Background Diastolic dysfunction is common immediately after coronary artery bypass surgery (CABG). The duration of this phenomenon is unknown. Intravenous calcium is frequently administered during separation from cardiopulmonary bypass (CPB). We sought to determine whether intravenous calcium influences perioperative diastolic function and whether diastolic dysfunction persists into the postoperative period. Methods and Results Patients undergoing first-time elective CABG (n = 29) were randomly assigned to receive intravenous calcium chloride (n = 13) or placebo (n = 16) during separation from CPB. Diastolic function was assessed by the pressure-area relation with transesophageal echocardiography and pulmonary capillary wedge pressure (PCWP) measured simultaneously. Left ventricular end-diastolic area (LVEDA) and Doppler indexes were measured at comparable PCWP (within 2 mm Hg) at baseline, after separation from CPB, after sternal closure, and 3 hours after surgery. After CABG, both groups had a significant decrease in LVEDA and mitral E-wave deceleration time that persisted at 3 hours. Because there were no significant differences between the calcium and control groups at any tune point, the data for the entire study cohort was analyzed. The LEDA decreased (stiffness increased) progressively from 16.9 +/- 3.4 cm(2) at baseline to 15.8 +/- 2.9 cm(2) after CPB, 14.9 +/- 2.5 cm(2) after sternal closure, and 14.3 +/- 3.1 cm(2) at 3 hours after surgery (P < .0001). The mitral E-wave deceleration time measured at the same time points was 168 47 ms, 136 +/-. 25 ms, 137 +/- 36 ms, and 111 +/- 44 ms (P = .0001). Conclusions An increase in left ventricular diastolic chamber stiffness is nearly universal after CABG, and it persists for at least 3 hours after surgery. An intravenous bolus of calcium chloride given during, separation from CPB has no measurable negative effect on diastolic function. In the setting of increased chamber stiffness, the PCWP alone sloes not adequately reflect the volume status and effective preload of the left ventricle.
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