Failure of argatroban anticoagulation during off-pump coronary artery bypass surgery.

Heparin-induced antibodies create vexing problems during cardiac surgery. Although alternative medications have been used for intraoperative anticoagulation, the results have been sufficiently variable that no one medication is recommended. In our case, due to the poor reversibility of the antithrombin agents, argatroban was chosen as a heparin substitute due to its short half-life and its anticoagulation assessment using the activated clotting time (ACT). Unfortunately, our experience was that argatroban does not provide adequate anticoagulation during off-pump coronary bypass surgery, even when the ACT is maintained at more than 380 sec.

The economic benefit of organizational restructuring of the cardiothoracic intensive care unit.

OBJECTIVES: Compare cost/benefits of organizational restructuring of the cardiac intensive care unit (CICU). DESIGN: Prospective, with a retrospective control period. SETTING: Academic medical center. PARTICIPANTS: Sixty-six CICU patients (prospective) and 57 patients who received care before restructuring (retrospective) were compared. Entrance criteria were constant for both study periods. INTERVENTIONS: The CICU was restructured from a level III ICU to a level I ICU with the initiation of a consultant CICU service. The CICU service provided an attending physician dedicated to ICU care daily. All cardiac patients admitted into the CICU received consultation by the CICU service. MEASUREMENTS AND MAIN RESULTS: The average postoperative intubation time decreased during the intervention period (61% extubated within 6 hours v 12%, p = 0.004). Pharmacy, radiology, laboratory, and ICU costs decreased 279 US dollars (p = 0.004), 196 US dollars (p = 0.003), 190 US dollars (p = 0.15), and 470 US dollars (p = 0.12), respectively. The ICU length of stay (0.28 days shorter) as well as the overall postsurgery stay (0.54 days shorter) were reduced in the intervention period (p = 0.11 and 0.10, respectively). CONCLUSIONS: The CICU service significantly reduced both total ICU-related costs ($1,173/patient) and overall costs (2,285 US dollars/patient) during the intervention period. Professional fees only reduced overall savings by 8%. These results indicate that organizational restructuring of the CICU to newer models can reduce costs associated with cardiac surgery.

Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow.

UNLABELLED: Dexmedetomidine is a selective alpha(2)-agonist approved for sedation of critically ill patients. There is little information on the effects of dexmedetomidine on cerebral blood flow (CBF) or intracranial hemodynamics, despite considerable other pharmacodynamic data. We hypothesized that therapeutic doses of dexmedetomidine would decrease CBF. Therefore, nine supine volunteers, aged 24-48 yr, were infused with a 1 micro g/kg IV loading dose of dexmedetomidine, followed by an infusion of 0.2 micro g. kg(-1). h(-1) (LOW DEX) and 0.6 micro g. kg(-1). h(-1) (HIGH DEX). Hemodynamic and CBF (via positron emission tomography) measurements were determined at each experimental time point. Dexmedetomidine decreased both cardiac output and heart rate during and 30 min after drug administration. Blood pressure decreased from 12% to 16% during and after the dexmedetomidine administration. Global CBF was decreased significantly from baseline (91 mL. 100 g(-1). min(-1) [95% confidence interval, 72-114] to 64 mL. 100 g(-1). min(-1) [51-81] LOW DEX and 61 mL. 100 g(-1). min(-1) [48-76] HIGH DEX). This decrease in CBF remained constant for at least 30 min after the dexmedetomidine infusion was discontinued, despite the plasma dexmedetomidine concentration decreasing 40% during this same time period (628 pg/mL [524-732] to 380 pg/mL [253-507]). IMPLICATIONS: Dexmedetomidine-induced sedation decreased cerebral blood flow (CBF) by congruent with 33%, which could be due to direct alpha(2)-receptor cerebral smooth muscle vasoconstriction or to compensatory CBF changes caused by dexmedetomidine-induced decreases in the cerebral metabolic rate.