Respiratory Insufficiency and Chronic Cor Pulmonale

Abstract

Because of newer technics of treatment, a small but ever increasing number of patients with chronic pulmonary disease are surviving long enough to develop chronic cor pulmonale. An attempt has been made to correlate the newer knowledge of aberrations of cardiocirculatory and respiratory physiology in chronic pulmonary disease. Respiratory insufficiency may be due to varying proportions to the following: (1) ventilatory dysfunction or impairment of the ability to move air into or out of the lungs; this may be of two types: (a) obstructive, due primarily to airway narrowing and (b) restrictive, due to disordered function of the thoracic bellows or diminished pulmonary distensibility; (2) unequal distribution of inspired air to the alveoli (intrapulmonary mixing); (3) uneven perfusion or distribution of capillary blood flow; (4) impaired diffusion or transfer of oxygen across the alveolar capillary barrier and (5) impaired cleansing of the lung. The same abnormal physiologic change may result from pathologic conditions which differ widely in etiology; furthermore, a particular disease may give rise to widely differing functional patterns. The types of pulmonary disease causing chronic cor pulmonale may be divided into two main categories: (1) Type I, pulmonary diseases associated with chronic diffuse obstructive emphysema. (2) Type II, pulmonary diseases in which the pathologic process tends to be localized in or about the pulmonary vessels. In some instances, a case belongs mainly in one category but may demonstrate some features of the other. The strain on the right ventricle is a result of: (1) increased resistance to pulmonary blood flow and (2) increased cardiac output (when present). Increased resistance to pulmonary flow may be due to: (a) reduction in caliber and distensibility of the pulmonary vascular bed which may be structural or related to hypoxia, (b) polycythemia and (c) intrapulmonary vascular shunts. Respiratory insufficiency may be suspected from the history. Physical and roentgenologic examinations may be confirmatory, but pulmonary function tests are necessary for a precise evaluation of the functional abnormalities. The recording of a physiologic, as well as a pathologic diagnosis, is a useful practice in the individual case. The presence of right ventricular enlargement can only be detected clinically when the chronic cor pulmonale is moderately advanced. However, clinical and roentgenologie evidence of pulmonary hypertension in chronic pulmonary disease indicates that right ventricular hypertrophy is probably present. The electrocardiogram may be helpful even in the absence of a definite right heart strain pattern since the electric position of the heart is often suggestive. Cardiac catheterization provides the best method for the early detection of pulmonary hypertension. The treatment of chronic cor pulmonale is much more hopeful today than in the past. It is most satisfactory when cor pulmonale is due to pulmonary disease of type I. Intensive therapy of the bronchopulmonary disease is as important as specific cardiac measures. The objectives of therapy are to combat infection, produce an adequate airway and improve effective alveolar ventilation. This may partially reverse many of the pathologic changes in the lung which are responsible for hypoxia and the anatomic reduction in the pulmonary vascular bed.