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DDAVP (0 3 mg/kg after bypass), DDAVP (0.3 mg/kg after bypass and a repeated dose 6 hours after surgery), or no drug (control) Aspirin-treated patients were included. Postoperative blood loss was not reduced in either of the 2 DDAVF patient groups Significant reduction in blood loss was observed in aprotlnintreated patients; however, the mean difference m 72-hour blood loss between aprotinin-treated patients and controls was less than 100 mL/M 2. Blood transfusion was reduced significantly only m the aprotmin group. The study is marked by large volumes of blood transfused (mean red cell transfusion 678 mL/M 2 in control patients) and unspecified transfusion triggers. Measures of fibrInolytic actwRy observed in both DDAVP-treated groups and control patients were attenuated m the aprotinm group.
Wolfer RS, Krasna M J, Hasnain JU, et al: Hemodynamic effects of carbon dioxide insufflation during thoracoscopy. Ann Thorac Surg 58:404-408, 1994 No significant effects on end-tidal C O 2 pressure, arterial oxygen saturation, heart rate, or blood pressure were observed in 32 patients undergoing thoracoseopy during one-lung ventilation and intrapleural CO2 insufftation at intrapleural pressures of 2 to 14 mmHg. Central venous pressure varied directly with mtrapleural pressure These results may differ from those observed during use of lntrapleural CO2 lnsufflatxon during thoracoscopy in the presence of two-lung ventilation via a single-lumen endotracheal tube when hemodynamic compromise has been reported
lppoiito G, DeCarli G, Puro V, et al: Device-specific risk of needle stick injury in Italian health care workers. J Am Med Assoc 272:607-610, 1994 A total of 2,524 injuries from hollow-bore needles were reported m 12 acute care hospitals over a 3-year period. Although &sposable syringes accounted for 60% of injuries, the rate of needle stick injury associated with syringes was low (3 8/100,000 devices used) Intravenous catheter stylettes had the highest needle stick injury rate (15.7/100,000) and accounted for 5% of all injuries Nurses, housekeepers, and physicians recewed 70%, 13%, and 10% of the needle stick injuries, respectwely Similar needle stick injury rates have been reported in the United States.
Aoki M, Jonas RA, Nomura F, et ah Effects of cerebroplegic solutions during hypothermic circulatory arrest and short-term recovery. J Thorac Cardiovase Surg 108:291-301, 1994 Cerebral adenosine triphosphate and intracellular pH recovery by phosphorus 31 magnetic resonance spectroscopy, microspheremeasured cerebral blood flow recovery, and cerebral oxygen consumption recovery were improved by intermittent crystalloid cerebroplegm (50 mL/kg at onset of hypothermic circulatory arrest and 10 mL/kg every 30 minutes during arrest) using 4°C saline and Umverslty of Wlsconsm organ preservation solutmn in 4-week-old piglets. Hypothermlc sahne cerebroplegla improved short-term recovery after 2 hours of circulatory arrest. Use of University of Wisconsin solution yielded further improvement in the recovery of cerebral blood flow and metabohsm. Addition of MK-801, an excitatory neurotransmitter antagonist, did not augment the protective effects of Unwersity of Wisconsm solution
LITERATURE REVIEW
Miller OI, Celermajer DS, Deanfield JE, et al: Very-low-dose inhaled nitric oxide: A selective pulmonary vasodilator after operations for congenital heart disease. J Thorac Cardiovasc Surg 108:487-494, 1994 Inhaled low-dose nitric oxide (2, 10, 20 ppm) in oxygen (FIO2 0.80) was administered 13 times to 10 infants (median age 6 months) at risk for postoperative pulmonary hypertension after congenital heart surgery. Pulmonary/systemic artery pressure ratio was a predictor of nitric oxide response; greater responses were observed in patients with a ratio > 0.50. Pulmonary vascular resistance decreased to similar degrees over the range of nitric oxide dose (2 to 20 ppm) administered. In children with a high pulmonary/systemic pressure ratio, mhalahon of nitric oxide 2 ppm reduced mean pulmonary vascular resistance 37% to 42%, systemic vascular resistance index by only 10%, and increased cardiac index 14% to 16% Higher nitric oxide doses reduced systemic vascular resistance index 36% to 40%
Higashiyama H, Yamaguchi M, Kumada K, et ah Functional deterioration of the liver by elevated inferior vena cava pressure: A proposed upper safety limit of pressure for maintaining liver viability in dogs. Intens Care Med 20:124-129, 1994 After modified Fontan operation, abnormally elevated central venous pressure can be considered an etiologic factor in the onset of acute hepatic failure. In 10 mongrel dogs, various degrees of central venous hypertension were produced by clamping the thoracic inferior cavil vein after creation of an active veno-venous shunt with a pump speed of 2.5 to 60 mL/kg/mm. The hepatic energy status was measured by the arterial ketone body ratio (acetoacetate/3-OH butyrate) as an estimate of the hepatic mltochondrial redox state From regression analysis between inferior cavil vein pressure monitoring and ketone body ratio, it was observed that an upper safety limit of inferior cavil vein pressure may lie around 20 5 mmHg An inferior cavil vein pressure below 27 mmHg appeared to be critical in order to maintain lwer viability with a ketone body ratio of 0.4
Inada E, D'Ambra M, Laraia P J, et al: Nitrous oxide does not depress left ventricular contractility in ischemic rat heart. J Anesth (Japan) 8:316-320, 1994 The direct effects of nitrous oxide on left ventrlcular contractility and myocar&al oxygen consumption (MVO2) in the ischemic isolated rat heart using a Langendorf method were studied. The heart was perfused with Kumpeis solution bubbled with 95% oxygen and 5% carbon dioxide (control phase) Left ventrlcular pressure, dP/dt, and coronary flow were measured, and MVO2 was calculated Global ischemia was induced by decreasing perfusion pressure to 40 mmHg (ischemlc phase). There were four groups of eight hearts each' control, nitrogen (50%), nitrous oxide (50%), and halothane (0.4%). After 15 minutes of the ischemic phase, the perfusion pressure was increased to 80 mmHg and the gas mixture was changed to the standard (reperfuslon phase). Nitrous oxide did not further depress myocardial contractility compared with nitrogen in the lschemic phase and did not alter MVO2 In the lschemic phase compared with nitrogen Halothane depressed myocardial contractility and decreased MVO2 in the ischemic phase compared with controls.