Abstract
Vasodilatinga medications have been shown to increase cardiac output (CO) and decrease pulmonary vascular resistance (PVR) in both stable and acutely ill patients with chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PHTN). Increasing CO raises the pulmonary arterial pressure (Ppa) more than normally expected in patients with pulmonary vascular disease. However, because PVR may decrease passively as CO increases, the specific vasodilating properties of a drug can only be assessed by measuring its effect on Ppa at comparable levels of CO.
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