Abstract
1. The weights and intraventricular volumes of the right ventricles have been determined from 198 hearts from patients with pulmonary diseases. 2. For diagnosis of concentric or eccentric cardiac hypertrophy the relative volume (the degree of dilatation) of a ventricle, i.e., intraventricular volume in ml/100 g ventricular muscle mass, serves as the most important criterion. 3. In cases of chronic cor pulmonale the hypertrophic right ventricle is more likely to be concentric than normal right ventricles, which have a postnatal physiological structural dilatation. 4. The adaptative hypertrophic growth of the right ventricle is associated with an increasing absolute intraventricular volume but the relative volume (the degree of dilatation) decreases. 5. As a result of pathological pressure load in chronic cor pulmonale the right ventricle develops a shape which resembles the normal left ventricle. This “left-ventricularisation” of a hypertrophied right ventricle is more pronounced in younger individuals. 6. In extreme systemic arterial hypertension the blood pressure rises to twice the normal and the weight of the hypertrophied left ventricle is 3–4 times above normal. In cor pulmonale blood pressure values can be 4–5 times and the weights of the hypertrophied right ventricle 5–6 times greater than normal. 7. Chronic failure of the hypertrophic left ventricle is combined with an increasing relative ventricular volume (i.e. eccentric structural dilatation). Failure of the hypertrophic right ventricle can develop although the relative ventricular volume of the degree of dilatation is less than in the normal (concentric hypertrophy compared with the normal right ventricle). 8. Calculations indicate that chronic cor pulmonale would require a weight of right ventricle muscle exceeding 10 times normal in order to maintain a long-term compensation. 9. Despite the good coronary blood supply of the right ventricle, with its excellent adaptative growth, hypertrophy accompanied by a decrease in the degree of dilatation is insufficient to compensate for the pressure load in chronic cor pulmonale and the primary physiological structural dilatation.
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