It is usually chronic but may be acute and reversible. Etiology Acute cor pulmonale usually results from massive pulmonary embolization but often occurs as acute reversible exacerbations of chronic cor pulmonale in patients with COPD, usually during acute respiratory infection. However, the most important mechanism leading to pulmonary hypertension is alveolar hypoxia, which results from localized inadequate ventilation of well-perfused alveoli or from a generalized decrease in alveolar ventilation. Alveolar hypoxia, whether acute or chronic, is a potent stimulus of pulmonary vasoconstriction, and chronic alveolar hypoxia also promotes hypertrophy of smooth muscle in the pulmonary arterioles. 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.