Anesthesiology
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Randomized Controlled Trial Comparative Study Clinical Trial
Paravertebral analgesia with levobupivacaine increases postoperative flap tissue oxygen tension after immediate latissimus dorsi breast reconstruction compared with intravenous opioid analgesia.
Directly measured tissue oxygen tension (Pto2) reflects the adequacy of local tissue oxygenation and influences surgical wound healing. Epidural analgesia increases Pto2 compared with intravenous morphine analgesia after abdominal surgery. The authors tested the hypothesis that paravertebral regional anesthesia and analgesia would increase Pto2 compared with intravenous opioid-based anesthesia and analgesia. ⋯ The postoperative latissimus dorsi flap Pto2 was higher for 20 h after breast reconstruction with paravertebral analgesia compared with intravenous morphine analgesia.
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Randomized Controlled Trial Clinical Trial
Epidural anesthesia, hypotension, and changes in intravascular volume.
The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available. ⋯ Thoracic epidural anesthesia per se does not lead to changes in blood volumes despite a reduction in blood pressure. When fluid is infused, there is a dilution, and the fluid initially seems to be located centrally. Because administration of hydroxyethyl starch and ephedrine has similar hemodynamic effects, the latter may be preferred in patients with cardiopulmonary diseases in which perioperative fluid overload is undesirable.
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Clinical Trial
Mixed-effects modeling of the intrinsic ventilatory depressant potency of propofol in the non-steady state.
Despite the ubiquitous use of propofol for anesthesia and conscious sedation and numerous publications about its effect, a pharmacodynamic model for propofol-induced ventilatory depression in the non-steady state has not been described. To investigate propofol-induced ventilatory depression in the clinically important range (at and below the metabolic hyperbola while carbon dioxide is accumulating because of drug-induced ventilatory depression), the authors applied indirect effect modeling to Paco2 data at a fraction of inspired carbon dioxide of 0 during and after administration of propofol. ⋯ Propofol at common clinical concentrations is a potent ventilatory depressant. An indirect response model accurately described the magnitude and time course of propofol-induced ventilatory depression. The indirect response model can be used to optimize propofol administration to reduce the risk of significant ventilatory depression.
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Randomized Controlled Trial Clinical Trial
Effects of epsilon-aminocaproic acid and aprotinin on leukocyte-platelet adhesion in patients undergoing cardiac surgery.
The administration of aprotinin during cardiopulmonary bypass (CPB) is hypothesized to decrease activation of leukocytes and platelets and possibly reduce their adhesion. Although epsilon-aminocaproic acid (EACA) shares the ability of aprotinin to inhibit excessive plasmin activity after CPB, its effect on leukocyte and platelet activation and leukocyte-platelet (heterotypic) adhesion is largely unknown. This study was performed to determine the relative effectiveness of the antifibrinolytics, aprotinin and EACA, at reducing leukocyte and platelet activation and leukocyte-platelet conjugate formation in patients undergoing CPB. ⋯ EACA seems to be as effective as aprotinin at reducing peak monocyte-platelet adhesion after CPB. Furthermore, inhibition of excessive plasmin activity seems to influence monocyte-platelet adhesion. The findings suggest that monocyte-platelet conjugate formation may be a useful marker of monocyte and platelet activation in this clinical setting.