The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Randomized Controlled Trial Clinical TrialPrevention of bleeding after cardiopulmonary bypass with high-dose tranexamic acid. Double-blind, randomized clinical trial.
This prospective, double-blind, randomized trial assessed the effectiveness of high-dose tranexamic acid given in the preoperative period on blood loss in patients undergoing cardiopulmonary bypass. One hundred fifty patients scheduled to undergo cardiac operations with cardiopulmonary bypass were randomized into three groups of equal size. The first group received 10 gm of tranexamic acid intravenously over 20 minutes before sternotomy and a placebo infusion over 5 hours. ⋯ Continued tranexamic acid infusion (10 gm over 5 hours) did not reduce bleeding further. There was no difference in the coagulation profile before operation between patients with and without excessive bleeding. However, coagulation tests done in the postoperative period indicated ongoing fibrinolysis and platelet dysfunction in patients with excessive bleeding.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Clinical TrialExtracorporeal membrane oxygenation as an adjunct treatment for primary graft failure in adult lung transplant recipients.
Primary graft failure is a catastrophic event in lung transplantation. Failure is characterized by profound abnormalities of gas exchange that are frequently unresponsive to alterations in mechanical ventilation. This condition can be fatal and, if less severe, is usually associated with significant permanent damage to the allograft. ⋯ In comparison, there were no survivors among six recipients placed on extracorporeal membrane oxygenation for late (> or = 7 days) graft dysfunction. Extracorporeal membrane oxygenation is a lifesaving adjunct in recipients with acute graft failure after lung transplantation. Ischemia-reperfusion injury and acute graft dysfunction after lung transplantation can be successfully reversed with early aggressive intervention.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Complications of extracorporeal life support systems using heparin-bound surfaces. The risk of intracardiac clot formation.
Extracorporeal life support with heparin-coated extracorporeal membrane oxygenation circuits are being used with increased frequency in patients who have cardiogenic shock. We report our experience in 30 patients with cardiogenic shock, looking specifically at the complications associated with this form of life support. Thirty patients with a mean age of 46.5 +/- 16.6 years received extracorporeal life support for a mean of 62.8 +/- 41.1 hours (range 0.5 to 159 hours). ⋯ Nine patients (30%) were discharged home. We conclude that the use of heparin-coated extracorporeal life support without systemic heparinization, especially after protamine has been used to reverse systemic heparinization in patients having postcardiotomy cardiogenic shock, may be dangerous. Extracorporeal life support has introduced new complications unique to itself specifically limb ischemia, oxygenator failure, and pump-head thrombus.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Desensitization of myocardial beta-adrenergic receptors and deterioration of left ventricular function after brain death.
Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. ⋯ Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
In acute lung injury, inhaled nitric oxide improves ventilation-perfusion matching, pulmonary vascular mechanics, and transpulmonary vascular efficiency.
Acute respiratory distress syndrome continues to be associated with significant morbidity and mortality related to ventilation-perfusion mismatch, pulmonary hypertension, and right ventricular failure. It has been suggested that inhaled nitric oxide, which is a selective pulmonary vasodilator, may be effective in the treatment of acute respiratory distress syndrome; however, the effects of nitric oxide on cardiopulmonary interactions are poorly understood. We therefore developed a model of acute lung injury that mimics the clinical syndrome of acute respiratory distress syndrome. ⋯ Although arterial oxygen tension increased, oxygen delivery did not improve significantly. These data suggest that by improving ventilation-perfusion matching and arterial oxygen tension while lowering pulmonary vascular resistance and impedance, nitric oxide may be beneficial in patients with acute respiratory distress syndrome. However, additional measures to enhance cardiac performance may be required.