ABSTRACT
From September 5 to November 4, 1991, four consecutive patients placed on centrifugal ventricular assist devices (VADs) for cardiac failure were supported with Biomedicus pumps coated with the Carmeda bioactive surface. The study included three men and one woman aged 52-65 years. Two patients were supported with a right VAD, one with a left VAD, and one with a biventricular VAD. Support ranged from 35.5 to 65.75 hr, and VAD flows ranged from 1.0-5.5 L/min. Three patients were weaned from the VADs, and two survived. At explant, all four systems had clots adherent to the surface of the tubing and connectors on the pump outflow side of the circuit. Two patients had clots in the pump. Some of the clots were firmly adherent, whereas others dislodged easily after being rinsed with saline. All patients received heparin for insertion, and in three patients, heparin was reversed with protamine. Two patients received no further anticoagulation, and two received continuous heparin within 24 hr of implant to maintain activated clotting times of 140-150 sec. All patients had bleeding complications before and after VAD placement, necessitating multiple blood product transfusions. One patient who was weaned and survived had multiple thromboembolic strokes. These data suggest that clots can form on surfaces coated with the Carmeda process, even if a low dosage of heparin is used.
Subject(s)
Heart-Assist Devices , Aged , Biocompatible Materials , Coronary Artery Bypass/adverse effects , Evaluation Studies as Topic , Female , Heart-Assist Devices/adverse effects , Heparin/administration & dosage , Humans , Male , Materials Testing , Middle Aged , Postoperative Complications/drug therapy , Postoperative Complications/etiology , Postoperative Complications/surgery , Surface Properties , Thrombosis/etiologyABSTRACT
Standard intracellular microelectrode techniques were used to study the effects of halothane on ouabain-induced delayed after depolarizations (DAD) in canine Purkinje fibers. Free running Purkinje fibers were superfused with 2 X 10(-7)M ouabain in Krebs-Henseleit buffer for 30-50 min until DAD appeared. Purkinje fibers were then paced for 20 beats at cycle lengths between 1,000 ms and 200 ms, and the amplitude of the DAD and coupling interval between the DAD and last paced beat were determined. Halothane (0.5, 1, and 2%) was then administered and measurements repeated. Halothane produced dose-related decreases in DAD amplitude without changing DAD coupling interval. The ability of calcium to antagonize the effects of halothane was evaluated by doubling buffer calcium concentration to 5 mM in the presence of halothane 2%. Doubling buffer calcium concentration to 5 mM antagonized the reduction of DAD amplitude caused by halothane. In several preparations, dysrhythmias occurred during ouabain superfusion. Halothane reversibly terminated these arrhythmias. Halothane antagonizes DAD and dysrhythmias induced in vitro by ouabain toxicity. This effect, in part, may account for the apparent effectiveness of halothane against ouabain-induced dysrhythmias in vivo.
