B
Backward failure, see Cardiac failure
Baclofen. Synthetic GABAB receptor agonist and skeletal muscle relaxant, used to treat muscle spasticity, e.g. following spinal injury and in multiple sclerosis. Acts at both spinal and supraspinal levels. Has also been used to treat alcohol withdrawal syndromes.
Bacteraemia. Presence of bacteria in the blood. May be present in SIRS and sepsis, but is not necessary for either diagnosis to be made.
Bacteria. Micro-organisms with a bilayered cytoplasmic membrane, a double-stranded loop of DNA and, in most cases, an outer cell wall containing muramic acid. Responsible for many diseases; mechanisms include the initiation of inflammatory pathways by endotoxins or exotoxins; direct toxic effects on/destruction of tissues or organ systems; impairment of host defensive mechanisms; invasion of host cells; and provocation of autoimmune processes. Early claims that bacterial infections had been conquered by the development of antibacterial drugs are now seen as premature in light of the increasing problem of bacterial resistance. Classified according to their ability to be stained by crystal violet after iodine fixation and alcohol decolorisation (Gram staining), various aspects of their metabolism and their morphology:
– aerobes:
– cocci (spherical-shaped), e.g. staphylococci, enterococci, streptococci species.
– bacilli (rod-shaped), e.g. bacillus, corynebacterium, mycobacterium species.
– cocci, e.g. peptococcus species.
– bacilli, e.g. actinomyces, propionibacterium, clostridium species.
– aerobes:
– cocci, e.g. neisseria species.
Bacterial contamination of breathing equipment, see Contamination of anaesthetic equipment
Bacterial resistance. Ability of bacteria to survive in the presence of antibacterial drugs. An increasingly significant problem in terms of cost, pressure on development of new antibiotics and impaired ability to treat infections both in critically ill patients and the community as a whole.
impermeability of the cell wall to the drug, e.g. pseudomonas and many antibiotics.
lack of intracellular binding site for the antibiotic, e.g. Streptococcus pneumoniae and penicillin resistance.
lack of target metabolic pathways, e.g. vancomycin is only effective against Gram-positive organisms because it affects synthesis of the peptidoglycan cell wall components that Gram-negative bacteria do not possess.
production of specific enzymes against the drug, e.g. penicillinase.
Factors that increase the likelihood of resistance occurring include indiscriminate use of antibacterial drugs, inappropriate choice of drug and use of suboptimal dosage regimens (including poor compliance by users, e.g. long-term anti-TB drug therapy). Regular consultation with microbiologists, use of antibiotic guidelines and infection control procedures, and microbiological surveillance may limit the problem. In the UK, the Department of Health has run several campaigns to increase awareness of the problem and encourage sensible prescribing of antibiotics. ‘Antimicrobial stewardship’ programmes (particularly in ITUs) strive to reduce the emergence of bacterial resistance, improve clinical outcomes and control costs, through the logical prescribing of antibacterial drugs.
Resistance may also occur in other micro-organisms, although the problem is greatest in bacteria.
Gandhi TN, DePestel DD, Collins CD, Nagel J, Washer LL (2010). Crit Care Med; 38 (Suppl.): S315–23
Bacterial translocation. Passage of bacteria across the bowel wall via lymphatics into the hepatic portal circulation, and thence possibly into the systemic circulation. Implicated in the pathophysiology of intra-abdominal or generalised sepsis and MODS, with increased bowel wall permeability resulting from inadequate oxygen delivery allowing bacteria or their components (e.g. endotoxins) to enter the circulation and activate various inflammatory mediator pathways, including cytokines. The inflammatory response may thus be initiated or maintained. Resting the bowel is thought to increase the chances of bacterial translocation; therefore early enteral feeding of critically ill patients (especially with a glutamine-enriched feed) is believed to be beneficial.
Although much evidence supports the occurrence of bacterial translocation, its actual significance in SIRS and MODS is disputed.
Bactericidal/permeability-increasing protein. Protein normally released by activated polymorphonuclear leucocytes. Binds to and neutralises endotoxin and is bactericidal against Gram-negative organisms (by increasing permeability of bacterial cell walls). May have a role in the future treatment of severe Gram-negative infections, e.g. meningococcal disease. Lipopolysaccharide-binding protein is closely related.
See also, Sepsis; Sepsis syndrome; Septic shock; Systemic inflammatory response syndrome
Bain breathing system, see Coaxial anaesthetic breathing systems
Bainbridge reflex. Reflex tachycardia following an increase in central venous pressure, e.g. after rapid infusion of fluid. Activation of atrial stretch receptors results in reduced vagal tone and tachycardia. Absent or diminished if the initial heart rate is high. Of uncertain significance but has been proposed to be involved in respiratory sinus arrhythmia and to act as a counterbalance to the baroreceptor reflex.
Balanced anaesthesia. Concept of using a combination of drugs and techniques (e.g. general and regional anaesthesia) to provide adequate analgesia, anaesthesia and muscle relaxation (triad of anaesthesia). Each drug reduces the requirement for the others, thereby reducing side effects due to any single agent, while also allowing faster recovery. Arose from Crile’s description of anociassociation in 1911, and Lundy’s refinement in 1926.
Ballistocardiography. Obsolete method for measurement of measure cardiac output and stroke volume via detection of body motion resulting from movement of blood within the body with each heartbeat.
Balloon pump, see Intra-aortic counter-pulsation balloon pump
Bar. Unit of pressure. Although not an SI unit, commonly used when referring to the pressures at which anaesthetic gases are delivered from cylinders and piped gas supplies.
Baralyme. Calcium hydroxide 80% and barium octahydrate 20%. Used to absorb CO2. Although less efficient than soda lime, it produces less heat and is more stable in dry atmospheres. Used in spacecraft. Carbon monoxide production may occur when volatile agents containing the CHF2 moiety (desflurane, enflurane or isoflurane) are passed over dry warm baralyme, e.g. at the start of a Monday morning operating session following prolonged passage of dry gas through the absorber.
Barbiturate poisoning. Causes CNS depression with hypoventilation, hypotension, hypothermia and coma.
Skin blisters and muscle necrosis may also occur.
general measures as for poisoning and overdoses.
forced alkaline diuresis, dialysis or haemoperfusion may be indicated.
Barbiturates. Drugs derived from barbituric acid, itself derived from urea and malonic acid and first synthesised in 1864. The first sedative barbiturate, diethyl barbituric acid, was synthesised in 1903. Many others have been developed since, including phenobarbital in 1912, hexobarbital in 1932 (the first widely used iv barbiturate), thiopental in 1934, and methohexital (methohexitone) in 1957.
• Substitutions at certain positions of the molecule confer hypnotic or other properties to the compound (Fig. 22). Chemical classification:
oxybarbiturates: as shown. Slow onset and prolonged action, e.g. phenobarbital.
Exist in two structural isomers, the enol and keto forms. The enol form is water-soluble at alkaline pH and undergoes dynamic structural isomerism to the lipid-soluble keto form upon exposure to physiological pH (e.g. after injection).
long-acting, e.g. phenobarbital.
medium-acting, e.g. amobarbital.
very short-acting, e.g. thiopental.
• Bind avidly to the alpha subunit of the GABAA receptor, potentiating the effects of endogenous GABA. Antagonism of AMPA-type glutamate receptors (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors) also contributes to CNS depression. Actions:
general CNS depression, especially cerebral cortex and ascending reticular activating system.
central respiratory depression (dose-related).
reduction of rapid eye movement sleep (with rebound increase after cessation of chronic use).
anticonvulsant or convulsant properties according to structure.
Oxidative and conjugative hepatic metabolism is followed by renal excretion. Cause hepatic enzyme induction.
Used mainly for induction of anaesthesia, and as anticonvulsant drugs. Have been replaced by benzodiazepines for use as sedatives and hypnotics, as the latter drugs are safer.
See also, γ-Aminobutyric acid receptors; Barbiturate poisoning
Bariatric surgery. Performed to induce significant and sustained weight loss in severe obesity, thereby preventing and indirectly treating the complications of obesity. Delivered as part of a multidisciplinary programme including diet/lifestyle modifications ± drug therapy.
• Indications (issued by NICE):
body mass index (BMI) ≥ 40 kg/m2 or 35–40 kg/m2 in the presence of related significant disease (e.g. diabetes, hypertension), where non-surgical measures have failed and patients are fit enough for anaesthesia and surgery.
BMI > 50 kg/m2 as first-line treatment, if patients are fit enough for anaesthesia and surgery.
malabsorptive: biliopancreatic diversion ± duodenal switch.
restrictive/malabsorptive: Roux-en-Y gastric bypass (laparoscopic or open).
Anaesthetic considerations are as for all patients with morbid obesity.
Barker, Arthur E (1850–1916). English Professor of Surgery at University of London. Helped popularise spinal anaesthesia in the UK. In 1907, became the first to use hyperbaric solutions of local anaesthetic agents, combined with alterations in the patient’s posture, to vary the height of block achieved. Studied the effects of baricity of various local anaesthetic preparations by developing a glass spine model. Used specially prepared solutions of stovaine (combined with 5% glucose) from Paris.
Baroreceptor reflex (Pressoreceptor, Carotid sinus or Depressor reflex). Reflex involved in the short-term control of arterial BP. Increased BP stimulates baroreceptors in the carotid sinus and aortic arch, increasing afferent discharge in the glossopharyngeal and vagus nerves respectively, that is inhibitory to the vasomotor centre and excitatory to the cardioinhibitory centre in the medulla. Vasomotor inhibition (reduced sympathetic activity) and increased cardioinhibitory activity (vagal stimulation) result in a lowering of BP and heart rate. The opposite changes occur following a fall in BP, with sympathetic stimulation and parasympathetic inhibition. Resultant peripheral vasoconstriction occurs mainly in non-vital vascular beds, e.g. skin, muscle, GIT.
The reflex is reset within 30 min if the change in BP is sustained. It may be depressed by certain drugs, e.g. halothane and possibly propofol.
Baroreceptors. Stretch mechanoreceptors in the walls of blood vessels and heart chambers. Respond to distension caused by increased pressure, and are involved in control of arterial BP.
carotid sinus and aortic arch:
– send afferent impulses via the carotid sinus nerve (branch of glossopharyngeal nerve) and vagus (afferents from aortic arch) to the vasomotor centre and cardioinhibitory centre in the medulla. Raised BP invokes the baroreceptor reflex.
– found in both atria. Involved in both short-term neural control of cardiac output and long-term humoral control of ECF volume.
– some discharge during atrial systole while others discharge during diastolic distension (more so when venous return is increased or during IPPV). The latter may be involved in the Bainbridge reflex. Discharge also results in increased urine production via stimulation of ANP secretion and inhibition of vasopressin release.
ventricular stretch receptors: stimulation causes reduced sympathetic activity in animals, but the clinical significance is doubtful. May also respond to chemical stimulation (Bezold–Jarisch reflex).
Other baroreceptors may be present in the mesentery, affecting local blood flow.
Barotrauma. Physical injury caused by an excessive pressure differential across the wall of a body cavity; in anaesthesia, the term usually refers to pneumothorax, pneumomediastinum, pneumoperitoneum or subcutaneous emphysema resulting from passage of air from the tracheobronchial tree and alveoli into adjacent tissues. Risk of barotrauma is increased by raised airway pressures, e.g. with IPPV and PEEP (especially if excessive tidal volume or air flow is delivered, or if the patient fails to synchronise with the ventilator). High frequency ventilation may reduce the risk. Diseased lungs with reduced compliance are more at risk of developing barotrauma, e.g. in asthma, ARDS; limiting inspiratory pressures at the expense of reduced minute volume and increased arterial PCO2 is increasingly used to reduce the risk of barotrauma in these patients (permissive hypercapnia). Evidence of pulmonary interstitial emphysema may be seen on the CXR (perivascular air, hilar air streaks and subpleural air cysts) before development of severe pneumothorax. In all cases, N2O will aggravate the problem.
Risk of barotrauma during anaesthesia is reduced by various pressure-limiting features of anaesthetic machines and breathing systems.
See also, Emphysema, subcutaneous; Ventilator-associated lung injury
Basal metabolic rate (BMR). Amount of energy liberated by catabolism of food per unit time, under standardised conditions (i.e. a relaxed subject at comfortable temperature, 12–14 h after a meal). May be expressed corrected for body surface area.
O2 consumption: the subject breathes via a sealed circuit (containing a CO2 absorber) from an O2-filled spirometer. As O2 is consumed, the volume inside the spirometer falls, and a graph of volume against time is obtained. O2 consumption per unit time is corrected to standard temperature and pressure. Average energy liberated per litre of O2 consumed = 20.1 kJ (4.82 Cal; some variation occurs with different food sources); thus BMR may be calculated. A similar derivation can be obtained electronically by the bedside ‘metabolic cart’, e.g. when calculating energy balance in critically ill patients.
• Metabolic rate is increased by:
circulating catecholamines, e.g. due to stress.
recent feeding (specific dynamic action of foods).
Measurement of metabolic rate under basal conditions eliminates many of these variables.
Basal narcosis, see Rectal administration of anaesthetic agents
Base. Substance that can accept hydrogen ions, thereby reducing hydrogen ion concentration.
Base excess/deficit. Amount of acid or base (in mmol) required to restore 1 litre of blood to normal pH at PCO2 of 5.3 kPa (40 mmHg) and at body temperature. By convention, its value is negative in acidosis and positive in alkalosis. May be read from the Siggaard-Andersen nomogram. Useful as an indication of severity of the metabolic component of acid–base disturbance, and in the calculation of the appropriate dose of acid or base in its treatment. For example, in acidosis:
See also, Acid–base balance; Blood gas analyser; Blood gas interpretation
Basic life support, adult (BLS). Component of CPR without any equipment or drugs (i.e. suitable for anyone to administer). Known as the ‘ABC’ of resuscitation. Use with simple equipment, e.g. airways, facemasks, self-inflating bags, oesophageal obturators, LMA; it has been defined as ‘basic life support with airway adjuncts’. Latest European recommendations (2010):
ensure own safety and that of the victim.
Breathing: check first – look, listen and feel for up to 10 s. If breathing, turn into the recovery position, unless spinal cord injury is suspected. Summon help, asking for an automated external defibrillator (AED) if one is available; a solo rescuer should ‘phone first’ since the chance of successful defibrillation falls with increasing delay (although children, trauma or drowning victims, and poisoned or choking patients may benefit from 1 min of CPR before calling for help). If not breathing, summon help and, on returning, start cardiac massage; after 30 compressions give two slow effective breaths (700–1000 ml, each over 1 s) followed by another 30 compressions. Rapid breaths are more likely to inflate the stomach. Cricoid pressure should be applied if additional help is available. Risk of HIV infection and hepatitis is considered negligible. Inflating equipment and 100% O2 should be used if available.
