Guidelines for sedation and/or analgesia by non-anaesthesiology doctors.

The still ever increasing demand for sedation and/or analgesia for diagnostic and therapeutic procedures puts high pressure on anaesthesia care providers all over Europe. Since the capacity to provide that service by anaesthetists is limited in most European countries, guidelines for non-anaesthetist doctors who want to sedate patients on a high-quality level and especially in a safe way are mandatory. This paper, produced by a working party of the European Board of Anaesthesiology of the European Union of Medical Specialists (EUMS/UEMS), gives direction to those practitioners who feel responsibilities in this area of medicine. Close cooperation with anaesthesiologists seems mandatory to achieve and sustain a high-quality standard for our patients undergoing medical or surgical procedures under sedation.

Hypoxia aggravates lipopolysaccharide-induced lung injury.

The animal model of inflammatory response induced by intratracheal application of lipopolysaccharide includes many typical features of acute lung injury or the acute respiratory distress syndrome. A number of experimental investigations have been performed to characterize the nature of this injury more effectively. In inflammatory conditions, hypoxia occurs frequently before and in parallel with pulmonary and non-pulmonary pathological events. This current study was designed to examine the in vivo effect of hypoxia as a potentially aggravating condition in endotoxin-induced lung injury. Lipopolysaccharide, 150 microg, was instilled intratracheally into rat lungs, and thereafter animals were exposed to either normoxia or hypoxia (10% oxygen). Lungs were collected 2, 4, 6 and 8 h later. Inflammatory response and tissue damage were evaluated by quantitative analysis of inflammatory cells and mediators, surfactant protein and vascular permeability. A significantly enhanced neutrophil recruitment was seen in lipopolysaccharide-animals exposed to hypoxia compared to lipopolysaccharide-animals under normoxia. This increased neutrophil accumulation was triggered by inflammatory mediators such as tumour necrosis factor-alpha and macrophage inflammatory protein-1beta, secreted by alveolar macrophages. Determination of vascular permeability and surfactant protein-B showed enhanced concentrations in lipopolysaccharide-lungs exposed to hypoxia, which was absent in animals previously alveolar macrophage-depleted. This study demonstrates that hypoxia aggravates lipopolysaccharide injury and therefore represents a second hit injury. The additional hypoxia-induced inflammatory reaction seems to be predominantly localized in the respiratory compartment, underlining the compartmentalized nature of the inflammatory response.

Anaesthetic preconditioning but not postconditioning prevents early activation of the deleterious cardiac remodelling programme: evidence of opposing genomic responses in cardioprotection by pre- and postconditioning.

BACKGROUND: Anaesthetic preconditioning (A_PreC) and postconditioning (A_PostC) both provide protection against ischaemia-reperfusion in the heart. However, post-ischaemic gene responses may differ between the two therapeutic strategies. METHODS: Isolated perfused rat hearts were exposed to 40 min test ischaemia followed by 3 h reperfusion and used to determine transcriptional changes in response to A_PreC and A_PostC. A_PreC was induced by 15 min of isoflurane 2.1 vol% followed by 10 min of washout, and A_PostC was induced by 15 min of isoflurane 2.1 vol% administered at the onset of reperfusion. Untreated hearts served as ischaemic control (ISCH). Coupled-two way clustering (CTWC) and principal component analysis (PCA) were used to identify gene expression patterns. RESULTS: A_PreC (7[sd 1]%) and A_PostC (6[2]%) produced a similar decrease in infarct size (ISCH 36[1]%, P<0.05). However, post-ischaemic genomic reprogramming was completely different. Few genes were jointly regulated (2.1 per thousand of upregulated genes and 1.3% of downregulated genes). Eight stable gene clusters including three subclusters emerged from CTWC and were related to inflammation, signalling, ion channels, transcription factors, long interspersed repetitive DNA, heat shock response and remodelling. Two stable sample clusters were identified for postconditioned hearts (first cluster) and for all other protocols (second cluster), emphasizing the unique cardiac phenotype elicited by A_PostC. PCA revealed a close genomic relationship between A_PreC and non-ischaemic healthy myocardium. CONCLUSIONS: A_PreC, but not A_PostC, induces a post-ischaemic gene expression profile similar to virgin myocardium and prevents activation of the deleterious cardiac remodelling programme. Hence A_PreC and A_PostC are not interchangeable with respect to their molecular outcome in the heart.

Complaints of sore throat after tracheal intubation: a prospective evaluation.

BACKGROUND AND OBJECTIVE: Sore throat and hoarseness rank, besides pain and nausea, among the most frequent subjective complaints after tracheal intubation for general anaesthesia. Our intention was to determine the incidence of postoperative sore throat from a large sample of patients and thus to identify the most important associated factors. METHODS: We prospectively followed up 809 adult patients who underwent elective surgical interventions and examined their history, the applied anaesthetic techniques, perioperative course and the occurrence, intensity and duration of postoperative throat complaints. The assignment and professional experience of the involved intubators were also assessed. The influence of a multitude of variables on postoperative throat complaints was statistically analysed. RESULTS: Postoperative sore throat was present in 40% overall being significantly higher in female than in male (44% vs. 33%; P = 0.001). The mean pain intensity in the affected patients (n = 323) was 28+/-12 mm on a visual analogue scale where 0 = no pain and 100 = extreme pain. The average duration was 16+/-11 h. Main factors associated with throat complaints were female sex; history of smoking or lung disease, duration of anaesthesia, postoperative nausea, bloodstain on the endotracheal tube and natural teeth. We could find no influence on the occurrence or intensity of throat complaints by the professional assignment or the length of professional experience of the personnel involved. CONCLUSIONS: Postoperative throat complaints frequently arise after tracheal intubation for general anaesthesia in the first 2 postoperative days, but they are of limited intensity and duration.

[Strategies for perioperative sympatho-modulation]. / Perioperative Strategien zur Regulierung des Sympathikotonus.

Despite the growing evidence for the efficacy of different sympatho-modulatory therapies to lower perioperative cardiac morbidity and mortality, such therapeutic strategies are rather infrequently used in daily clinical practice. Most physicians involved in perioperative medicine are aware of the increasing literature related to this topic, but only few comply with current clinical practice guidelines even in the absence of contraindications. This review discusses possible explanations for this reluctance and again summarizes the basic and clinical principles of current sympatho-modulatory therapies including alpha(2)-agonism, beta-adrenergic antagonism, and regional anesthetic techniques in modern anesthetic practice. In addition, the emerging perioperative concept of a patient-tailored individualized pharmacotherapy based on "gene profiling", particularly the adrenergic polymorphisms, is discussed.

Preconditioning with sevoflurane decreases PECAM-1 expression and improves one-year cardiovascular outcome in coronary artery bypass graft surgery.

BACKGROUND: Cardiac preconditioning is thought to be involved in the observed decreased coronary artery reocclusion rate in patients with angina preceding myocardial infarction. We prospectively examined whether preconditioning by sevoflurane would decrease late cardiac events in patients undergoing coronary artery bypass graft (CABG) surgery. METHODS: Seventy-two patients scheduled for elective CABG surgery were randomized to preconditioning by sevoflurane (10 min at 4 vol%) or placebo. For all patients, follow-up of adverse cardiac events was obtained 6 and 12 months after surgery. Transcript levels for platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31), catalase and heat shock protein 70 (Hsp70) were determined in atrial biopsies after sevoflurane preconditioning. RESULTS: Pharmacological preconditioning by sevoflurane reduced the incidence of late cardiac events during the first year after CABG surgery (sevoflurane 3% vs 17% in the placebo group, log-rank test, P=0.038). One patient in the sevoflurane group and three patients in the placebo group experienced new episodes of congestive heart failure and three additional patients had coronary artery reocclusion. Perioperative peak concentrations for myocardial injury markers were higher in patients with subsequent late cardiac events [NTproBNP, 9031 (4125) vs 3049 (1906) ng litre(-1), P<0.001; cTnT, 1.31 (0.88) vs 0.46 (0.29) microg litre(-1), P<0.001]. Transcript levels were reduced for PECAM-1 and increased for catalase but unchanged for Hsp70 in atrial biopsies after sevoflurane preconditioning. CONCLUSIONS: This prospective randomized clinical study provides evidence of a protective role for pharmacological preconditioning by sevoflurane in late cardiac events in CABG patients, which may be related to favourable transcriptional changes in pro- and antiprotective proteins.

The airway compartment: chambers of secrets.

The adhesion molecule intercellular adhesion molecule-1 (ICAM-1) is known to play a crucial role in lung inflammation such as endotoxin-induced injury. Although ICAM-1 has been characterized on endothelial cells, limited information is available regarding its expression in the epithelial compartment. The present review provides novel views on this aspect.

Effect of rofecoxib on platelet aggregation and blood loss in gynaecological and breast surgery compared with diclofenac.

BACKGROUND: Non-selective cyclooxygenase (COX) inhibitors or non-steroidal anti- inflammatory drugs (NSAIDs) are frequently omitted for perioperative pain relief because of potential side-effects. COX-2-selective inhibitors may have a more favourable side-effect profile. This study tested the hypothesis that the COX-2-selective inhibitor rofecoxib has less influence on platelet function than the NSAID diclofenac in gynaecological surgery. In addition, analgesic efficacy and side-effects of the two drugs were compared. METHODS: In this single-centre, prospective, double-blind, active controlled study, women undergoing vaginal hysterectomy (n=25) or breast surgery (n=25) under general anaesthesia received preoperatively 50 mg of rofecoxib p.o. followed 8 and 16 h later by two doses of placebo or three doses of diclofenac 50 mg p.o. at the same time points. We assessed arachidonic acid-stimulated platelet aggregation before and 4 h after the first dose of study medication, estimated intraoperative blood loss, and haemoglobin loss until the first morning after surgery. Analgesic efficacy, use of rescue analgesics, and side-effects were also recorded. RESULTS: In the rofecoxib group, stimulated platelet aggregation was disturbed less (P=0.02), and estimated intraoperative blood loss (P=0.01) and the decrease in haemoglobin were lower (P=0.01). At similar pain ratings, the use of anti-emetic drugs was less in the rofecoxib group (P=0.03). CONCLUSION: Besides having a smaller effect on platelet aggregation, one oral dose of rofecoxib 50 mg given before surgery provided postoperative analgesia similar to that given by three doses of diclofenac 50 mg and was associated with less use of anti-emetics and less surgical blood loss in gynaecological surgery compared with diclofenac.

Release of inflammatory mediators in irradiated cell salvage blood and their biological consequences in human beings following transfusion.

BACKGROUND AND OBJECTIVE: Irradiation of intraoperative cell salvage blood has recently been used to inactivate tumour cells before retransfusion, during cancer surgery. No information is available about a potential inflammatory response of the recipient to the retransfusion of irradiated intraoperative cell salvage blood. This pilot study was conducted to investigate the possible release of the pro-inflammatory mediators, tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), eotaxin and monocyte chemo-attractant protein-1 (MCP-1), in the serum of recipients by intraoperative retransfusion of irradiated intraoperative cell salvage blood. METHODS: Nine patients undergoing gynaecological cancer surgery were included in this study. Intraoperative cell salvage blood was irradiated with 50 Gy and retransfused to the patient. Serum and intraoperative cell salvage blood concentrations of TNF-alpha, IL-1beta, eotaxin and MCP-1 were repeatedly analysed before and after retransfusion, respectively before and after irradiation. RESULTS: Traces of mediators were detected in intraoperative cell salvage blood but no increase due to irradiation was observed. Following transfusion of intraoperative cell salvage blood, minute quantities (all < 30 pg mL(-1) of mediators were detected in the serum of patients. However, there was no significant upregulation compared to serum values before retransfusion. CONCLUSIONS: These results provide evidence that retransfusion of irradiated intraoperative cell salvage blood might represent a blood-saving strategy in cancer surgery without an immunological inflammatory response as shown by a lack of upregulation of inflammatory mediators.

Patient well-being after general anaesthesia: a prospective, randomized, controlled multi-centre trial comparing intravenous and inhalation anaesthesia.

BACKGROUND: The aim of this study was to assess postoperative patient well-being after total i.v. anaesthesia compared with inhalation anaesthesia by means of validated psychometric tests. METHODS: With ethics committee approval, 305 patients undergoing minor elective gynaecologic or orthopaedic interventions were assigned randomly to total i.v. anaesthesia using propofol or inhalation anaesthesia using sevoflurane. The primary outcome measurement was the actual mental state 90 min and 24 h after anaesthesia assessed by a blinded observer using the Adjective Mood Scale (AMS) and the State-Trait-Anxiety Inventory (STAI). Incidence of postoperative nausea and vomiting (PONV) and postoperative pain level were determined by Visual Analogue Scale (VAS) 90 min and 24 h after anaesthesia (secondary outcome measurements). Patient satisfaction was evaluated using a VAS 24 h after anaesthesia. RESULTS: The AMS and STAI scores were significantly better 90 min after total i.v. anaesthesia compared with inhalation anaesthesia (P=0.02, P=0.05, respectively), but equal 24 h after both anaesthetic techniques (P=0.90, P=0.78, respectively); patient satisfaction was comparable (P=0.26). Postoperative pain was comparable in both groups 90 min and 24 h after anaesthesia (P=0.11, P=0.12, respectively). The incidence of postoperative nausea was reduced after total i.v. compared with inhalation anaesthesia at 90 min (7 vs 35%, P<0.001), and 24 h (33 vs 52%, P=0.001). CONCLUSION: Total i.v. anaesthesia improves early postoperative patient well-being and reduces the incidence of PONV.

Anaesthetics and cardiac preconditioning. Part I. Signalling and cytoprotective mechanisms.

Cardiac preconditioning represents the most potent and consistently reproducible method of rescuing heart tissue from undergoing irreversible ischaemic damage. Major milestones regarding the elucidation of this phenomenon have been passed in the last two decades. The signalling and amplification cascades from the preconditioning stimulus, be it ischaemic or pharmacological, to the putative end-effectors, including the mechanisms involved in cellular protection, are discussed in this review. Volatile anaesthetics and opioids effectively elicit pharmacological preconditioning. Anaesthetic-induced preconditioning and ischaemic preconditioning share many fundamental steps, including activation of G-protein-coupled receptors, multiple protein kinases and ATP-sensitive potassium channels (K(ATP) channels). Volatile anaesthetics prime the activation of the sarcolemmal and mitochondrial K(ATP) channels, the putative end-effectors of preconditioning, by stimulation of adenosine receptors and subsequent activation of protein kinase C (PKC) and by increased formation of nitric oxide and free oxygen radicals. In the case of desflurane, stimulation of alpha- and beta-adrenergic receptors may also be of importance. Similarly, opioids activate delta- and kappa-opioid receptors, and this also leads to PKC activation. Activated PKC acts as an amplifier of the preconditioning stimulus and stabilizes, by phosphorylation, the open state of the mitochondrial K(ATP) channel (the main end-effector in anaesthetic preconditioning) and the sarcolemmal K(ATP) channel. The opening of K(ATP) channels ultimately elicits cytoprotection by decreasing cytosolic and mitochondrial Ca(2+) overload.

Anaesthetics and cardiac preconditioning. Part II. Clinical implications.

There is compelling evidence that preconditioning occurs in humans. Experimental studies with potential clinical implications as well as clinical studies evaluating ischaemic, pharmacological and anaesthetic cardiac preconditioning in the perioperative setting are reviewed. These studies reveal promising results. However, there are conflicting reports on the efficacy of preconditioning in the diseased and aged myocardium. In addition, many anaesthetics and a significant number of perioperatively administered drugs affect the activity of cardiac sarcolemmal and mitochondrial K(ATP) channels, the end-effectors of cardiac preconditioning, and thereby markedly modulate preconditioning effects in myocardial tissue. Although these modulatory effects on K(ATP) channels have been investigated almost exclusively in laboratory investigations, they may have potential implications in clinical medicine. Important questions regarding the clinical utility and applicability of perioperative cardiac preconditioning remain unresolved and need more experimental work and randomized controlled clinical trials.

[A short history of the Swiss Society of Anaesthesiology and Reanimation (SSAR)]. / Kurze Geschichte der Schweizerischen Gesellschaft für Anästhesiologie und Reanimation (SGAR).

In common with most continental countries, anaesthesia in post-World War II Switzerland was clearly in arrears in comparison to the Anglo-American and Scandinavian countries. As early as in 1947, however, motivated young physicians left Switzerland for England, Scandinavia and the USA to familiarise themselves with the advances made in modern anaesthesia. In March, 1951, three of these pioneers, Ch. Bovay (Lausanne), W. Hügin (Basel), and K. Zeller (Winterthur), founded the Professional Association of Swiss Anaesthesiologists, thus preparing the ground for the Swiss Society of Anaesthesiology which was founded on July 5 th, 1952, on the occasion of the annual meeting of the Swiss Society of Surgery held in Zurich. Members of the first Executive Committee were Ch. Bovay, K. Zimmermann (Zurich), and W. Hügin. In 1963, the latter was appointed first Professor of Anaesthesiology in Switzerland by the University of Basel. Looking back, the 18 physicians involved in the foundation of the Society were indeed most courageous. This step towards independence is all the more admirable since the Swiss Society of Surgery, by founding a Section of Anaesthesiology, attempted to retain sovereignty over this small and new group of specialists. Only in 1954 anaesthesiology was recognised by the Swiss Medical Association as a medical specialty in its own right. In 1967 the name was changed to Swiss Society of Anaesthesiology and Reanimation (SSAR). Since coming into existence, the Society has grown more than 40-fold, with a total membership approaching 800 by 2002 end. In recent years, the SSAR took a particular interest in promoting both the training and CME of anaesthesiologists, in supporting research by its young members and in improving the quality and safety of anaesthesia.

Decreased alveolar oxygen induces lung inflammation.

Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well defined. Therefore, effects of alveolar hypoxia were studied in rat lungs, exposing rats to 10% oxygen over periods of 1, 2, 4, 6, and 8 h. An increase in the number of macrophages in bronchoalveolar lavage fluid of hypoxic animals was shown between 1 and 8 h. Extravasation of albumin was enhanced after 1 h and remained increased throughout the study period. NF-kappaB-binding activity as well as mRNA for TNF-alpha, macrophage inflammatory protein (MIP)-1beta, and monocyte chemoattractant protein (MCP)-1 were increased within the first 2 h of exposure to hypoxia. Hypoxia-inducible factor (HIF)-1alpha and intercellular adhesion molecule (ICAM)-1 mRNA were upregulated between 1 and 6 h. Elimination of alveolar macrophages by intratracheal application of liposome-encapsulated clodronate led to a decreased expression of NF-kappaB binding activity, HIF-1alpha, TNF-alpha, ICAM-1, and MIP-1beta. In summary, alveolar hypoxia induced macrophage recruitment, an increase in albumin leakage, and enhanced expression of inflammatory mediators, which were mainly macrophage dependent. Alveolar macrophages appear to have a prominent role in the inflammatory response in hypoxia-induced lung injury and the related upregulation of inflammatory mediators.

Role of alveolar epithelial ICAM-1 in lipopolysaccharide-induced lung inflammation.

Intercellular adhesion molecule-1 (ICAM-1) is known to play a central role in lung inflammation. Limited information, however, is available regarding the expression and biological function of ICAM-1 in the alveolar epithelial compartment. The current report analyses the expression pattern of ICAM-1 in primary cultures of rat alveolar epithelial cells (AECs) and in the rat lung following instillation of bacterial endotoxin (lipopolysaccharide (LPS)) in order to better define the role of alveolar epithelial ICAM-1. AECs stimulated in vitro with LPS were evaluated for ICAM-1 and ICAM-1 messenger ribonucleic acid content. Adherence assays with neutrophils and macrophages were performed. Endotoxin-induced ICAM-1 upregulation on AECs was demonstrated in vivo by immunofluorescence staining. In addition, the effect of intratracheally-instilled anti-ICAM-1 was assessed. Significant upregulation of ICAM-1 occurred in vitro and in vivo on AECs after LPS stimulation. Adherence assays showed a 114% increase in adhesion of neutrophils to AECs. Antibody directed against ICAM-1 reduced this adhesion by 40%. A significant reduction in the number of neutrophils in bronchoalveolar lavage fluid and whole lung was seen under airway ICAM-1 blockade. These data indicate that intercellular adhesion molecule-1 participates in the inflammatory response to lipopolysaccharide-induced lung injury in the distal airways by interacting mainly with neutrophils.

Late oesophageal perforation after intraoperative transoesophageal echocardiography.

Serious haemodynamic instability occurred during emergency surgery for a perforated duodenal ulcer in a 72-year-old man with acute myocardial infarction. Intraoperative transoesophageal echocardiography was crucial for diagnosis of the location of myocardial infarction in the right ventricle and the subsequent haemodynamic management. Postoperatively, a thrombus in the right coronary artery was removed by coronary angiography. The patient's trachea was extubated on the fourth postoperative day. Another 4 days later a leak in the lower oesophagus was suspected because of pleural empyema, and verified. The patient's trachea had to be re-intubated and an oesophageal stent was inserted. The patient was discharged, fully recovered, 2 months after the operation.

[Participation--oriented analysis of the anesthesia workplace. A work system for anesthesia in a multidisciplinary operating room]. / Beteiligungsorientierte Arbeitsplatzanalyse. Schwachstellen im Arbeitssystem der Anästhesie in einem multidisziplinären OP-Trakt.

INTRODUCTION: The aim of this study was the detection and understanding of weak points in the ergonomic design of anaesthesia workplaces in a multidisciplinary operating room facility. METHODS: Analysis of workplaces and of working processes by means of observations, computer-supported task recording and video-photo documentation. During guided interviews the participants were provided with material for naming-by-pointing and drawing. Subsequently, the background of the problems encountered and possible improvements were visualised. RESULTS: Important deficits were devices not positioned within reach and view, difficulties in operating the lines connecting the patient and the devices, and inconsistent workplace layouts. These were caused by erroneous planning of the facility and disregarding ergonomic principles in equipment design. The initial improvements implemented were the development of a new concept for a flexible equipment positioning and the design of a tool for cable handling. DISCUSSION AND CONCLUSION: Although from the very beginning of the study the anaesthesia personnel quoted the handling of the lines connecting patients and devices as the main cause for working difficulties, the external ergonomist could contribute to a broader view of the problems. The method presented here initiated a mutual learning process between ergonomist and users and resulted in a common understanding of the problems and their causes. Compared to the traditional consulting process, more time and efforts were necessary but were offset by the users' acceptance of the improvements and the prevention of design errors.

Changes in intrathoracic blood volume associated with pneumoperitoneum and positioning.

BACKGROUND: It is still controversial whether elevated cardiac filling pressures after the onset of pneumoperitoneum are the consequence of increased intrathoracic pressure or of increased venous return. The aim of this study was to assess the effects of pneumoperitoneum and body positioning on intrathoracic blood volume (ITBV). METHODS: Thirty anesthetized patients were randomly assigned to have CO2-pneumoperitoneum (13 mmHg) either in a supine, in a 15 degrees head-up tilt or in a 15 degrees head-down tilt position. Measurements of ITBV and hemodynamics by the double indicator method were recorded after induction of anesthesia and application of a fluid bolus (Lactated Ringer's solution 10 ml/kg), after positioning and after induction of pneumoperitoneum. RESULTS: Intrathoracic blood volume index (ITBVI) increased significantly after induction of pneumoperitoneum in all body positions (supine: from 18.5 +/- 3.3 -20.2 +/- 5.2 ml/kg (+6%) head-up from 16.7 +/- 3.8 - 17.4 +/- 3.7 ml/kg (+16%) and head-down: from 19.8 +/- 5.6 - 20.5 +/- 5.9 ml/kg (+14%)). Heart rate did not change significantly in any of the groups. Cardiac index showed a statistically significant change in the head-down position with pneumoperitoneum (-11%). A good correlation was found for stroke volume (SV) with ITBV (r = 0.79), but not with central venous pressure (r = 0.26). Systemic vascular resistance index increased significantly in all three groups (supine +6%, head-up +16%, head-down position +14%). CONCLUSION: The present study indicates that the onset of pneumoperitoneum, even with moderate intra-abdominal pressures, is associated with an increased intrathoracic blood volume in ASA I/II patients.

Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action.

This review focuses on the mechanisms and sites of action underlying beta-adrenergic antagonism in perioperative medicine. A large body of knowledge has recently emerged from basic and clinical research concerning the mechanisms of the life-saving effects of beta-adrenergic antagonists (beta-AAs) in high-risk cardiac patients. This article re-emphasizes the mechanisms underlying beta-adrenergic antagonism and also illuminates novel rationales behind the use of perioperative beta-AAs from a biological point of view. Particularly, it delineates new concepts of beta-adrenergic signal transduction emerging from transgenic animal models. The role of the different characteristics of various beta-AAs is discussed, and evidence will be presented for the selection of one specific agent over another on the basis of individual drug profiles in defined clinical situations. The salutary effects of beta-AAs on the cardiovascular system will be described at the cellular and molecular levels. Beta-AAs exhibit many effects beyond a reduction in heart rate, which are less known by perioperative physicians but equally desirable in the perioperative care of high-risk cardiac patients. These include effects on core components of an anaesthetic regimen, such as analgesia, hypnosis, and memory function. Despite overwhelming evidence of benefit, beta-AAs are currently under-utilized in the perioperative period because of concerns of potential adverse effects and toxicity. The effects of acute administration of beta-AAs on cardiac function in the compromised patient and strategies to counteract potential adverse effects will be discussed in detail. This may help to overcome barriers to the initiation of perioperative treatment with beta-AAs in a larger number of high-risk cardiac patients undergoing surgery.