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Ann Thorac Surg 1984;37:133-140
© 1984 The Society of Thoracic Surgeons
From the Section of Cardiothoracic Surgery and the Department of Anesthesiology, Mayo Clinic and Mayo Foundation, Rochester, MN
* Address reprint requests to Dr. Shapira, Deborah Heart and Lung Center, Browns Mills, NJ 08015
To determine the hemodynamic effects of intravenous injection of calcium chloride, 26 patients were studied immediately after termination of extracorporeal circulation. Eighteen patients (Group A) had injection of a single bolus of CaCl2; in the other 8 patients (Group B), the bolus injection was followed by infusion of CaCl2 at a rate of 1.5 mg/kg/min for 10 minutes. Myocardial contractile element velocity (Vpm), aortic blood flow, electrocardiograms, and left ventricular, systemic arterial, pulmonary arterial, and left atrial pressures were recorded continuously. The baseline ionized calcium level after bypass was 3.6 ± 0.6 mg/100 ml (normal range, 3.9 to 4.5 mg/100 ml); this increased to 5.4 ± 0.5 mg/100 ml 1 minute after CaCl2 injection. The ionized calcium level was 4.7 ± 0.6 mg/100 ml 6 minutes after CaCl2 injection in Group A, and was 5.9 ± 0.2 mg/100 ml and 6.4 ± 0.2 mg/100 ml at 6 and 10 minutes, respectively, in Group B. There was significant early hemodynamic improvement after CaCl2 injection, including increases in Vpm (p < 0.001), cardiac index (p < 0.001), mean blood pressure (p < 0.01), and stroke volume index (p < 0.001).
A similar pattern of hemodynamic response was observed in both groups. Approximately 1 minute after CaCl2 injection, cardiac index returned to control level, Vpm and mean blood pressure remained elevated, and heart rate declined (p < 0.01). Systemic vascular resistance gradually increased and was significantly elevated (p < 0.05) in Group B at 3 minutes and in Group A at 6 minutes.
We conclude that after cardiopulmonary bypass, injection of CaCl2 causes both immediate and sustained enhancement of myocardial performance and blood pressure. A transient elevation of cardiac index is followed by a gradual increase in systemic vascular resistance.
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