These hypertrophied vessels respond to subsequent acute hypoxia. Hypercapnic acidosis augments the pulmonary vasoconstriction. During chronic hypoxia, pulmonary hypertension may be intensified by increased blood viscosity arising from secondary polycythemia and by increased cardiac output. However, increased pulmonary capillary pressure does not contribute per se to the pathogenesis of pulmonary arterial hypertension in cor pulmonale. Hypoxemia and acidosis often aggravate independent disease of the LV and intensify respiratory insufficiency if LV failure induces pulmonary edema.
Exertional dyspnea is the most common symptom of pulmonary hypertension.
Some patients suffer syncope or fatigue on exertion, and substernal anginal pain is common. Physical signs include left parasternal systolic lift and a loud pulmonic second sound. Murmurs due to functional tricuspid and pulmonic insufficiency may occur. These signs of right heart enlargement appear early and are readily discernible in acute cor pulmonale. Chest x-rays show RV and proximal pulmonary artery enlargement with distal arterial attenuation.