Drug-induced prolongation of cardiac repolarization may trigger malignant ventricular arrhythmias, such as torsade de pointes. The duration of QT interval, QT corrected for heart rate (QTc), JT interval, QT dispersion (QTd), QT variability index, and transmular dispersion of repolarization (TDR) are ECG markers of torsadogenicity. All volatiles, especially isoflurane and desflurane, have been found to prolong QTc and QTcd, while sevoflurane has probably no effects on TDR. Among i.v. anaesthetics, propofol seems superior due to its minimal effects on QTc and TDR; moreover, a decrease in QTc and QTcd has been demonstrated in many studies. Regarding opioids, fentanyl, alfentanil, and remifentanil produce no effects on QTc, while sufentanil, at high doses, may induce QT prolongation. Succinylcholine, but not the non-depolarizing neuromuscular blockers, produces QTc prolongation which can be attenuated by opioids and β-blockers. Reversal of neuromuscular block with anticholinesterase-anticholinergic combinations has been associated with significant QTc prolongation, while such an effect has not been demonstrated for sugammadex, even at high doses. Local anaesthetics have probably no intrinsic action on duration of repolarization; nevertheless, an extensive subarachnoid sympathetic block may increase the duration of QTc. On the contrary, thoracic epidural anaesthesia has been associated with a decrease in both QTc and TDR. Among adjuvants, midazolam seems to have no effect on QTc and TDR, while commonly used antiemetics, such as droperidol, domperidone, and most 5-HT3 antagonists, produce significant QT prolongation. The effects of anaesthetic drugs and techniques on electrocardiographic torsadogenic markers should be considered in the perioperative management of patients with preexisting repolarization abnormalities.

Patients with inherited cardiac channel disorders are at high risk of perioperative lethal arrhythmias. Preoperative control of symptoms and a multidisciplinary approach are required for a well-planned management. Good haemodynamic monitoring, adequate anaesthesia and analgesia, perioperative maintenance of normocarbia, normothermia, and normovolaemia are important. In congenital long QT syndrome, torsades de pointes should be prevented with magnesium sulphate infusion and avoidance of drugs such as droperidol, succinylcholine, ketamine, and ondansetron. Propofol and epidural anaesthesia represent safe choices, while caution is needed with volatile agents. In Brugada syndrome, β-blockers, α-agonists, and cholinergic drugs should be avoided, while isoproterenol reverses the ECG changes. Propofol, thiopental, and volatiles have been used uneventfully. In congenital sick sinus syndrome, severe bradycardia resistant to atropine may require isoproterenol or epinephrine. Anaesthetics with vagolytic properties are preferable, while propofol and vecuronium should be given with caution due to risk of inducing bradyarrhythmias. Neuraxial anaesthesia should produce the least autonomic imbalance. Arrhythmogenic right ventricular dysplasia/cardiomyopathy induces ventricular tachyarrhythmias, which should be treated with β-blockers. Generally, β-adrenergic stimulation and catecholamine release should be avoided. Halothane and pancuronium are contraindicated, while large doses of local anaesthetics and epinephrine should be avoided in neuraxial blocks. In catecholaminergic polymorphic ventricular tachycardia, β-blocker treatment should be continued perioperatively. Catecholamine release and β-agonists, such as isoproterenol, should be avoided. Propofol and remifentanil are probably safe, while halothane and pancuronium are contraindicated. Regional anaesthesia, without epinephrine, is relatively safe. In suspicious cardiac deaths, postmortem examination and familial screening are recommended.

Compared with LEA-lidocaine or placebo, intravenous lidocaine offered no clinically significant benefit in terms of analgesia and bowel function.

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Cardiac arrest (CA) is not a uniform condition and its pathophysiology strongly depends on its cause. In this work we have used a metabolomics approach to study the dynamic metabolic changes occurring in the plasma samples of a swine model following two different causes of CA, namely asphyxia (ACA) and ventricular fibrillation (VFCA). Plasma samples were collected at baseline and every minute during the experimental phases. In order to identify the metabolomics profiles characterizing the two pathological entities, all samples were analysed by 1H NMR spectroscopy and LC-MS/MS spectrometry.The metabolomics fingerprints of ACA and VFCA significantly differed during the peri-arrest period and the resuscitation phase. Major alterations were observed in plasma concentrations of metabolites related to tricarboxylic acid (TCA) cycle, urea cycle, and anaplerotic replenishing of TCA. ACA animals showed significant metabolic disturbances during the asphyxial and CA phases, while for VFCA animals this phenomenon resulted shifted at the resuscitation phase. Interestingly, starting from the asphyxial phase, the ACA animals were stratified in two groups based on their metabolomics profiles that resulted to be correlated with the clinical outcome. Succinate overproduction was observed in the animals with the worse outcome, suggesting a potential prognostic role for this metabolite.

The combination of centhaquin 0.015 mg/kg and HES 130/0.4 resulted in shorter time to target MAP, lower wet-to-dry ratio, and better survival rates after resuscitation from hemorrhagic shock.

SummaryIn thalassaemic patients, multiple organ systems may be affected by the disease, blood transfusion, iron overload and chelating therapy. Patients may develop cardiomyopathy, pulmonary hypertension or heart failure requiring preoperative echocardiography or cardiac catheterisation. Restrictive lung dysfunction is commonly encountered, especially in patients with splenomegaly. Haemoglobin level should be optimised pre-operatively and maintained at adequate levels with transfusion and blood-saving strategies. Susceptibility to infections should be managed with broad-spectrum antibiotics. Thromboembolic events due to hypercoagulability should be prevented by simple measures, such as graduated compression stockings, intermittent pneumatic compression and early mobilisation, and possibly anticoagulant drugs. When general anaesthesia is administered, the risk of difficult intubation due to orofacial malformation should be considered. Cardiovascular depression due to negative inotropic and vasodilating effects of general anaesthesia should be minimised. Neuraxial techniques may also be challenging due to spinal skeletal abnormalities and extramedullary haemopoiesis. A multidisciplinary pre-operative approach, clinical optimisation and a carefully planned strategy are mandatory.