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ARTICLE |

THE RIGHT VENTRICLE IN PULMONARY TUBERCULOSIS

ERNST P. BOAS, M.D.; HUBERT MANN, M.D.
Arch Intern Med (Chic). 1921;28(1):62-70. doi:10.1001/archinte.1921.00100130067006.
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Current medical opinion, in so far as it is directed to the heart in the tuberculous patient, seems to take it for granted that in chronic phthisis there is frequently found a dilatation and hypertrophy of the right ventricle. This is explained usually by the assumption that with extensive pulmonary disease there is a partial obliteration and obstruction of the pulmonary stream bed which exacts an increased amount of work from the right ventricle to maintain the circulation. This mechanism would be analogous to the left ventricular hypertrophy that accompanies arterial hypertension. Thus Bohland1 states that such a hypertrophy is present in chronic phthisis, that it is compensatory in its nature, and that the enlarged right ventricle, having little reserve, easily becomes insufficient. Krehl,2 too, mentions that such hypertrophy is of frequent occurrence.

On analysis, the evidence for this belief is found to be conflicting and for the most part

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