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Pulmonary hypertension , an abnormal elevation in pulmonary artery pressure, may be the result of left heart failure, pulmonary parenchymal or vascular disease, thromboembolism, or a combination of these factors. Whether the pulmonary hypertension arises from cardiac, pulmonary, or intrinsic vascular disease, it generally is a feature of advanced disease. Because the causes of pulmonary hypertension are so diverse, it is essential that the etiology underlying the pulmonary hypertension be clearly determined before embarking on treatment.
Cor pulmonale is a term used to indicate right ventricular (RV) enlargement secondary to any underlying cardiac or pulmonary disease. Pulmonary hypertension is the most common cause of cor pulmonale. Advanced cor pulmonale is associated with the development of RV failure.
The right ventricle responds to an increase in resistance within the pulmonary circulation by increasing RV systolic pressure as necessary to preserve cardiac output. Over time, chronic changes occur in the pulmonary circulation that result in progressive remodeling of the vasculature, which can sustain or promote pulmonary hypertension even if the initiating factor is removed.
The ability of the RV to adapt to increased vascular resistance is influenced by several factors, including age and the rapidity of the development of pulmonary hypertension. For example, a large acute pulmonary thromboembolism can result in RV failure and shock, whereas chronic thromboembolic disease of equal severity may result in only mild exercise intolerance. Coexisting hypoxemia can impair the ability of the ventricle to compensate. Several studies support the concept that RV failure occurs in pulmonary hypertension when the RV myocardium becomes ischemic due to excessive demands and inadequate right ventricular coronary blood flow to the RV. The onset of clinical RV failure, usually manifest by peripheral edema, is associated with a poor outcome.
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