerve is thus the carrier of both inhibitory and exciting stimuli.

As the physiological function of breathing is to bring oxygen to and remove carbon dioxide from the blood, it would naturally be expected that breathing would be regulated in accordance with the amount of oxygen required and of carbon dioxide formed; but until quite recently the actual mode of regulation was by no means clear. It was commonly supposed that afferent nervous impulses in some way regulated the otherwise automatic action of the centre, want of oxygen or excess of CO₂ in the blood being only an occasional and relatively unimportant factor in the regulations. The phenomenon of “apnoea” or complete cessation of natural breathing which occurs after forced breathing, was attributed mainly to the already mentioned distension effect through the vagus nerves. To go further back still, it was even supposed that the rate and depth of breathing, and the percentage of oxygen in the inspired air, determine the consumption of oxygen and formation of carbon dioxide in the body, just as the air-supply to a fire determines the rate of its combustion. This old belief is still often met with-for instance, in the reasons given for recommending “breathing exercises” as a part of physical training.

It is evident that if the breathing did not increase correspondingly with the greatly increased consumption of oxygen and formation of CO₂ which occurs, for instance during muscular work, the percentage of oxygen in the air contained in the lung cells or alveoli (alveolar air) would rapidly fall, and the percentage of carbon dioxide increase. The inevitable result would be a very imperfect aeration of the blood. Investigation of the alveolar air has furnished the key to the actual regulation of breathing. Samples of this air can be obtained by making a sudden and deep expiration through a piece of long tube, and at once collecting some of the air contained in the part of this tube nearest the mouth. By this means it has been found that during normal breathing at ordinary atmospheric pressure the percentage of carbon) dioxide (about 5·6% on an average for men) is constant for each individual, though different persons vary slightly as regards their normal percentage. The breathing is thus so regulated as to keep the percentage of carbon dioxide constant; and under normal conditions this regulation is surprisingly exact. The ordinary expired air is a mixture of alveolar air and air from the “dead space” in the air passages. The deeper the breathing happens to be, the more alveolar air there will be in the expired air, and the higher, therefore, the percentage of carbon dioxide in it, so that the expired air is not constant in composition, though the alveolar air is. If air containing 2 or 3% of carbon dioxide is breathed, the breathing at once becomes deeper, in such a way as to prevent anything but a very slight rise in the alveolar carbon dioxide percentage. The difference is scarcely appreciable subjectively, except during muscular exertion. The effect of 1% of carbon dioxide in the inspired air is so slight as to be negligible, and there is no foundation for the popular belief that even very small percentages of carbon dioxide are injurious. With 4 or 5% or more of carbon dioxide, however, much panting is produced, and the alveolar carbon dioxide percentage begins to rise appreciably, since compensation is no longer possible. As a consequence, headache and other symptoms are produced. If, on the other hand, the percentage of carbon dioxide in the alveolar air is abnormally reduced by forced breathing, the condition of apnoea is produced and lasts until the percentage again rises to normal, but no longer. Forced breathing with air containing more than about 4% of carbon dioxide causes no apnoea, as the alveolar carbon dioxide does not fall.

If oxygen is breathed instead of air there is no appreciable change in the percentage of carbon dioxide in the alveolar air, and no tendency towards apnoea. Want of oxygen is thus not a factor in the regulation of normal breathing. During muscular work the depth and .frequency of breathing increase in such a way as to prevent the alveolar carbon dioxide from rising more than very slightly. It is still the carbon dioxide stimulus that regulates the breathing, although with excessive muscular work other accessory factors may come in to some extent.

Under increased barometric pressure the percentage of carbon dioxide in the alveolar air no longer remains constant; it diminishes in proportion to the increase of pressure. For instance, at a pressure of 2 atmospheres it is reduced to half, and at 6 atmospheres to a sixth; while at less than normal atmospheric pressure it rises correspondingly unless symptoms of want of oxygen begin to interfere with this rise. These results show that it is not the mere percentage, but the pressure (or “partial pressure”) of carbon dioxide in the alveolar air that regulates breathing. The pressure exercised by the carbon dioxide in the alveolar air is of course proportional to its percentage, multiplied by the total atmospheric pressure. It follows from this law that at a pressure of 6 atmospheres 1% of carbon dioxide in the inspired air would have the same violent effect as 6% at the normal pressure of I atmosphere. To take a concrete practical application, if a diver whose head was just below water were supplied with sufficient air to keep the carbon dioxide percentage in the air of his helmet down to 3% at most, he would be quite comfortable. But if, with the same air supply as measured at surface, he went down to a depth of 170 ft., where the pressure is 6 atmospheres, he would at once experience great distress culminating in loss of consciousness, owing, not to the pressure of the water, which has trifling effects, but to the pressure of carbon dioxide in the air he Was breathing. The air supply must be increased in proportion to the increase of pressure if these effects are to be avoided, and ignorance of this has led to the common failure of diving work at considerable depths.

The foregoing, facts enable us to understand the regulation of breathing under normal conditions. The pressure of carbon dioxide in the alveolar air evidently determines that of the carbon dioxide in the arterial blood, and the latter in its turn determines the carbon dioxide pressure in the respiratory centre, which is very richly supplied with blood. The centre itself is extremely sensitive to the slightest increase or diminution in carbon dioxide pressure; and thus it is that the alveolar carbon dioxide pressure is so important. That the stimulus of carbon dioxide is from the blood and not through nerves is proved by many experiments. The function of the vagus nerves in regulating the breathing is apparently to, as it were, guide the centre in the expenditure of each separate inspiratory or expiratory effort; for as soon as inspiration or expiration is completed the inspiratory or expiratory effort is cut short by impulse proceeding up the vagus nerve, and much waste of muscular work and risk of injury to the lungs is thereby prevented. Under ordinary conditions the regulation of carbon dioxide pressure in the alveolar air ensures at the same time a normal pressure of oxygen, since absorption of oxygen and giving off of carbon dioxide normally run parallel to one another. If, however, air containing abnormally little oxygen is breathed, the normal relation between oxygen and carbon dioxide in the alveolar air is disturbed. A similar state of affairs is brought about by any considerable diminution of atmospheric pressure. Not only does the partial pressure of oxygen in the inspired air fall, but this fall is proportionally much greater in the alveolar air; and the effects of want of oxygen depend on its partial pressure in the alveolar air. It has been known for long that any great deficiency in the proportion of oxygen in the air breathed increases the depth and frequency of the breathing; but this effect is not apparent until the percentage of oxygen or the barometric pressure is reduced by more than a third, which corresponds to a reduction of more than half in the alveolar oxygen pressure. In contrast with this an increase of a fiftieth in the alveolar carbon dioxide pressure has a marked effect on the breathing. Along with the increased breathing caused by deficiency of oxygen there is more or less blueness of the skin and abnormal effects of various kinds, such as partial loss of sensibility, memory and power of thinking. Long exposure often causes headache, nausea, sleeplessness, &c.—a train of symptoms known to mountaineers as “mountain sickness.” That the primary cause of “mountain sickness” is lack of oxygen owing to the low atmospheric pressure there is not the slightest doubt. Lack of oxygen is thus not only an important, but also an abnormal form of stimulus to the respiratory centre, since it is accompanied by quite abnormal symptoms. A further analysis of the special effect of lack of oxygen on the respiratory centre has shown that this effect still depends on the partial pressure of carbon dioxide in the alveolar air. The lack of oxygen appears, in fact, to have simply increased the sensitiveness of the centre to carbon dioxide, so that a lower partial pressure of carbon dioxide excites the centre, and the breathing is correspondingly increased. By prolonged forced breathing so much carbon dioxide is washed out of the body that the subsequent apnoea lasts until the oxygen in the alveolar air is nearly exhausted. The subject of the experiment becomes very blue in the face and is partially stupefied by want of oxygen before he has any desire to breathe. The probable explanation of these facts is that want of oxygen does not itself excite the centre, but that some substance very probably lactic acid, which is known to be formed abundantly —is produced abnormally in the body during exposure to want of oxygen and aids the carbon dioxide in exciting the centre. Itis known that the blood becomes less alkaline at high altitudes, and that acids in general excite the centre. A person on a high mountain thus gets out of breath much more easily than at sea-level. The extra stimulus to the centre during work still comes from the extra carbon dioxide formed, but has a greater effect than usual on the breathing. If the extra stimulus came directly from Want of oxygen the person on the mountain would probably turn blue and lose consciousness on the slightest exertion. By analysing the alveolar air it can be shown that after a time even a height of 5000 to 6000 ft., or a diminution of only a sixth in the barometric pressure, distinctly increases the sensitiveness of the respiratory centre to carbon dioxide, so that there seems to be a. slow accumulation of acid in the blood. The effect also passes off very slowly on returning to normal pressure, although the lack of oxygen is at once removed. The blueness of the skin (“ cyanosis ”) produced by lack of oxygen is due to the fact that the haemoglobin of the red corpuscles is imperfectly saturated with oxygen. Haemoglobin which is fully saturated with oxygen has a bright red colour, contrasting with the blue colour which it assumes when deprived of oxygen. According to the existing evidence the saturation of the haemoglobin is practically complete under normal conditions in the lungs, or when thoroughly shaken at the body temperature and normal atmospheric pressure with air of the same composition as normal alveolar air. As the partial pressure of the oxygen in this air falls, however, the saturation of the haemoglobin becomes less and less complete, and the arterial blood assumes amore and more blue tinge, which imparts a blue or leaden colour to the skin, accompanied by the symptoms, already referred to, of lack of oxygen. Normal arterial blood in man yields about 19 volumes of physiologically available oxygen for each 100 volumes of blood. Of these 19 volumes about 18% are loosely combined with the haemoglobin of the red corpuscles, the small remainder being in simple solution in the blood. Venous blood, on the other hand, yields only about 12 volumes. The combination of haemoglobin with oxygen is only stable in the presence of free oxygen at a pressure of about that in normal alveolar air. As this pressure falls the compound is progressively dissociated. From this it can be readily understood why the blood loses its oxygen in passing through the tissues, which are constantly absorbing free oxygen, and regains it in the lungs. The marked effects produced by abnormal deficiency in the pressure of oxygen in the alveolar air are also readily intelligible; for even although the arterial blood still contains sufficient oxygen to cover the normal difference between the oxygen content of arterial and that of venous blood, yet this oxygen is given off to the tissues less readily—i.e. at a lower pressure, and thus fails to supply their demands completely. It is evident also that in pure air at normal pressure increased ventilation of the lungs does not appreciably increase the supply of oxygen to the blood, whereas in air largely deprived of its oxygen, or at low pressure, the increased alveolar oxygen pressure produced by deep breathing helps greatly in saturating the blood with oxygen, and may thus relieve the symptoms of Want of oxygen. Hence it is that the increased sensitiveness of the respiratory centre to carbon dioxide, and consequent increased depth of breathing, at high altitudes compensates to a large extent for deficiency in the oxygen pressure. Addition of carbon dioxide to the inspired air produces exactly the same result. Indeed Professor Angelo Mosso was led by observation of the beneficial effects of carbon dioxide at low atmospheric pressure to attribute mountain sickness to lack of carbon dioxide, a condition which he designated by the word “ acapnia. ” When impure air is vitiated, not only by deficiency of oxygen, but also by carbon dioxide, the carbon dioxide causes panting, which not only gives warning of any danger, but prevents the alveolar oxygen percentage from falling in the way it would do if the carbon dioxide were absent. In this Way the carbon dioxide greatly lessens the danger. To give instances, air progressively and very highly vitiated by respiration is much less likely to cause danger if the carbon dioxide is not artificially absorbed, and not nearly so dangerous as the great diminution of atmospheric pressure (and consequently of oxygen pressure) which occurs in a very high balloon ascent. Indeed the dangers of a very high balloon ascent are notorious, and a number of deaths or very narrow escapes are on record.

]ust as oxygen forms a dis sociable compound with the haemoglobin of the blood, so does carbon dioxide form dis sociable compounds. One of' these compounds appears to be with haemoglobin itself, and another is sodium bicarbonate, which is far more easily dissociated in the blood than in a simple watery solution, owing to the presence of proteid and possibly other substances which act as weak acids and thus help the dissociation process. The whole of the carbon dioxide can therefore be removed from the blood by a vacuum pump, just as the whole of the oxygen can. Venous blood contains roughly speaking about 40 volumes of carbon dioxide per 100 of blood, and arterial blood about 34 volumes. Of this carbon dioxide only about 3 volumes can be in free solution, the rest being loosely combined. The conveyance of carbon dioxide from the blood to the lungs is thus readily intelligible, as well as the fact that any increase or diminution of the pressure of carbon dioxide in the alveolar air will naturally lead to a damming back or increased liberation of carbon dioxide from the blood, and that by forced breathing carbon dioxide can be washed out of the blood to such an extent that a prolonged cessation of natural breathing (apnoea) follows, since even in the venous blood the partial pressure of carbon dioxide has become too low to excite the respiratory centre. It will be evident from the foregoing that in order to supply efficiently the respiratory requirements of the tissues not only must the breathing, but also the circulation, be suitably regulated. In hard muscular work the consumption of oxygen and output of carbon dioxide may be increased eight or ten times beyond those of rest. Unless, therefore, the blood supply to the active tissues were correspondingly increased, deficiency of oxygen would at once arise, since the amount of oxygen carried by a given volume of the arterial blood is very limited, as already explained. It is known that the supply of blood to each organ is always increased during its activity. This; increase can, for instance, readily be seen and measured in the case of contracting muscles or secreting glands; and the volume and frequency of the pulse are greatly increased during muscular work. But while it is evident enough that the flow of blood through the body is determined in accordance with the metabolic activities of each tissue, our knowledge is as yet very scanty as to the means by which this determination is brought about. Probably, however, carbon di.oxide may be nearly as important a factor in the regulation of the circulation as in that of breathing. Just as the rate of breathing was formerly supposed to determine, and not to be determined by, the fundamental metabolic processes of the body, so the circulation was supposed to be another independent determining factor; and under the influence of these mechanistic conceptions the direction of investigation into the phenomena of respiration and' circulation has been largely diverted to side issues.

Since the circulation, no less than the breathing, is concerned in the supply of oxygen to and removal of carbon dioxide from the tissues, it can readily be understood that defective circulation, such as occurs, for instance, in uncompensated valvular affections of the heart, may affect the breathing and hinder the normal respiratory exchange. Conversely, also, defects in the aeration or oxygen-carrying power of the blood may be compensated for by increase in the circulation. For instance, in the very common condition known as anaemia, where the percentage of haemoglobin, and consequently the oxygen-carrying power of the blood, is often reduced to a third or less, the respiratory disturbances may be so slight that the patient is going about his or her ordinary work. A miner suffering from the now well-known “ worm disease, ” or ankylostomiasis (g.v.), may be working underground, or a. housemaid suffering from chlorosis may be doing her work, with only a third of the normal oxygen-carrying power of the blood. There seems to be no doubt that in such cases an increased rate of blood circulation compensates for the diminished oxygen-carrying power of the blood. It is well known that at high altitudes a gradual process of adaptation to the low pressure occurs, and the shortness of breath and other symptoms experienced for the first few days gradually become less and less. This adaptation is .partly, at least, due to a. marked increase in the percentage of haemoglobin in the blood, though probably circulatory and perhaps other compensatory changes are also involved.

In connexion with respiration the action of certain poisons is of great interest. One of these, carbon monoxide, is of very common occurrence, and causes numerous cases of poisoning. Like oxygen, it has the property of combining with the haemoglobin of the blood, but its affinity for haemoglobin is far more strong than that of oxygen. In presence of air containing as little as -05% of carbon monoxide, the haemoglobin will become about equally shared between oxygen and carbon monoxide, so that, since air contains 20.9% of oxygen, the affinity of carbon monoxide for haemoglobin may be regarded as abou-t 400 times greater than that of oxygen. The blood of a person breathing even a small percentage of carbon monoxide may thus become gradually saturated to a dangerous extent, since the haemoglobin engaged by the carbon monoxide is for the time useless as an oxygen-carrier. Air containing more than about o.r % of carbon monoxide is thus more or less dangerous if breathed for long; but the blood completely recovers in the course of a few hours if pure air is again breathed. The poisonous action of carbon monoxide can be abolished by placing the animal exposed to it in oxygen at an excess pressure of about an atmosphere. The reason for this is that, in consequence of the increased partial pressure of the oxygen, the amount of this gas in free solution in the blood is greatly increased in accordance with Dalton's law, and becomes sufficient to supply the tissues with oxygen quite independently of the haemoglobin. Even at ordinary atmospheric' pressure the extra oxygen dissolved in the blood when pure oxygen is breathed is of considerable importance. Carbon-monoxide poisoning is the chief cause of death in Colliery explosions and fires, and the sole cause in poisoning by lighting gas and fuel gas of various kinds. Its presence in dangerous proportions may be readily detected with the help of a small bird, mouse or other small warm-blooded animal. In such animals the respiratory exchange is so rapid that symptoms of carbon-monoxide poisoning are shown far more quickly than in man. The small animal can thus be employed in mines, &c., to indicate danger from carbon monoxide. A lamp is useless for this purpose. There are various other poisons, such as nitrites, chlorate's, dinitrobenzol, &c., which act by disabling the haemoglobin, and so cutting 05 the oxygen supply to the tissues.

Between the air in the air-cells of the lungs and the blood of the lung capillaries there intervenes nothing but a layer of very thin, fattened cells, and until recently it was very generally believed that it was by diffusion alone that oxygen passes inwards and carbonic acid outwards through this layer. Similar simple physical explanations of processes of secretion and absorption through living cells have, however, turned out to be incorrect in the case of other organs. It is known, moreover, that in the case of the swimming-bladder of fishes oxygen is secreted into the interior against enormous pressure. Thus, in the case of a

fish caught at a depth of 4500 ft., the partial pressure of the

oxygen present in the swimming bladder at this depth was 127 atmospheres, whereas the partial pressure of oxygen in sea-water is only about O~2 atmosphere. Diffusion can therefore have nothing to do with the passage of gas inwards, which is known to be under the control of the nervous system. The cells lining the interior of the swimming bladder are developed from the same part of the alimentary tract as those lining the air-cells of the lungs, so that it seems not unlikely that the lungs should possess the power of actively secreting or excreting gases. The question whether such a power exists, and is normally exercised, has been investigated by more than one method; and although it is not possible to go into the details of the experiments, there can be no doubt that the balance of the evidence at present available is in favour of the View that diffusion alone is incapable of explaining either the absorption of oxygen or the excretion of carbon dioxide through the lining cells of the lungs. The partial pressure of oxygen appears to be always higher, and of carbon dioxide often lower, in the blood leaving the lungs than in the air of the air-cells; and this result is inconsistent with the diffusion theory. As to the causes of the passage of oxygen and carbonic acid through the walls of the capillaries of the general circulation, we are at present in the dark. Possibly diffusion may explain this process.

II. Although we cannot trace the exact changes which occur when oxygen passes into living cells, yet it is possible to obtain a clear general view of the origin and destiny of the material concerned in the process, and of the physiological conditions which determine it.

The oxidizable material within the body consists, practically speaking, of proteids (albumen-like substances, with which the collagen of connective tissue may be included), fats and carbohydrates (sugars and glycogen). All of these substances contain carbon, hydrogen and oxygen in known, though different, proportions, and the former also contains a known amount of nitrogen and a little sulphur. Nitrogen is constantly leaving the body as urea and other substances in the urine and faeces; and a small but easily measurable proportion of carbon passes off in the same manner. The rest of the carbon passes out as carbon dioxide in respiration. Now carbohydrates and fats are oxidized completely in the body to carbon dioxide and water. This follows from the fact that, practically speaking, no other products into which they might have been converted leave the body except carbon dioxide and water. Moreover, a given weight of carbohydrate requires for its oxidation a definite weight of oxygen, and produces a definite weight of carbon dioxide. There is thus a definite relation between the weight of oxygen used up and the weight of carbon dioxide formed in this oxidation. The same is true for the oxidation of fat and of proteid, allowing in the latter case for the fact that the nitrogen, together with part of the carbon and hydrogen, passes out as urea, &c., in an incompletely oxidized form. From all this it follows that if we measure over a given period (1) the discharge of nitrogen from the body, (2) the intake of oxygen and (3) the output of carbonic acid, We can easily calculate exactly what the ultimate destiny of the oxygen has been, and at the ultimate expense of what material the carbonic acid has been formed. What the intermediate stages may have been we cannot say, but this in no way affects the validity of the calculation. If, during the period of measurement, food is taken, the basis of the calculation is still substantially the same, as the oxidizable material in food consists of practically nothing else except proteids, carbohydrates and fats.

Liberation of Energy.-From experiments made outside the body, we know that in the oxida-tion of a given weight of proteid, carbohydrate or fat, a definite amount of energy is liberated. In the article on Dmrnrrcs it is shown that precisely the same liberation of energy occurs in the living body, due allowance being made for the fact that the oxidation of proteid is not quite complete. The following table shows the respiratory quotients (the respiratory quotient being the ratio between the volume of carbon dioxide formed and that of oxygen used up) and energy expressed in units of heat (calories) liberated per gramme of carbon dioxide produced and oxygen consumed in the living body during the oxidation of proteid, fat and a typical carbohydrate:-

7 Calories per Calories per

Substance oxidized. Rgiggziffy §§ '§ ;';fof'f gr;'X“;, ';§ n°f duced. consumed.

1;';“*“' .; li ;:;§ I 3:23

Cane-sugar . I ~oo 2- 59 3~ 56

In the oxidation of non-living substances the rate varies, within wide limits, according to that at which oxygen is supplied. Thus a fire burns the faster the more air is supplied, and the higher the percentage of oxygen in the air. It was for long believed that in the living body also the rate of oxidation must vary according to the oxygen supply. It has been found, however, that this is not the case. Provided that a certain minimum of oxygen is present in the air breathed, or in the blood supplied to the tissues, it is, practically speaking, indifferent whether the oxygen supply be increased or diminished: only a certain amount is consumed. It might be supposed that the reason for this is that the available oxidizable material in the body is limited, and that if the food supply were increased there would be a corresponding increase in the rate of oxidation. This hypothesis is apparently supported by the fact that, when an increased supply of proteid is given as food, the amount of nitrogen discharged in the urine is almost exactly correspondingly increased, so that evidently the oxidation of proteid increases correspondingly with the supply. Similarly, when carbohydrate food is given, the alteration in the respiratory quotient shows that more carbohydrate than before is being oxidized. Closer investigation in recent times has, however, brought out the very striking fact that, if oxidation be measured in terms of energy liberated by it in the body, it makes but little difference, other things being equal, whether the animal is fasting or not. If more proteid or carbohydrate is oxidized at one time, correspondingly less fat is oxidized, but the total energy liberated as heat, &c., in the body is about the same, unless the diet is very excessive, when there is a slight increase of oxidation. Even after many days of st.arvation, the rate of oxidation per unit of body weight has been found to remain sensibly the same in man. When more food is taken than is required, the excess is stored upfchiefiy in the form of fat, into which carbohydrate and possibly also proteid are readily converted in the body. When less food is taken than is needed, the stock of fat is drawn upon, and supplies by far the greater proportion of the energy requirements of the body.

During the performance of muscular work oxidation is greatly increased, and may amount to ten times the normal or more. Even the slight exertion of easy walking increases oxidation to three times. When the energy represented by the external work done in muscular exertion is compared with the extra energy liberated by oxidation in the body, it is found, as would be expected, that the latter value largely exceeds the former. In other words, much of the energy liberated is wasted as heat. Nevertheless the muscles are capable of working with less waste than any steam or gas engine. In the work of climbing, for instance, it has been found in the case of man that 3 5 % of the energy liberated is represented in the work done in raising the body. Muscular work, if at all excessive, leads to fatigue, and consequent rest. On the other hand, unnatural abstinence from muscular activity leads to restlessness and consequent muscular work. Hence on an average of the twenty-four hours the expenditure of energy by different individuals, with different modes of life, does not as a rule differ greatly. The rate of oxidation per unit of body weight varies considerably according to size and age. If we compare different warmblooded animals, we find that the rate of oxidation is relatively to their weight far higher in the smaller ones. In a mouse-or small bird, for instance, the rate is about twenty times as great as in a man. The difference is in part due to the fact that the smaller an animal is the greater is its surface relatively to its mass, and consequently the more heat does it require to keep up its temperature. The smaller animal must therefore produce more heat. Even in cold-blooded animals, however, oxidation appears to be more rapid the smaller the animal. In the case of man, oxidation is relatively more than twice as rapid in children than in adults, and the difference is greater than would be accounted for by the difference in the ratio of surface to mass. Allowing for differences in size, oxidation is about equally rapid in men and women.

It was for long believed that the special function of respiratory oxidation was (1) the production of heat, and (2) the destruction of the supposed “waste products.” Further investigation has, however, tended to show more and more clearly that in reality respiratory oxidation is an essential and intimate accompaniment of all vital activity. To take one example, secretion and absorption, which were formerly explained as simple processes of filtration and diffusion, are now known to bel accompanied, and necessarily so, by respiratory oxidation in the tissues concerned. The respiratory oxidation of an animal is thus a very direct index of the activity of its vital processes as a whole. Looking at what is known with regard to respiratory oxidation, we see that what is most striking and most characteristic in it is its tendency to persist-to remain on the whole at about a normal level for each animal, or each stage of development of an animal. The significance of this cannot be over-estimated. It indicates clearly that just as an organism differentiates itself from any non-living material system by the manner in which it actually asserts and maintains its specific anatomical structure, so does it' differentiate itself from any mere mechanism by the manner in which it asserts and maintains its specific physiological activities.

Authorities.—For further general information the reader may be referred to the sections by Pembrey and by Gamgee in Schafer's Handbook of Physiology, vol. i., and by Bohr in Nagel's Handbuch der Physiologie, vol. i. The following additional references are to recent investigations: Regulation of Breathing, Haldane and Priestley, Journal of Physiology, xxxii. 225 (1905). Respiration at High Altitudes and Effects of Want of Oxygen, Zuntz, Loewy, Caspari, and Müller, Das Höhenklima (1905); Boycott and Haldane, Ward, and Haldane and Poulton, Journal of Physiology, xxxvii. (1908). Respiration at High Pressures, “Report to the Admiralty of the Committee on Deep Diving" (1907). Respiratory Exchange and Secretion, Barcroft, Journal of Physiology, xxvii.-31 (1901); Barcroft and Brodie, Journal of Physiology, xxvii. 18, and xxxiii.,52 (1905). Excretion of CO₂ by the Lung Epithelium, Bohr, Zentralblatt fur Physiologie. 337 (2907). “Normal Alveolar CO₂ Pressure in Man, ” Mabel Fitzgerald and J. Haldane in Physiological Journal (1905).  (J. S. H.) 

(3) Movements of Respiration

Normal Respiration.—If the naked body of a person asleep or in perfect inactivity be carefully watched, it will be found that the anterior and lateral walls of the chest move rhythmically up and down, while air passes into and out of the nostrils (and mouth also if this be open) in correspondence with the movement. If we look more closely we shall find that with every uprising of the chest walls the membranous intercostal portions sink slightly as if sucked in, while at the same time the flexible walls of the abdomen bulge as if protruded by some internal force. If respiration be in the slightest degree hurried, these motions become so marked as to escape the attention of no one. The elevation of the chest walls is called inspiration, their depression, expiration. Inspiration is slightly shorter than expiration, and usually there is a slight pause or momentary inaction of the chest between expiration and the following inspiration. Apparatuses for measuring the excursion of a given point of the chest wall during respiration are called thoracometers or stethometers. Apparatuses for recording the movements of the chest are called stethographs or pneumographs.

Frequency of Respiration.—The frequency of respiration during perfect rest of the body is 16 to 24 per minute, the pulse rate being usually four times the rate of respiration; but the respiratory rhythm varies in various conditions of life. The following are the means of many observations made by Lambert Adolphe Quételet (1796–1874): at the age of one year the number of respirations is 44 per minute; at 5 years, 26; from 15 to 20 years, 20; from 25 to 30, 16; from 30 to 50, 18.1. Muscular exertion always increases the frequency of respiration. The higher the temperature of the environment the more frequent is the respiration. Paul Bert (1833–1886) has shown that with higher atmospheric pressures than the normal the frequency of respiration is diminished while the depth of each inspiration is increased. The frequency of respiration diminishes until dinner-time, reaches its maximum within an hour of feeding, and thereafter falls again; if dinner is omitted, no rise of frequency occurs. The respiratory act can be interrupted at any stage, reversed, quickened, slowed and variously modified at will, so long as respiration is not stopped entirely for more than a short space of time; beyond this limit the will is incapable of suppressing respiration., Depth of Respiration.-The depth of respiration is measured by the quantity of air inspired or expired in the act; but the deepest expiration possible fdoes not suffice to expel all the air the lungs contain. The following measurements have been ascertained, and are here classified according to the convenient terminology proposed by John Hutchinson (1811–1861). (1) Residual air, the volume of air remaining in the chest after the most complete expiratory effort, ranges from 100 to 130 cub. in. (2) Reserve or supplemental air, the volume of air which can be expelled from the chest after an ordinary quiet expiration, measures about 100 cub. in. (3) Tidal air, the volume of air taken in and given out at each ordinary respiration may be stated at about 20 cub. in. (4) Complemental air, the volume of air that can be forcibly inspired over and above what is taken in at a normal inspiration, ranges from about Ioo to 130 cub. in. By vital capacity, which once had an exaggerated importance attached to it, is meant the quantity of air which can be expelled from the lungs by the deepest possible expiration after the deepest possible inspiration; it obviously includes the complemental, tidal and reserve airs, and measures about 230 cub. in. in the Englishman of average height, i.e. 5 ft. 8 in. (Hutchinson). It varies according to the height, body weight, age, sex, position of the body and condition as to health of the subject of observation.

Vital capacity is estimated by means of a spirometer, a graduated gasometer into which air may be blown from the lungs. The residual air, which for obvious reasons cannot be actually measured, may be estimated in the following way (Emil Harless, 1820–1862; Louis Gréhant, b. 1838). At the end of ordinary expiration, apply the mouth to a mouthpiece communicating with a vessel filled with pure hydrogen, and breathe into and out of this vessel half a dozen times-until, in fact, there is reason to suppose that the air in the lungs at the time of the experiment has become evenly mixed with hydrogen. Then ascertain by analysis the proportion of. hydrogen to expired air in the vessel and estimate the amount of the air which the lungs Contained by the following formula:—

v : V+v = p : 100;

V=v(100−p)/p;

where V=volume of air in the lungs at the time of experiment, v=volume of the vessel containing hydrogen, p=proportion of air to hydrogen in the vessel at the end of the experiment. V, then, is the volume of air in the lungs after an ordinary expiration; that is, it includes the residual and the reserve air; if we subtract from this the amount of reserve air ascertained by direct measurement, we obtain the 100–130 cub. in. which Hutchinson arrived at by a study of the dead body.

Volume of Respiration.—It is clear that the ventilation of the lungs in ordinary breathing does not merely depend on the quantity of air inspired at each breath, but also on the number of inspirations- in a given time. If these two values be multiplied together we get what might be called the volume of respiration (Athmungsgrösse, Isidore Rosenthal, b. 1836), in contradistinction to depth of respiration and frequency of respiration. Various instruments have been devised to measure the volume of respiration, all more or less faulty for the reason that they compel respiration under somewhat abnormal conditions (Rosenthal, Gad, Peter Ludwig, Panum (1820-1885), Ewald Hering (b. 1834). From the data obtained we may conclude that the respiratory volume per minute in man is about 366 cub. in. (6000 cub. centim.). In connexion with this subject it may be stated that, after a single ordinary inspiration of hydrogen gas, 6-ro respiration's of ordinary air must occur before the expired air ceases to contain some trace of hydrogen.

Types of Respiration.—The visible characters of respiration in man vary considerably according to age and sex. In men, while there is a moderate degree of upheaval of the chest, there is a considerable although not preponderating degree of excursion of the abdominal walls. In women the chest movements are decidedly most marked, the excursion of the abdominal walls being comparatively small. Hence we may distinguish two types of respiration, the costal and the abdominal, according to the preponderance of movement of one or the other part of the body wall. In forced respiration the type is costal in both sexes, and so it is also in sleep. The cause of this difference between men and women has been variously ascribed (a) to constriction of the chest by corsets in women, (b) to a natural adaptation to the needs of child-bearing in women, and (c) to the greater relative flexibility of the ribs in women permitting a wider displacement under the action of the inspiratory muscles.

Certain Concomitants of Normal Respiration.—If the ear be placed against the chest wall during ordinary respiration we can hear with every inspiration a sighing or rustling sound, called "vesicular," which is probably caused by the expansion of the air vesicles; and with every expiration a sound of a much softer sighing character. In children the inspiratory rustle is sharper and more pronounced than in adults. If a stethoscope be placed over the trachea, bronchi or larynx, so that the sounds generated there may be separately communicated to the ear, there is heard a harsh to-and-fro sound during inspiration and expiration which has received the name of "bronchial."

In healthy breathing the mouth should be closed and the ingoing current should all pass through the nose. When this happens the nostrils become slightly expanded with each inspiration, probably by the action of the M. dilatatores naris. In some people this movement is hardly perceptible unless breathing be heavy or laboured. As the air passes at the back of the throat behind the soft palate it causes the velum to wave very gently in the current; this is a purely passive movement. If we look at the glottis or opening into the larynx during respiration, as we may readily do with the help of a small mirror held at the back of the throat, we may notice that the glottis is wide open during inspiration and that it becomes narrower by the approximation of the vocal chords during expiration. This alteration is produced by the action of the laryngeal muscles. Like the movements of the nostril, those of the larynx are almost imperceptible in some people during ordinary breathing, but are very well marked in all during forced respiration.

The Mechanics of Respiration.—The thorax is practically a closed box entirely filled by the lungs, heart and other structures contained within it. If we were to freeze a dead body until all its tissues were rigid, and then were to remove a portion of the chest wall, we should observe that every corner of the thorax is accurately filled by some portion or other of its contents. If we were to perform the same operation of removing a part of the chest wall in a body not first frozen we should find, on the other hand, that the contents of the thorax are not by any means in such circumstances bulky enough to fill up the space provided for them. If we were to measure the organs carefully we should find that those which are hollow and whose cavities communicate with the regions outside the thorax are all larger in the frozen corpse than in that which was not frozen. In other words, the organs in the thorax are distended somewhat in order that they may completely fill the chest cavity; and the nature of this curious and important condition may best be illustrated by the simple diagrams, figs. 7 and 8 (from Hermann's Physiologie des

Fig. 7.	Fig. 8.

Menschen),—where t is the trachea, l the lung, v the auricle of the heart, k the ventricle, i an intercostal space with its flexible membranous covering. When the interior of the vessel is rendered vacuous by exhaustion through the tube o, the walls of the lungs and heart are expanded until the limits of the containing vessel are accurately filled, while all flexible portions of the walls of the vessel (corresponding to the intercostal membranes and the diaphragm of the thorax) are sucked inwards.

From this description it follows that the lungs, even when the thorax is most contracted, are constantly overs distended, and that, when the cause of this over-distension is removed, the lungs, being elastic, collapse. It further follows that if the thorax is dilated, the flexible hollow organs it contains must perforce be still more distended-a distension which in the case of the lungs is followed by an in drawing of air through the trachea in all cases where the trachea is open. Thus, as the act of respiration is primarily a dilatation of the thorax, the part played by the lungs is, as Galen knew, a purely passive one.

How is dilatation of the thorax effected? It has been pointed out that the rib-planes decline from the horizontal in two directions, viz. from behind forwards, and from the anteroposterior mesial plane outwards; a glance at fig. 9 will make this double sloping clear to the reader. It has, moreover, been explained that the diaphragm arches upwards into the thorax in such a manner that the lateral parts of the arch are vertical and in contact with the inner face of the thoracic walls. This being the structure of the thorax, the enlargement of its cavity is brought about (1) by raising the rib planes until they approach the horizontal, and (2) by depressing the diaphragm and making its rounded dome more cone-like in outline. A moment's consideration will show how these actions enlarge the boundaries of the-thorax. (a) When the postero-anterior slope of the rib-planes is diminished by the raising of the anterior ends of the ribs, the whole sternum is thrust upwards and forwards, and the antero-posterior diameter of the thorax is increased. (b) When the lateral slope of the rib-planes is diminished by the ribs being moved upwards about an axis passing through their sternal and vertebral extremities, it is evident that the lateral diameter of the thorax must be increased. (c) When the muscular portion of the diaphragm contracts, the curves of its dome-like shape are straightened, the whole diaphragm comes to look more conical on section, and the apposition of its lateral parts to the inner surface of the

From Hermann's Handbuch.

Fig. 9.—Showing Slope of Ribs.

thorax is destroyed; the two apposed surfaces are drawn apart much as the leaves of a book might be, and a space is formed between them, into which some portion of the lung slips. (d) When the diaphragm descends it draws with it the whole contents of the thorax; inasmuch as the contents as a whole are conical in shape with the apex upward and are fitted into the conical space of the thoracic cavity, it is clear that the descent of the contents will tend to create a space between them and the thoracic walls; for each stratum of lung, &c., which is adapted to fit a certain level of thorax, will thereby be brought into a lower and (as the thorax is conical) a more spacious level. Hence the descent of the diaphragm causes a much greater enlargement of the thorax than is measured by the mere elongation of the vertical diameter. In this manner the thorax is distended and air is drawn into the lungs. The contraction of the thorax in expiration is brought about by the return of the ribs and diaphragm to their original position of rest.

How the Inspiratory Movements are Produced.—The Rib Movements.—These are caused by the contraction of muscles which are fixed either to the central axis of the body (including under that term the head and vertebral column) or to some point rendered sufficiently stable for the purpose by the action of other adjuvant muscles. Thus the M. levatores costarum arise from the transverse processes of the 7th cervical and eleven upper dorsal vertebrae, and are attached to the ribs below in series; the M. scaleni spring from the cervical vertebrae, and are attached to the anterior parts of the first and second ribs; the M. sternocleido-mastoidei arise from the side and back of the skull, and are inserted into the upper part of the sternum and the clavicle; the M. pectoral is minor arises from the coracoid process of the scapula, and is inserted into the anterior ends of some of the ribs; the M. serratus posticus superior arises from certain of the cervical and dorsal vertebrae, and is inserted into the posterior part of certain of the ribs; the M. cervical is ascend ens (part of the M. erector spinae) arises from certain of the cervical vertebrae, and is inserted into the posterior part of certain ribs. The M. serratus magnus and the M. pectoral is major, which are affixed on the one hand to the upper arm and to the scapula respectively, and on the other to the ribs and to the sternum respectively, may in certain elevated positions of the arm and shoulder act as inspiratory muscles. When all these muscles contract, the ribs are raised in the twofold way already described, some pulling up the anterior ends of the ribs, and others causing the arched ribs to rotate about an axis passing through their vertebral and sternal joints. In addition to the muscles just enumerated, the M. inter cost ales externi are undoubtedly inspiratory muscles. Every external intercostal muscular fibre between a pair of ribs must, when it contracts, of necessity raise bath ribs, as is clearly shown by the accompanying diagram (fig. ro). Here a'b' must be shorter than ab, for if angle BAa=x, then ab2=AB2+ (Bb-Aa)2+2AB(Bb-Aa)cos x; hence ab will be larger the smaller the angle x, for the cosine increases as the angle diminishes. an

Fig. 10.	Fig. 11.

By a similar geometrical treatment of the question it may be shown that the internal intercostal muscles when they contract must of necessity depress both the ribs to which they are attached. If the angle BAc' =x(fig, 11), then c'd'2=AB2-|- (Ac' -Bd')2-2AB(Ac'-Bd') cos x; hence c'd' will be larger the larger the angle x. . The case, however, is not so clear with reference to the anterior portions of the internal intercostals which lie between the cartilages; for it is evident that these fibres have the same direction with regard to the sternum as an axis as the external intercostals have with regard to the vertebral column as an axis; that is to say, the geometrical diagram in fig. ro applies to the inter-cartilaginous internal intercostals as perfectly as it does to the inter-osseous parts of the external intercostals, the inference being that the inter-cartilaginous internal intercostals tend to elevate the pair of ribs between which they stretch. The geometrical argument is, however, overborne by physiological experiment: Martin and Hartwell have observed in the dog and the cat that the internal intercostals throughout their whole extent contract (not synchronously) but alternately with the diaphragm; hence we must conclude that their function throughout is not inspiratory like that of the diaphragm, but expi-ratory.

The Movements of the Diaphragm.—The muscular fibres of the diaphragm are arranged in a radial manner, or, more strictly speaking, in a manner like the lines of longitude on a terrestrial globe. The central tendon of the diaphragm corresponds to the pole of such a globe. The contraction of the fibres is expendcd on straightening the longitudinal curves rather than on pulling down the central tendon to a lower level; in fact, the central tendon moves very little in ordinary respiration. H ow the Expiratory Movements are Produced.-The action of inspiration disturbs many organs from the position of rest into which gravity and their own physical properties have thrown them. The ribs and sternum are raised from the position of lowest level; the elastic costal cartilages are twisted; the elastic lungs are put upon the stretch; the abdominal organs, themselves elastic, are compressed and thrust against the elastic walls of the belly, causing these to bulge outwards. In short the very act of inspiration stores up, as it were, in sundry ways the forces which make for expiration. As soon as the inspiratory muscles cease to act these forces come into play, and the position of rest or equilibrium is regained. It is very doubtful whether any special expiratory muscles are called into action during ordinary respiration. The internal intercostals may in man be exercised in ordinary expiration (although they are certainly not so exercised in the dog and the cat); but in laboured expiration many muscles assist in the expulsive effort. The muscles forming the belly-walls contract and force the abdominal contents against the relaxed diaphragm in such a manner as to drive it farther and farther into the thorax. At the same time by their attachment to the lower edge of the thorax these same muscles pull down the ribs and sternum. The M. triangular is sterni, which arises from the back or thoracic aspect of the sternum and lower costal cartilages and is inserted into the costal cartilages higher up, can obviously depress the ribs. So also can the M. serratus posticus inferior, which arises from the thick fascia of the loins and is inserted into the last four ribs. So also can the M. quadratus lumborum, which springs from the pelvis and is attached to the last rib. Indeed there is hardly a muscle of the body but may be called into play during extremely laboured respiration, either because it acts on the chest, or because it serves to steady some part and give a better purchase for the action of direct respiratory muscles.

Certain Abnormal Forms of Respiration.

Coughing.—There is first a deep inspiration followed by closure of the glottis. Then follows a violent expiratory effort which bursts open the glottis and drives the air out of the lungs in a blast which carries away any light irritating matter it may meet with. The act is commonly involuntary, but may be imitated exactly by a voluntary effort.

Hawking, or Clearing the Throat.—In this act a current of air is driven from the lungs and forced through the narrow space between the root of the tongue and the depressed soft palate. This action can only be caused voluntarily.

Sneezing.—There is first an inspiration which is often unusually rapid; then follows a sudden expiration, and the blast is directed through the nose. The glottis remains open all the time. The act is generally involuntary, but may be more or less successfully imitated by a voluntary effort.

Snoring is caused by unusually steady and prolonged inspirations and expiration's through the open mouth, -the soft palate and uvula being set vibrating by the currents of air.

Crying consists of short deep inspirations and prolonged expiration's with the glottis partially closed. Long-continued crying leads to sobbing, in which sudden spasmodic contractions of the diaphragm cause sudden inspirations and inspiratory sounds generated in larynx and pharynx.

Sighing is a sudden and prolonged inspiration following an unusually long pause after the last expiration.

Laughing is caused by a series of short expiratory blasts which provoke a clear sound from the vocal chords kept tense for the purpose, and at the same time other inarticulate but very characteristic sounds from the vibrating structures of the larynx and pharynx. The face has a characteristic expression. This act is essentially involuntary, and often is beyond control; it can only be imitated very imperfectly.

Yawning is a long deep inspiration followed by a shorter expiration, the mouth, fauces and glottis being kept open in a characteristic fashion. It is involuntary, but may be imitated.

Hiccough is really an inspiration suddenly checked by closure of the glottis; the inspiration is due to a spasmodic contraction of the diaphragm. The closure of the glottis generally leads to a characteristic sound.  (A. G.*) 

(4) Pathology of the Respiratory System

In the following article we have to give an account of the more important pathological processes which affect the lungs, pleurae and bronchial tubes. In the aetiology of pulmonary affections, the relations between the lungs and the external air, and also between them and the circulatory system, are important. The lungs are, so to speak, placed between the right and left cavities of the heart, and the only way for the blood to pass from the right ventricle to the left side of the heart, except in cases of a patent foramen ovale or other congenital defect forming a communication between the two sides of the organ, is by passing through them. The result is that not only may they become diseased by foreign material carried into them by the blood, but any obstruction to the flow of blood through the left side of the heart tends sooner or later to engorge or congest them, and lead to further changes. Through the nose and mouth they are in direct Connexion with the external atmosphere. Hence the variable condition of the air as regards temperature, degree of moisture, and density, is liable to produce directly various changes in the lungs, or to predispose them to disease; and the contamination of the air with various pathogenic germs and irritating particles in the shape of dust, is a direct source of many lung affections.

Bronchitis, or inflammation of the mucous membrane of the bronchial tubes, has been generally attributed to exposure to atmospheric changes. It occurs with great frequency in the extremes of life, and it is in early childhood and in old age that it is more liable to be fatal. Bronchitis may often follow exposure to cold, but that low temperature in itself is not sufficient to cause it is shown by the fact that the crews of arctic expeditions have been singularly free from diseases usually attributed to cold, but on their return to moist germ-laden atmospheres have at once been affected. Children reared in heated rooms with lack of ventilation are peculiarly susceptible to attacks on the slightest change of temperature. Bronchitis is also frequently caused by cardiac and renal diseases, and by the extension of inflammatory diseases of the upper air passages (as rhinitis, laryngitis or pharyngitis), while blockage of the nasal passages by adenoid or other growths may, by causing persistent mouth-breathing, lead to bronchial infection. Before the bacterial origin of disease was understood, bronchitis was attributed solely to what is termed “catching cold,” and the exact relation of the chill to the bacterial infection is still unknown. It is probable that the chilling of the surface of the body by exposure causes congestion of the mucous membrane, the presence of a virulent micro-organism being then all that is required to produce bronchitis. It is generally accepted that in persons living in the pure air of the country the small bronchi and air-cells are sterile (Barthel in the Zentralblatt für Bakteriologie, vol. xxiv.). Bacteria are arrested on their way by the leukocytes of the nasal mucous membrane and by the vibration of the ciliated epithelium of the upper air passages. The mucous membrane of the upper bronchi is, however, tenanted by various micro-organisms such as the diplo-bacillus of Friedlander, bacillus coli communis, micrococcus tetragenus, &c., and it is considered by William Ewart that these organisms may in certain conditions of their host become virulent. “Specific” bronchitis occurs in the course of a specific infective disease (e.g. influenza, measles or whooping cough) and is due to the specific micro-organism gaining access by the mucous membrane of the respiratory tract. Cases have been known in which the diphtheria bacillus has been so localized. In glanders, small-pox, syphilis and pemphigus, the infective micro-organism is carried to the bronchi by the blood stream. In common or “nonspecific” bronchitis, streptococci, pneumococci and staphylococci are found in the sputum together with Friedlander's bacillus and the bacillus coli communis. Microscopically the bronchi show hyperaemia of the mucous and sub mucous coats, and the whole wall becomes infiltrated with polymorphonuclear leukocytes and round cells- Many cells undergo mucoid degeneration, and there is abundant epithelial proliferation. A large quantity of mucus is secreted by the glands, and the lumen of the bronchi contains an exudate consisting of mucus, degenerated leukocytes and cast-off epithelial cells.

In the rare form of bronchitis known as fibrinous or plastic bronchitis a membranous exudate is formed which forms casts of the bronchi, which may be coughed up. The casts vary from an inch to six or seven inches in length, with branches corresponding to the divisions of the bronchi from which they come. The cast consists of mucus and fibrin in varying proportions. The exact pathology of this variety is still undetermined.

Bronchitis may affect the whole bronchial tract, or more especially the larger or the smaller tubes. It may occur as an acute or as a chronic affection. In the acute form the inflammation may remain limited to the bronchial tubes and gradually subside, or it may lead to inflammation of the surrounding lung tissue, giving rise to disseminated foci of inflammation of greater or less extent throughout the lungs (catarrhal or bronchopneumonia). This is a common complication of bronchitis, especially where the smaller tubes are affected, and is more frequently seen in children than adults. In cases of chronic bronchitis the affection, as a rule, begins as a slight ailment during the winter, and recurs in succeeding Winters. The intervals of freedom from the trouble get shorter, and in the course of a few years it persists during the summer as well as the winter months. A condition of chronic bronchitis is thus established. The persistent cough which this occasions is one of the chief causes of the development of the condition of emphysema, where there is a permanent enlargement of the air-cells of the lungs with an atrophy of the walls of the air vesicles. The emphysema occasions an increase in the shortness of breath from which the person had previously suffered, and later, in consequence of the greater difficulty with which the blood circulates through the emphysematous lungs, the right side of the heart becomes dilated, and from that we have the development of a general dropsy of the subcutaneous tissues, and less and less perfect aeration of the blood.

The death rate from bronchitis in England and Wales during 1908 was: males 1102, females IO83 per million living. The death rate for the five years 1901-1905 was 1237 per million for all sexes. The death rate for the twenty years 1888'I9OS consistently showed a slight decline.

Diseases of Occupations.-We all inhale a considerable amount of carbonaceous and other foreign particles, which in health are partly got rid of by the action of the ciliated cells lining the bronchial tubes, and are partly absorbed by cells in the wall of the tubes, and carried in the lymph channels to the bronchial lymphatic glands, where they are deposited, and cause a more or less marked pigmentation of the tissues. Part of such pigment is also deposited in the walls of the bronchial tubes and the interstitial tissue of the lungs, giving rise to the grey appearance presented by the lungs of all adults who live in large cities. In certain dusty occupations, such as those of stone masons, knife-grinders, colliers, &c., the foreign particles inhaled cause trouble. The most common affection so produced is chronic bronchitis, to which becomes added emphysema. In some cases not only is bronchitis developed, but the foreign particles lead to an increase of the fibrous tissue round the bronchi and in the interstitial tissue of the lungs, and so to a greater or lesser extent of fibroid consolidation. As this fibrous tissue may later undergo softening and cavities be formed, a form of consumption is produced, which is named according to the particular occupation giving rise to it; e.g. stonemasons' phthisis, knife-grinders phthisis, colliers' phthisis. It should, however, be pointed out that these dusty occupations are probably not so frequently the cause as was at one time taught of these simple inflammatory fibroid changes in the lungs with their subsequent cavity formation; individuals engaged in such occupations are apt to suffer from a chronic tuberculosis of the lung associated with the formation of much fibrous tissue, and the occupation simply predisposes the lung to the attacks of the tubercle bacillus. The term pneumonia is frequently used of different forms of inflammation of the lungs, and includes affections which pimp run different clinical courses, present diverse appearmon, , ances after death, and probably have different exciting causes. It would be better if the term acule pneumonia or pneumonia fever were reserved for that form of acute inflammation of the lungs which is usually characterized by sudden onset, and runs an acute course, which terminates generally by crisis from the fifth to the tenth day, the inflammation leading to the consolidation by fibrinous effusion of the greaser part or whole of one lobe of a lung. Acute pneumonia usually occurs in a sporadic form, and is most prevalent in the United Kingdom from November to March. Occasionally it is epidemic, and there is evidence to show that sometimes it is an infective disease. There' is great difficulty, however, in being quite certain that the occurrence of the disease in those who have been attending upon or brought into intimate Connexion with sufferers from pneumonia is the result of infection, for such cases may be due to an epidemic of the disease, or to the various individuals attacked having been exposed to the same cause.

Formerly acute croupous or lobar pneumonia was thought to be due to “catching cold", we now know it to be an infectious disease resultant on the invasion of one or more specific micro-organisms. The chief micro-organisms which have been found to be present during an attack of acute pneumonia are the micro coccus lanceolatus or pneumococcus of Frankel and Weichselbaum, which is found in the inflamed lung in a large majority of cases and is capable of producing pneumonia when inoculated into guinea-pigs. Sternberg demonstrated the presence of the pneumococcus in the saliva of healthy individuals; it tends, however, in this case to vary in form. The micro-organism differs in virulence in given strains; thus one epidemic may be more severe than another; and it tends to increase in virulence in its passage through the human subject. The exact conditions necessary for the production of increased virulence in the organism causing an attack of lobar pneumonia are not yet determined, but are usually ascribed to lowered states of the health and to atmospheric conditions. The pneumococcus produces in the human organism an intracellular toxin, but the question as to whether it can also produce a soluble toxin in the living body is still debated. The difficulty of obtaining sufficient quantities of the toxins of this organism has prevented the production of antisera of high potency. In lower animals, less potent sera have proved successful in protecting against a fatal dose of pneumococci. The change effected by the administration of a serum is produced by causing a change in the pneumococci, which causes them to be more easily destroyed by the phagocytes. The element which brings about this change is termed an opsonin; see BLOOD and BACTERIOLOGY (ii). The bacillus pneumonia of Friedliinder is also said to be found in a certain percentage of cases, but a number of observers deny its presence in pure culture in primary croupous pneumonia.

Unlike many acute diseases, pneumonia does not render a person less liable to future attacks; on the contrary, those who have been once attacked must be looked upon as more prone to be affected again. Acute pneumonia usually attacks the whole or greater part of one lobe 'of one lung, but more than one lobe may be affected, or both lungs may be involved. The disease produces a solid and airless condition of the affected part owing to a fibrinous exudation taking place into the aircells and smaller bronchial passages. In favourable cases the exudationfis partly absorbed and partly expectorated, and the lung returns to its normal healthy condition; in others, death may ensue from the extent of lung affected, or from the/ spread of the inflammation to other parts, as for instance the pericardium or meninges of the brain. In such cases it is interesting to note that the same micro-organism has been found in the inflammatory exudation in the pericardium or on the meninges as in the pneumonia lung; probably the organism had been absorbed from the lung, and was the cause of the secondary inflammations. In cases of death from uncomplicated pneumonia a very variable extent of lung is involved. In some cases this result may be ascribed to the weakness of the individual and especially of the heart, but in others the virulence of the micro-organisms and the toxins which they have produced is probably the more correct explanation. The improvement in a patient suffering from pneumonia usually commences suddenly, with a rapid fall in the temperature. The day on which this “ crisis” takes place varies, but most commonly it appears to be the seventh from the initial rigor (22 % of the cases, Iiirgensen). It may, however, occur a few days earlier or later, being observed in about 74% between the fifth and the ninth day of the disease (jiirgensen). The disease occasionally ends in the formation of an abscess, in gangrene, or in fibroid induration of the lung, but these terminations are rare.

The death rate of acute pneumonia for England and Wales in 1908 was 1383 per million living of the population., Broncho-pneumonia.-jlt is usual to recognize a form of inflammation of the lungs which differs from the above lobar pneumonia. and in which small patches of consolidation are usually scattered throughout the lower lobes of both lungs. This broncho- or catarrh all pneumonia is usually preceded by an attack of bronchitis, to which it bears an intimate relation. In some cases the small foci of inflammation may run together so as to affect the greater part of a lobe of a lung, and the distinction between such a form of broncho-pneumonia and lobar pneumonia presents such difficulties in the view of some observers, that they have refused to recognize any essential difference between the two. Usually, however, it is not difficult to distinguish the two affections both clinically and anatomically. Broncho-pneumonia is especially seen as a. complication of bronchitis, and while it more frequently attacks children than young adults, it is not uncommon in old people, especially secondary to bronchitis. It is frequent in children after acute infectious fevers, especially measles and diphtheria, and in cases of whooping-cough. It differs from the above-mentioned pneumonia in that it does not usually attack the whole of a lobe of a lung, but occurs in small disseminated patches more especially throughout the lower lobe of both lungs. The accompanying fever is more irregular than in the preceding form, and the disease usually runs a more prolonged course. It is an extremely fatal affection in both the very young and old. Young persons who have suffered from it are not infrequently attacked by pulmonary tuberculosis subsequently. It must be admitted that we are even less certain of its bacteriology than we are of that of lobar pneumonia. In some cases Frankel's pneumococcus is found, and in others various other micro-organisms. Many of the latter are doubtless saprophytic, and are not the essential cause of the disease, but it is not probable that any one particular form of organism accounts for all forms of broncho-pneumonia.

The bacteriology of broncho-pneumonia presents no one micro-organism which can be definitely said to cause the disease. The micro-organism most frequently found, either alone or associated with other bacteria, is the pneumococcus, which occurred in 67% of a series investigated by Wollstein. Other organisms found are the streptococcus, particularly in bronchopneumonia following infectious fevers, the staphylococcus aureus and albus, and Friedlander's bacillus. In some cases the bacillus infiuenzae alone has been found, and the Klebs-Lofiier bacillus in cases following upon diphtheria. When the disease is associated with pulmonary tuberculosis the tubercle bacillus is found.

The tuberculous virus, the tubercle bacilli, may gain entrance to the lungs through the inspired air or by means of the blood Tube" or lymph currents. Also in some cases it has been cu,0s, s demonstrated that tubercle bacilli may infect the glands of the mesentery following the ingestion of the milk of tuberculous cattle. In this the Government Commissions of Great Britain and Germany as well as the United States Bureau of Animal Industry confirm the findings of private investigators. It may be well here to summarize the views generally held as to infection. In the first place, the doctrine of inherited disease is discredited, and the doctrine of specific susceptibility is in doubt. Infants are known to be extremely susceptible, and this susceptibility lessens with increasing age, adults requiring prolonged exposure. As a mode of infection the sputum of diseased persons is of great importance. Infected food, especially milk, comes next, together with food infected by flies; and the mother's milk is a minor source. Infection is not often received through the skin, but most frequently through the mucous membrane of the mouth, air passages and intestine; occasionally the infection is alveolar. Pulmonary tuberculosis is often secondary to a latent lymphatic form. The tubercle bacillus was discovered by Koch in 1882, and since then it has become generally accepted that the bacillus varies in type. The bacilli have been classified by A. G. Foullerton into (a) occurring in fishes and cold-blooded animals, (IJ) in birds, (0) in rats, (d) in cattle, (e) in man. Exactly how far they

• The term catarrhal pneumonia has been usually regarded as

synonymous with the term broncho-pneumonia, and this usual nomenclature has been maintained in the present article. We must, however, recognize that all simple acute broncho-pneumonia's are not purely catarrhal in the strict pathological sense. For instance, a considerable amount of fibrinous exudation is not infrequently present in the patches of broncho-pneumonia, and some of the cases of septic broncho-pneumonia can scarcely be accurately termed Cdlllffhdl.

are interchangeable and can affect the human race is not definitely settled. They may be different varieties of the same species caused by differentiated strains of a common stock, or may be distinct but generically allied species. Von Behring considers that the bovine type may undergo modification in the human body, a theory which may lead to a complete change in our beliefs in the mode of entry of the bacillus. Recent investigators have put forward the view that the tubercle bacillus is not a bacterium, but belongs to the higher group known as streptotricheae or mould fungi.

The action of the tubercle bacillus upon the tissues, like most other infectious agents, gives rise to inflammatory processes and anatomical changes, varying with the mode of entry and virulence of the micro-organism. The most characteristic result is the formation throughout the lungs in the form of small scattered foci forming the so-called miliary tubercles. Such miliary tuberculosis of the lungs is frequently only 3. part of a general tuberculosis, a similar tuberculous affection being found in other organs of the body. In other cases the lungs may be the only or the principal seat of the affection. The source whence the tuberculous virus is derived varies in different cases. Old tubercular glands in the abdomen, neck and elsewhere, and tuberculous disease of bones or joints, are common sources whence tubercle bacilli may become absorbed, and occasion a general dissemination of miliary tubercles in which the lungs participate. Where the source of infection is an old tuberculous bronchial gland or a focus of old tubercle in the lung, the pulmonary organs may be the only seat of- the development of miliary tuberculosis for a time; but even then, if life is sufficiently prolonged, other parts of the body become involved. Acute miliary tuberculosis of the lungs is not infrequently a final stage in the more chronic tuberculous lesions of the different forms of pulmonary phthisis.,

In pulmonary phthisis, or consumption, the disease usually commences at the apex of one lung, 'but runs a very variable course. In a large majority of cases it remains conhned to one small focus, and not only does not spread, but undergoes retrograde changes and becomes arrested. In such cases fibrous tissue develops round the focus of disease and the tuberculous patch dries up, often becoming the seat of the deposit of calcareous salts. This arrest of small tuberculous foci in the lung is doubtless of very frequent occurrence, and in post mortem examinations of persons who have died from injuries or various diseases other than tubercle it is common to find in the lungs arrested foci of tubercle, which in the majority of instances have never been suspected during life, and probably have occasioned few, if any, symptoms. It has been shown that in more than 37% of persons, over 21 years of age, dying in a general hospital of various diseases, there is evidence of arrested tubercle in the lungs. As such persons are chiefly drawn from the poorer classes, among whom tubercle is more common than among the well-to-do, this high percentage may not be an accurate indication of the frequency with which pulmonary tubercle does become arrested. It does, however, show that the arrest and the healing of tuberculosis of the lungsis by no means infrequent, and that it occurs among those who are not only prone to become infected, but whose circumstances are least favourable to the arrest of the disease. These facts indicate that the human organism does offer a resistance to the growth of the tubercle bacilli. A focus of pulmonary tubercle may become arrested for a time and then resume activity. In many cases it is difficult to say why this is so, but often it is clearly associated with. a lowering in the general health of the individual. It cannot be too strongly insisted that the arrest of a tuberculous focus in the lung is a slow process and requires a long time. Commonly a person in the early stage of phthisis goes away to a health resort, and in the course of a few weeks or months improves so much that he returns to a densely populated town and' resumes his former employment. In a short time the disease shows renewed activity, because the improved conditions were not maintained long enough to ensure the complete arrest of the disease.

Instead of the tuberculous focus becoming arrested, it may continue to spread. The original focus and the secondary ones are at first patches of consolidated lung. Later, their central parts soften and burst into a bronchus; then the softened portion is coughed up, and a small cavity is left, which tends gradually to increase in size by peripheric extension and by merging with other cavities. This process is repeated again and again, and sooner or later the other lung becomes similarly affected. At any stage of the softening process the blood vessels may become involved and give rise by rupture to a large or a small hemorrhage (haemoptysis). It not infrequently happens that such haemoptysis may be the first symptom that seriously attracts attention. At a later period hemorrhage frequently takes place in large or small amounts from the rupture of vessels, which frequently are dilated and form small aneurysms in the walls of cavities. A fatal termination may be hastened by the absorption by means of the blood vessels and lymphatics of the tuberculous virus from some of the foci of disease, and the occurrence therefrom of a local miliary tuberculosis of the lungs or a general tuberculosis of other organs. The rapidity with which the destructive process spreads throughout the lung varies considerably. We therefore recognize acute phthisis, or galloping consumption, and chronic phthisis. In the acute cases the softening progresses rapidly and is associated with the development of very little fibrous tissue; probably various forms of microorganisms other than the tubercle bacilli assist in the rapid softening. In the more chronic cases there is development of much fibroid tissue, and the disease is associated with periods of temporary arrest of the tubercular process. The expectoration from cases of pulmona phthisis contains tubercle bacilli, and is a source of danger torfiealthy individuals, in whom it may produce the disease. Attendance on persons suffering from pulmonary phthisis involves very little risk of infection if prqper care is taken to prevent the expectoration becoming dry an disseminated as dust; perfect cleanliness is therefore to be insisted upon in the rooms inhabited by a phthisical person. The tubercle bacilli soon lose their virulence in the presence of fresh air and sunshine, and therefore these agents are not only desirable for the direct benefit of the phthisical patient, but also are agents in preventing the development of fresh disease in healthy individuals.

Although the tubercle bacilli are the essential agents in the development of pulmonary tuberculosis, there are other conditions which must be present before they will roduce the disease. It is probable that large numbers of individiials are exposed to the action of tubercle bacilli which gain entrance to the pulmonary tract, and yet do not give rise to the disease, because the conditions of their growth and multiplication do not exist. In such cases we may consider that the seed is present, but that the soil is unsuitable for its growth. Certain families appear more predisposed to tuberculosis than others.

The most important circulatory disturbances met with in the lungs are those seen in cases of dilated heart, with or without disease of the mitral valve, when engorgement g;°;;, m of the pulmonary vessels sets up a condition of venous engorgement of the lungs. This may lead to various changes. After it has lasted a. variable time, and if it is very intense, serous transudation occurs into the substance of the lung and the alveoli, and thus a condition of pulmonary dropsy or oedema is established. The venous engorgement also predisposes the subjects of such heart affections to bronchitis and pneumonia. In disease of the mitral valve, in cardiac dilatation and in simple feebleness of the heart, such as is seen in old age and after debilitating fevers, especially typhoid, there is commonly developed a venous congestion of the bases of the lungs, forming the so-called hypo static congestion of those organs, and to this is frequently added pneumonia. In long-standing cases of pulmonary congestion brought about by disease of the mitral valve and dilatation of the heart, a certain amount of fibrous tissue may be found in the interstitial tissue of the lungs, and from transudation of certain elements of the blood we get the formation in the newly formed fibrous tissue of blood pigment. In these cases blood pigment is found in the cells, in the pulmonary alveoli, and such cells also carry the pigment into the interstitial tissue. This condition constitutes the state known as brown induration of the lungs. Acute congestion of the lungs occurs as part of the first stage of pneumonia. It also probably exists during violent exertion, and may possibly be brought about by excitement.

Another circulatory disturbance of great importance is that arising from blocking of the pulmonary artery. or its branches by an embolus or a thrombus. Where the Embousm obstruction takes place in the main vessel, death and rapidly ensues. Where, however, a small branch of Thromthe vessel is occluded, as frequently occurs from a "sl" coagulum forming in the right side of the heart, or in the pulmonary vessels in cases of disease of the mitral valve, or in dilatation of the heart, or from the detachment of a small veget.ation from disease of the tricuspid or pulmonary valves, a hemorrhagic exudation takes place, forming a patch of consolidation in the lung (hemorrhagic infarct). As this hemorrhagic exudation takes place not only into the substance of the lung, but also into the bronchial tubes, such lesions are usually associated with spitting of blood (haemoptysis), The increased tension produced in the pulmonary vessels in cases of mitral disease may also probably lead to the formation of hemorrhagic exudation's into the lungs, apart from the occurrence of embolism or thrombosis. Usually the occurrence of pulmonary embolism and the formation of hemorrhagic infarcts in the lungs mark an important epoch in the course of a case of heart disease. It usually occurs at a late stage of the affection, " and not infrequently contributes materially to a fatal termination. It is probable that many of the cases of pneumonia and pleuritic effusion, coming on in cases of valvular heart disease and of cardiac dilatation, owe their origin to an embolus and to the formation of a hemorrhagic infarct.

The term asthma is commonly applied to a paroxysmal dyspnoea of a special type which is associated with a variety of conditions. In true spasmodic asthma there A th may be no detectable organic disease, and the par- S ma oxysms are generally believed to be due to a nervous influence Which, acting upon the bronchial muscles, produces a spasm of the tubes, or, acting through the vaso-motor branches of the sympathetic, produces a congestion of the bronchial mucous membrane. The most probable theory is that lately advanced, that it is caused by a profound toxaemia. An'organism has been isolated, which is said to be the cause of certain cases of asthma, and the fact that benefit has been said to follow treatment by a vaccine is in favour of this view. The 'exciting cause may not be at all apparent, even on the most careful observation and examination of the sufferer, but in other cases the attacks may be brought about by some reflex irritation. Nasal polypi and other diseases of nasal mucous membrane have been shown in some cases to be a cause of asthma. Irritation of the bronchial mucous membrane appears to be one of the most common, but it is usually difficult to say exactly in what the irritation consists. .

The sputum in true asthma is typical, consisting of white translucent pellets like boiled tapioca. These pellets consist of mucus arranged in a twisted manner and known as Curschmann spirals; they also contain Charcot-Leyden crystals, degenerated epithelium and leukocytes, of which the majority are eosinophiles. The spirals consist of a central solid thread round which the mucus is arranged in spiral form. The twisting has been attributed to a rotatory motion of the cilia, helped by the spasm of the bronchial muscles. Allied to true asthma is the bronchial asthma frequently met with in the subjects of bronchitis and emphysema. In such cases the irritation evidently proceeds from the inflamed bronchial mucous membrane. Hay asthma is the variety in which the pollen of certain plants, especially grasses, is the exciting cause of the paroxysms. In cardiac feebleness, in valvular disease of the heart, and in cardiac dilatation, we may get dyspnoeic attacks of a more or less paroxysmal nature, to which the- term cardiac asthma has been applied. Similarly, to a form of dyspnoea met with occasionally as a manifestation of uraemia in chronic Bright's disease the term of renal asthma has been given.

Pleurisy, or inflammation of the pleura, is a very common affection, and is met with under different forms. In many p|em, sy instances we have simply the pouring out, over a greater or less area of the surface of the pleura, of a fibrinous exudation which may become absorbed or undergo organisation, a certain amount of thickening of the pleura, and adhesion's of the two layers resulting. Such cases form the group known as cases of dry pleurisy. In other instances a greater or lesser amount of serous exudation takes place into one or other pleural cavity, forming the cases of serous pleuritic effusion. In others the exudation into the pleural cavity is purulent, giving rise to the condition known as empyema or purulent pleuritic effusion. The occurrence of dry pleurisy is probably very frequent, and leads to small pleural adhesion's which cause little or no inconvenience. In post-mortem examinations of persons who have died from various diseases it is common to find such pleural adhesion's present, although they have never been suspected during life. Pleurisy in one or other of the above forms may come on in a person apparently in good health (idiopathic pleurisy), or it may follow a fracture of the ribs or other injury to the chest. It is not uncommonly secondary to some other disease; thus it is almost a constant accompaniment of acute lobar pneumonia. In such cases the effusion is most commonly a simple fibrinous one, which with the subsidence of the primary disease is in great part absorbed. In other cases of pneumonia we get a certain amount of serous effusion into the pleura; and sometimes, especially in children, the pneumonia is followed by the development of an empyema. Pleurisy with effusion is also frequently a complication of valvular heart disease and dilatation of the heart, and in such cases is often associated with the formation of superficial pulmonary infarcts. It is also seen in many other diseases of the lungs. For instance, in chronic pulmonary phthisis pleuritic adhesion's over various parts of the lungs are the rule; and we also frequently get serous effusion into the pleura as a complication of the various forms of pulmonary tuberculosis. Purulent effusion is less common in phthisis, but it is the rule where the pleura is perforated by the necrosis of a tuberculous focus in the lung and the establishment of a communication between the pleura and a tuberculous cavity and the bronchial tubes (pyopneumrmolhorax), a combination in which there is both air and pus in the pleural cavity. Secondary pleurisy is also seen in an extension of the disease from neighbouring parts, as from peritonitis, sub-diaphragmatic abscess, and suppuration in the liver or spleen. As a secondary disease, pleurisy is also known in the course of various forms of nephritis, rheumatism, and the acute specific diseases.

Cases formerly classed as idiopathic pleurisy are now known to be caused by certain micro-organisms. These vary in relation to the character of the effusion. The most frequent is the tubercle bacillus, which is generally present in sero-fibrinous effusions. In this case the pleurisy is really secondary to a possibly unrecognized tuberculous infection either of the lung or pleura. In purulent effusions the pneumococcus may occur as a pure infection, or the streptococcus pyogenes or the staphylococcus may be present. Mixed infections occur in 21% of purulent effusions, and varieties of other organisms, such as the influenza bacillus, the typhoid bacillus, the Klebs-Lofiler bacillus and the colon bacillus, have been occasionally found. There are at least five types of pulmonary emphysema; (1) hypertrophic, idiopathic or large-lunged emphysema; (2) senile or small-lunged emphysema; (3) compensatory emphysema; (4) acute vesicular emphysema; (5) interstitial or interlobular emphysema. Two points are usually admitted: that emphysema appears only in lungs that are congenitally weak, and that the exciting cause is increased intravesicular tension. When one or more lobules are cut off from the working part of the lung the neighbouring vesicles become distended. Should the plugging of the lobule remain permanent, typical emphysema results. This happens in illnesses inducing violent respiratory efforts, such as chronic bronchitis, whooping cough and asthma. In large-lunged emphysema the lung is excessively large, and does not collapse on opening the chest wall. Microscopically two lesions are notable. The septa between the vesicles are atrophied, many have disappeared and the vesicles have coalesced; the loss in lung tissue diminishes the vascular field of the lung and tends to imperfect aeration, whence the dyspnoea. The elastic tissue of the lung is also lost. In small lunged emphysema there is a condition of senile atrophy. The lung is smaller than normal, and the intravesicular septa are destroyed. In this case the primary cause is atrophy of the bronchi, and increased air pressure is not a factor. Compensatory emphysema is that which develops in a portion of a lung in which the other portion is the seat of a lesion, such as pneumonia. Occasionally it is merely physiological, but sometimes here too the septa undergo atrophic changes. Acute vesicular emphysema is hardly a pathological variety, and is really rapid distension coming on during an attack of asthma or angina pectoris. The variety is temporary only. Interstitial emphysema is characterized by the presence of air in the inter stitial connective tissue of the lung. It is usually due to rupturl of the air vesicles during paroxysms of coughing. (T. H *; H. L. H.)

(5) SURGERY or THE RESPIRATORY SYSTEM

About the middle of the 19th century, Manuel Garcia demonstrated the working of the vocal cords in the living subject, by placing a flat mirror of about the size of a shilling at the back oi the mouth, and throwing strong light on to it from a concave mirror fixed upon the observer's forehead. By the use of a laryngoscope and a cocaine spray the most irritable throat can now be made tolerant of the presence of the small mirror, and thus the medical man is enabled to make a prolonged and thorough examination of the interior of the larynx and even to perform delicate operations upon it. Foreign bodies which have become caught in the larynx can thus be seen and extracted, and small growths can be satisfactorily removed even from the vocal cords themselves.

A foreign body in the air-passages may be impacted above the vocal cords, and the prompt thrusting down of a finger may dislodge it and save the person from death by suffocation. If there is doubt as to the site of the impaction, and the symptoms are urgent (as is likely to be the case) immediate laryngotomy should be done. In this operation a tube is introduced through the crevice which can easily be felt in the middle line of the neck, between the thyroid and cricoid cartilages. The procedure is easily and quickly accomplished. It is, moreover, often resorted to when the surgeon is about to perform some extensive operation in the mouth which must needs be accompanied by free hemorrhage. Laryngotomy having been done, and the pharynx having been plugged with gauze, the air passages can be kept free of blood during the whole operation. If the foreign body be such a thing as a button, cherry-stone, sugar-plum or coin, it may at once set up alarming symptoms of spasmodic suffocation. But when the first alarm has quieted down, the attacks are likely to be only occasional, as when the article, drawn up with the expired air, comes in contact with the under aspect of the vocal cords. It may be that in a violent fmt of coughing it will be expelled, but, if not, the surgeon must be at hand ready to perform tracheotomy when the urgency of the symptoms demands it. Tracheotomy is the making of an opening into the trachea, the air-tube below the larynx. It is unsafe to leave a child with a foreign body loose in its windpipe, on account of the risk of sudden and fatal asphyxia. Possibly the X-rays may show its exact position and give help in its removal. But, in any case, the safest thing will be to perform tracheotomy and to leave the edges of the opening into the windpipe wide asunder, so that the object may be coughed out -the nurse being on guard all the while. The operation of tracheotomy is sometimes urgently called for in the case in which the air-way has become blocked by a child having sucked hot water from the spout of a kettle or teapot, or in the case of obstruction by the swelling of the acute inflammation of laryngitis or of diphtheria. Should the air-way through the larynx become narrowed by the presence of a growth which does not diminish under the influence of iodide of potassium, the question may arise as to whether it should be dealt with by splitting the thyroid cartilage and holding the wings apart, or by the removal of the whole larynx. For such growths are often malignant. If the wide infection of the lymphatic glands of the neck suggests that no radical operation should be undertaken, a bent silver tube may be introduced below the growth (tracheotomy) in order to provide for the entrance of air. This will get over the difficulty of breathing, but it cannot, of course, do more than that.

Acute laryngitis is very often due to diphtheria. The symptoms are those of laryngeal obstruction, together with constitutional disturbances of various kinds. The old-fashioned nurse called the disease “croup”—a term devoid of scientific meaning (see Diphtheria). In an ordinary catarrhal case, leeches and fomentation's may suffice, though sometimes tracheotomy or incubation is called for. But if bacteriological examination shows the presence of diphtheritic bacilli, antitoxin must at once be injected. (See also Lung.)  (E. O. *)