Etiology and classification of pulmonary hypertension

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Pulmonary hypertension is the consequence of either acute or chronic athological mechanisms resulting in a loss of the independence of pulmonary artery pressure and cardiac output. Although pulmonary hypertension can be characterized by more or less arbitrary pulmonary artery pressure limits under static conditions, it is better defined by an increasingly linear relationship between vascular resistance and cardiac output when blood flow is elevated ( Table 1). Whereas in healthy subjects the cross-sectional area of the pulmonary vascular bed increases with elevated cardiac output owing to recruitment of apical vessels, a restriction of this mechanism causes a linear dependence of blood flow and pulmonary artery pressures which correlates with disease severity. The pulmonary circulation then behaves like the systemic circulation and no longer as a 'high-flow-low-pressure system' ( Edsod 1989).

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Table 1 Definition of pulmonary hypertension

Pulmonary hypertension can be differentiated by (a) its underlying pathophysiological mechanism ( Table.2), (b) clinically by its pulmonary or extrapulmonary origin (Table.. ..3), or (c) its anatomical location (i.e. pre- or postcapillary). Many pathological conditions can eventually result in pulmonary hypertension, but in the intensive care unit (ICU) most patients develop pulmonary hypertension in relation to the acuteness of the underlying disease. Other patients, in whom pulmonary hypertension is either latent or develops subacutely, are clinically asymptomatic unless severe structural changes in pulmonary vasculature result in progressive deterioration of pulmonary or cardiovascular function. Advanced stages of chronic pulmonary hypertension represent a major therapeutic challenge because of vascular remodeling and compensatory transformation of the pulmonary circulation including the right ventricle.

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Table 2 Causes of pulmonary hypertension

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