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The pulmonary vascular bed is normally a low-resistance, high-capacitance circuit capable of accommodating the entire cardiac output at pressures approximately 15%–20% of those in the systemic circulation. In pulmonary hypertension (PH), elevated pulmonary arterial pressure places a burden on the normally thin-walled right ventricle as it works to maintain normal blood flow. Without effective therapy, right heart dysfunction leads to progressive symptoms and is often fatal. Pulmonary hypertension is frequently a result of common left-sided heart or lung diseases. Less frequently, it results from a disease process intrinsic to the pulmonary vasculature itself. Differentiating among the several causes of PH requires methodical evaluation. Differentiation is essential because management varies according to the underlying cause, and misapplication of therapy can cause serious harm.
Apical 4-chamber view of an echocardiogram from a patient with idiopathic pulmonary arterial hypertension (left panel).
Dilatation of both the right atrium (RA) and right ventricle (RV) is appreciated when compared with an apical four chamber view from a healthy individual (right panel). Other echocardiographic findings in patients with pulmonary hypertension can include RV hypokinesis, septal flattening or bowing toward the left ventricle, tricuspid regurgitation, pulmonary insufficiency, and midsystolic closure of the pulmonary valve.
Electrocardiogram of a 31-year-old woman presenting with dyspnea, demonstrating right axis deviation, right atrial enlargement, and right ventricular hypertrophy with repolarization abnormality, suggesting pulmonary hypertension.
Posteroanterior chest radiograph in a patient with idiopathic pulmonary arterial hypertension.
Central pulmonary arteries are enlarged (top arrows), and the laterally shifted right heart contour (bottom left-hand arrow) suggests right atrial and right ventricular enlargement.
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