Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 9)

Chronic lobular emphysema is chiefly of interest in connection with the other pulmonary diseases which give rise to it. The mechanism of its production is like that of acute lobular emphysema, but the diseases occasioning it being chronic the emphysema to which they give rise is equally permanent. At the apex of the lung, its most common situation, it is very often associated with tubercle in a calcareous state. The changes accompanying this deposit of tubercle favor the loss of elasticity in the vesicles of the apex, and the violent expiratory efforts, with closure of the glottis, occurring in the attacks of cough to which phthisical patients are subject, force the air into this part especially, and also into other regions of less resistance, and thus occasion permanent distension of the vesicles.

SYMPTOMS AND SIGNS.—The signs of this form of emphysema are so often masked by those proper to phthisis that the detection of the former is difficult or impossible. This, however, is of no practical importance in respect to treatment. At times the distension of the vesicles at the apex is so great as to produce bulging in the supra-clavicular region and to overcome the dulness due to deposit by the resonance it occasions.

TREATMENT.—No special treatment beyond that of the causative affections is required.

3. Hypertrophic Lobar Emphysema.

This is a substantive affection, and is much the most important form of the disease, both in its origin and development and in the consequences to which it leads. Though sometimes limited to one lung, or even to a single lobe of one lung, yet it more commonly involves the greater part of both lungs, which are increased in size, as shown by the alteration of the contour of the chest during life and by the appearance of the organs after death. This enlargement of a lobe or of a whole lung is of course the aggregate of the increase in size of the individual vesicles, the changes in which form the pathological units of the disease.

ETIOLOGY.—In no disease is the study of etiology as throwing light on treatment, both medicinal and hygienic, of more value than in emphysema, the important question being as to whether it takes its origin from some immediate mechanical cause acting upon the healthy cell-walls, and thus distending them, or whether they suffer such distension only when they have been previously weakened by some degenerative process in their tissue. The importance of determining this point correctly with reference to treatment is obvious.

In partial and lobular emphysema the change may have been wrought by causes mechanical in their nature and directed specially to the affected parts, such as have been already referred to; but in the general diffused or lobar form of the disease, in which by degrees the greater part or the whole of a lung is involved, we are almost compelled to assume the existence of some degenerative process or tendency coextensive with the malady and determining its existence. That any one form of degeneration is present in all cases has never been proved; indeed, it may be said to have been disproved. Rainey's view, that the change in the air-cells is essentially dependent on fatty degeneration of their walls, was based mainly on observations made upon a single case, and, although favored by the eminent authority of C. J. B. Williams, it has not been substantiated. The same thing must be said of Sir William Jenner's teaching, that fibroid degeneration is the essential lesion. Though both fibroid and fatty changes are found in not a few cases, yet in others a careful examination has failed to detect either the one or the other of them, so that neither can be regarded as the essential condition explaining all cases. Nevertheless, it is probable in the highest degree that a degenerative change of some kind, due to imperfect or perverted nutrition of the cell-walls, always exists in general lobar emphysema, though its nature may sometimes elude observation.

In cases of well-marked emphysema there may be no discoverable morphological changes in the walls of the alveoli, though, as remarked by Hertz,² "a tissue-relaxation may be present in the lung without our being able to recognize any corresponding microscopic abnormality."

² Ziemssen's Cyclop., vol. v. p. 373.

It may be said, then, that while in partial or local emphysema the alteration in the air-vesicles may be effected by extraordinary efforts brought to bear upon healthy cell-walls, in general or lobar emphysema, on the other hand, it may be produced by ordinary efforts acting upon weakened and diseased cell-walls. The morbid change is probably not in all cases alike, being sometimes fatty, sometimes fibroid, degeneration, and in other cases of a kind not ascertained.

In addition to other considerations, the markedly hereditary nature of emphysema in not a few instances would of itself render the existence of some constitutional predisposing cause highly probable. On this point A. T. H. Waters³ quotes the observations of Greenhow and Jackson. Out of 42 cases collected by Greenhow, 23 showed an hereditary tendency, and in 28 reported by Jackson, 18 were of emphysematous parentage. In stating his belief that substantive or general emphysema is the result of some degenerative process, Waters bases it on the following considerations: 1st. The high degree of development which the disease often reaches, without any previous history of violent or long-standing cough, in connection with either bronchitis, whooping cough, or any similar affection. 2d. The frequency with which the disease attacks the whole of both lungs, and the uniform character of the morbid changes often observed throughout all parts of the lungs. 3d. The hereditary nature of the disease, as shown by observations. 4th. The manner in which the disease is influenced by certain remedial measures which are known to act beneficially on other diseases attended with degeneration of tissue.

³ Diseases of the Chest, pp. 122, 123.

As to the nature of the immediate exciting cause of emphysema, whether in the general or local form, different views have been maintained. The most important of these are the inspiratory and expiratory theories.

The former of these theories, that in accordance with which the disease is referred to inspiratory action, was maintained by Laennec, and under the influence of his authority was at one time generally accepted. In accordance with this view, the existence of bronchitis is an important factor in the production of emphysema, as undoubtedly it often is in the lobular form. The dilatation of the air-vesicles was attributed to their over-distension by inspiratory efforts allowing the free entrance of air, the escape of which was impeded by bronchial mucus. Inspiration was thus regarded as a more powerful act than expiration, which was considered too feeble to drive the air beyond the accumulated mucus. In this way the air was supposed to accumulate in gradually increasing amount within the cells, which thus became distended.

But in opposition to this view it has been shown by Hutchinson's researches that Laennec was wrong in supposing inspiratory power to be greater than that of expiration; and it is further opposed by the researches of Mendelssohn and Traube, and those of Gairdner, which have shown conclusively that the presence of a pledget of mucus in a bronchial tube, so far from causing distension of the air-vesicles to which it leads, must ultimately ensure their collapse. The collapse thus occasioned, which is most common in the lower parts of the lungs, may lead, partly perhaps through inspiratory pressure, to vicarious emphysema in the upper portions, which receive a relatively larger quantity of air, in accordance with Williams' theory of negative inspiratory pressure.

It is true, then, as maintained by Laennec, that bronchitis may occasion emphysema, but the emphysema does not occur in the vesicles to which the affected tubes directly lead, nor from the force of inspiration applied to these vesicles, as Laennec taught, but in other portions of the lungs.

The expiratory theory affords a more satisfactory explanation of emphysema than does the inspiratory theory, and one more completely in accordance with the physiology of respiration and the anatomy of the thorax.

In ordinary expiration, in which the lungs are uniformly and equably compressed by the chest-walls, there is nothing tending to force air into one part of these organs more than into another, and thus produce emphysematous dilatation. But in forced expiration, such as occurs in the act of coughing, it may be plainly seen, if the chest be uncovered, that the air is driven upward to the top of the lungs, so as to produce a perceptible bulging in the supra-clavicular region. This bulging is notably increased in the coughing-spells of emphysematous subjects; and this fact is urged by Sir William Jenner both as throwing light upon the expiratory act as a principal factor in the disease, and as accounting for the special frequency of emphysema in the upper parts of the lungs. The explanation of this phenomenon is found in the circumstance that in the strong expiratory efforts of coughing the abdominal muscles force the diaphragm upward, and thus compress the lungs from below; at the same time the strong lateral anterior and posterior thoracic walls resist pressure, while the superior part of the thorax, covered over with fascia, but not completely protected by a bony structure, offers least resistance. To this unprotected part of the lungs and to the free margins and borders, which contain normally the smallest amount of air, will the strong currents produced by violent expiratory efforts be driven, so as to cause distension of their vesicles. Thus, the frequent coughing-spells of bronchial catarrh, so commonly associated with emphysema, give rise to the expiratory efforts which are the immediate cause of the emphysema.

While, therefore, it is probable that in some cases and to a certain degree inspiration may have a share in occasioning emphysema, yet expiration is to be regarded as a more important and more frequent factor in its production. This, at least, is probably the case in partial and lobular emphysema, and in some instances of the lobar form where the disease gradually spreads throughout a lobe. But in rapidly-diffused and extensive lobar emphysema such an explanation cannot always be admitted, because sometimes the disease advances steadily, so as to involve the greater part of one or both lungs without the occurrence of any paroxysms of cough which could distend the air-cells by their violent expiratory efforts. In such cases the only distending force would seem to be that of ordinary inspiration, which, while it might have no effect upon healthy lung-tissue, may easily be supposed to exercise sufficient dilating power upon air-cells, the walls of which are in a state of degeneration, and, thus being unnaturally weak, yield to pressure.

SYMPTOMS AND SIGNS.—One of the earliest symptoms of emphysema is shortness of breath; and, though at first it may not be very marked, yet as the disease advances it becomes more and more urgent, especially on going up stairs or walking up hill. Distension of the stomach by a full meal is likely to induce it, and even a slight degree of bronchial catarrh may render it extremely distressing. This symptom is due chiefly to two causes: First, the obliteration of numerous capillaries in the pulmonary system, occasioned by the thinning and destruction of the cell-wells in which they ramify, interferes with oxygenation, so that an increased number of inspiratory acts is required to supply the deficiency, and thus respiration is hurried; and, secondly, the impairment of the natural elasticity of the air-vesicles prevents the expulsion of their contents; the residual air remains, therefore, unchanged, and cannot supply oxygen to the blood; and thus increased expiratory efforts are made in order to expel the stagnant air and obtain a fresh supply. Notwithstanding this increase of both inspiratory and expiratory action, the movements of the chest are but slight. As far as bronchial catarrh is a cause of dyspnoea in emphysematous patients, improvement may take place in the warm dry weather of summer, when this symptom is often much mitigated.

Cough is a very constant symptom, varying in degree with the extent of bronchial catarrh. The act of coughing is feeble and expectoration is effected with difficulty—so much so that sometimes the retained secretion threatens suffocation.

Asthma occurs in paroxysms, and as a distinct phenomenon from the dyspnoea which is more or less constant. The asthmatic seizures often come on in the night after the patient has been asleep; they are characterized by orthopnoea and constriction in the chest, and generally subside with free expectoration.

The physical signs of emphysema are highly characteristic and of great importance. On inspection a peculiar conformation of the chest is observed when the emphysema has lasted for some time, the departure from the normal form gradually increasing in the progress of the disease until, in advanced cases, a degree of deformity is produced which is strikingly characteristic. In the earlier stages, or if the emphysema is local and partial, the alteration in the chest-wall consists only of a prominence corresponding with the dilated portion of the lung. But when the disease is general and occupies a considerable portion of both lungs, a rounded, convex, or barrel-like form of the thorax is produced, most noticeable in the upper part, and due to increased prominence of the ribs. The thoracic portion of the spine becomes more curved, and thus throws the shoulders forward, producing a stooping attitude. The intercostal spaces at the upper part of the chest are frequently effaced by the pressure of the enlarged lung, while at the lower part the depression of these spaces may be increased, especially during inspiration, by the action of the diaphragm. The enlargement of the thorax as a whole is chiefly due to the changes in its upper part, the lower part appearing sometimes by contrast to have lessened in volume. This, however, is in most cases apparent rather than real; but in some instances the dimensions in the lower part of the chest are actually lessened.

The respiratory movements in well-marked emphysema are characteristic and peculiar. The dilatation of the chest which is sought to be accomplished by muscular action is small and disproportioned to the amount of effort put forth, notwithstanding that the need for air keeps the sterno-mastoid and scaleni muscles in constant action. The reason of this is that, the lungs being distended nearly to their utmost capacity, there is but little room for further expansion. As there is only slight enlargement on inspiration, so with expiration the walls of the thorax contract but little at their upper part.

The result, therefore, of their muscular efforts is that the ribs are lifted and the sternum carried forward, so that the whole chest rises and falls in respiration as if its walls formed a solid case. But the character of respiration is by no means the same in all cases of emphysema. More than forty years ago Stokes⁴ called attention to the different modes of breathing in different cases accordingly as there is or is not displacement of the diaphragm; and his observations have more recently been reaffirmed by Waters⁵ and others. In the one class of cases the diaphragm retains its normal position and the upper part of the chest is very prominent, probably because the disease is chiefly in the upper portion of the lungs. Here there is but little descending movement of the diaphragm in inspiration and the abdomen remains flat. In the other class the diaphragm has been displaced and pushed downward by the enlarged lungs, which have probably been involved in the disease throughout their whole extent. In these cases the abdomen is protruded more or less with every inspiration. The difference between the two types of breathing is important, as in the latter class of cases there is more advanced and extensive disease than in the former, the symptoms being more urgent, and especially the dyspnoea greater. Inspection of the chest shows that the movement of inspiration is more quickly accomplished than that of expiration, which is prolonged, labored, and often wheezing in character.

⁴ Diseases of Chest, 2d ed., p. 173.

⁵ Diseases of Chest, p. 140.

Percussion and auscultation furnish signs of the utmost importance for determining the existence of emphysema which are in direct accordance with the physical conditions giving rise to them.

Increased resonance on percussion is observable over all portions of the lungs when the disease is general, but it is most marked at the upper part and along the anterior borders. When the disease is partial, the increased resonance is limited to the portions of the chest-wall over the affected areas. This sign is of course due to the greater amount of air in the distended vesicles. In very marked cases the resonance sometimes loses the vesicular and approaches the tympanitic character. There is very little, if any, further increase of the resonance on full inspiration. This is unlike what occurs in health, and is due to the fact that the capacity of the distended lungs is not relatively increased in emphysema, as it is in health, by the act of inspiration.

Over the cardiac region the normal dulness on percussion is lessened or entirely superseded by resonance from the overlapping of the heart by the distended lung. In partial emphysema the heart may escape this encroachment and its area of dulness may not be lessened; and even in some rare cases where the disease is general and far advanced the same thing may be observed, from the lung being bound by pleuritic adhesions, so that it cannot expand in the direction over the heart. But, as a very general rule, it will be found in hypertrophic emphysema that the normal præcordial dulness is lessened or absent. When this is observed the heart is in some cases forced downward, its beat being felt most distinctly in the epigastrium; and in other cases it is carried directly backward, so that its impulse can hardly be detected at all.

Over the posterior wall of the chest percussion gives a clear note at a lower level than in health, because the dilated lung extends farther down toward the bottom of the thorax.

The signs afforded by auscultation are highly characteristic of emphysema, and, like those of percussion, in direct relation with the physical condition of the lungs. The respiratory sounds are notably feebler, because the amount of air entering and leaving the lungs at each act of respiration is less than in health. The distended lungs can admit only a small amount of air at each inspiration, and from their diminished elasticity they can expel but a small amount at each expiration. This feebleness is directly proportioned to the degree of the disease, or, in other words, to the amount of distension; for the greater the distension, the less movement of the lungs and the less play of air. If the disease be unequally advanced on the two sides of the chest, the respiratory murmur will correspondingly vary, being feebler on the side where the disease is most advanced.

Besides this change in intensity, there is also an alteration in the rhythm of the respiratory acts corresponding to what has been referred to above as observable on inspecting the chest. The ratio of inspiration and expiration is always changed in well-marked emphysema—so much so as to be in many instances reversed, the expiratory occupying more than double the time of the inspiratory act. Inspiration is short and quick, because the air enters freely and the limit of the possible expansion of the lungs is speedily reached. Expiration is prolonged, because there is a loss of their normal elasticity, and an effort is made by voluntary action of the expiratory muscles to expel the stagnant residual air. This alteration in rhythm is eminently characteristic of emphysema when the disease is far advanced and occupies a considerable portion of the lungs. Feebleness of respiratory murmur is an earlier sign than alteration in rhythm, and may be observed before any marked prolongation of the expiratory act occurs and before there is any very positive increase of resonance on percussion. Hence it is of great importance if not otherwise explicable, as it sometimes is by unusual thickness of the chest-walls, because it indicates, taken by itself, an early stage of emphysema in which treatment may be most likely to be beneficial. It is sometimes found in very advanced stages of emphysema that the respiratory sounds are almost totally inaudible; but in general, while both murmurs are feeble, expiration is more appreciable than inspiration. If, however, the disease is associated with bronchitis, either constantly or intermittingly, the proper auscultatory signs of the accompanying affection may be observed, though modified by the emphysema. Thus, moist and dry râles according to the stage of the bronchitis, sibilant or sonorous, subcrepitant or mucous râles according to the size of the bronchial tube involved, may be heard, the abnormal sounds being notably prolonged during expiration.

It can hardly be doubted that the sign referred to by Laennec as "perfectly pathognomonic of emphysema," and described by him as "the dry crepitant râle with large bubbles" (râle crépitant sec à grosses bulles), is in most cases, if not always, dependent upon coexistent bronchitis. Certainly, many cases of emphysema are met with in which, in the absence of bronchitis, no such sound is heard. The signs or combination of signs which are indeed "perfectly pathognomonic of emphysema" are increased resonance upon percussion, associated with marked feebleness of respiration and prolonged expiration. This association of signs is always indicative of emphysema, because it can be explained only by the physical conditions involved in this disease.

Auscultation of the cardiac region gives results corresponding with those afforded by percussion and palpation. When the lung is distended sufficiently to overlap the heart, the sounds belonging to the latter organ will be more or less indistinct and distant, and sometimes scarcely audible. If the heart be pushed to the right or downward instead of being driven backward, the sounds may still be distinct, but they are out of place and have their greatest intensity under the sternum or at the epigastrium. The proper signs of hypertrophy or dilatation of the heart, which may be revealed on post-mortem examination, and the mechanism of which will be referred to farther on, are to a great degree masked during life; for the overlapping lung prevents the detection of increased cardiac dulness by percussion or increased impulse by auscultation.

Palpation of the chest serves to confirm the evidence supplied by inspection. The effacement of the intercostal spaces, the lessened mobility of the ribs, and the situation of the apex-beat of the heart are signs of importance of which the sense of touch takes cognizance.

COMPLICATIONS AND SEQUELÆ.—Bronchitis is one of the most frequent of the affections complicating emphysema. In the partial form of the malady it often sustains, as has been already seen, a direct causal relation to the emphysema. When the disease is diffused and general, bronchitis is sooner or later almost always encountered, and is then of a congestive rather than an inflammatory type, being often unaccompanied by fever, and in part due to interference with the circulation through the smaller bronchial arteries. For, as some branches of these vessels are distributed in the interlobular areolar tissue, and others ramify upon the walls of the smallest bronchial tubes, a constant pressure may be made upon them by the dilated air-vesicles, and this obstruction of the circulation through them may occasion passive congestion. The bronchitis accompanying advanced emphysema is generally attended with free secretion, amounting in some cases to a bronchorrhoea so profuse as seriously to imperil life by suffocation, the danger being increased by the difficulty in expectorating that exists. The discharge from the bronchi is often in such cases of a muco-purulent character. So urgent is the danger sometimes arising from this complication that unless it be relieved death may quickly ensue. The face and other portions of the surface become livid or leaden, the whole body more or less cool, the pulse weak and hurried, and copious râles are audible even without applying the ear to the chest. Life is threatened both by the accumulation in the respiratory passages obstructing the entrance of air, and by the tendency to the formation of heart-clots from the embarrassment to the pulmonary circulation and the consequent malaëration of the blood.

Another very common complication of emphysema is asthma, which, indeed, is sure to occur in greater or less degree of violence and at longer or shorter intervals in all cases where the disease has become extensive. The attacks often come on in the night, arousing the patient from sleep. The tendency to a nocturnal occurrence of asthma may be due to the recumbent position favoring passive congestion of the lungs, and to the diminished activity of the respiratory process during sleep when it is not aided by voluntary effort. From both these causes an irritation may be set up determining reflex spasm of the bronchi. Moreover, the paroxysmal occurrence of asthmatic attacks is an illustration of the general law in accordance with which morbid neurotic conditions frequently occur intermittingly, though the eccentric cause of them is constantly existing, as witnessed in the subjects of epilepsy or angina pectoris. The frequent recurrence of these attacks of spasmodic asthma is in all probability the cause of the hypertrophic state of the muscular tissue in the bronchial tubes which is often met with as a part of the morbid anatomy of emphysema.

The structural alterations of the heart that occur in emphysema are the results, more or less directly, of the mechanical conditions involved in the disease. Earliest in the sequence of changes affecting this organ are non-compensative hypertrophy and dilatation of its right chambers; and by some writers it has been maintained that the alterations due to emphysema are found only on this side of the organ. This, however, has been completely disproved by extended observations, and it has been shown that left hypertrophy and dilatation, while not such direct consequences of emphysema as the corresponding changes on the right side, are yet frequently encountered, and are plainly due to the disease in the lungs.

The hypertrophy and dilatation of the right chambers of the heart are easily understood when it is considered that the constant pressure of the enlarged air-vesicles of the emphysematous lungs interferes more and more with the circulation through the pulmonary capillaries, and that there is thus a constant impediment to the onward course of the blood from the pulmonary artery, and a continuous backward pressure within the right ventricle and auricle. The effort to overcome this pressure leads to hypertrophy, and ultimately, as this effort is less and less effective, to dilatation of the right chambers.

It would appear as though the readiness with which the alterations on the right side of the heart may be explained has led, if not to their being more frequently observed, yet at any rate to their being more emphasized, than are the corresponding changes on the left side. Some writers have referred only to those on the right side, giving the correct explanation of them, but making no mention of the similar condition on the other side. Thus, Rokitansky⁶ refers to the obstruction to the circulation occasioned by the expansion of the air-cells in pulmonary emphysema as one of the causes of dilatation of the right ventricle and auricle, but says nothing of similar changes on the left side. Other pathologists, however, as Lebert and Gairdner, have shown that at least in long-standing emphysema the left side is also not infrequently involved in disease.

⁶ Path. Anat., vol. iv. p. 130.

What explanation, then, is to be given of those changes in the left chambers which, if less frequent than hypertrophy and dilatation on the right side, are yet certainly not uncommon? Evidently, they cannot be referred to obstruction in the pulmonary circulation; for this, while producing backward pressure into the right compartments, must, on the contrary, lessen the amount of blood received by the left chambers, which therefore have no excessive labor thrown upon them from this cause, and so cannot become hypertrophied in such a manner.

The explanation is probably to be found partly, as suggested by Waters,⁷ in the altered position of the heart occasioned by the emphysema, and partly in the remora of the venous circulation.

⁷ Diseases of the Chest, p. 152.

There are thus two factors to be considered, the first of which applies to the right heart as well as to the left. As to this first, the more extensive the emphysema the greater is the degree of displacement that the heart undergoes; and as the normal position of the ventricles with reference to the arteries emanating from them offers the easiest course to the blood-currents, any departure from this position causes an embarrassment, and consequently increased labor, in the left chambers as well as the right; hence one explanation of the hypertrophy on both sides. As to the second factor, the obstruction to the general capillary circulation necessitates an increased effort of the left ventricle to overcome it; and so, as far as it is concerned, another cause of hypertrophy is in operation.

It is frequently observed in advanced emphysema that there is a marked disproportion between the forcible heart-beat and the feeble radial pulse, the former being due to the hypertrophy, and the latter to the small amount of blood received and propelled by the heart.

Besides these changes in the size of the heart and the thickness of its walls, constituting hypertrophy or dilatation as the case may be, a displacement of the entire organ is a not uncommon consequence of emphysema. The direction of this displacement may vary, so that it may be either directly backward, the heart being overlapped by the distended lung, or it may be downward or to the right of the sternum. A much greater degree of displacement of the heart may result from the pressure of pleural effusion than from emphysema of the lung; but when due to pleurisy it is generally of shorter duration and admits of perfect restoration, whereas when caused by emphysema it is usually permanent. The writer has at present under his care a case of extreme displacement of the heart to the right, the apex-beat being felt and seen to the right of the sternum; but in this patient, while extensive supplementary emphysema of the left lung, due to the almost complete incapacitation of the right lung, has probably had a share in causing the displacement, yet a more important cause of it has been contraction of the right side of the chest, the result of absorption of an old pleural effusion which has left the lung bound back and adherent. This case closely resembles one reported by Stokes as presenting "the singular phenomenon of the displacement of the heart to the right side, consequent on the removal of an effusion of the right side."⁸

⁸ Diseases of the Chest, p. 467.

Dropsy is to be regarded as one of the most notable complications and consequences of emphysema; for when the disease is of long standing the loss of balance between the arterial and venous circulation occasioned by the obstruction to the passage of blood through the lungs gives rise ultimately to effusion of the serum, which is first seen in the lower extremities, and may subsequently become general.

In consequence of the disturbances in the circulation and respiration which have been considered, it is not surprising that the nutritive function should be impaired, as is found often to be the case in the subjects of old emphysema, who present a cachectic and anæmic appearance, partly due to malaëration of the blood, and partly to imperfect performance of the assimilative functions occasioned by passive congestion of the alimentary tract. Still another cause may be found, as suggested by Hertz,⁹ in the insufficient supply of the elements received from the lymph through the imperfect emptying of the thoracic duct into the distended left subclavian vein.

⁹ Ziemssen's Cyclop., vol. v. p. 382.

There has been much discussion as to the connection between emphysema and pulmonary phthisis, some pathologists having held that the two affections are incompatible with each other, and that emphysema may thus exercise a prophylactic influence against phthisis. Careful and extensive observations furnish no valid grounds for such a belief. So far as supplementary emphysema is concerned, it is a common thing to find emphysematous patches at the bases and along the margins of lungs the apices of which are tuberculous. In such cases the increased inspiratory labor thrown upon some portions of the lungs in consequence of impaired function of other parts accounts for the emphysema. But, besides this common condition, cases are met with in which the emphysematous portions are themselves beset with tubercle. Such a case is reported by Waters,¹⁰ in which an emphysematous lung was found studded with tuberculous matter, which on microscopic examination was seen in the air-sacs and ultimate bronchial tubes.

¹⁰ Diseases of the Chest, p. 156.

While emphysema ensures no absolute immunity from tuberculous diseases of the lungs, yet the physical condition involved in it does lessen the liability to tuberculous deposit, which is favored by active hyperæmia, and active hyperæmia is not apt to occur in an emphysematous part of a lung. It likewise lessens the liability to such pulmonary affections as hæmoptysis, oedema, and perhaps pneumonia. The diminished pulmonary circulation occasioned by the shrinking and obliteration of the capillaries explains the infrequency of hæmoptysis. The same cause, together with the smaller amount of interlobular areolar tissue that the emphysematous lung contains, lessens the liability to oedema, because there are both less blood from which the serum can be effused and less of the tissue in which it can be collected and held. And the infrequency of pneumonia in an emphysematous lung is owing to the absence of conditions favoring hyperæmic changes.

DURATION AND TERMINATIONS.—No definite limit can be assigned to the duration of emphysema, as the progress of the disease varies very much in different persons according to the underlying cause, and according also to the care taken in avoiding those influences which promote its development, such as physical exertion or exposure to cold and damp. Many persons with extensive emphysema, if they can secure favorable climatic conditions, and thus escape attacks of bronchial catarrh, will live on for years in comparative comfort, whereas in others the disease may advance with rapidity to a fatal issue if their situation in life necessitates hard work or exposure to causes that induce frequent attacks of bronchitis. The immediate cause of a fatal termination is generally either apnoea resulting from extensive bronchitis, or asthenia from impaired action of the heart, or both of these conditions together.

PATHOLOGY AND MORBID ANATOMY.—From examinations made at various stages of the disease in those who have died of emphysema it is seen that the earliest change is a dilatation of the air-sacs, which become gradually more distended, their walls growing thinner, until they may yield at some points and perforations occur. As the disease advances the perforations become larger and more numerous, until the walls are so far destroyed that several sacs or even lobules are blended together, forming only one cavity. The alveoli may be dilated to the size of a mustard-seed, or even a pea, without undergoing rupture, and may thus become visible by the unaided eye; but when the emphysematous spaces are as large as a hazelnut or small walnut they consist of numerous air-sacs, or even of several lobules, fused together by the atrophy and breaking down of the interalveolar and interlobular tissues. When the cavities thus produced by the fusion of several sacs or lobules are in the subpleural portion of the lung, they will sometimes project beyond the adjacent surface, so as to form appendages of the size of a small walnut which appear to be connected with the lung by a pedicle. It is remarked by Waters that perforation of the cell-walls is much more common in lobar than in lobular emphysema, even though the dilatation of the sacs may be as great or greater in the latter than in the former affection; which is due, no doubt, to the fact that the extensive and diffused changes in the lobar form are dependent upon a degenerative process, in consequence of which the walls are specially prone to give way.

All the changes just referred to, from the earliest and slightest degree of distension to extreme attenuation and perforation of the walls, with final coalescence of several sacs and the formation of appendages, may be met with at the same time in different parts of the same lung. The most advanced changes are found most commonly at the apices and free margins of the lungs, while in the deeper parts an earlier stage only may have been reached.

The blood-vessels in the cell-walls are diminished in calibre by the atrophy of these walls and by the constantly-increasing air-pressure, so as to admit only the watery part of the blood; and thus is explained the pigmentary change in the surrounding tissues where the blood-corpuscles collect. Ultimately, many of the vessels are obliterated, and the backward pressure thus induced extends to the pulmonary artery, and thus gives rise to hypertrophy and dilatation of the right side of the heart, as already explained. It is this pressure on the vessels in the alveolar walls that causes also passive hyperæmia of the bronchial mucous membrane, and thus produces a tendency to bronchitis, which so often occurs as a consequence of emphysema, while, again, primary bronchitis is frequently a factor in the production of the disease. The principal change in the bronchial tubes, in addition to the hyperæmia and softening of their mucous membrane due to coexisting bronchitis, is a hypertrophic thickening of their muscular coat, the result probably of repeated spasmodic action in the asthmatic attacks.

DIAGNOSIS.—The chief points by which the diagnosis of emphysema is determined have already been referred to under the head of Symptoms and Signs. The most important of these are the auscultatory signs; for, although the general symptoms and history of the case may point with probability to the nature of the malady, yet if these alone be regarded other affections may easily be confounded with it.

The auscultatory signs proper to emphysema are increased resonance upon percussion, feeble respiratory murmur, and prolonged expiration. Any one of these physical signs may be met with in other affections than emphysema, but when they occur conjointly they point only to this disease. In addition to them the alteration in the form of the chest-wall, so that it becomes rotund or barrel-shaped, and the asthmatic character of the breathing, are important indications. The diseases most likely to be mistaken for emphysema are phthisis, bronchitis, pneumothorax, and pleural effusion.

In the early stage of phthisis feebleness of respiratory murmur with prolonged expiration might suggest the existence of emphysema; but, apart from the fact that these signs at any time when a doubt might be felt are generally confined to the top of the lung in phthisis, the diminished percussion resonance, the bronchial or broncho-vesicular breathing, the bronchophony or bronchial whisper, and increased vocal resonance and fremitus—all of them proper signs of phthisis and all wanting in emphysema—would by their presence or absence clearly establish the differential diagnosis between the two affections. In more advanced phthisis, when softening has taken place and a cavity exists, difficulty in discriminating between the two diseases could hardly arise.

Emphysema is so frequently associated with chronic bronchitis and with intercurrent attacks of acute bronchitis that it is often important to determine whether these latter affections exist independently or are complications of the emphysema. The question is in general settled by the history of the case and by the conformation of the chest, showing whether previous dilatation of the air-cells has taken place or not; as also by the presence or absence of the special signs of emphysema when those of the bronchial affection are encountered.

Capillary bronchitis, from the urgent dyspnoea attending it and the vesiculo-tympanitic resonance which it sometimes presents, especially in the upper and anterior parts of the chest, may possibly be mistaken for emphysema, from which, however, it may be distinguished by the quickened pulse and high temperature that belong to this form of bronchitis, as also by the rapid diffusion of the subcrepitant râle over both sides of the chest in capillary bronchitis; whereas this sign is absent or less marked in emphysema. Moreover, capillary bronchitis is most common in childhood, when diffused emphysema is less frequently met with.

Pneumothorax is characterized by distension of the chest and increased percussion resonance—signs which belong also to emphysema; but the possibility of error is avoided by the consideration that whereas in emphysema the respiratory sound is feebler than natural, in pneumothorax it is strongly exaggerated and amphoric in character; and there are also the additional signs of metallic tinkling and the plashing noise or "Hippocratic succussion sound" made by moving the body backward and forward. Moreover, even as regards the sign in which the affections would appear to resemble each other, a difference may be observed on careful examination; for the percussion note of pneumothorax is purely tympanitic, while in emphysema the increased resonance has still a vesicular character to some degree. Pneumothorax, again, is always a unilateral affection, and emphysema is almost as constant in its occurrence on both sides of the chest.

It might appear that there would be little liability to confuse emphysema with pleural effusion, in view of the very general presence of dulness on percussion in the latter affection and of resonance in the former. But in some cases of fluid effusion in the chest a degree of tympanitic resonance is met with, more especially in children. J. Lewis Smith remarks that "as a rule in the pleuritis of children, at a certain stage of the effusion, percussion produces a sound which is either decidedly tympanitic or which partakes of the tympanitic character."¹¹ In both affections, moreover, there may be enlargement of the chest. The doubt, if it arise, may be settled by the consideration that in emphysema the altered resonance and the enlargement are on both sides; whereas in pleurisy these signs are in general on one side only; and, further, the enlargement is more marked at the top of the chest in emphysema and at its base in pleural effusion.

¹¹ Diseases of Children, 5th ed., p. 607.

In concluding the account of the diagnosis it may be said that when the history of a case, the frequent or constant occurrence of dyspnoea, and the more or less rounded conformation of the chest make the existence of emphysema probable, this probability may be converted into a certainty by the discovery of resonance on percussion, feeble respiratory murmur, and prolonged expiration.

PROGNOSIS.—The circumstances, apart from treatment, which especially affect the prognosis of emphysema are the form in which the disease occurs and the ability of the patient to secure immunity from influences which may increase the malady itself or the attendant bronchitis, such as hard work, great exertion of the respiratory organs, and exposure to cold and damp.

Acute supplementary emphysema, even when it affects considerable portions of both lungs, may entirely disappear and the vesicles be restored to their integrity on the removal of the underlying cause. Thus, the vicarious dilatation of air-cells following acute bronchitis or whooping cough in children may leave no sign of its previous existence after recovery from these diseases. In general, the shorter the duration of the causal diseases, the more likely is the emphysema to disappear; for if it be maintained for a considerable time, the elasticity of the cells may be so damaged that they may never return to their natural size.

In hypertrophic lobar emphysema the prognosis in most cases is unfavorable as regards perfect recovery; while yet the disease may not materially shorten life, and with proper care may be compatible with a fair degree of comfortable existence. And, indeed, even in this form of the disease, provided it do not affect a great extent of lung and have not been of very long duration, there is in some cases ground for hope of ultimate recovery, with restoration of the air-cells to their normal condition. Modern methods of treatment have rendered the prognosis in such cases somewhat less unfavorable than it was once held to be.

TREATMENT.—The treatment of emphysema comprises several distinct objects: 1st, the arrest of the degenerative changes which may be going on in the walls of the air-vesicles, and which favor their dilatation; 2d, the restoration, as far as is possible, of the integrity of the lungs, so that they may resume their natural size; 3d, the relief of bronchitis, asthma, and dropsy, which are associated as secondary affections with the primary disease.

To meet the first of these indications, the arrest of degenerative change, iron is among medicinal agents the one most to be relied upon; for, though neither it nor any other means has power to restore loss of tissue or to reproduce integrity of structure when several alveoli are fused into one cavity by the breaking down of their partition-walls, yet by enriching the blood it may improve the nutrition of these cell-walls so that the tendency to dilatation and rupture may be checked. Iron steadily administered in small doses is the best means for effecting this end, and if the patient object to one form of the metal after using it for some time, it may be changed for another. The best preparation of the drug is probably the tincture of the chloride, and one of the best forms for administering this medicine is the mixture of acetate of iron and ammonium (Basham's mixture) introduced into the U. S. Pharmacopoeia of 1880. This is especially valuable, when any dropsical effusion exists, on account of its gentle diuretic action. In addition to iron, other agents promotive of nutrition, such as cod-liver oil and the hypophosphites, may be used with the same view. Stomachic tonics, such as the simple bitters and pepsin, may be useful by aiding digestion and nutrition; and at the same time, by preventing the formation of flatus, they may relieve the dyspnoea caused by upward pressure on the diaphragm. That real benefit may be derived from such measures is beyond doubt; and it is to be feared that some practitioners, in their conviction that no cure can be wrought in those parts of the lung which have actually undergone wasting and rupture, have to too great an extent neglected the use of means which may at least prevent the advance of similar changes in other parts, and thus tend to stay the progress of the disease.

Deep and hurried respiration will increase the air-pressure within the yielding vesicles; for this reason active exercise is objectionable, especially walking up hill, and the use of wind instruments is to be strictly prohibited. Indeed, as regards this last cause of respiratory pressure the patient's inability to practise is in general warning enough, but in the early stages of the affection a caution against it may be necessary.

The suggestion of the use of strychnia against emphysema is not founded on a correct knowledge of the mode of action of this drug; for, although it may stimulate muscular contractility, it has no influence upon the elasticity of the air-cells and no power to restore them to their natural size. Whatever benefit may result from it is due solely to its action on digestion and the improvement in nutrition to which it may thus contribute.

The second indication of treatment, the restoration of the dilated air-cells to their natural size, is possible, if at all, only at an early period of the disease or in portions of the lung which have not gone beyond a moderate degree of cell-dilatation. An enlarged space formed by the fusion of several cells cannot be lessened in size by any means, medical or mechanical, and the loss of respiratory power from the destruction of the cell-walls in which oxygenation is effected does not admit of permanent relief. Where, however, such destruction has not yet taken place and distension is not extreme, there is reason to believe that a return of the cells to their natural size may in some cases be accomplished. The inhalation of condensed air has been recommended with this view; and no doubt good may result from it, due chiefly to the retardation of the breathing and of the heart's action which it occasions, while dyspnoea is relieved by the larger supply of oxygen taken in at each inspiration. This improvement in respiration causes more complete tissue-metamorphosis, and thus aids nutrition and all the functions.

Still greater benefit is to be derived from the exhalation into rarefied air—a measure which acts upon mechanical principles, and has been found to give relief not only to the symptoms of emphysema, but to the organic disease itself; for the retention and stasis of the residual air, which is far larger in amount in emphysema than it is in health, serve at once to keep up the dilatation of the cells and to increase the dyspnoea; and therefore any means which will effect the withdrawal of this air will favor the return of the cells to their normal size, and at the same time relieve the dyspnoea. This benefit is accomplished by the method of expiration into rarefied air, which acts by suction—or pneumatic aspiration, as it may be termed—drawing out the air from the distended vesicles, and relieving them of the continual presence and pressure of this air. Better results would appear to be gotten from the conjoint use of the two methods—the inspiration of compressed air and expiration into rarefied air—than from either one alone.

By the persistent use of these means in cases which have not advanced so far as to defy all treatment not only may the symptoms of dyspnoea, cough, asthma, and impaired nutrition be improved, but the size of the chest may be diminished, as shown by measurement; and this can result only from the return of the distended air-cells, in some degree at least, to their normal capacity.

The apparatus best fitted to effect this double purpose is that of Waldenburg, as modified by Tobold.¹² The method of using it is simple, and can readily be understood by examining the instrument. It must be said that the most valuable action of this apparatus consists in the withdrawal of the air from the cells which it effects, for this tends to produce an organic change for the better—viz. the diminution of the enlarged cells by a sort of suction; while its other action, the supply of condensed air, gives relief to symptoms mainly. In emphysema the expiratory act is relatively more impaired than the inspiratory, and the apparatus is best adapted to the relief of this greater deficiency. Henry Saltzer, formerly of Germany and now of Baltimore, has recently obtained very favorable results from its use in emphysema, not only as regards the dyspnoea and other symptoms, but also in the way of lessening the size of the chest as determined by measurements.¹³

¹² This instrument is made by Messrs. J. Reynders & Co. of New York.

¹³ A reference to Saltzer's observations and measurements may be found in Weil's Handbook of Topographical Percussion, pp. 107, 108, Leipzig, 1880.

The third indication of treatment has reference to the complications of emphysema. Of these the most common, and one of the most important, is bronchitis, which is to be treated in the same way as when it occurs as an independent affection. Expectorants to promote and remove secretion and agents to allay cough are very important means, because the retention of secretion and the effort of cough to expel it cause a strain upon the air-cells, and thus increase the emphysema. The local use, by inhalation or spray, of opiates, belladonna, hyoscyamus, and other agents of this class, is often most serviceable by giving relief to the cough without disturbing digestion. As bronchitis is in many emphysematous patients a very chronic affection, and is attended with submucous thickening in the bronchial tubes and consequent diminution of their calibre, the iodide of potassium is an agent of special value for its relief. Whether the influence of this remedy is due to a sorbefacient power or to some other unexplained mode of action, there is no doubt of its great value in chronic bronchitis, so that for this complication of emphysema it claims a very high rank among medicines. The rapidity with which relief is afforded to the cough and dyspnoea of bronchitis, and to the asthmatic paroxysms attending it, by full doses of 10 or 15 grains of iodide of potassium at intervals of four hours, makes it probable that its action is partly neurotic in character. It is remarked by Austin Flint, Sr., that when the iodide has effected a marked improvement in the chronic bronchitis he has known the characteristic deformity caused by the emphysema to be notably diminished.¹⁴

¹⁴ Clinical Medicine, p. 131.

A dangerous symptom which sometimes arises in the course of the chronic bronchitis accompanying emphysema is profuse bronchial catarrh, which may destroy life by producing apnoea, the surface becoming cold and the pulse feeble and vanishing as the patient seems to be drowning in his own secretion. In this condition the writer has in several instances found prompt and unmistakable benefit from the hypodermic injection of hydrobromate of quinia, and he would strongly advise the use of this agent. The solution he has employed is of the strength of 4 grains of the salt to 20 minims, and of this 15 to 20 minims has been the dose given. Under the action of this remedy the pulmonary capillaries would appear to be so toned that further effusion is checked, and the gasping and cyanotic condition has been speedily succeeded by comfortable breathing. For the same symptom Waters advises the use of moderately large doses of turpentine (drachm doses in aromatic water every two hours) on a plan suggested by Sir D. Corrigan of Dublin.¹⁵

¹⁵ Diseases of the Chest, p. 172.

As bronchitis has so much power to produce emphysema when the conditions favorable to its occurrence exist, and to increase it when already established, everything tending to prevent it is of great importance. With this view the avoidance of cold and wet, and, when practicable, recourse to a mild climate in winter, are advisable.

The attacks of asthma to which emphysematous patients are subject are to be treated in the same way as the purely spasmodic form occurring independently of discoverable organic disease. If the difficult breathing has come on suddenly and the patient is not laboring under advanced dilatation of the heart, prompt relief may be given by a hypodermic injection of morphia; but if the heart is much dilated, this might endanger too great depression. Chloral is generally unsafe for the same reason. The bromides in full doses may be serviceable in the less severe attacks, and the tincture of lobelia in doses of 10–20 drops every fifteen minutes until slight nausea is felt is often of great benefit, as is also the smoking of stramonium-leaves.

The dropsy met with in advanced stages of emphysema may be so prominent a symptom as to require special treatment. Its cause is found in dilatation and weakness of the right chambers of the heart, which result from obstruction to the circulation through the lungs when compensative hypertrophy is no longer efficient, for then these give rise to passive congestion of the liver and kidneys and remora of the general venous system, with dropsical leakage, seen first and chiefly in the lower extremities. Treatment is therefore to be directed chiefly to increasing the tone of the heart; and for this purpose digitalis is most useful, as it is in other forms of cardiac dropsy. The chief indication of its beneficial action is seen in the better action of the kidneys consequent upon the increased impulsive force given to the heart. When acting favorably, marked relief both of the dropsy and the dyspnoea may be obtained from the use of this agent in the dose of 2 to 4 drachms of the infusion or 10 or 15 drops of the tincture every three or four hours. If the stomach should not bear the digitalis, as is sometimes the case, or if it fail to act or lose its power, the fluid extract of convallaria, recently introduced as synergistic with foxglove, may be employed as a substitute for it.

Under similar circumstances, if the patient's strength will admit of it, great benefit will sometimes result from a mercurial purge, by which passive congestion of the portal system may be relieved and the upward pressure of an engorged liver in some degree lessened.

4. Atrophic Lobar Emphysema.

This disease differs from the hypertrophic form of emphysema in the circumstance that the bulk of the affected lungs has undergone diminution from waste or atrophy of their tissue. Absolutely, the lungs may contain no more air than they should in health—they may even contain less—but, relatively, there is an increased amount of air in them in consequence of the diminished amount of the lung-tissue. Such relative increase of air in a given area of the lung may be very considerable from the atrophy and destruction of the cell-walls, the alveoli coalescing so as to form cavities, while the individual air-cells are not dilated. The entire lung, however, is shrunken, the chest-wall correspondingly depressed and contracted, and the thoracic muscles atrophied. The function of the affected lungs is impaired in consequence of their loss of size and the diminution of the respiratory movements. This is of course especially noticeable when exertion is made, while under other circumstances there may be little or no embarrassment of breathing unless the disease is far advanced and has involved a large amount of both lungs. But, in general, this form of disease causes less distress and is a less formidable affection than hypertrophic emphysema. In some cases a mingling of the two forms is found, as when a person the subject of general atrophic emphysema has a local vesicular dilatation developed at the top and margins of the lungs.

The shrunken state of the lungs in atrophic emphysema prevents the heart from being overlapped, so that the area of cardiac dulness is not lessened, as it is in the hypertrophic form; and as the general waste of the system is attended with a diminution of the amount of blood, dilatation of the right ventricle, and consequent dropsy, are not apt to occur, as they are in hypertrophic emphysema.

ETIOLOGY.—Atrophic emphysema is always due to constitutional causes. It is found chiefly in old persons or in those in whom impaired nutrition has produced the degenerative changes of old age. Hence it is described by some writers as senile emphysema or senile atrophy of the lungs.

SYMPTOMS.—Of the general symptoms of atrophic emphysema, apart from those which belong also to the hypertrophic form, the most marked are—first, the lessened size of the thorax; and, second, the character of the dyspnoea, which is not urgent, and is not apt to occur except on making exertion. The blood is lessened in amount from the general impairment of nutrition, and is therefore adapted, so to speak, in quantity to the diminished aërating space. Percussion in general gives exaggerated resonance, from the relative increase of air in the lung and the thinness of the thoracic wall, which thus vibrates more perfectly. In some cases, however, from loss of elasticity in the cartilages of the ribs, the resonance is even diminished. On auscultation there are found somewhat prolonged expiration and, in general, feeble inspiratory murmur—signs which belong also, but in greater degree, to true hypertrophic emphysema, from which, however, the atrophic form is to be distinguished by the contraction of the chest that is seen throughout its entire contour.

In some cases of hypertrophic emphysema there may be, it is true, an appearance of partial contraction of the chest-wall, since where the emphysema has produced a marked bulging of the upper portion of the thorax the part below may seem by contrast to be contracted. But in the atrophic form of the disease no distension is seen at any part of the chest-wall, the whole surface being more or less sunken and contracted. Even in hypertrophic emphysema with distension of the thorax, when the disease has lasted a long time there may be some degree of wasting of the lung-tissue; but this condition does not constitute true atrophic emphysema, which is such from the beginning without any preceding stage of hypertrophy.

DIAGNOSIS.—The diagnosis of atrophic emphysema is to be made by the physical signs studied in connection with the conformation of the chest.

PROGNOSIS.—The prognosis of this affection is hopeless as regards a cure, since the organic change is due to the degeneration of age; yet the disease may continue for years without materially or at all affecting the duration of life.

TREATMENT.—The atrophied lungs can never be restored to their integrity; treatment is therefore limited to the use of tonics and nutriment in order to hold in check the process of waste; and to the relief of bronchial catarrh, which is apt to be attended with profuse purulent secretion. The agents best suited to these two purposes have already been considered.

II. INTERLOBULAR OR EXTRA-VESICULAR EMPHYSEMA.

Interlobular or extra-vesicular emphysema is, as has been previously stated, an affection differing anatomically and pathologically from the form of disease already described. In the vesicular form air is present where it normally belongs, but in undue amount; in the interlobular form it is present where it ought not to be—that is, in the meshes of the connective tissue between the lobules, beneath the pleura, and around the bronchial tubes and pulmonary vessels. These situations may be reached by the air through a rupture of the vesicles, and thus in some cases vesicular may be associated with interlobular emphysema, the rupture having occurred from violent cough; or the emphysematous infiltration may be gaseous, as the result of gangrene occurring during life or of decomposition after death.

DIAGNOSIS.—The presence of air in the connective tissue of the lungs cannot be determined by any signs or symptoms; if, however, it should be discovered in the subcutaneous tissue of the neck, face, or chest, giving rise to puffiness and crackling of the integument, its presence in the areolar tissue of the lungs may be suspected, especially if there be coexisting vesicular emphysema, the air having passed into the mediastinum and thence into the tissue beneath the skin.

The existence of interlobular emphysema is not, in general, of serious significance, as the air commonly disappears from the subcutaneous tissue in a few days; whence it may be inferred that it likewise disappears from the connective tissue of the lung, the opening which had admitted it there having become closed. If present in large amount in the lung-substance, it may, however, increase the difficult breathing of an emphysematous subject by compressing a number of the air-vesicles. Or, again, if the interstitial emphysema be subpleural, the bulla may burst, and the air, escaping into the cavity of the chest, may occasion pneumothorax, or even hydro-pneumothorax, from the resulting inflammation. Such an occurrence is, however, very uncommon.

Even when the diagnosis of interlobular emphysema is established, no treatment is needed or practicable.

COLLAPSE OF THE LUNG (ATELECTASIS).

BY SAMUEL C. CHEW, M.D.

DEFINITION.—The term atelectasis is derived from [Greek: atelês], incomplete, and [Greek: echtasis], expansion, and designates a condition in which the lung has failed to expand or has returned in part or throughout its whole extent to the state of non-expansion which is normal in foetal life. In the former case the state is one of congenital atelectasis, and is of course met with only in the new-born; in the latter it is acquired atelectasis, or collapse of the lung, a portion or portions of the organ which have once been expanded having the air excluded from their alveoli, so that these collapse and return to the pre-natal state. To this condition of acquired atelectasis the term apneumatosis, from [Greek: a] negative, and [Greek: pneumatôsis], filling with air, was applied by Fuchs in 1849, and it has since been adopted by Graily Hewitt.

HISTORY.—For a long time this affection was regarded as a peculiar form of pneumonia, for the reason that at post-mortem examinations patches of collapsed lung-tissue were found which appeared to have undergone solidification. Inasmuch as the condition was most frequently met with in young children, and the supposed solidification was often limited to certain lobules of the lung with intervening healthier spaces, it was described as the lobular pneumonia of children.

The secondary nature of the affection, and the fact that it is very generally preceded by bronchitis, and sometimes by catarrhal pneumonia, were pointed out by Barthez and Rilliet in 1838. Some other important distinctions between this affection and general or lobar pneumonia had been referred to by various writers, but it was not until 1844 that its true nature was satisfactorily elucidated by Bailly and Legendre, who showed, by blowing air into the lungs after death, that the lobules supposed to be hepatized were not really solidified by exudation, but had simply collapsed for want of air.

ETIOLOGY.—The congenital atelectasis of new-born children may be due to original feebleness, to protraction of labor interfering with the blood-supply through the cord, or to obstruction of the air-passages by mucus or other substances. In any case, it is the result of non-expansion of the chest, so that the lungs are not unfolded. This constitutes atelectasis in the strict sense.

Acquired atelectasis, apneumatosis or collapse of the lung, is an affection most frequent in early infancy, though not limited to that period of life, since bronchitis with defective innervation and great impairment of strength, the essential factors in the production of the disease, may occur at any period of life.

It is probably in almost every case secondary to bronchitis, and due to the occlusion of the smaller bronchi by the presence of mucus allowing the egress, but impeding the ingress, of air, so that the lobules to which they lead are gradually evacuated of air, and thus finally collapse.

Obstruction of a bronchial tube by a foreign body or by the pressure of a morbid growth within the lung may produce collapse of the lobules to which such tube leads, a smaller or larger part of the lung being involved in proportion to the size of the obstructed bronchus. Such cases are, however, very rare, and they more closely resemble the condition brought about by the pressure of a pleural effusion giving rise to the state of carnification, which is, in effect, an atelectasis involving the greater part or the whole of a lung, and not limited to certain lobules nor taking place lobule by lobule.

The principal cause of lobular collapse is no doubt bronchial catarrh, the action of which is aided by impairment of the general strength and of muscular respiratory power; for the natural elasticity of the lung-tissue would favor the exit and oppose the entrance of air unless it were counterbalanced by muscular action in inspiration. If, then, this inspiratory action is lessened, the requisite amount of air will not enter the alveoli, and that which they already contain will be in part driven out, and perhaps in part absorbed into the blood, by the pressure to which it is subjected. Deficient innervation and lower vital power are thus important elements in determining collapse, which is most common in very young infants or in those who, though somewhat older, have had their nutrition impaired by malhygienic influences or by other diseases.

The mechanism of the production of lobular collapse by the presence of mucus in the bronchial tubes has been well explained by the classical observations and experiments of Gairdner and of Hutchinson. They showed that the physical result of collapse is in part due to the force of expiration being greater than that of inspiration, and in part to the anatomical formation of the bronchial tree. As to the former of these causes, it was shown by the experiments of Hutchinson, already alluded to in the article on EMPHYSEMA, that the force of expiration capable of being applied for the overcoming of obstruction in the bronchial tubes is greater than that of inspiration—in opposition to the teaching of Laennec, who regarded the inspiratory as the greater force. Repeated efforts to clear the bronchial tubes of accumulated secretion by the forced expiration of coughing must therefore remove air from the alveoli in greater amount than it can be returned to them by inspiration, and so they must ultimately be evacuated of their contents and consequently collapse.

The second mechanical cause to which Gairdner refers is found in the shape of the bronchial tubes, which taper in size as they advance toward the air-cells. The mucus contained within a tube may in consequence of this shape act as a ball-valve, being displaced forward in the direction of the greater diameter by the expiratory efforts, thus allowing the exit of air, the entrance of which will be impeded because inspiratory action will at once close the valve. This valve-action of a plug of mucus is well illustrated and proved by the experiments of Mendelssohn and Traube. In one of these a shot was introduced into the left bronchus of a dog, and in two days the left lung was found collapsed and the right one in a state of supplementary emphysema. The collapsed lung was afterward distended by inflation. In a like manner pledgets of mucus may establish an air-pump action that will empty the cells to which the obstructed tubes lead and cause them to collapse. It is, moreover, not improbable that a portion of the contained air is absorbed by the blood-vessels, as is maintained by Fuchs.

As a predisposing cause age has a remarkable influence in producing atelectasis, the condition being much more frequent under five or six years of age than after that time. This is explained by two considerations: The first is the greater prevalence of catarrhal affections of the air-passages in young children than in other subjects; the second is the fact that the chest-walls in a child are more pliable and less firm and resistant than those of an adult, so that when the diaphragm descends in inspiration a portion of the chest-wall may sink in, and the lung immediately beneath such portion will not expand to meet the costal wall as it does in older persons. According to Graily Hewitt, the part at which the chest-wall is most depressed is "at the junction of the cartilages with the ribs, and the ribs which more especially exhibit this want of power to resist the atmospheric pressure are those just above and below the nipple, the fourth to the seventh inclusive."¹

¹ Reynolds's Syst. Med., vol. iii. p. 872.

The principal cause of collapse involving an entire lobe or the whole lung is the presence of liquid in the thorax in the form either of inflammatory serous effusion, empyema, or hydrothorax. The admission of air into the cavity of the chest by perforation of the lung or by a penetrating wound of the thorax may also lead to the same result by allowing atmospheric pressure on the lung. In such cases the lung may again expand on the absorption or withdrawal of the liquid or air, but it sometimes remains permanently compressed and carnified.

SYMPTOMS.—It is probable that atelectasis in very limited degree may exist without being discovered or suspected, the amount of lung involved being insufficient to interfere by its loss of function with respiration or to give rise to appreciable symptoms.

In congenital atelectasis the symptoms are obvious from the moment of birth, and all point to obstructed or imperfect respiration; but they vary in degree. Should expansion of the chest not take place at all, the heart, which at first may be felt feebly beating, will soon stop, and death will occur. In other cases, in which the atelectasis is not absolute, but yet expansion is not accomplished sufficiently for respiration to be kept up, the infant is more or less cyanotic, especially about the lips and face and at the extremities. The movements of the thorax are slight in degree, and the cry is weak and suppressed, and at last inaudible. In such cases death usually occurs in a few hours, but sometimes life is protracted for several days. The symptoms then are like those of acquired atelectasis or collapse of the lung.

In this condition—which, as already stated, is generally the result of bronchitis occurring in debilitated children—the symptoms show malaëration of the blood. Sometimes they are gradually developed, and sometimes they occur quite suddenly, according to the rapidity with which the collapse spreads through the lung and the number of lobules involved in it.

The signs of bronchitis are present before the occurrence of collapse, and are more or less mingled with those pointing to the collapsed state. The hurried respiration so often met with in bronchitis is increased by the collapse of any considerable numbers of lobules in the lung. The evidences of imperfect oxygenation of the blood, which in children are often apparent in bronchitis, are greatly augmented on the occurrence of collapse, the breathing becoming more rapid and oppressed, the working of the alæ nasi increased, and the dusky hue of the surface spreading and becoming deeper. The character of the respiration is modified in a very remarkable way, as pointed out by George A. Rees of London, in consequence of the pliable and yielding condition of the chest-walls in early childhood. When the upper part of the chest is elevated in inspiration and the diaphragm descends, the space thus produced cannot be filled by the lungs in consequence of their partially collapsed state; and for this reason the intercostal spaces and the lower end of the sternum are sunken by the atmospheric pressure at each inspiratory act. This character of breathing may also be observed in older subjects of collapse as regards the depression of the intercostal spaces, though in less degree than in children, in consequence of the greater rigidity of the thorax after childhood.

As collapse of the lung in very limited degree may be unattended with general symptoms, so likewise it may have no positive auscultatory signs. A moderately extensive tract of the lungs must be affected in order to produce these to an appreciable extent. This amount cannot be stated exactly, but, according to Gerhardt, it is from an eighth to a sixth of one lung.²

² Ziemssen's Cyclop., vol. v. p. 332.

Dulness on percussion, varying in degree and extent with the number of affected lobules and their nearness to each other, is a very constant sign of collapse; but it must be kept in mind that if the collapsed lobules are disseminated or central the dulness may be hardly observable. Sometimes there is difficulty in detecting dulness, because from the bilateral character of the bronchitis the collapse of lobules may take place in about equal degree on both sides, so that one side cannot be contrasted with the other. Ordinarily, however, there is a difference in the degree of dulness between the two sides, because the affection is more extensive in one than in the other; and in general the loss of resonance over the collapsed lobules is determinable without comparison of the two sides. Not uncommonly, patches of dulness are found with intervals of comparatively clear resonance.

On auscultation the respiratory sounds are feeble or entirely absent in an area in which a number of adjacent lobules are involved together in collapse.

When a considerable part of a lobe is affected, bronchial breathing may sometimes be heard, but this is in general less marked than the degree of dulness and the amount of condensation would lead the examiner to expect, because the breathing is too feeble to give rise to the vibrations necessary for the production of this sign.

An important indication of lobular collapse is the rapidity with which the signs just described are developed; a part or parts of the lung which had been clear on percussion and normal in respiratory character becoming in a day, or sometimes in a few hours, dull and nearly silent to the ear. This very suddenness with which the physical signs are developed in a case of bronchitis or catarrhal pneumonia in a child points very plainly to the occurrence of collapse of the lung.

PATHOLOGY.—The pathological appearances in collapse of the lung vary according to the extent of tissue involved in the change, and also according to the cause which has induced it. In the disseminated lobular form which is due to bronchitis the collapsed portions are chiefly seen on the surface and at the margins of the lung, and they extend more deeply into the organ as it becomes more involved in the atelectatic condition. On the surface or on a section the collapsed patches are depressed somewhat below the surrounding parts and are of a darker hue, so that they are readily seen as dark-red or purplish spots surrounded by the lighter healthy tissue. The contrast is sometimes enhanced by the fact that the non-collapsed parts are even paler than natural from the vicarious emphysema that has been established in them.

The consistence of the affected part varies in different cases. If the change has occurred without previous congestion, the texture may be somewhat flaccid; but if there has been hyperæmia, the part will be leathery, non-crepitant, and resisting pressure. If no crepitation can be detected the part will sink in water from the complete expulsion of air from the affected lobules. A cut surface is smooth and does not present the granular appearance of a hepatized lung, nor can exudation-matter be pressed or scraped from it.

The collapsed lobules may be made to swell up and resume their normal appearance and rosy color by forcing air with a blowpipe into the bronchus leading to them. This is so generally true, at least, that it has been regarded as a certain test by which to discriminate between atelectasis and pneumonic consolidation when there may be a doubt at a post-mortem examination as to which condition exists. In general, the attempt to inflate will succeed when the air is directed into a collapsed lobule; but the test is of less value than it was once held to be because it has been shown, on the one hand, that lobules which have been collapsed for some time will not always expand under the inflating force, and, on the other, that in recent catarrhal pneumonia the alveoli may for a time still be inflated with air.

Meigs and Pepper, while stating that in general the results of the attempt to produce inflation are altogether different in the two conditions, yet hold, in accordance with Gairdner's teaching, that "partially pneumonic lung may be inflated when the affection is recent and combined, as it frequently is, with bronchitic collapse; while in the latter lesion—i.e. collapse of lobules—in its purest forms complete inflation is often very difficult or impossible after the collapsed state has been of some duration."³

³ Diseases of Children, p. 143, 4th ed.

Nevertheless, the test is of value when applied along with others; for, as stated by J. Lewis Smith, "the inflated pneumonic lung is more solid and resisting when pressed between the thumb and fingers than is the collapsed lung."⁴

⁴ Diseases of Children, p. 570, 5th ed.

The chief differences between the two conditions are—1st, the color, which in collapsed lobules is purplish or livid, and in pneumonia reddish-brown; 2d, the microscopic appearance, showing the alveoli filled with cell-proliferation in pneumonia and free from change in collapse; and 3d, the state of the adjacent pleura, which is inflamed and often covered with lymph in pneumonia, while it is entirely healthy in non-complicated collapse.

The bronchial tubes present the appearances met with in bronchitis, being more or less congested, showing a softened state of their lining membrane, and containing liquid mucous secretion and sometimes firmer pledgets which have caused the obstruction.

As regards changes in the heart, extensive atelectasis may prevent closure both of the foramen ovale and of the ductus arteriosus. From the obstruction to the flow of venous blood offered by the collapsed portions of the lungs the right ventricle may become so distended that a portion of its blood may still be forced through the ductus arteriosus, and another portion backward into the auricle and through the foramen ovale, so that both of these channels may be kept pervious.

DIAGNOSIS.—Congenital atelectasis, if complete, cannot be mistaken for any other condition occurring at birth, and is sufficiently denoted by the signs already described.

Imperfect expansion of the lungs continuing for some days after birth might suggest patency of the foramen ovale from the purplish hue of the surface common to both conditions. The expansion of the chest and the resonance that it yields on percussion in the cardiac affection will be sufficient to discriminate them except in those cases in which they exist together.

Acquired atelectasis or collapse of the lung may require to be distinguished from bronchitis, from pleural effusion, and from catarrhal pneumonia.

Even uncomplicated bronchitis is in children sometimes accompanied with so much dyspnoea as to cause apprehension that collapse of lobules has taken place, but the absence of percussion dulness, either diffused or in patches, will exclude the supposition.

From pleural effusion collapse of the lung may be distinguished by the fact that the dulness due to pleurisy is generally on one side only, that it is more intense and diffused than that of collapse, and that its line of demarcation may often be made to shift with the position of the patient.

Catarrhal pneumonia is in general distinguishable from collapse by the history, course, and symptoms of the disease, especially the sudden rise of temperature that belongs to pneumonia; as also by the auscultatory signs. The percussion dulness of pneumonia is more extensive than that of collapse, and is accompanied with bronchial breathing; whereas in collapse the respiratory sounds are feeble and mingled with moist râles.

PROGNOSIS.—In congenital atelectasis, if there be no expansion of the lungs within the first few minutes after birth, the prognosis is generally bad. In some apparently hopeless cases, however, the persistent employment of means tending to arouse the respiratory function, and especially of those acting through a reflex influence, is crowned with success. The prognosis varies according to the amount of unexpanded lung; for even when some respiratory efforts have been made, if the air enter only a limited extent of the lungs, the infant will drag on a feeble existence for perhaps a few days, and then perish from apnoea and exhaustion. When the lungs are once fully inflated the danger from congenital atelectasis is past.

In acquired collapse of the lung the prognosis is dependent both upon the number of lobules involved and upon the amount of strength possessed by the patient. A larger amount of disease may be recovered from if the nutrition and nervous system be not much depressed, while a smaller amount may prove fatal in less favorable conditions of the general system. Much also depends upon the extent and duration of the coexisting bronchitis, and the degree to which it has affected the constitutional powers.

TREATMENT.—In the treatment of congenital atelectasis the main endeavor must be directed to arousing the respiratory function; and this is best accomplished by means acting reflexively through the centres of respiration. Sprinkling the chest and back with cold water, the application of cold water to the spine by a sponge or by affusion, or the alternate use of cold and hot water in the same way, will often induce a deep inspiration by which the lungs will be unfolded and respiration perfectly established. If this be not fully accomplished, it is of the utmost importance that the child should be carefully watched as long as the atelectasis continues in any degree, and that the same means should be again resorted to when the failure of respiration is threatened. The temperature of the surface should be maintained by artificial heat and woollen wrappings, as a depression below the normal standard easily takes place, and serves to lower all the vital processes and increase the difficulty of keeping up respiration.

In acquired atelectasis treatment must to a great degree be directed to the superinducing bronchial catarrh. Counter-irritation of the chest may be practised with Stokes's liniment, which consists of equal parts of oil of turpentine, acetic acid, and camphor liniment, or with mustard poultices prepared with special reference to the sensitiveness of a child's skin by mixing the mustard with a double portion of flour or Indian-corn meal. With the same view, dry cups may sometimes be advantageously used.

Expectorants are serviceable by relieving the bronchitis, the best being the syrup or wine of ipecacuanha in the dose of 5 to 10 drops, or the muriate of ammonia in the dose of 1 to 3 grains in simple syrup or syrup of liquorice, every two or three hours.⁵ These agents may modify the inflammatory state of the bronchial mucous membrane, and thus prevent the extension of the collapse. If bronchial secretion be profuse, the question of the use of emetics becomes very important. When employed judiciously with reference to the real needs of the case, they may be eminently beneficial, acting partly by removing the accumulation in the bronchi which may have occasioned the collapse and may favor its further extension, and partly perhaps by the deep inspiration which precedes emesis serving to expand the collapsed lobules. It must be remembered, however, that there is always a tendency to failure of the vital powers in acquired atelectasis, and that this may be dangerously increased by emetics of a depressing character. The best for the purpose are alum, sulphate of zinc, and ipecacuanha. The repetition of the emetic must be determined by its effect on the breathing and on the patient's strength.

⁵ One of the following formula may be used:

Rx. Syr. ipecac. drachm i–ij;

Syr. prun. virginian. drachm vj;

Ammon. muriat. drachm ss;

Aquæ, ounce j. M.

Dose, teaspoonful for a child of three to six months.

Or,

Rx. Ammon. muriat. drachm ss–drachm j;

Syr. glycyrrhiz. Aquæ, aa ounce j. M.

Dose, as above.

Tonics and supporting measures are always called for in the treatment of atelectasis, in view of the fact that the condition is essentially dependent on failure of constitutional strength. Milk, wine-whey, and animal broths are appropriate articles of food; alcoholic stimulants are generally required; and in emergencies, if sudden increase of prostration occur, the carbonate of ammonia in the dose of 1 or 2 grains may be given.

During the whole course of the malady such tonics as quinia or the compound tincture of cinchona or one of the soluble salts of iron may be administered.

Brown Induration of the Lungs.

DEFINITION.—Increased density of certain portions of the lungs, which are of a reddish color, with brown or yellowish-brown spots scattered throughout the indurated tissue.

SYNONYMS.—Pigment induration; Congestive carnification.

HISTORY.—This affection is a form of passive congestion of the lungs, in regard to which it is somewhat uncertain whether the morbid process is simply one of congestion or whether along with this an inflammatory element is likewise present. It is beyond question, however, that the changed condition of the lung is primarily and chiefly congestive, and that it originates from causes which produce congestion.

ETIOLOGY AND MORBID ANATOMY.—The etiology and morbid anatomy of this affection are so closely related that they are best considered together. The most important fact both in the etiology and pathology of brown induration of the lungs is that it is gradually brought about as the consequence of obstruction to the pulmonary circulation from disease of the mitral valve, either constrictive or regurgitant in character. Interference with the return of the blood to the left side of the heart is in this way produced, with consequent stasis in greater or less degree within the pulmonary capillaries.

The most marked changes observed in lungs which have undergone this form of congestion are that they do not collapse when the chest is opened, and that they are more compact and less elastic and crepitant than healthy lungs. On section they present a reddish color interspersed with spots of yellowish- or reddish-brown, which sometimes are of a very dark hue.

Microscopic examination shows an increased size of the capillaries of the lung, which seem to encroach upon the air-cells and thus lessen their capacity. Whether the walls of the alveoli have themselves undergone thickening is a question about which different opinions have been entertained. Rokitansky states that "when stasis has continued for a longer period the walls of the air-cells and the interstitial tissue become swollen, so that the former may become perfectly impermeable to air;"⁶ and although, in the passage quoted, he is writing of pulmonary congestion in general, and not of this form in particular, yet, as he is describing a stasis which has continued for some time, the observation would seem applicable to the affection under consideration.

⁶ Path. Anat., vol. iv. p. 59.

Wilson Fox affirms that he has found alveolar thickening in considerable tracts in this affection, with a distinct increase of fibrous tissue in the walls of the alveoli; but this change, he goes on to say, is not uniformly present, and in some places the alveoli are found filled with epithelial products like those of catarrhal pneumonia.

The true explanation of the condition is probably this: that, beginning as a passive congestion, such as might be expected to result from the mitral disease with which it is almost constantly associated, the affection afterward assumes an inflammatory condition of a low type with epithelial proliferation, and in some cases with thickening of the alveolar walls and the interlobular connective tissue. Passive hyperæmia is, however, always the basis of the disease. The brownish spots visible in a section are caused by the leakage of blood from the congested capillaries into the alveoli or interstitial tissue without the occurrence of any large extravasation. The blood thus exuded undergoes pigmentary change, with the production of hæmatoidin, the shades of color varying accordingly as the exudation has been recent or of longer duration.

The failure of the lungs to collapse is due to the encroachment of the dilated capillaries on the air-cells, and perhaps to the thickening of the cell-walls and the partial occupation of the cells themselves by epithelial products.

SYMPTOMS.—The general symptoms and the physical signs of this affection are of the same character as those that occur in other forms of pulmonary congestion. Dyspnoea is felt, especially on making exertion; and this may be attributable in part to the associated cardiac disease as well as to the condition of the lungs. Loss of resonance on percussion and feebleness of respiratory murmur are observable; and when the condensation is great bronchial breathing may be heard.

DIAGNOSIS.—It is evident that there is nothing in these signs distinctive of this particular form of congestion, which is, in fact, not diagnosticable with absolute certainty during life. The probability of its existence may, however, be inferred if along with the above symptoms and signs a presystolic or regurgitant mitral murmur is heard, showing constriction or incompetency of the mitral valve.

PROGNOSIS.—The prognosis of this affection is of course always unfavorable, because the condition depends upon mechanical disease of the heart of an incurable nature. Temporary improvement may, however, sometimes take place under proper treatment.

TREATMENT.—Such treatment must be used as serves to support the weakened heart and hold in check the tendency to dilatation. With this view digitalis or convallaria may be employed, with tonics and alcoholic or ammoniacal stimulants as occasion may require. Counter-irritation over the lungs may be used and expectorants may be given. If dyspnoea be urgent, the preparations of ether, such as Hoffman's anodyne, or the carbonate of ammonia, may be administered.

CONGESTION AND OEDEMA OF THE LUNGS (HYPOSTATIC PNEUMONIA).

BY SAMUEL C. CHEW, M.D.

Congestion and oedema of the lungs are often found together, but they are different morbid conditions, and each may occur independently of the other. It is best, however, to consider them in connection with each other.

DEFINITION.—By congestion of the lungs is meant an active or passive hyperæmia of the pulmonary vessels, which are surcharged with blood.

Oedema of the lungs signifies an effusion of fluid consisting mainly of the serum of the blood into the air-vesicles and, to some extent, into the pulmonary connective tissue. Congestion is at times the determining cause of oedema, but the latter condition may arise from causes not tending to produce the former.

HISTORY AND ETIOLOGY.—As pulmonary congestion and oedema are almost always secondary and dependent affections, their etiology is an essential part of their history, so that these subjects will be best considered together.

Active congestion of the lungs may result from any cause producing an increased afflux of blood to these organs, such as hypertrophy or functional over-action of the heart, or the sudden recession of the blood from the surface and perhaps from other internal organs, such as may take place under the influence of cold. Violent exercise, rapid walking up hill, or even mental excitement, may in some impressible subjects suffice to produce it.

Why vascular congestion should occur in a greater degree and more readily in the lungs than elsewhere from the effect of cold is sufficiently evident when it is considered that the pulmonary capillaries are not supported by surrounding tissue, as those of other parts are. And for the same reason the direct action upon them of cold air or of certain irritant gases, such as ammonia or chlorine, may suffice to cause an undue afflux of blood to them.

How far a neurotic influence exercised reflexively through the vaso-motor system may serve to produce active congestion has not yet been fully determined; but it is probable that the sudden pulmonary congestions which have been known to follow the drinking of a large quantity of cold water when the body is heated may be attributed to such an action.

Passive congestion may be occasioned by a retardation of the blood-flow from the lungs; as, for example, by a hindrance to its onward passage through the left chambers of the heart in consequence of obstructive valvular disease, especially a great degree of mitral or aortic stenosis. So also mitral or aortic incompetency, by allowing the blood to be crowded backward in the pulmonary veins, may interfere with its passage through the lungs, and in this way set up passive hyperæmia.

By some writers mere weakness of the heart is spoken of as a cause of passive congestion of the lungs; but it can hardly be regarded as such apart from influences affecting the blood itself or the tonicity of the pulmonary vessels; for it is to be considered that while weakness of the left chambers of the heart might impede the onward course of the blood received from the lungs, yet at the same time the right chambers, if weakened in a corresponding degree, would send less blood into those organs, and then the conditions of passive hyperæmia would not exist. It is well known, moreover, that cardiac weakness coming on suddenly as in syncope, or gradually as in various asthenic diseases, may be present without the occurrence of any signs of pulmonary congestion. Yet it is not impossible that there may be a disturbance of the balance between the actions of the right and left sides of the heart, and that thus passive congestion of the lungs may result from a relatively greater weakness on the left than on the right side of the heart, so that the left auricle and the pulmonary veins may be obstructed, and backward pressure produced while the right ventricle is still sending blood into the lungs.