action for its special construction. If it assume the tubular or semi-tubular character; if it line a cavity, as an added layer; if it be made up of distinct layers; if it have a firm attachment, mechanical or by vessel; if it have impressed on it a model of valve-structures; if it assume a spiral character: under all or any of these circumstances, it has been formed before death.

Again, a concretion may commence in the course of the circulatory canals, and may be built up in opposition to the current; in which case it will be a plug or solid cord. Or, commencing on some point of obstruction, as the side of the auricle, it may go with the stream, and be deposited with it; in which case it will be deposited in layers, and assume, more or less, a tubular character.

Lastly, a portion of concretion dislodged from the heart, may be carried into the finer ramifications of the systemic arteries; or a portion detached from a vein may (but this is rare) be carried into the right heart, and thence into the pulmonary artery and its ramifications. At the same time, concretions admit of being formed at the actual points where they are found; and in many cases are thus formed and deposited.

Conditions which lead to Deposition of Fibrin.

In chapter III, there are briefly sketched out the leading physical conditions which favour the deposition of fibrin in the circulation; viz. actual increase of fibrin, relative increase, and impeded motion. We are prepared now to see a little better the way in which these conditions assist in the act of deposition.

The simple fact of deposition from absolute increase of the fibrinous constituent is very simple. The excess of fibrin cannot be held in solution; it is out of pro

portion to its solvent, and deposition becomes a mere mechanical result, taking place at such parts as afford most resistance, such as a point of exuded matter, or a thickened valve. When the excess is relative, the effect is virtually the same; except in special cases, cholera for instance, where the diminution of water is attended with increase in the amount of alkali; or in cases where the respiration is much impeded. In the third class, where an obstruction to the current of normal blood gives rise to the deposition, the deposition is the result of partial stasis of blood at the obstructed point. The blood, thus checked, yields up its solvent to the blood-current which does pass along the tube, as the blood in the test-tube beneath a current of blood-vapour yields up its solvent to the upper and fluid stratum, and straightway solidifies. In the aneurismal cavity, this process of separation is exceedingly simple. Lancisi, and also Dr. Baillie, were aware that the deposition in the aneurismal tumour is most marked at the point where the current is most feeble. But Lancisi attributed the effect to a mere statical cause; and stasis is, after all, the primary element. But stasis in itself would never lead to deposition if the fluid were permanent; nay, it does not even lead to the final deposition of blood-corpuscles, for these are washed away with the stream; but it is sufficient to lead to the deposition of the plastic fibrin, held as it is but temporarily fluid by a solvent which, under favouring physical conditions, is diffused and borne away. In instances where the fibrinous deposition is the mere result of an enfeebled circulation, there may yet be other conditions favourable to deposit. There may be, for example, as in phthisis pulmonalis (in which disease these depositions

in the heart ordinarily are found in the last stages of life), an absolute loss of the blood-solvent, either by its rapid elimination, or by an arrest of the process by which it is normally supplied to the blood.

The effect of some septic agents in inducing fibrinous deposition is a point which must not be overlooked, however little we may know concerning the influence of such agents. I presume, but on this I have not sufficient experimental data to lead to any positive conclusion, that a poison having weak acid properties, or having the power of giving rise to the formation of an acid on being introduced into the circulation, would by its presence lead to a deposition of fibrin. Experiments differ in regard to poisons thrown into the blood. Gaspard and Lee found that the injection of pus gave rise to fibrinous deposit. Magendie injected putrid fluids, and produced permanent fluidity. All may depend on the condition of the fluid used at the time of its injection. Pus having an acid reaction, as sometimes obtains, produces, when added to blood newly drawn, instant coagulation. A little more of the same specimen of pus, allowed to stand till decomposition has commenced, and it has acquired an alkaline reaction, on being added to blood in the same proportion, retards coagulation, or stops it altogether.

Lastly, there is a condition which has long been known to favour coagulation and fibrinous deposition. I mean loss of blood, and syncope or exhaustion during impoverished states of body. The explanation here is, that these states are attended, as a general rule, by an excess of fibrin in the blood as well as by an excess of water. The fibrin solvent is thus widely distributed, the density of the blood is reduced, the fibrin super

abounds, and stasis only is required to give all the circumstances favourable to deposition.

Symptoms and Diagnosis of Fibrinous Concretions in

the Heart.

The symptoms produced by fibrinous deposition in the heart are strikingly characteristic when they are once understood. But as they are commonly superadded to other symptoms, and appear at the acme or near the end of a disease, they occasion great perplexity to all who are not prepared to read them off, and whose attentions are bent to some mere local mischief, by which the disease perchance is misnamed, rather than to the grand changes which are occurring in the body as a whole.

Whatever be the disease, the effects of a fibrinous deposition are in the main the same, according to the manner in which the deposit itself is laid down. In other words, the symptoms depend on the position, form, and character of the deposit, less than on the preexisting malady.

Whenever fibrinous deposition takes place in the heart during the course of a disease, the pure symptoms of the disease are lost or masked by the new symptoms which are set up, and which take to themselves a general representative position.

The advantages which I have had for tracing out the symptoms produced by concretion, and for confirming by dissection the diagnosis instituted, have been confined mainly to cases where active inflammatory mischief (hyperinosis) has been the forerunning disorder. I write, therefore, from these sources of natural information.

All symptoms of acute inflammatory disease are attended with some risk of fibrinous deposition. Taking the majority of such cases, the risk certainly is small; but it is present in each case, and what renders the risk more serious is, that such risk or tendency to deposition cannot be measured by the local indications of inflammatory mischief in any given case, nor yet by the general symptoms which accompany the local. The symptoms of concretion may supervene in the mildest as in the severest cases. They may creep on insidiously; they may take effect in a sudden and unexpected outbreak. The following is an outline of a case in which the symptoms are unexpected. I write as I have seen, and as others have seen.

A patient is suffering from an acute inflammatory attack. The local mischief, be it pneumonia, bronchitis, erysipelas, peritonitis, rheumatism, is not in itself such as to cause immediate alarm. The symptoms go on from visit to visit, and the patient is left on one of these occasions not apparently in imminent danger. Unexpectedly, there is a sudden call for the practitioner. He goes, and in the universal change that has occurred he reads off the death-signals. The man will sink. The fact as it is written in the patient is not to be described in words, but is easily learned from experience; it is written in the face of the sick man, in the restlessness, in the expression altogether. Whoever knows disease, knows at once, without further comment, what I mean. It is my business to show how far this finale of inflammatory disorders results from fibrinous deposit, and to indicate how the symptoms, when studied in detail, yield the diagnosis of concretion.

If my observation of the last symptoms and of the