Acute Pulmonary Hypertensive Heart Disease: Pathophysiology

¹ Department of Cardiopulmonary Diseases, National Institute of Cardiology

The term "acute pulmonary hypertensive heart disease" is proposed to identify the condition characterized by the sudden appearance of functional alterations of the right ventricle with or without dilatation of its cavity due to a sudden elevation of the pulmonary arterial pressure.

The cardiopulmonary pathophysiologic alterations (hemodynamic, respiratory and humoral) produced by pulmonary thromboembolism, are directly related to the number of vessels occluded, the caliber of these, as well as to the secondary vascular reaction in the arterial section of the lung.

Experimental evidence has proved that if more than 60 per cent of the pulmonary arterial section is occluded, the right ventricle will dilate and the left ventricular output consequently will be reduced.

Clinical and experimental findings coincide in concluding that the vascular occlusion increases the resistance in the pulmonary arterial section through a double mechanism. One of these, purely mechanical in nature, is caused by the vascular obstruction through the emboli and the other one is functional and a consequence of the first; there being a vascular reaction probably produced by the liberation of chemical agents (serotonin and others).

Apparently the vasoconstriction, which may be local, regional or even generalized, only appears when the embolism is lodged in the vessels of less than 250 microns.