junction being occupied by the heart (see Fig. 42, p. 143); the cavity of the lungs contains: 1. All that portion of the circulation called pulmonary, that is, the upper circle; 2. The point of junction of these two circles, viz., the heart; and 3. The lateral origins of the lower circle, or the summit of the arterial and of the venous cone. The changes in intrathoracic pressure affect all these three portions.

This influence is counteracted, however, in the case of the circulation of the thorax, by the fact that the venous cone of this circulation is subjected to the same variations, and simultaneously, as the arterial cone; and as the differences of intravascular pressure which produce the circulation remain the same, no change in the circulation occurs; the circulation is but slightly influenced, except by the more or less complete expansion of the alveoli, which occasions a greater or less permeability of the capillary vessels, or, in other words, of the base of the pulmonary cone.

The influence of respiration is much more sensibly felt in the heart an expiration made with force, as in any great exertion, causes immense pressure upon the heart, and as the coats of this cavity are thin, and easily compressed, a deformation ensues. Weber has made experiments to show this, by first making an extremely deep inspiration, and then very forcible movements of expiration, the glottis being closed, and the arms kept fixed against his sides. After the lapse of a few seconds, a change is observed in the pulse, which becomes slower, and, at length, ceases entirely; if the ear is placed over the chest, no sound is heard, whence we may infer that the heart has ceased to beat. If the experiment be continued, the person loses consciousness, and thus, in spite of himself, returns to his original state of life and circulation.

If, however, the person remains passive, the stoppage of the heart continues, and may end in death; this is probably the case with persons who are squeezed to death in a turbulent crowd, the outside pressure being continued even after syncope has been produced. In experiments or accidents of this kind, the stoppage is not the same in all parts of the

1 A case has been reported by the American editor (" Boston Med. & Surg. Journal," Dec. 11, 1873, p. 577), in which a rupture of the right auricle was caused by compression of the thoracic walls. Another accident (reported in the Gaz. Hebd.,' " March 27, 1874, p. 199, by MM. Doubre and Charpentier) of compression of the thorax between a wheel and the ground, resulted also in the rupture of the right auricle.

heart it takes place chiefly in the right auricle. The effect produced may be shown by exposing the heart of a frog, and compressing it at the point of the opening of the vena cava, and thus preventing the entrance of the blood: the entire heart then ceases to beat, because the ventricle, as well as the auricle, receiving no more blood, there is no longer on the inner surface of these cavities any impression which may serve as a point of origin of the reflex action which causes the pulsation of the heart. If the man or animal, however, is in a state of perfect health, it is not very likely that this mechanism of compression will produce death. Indeed, though the heart stops, the arteries by means of their elasticity drive their contents into the veins, which become turgid, while the summit of the venous cone quickly pours into the heart a mass of blood, thus setting the heart in motion again. The mechanism which we have described, however, explains the so-called voluntary stoppage of the heart, of which some persons have professed to be capable: the will acts upon the heart, in this case, only through the medium of respiration.

Respiration produces a similar effect on the general circulation, the top of the two cones (the arterial and the venous) being included in the thorax. We know that at the top of the venous cone the pressure is so slight that it may be represented by 0 or 1; at the top of the arterial cone, on the other hand, the contraction of the ventricle produces a pressure which may be reckoned as 25 (see p. 143).

10%

Let us suppose that, by means of a strong expiration, a pressure of is produced in the cavity of the thorax: the pressure at the top of the venous cone will then be, an enormous pressure for this part of the circulating system, an essential feature of its working condition being the absence of all pressure. The consequence will be a considerable reflux into the veins; this reflux into the veins near the heart is prevented by the numerous valves with which they are furnished, and it is only at the top of the cone that the pressure is made. As the blood continues to flow, and finds an obstruction to its further progress, stagnation follows, accompanied by distention of the veins adjacent to the thorax. This is chiefly seen in straining, and in those processes which are accompanied by it, as parturition, defecation, &c.; the signs of the stagnation of the blood are injection of the eyes, redness of the face, cessation of the cerebral circulation, and, finally, the suppression of the functions of the brain (vertigo and even apoplexy): a state of less entire stagnation, often

repeated, causes dilatation of the veins, varices, vascular hypertrophy of the thyroid gland, &c.

This influence of expiration produces equally marked effects in the arterial cone. At the top of this cone, the pressure produced by the ventricle is 25. If we assume the pressure in the thorax at, in the arterial cone it will be 10%; this causes the arterial blood to flow much faster, there being here nothing which can counteract or delay the effect of this increase of pressure; and the fluid is forced into the arteries by two pumps, the heart and the thorax. It is true that the slackening of the flow of the blood in the veins has a tendency to counterbalance its increased rapidity in the arteries, but, in spite of this, immense pressure is produced on the entire current of the circulation, accompanied by a strong tendency to hemorrhage, ruptures of aneurisms, varicose dilatations, &c.1

The phenomena which follow a diminution of pressure in the thorax, produced by a violent inspiratory movement, are entirely different from the above. The pressure at the top of the venous cone then becomes less than 0, or, in fact, aspiration of blood by the veins, an increased acceleration of the circulation of the venous blood; if the blood does not flow in sufficient quantity to satisfy this aspiratory demand, the coats of the veins become relaxed, and show a tendency to collapse. In the veins which are near the thorax, and are especially under the influence of this aspiration, the relations between the coats of the veins and the aponeuroses are such that these vessels remain constantly open: the aspiration is thus continued to veins more remote from the heart. In a surgical operation, therefore, if one of the veins near the thorax be opened, the outer air, at the moment of inspiration, may be drawn into the interior of the vessel, an occurrence which is generally followed by speedy death.

Under the influence of this inspiratory aspiration, the aortic pressure, which is, falls to, or, causing a slackening of the circulation, diminished tension of the vessels, feebleness of the pulse, &c. But while the conditions of expiration were favorable to hemorrhage, these resist it, and, in order to arrest the flow of blood, it is sometimes only necessary to cause the patient to make several deep inspirations.

These results, at which we have arrived by simple reason

1 See F. Guyon, "Note sur l'Arrêt de la Circulation Carotidienne pendant l'Effort." Archives de Physiologie, 1866.

ing, have been experimentally verified by Marey, by means of the graphic method. This physiologist has reached the following conclusions in regard to the effect produced on the circulation by respiration. Respiration affects the pulsation of the heart; it not only causes variation in the line of the whole tracing, but imparts to the pulsations produced during inspiration an amplitude and a form which differ from those observed during expiration; when respiration is stopped, the pulsation of the heart slackens and diminishes in intensity: these modifications are explained by the fact that the blood passes less readily through the lung when the latter is not in action. After an effort (forcible attempt at expiration, the glottis being closed) the pulsation of the heart assumes special features. The left ventricle makes its action intensely perceptible, while the blood in the auricle is violently precipitated at the period at which the diastole begins. If the person experimenting breathe through a narrow tube, the relation between the pulsation of the heart and the respiratory movements is changed: while the respiration becomes less frequent, the pulsations become more rapid.

We also find in the pulse differences corresponding to the different respiratory types (thoracic and abdominal types, see p. 295). The thoracic type exhibits a diminution of pressure during inspiration, the whole extent of the line traced rising again during expiration. The abdominal type produces exactly the contrary effect (Marey). We give (Fig. 83) a

P. normal.

Inspiration.

Expiration

Fig. 83. Abdominal type.

graphic tracing of the pulse, while respiration is taking place during forcible contraction of the diaphragm. We see that in the abdominal type (as in the thoracic) the pulsation diminishes, and, finally, disappears, while the arterial tension increases.1

We may mention, in conclusion, and rather as an experi

1 P. Lorain, Etudes de Médecine Clinique." Le Pouls, 1870.

mental curiosity than as an important physiological fact, the influence, in a contrary direction, which may be observed to exist between the heart and the lungs. "We know that the pulsation of the heart changes the condition of the intrathoracic pressure; supposing the thorax to be immovable, the afflux of blood which takes place at each diastole, should compress the air in the lungs, and, if the glottis is open, give rise to a slight expiration; in the same manner, when the heart is suddenly emptied, the blood which gushes out of the thorax is replaced by a certain quantity of air which enters through the trachea. In the normal condition, we are scarcely sensible of this, on account of the constant modifications produced by respiration in the respiratory capacity of the thorax. The fact, however, can easily be made plain, by placing the trachea of a dog in communication with the registering apparatus, and then puncturing or severing the medulla oblongata of the animal by a single stroke: respiration ceases immediately, while the heart continues to beat for some minutes, its pulsations being registered through the medium of the air in the trachea" (P. Bert).

IV. CHEMICAL PHENOMENA OF RESPIRATION.

WE understand how the air and the blood are brought into contact with each other, and also by what mechanism they are constantly renewed; we have now to examine the gaseous exchanges which are produced by this contact taking place in the lungs: what these are we shall see by ascertaining the changes made in the air and in the blood, during their passage through the lungs.

A. Modifications in the air exhaled.

We know that 10 cubic metres (10,000. litres) of air are received into the lungs daily, and that nearly an equal quantity is expelled: we thus retain about or of the air inhaled; at the first examination, however, the exhaled gas is found undiminished in quantity, on account of the vapor contained in it, which occupies a considerable space. A still more important change which takes place in the air is the loss of oxygen, which is replaced in a great measure by carbonic acid, one-fifth of the amount of the 10 cubic metres of air inhaled is oxygen (21 parts of O. to 79 parts of N.); this is equal by weight to 2 kilos. of oxygen. In the air ex