The use of extracorporeal membrane oxygenation (ECMO) has recently increased exponentially. ECMO has become the preferred mode of organ support in refractory respiratory or circulatory failure. The fragile balance of haemostasis physiology is massively altered by the patient’s critical condition and specifically the aetiology of the underlying disease. Furthermore, an application of ECMO conveys another disturbance of haemostasis due to blood-circuit interaction and the presence of an oxygenator. The purpose of this review is to summarise current knowledge on the anticoagulation management in patients undergoing ECMO therapy. The unfractionated heparin modality with monitoring of activated partial thromboplastin tests is considered to be a gold standard for anticoagulation in this specific subgroup of intensive care patients. However, alternative modalities with other agents are comprehensively discussed. Furthermore, other ways of monitoring can represent the actual state of coagulation in a more complex fashion, such as thromboelastometric/graphic methods, and might become more frequent. In conclusion, the coagulation system of patients with ECMO is altered by multiple variables, and there is a significant lack of evidence in this area. Therefore, a highly individualised approach is the best solution today.
To evaluate the predictive performance of the Eleveld target-controlled infusion model for propofol during deep hypothermia, characterise temperature-dependent changes in propofol pharmacokinetics, and explore the relationship between depth of anaesthesia monitoring and the perioperative stress response during deep hypothermic circulatory arrest. Prospective, single-centre, low-intervention study. Tertiary cardiac surgery centre. Thirty adult patients undergoing elective pulmonary endarterectomy with cardiopulmonary bypass and deep hypothermic circulatory arrest. Serial blood samples (T0-T13) were obtained to determine propofol serum concentrations and endogenous norepinephrine levels. Model performance of the Eleveld target-controlled infusion system was assessed using linear regression across temperature phases, and population pharmacokinetic analysis was performed using nonlinear mixed-effects modelling. Predictive performance deteriorated during cooling and improved during rewarming. A two-compartment model identified temperature as a significant covariate on propofol clearance, with marked reduction during hypothermia and relative increase during rewarming. Processed EEG monitoring demonstrated profound cortical suppression (mean suppression ratio 98.4%, PSI 0.4). Despite this, norepinephrine levels decreased during cooling and increased significantly during reperfusion, indicating activation of the stress response in the absence of cortical activity. No intraoperative awareness was detected. Deep hypothermia alters propofol pharmacokinetics, reducing clearance and impairing model performance, while rewarming increases clearance. Autonomic stress responses may occur despite profound cortical suppression, highlighting limitations of EEG-based depth of anaesthesia monitoring during deep hypothermic circulatory arrest. These findings support temperature-adaptive dosing and warrant confirmation in prospective randomised studies.
Pulmonary endarterectomy is an established treatment for selected patients with chronic thromboembolic pulmonary hypertension. And bleeding into the airway