Martin Pavlík

Pesticide Biosensor Based on Coimmobilized Acetylcholinesterase and Butyrylcholinesterase

Abstract The detection of organophosphate and carbamate pesticides using amperometric biosensors based on immobilized cholinesterases (ChE) was investigated. If only one type of ChE was used for analysis, the sensitivities for some pesticides were not sufficient. We have prepared biosensors with immobilized acetylcholinesterase or butyrylcholinesterase and with both ChEs coimmobilized in the same enzyme layer. Both coimmobilized ChEs function simultaneously in the presence of acetylthiocholine and these biosensors exhibit high response to a wider group of pesticides compared with sensors containing only one type of ChE.

Temperature corrected thromboelastography in hypothermia: is it necessary?

Context Hypothermia is known to influence thromboelastography (TEG). TEG reproducibility is generally low. Objective The aim of this study was to evaluate the rationale of TEG temperature adjustment in patients during hypothermia. We hypothesised that temperature adjustment would not be important because of low TEG reproducibility. Design Prospective observational study. Setting Single-centre, secondary care study performed 01/2009 to 07/2010. Patients Survivors of cardiopulmonary resuscitation in whom therapeutic hypothermia (32 to 34°C) was indicated for 24 h were recruited to the study which lasted 36 h. Four hundred samples from 30 patients (22 men and eight women) were obtained. No specific exclusion criteria were defined. Main outcome measures Temperature adjusted and non-adjusted Kaolin–Heparinase and Rapid-TEG were done at 12-h intervals during the first 36 h. Results Bland–Altman plots were used for analysis. During hypothermia, the bias of adjusted measurements was greater in clot formation variables for both Kaolin–Heparinase-TEG (from −15 to −19%) and Rapid-TEG (−9 to −25%) compared to normothermia (from −3 to 3% for Kaolin–Heparinase-TEG and −10 to 2% for Rapid-TEG). Bias of clot strength variables was not influenced by temperature adjustment (median −1%). The 95% limits of agreement were wide for clot formation variables and independent of temperature. In Kaolin–Heparinase-TEG (R −42 to 40% normothermia, −47 to 18% hypothermia) and in Rapid-TEG (R −117 to 97% normothermia, −114 to 95% hypothermia). Limits of agreement of clot strength variables were narrower and independent of temperature in Kaolin–Heparinase-TEG (MA −16 to 13% normothermia, −9 to 10% hypothermia) and also in Rapid-TEG (MA −27 to 24% normothermia, −18 to 20% hypothermia). Conclusion Although TEG analysis with temperature adjusted to the in-vivo value during hypothermia yields results with small systematic bias, the importance of temperature adjustment in clinical routine is low because of the precision limits of TEG measurement itself. Therefore, we see no need to perform TEG analysis at the in-vivo temperature.

The impact of sedation on pulse pressure variation.

OBJECTIVE Pulse pressure variations (PPV) are mainly influenced by ventilation. The impact of sedation on PPV is not known. The aim of the study was to test the influence of sedation on pulse pressure variation in mechanically ventilated critically ill patients and to compare PPV in critically ill and brain dead patients. Beside the absolute value of PPV, the adjusted values of pulse pressure were used to eliminate influence of ventilation. DESIGN AND INTERVENTION Mechanically ventilated patients received four different breath frequencies. At each frequency airway pressure was adjusted to keep the end-tidal CO2 stable. In critically ill patients the frequencies were applied at basal (bispectral index - BIS median 38) and deeper sedation (BIS 29). MAIN OUTCOME MEASURES Simultaneous haemodynamic and respiratory data including oesophageal pressure were recorded, adjusted PPV were calculated as PPV/VT, PPV/dPair, PPV/dPes where VT is tidal volume, dPair and dPes are airway and oesophageal driving pressures. SETTING University Hospital, ICU. PARTICIPANTS 30 critically ill and 23 patients with a diagnosis of brain death. RESULTS The pulse pressure variation did not change significantly during deep sedation compared to basal sedation (median 10.3 vs 10.9%) whereas PPV/dPair increased from 0.7 to 0.8%/cmH2O and PPV/dPes from 1.9%/cmH2O to 2.4%/cmH2O (p=0.04). Patients with a diagnosis of brain death had higher PPV and adjusted PPV than critically ill patients. CONCLUSION Deeper sedation increases values of adjusted pulse pressure variation.