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The relationship between left ventricular filling pressure and plasma colloid osmotic pressure to pulmonary edema was examined in a group of 37 patients, the majority of whom were hypovolemic. Sixteen patients developed pulmonary edema during fluid infusion. In the 21 patients who did not develop pulmonary edema, the left ventricular filling pressure was slightly elevated but the colloid osmotic pressure was not reduced. The majority of these patients were treated with colloid solutions (group I). In five of the 16 patients who developed pulmonary edema, the left ventricular filling pressure was elevated and there was no reduction in the plasma colloid osmotic pressure. These patients received only colloids (group II). In the other 11 patients who developed pulmonary edema, the left ventricular filling pressure was normal but the plasma colloid osmotic pressure was reduced to 16 +/- 2 torr (group III). The colloid osmotic pressure in this group was significantly less than in the other two groups (P less than 0.01). Most of these patients received large volumes of crystalloid solutions. After administration of furosemide, clearing of pulmonary edema in this group was associated with normalization of the plasma colloid osmotic pressure. Infusion of large volumes of crystalloids in hypovolemic patients can be hazardous, for reduction of the plasma colloid osmotic pressure may predispose to the development of pulmonary edema even when the left ventricular filling pressure remains normal.

of rupture of the pulmonary artery by pulmonary artery balloon-tipped catheters. Anesth Analg 1983;62:925-30. 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 k 720 mm Hg (mean 5 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 2 600 mrn Hg in the distal pulmonary artery), (P < 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 Hgor 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.

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