Pulmonary hypertension in chronic obstructive lung disease

Abstract

Pulmonary hypertension in chronic pulmonary lung disease (COPD) is caused by alveolar hypoxia and pulmonary vasoconstriction. The result is remodeling of smaller pulmonary arteries, with nicotine being a major contributing factor. Hypoxic pulmonary hypertension is enhanced by respiratory acidosis. There is inter-individual variability in the susceptibility of pulmonary vessels to hypoxia. Genetic differences may also be responsible for varying degrees of pulmonary vascular remodeling. This may partly explain the various degrees of pulmonary hypertension associated with the same degree of respiratory insufficiency. Pulmonary hypertension in COPD is usually mild. Mean pulmonary artery pressure is in the range of 20-35 mmHg; progression of pulmonary hypertension is slow. Initially, mean pulmonary artery pressure at rest is normal while increasing, at a workload of 40 W and at steady state, to levels over 30 mmHg; this is referred to as exercise-induced pulmonary hypertension. Those with exercise-induced pulmonary hypertension are more likely to develop resting pulmonary hypertension. Repeat increases in pulmonary artery pressure have been suggested to contribute to the development of heart failure. Pulmonary hypertension also becomes more severe during sleep (particularly during REM sleep) as does hypoxemia. Pulmonary hypertension tends to deteriorate during acute episodes of airway infection in parallel with deteriorated respiratory function whereby mean pulmonary artery pressure rises by as much as 20 mmHg. These episodes may contribute to the development of right-heart failure. Recent findings suggest that pulmonary embolism may be a relatively frequent cause of acute exacerbation of cor pulmonale. Severe pulmonary hypertension is present in no more than 5-10% COPD patients except for situations when they are assessed during acute exacerbation; exceptions include associated left-heart disease and embolism. Vascular remodeling in these patients resembles the pulmonary vascular remodeling in pulmonary arterial hypertension. Although pulmonary hypertension is usually mild in lung disease, less often moderate, and seldom severe, mean pulmonary artery pressure is the most reliable prognostic predictor also in multivariate analysis. While Doppler echocardiography was a major advance in non-invasive diagnosis of pulmonary hypertension, it may be occasionally associated with no negligible problems in COPD patients. The absence of abnormal right ventricular size and function will usually rule out pulmonary hypertension. Right ventricular function at rest and during exercise can be assessed using radionuclide ventriculography and echocardiography. Alternatively, right ventricular function and size can be assessed by spiral CT angiography or, ideally, by magnetic resonance imaging. In conclusion, this overview points to problems encountered in the diagnosis of right-heart failure and outlines the potential role of vasodilator therapy, particularly in patients with severe pulmonary hypertension.