Effects of calcium on left ventricular function early after cardiopulmonary bypass.

OBJECTIVES: Evaluation of the effects of intravenous CaCl2 on systolic and diastolic function early after separation from cardiopulmonary bypass (CPB) DESIGN: Prospective study SETTING: University hospital PARTICIPANTS: Twenty patients scheduled for elective coronary artery surgery INTERVENTIONS: Left ventricular (LV) pressures were measured with fluid-filled catheters. Data were digitally recorded during pressure elevation induced by tilt-up of the legs. Transgastric short-axis echocardiographic views of the LV were simultaneously recorded on videotape. Measurements were obtained before the start of CPB, 10 minutes after termination of CPB, after intravenous administration of CaCl2, 5 mg/kg, and 10 minutes later. MEASUREMENTS AND MAIN RESULTS: Systolic function was evaluated with the slope (Ees, mmHg/mL) of the systolic pressure-volume relation. Diastolic function was evaluated with the chamber stiffness constant (Kc, mmHg/mL) of the diastolic pressure-volume relation. CaCl2 increased Ees from 2.62 +/- 0.46 to 5.58 +/- 0.61 (mean +/- SD), but induced diastolic dysfunction with an increase in Kc from 0.011 +/- 0.006 to 0.019 +/- 0.007. These changes were transient and had disappeared within 10 minutes after administration of CaCl2. CONCLUSIONS: CaCl2 early after CPB transiently improved systolic function at the expense of an increase in ventricular stiffness, suggesting temporary diastolic dysfunction.

Effects of lidoflazine on left ventricular function in patients.

OBJECTIVE: The present study evaluated the effects of the nucleoside transport inhibitor, lidoflazine, at a dose of 1 mg/kg, on left ventricular function. DESIGN: Patients were randomly assigned to receive either lidoflazine or saline in a double-blind manner. SETTING: A university hospital. PARTICIPANTS: The study was performed in 32 patients scheduled for elective coronary artery bypass surgery. INTERVENTIONS: Left ventricular pressures were measured with fluid-filled catheters. Data were digitally recorded during pressure elevation induced by tilt-up of the legs. Transgastric short-axis echocardiographic views of the left ventricle were simultaneously recorded on videotape. Systolic function was evaluated with the slope (Ees, mmHg/mL) of the systolic pressure-volume relationship. Diastolic function was evaluated with the chamber stiffness constant (Kc, mmHg/mL) of the diastolic pressure-volume relationship. Cardiac function was assessed at baseline and after administration of either lidoflazine (group A [n = 16]) or placebo (group B [n = 16]). Data were compared using two-factor analysis of variance. MEASUREMENTS AND MAIN RESULTS: At baseline, diastolic and systolic function were comparable in both groups. Lidoflazine increased Kc from 0.079 +/- 0.015 to 0.125 +/- 0.017 mmHg/mL and decreased Ees from 2.481 +/- 0.213 to 1.217 +/- 0.211 mmHg/mL (p = 0.009 and p = 0.004, respectively). None of these changes occurred when placebo was administered. CONCLUSIONS: Administration of lidoflazine before the start of cardiopulmonary bypass impaired left ventricular systolic function but also increased diastolic stiffness.

Inotropic effects of sodium nitroprusside: a clinical study on coronary surgery patients.

OBJECTIVE: Sodium nitroprusside (SNP) induces release of nitric oxide and is widely used as a vasoactive drug. Recent research analyzed effects of SNP on cardiac muscle and described variable inotropic effects. The present study evaluated effects of SNP on left ventricular (LV) function in patients undergoing coronary artery surgery. METHODS: The study was performed in 100 patients with a preoperative ejection fraction > 40%. LV pressures were measured with a fluid-filled catheter in the LV cavity. Hearts were placed in AV sequential mode at a rate of 90 beats/min. Measurements were obtained at end-expiration and consisted of a control tracing and a tracing obtained after a 5 min infusion of SNP 0.5 microgram.kg-1.min-1. These measurements were obtained before and after cardiopulmonary bypass (CPB). An average of 5 consecutive beats was obtained for analysis. Ventricular function was assessed with LV pressure and dP/dt. Data were analyzed using two factor analysis of variance for repeated measurements. RESULTS: 1. Baseline patient data (n = 80). Before CPB, a variable inotropic response to SNP was observed. The direction of the inotropic response was related to preoperative beta-blocking medication. LVP and dP/dtmax increased with SNP in patients without preoperative beta-blocking medication. In patients on preoperative beta-blocking medication, SNP did not alter LVP and dP/dtmax. After CPB, a positive inotropic response was not observed in any of the patients. 2. Postoperative patient data under dobutamine (n = 20). Data of these separate observations were similar to baseline data before CPB. After CPB and under dobutamine administration (5 micrograms.kg-1.min-1) all 20 patients developed a positive inotropic response to SNP. CONCLUSIONS: In coronary surgery patients, SNP induced variable inotropic effect. The direction of the inotropic response appeared to be modulated by the beta-adrenergic drive.

Retrograde cerebral perfusion does not perfuse the brain in nonhuman primates.

BACKGROUND: Recently retrograde cerebral perfusion (RCP) has been advocated as an alternative to complete circulatory arrest during aortic arch surgery. METHODS: In 19 baboons, we compared brain protection using hypothermic circulatory arrest or RCP. Animals were placed on cardiopulmonary bypass, cooled to 18 degrees C, underwent 1 hour of circulatory arrest or RCP, and were reperfused for 3 hours. Biochemical variables, cerebral blood flow (colored microsphere technique), and brain histology were assessed. RESULTS: Release of the brain-specific ischemic marker CK-BB was similar in both groups (peak values, 123 +/- 97 U/L in the circulatory arrest group and 164 +/- 88 U/L in the RCP group; p > 0.05), as were the arteriovenous differences in glucose uptake and lactate production (p > 0.05). During RCP, significant brain flow could not be detected (0.5 +/- 0.5 mL.min-1 x 100 g-1). About 90% of the blood was shunted to the inferior caval vein, and an equilibrium in circulating microspheres was found between RCP inflow and caval vein outflow. Less than 1% of the RCP inflow returned to the aortic arch. Histologic signs of brain damage were minimal in both groups, although slightly more glial edema was found in the RCP group. CONCLUSIONS: These data suggest that in nonhuman primates, retrograde cerebral perfusion does not perfuse the brain because of venovenous shunting.