Pathophysiology of Rupture of the Pulmonary Artery by Pulmonary Artery Balloon-Tipped Catheters

Abstract

High pressures have been reported in pulmonary artery catheter balloons. This study was undertaken to determine the in vitro rupturing pressures of human peripheral pulmonary arteries and to evaluate whether such pressures could be generated under clinical conditions. The in vitro model then was confirmed in vivo in the dog and the evolution of a rupture of a peripheral pulmonary artery studied. In vitro, pulmonary arteries of subjects under age 60 yr are remarkably resistant and tolerate intra-balloon pressures of 2700 mm Hg in the one mid-pulmonary artery studied and up to 4219 +/- 720 mm Hg (mean +/- SD) in the distal pulmonary artery. Subjects over the age of 60 yr have significantly lower rupturing pressures (1965 +/- 540 mm Hg in the mid-pulmonary artery, and 2498 +/- 600 mm Hg in the distal pulmonary artery), (P less than 0.05). Thus overdistension by the balloon may explain most ruptures. Preexisting pulmonary hypertension did not affect in vitro rupturing pressures. Clinicians generated intraballoon mean pressures of 795 +/- 130 mm Hg, with 20% of them generating higher and potentially dangerous pressures (1000 mm Hg or more). The in vitro model was confirmed by in vivo studies in dogs with pressures that cause pulmonary artery rupture. Furthermore, in normal dogs, rupture of a peripheral pulmonary artery was without complications. This suggests that rupture of the peripheral pulmonary artery may occur clinically more frequently than reported. The user of flotation pulmonary arterial catheters should be aware of the dangers associated with this diagnostic tool. In particular, liquids must never be used to inflate pulmonary arterial catheter balloons.