Limited evidence supports the use of hemodynamic variables that correlate with delayed cerebral ischemia or pulmonary edema after aneurysmal subarachnoid hemorrhage. The aim of this study was to identify those hemodynamic variables that are associated with delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage.Design:
A multicenter prospective cohort study.Setting:
Nine university hospitals in Japan.Patients:
A total of 180 patients with aneurysmal subarachnoid hemorrhage.Interventions:
None.Measurements and Main Results:
Patients were prospectively monitored using a transpulmonary thermodilution system in the 14 days following subarachnoid hemorrhage. Delayed cerebral ischemia was developed in 35 patients (19.4%) and severe pulmonary edema was developed in 47 patients (26.1%). Using the Cox proportional hazards model, the mean global end-diastolic volume index (normal range, 680–800 mL/m2) was the independent factor associated with the occurrence of delayed cerebral ischemia (hazard ratio, 0.74; 95% CI, 0.60–0.93; p = 0.008). Significant differences in global end-diastolic volume index were detected between the delayed cerebral ischemia and non–delayed cerebral ischemia groups (783 ± 25 mL/m2 vs 870 ± 14 mL/m2; p = 0.007). The global end-diastolic volume index threshold that best correlated with delayed cerebral ischemia was less than 822 mL/m2, as determined by receiver operating characteristic curves. Analysis of the Cox proportional hazards model indicated that the mean global end-diastolic volume index was the independent factor that associated with the occurrence of pulmonary edema (hazard ratio, 1.31; 95% CI, 1.02–1.71; p = 0.03). Furthermore, a significant positive correlation was identified between global end-diastolic volume index and extravascular lung water (r = 0.46; p < 0.001). The global end-diastolic volume index threshold that best correlated with severe pulmonary edema was greater than 921 mL/m2.Conclusions:
Our findings suggest that global end-diastolic volume index impacts both delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage. Maintaining global end-diastolic volume index slightly above normal levels has promise as a fluid management goal during the treatment of subarachnoid hemorrhage.