It is hypothesized that tissue dysoxia and O2 debt are major factors in the development and the propagation of multiple organ failure in critically ill patients. Dysoxia is the result of an abnormal relationship between O2 supply (DO2) and O2 demand and translates into increased anaerobic metabolism and tissue and blood lactate concentration. First-line therapeutic strategies used to avoid the development of an O2 debt involve correction of cardiac output, haemoglobin, and O2 saturation in order to increase DO2 above its critical value. They are not sufficient, however, to ensure appropriate end-organ perfusion and oxygenation. The adequacy of cardiac output towards tissue metabolic requirements may be appreciated by venous-to-arterial and gut mucosal-to-arterial PCO2 differences. This review details these strategies and discusses their usefulness in current practice.

The retrospective analysis of 1700 forensic autopsies over 17 years (1981–97) following unexpected sudden cardiac death revealed a group of 50 cases that could have been related to surgery and/or anaesthesia. Patients were young with no history of cardiac disease. Surgery was performed for uncomplicated disorders, all classified as ASA 1. Cardiac arrest took place at induction of anaesthesia in 16% of cases, during surgery in 64% and at the end of surgery in 20%. Investigation and expertise reports ordered by the public prosecutor revealed none of the typical causes of death usually associated with surgery or anaesthesia. Pathological examination showed cardiac lesions in 47 cases: arrhythmogenic right ventricular cardiomyopathy in 18 cases, coronary artery disease in 10 cases, cardiomyopathy in eight cases, structural abnormalities of the His bundle in nine cases, mitral valve prolapse in one case, and acute myocarditis in one case. Identification of the cause of death of patients at low risk may provide major relief to the family of the patient and the medical staff.

In order to compare the effect of atropine and sodium chloride on the dynamic compliance of the respiratory system after tracheal intubation, we studied 20 patients allocated randomly into two groups to receive either: atropine after 5 min of steady state and sodium chloride after 10 min (group A) or in reverse order (group B) intravenously. The study was conducted in a randomized double-blinded manner. The patients were anaesthetized with thiopental 5 mg kg−1 followed by thiopental 50 mg intravenously, as required. Intubation was facilitated by atracurium 0.5mg kg−1 intravenously and fentanyl 200 μg intravenously. During fixed volume ventilation (100 mL kg−1, f=10), compliance and end-tidal carbon dioxide were measured every 10 s by a Datex AS/3-respiratory module connected to a portable IBM-pc. Five minutes was allowed to establish a steady state then either atropine or sodium chloride was administered according to the protocol. Respiratory dynamic compliance increased significantly after intravenous administration of atropine (P < 0.05). We conclude that atropine 1.0 mg given intravenously provides protection against an intubation-induced decline in respiratory dynamic compliance.

The intraoperative effects of continuous spinal anaesthesia, and the efficacy of postoperative continuous spinal analgesia in 48 elderly high risk patients undergoing major abdominal, vascular or orthopaedic surgery is reported. Intraoperative anaesthetic technique proved to be safe and provided satisfactory results in the immediate postoperative period. Furthermore, the postoperative analgesic regimen which involved intrathecal fentanyl and bupivacaine, and intravenous tenoxicam, provided effective analgesia for all patients. The intrathecal analgesic regimen was administered continuously through a PCA pump which had the facility to provide bolus doses when requested in predetermined lockout intervals. The mean doses of fentanyl and bupivacaine infused intrathecally for the first 24 h postoperatively were 14.5±1.5 μg h−1 (mean±SD) and 0.72±0.08mg h−1 (mean±SD), respectively, while the requirements for analgesia decreased progressively over time but lasted for 118 h. The technique provided effective analgesia with low pain scores that was reflected by the ease in performing physical exercises and the pleasant co-operation with the physiotherapist. Only minor complications related to anaesthesia/analgesia were encountered.

We studied the direct effect of intravenous anaesthetics, local anaesthetics and premedication drugs in common use for major surgery, on the spontaneous versus lectin induced proliferation of cultured normal rat peripheral blood mononuclear cells, not exposed to surgical or any other trauma prior to culture. Peripheral blood mononuclear cells were incubated in cell-culture medium in the presence or in the absence of propofol, ketamine, fentanyl, midazolam, thiopental sodium, lidocaine or etomidate. The cells proliferated either spontaneously or under stimulation with a lectin phytohaemagglutinine P for 72 h. The proliferation rate was evaluated by 2H-Thymidine incorporation. Fentanyl, thiopental sodium, lidocaine and etomidate significantly inhibited phytohaemagglutinine P induced 3H-Thymidine incorporation in cultured rat peripheral blood mononuclear cells. Counts per minute of the cultures treated with these drugs were 1667.80±745.72, 1614.1±615.00, 1688.0±615.0 and 1549±560.41, respectively, compared with the phytohaemagglutinine P stimulated positive control counts per minute, 13488±4305.6 (P<0.001 in each comparison). Propofol, ketamine and midazolam inhibited the lectin-induced cell proliferation to levels not statistically different from the baseline. Counts per minute of these cultures were 1361.90±745.73; 1108.90±751.33 and 1518.10±848.88, respectively. Compared either with the baseline 972.57±356.73 counts per minute or to the positive control culture counts per minute, 13488±4305.6 the difference was statistically significant (P<0.001) in each comparison. All the substances tested in this study proved capable of exerting direct inhibitory effect on circulating immunocompetent cells, because the latter were not subjected to any other immunosuppressive factor, be it operative trauma, blood transfusion, malnutrition, drug abuse, prior to culture. The possible theoretical and practical implications are discussed in this study.

We have studied the acid-base equilibrium in 12 patients with end-stage renal failure (ESRF) during capnoretroperitoneoscopic nephrectomy. Bupivacaine (12 mL, 0.375%) and morphine (2 mg) were given in the lumbar epidural space, and fentanyl (0.5 μg kg−1) and midazolam (50 μg kg−1) were given intravenously. Anaesthesia was induced by thiopental, maintained with halothane carried by oxygen enriched air (inspired oxygen fraction = 0.35), and ventilation was achieved with a tidal volume of 10 mL kg−1 at a rate of 12 min−1. This procedure resulted in a mild degree of respiratory acidosis that was cleared within 60 min. We conclude that capnoretroperitoneoscopic nephrectomy can be performed in patients with end-stage renal failure with minimal transient respiratory acidosis that can be avoided by increased ventilation.

A prospective observational study of 101 women having breast surgery under general anaesthesia was performed to assess the extent of postoperative nausea and vomiting in this group of women. The overall rate of postoperative nausea and vomiting was high, 56% and 41%, respectively, and was significantly associated with length of surgical procedure and morphine use. Techniques to reduce morphine requirement should be evaluated to try and reduce this cause ofmorbidity.

The management of surgical embolization of a post-traumatic carotid-cavernous fistula is reported in this study. The procedure was successfully performed with the aid of a fibreoptic intravascular catheter, which was monitoring continuously the changes of the jugular venous oxygen saturation. Jugular venous oxygen saturation monitoring effectively confirmed the success of embolization without the need for intraoperative angiography, by manifesting an abrupt return of oxygen saturation from arterial to normal venous values immediately after embolization.

Extracorporeal membrane oxygenation is the recommended treatment for fulminant pulmonary failure due to varicella pneumonia. However, in pregnancy fetal viability during extracorporeal membrane oxygenation is generally poor resulting in either therapeutic or spontaneous abortion. The present case is to our knowledge the first report on the treatment with nitric oxide to improve oxygenation in a pregnant woman with fulminant pulmonary failure due to varicella pneumonia. Adding 20 parts per million nitric oxide to the inspiratory gas increased arterial oxygen saturation from 75 to 88%, and it could be kept at this level. Due to a vaginal bleeding, an emergency Caesarean section was performed with successful outcome for the fetus. The mother started to improve after delivery and could be weaned from nitric oxide after 5 days. We conclude that inhalation of nitric oxide may be a good alternative to extracorporeal membrane oxygenation in the treatment of fulminant pulmonary failure due to varicella pneumonia in pregnancy.