What is the role of cardiac catheterization in the diagnosis of pulmonary veno-occlusive disease (PVOD)?

Updated: Oct 16, 2018
  • Author: Hakim Azfar Ali, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Interestingly, a clue to the diagnosis of pulmonary veno-occlusive disease (PVOD) is the inability to accurately measure the wedge pressure during cardiac catheterization. Multiple wedge pressure measurements or a distal wedge reading confirmed by a partial pressure of oxygen similar to arterial blood should be performed to determine the correct wedge pressure.

A correctly performed pulmonary capillary wedge pressure measurement generally reveals normal or decreased wedge pressure, despite the fact that the pulmonary capillary pressures (in the absence of a static blood column) are elevated. Occasionally, an elevated wedge pressure may be obtained, depending on the degree of venous occlusion and collaterals. This may occur because of the patency of the larger pulmonary veins. [27]

In PVOD, the use of a short-acting pulmonary arterial vasodilator, such as inhaled nitric oxide or intravenous epoprostenol or adenosine, during acute vasoreactivity testing may precipitate acute pulmonary edema. The edema results from increased transcapillary hydrostatic pressures in the setting of acute arterial vasodilation and preexisting venous occlusion. The development of pulmonary edema in response to a pulmonary vasodilator, therefore, is strongly suggestive of the diagnosis of PVOD. [46] This complication in association with the poor response of PVOD patients to PAH-specific therapy argues against vasodilator testing in patients in whom PVOD is strongly suspected.

The development of acute fulminant pulmonary edema, and even death, has been reported with infusion of even a very low dose of intravenous epoprostenol. Hence, great caution should be used in patients with suspected PVOD while administering intravenous epoprostenol. [47]

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