Calcium inhibits the cardiac stimulating properties of dobutamine but not of amrinone. Ionized calcium concentration and cardiovascular function after cardiopulmonary bypass. Calcium attenuates epinephrine's beta-adrenergic effects in postoperative heart surgery patients. Effects of single dose calcium gluconate infusion in hypocalcemic preterm infants. Effect of calcium therapy in the sick premature infant with early neonatal hypocalcemia.
To contrast the effect of increasing blood calcium concentrations on the cardiovascular actions of intravenous beta-adrenergic agonists and phosphodiesterase inhibitors, 46 patients recovering from aortocoronary bypass surgery received either dobutamine or amrinone both in the presence and absence of a calcium infusion. Cardiac output, systemic arterial pressure, pulmonary arterial pressure, central venous pressure, pulmonary artery occlusion pressure, heart rate, and blood ionized calcium concentration were measured before and during infusions of dobutamine (2.5 and 5.0 micrograms/kg/min) and amrinone (0.75 mg/kg bolus + 10 micrograms/kg/min or 2.25 mg/kg bolus + 20 micrograms/kg/min). After the initial dobutamine infusion period, patients were randomly and blindly assigned to receive either a calcium or placebo infusion, and the dobutamine infusions were repeated. Because of the long duration of amrinone's actions, the amrinone maintenance infusion was continued while randomized, blinded infusion of either calcium or placebo was added. Dobutamine (5 micrograms/kg/min) increased cardiac output from 7.1 +/- 0.3 L/min to 9.1 +/- 0.4 L/min, and increased heart rate from 93 +/- 4 beats/min to 107 +/- 4 beats/min. Systemic vascular resistance decreased and stroke volume increased. Dobutamine had no significant effects on other hemodynamic values. Amrinone (2.25 mg/kg bolus + 20 micrograms/kg/min) increased cardiac output from 5.6 +/- 0.4 L/min to 6.9 +/- 0.5 L/min, and increased heart rate from 87 +/- 3 beats/min to 98 +/- 3 beats/min. Amrinone decreased mean arterial pressure, systemic vascular resistance, pulmonary artery occlusion pressure, central venous pressure, and pulmonary artery pressure. Calcium infusion increased arterial pressure (8 to 13 percent) but had no significant effects on any other hemodynamic parameters. Calcium reduced the increase in cardiac output produced by dobutamine by 30 percent, but it did not alter the cardiotonic actions of amrinone. Thus, calcium inhibits the cardiotonic actions of certain beta-adrenergic agonists, most likely by interfering with signal transduction through the beta-adrenergic receptor complex. Patients who required cardiopulmonary bypass were studied to determine the postoperative incidence of hypocalcemia and to quantify the effects of intravenous (IV) calcium chloride on ionized calcium (Ca++) concentration in blood and on cardiac function. Patients either received no calcium chloride postoperatively (control), or received it as an intermittent IV bolus (5 mg/kg) or as a constant infusion (0.5 mg/kg/min) whenever Ca++ concentration was less than 1.8 mEq/L. Hemodynamic profiles were determined every 15 minutes during the first two postoperative hours. Regardless of Ca++ concentration and therapy, cardiac indices, stroke indices, and vascular resistances of all patients never differed significantly. No variable changed consistently, other than Ca++ concentration, in those patients receiving calcium chloride. We conclude that postoperative hypocalcemia occurs frequently after cardiopulmonary bypass surgery, but not to the degree that would be expected to cause cardiovascular depression, and is readily corrected with IV calcium chloride. Myocardial depression occurred in all patients, but likely resulted from other causes. Epinephrine and calcium possess both cardiac inotropic and vasopressor activity. In addition, epinephrine's cardiovascular effects are mediated via increases in intracellular calcium. As a result, many clinicians administer the two agents together in an attempt to augment their effects. Although this approach seems rational, it has never been proven effective. We evaluated the cardiovascular and hyperglycemic actions of epinephrine (10 and 30 ng/kg/min), with and without calcium chloride administration (10 mg/kg bolus followed by 2 mg/kg/hr infusion), in a prospective, randomized, blinded, crossover designed study. Twelve adult patients were studied 1 day after aortocoronary bypass surgery. Calcium chloride raised ionized calcium levels from 1.06 +/- 0.03 (mean +/- SEM) to 1.44 +/- 0.05 mM (p less than 0.05). Calcium raised mean arterial pressure from 85 +/- 1 to 94 +/- 2 mm Hg (p less than 0.05) but had no significant effect on cardiac index. Epinephrine alone at 10 and 30 ng/kg/min significantly raised cardiac index from 2.7 +/- 0.2 to 3.0 +/- 0.2 (p less than 0.05) and 3.6 +/- 0.3 (p less than 0.05) l/min/m2. After calcium, epinephrine failed to significantly increase cardiac index. Epinephrine at 30 ng/kg/min significantly increased mean arterial pressure from 87 +/- 1 to 95 +/- 2 mm Hg (p less than 0.05). After calcium, epinephrine had no significant effect on blood pressure. In addition, epinephrine's hyperglycemic effect was blunted by calcium. Plasma epinephrine levels were similar during control and calcium infusions. We conclude that calcium blunts epinephrine's beta-adrenergic actions in postoperative cardiac surgery patients. We conducted a prospective, double-blind study of 43 preterm infants to examine the effect of a single calcium gluconate infusion as therapy for neonatal hypocalcemia on serum calcium concentrations and hypocalcemic signs in preterm infants with low total serum calcium concentrations. Total and ionized serum calcium was measured and signs of irritability, jitteriness, and twitching were scored (scale 0-9) by blinded observers before and after receiving one dose of either calcium gluconate (100 mg/kg) or placebo (normal saline). Total and ionized serum calcium increased 3 to 6 hours following the calcium, but not the placebo, infusion. Of the infants with hypocalcemic signs, the average score of hypocalcemic signs decreased in the 11 calcium-treated infants; the 12 infants with hypocalcemic signs showed no change of hypocalcemic signs following treatment with placebo. We conclude from this study that a single dose of calcium gluconate (100 mg/kg) in hypocalcemic preterm infants raise total and ionized serum calcium and decrease clinical signs of hypocalcemia. Twenty-seven sick premature infants with serum calcium concentrations less than 6.0 mg/dl during the first day of age were enrolled in a prospective controlled study involving two treatment regimens--calcium given as a bolus or a drip--or no treatment. Mean total calcium concentration was 5.5 +/- 0.8 mg/dl, and ionized calcium was 3.1 +/- .3 mg/dl, with no significant difference between treatment groups. By 24 hours, in all groups total calcium had increased to greater than 6.0 mg/dl (bolus 6.5 +/- 1.1, drip 7.0 +/- 0.4, control 6.6 +/- 0.4) and ionized calcium to greater than 3.5 mg/dl (bolus 3.9 +/- 0.3, drip 3.6 +/- 0.6, control 3.6 +/- 0.3). Ionized and total calcium concentrations were significantly correlated (r = 0.562; P less than 0.001), but total calcium did not predict ionized calcium in any group. These data support the concept that, even in sick infants, early neonatal hypocalcemia is a physiologic phenomenon that may not require treatment.
There is no clear evidence that parenteral calcium supplementation impacts the outcome of critically ill patients.