R. A. Bouwman

Anaesthetic management during open and percutaneous irreversible electroporation

BACKGROUND Irreversible electroporation (IRE) is a novel tumour ablation technique involving repetitive application of electrical energy around a tumour. The use of pulsed electrical gradients carries a risk of cardiac arrhythmias, severe muscle contractions, and seizures. We aimed to identify IRE-related risks and the appropriate precautions for anaesthetic management. METHODS All patients who were treated with IRE were prospectively included. Exclusion criteria were arrhythmias, congestive heart failure, active coronary artery disease, and epilepsy. All procedures were performed under general anaesthesia with complete muscle relaxation during ECG-synchronized pulsing. Adverse events, cardiovascular effects, blood samples, cerebral activity, and post-procedural pain were analysed. RESULTS Twenty-eight patients underwent 30 IRE sessions for tumours in the liver, pancreas, kidney, and lesser pelvis. No major adverse events occurred during IRE. Median systolic and diastolic blood pressure increased by 44 mm Hg (range -7 to 108 mm Hg) and 19 mm Hg (range 1-50 mm Hg), respectively. Two transient minor cardiac arrhythmias without haemodynamic consequences were observed. Muscle contractions were mild and IRE caused no reactive brain activity on a simplified EEG. Pain in the first 24 h after percutaneous IRE was generally mild, but higher pain scores were reported after pancreatic treatment (mean VAS score 3; range 0-9). CONCLUSIONS Side-effects during IRE on tumours in the liver, pancreas, kidney, and lesser pelvis seem mild and manageable when current recommendations for anaesthesia management, including deep muscle relaxation and ECG synchronized pulsing, are followed. Electrical pulses do not seem to cause reactive cerebral activity and evidence for pre-existing atrial fibrillation as an absolute contra-indication for IRE is questionable.

Minimally invasive intraoperative estimation of left-ventricular end-systolic elastance with phenylephrine as loading intervention

BACKGROUND Left-ventricular end-systolic elastance (Ees) is an index of cardiac contractility, but the invasive nature of its assessment has limited perioperative application. We explored the feasibility of a minimally invasive method of Ees estimation for perioperative assessment of cardiac function and evaluated the suitability of phenylephrine as a loading intervention. METHODS In 17 surgical patients, Ees was determined as the slope of the end-systolic pressure-volume relation, which was obtained from non-invasive or invasive continuous arterial pressure measurements and left-ventricular volume determinations using transoesophageal echocardiography (TOE). Ees was determined using as loading interventions preload reduction by inferior vena cava compression (IVCC) and afterload increase by phenylephrine administration. RESULTS Median invasive Ees determined with phenylephrine estimated 1.05 (0.59-1.21) mm Hg ml(-1) and with IVCC 0.58 (0.31-1.13) mm Hg ml(-1). Bland-Altman analysis to evaluate the level of agreement between minimally invasive and invasive Ees estimation revealed a bias of -0.03 (0.12) mm Hg ml(-1) with limits of agreement from -0.27 to 0.21 mm Hg ml(-1) and the percentage error was 33%. Agreement between Ees obtained with phenylephrine and IVCC revealed a bias of 0.15 (0.69) mm Hg ml(-1) with limits of agreement from -1.21 to 1.51 mm Hg ml(-1) and a percentage error of 149%. CONCLUSIONS It is feasible to determine Ees combining continuous non-invasive arterial pressure measurements and left-ventricular volume determinations with TOE. However, administration of phenylephrine cannot substitute IVCC as a loading intervention, indicating that estimation of Ees in the intraoperative setting remains a challenge.

Sevoflurane-induced cardioprotection is mediated by protein kinase C-alfa via production of reactive oxygen species: 4AP3-6

35 minutes of global ischaemia followed by 60 minutes of reperfusion (I/R). The hearts were randomly divided into 4 groups: (1) control (CON, n 8); (2) sevoflurane preconditioning (SEVO, n 8) receiving three times 5-minute episodes of sevoflurane (2,5 vol%) before I/R; (3) pre-treatment 1 g/ml bupivacaine during 40 minutes before I/R combined with sevoflurane preconditioning (BUPI-SEVO, n 8); and (4) bupivacaine pre-treatment alone (BUPI, n 4). After I/R, cardiac function was determined as recovery of left ventricular pressures (LVP, expressed as percentage to values before I/R) and cellular injury was determined by infarct size with triphenyltetrazolium chloride (TTC) staining. Results: After I/R, the SEVO group showed increased recovery of LVP (53 3% SEVO vs. 46 3% CON, n 8, p 0.05), as well as a reduced infarct size (25 8% SEVO vs. 59 6% CON, n 6, p 0.01). Interestingly, in the BUPI-SEVO and BUPI group infarct size was reduced to a similar extent as the SEVO group (24 7% BUPI-SEVO n 8 and 34 3% BUPI n 4 vs. CON, p 0.05), whereas LVP were unaltered compared to controls. Conclusion: The efficacy of the volatile anaesthetic sevoflurane-induced cardioprotection against ischaemia-reperfusion injury was not affected by the local anaesthetic bupivacaine. Therefore, we suggest that both anaesthetics might induce similar cardioprotective signalling pathways.