Royster R L, Butterworth J F, Prielipp R C, Robertie P G, Kon N D, Tucker W Y, Dudas L M, Zaloga G P
Department of Anesthesia, Wake Forest University Medical Center, Bowman Gray School of Medicine, Winston-Salem, North Carolina 27157-1009.
Anesth Analg. 1992 Jan;74(1):3-13. doi: 10.1213/00000539-199201000-00003.
Forty hemodynamically stable patients were randomized to receive an intravenous bolus of either calcium chloride (5 mg/kg) (n = 20) or placebo (n = 20) (phase I). Six minutes later, they received either an epinephrine (30 ng.kg-1.min-1) (n = 20) or placebo (n = 20) infusion (phase II). Hemodynamic and ionized calcium measurements were obtained in phase I at baseline and at 3 and 6 min after the bolus, and in phase II, at 3 and 6 min (study times 9 and 12 min) after initiation of the infusion. Compared with placebo, calcium did not significantly increase cardiac index but significantly increased mean arterial pressure. Calcium improved cardiac index from 2.46 +/- 0.12 (mean +/- SEM) to 2.74 +/- 0.12 L.min-1.m-2; likewise, placebo improved cardiac index from 2.51 +/- 0.15 to 2.74 +/- 0.15 L.min-1.m-2. Mean arterial blood pressure increased with calcium from 74 +/- 2 to 82 +/- 3 mm Hg compared with a placebo change of 74 +/- 2 to 76 +/- 2 mm Hg. Patients who received the epinephrine infusion (n = 20) demonstrated a significant increase in cardiac index at time 12 min compared with patients receiving only placebo (n = 20). Cardiac index of the epinephrine group increased from 2.56 +/- 0.15 to 2.92 +/- 0.22 L.min-1.m-2, whereas in the placebo group it decreased from 2.86 +/- 0.13 to 2.78 +/- 0.12 L.min-1.m-2. Prior administration of calcium did not alter the subsequent response to epinephrine (n = 10) compared with patients receiving epinephrine alone (n = 10). We conclude that cardiac index improves with time without drug therapy after bypass. Calcium chloride increases mean arterial blood pressure but not cardiac index immediately after cardiopulmonary bypass, whereas low-dose epinephrine significantly increases both cardiac index and mean arterial blood pressure without causing tachycardia in these patients. Calcium chloride (5 mg/kg) did not augment or inhibit the hemodynamic response to an epinephrine infusion.
40名血流动力学稳定的患者被随机分为两组，分别接受静脉推注氯化钙（5mg/kg）（n = 20）或安慰剂（n = 20）（I期）。6分钟后，他们接受肾上腺素（30ng·kg-1·min-1）（n = 20）或安慰剂（n = 20）输注（II期）。在I期，于基线、推注后3分钟和6分钟测量血流动力学和离子钙；在II期，于输注开始后3分钟和6分钟（研究时间9分钟和12分钟）测量。与安慰剂相比，氯化钙未显著增加心脏指数，但显著增加平均动脉压。氯化钙使心脏指数从2.46±0.12（均值±标准误）提高到2.74±0.12L·min-1·m-2；同样，安慰剂使心脏指数从2.51±0.15提高到2.74±0.15L·min-1·m-2。氯化钙使平均动脉血压从74±2mmHg升高到82±3mmHg，而安慰剂组从74±2mmHg升高到76±2mmHg。接受肾上腺素输注的患者（n = 20）在12分钟时的心脏指数较仅接受安慰剂的患者（n = 20）显著增加。肾上腺素组的心脏指数从2.56±0.15升高到2.92±0.22L·min-1·m-2，而安慰剂组从2.86±0.13降低到2.78±0.12L·min-1·m-2。与单独接受肾上腺素的患者（n = 10）相比，预先给予氯化钙并未改变随后对肾上腺素的反应（n = 10）。我们得出结论，体外循环后未经药物治疗心脏指数随时间改善。氯化钙在体外循环后即刻增加平均动脉血压但不增加心脏指数，而低剂量肾上腺素在这些患者中显著增加心脏指数和平均动脉血压且不引起心动过速。氯化钙（5mg/kg）未增强或抑制对肾上腺素输注的血流动力学反应。
