Louise M. Dudas

Heparin management protocol for cardiopulmonary bypass influences postoperative heparin rebound but not bleeding

A group of 63 adult patients undergoing cardiac surgical procedures requiring cardiopulmonary bypass (CPB) were studied to examine the relationship between heparin doses administered and postoperative bleeding. Patients were randomly assigned either to receive heparin 200 U/kg and additional heparin as needed to reach and maintain an activated clotting time (ACT) greater than 400 s for CPB (group A, n = 30), or to receive heparin 400 U/kg and additional heparin as needed to reach and maintain a whole blood heparin concentration greater than 4.0 U/ml for CPB (group H, n = 33). Groups were compared for the amount of postoperative bleeding, heparin rebound, homologous transfusion requirements, and standard laboratory coagulation tests. In the last 33 patients studied, additional tests of platelet aggregation and plasma levels of beta thromboglobulin (BTG), antithrombin III, and several markers of fibrinolysis were measured and compared by group. The mean heparin dose was 28,000 +/- 4,800 U for group A and 57,000 +/- 10,700 U for group H (P less than 0.05 for group A vs. group H). At 8 and 24 h postoperatively, mediastinal drainage did not differ significantly between groups (mean 24-h drainage +/- SD = 901 +/- 414 ml in group A, 1035 +/- 501 ml in group H), nor did the incidence of transfusion with homologous blood products.(ABSTRACT TRUNCATED AT 250 WORDS)

A randomized, blinded, placebo-controlled evaluation of calcium chloride and epinephrine for inotropic support after emergence from cardiopulmonary bypass

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.

Normal Parathyroid Hormone Responses to Hypocalcemia during Cardiopulmonary Bypass

To determine whether the calcium-magnesium-parathyroid hormone-calcitriol (vitamin D) axis responds appropriately to the hypocalcemia that routinely follows initiation of cardiopulmonary bypass (CPB), we measured blood ionized calcium (CaI), total calcium (CaT), total magnesium (MgT), ultrafilterable magnesium (MgI), total protein, intact parathyroid hormone (PTH), and calcitriol concentrations at eight defined time points in 28 patients undergoing elective cardiac surgery. With the onset of CPB, CaI decreased from 1.14 +/- 0.02 to 0.91 +/- 0.03 mM, P less than 0.05) (n = 17), and then gradually returned to a normal value by the time of separation from CPB (0.98 +/- 0.01 mM). CaT, MgI, MgT, and total protein concentrations declined significantly upon initiation of CPB and remained depressed thereafter. PTH initially decreased upon initiation of CPB (from 50 +/- 8 to 24 +/- 9 pg/ml, n = 9, P less than 0.05), remained inappropriately decreased during the early phases of CPB, and then gradually increased to maximal concentrations in response to hypocalcemia (103 +/- 15 pg/ml) before emergence. Calcitriol concentrations (n = 8) were unchanged during surgery. Based on these initial results, which suggested an association between hypomagnesemia and the slow PTH response to hypocalcemia, measurements were repeated in 10 additional patients, to whom magnesium (Mg) (1 g MgSO4 in two separate intravenous doses) was administered. Mg administration neither altered the PTH response to ionized hypocalcemia nor hastened the return of CaI to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Magnesium inhibits the hypertensive but not the cardiotonic actions of low-dose epinephrine

Intravenous magnesium supplementation is often used to control cardiac arrhythmias and coronary artery vasospasm resulting from disturbances of magnesium homeostasis after coronary artery bypass surgery. Many such patients also require inotropic drug support of depressed myocardial function. However, increased serum magnesium concentrations directly depress cardiac contractility in animals and may interfere with catecholamine actions. To determine whether small intravenous doses of magnesium sulfate (MgSO4) interfere with the cardiotonic actions of epinephrine, we examined the hemodynamic effects of MgSO4 and epinephrine infusion in 17 cardiac surgical patients on their 1st postoperative day in a prospective, controlled study. In 11 patients, infusion of MgSO4 (7-mg.kg-1 bolus followed by 10 mg.kg-1.h-1 as a continuous infusion) increased serum magnesium concentrations by 44% (mean +/- standard error of the mean [SEM] of 0.8 +/- 0.1 to 1.2 +/- 0.1 mM; P less than 0.01) but had no significant effect on heart rate; mean arterial, central venous, or pulmonary arterial occlusion pressures; or cardiac output. Epinephrine infusion (30 ng.kg-1.min-1) significantly increased cardiac index (2.7 +/- 0.1 to 3.1 +/- 0.21.min-1.m-2; P less than 0.05); this effect was not altered by MgSO4 administration (n = 11). However, MgSO4 significantly blunted epinephrines hypertensive action and prevented a significant increase in mean arterial pressure during concurrent MgSO4-epinephrine administration. Six placebo control patients were given two sequential infusions of epinephrine separated by a placebo infusion to rule out an effect of time on the hemodynamic response to epinephrine. Mean arterial pressure and cardiac index responses to epinephrine were identical before and after placebo infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart rate-right ventricular volume relation with myocardial revascularization

Whether increasing pacing frequency in cardiac surgical patients effectively improves right ventricular cardiac index depends on the interrelationships between heart rate, stroke volume index, and end-diastolic volume index. If an inverse relation exists between heart rate and right ventricular volume then the decrease in right ventricular ejection fraction described after bypass may be due, in part, to changes in heart rate. We evaluated the effects of pacing at 80, 95, and 110 beats/min using a thermodilution volumetric catheter in 16 patients undergoing myocardial revascularization. End-diastolic volume index, stroke volume index, and stroke work index were significantly greater after bypass than before bypass, whereas right ventricular ejection fraction remained constant. Before and after bypass, sequentially increasing pacing frequency from 80 to 110 beats/min decreased stroke volume index by 28% to 35% (p less than 0.001), end-diastolic volume index by 12% to 14% (p less than 0.001), and right ventricular ejection fraction by 18% to 24% (p less than 0.001). Right ventricular performance, assessed by comparing the stroke volume index to end-diastolic volume index and stroke work index to end-diastolic volume index relations generated during pacing, was not altered by bypass. We conclude that sequentially increasing heart rate from 80 to 110 beats/min fails to improve stroke volume index and consequently cardiac index before or after cardiac operations. Intraoperatively, in patients with normal left ventricular function, increasing pacing frequency decreases right ventricular ejection fraction due to simultaneous reductions in stroke volume index and end-diastolic volume index.