Cyanosis, Or The Abnormal Formation Of The Heart on which it depends, may terminate in death, either suddenly and rapidly, or slowly, in the same manner as in acquired heart-diseases.

There is an anomalous form of cyanosis depending on original narrowness of the arterial trunks, associated with a normal formation of the heart, which constitutes a transition stage from the cyanosis, arising from malformations of the heart and of the arterial trunks to that form of cyanosis which is a symptom of acquired heart-disease. This anomalous narrowness, associated with a normal formation of the heart, extends in various degrees to the aortic trunk; and, like many other phenomena of cachexia, occurs most commonly during childhood and in puberty.

Finally, cyanosis is a common symptom of many heart-diseases, such as dilatations and hypertrophies of a higher degree, together with the anomalies of the valves, from which they originate. These diseases also commonly give rise to acquired anomalies of the vascular trunks, such as contraction and obliteration, acquired communications of the aorta with the pulmonary artery and with the Venae cavae, and the consequent entrance of arterial blood into the two last-named vessels. These forms of cyanosis very frequently do not appear decidedly until advanced periods of life, although the heart-disease may have been acquired in early childhood, if it be not even congenital. It is still problematical whether this form of cardiac cyanosis can be acquired by the reopening of the closed Foramen ovale and by a morbid perforation of the septum, owing either to inflammation and suppuration, or to a fissure. This view of the possibility of the reopening of the Foramen ovale originated at a period when too much importance was attached to its patency, and would appear to be especially designed to serve for the completion of the whole theory. The cases recorded of acquired morbid perforation of the septa are certainly not wholly improbable, but the previous history of these cases affords us no convincing grounds for the assumption of the process of inflammation and suppuration or the existence of a fissure. These cases are also incapable of solving the questions whether these processes may not date from the period of foetal life, and whether, therefore, the morbid perforation may not be a congenital heart-disease; nor do they show whether the case may not be one in which the products and residua of inflammation belonged to a process subsequent to the perforation rather than to one by which this process was effected. This perforation deserves the more consideration, since traces of old or recent endocarditis have not unfrequently been found in hearts presenting such anomalies of formation.

Cyanosis may not only be derived from the heart (where it most commonly originates in the right side), but it may also depend on the most various congenital and acquired diseases of the lungs, which impede the circulation of the blood in the capillaries. The insufficiency of the pulmonary capillaries to carry the blood from the right side of the heart, causes an impediment in the discharge of the venous system into the right cavities of the heart, and thus gives rise to cyanosis; and it, moreover, as is clearly observed when of long continuance, induces active dilatation of the right side of the heart, the intensity of which corresponds to the degree of the impermeability of the pulmonary capillaries. We purpose in a future page to treat this subject more in detail.

Diseases of the left side of the heart, such as dilatation and hypertrophy of the ventricle, but more particularly contraction of the auriculo-ventricular opening, occasion the right side of the heart to be over-filled, in consequence of the obstruction opposed to the discharge of the blood from the capillaries of the lungs; and hence we have the phenomena of cyanosis, usually with extension of disease (dilatation and hypertrophy) to the right side of the heart.

Cyanotic Phenomena

Cyanotic Phenomena of various degrees of intensity may also depend on conditions of excessive density, and on continued compression of the lung (as for instance from exudations), on atelectasis of the lung, on catarrh and bronchial dilatation, emphysema of the lung, extensive pneumonia and pneumonic induration, pulmonary tuberculosis, etc, in like manner as on narrowness and closing of the arterial trunk, and admit of an equally easy mode of explanation. These phenomena of cyanosis may, moreover, either when congenital or acquired soon after birth, obstruct or wholly prevent the involution (closure) of the foetal passages.

All cyanoses, or rather all forms of disease of the heart, vessels, or lungs, inducing cyanosis of various kinds and degrees, are incompatible with tuberculosis, against which cyanosis offers a complete protection, and herein we find a key for the solution of the immunity against tuberculosis afforded by many conditions which at first sight appear to differ so widely from one another.