It has been repeated so often that death from pneumonia is the result of heart failure that this view seems to be accepted generally by the medical profession.1 The frequent observation of a dilated right side of the heart, with more or less evidence of toxic myocarditis at autopsy seems to be the basis for this assumption. If it is true that the patient with pneumonia dies only because the heart muscle gives way, the clinical data observed during life should corroborate this fact. If it is not true, it is important, from the standpoint of both therapy and prognosis, that the true pathologic physiology of the disease should be understood.
The terminal dilatation of the heart is commonly believed to result from the combined effect of two factors: (a) the impairment of functional integrity through the injurious action of the toxins of the infection on the muscle tissue of
RANDOLPH BM. THE CARDIOVASCULAR PROBLEM IN PNEUMONIA. Arch Intern Med (Chic). 1929;43(2):249–266. doi:10.1001/archinte.1929.00130250107008
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