VOLUME EXPANSION INCREASES RIGHT-VENTRICULAR INFARCT SIZE IN DOGS BY REDUCING COLLATERAL PERFUSION

Study objective: Plasma volume expansion is frequently recommended to correct the low output state resulting from right ventricular (RV) inf arction. However, any subsequent increase in pericardial and RV fillin g pressures from volume expansion could impair RV collateral blood flo w. We examined whether volume expansion in dogs before right coronary Ligation reduced collateral perfusion and worsened the extent of RV ne crosis. Design: Randomized experimental study. Setting: Animal researc h laboratory in university medical center. Participants: Forty anesthe tized, closed-chest dogs were randomly assigned to normovolemic, peric ardium opened (n=10) or intact (n=10) groups, and hypervolemic, perica rdium opened (n=10) or intact (n=10) groups. Interventions: Hypervolem ic animals received 24 mL/kg of 6% hetastarch. All animals underwent 9 0 min right coronary ligation, followed by 120 min reperfusion. Collat eral coronary blood flow (radioactive microspheres) and area of necros is (An) were determined in the area at risk (Ar). Measurements and res ults: Stroke volume decreased in all groups with ischemia but remained 25 to 40% greater in both hypervolemic groups than in normovolemic an imals (p<0.05). In hypervolemic animals with intact pericardium, RV en d-diastolic pressure increased to 10.4+/-2.1 mm Hg (mean+/-SD), a valu e that significantly exceeded those of the other three groups. During RV ischemia, collateral perfusion in the Ar was similar in both normov olemic groups and in hypervolemic animals with opened pericardium (mea n range, 12.9+/-8.8 to 13.8+/-7.6 mL/min/100 g; p=NS), and the An/Ar v aried from 11.8+/-6.3 to 18.6+/-17.4% (p=NS). In contrast, in hypervol emic animals with intact pericardium, collateral perfusion decreased t o 7.2+/-3.5 mL/min/100 g and the An/Ar was increased to 38.2+/-18.6% ( p<0.05 compared with other groups, respectively). Overall, An/Ar was i nversely related to collateral blood flow in the Ar (r=-0.46; p<0.05) and correlated positively with RV end-diastolic pressure (r=0.61; p<0. 05). Conclusions: Volume expansion preserved stroke volume during RV i schemia, independent of pericardial integrity. However, volume expansi on in animals with an intact pericardium increased RV infarct size by twofold to threefold secondary to reduced periischemic collateral perf usion. This detrimental effect of volume expansion on infarct size was prevented by opening the pericardium.