Our understanding of perioperative coagulopathy, diagnostic tools, and therapeutic approaches has evolved in recent years. Additional multidisciplinary efforts are required to understand the optimal combinations, cost-effectiveness, and safety profiles of allogeneic components, and available factor concentrates.

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Plasma AT activity is severely decreased after CPB with DHCA. Our data suggest that the administration of coagulation factor components without AT repletion may lead to excessive thrombin generation, which clinically, may potentially lead to a hypercoagulable state.

Background Arterial blood pressure (BP) measurement at least every five minutes is part of the American Society of Anesthesiologists' (ASA) monitoring standard, but prolonged BP gaps in electronic anesthesia records have been noted. We undertook multicenter studies to determine the frequency of cases with at least one interval ≥ 10 minutes between successive BP measurements and then to ascertain if educational feedback via an electronic, near real-time notification system alerting providers to the presence of such gaps would reduce their incidence. Methods We evaluated 212,706 electronic anesthesia records from three large academic centers. We determined the fraction of cases with ≥ 10 minute BP monitoring gaps at baseline and did a root cause analysis to determine common causes for these lapses. We then designed and implemented automated systems at two of the hospitals to notify point-of-care providers immediately after such 10-minute gaps occurred and determined the subsequent impact of this feedback on BP gap incidence, compared to baseline. Results At Hospital A, the notification system reduced the incidence of cases with at least one BP gap (1.48% ± 0.19% SD vs 0.79% ± 0.36% SD, p<0.0001). At Hospital B, the gap incidence was not significantly altered when notification was provided after a 10-min gap had already occurred (2.72% ± 0.60% SD vs. 2.45% ± 0.48% SD, P=0.27), but the incidence was reduced when such notification was provided after 6 minutes without a BP reading (2.72% ± 0.60% SD vs 1.54% ± 0.19% SD, P<0.0001). At Hospital C, where notification was not implemented, the baseline rate of BP gaps was consistent across the preintervention and follow-up periods (7.03% ± 1.27% SD vs. 7.13% ± 0.11% SD, p=0.74). Although monitors disconnected during position change was the most common identifiable cause of BP gaps, reasons for the missing BPs were often not documented. During a week when the electronic charting system was temporarily inoperable, no BP gaps were noted on a convenience sample of 500 paper records from Hospital A (99% upper confidence limit = 0.83%). Conclusions BP gaps of ≥ 10 minutes were common in electronic anesthesia records, and their incidence was reduced but not eliminated by near real-time feedback to providers. The ASA standard for every 5 min BP documentation may not be achievable with current practices and technology. Anesthesia information management systems users need to be cognizant of the potential for gaps in BP measurement, take steps to minimize their occurrence, and document an explanation when such failures occur.

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Thrombin is a key hemostatic enzyme, which propagates its own generation by activating factors V, VIII, and XI. Sustained thrombin generation also activates thrombin-activatable fibrinolysis inhibitor (TAFI), which stabilizes fibrin clot against fibrinolysis. Recombinant activated factor VII (rFVIIa) is considered a novel hemostatic intervention for refractory bleeding, but rebleeding episodes related to fibrinolysis still occur. The present study aimed to investigate the antifibrinolytic effects of rFVIIa in relation to thrombin generation. Using thrombelastography, the effects of rFVIIa on thrombin-activated fibrin formation and on fibrinolysis induced by tissue plasminogen activator were evaluated in various factor-deficient plasma samples. A Thrombinoscope was used to quantitate thrombin generation. Thrombin increased antifibrinolytic activity in a concentration-dependent manner as demonstrated by a longer clot lysis time. In plasma deficient in factors V, VIII, IX, X, or XI, clot lysis occurred early (< 20 min), and rFVIIa addition had minimal effect, except for improved antifibrinolytic effect in factor-XI-deficient plasma. A normal clot lysis time was observed in factor-XIII-deficient or dual antithrombin/factor-VIII-deficient plasma. Inhibition of TAFI increased the rate of fibrinolysis. Thrombin generation was delayed or decreased in single factor-deficient plasma except for factor XIII deficiency. After rFVIIa addition, the peak thrombin generation reached over 100 nmol/l in factor-XI-deficient plasma, but not in plasma deficient in factors V, VIII, IX, or X. Thrombin generation and subsequent activation of TAFI were important for clot stability. We conclude that rFVIIa therapy does not compensate for increased susceptibility to fibrinolysis due to lack of factor(s) necessary for the formation of tenase and prothrombinase.

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