Nordic guidelines for neuraxial blocks in disturbed haemostasis from the Scandinavian Society of Anaesthesiology and Intensive Care Medicine.

BACKGROUND: Central neuraxial blocks (CNBs) for surgery and analgesia are an important part of anaesthesia practice in the Nordic countries. More active thromboprophylaxis with potent antihaemostatic drugs has increased the risk of bleeding into the spinal canal. National guidelines for minimizing this risk in patients who benefit from such blocks vary in their recommendations for safe practice. METHODS: The Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI) appointed a task force of experts to establish a Nordic consensus on recommendations for best clinical practice in providing effective and safe CNBs in patients with an increased risk of bleeding. We performed a literature search and expert evaluation of evidence for (1) the possible benefits of CNBs on the outcome of anaesthesia and surgery, for (2) risks of spinal bleeding from hereditary and acquired bleeding disorders and antihaemostatic drugs used in surgical patients for thromboprophylaxis, for (3) risk evaluation in published case reports, and for (4) recommendations in published national guidelines. Proposals from the taskforce were available for feedback on the SSAI web-page during the summer of 2008. RESULTS: Neuraxial blocks can improve comfort and reduce morbidity (strong evidence) and mortality (moderate evidence) after surgical procedures. Haemostatic disorders, antihaemostatic drugs, anatomical abnormalities of the spine and spinal blood vessels, elderly patients, and renal and hepatic impairment are risk factors for spinal bleeding (strong evidence). Published national guidelines are mainly based on experts' opinions (weak evidence). The task force reached a consensus on Nordic guidelines, mainly based on our experts' opinions, but we acknowledge different practices in heparinization during vascular surgery and peri-operative administration of non-steroidal anti-inflammatory drugs during neuraxial blocks. CONCLUSIONS: Experts from the five Nordic countries offer consensus recommendations for safe clinical practice of neuraxial blocks and how to minimize the risks of serious complications from spinal bleeding. A brief version of the recommendations is available on http://www.ssai.info.

[Hemo- and cardiodynamic effect of nifedipine in halothane or isoflurane anesthesia. An animal experiment study]. / Hämo- und kardiodynamische Wirkung von Nifedipin unter Halothan- oder Isoflurananästhesie. Eine tierexperimentelle Studie.

OBJECTIVE: The present experimental study on 16 acutely instrumented dogs was designed to determine the haemo- and cardiodynamic changes after an intravenous infusion of nifedipine during halothane or isoflurane anaesthesia. METHODS: General anaesthesia was induced with ketamine (10 mg/kg) and fentanyl (0.02 mg/kg) and maintained with fentanyl (0.3 micrograms/kg/min), 3:1 N2O/O2 inhalation mixture, and pancuronium (300 micrograms/kg/h). A left thoracotomy was performed and a needle force probe was placed in the left ventricular wall to measure myocardial force of contraction. A Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The animals were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Three hours after instrumentation baseline haemodynamic measurements were performed and repeated 30 min after either halothane 0.8 vol.% (n = 8) or isoflurane 1.5 vol.% (n = 8). Then nifedipine (10 micrograms/kg i.v.) was administered and haemodynamic measurements were repeated. RESULTS: Both volatile anaesthetic agents caused a decrease in MAP, CO, LVP, LVFS, and dP/dtmax. Heart rate, CVP, PAOP, and the diastolic diameter of the heart did not change with halothane and isoflurane. Isoflurane led to a decrease of SVR that was not seen with the administration of halothane. Nifedipine during halothane anaesthesia caused a further decrease in MAP, SVR, LVP, dP/dtmax, and LVFS compared to the already reduced values with halothane alone. However, SV did not decrease any further. If nifedipine was added to isoflurane a further decrease in CO and SV was observed despite a constant SVR. CONCLUSION: Halothane, isoflurane and nifedipine are cardiac depressant drugs. Isoflurane induces vasodilation and appears to be less cardiodepressant than halothane in the clinical situation. However, if nifedipine is added, the vasodilation caused by nifedipine offsets its own negative inotropic effect and in parts the cardiac depression of halothane. Combined with isoflurane the vasodilatory effect of nifedipine is insignificant and the negative inotropic effects of both drugs are additive resulting in a profound decrease in SV and CO.

Prolonged total extracorporeal lung assistance without systemic heparinization.

A 16-year-old female developed severe ARDS in her single remaining lung following pneumonectomy for blunt trauma. Total extracorporeal lung assist (ECLA) for 40 days using a covalently heparin-coated circuit proved lifesaving. Systemic heparinization was not applied, as the heparinized surface by itself prevented clotting of the extracorporeal circuit. Systemic primary fibrinolysis developed but was not associated with major bleeding. A veno-right ventricular cannulation technique was used and maximum venous drainage for the extracorporeal circulation was achieved by elevating the bed 50 cm from the floor. This allowed extracorporeal blood flow (ECBF) approaching cardiac output (CO) and complete extracorporeal replacement of lung function. After 40 days, lung recovery allowed discontinuation of ECLA. Five days later the patient suffered serious lung collapse and was operated for a bronchopleural fistula. The patient was extubated 4 weeks after terminating ECLA and discharged in good condition 5 weeks later.

[Alfentanil combination anesthesia in infants]. / Zur Alfentanil-Kombinationsanästhesie im Säuglingsalter.

In the last few years new narcotic agents with more favourable pharmacokinetic properties have been introduced into clinical practice. Short half-lives and smaller distribution volumes facilitate control of anaesthetic depth and shorten the recovery period. One of these narcotics is alfentanil. This study was performed on the effects of alfentanil when used during anaesthesia in infants under the age of one year. After induction and relaxation alfentanil 20 mcg/kg were given i.v. initially. The same dose was repeated as needed until 15 min. before surgery ended. The patients were ventilated with N2O/O2 (2:1). Muscle relaxation was maintained at 90-95% with vecuronium, monitoring "train of four" twitch response. The effects of alfentanil on airway pressure, pulse and blood pressure were measured during and without muscle relaxation. The time from end of surgery until full recovery was recorded. Percutaneous CO2-tension was measured in the recovery room. There were no clinical problems with induction or recovery. The average time until the infants opened their eyes and started moving was 1.8 min. No significant changes in pulse and blood pressure occurred during surgery. Airway pressure showed minimal increases when muscle relaxation decreased. These data suggest that alfentanil/N2O anaesthesia can be considered as an alternative if halogenated hydrocarbons are rated unsuitable in paediatric anaesthesia.

[Hemo- and cardiodynamic action of halothane or isoflurane following peroral long-term pretreatment with nifedipine. An animal experimental study]. / Hämo- und kardiodynamische Wirkung von Halothan oder Isofluran nach peroraler Langzeitvorbehandlung mit Nifedipin. Eine tierexperimentelle Studie.

This study investigated the influence of chronic oral nifedipine on the hemodynamic effects of halothane or isoflurane anesthesia in dogs. Under general anesthesia with fentanyl 0.3 microgram/kg/min i.v. and 3:1 N2O/O2 inhalation mixture a left thoracotomy was performed and two needle force probes were placed in the left ventricular wall to measure myocardial force of contraction. In the halothane group (n = 12) a Hall-effect sensor was placed on the anterior surface of the left ventricle, which in combination with a magnet on the posterior surface allowed measurements of left ventricular diameter. In the isoflurane group (n = 15) a Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The dogs were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Prior to surgery, in the halothane group 6 dogs were pretreated with nifedipine 6 mg/kg p.o. for 10 days; the other 6 served as controls. In the isoflurane group, 8 dogs were pretreated with nifedipine in the same way and 7 served as controls. Three hours after instrumentation baseline hemodynamic measurements were performed and repeated 15 min after adding 1 MAC and then 2 MAC halothane or isoflurane. Oral pretreatment with nifedipine caused vasodilation with a significant decrease in systemic vascular resistance (SVR) and mean arterial pressure (MAP); heart rate (HR) and dp/dt max were unchanged in comparison to the control group. The cardiac output (CO) increased. Halothane (1 MAC/2 MAC) had a dose-related circulatory depressant effect. This occurred to the same extent in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic and cardiodynamic effects of propofol and etomidate: negative inotropic properties of propofol.

The hemodynamic effects of an induction dose of propofol, 2.5 mg/kg, or etomidate, 0.3 mg/kg, were studied in eight dogs. In addition, cardiodynamic changes were measured using a left ventricular catheter and needle force probes. Propofol was associated with significant decreases in systolic (19.9%) and diastolic (25.3%) arterial pressures associated with a 17.3% decrease in cardiac output (CO) and a 11.6% reduction in systemic vascular resistance (SVR) without change in pulmonary capillary wedge pressure (PCWP). These changes were most pronounced 1 min after the injection of propofol. At 5 and 10 min after the administration of propofol, heart rate (HR) decreased significantly. Minimal changes in hemodynamics were observed with etomidate. Propofol lowered systolic left ventricular pressure (LVPsys) by 17.6%. Signals generated by the force probes in the left ventricular myocardium showed a significant reduction (16.3%) in left ventricular force (LVF) and a decrease in early systolic rates of increase in force (dF/dt max) by 23.5% associated with propofol. In the presence of an unchanged preload, an unchanged HR, and a decreased SVR, the reduction in CO suggests that propofol has a negative inotropic effect. This negative inotropic effect was confirmed by a reduction in LVF and dF/dt max.

[Flow resistance in pediatric oro- and nasotracheal tubes]. / Strömungswiderstände pädiatrischer Oro- und Nasotrachealtuben.

Flow resistances of different endotracheal tubes used in paediatric anaesthesia were determined with varying gas flows of 3 to 10 lit. per minute. We found no significant differences between preformed orotracheal and nasotracheal tubes and ordinary endotracheal tubes consisting of PVC plastic and spiral tubes made of silicone material, respectively. Woodbridge tubes showed significantly higher resistance to all gas flows used. Because of their less favourable material and flow resistance properties, Woodbridge tubes cannot be recommended for paediatric anaesthesia.

Pulmonary blood flow reduction by prostaglandin F2 alpha and pulmonary artery balloon manipulation during one-lung ventilation in dogs.

The purpose of this experimental study was to compare two methods of pulmonary blood flow manipulation during one-lung ventilation (OLV), either reducing pulmonary blood flow to the non-ventilated lung by inflation of a pulmonary artery catheter balloon (PAB) or by infusion of prostaglandin F2 alpha (PGF2 alpha). Seven anaesthetized dogs were intubated with a Kottmeier endobronchial tube and ventilated with 66% O2. Systemic and pulmonary pressures and blood gases, cardiac output and airway pressure were measured, and the venous admixture (QSP/QT) was calculated. During two-lung ventilation (TLV) Pao2 was 43.6 +/- 1.9 kPa (mean +/- s.d.) and (QSP/QT) was 11 +/- 3%. OLV reduced Pao2 to 12.1 +/- 1.6 kPa (P less than or equal to 0.001) and increased QSP/QT to 40 +/- 4% (P less than or equal to 0.001). Mean pulmonary artery pressure and airway pressure increased. PAB inflation caused an increase in Pao2 to 19.9 +/- 2.9 kPa (P less than or equal to 0.02) and a decrease in QSP/QT to 27 +/- 6% (P less than or equal to 0.001). PGF2 alpha infusion (1.2 micrograms kg-1 min-1) into the pulmonary artery of the non-ventilated lung increased Pao2 to 22.4 +/- 3.3 kPa (P less than or equal to 0.001) and decreased QSP/QT to 25 +/- 4 (P less than or equal to 0.001). PGF2 alpha infusion resulted in a small increase in mean systemic and pulmonary artery pressures. During the infusion of 1.2 micrograms kg-1 min-1 of PGF2 alpha no signs of bronchoconstriction were observed. PAB inflation and PGF2 alpha infusion were equally effective in improving oxygenation and reducing venous admixture during OLV.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin F2 alpha improves oxygen tension and reduces venous admixture during one-lung ventilation in anesthetized paralyzed dogs.

The authors investigated the effect of prostaglandin F2 alpha infused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, PaO2 was 327 +/- 15 mmHg (mean +/- SD) and venous admixture (Qsp/Qt) was 11 +/- 3%. One-lung atelectasis reduced PaO2 to 91 +/- 12 mmHg and increased Qsp/Qt to 40 +/- 4%. Prostaglandin F2 alpha in doses of 0.4, 0.6, 1.2, and 1.8 micrograms X kg-1 X min-1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 micrograms X kg-1 X min-1 there was a dose-dependent reduction in Qsp/Qt to a minimum of 25 +/- 4% and an increase in PaO2 to 168 +/- 25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 micrograms X kg-1 X min-1 decreased PaO2 to 156 +/- 32 mmHg and increased Qsp/Qt to 32 +/- 9%. Increased systemic effects of prostaglandin F2 alpha were observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.