In the presence of postcapillary pulmonary hypertension, physiologic disturbances may begin when the total intravascular pressure exceeds the oncotic pressure of the blood. As a result, fluid leaks out of the vessels and collects in the interstitium before pouring into the alveoli.

Pulmonary edema interferes with gas exchange, resulting in a state of hypoxemia. Alveolar hypoxia has a profound influence on the pulmonary vessels, causing them to constrict. Since there is greater alveolar hypoxia in the lung bases than in the apices, the basilar vessels constrict significantly, forcing the blood to flow upward. This phenomenon actually represents a reversal of the normal PBF pattern: redistribution or cephalization of the pulmonary vascularity.

Cephalization occurs in any of three conditions: (1) left-sided obstructive lesions, e.g., mitral stenosis^! (see Fig. 12-3/1) or aortic stenosis, (2) left ventricular failure, e.g., coronary heart disease or cardiomyopathies, and (3) severe mitral regurgitation even before pump failure of the left ventricle occurs. It should be emphasized that unless there is obvious constriction of the lower-lobe vessels, the diagnosis of cephalization should not be made. Dilatation of the upper-lobe vessels is of secondary importance and can be found without narrowing of the basilar vessels in a number of entities, most noticeably left-to-right shunts.

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