19 Sturges, Pneumonia, loc. cit.
An analogy has been noted by some observers between pneumonia and acute rheumatism. Trousseau sees an analogy between erysipelas and pneumonia.20 But apart from their etiology it is difficult to recognize any constant resemblances between them. Sturges places "pneumonia in a middle place between the specific fevers, so called, and the local inflammations," and adds that it has something in common with both. Cohnheim classes croupous pneumonia among the miasmatic contagious diseases.
20 Clinical Lectures, vol. iii. p. 353.
The idea of its being a specific disease dates from the latter part of the eighteenth century:21 it is not by any means a modern thought, although it has within the last ten years received a new impulse and given rise to extended discussions.
21 C. Strackius in Nov. Theo. Morg., 1786.
It seems to me that the resemblance of pneumonia to the acute general diseases is to be found for the most part in its nervous phenomena, and that the complications which render pneumonia dangerous are those which interfere directly with the muscular power of the heart or diminish its nerve-supply.
In order that the influence exerted by an abnormal nerve-supply upon the contractility of the cardiac muscles may be more apparent, let us glance at a few modern physiological facts. When the inhibitory nerve of the heart, the pneumogastric, is cut, the heart beats wildly. When the peripheral cut end is stimulated, the heart stops in diastole. But neither of these phenomena instantly follows the operations, on account of the intervening cardiac ganglia, the part of the vaso-motor system which has its centre in the medulla oblongata. Afferent inhibitory filaments (the depressor branch) of the vaso-motor centre are also in the vagus. Now, by injecting atropine into the blood we so influence these cardiac ganglia (which intervene between the conditions of the vagus and the resulting action upon the heart-beat) that the inhibitory action is entirely checked. Thus an intimate connection is apparent between the local heart-mechanisms, the general vaso-motor system, and some filaments of the vagus. Again, we know that the natural explosive decompositions of the nerve-cells of the respiratory centre may be either augmented or enfeebled according to the condition of the blood supplying this ganglion. Now divide the cervical portion of the pneumogastric, and there results, after a more or less prolonged period, an extensive pulmonary consolidation (hepatization), which is not accompanied by the least sign of heart-failure. It is to be remembered that such pulmonary consolidation has none of the essential pathological characteristics of croupous pneumonia.22
22 Michael Foster, Wagner, Goetz, Heidenhain, Du Bois-Reymond, Ludwig, and Pflüger.
From these experiments the following deductions seem at least reasonable: The tonic influence normally held by the vaso-motor system of nerves over the vascular system is either lessened or destroyed by an altered blood-state or by some morbific agent in the blood introduced from without. The large quantity of blood which would then be retained in the arterioles throughout the body, and which could not be returned to the heart, may cause so great a diminution in the blood-pressure as in itself to cause heart-failure. But in addition, and in connection with this, may not the action of a morbific material in the blood upon the intrinsic cardiac ganglia so interfere with their function, or so act upon the medullary vaso-motor centre itself, that the movements of the heart are deranged and its power is more or less diminished?
It would seem that this materies morbi in the blood may as well act upon both the medullary centre of the vaso-motor system and the ganglia in the wall of the heart as upon either alone. The phenomena of asphyxia are brought about by influences acting solely on the medullary centre. Again, the large amount of urea excreted, the result of excessive tissue-change throughout the body, may also be due to deranged nerve-function.