Commonly used IV anesthetic agents Propofol (2,6-diisopropylphenol; t =30 \200\223600min)1 This lipophilic phenol deriva- tive is produced commercially as an emulsion in soybean oil and has become the most commonly used IV anesthetic agent in the developed world. Its good recovery characteristics and anti-emetic eff ect make it popular, espe- cially in day-case surgery. 24 It is fast-acting and its off set of action is due to rapid redistribution, an d not metabolism. \200 Dose examples: Induction = 2mg/kg IVI at 2 \200\2234mg/ sec. Maint enance = 4 \200\22312mg/kg/h IVI. NB: \200\207Rapid injection can cause cardiovascular dep ression ( \200\201BP), and respiratory depression can occur when combined with IV narcotics . For procedural seda- tion: 0.5 \200\2231mg/kg IVI over 1 \200\2235min. Dose needs to be r educed in the elderly, debilitated and shocked. Dose also depends partly on premed use: wit h midazolam induction dose requirements for propofol are reduced by 20 \200\22350%. This ef f ect seems to be more pronounced in the elderly. 26,27 \200 Uses: It is used in inductio n and maintenance of GA, and for sedation dur- ing regional anesthesia, short procedures, a nd as a sedative in ITU (though contraindicated in children for this last use). Once opened , use ampoules or discard, because of the risk of bacterial growth. 620 \200 \200\207Contraindications: \200 Extremes of age \200 <17yr for sedation \200 Egg or soy allergy 25 \200 Compromised airway2 a i s e h t s e a n A Problems: Pain on injection occurs in up to 40% of patients. This can be minimized by eithe r adding a small amount of lidocaine (eg 2mL of 1%) to the propofol, or by pre-injection of local anesthetic. 28 Thiopental sodium (t =11h) a barbiturate that is typically mixed wit h water to give a 2.5% solution (ie 25mg/mL). It has a rapid onset of action (arm \200\223 brain circulation time about 30sec). Eff ects last 3 \200\2238min, and awakening is due lar gely to redistribution, not metabolism. Some 30% of the injected dose is still present in t he body after 24h, giving rise to a hangover eff ect. It has been replaced by propofol as t he most popular induction agent. \200 Dose examples: 100 \200\223150mg (less if elderly/d ebilitated) IV over 10 \200\22315sec (longer if elderly/debilitated), followed by further q uantity if needed accord- ing to response after 30 \200\22360sec (or up to 4mg/kg; max 500m g). Uses: Induction of GA; it is also a potent anticonvulsant \200\224used in status epi- lepticus management when other measures have failed (p208). Problems: Anaphylaxis is rare (1 in 20,000). Is a negative inotrope so can drop cardiac out put by 20%. May also lead to bronchoconstriction. \200\207Intra- arterial injection produc es pain and blanching of the hand/limb below the level of injection due to arterial spasm, followed by ischaemic damage and gangrene \200\224following inadvertent brachial artery pun cture in the antecubital fossa. This is less of a problem now that an indwelling cannula is ob- ligatory (compared with the historical use of a needle). \200\207Contraindications: \200 Airway obstruction \200 Barbiturate allergy \200 Fix ed cardiac output states \200 Hypovolaemia/ \200\201BP \200 Porphyria \200 Compromised airway2 Treatment: 1 Leave the needle in the artery and inject a vaso- dilator, eg papaverine. 2 Ask an experienced colleague to perform, bra- chial plexus or stellate ganglion block. (T his should dilate vessels and \200\201ischaemia.) 3 Heparin IV to stop thrombus forming. 4 Give pain relief \200\224postpone surgery unless desperate. Extravascular injection causes severe pain and local necrosis. \200\207Get expert help. In \201 ltrate with hyaluronida se 1500IU dissolved in 1mL water through the cannula. 1 The pharmacokinetics are best modeled by a three-compartment model. 2 A compromised airwa y is a relative contraindication to any iv induction, regardless of the agent used. 621 Other IV anesthetic agents Etomidate (t =3.5h) This is a carboxylated imidazole and is use d as an induc- tion agent. Dose: 0.15 \200\2230.3mg/kg. Uses: Histamine release is not a fe ature, but rapidity of recovery and cardiovascular stability are; therefore it is often use d in emergent patients with trauma/head injuries for whom avoidance of even a brief episode of hypotension is important. Problems: Be aware it can induce involuntary muscle movements , nausea, and adrenal suppression. 29,30 Local thrombophlebitis can occur after injection. Ketamine (a phencyclidine derivative, produced as a racemic mixture; N-methyl-d-aspartate r eceptor antagonist; t =2.2h) Dose example: 2mg/kg usually gives 5 \200\22310min of surgica l anesthesia (for long procedures \200\224see BNF 15.1.1). Uses: Mainly for pediatric anest hesia and procedural sedation. Car- diac output is unchanged or increased, and so it is a g ood \200\230on site \200\231 or \200\230in the \201 eld \200\231 agent, as it can be gi ven IM, producing profound analgesia without com- pounding shock. Ketamine has potent bronc hodilatory properties, so can be considered during intubation in status asthmaticus. 31 Pro blems: Hypertonus and salivation, but there is some maintenance of laryngeal re \202 exes (but do not rely on this). Recovery is slow. Emergence phenomena are troublesome (de- liriu m, hallucinations, nightmares; all made worse if the patient is disturbed during recovery). \200\207Avoid in the hypertensive patient, those with a history of stroke or raised intra cranial pressure (further \200\200 produced), patients with a re- cent penetrating eye inj ury (risk of \200\200 intra-ocular pressure), and psychiatric patients. Avoid adrenaline i n \201 ltrations. In the UK, the Home Offi ce classi \201 es it as a class C drug as it i s prone to misuse ( \200\230Special-K \200\231). Ideal weight and drug dosages To avoid exc essive dosage in obese patients it may be best to calculate the dose on the basis of ideal body weight (IBW). a i s e h t s e a n A Ideal body weight in kg: \200 = 50kg + 2.3kg for each inch over 5 feet tall. \200 = 45. 5kg+2.3kg for each inch over 5 feet tall. See www.globalrph.com The ideal (but imaginary) IV anesthetic agent The ideal IV agent would be stable in solutio n and in the presence of light, be water-soluble and have a long shelf-life. It would be pa inless when given IV; non-irritant if injected extravascularly (with a low incidence of thr ombosis) with some pain (as a warning) if given intra-arterially. Furthermore: \200 It sh ould act rapidly within one arm \200\223brain circulation. \200 Recovery should be quick and complete with no hangover eff ect. \200 It should provoke no excitatory phenomena. \200 Analgesic properties are advantageous. \200 Respiratory and cardiovascular eff ects should be minimal. \200 It should not interact with other anesthetic agents. \200 Ther e should be no hypersensitivity reactions. \200 There should be no post-op phenomena, eg nausea or hallucinations. The ideal (but imaginary) inhaled anesthetic agent 32 Inhaled agents have advantages (eg no IV access required, more precise con- trol) and disadvantages (eg claustrophobic) over IV agents. The ideal inhaled agent should: \200 Have low solubility in blood and tissues (to allow rapid recovery). \200 Be resistant to any degradation. \200 Have no injurious ef f ects on vital tissues. \200 Be administrable in a reliable and known concentration. Neuromuscular blockers These act on the post-synaptic receptors at the NMJ. There are two m ain types: Depolarizing agents Suxamethonium (=succinylcholine) is the only one com- monly used. It is a partial agonist for acetylcholine receptors and causes ini- tial fasciculatio n through depolarization of the post-synaptic membrane, then paralysis by inhibiting the re storation of normal membrane polarity. Suxam- ethonium is rapidly inactivated by plasma cho linesterases. Dose: 1 \200\2231.5mg/kg IV uses: It has been the most popular paralytic agen t in rapid sequence induc- tions (RSI) for several decades due to its rapid onset (30 \200 \22360sec), and short du- ration (3 \200\2235min). Both these aspects are important in rapi d sequence induction. The rapid onset lessens the time between induction and intubation \200\224decreas- ing the risk of aspiration and potential hypoxia. The short duration means that if intubation is impossible, the patient regains muscle tone, and starts pro- tecting their own airway again. Its popularity may start to wane with the increasing use of rocuro nium (below). Side effects: \200\200K+ (enough to raise the plasma K+ by 0.5 \200\2231.0m mol/L \200\224avoid in paraplegia and burns!). Beware that K+ liberation is increased with multiple sclerosis, Guillain \200\223Barr , stroke, and crush injury. Suxamethonium increa ses intra-ocular pressure (eg increases risk of vitreous extrusion). 30% of patients get po st-operative muscle pains. Repeated doses of suxamethonium may lead to bradycardia \200\224 more common in children \200\224treat with atropine. \200\207Beware suxamethonium apnoea ( p628). Non-depolarizing agents These drugs are competitive antagonists of ace- tylcholine ( ACh) \200\224that is they compete with ACh at the NMJ \200\224but without pro- ducing initi al depolarization (so no fasiculations). Their action can be reversed by anticholinesterase s (eg neostigmine) which lead to an increase in the amount of ACh available at the NMJ. The y are used during balanced anesthesia to facilitate IPPV and surgery. Examples include: Roc uronium: Lasts 10 \200\22315min. Typically given at dose of 0.6mg/kg IBW (ideal body weight p621) \200\224although in RSI has been used at doses of 0.9 \200\2231.2mg/kg to produce in tubating conditions within 60 sec. Rocuronium has few side eff ects \200\224although has be en known to cause anaphylaxis. Excretion is via the liver. Historically, rocuronium has not been used for RSI due to its duration of action. The availability of Sugamma- dex (a rever sal agent for rocuronium) is allowing this to change. At doses of 16mg/kg (given 3 \200\223 5min post rocuronium) sugammadex is able to reverse rocu- ronium faster than the time taken for suxamethonium to wear off . 33 Given its lower side eff ect pro \201 le, RSI with roc uronium could be considered an attrac- tive alternative to RSI with suxamethonium. Vecuroni um: Lasting 20 \200\22330min, it is used if cardiovascular stability is important. Adult do se: 0.1mg/kg IV then 20 \200\22330 g/kg IV as needed. Sugammadex also reverses vecuronium. Atracu- rium: Lasting 20min. Metabolism is by Hoffman elimination (spontaneous molecular breakdown), so it is the drug of choice in renal and liver failure. Dose: 0.5mg/kg IBW IV t hen 100 \200\223200 g/kg IBW IV as needed. Other non-depolarizing agents include cisatracu rium and mivacurium. Note on neuromuscular blockers in those with myasthenia In general, th ese patients are resistant to suxamethonium and very sensitive to non-de- polarizing relaxa nts (action may be prolonged: lower doses may be needed). Warn patients that mechanical ven tilation may be needed post-op. Liaise closely with a senior anesthetist. A small dose of a tracurium is most com- monly used. 622 \200 a i s e h t s e a n A 623 Action at the NMJ: mayhem, mischief or medication? Procession at the synapse ( \201 g 1) W ith the arrival of an ac- tion potential at the nerve terminal comes the release of ace- (A Ch) by tylcholine exocytosis of vesicles at the presynaptic membrane. ACh then diff uses ac ross the synaptic cleft ( 75nm wide), its fate then being one of: Schwann cell Axon Part of Schwann cell Prejunction membrane Basal lamina Choline uptake Postjunctional membra ne Densa projection Fig 1. Procession at the synapse Membrane recycling ACh receptor ACh esterase on basal lamina ACh molecules a i s e h t s e a n A 1 Hydrolysis in the synaptic cleft by acetylcholinesterase (AChE) to choline and acetate. 2 Diff usion into circulation (to be broken down by pseudocholinesterase). 3 Binding to pos t-synaptic nicotinic ACh receptors (NAChRs). 4 It is the last of these that continues the s ignal procession at the post- synaptic membrane by opening an ionophore channel linked to t he re- ceptor, allowing the in \202 ux of Na+ cations. Membrane depolarization en- sues, c reating an endplate potential that results in muscle contraction. Hydrolysis of ACh whilst bound to the receptor causes termination of the endplate potential, bringing the trigger to contraction to an end. Although there is a degree of receptor redundancy in the system for safety, the skeletal ne uromuscular junction is nonetheless a site where lethal paraly- sis can take place. But age nts that meddle here are not all bad. Mayhem \200 \200 Curare: eg tubocurarine, reversib le NAChR blocker; poison used in South America extracted from plants (eg Chondrodendrum tom entosum, Strychnos toxifera) and used to tip darts for hunting. \200 \200 -Neurotoxoins: eg \200 -bungarotoxin, irreversible NAChR blockers found in snake venom (eg Taiwanese ban ded krait, Bungarus multicinctus); multiple research uses, including immunostaining techniq ues (see \201 g 1, p612). Botulinum toxin: produced by Clostridium botulinum; blocks exocytosis. \200 Organophospha tes: insecticides which irreversibly inhibit AChE, causing pro- longed binding of ACh at th e post-synaptic membrane and depolarization. Sarin: odorless and colorless high SVP agent (see p619), infamous as a nerve gas; related to organophosphates. \200 mischief \200 Nicotine: mimics the eff ect of acetylcholine at the receptor. \200 Myasthenia gravis: au toimmune depletion of NAChRs on the post-synaptic membrane (OHCM p516). Eaton \200\223Lambert syndrome: defective ACh release at the pre-synaptic mem- brane; paran eoplastic or autoimmune syndrome, with antibodies vs the pre-synaptic voltage-gated Ca2+ ch annels \200\224OHCM p516. \200 or medication? Suxamethonium: depolarizing NAChR blocker (see OPPOSITE). \200 Vecuronium: non-depolarizi ng NAChR blocker (see OPPOSITE). \200 Neostigmine: anticholinesterase that prevents break down of ACh in the synaptic cleft, increasing the effi cacy of ACh. Edrophonium: another anticholinesterase, which was used diagnostically in myasthenia gravis (Tensilon test); also used to reverse eff ects of non-depolarizing blockers, though wors ens eff ect of depolarizing blockers. \200 Botulinum toxin: used to relieve disability fr om focal spasticity, and in blepharospasm, spasmodic torticollis and severe hyperhidrosis. Practical conduct of anesthesia I The practitioner administering the anesthetic is responsi ble for the suitabil- ity of the surroundings, the adequacy of the available equipment, and his or her own competence to deal with potential complications. The presence of a skilled dedicated assistant with the anesthetist is also vital. \200\207Equipment must be checked before even the shortest anesthetic proce- dure, see p618. Induction May be IV OR inhalatio nal (though IM is possible with ketamine, p621). Intravenous: \200 Establish IV access. \200 Pre-oxygenate, and give co-induction agents (e.g. fentanyl/midazolam) \200 Give a s leep-inducing dose of eg propofol. \200\207Beware: Stimulation before anesthesia can have drastic consequences (coughing, breath-holding, laryngospasm). Remember: noise is a stimulu s too. Gaseous: \200 Either start with sevo \202 urane in oxygen according to age and cl ini- cal state. \200 Or give nitrous oxide: oxygen 60% : 40% mixture with a volatile agen t, eg sevo \202 urane. In children, it is less frightening to start with a hand cupped fro m the end of the circuit onto the face than to apply the mask direct to the face. \200 Es tablish IV access as soon as asleep. Indications for gaseous induction \200 At the patien t \200\231s request. \200 Diffi cult IV access \200 Children \200 Some patients with partial airway obstruction (actual or potential, eg for- eign body, tumor, or abscess), tho ugh awake \201 bre-optic intubation is an option. 624 \200 a i s e h t s e a n A Airway control This is maintained by holding a mask onto the face, by in- serting a larynge al mask airway, or by intubation (p627). To prevent airway obstruction, standard chin lift and/or jaw thrust maneuvers are used. It may be facilitated by the use of an airway adjunct (eg oropharyngeal or naso- pharyngeal), \200\207but this may produce vomiting or laryngos pasm at light levels of anesthesia. Ensure the patient is adequately anesthetized (see p626 ), as laryngoscopy and tracheal intubation can produce a harmful adrenergic stress response with adverse increases in pulse and BP. Concurrent short-acting opiates or es- molol IVI c an attenuate this in a dose-dependent way. 34 Aspiration Aspiration of foreign material into the respiratory tract can occur at any time around anes thesia. It is unlikely to occur if a tracheal tube is in situ. It may occur with a LMA (p62 7). It can be the result of passive regurgitation, or of active vomiting. If suspected (dir ect visualization at laryngoscopy, cough- ing, vomiting, laryngospasm, bronchospasm, SAO2 \200\201, tachypnoea, wheeze and crepitations on auscultation), then immediately do the fol lowing: \200 Apply cricoid pressure, unless actively vomiting (risks oesophageal rupture). \200 Use suction to clear the mouth of debris. \200 Intubate with an ET tube, use soft c atheters to suction out the upper air- way. \200 Refrain from ventilating whilst undertaking these procedures, providing oxygenation levels are acceptable (to prevent dispersion of aspirate). \200 Empty the stomach with an NGT at the \201 rst available opportunity. \200 Put the patient head down and in the left lateral position. \200 Cancel surgery, unless it is for an emergency. \200 Consider ongoing ventilatory support to ensure adequate oxygenation. \200 Arrange a CXR. Further investigation may be needed, eg bronchoscopy. \200 In the abse nce of fecal contamination of the airway, consider withholding antibiotics until sensitivities are known (eg from bronchial lavage). 625 Mechanical ventilation Indications Ventilators are used in anaes- thesia when there is an o perative need for muscle paralysis, or when muscle paralysis is part of a balanced GA for a long operation. (Ventilators are used in intensive care for ventilatory support in reversi ble acute respiratory failure \200\224this is a diff erent topic: see eg p110.) Modes1 \200 Whenever the patient is paralyzed and intubated, intermittent positive pressure venti lation (IPPV) is mostly used. These ventilators have controls to alter: Overview of ventilator modes: \200 Pressure controlled \200 Volume controlled a i s e h t s e a n A Tidal volume \200\224which provides precise control of volume and PaCO2 (ie volume controll ed) \200 Pressure necessary to in \202 ate the lungs (ie pressure controlled) \200\224whi ch reduces risk of barotrauma. Other controls may be available to adjust: \200 Respiratory rate \200 Inspiratory time \200 Inspiratory \202 ow waveform \200 End-tidal pause \200 I:E ratio (I:E = the ratio of inspiratory to expiratory time). Another form is controlled mandatory ventilation (CMV), which controls the drive and rate o f ventilation in the presence of paralyzed spontaneous breathing, and is in practice the sa me as IPPV. Some ventilators deliver synchronized intermittent mandatory ventila- tion (SIMV) which all ows the patient to start breathing spontaneously when paralysis wears off , providing assis tance if these breaths are inadequate. These are less common in theater, and more often use d in intensive care units. \200\207It is mandatory for ventilators to have disconnect, hig h-pressure, and oxy- gen failure alarms. Whichever mode is used, positive end expiratory pr essure (PEEP) is often a useful adjunct. PEEP allows a pressure to be exerted at the end of expiration, which help splint open alveoli, increasing the surface area available for gas exchange, thereby reducing the amount of "shunt" (areas of lung which are perfused but not ventilated). A typical PEEP value would be 5cm H2O. High levels of PEEP may lead to re- du ced venous return due to a rise in intratho- racic pressure. Familiarity with ventilators a nd ventilation is best gained from direct observation of their use. If you are interested i n \201 nding out more, then pursue the opportunity of a placement in the intensive care u nit. Lung compliance Compliance = change in volume change in pressure This is a useful concept in ventilation, as it relates to the behavior of various parts of the respiratory tract. Poor compliance means only a sma ll change in volume for a big change in pressure. 1 High-frequency oscillatory ventilation (HFOV) is used in preterm infants and neonates (p1 10).35 Practical conduct of anesthesia II Intubation Passing an ET tube through the cords into the trachea protects the airway and ensures that ventilation can take place. Most commonly nee d- ed in: \200 Risk of vomiting/aspiration ( \200 p 624) of gastric contents: eg re \202 ux oesophagitis, abdominal disease, major trauma, non-fasted, hiatus hernia, pregnant >15w ks. \200 Management of diffi cult airways. If diffi culty is suspected, ensure senior hel p 626 \200 is available and consider \201 bre-optic or awake intubation. An inaccessible or shared airway (eg as in head and neck surgery). \200 Conditions when m uscle paralysis facilitates surgery, eg abdominal surgery. \200\207Paralyzed patients cann ot breathe \200\224and so require ventilation. Muscle relaxation increases the ease of intu bation \200\224the norm is a short- or long-acting muscle relaxant, as appropriate: Short-a cting: Suxamethonium, typically 1 \200\2231.5mg/kg IV. Use if risk of vomiting \200\200 or when diffi culty with in- tubation is anticipated. Long-acting: Many are available, eg roc uronium/ve- curonium (see p622), but they take longer to provide suitable conditions for in tubation. Rocuronium provides suitable intubating conditions in 60 \200\22390s, but vecuron ium may take >2min. Rapid sequence induction (RSI) Used where the risk of aspiration is hig h. \200 Pre-oxygenate with 100% O2 for 3min to provide an O2 reservoir in the lungs a i s e h t s e a n A for use during the period of induced apnoea. Sellick \200\231s maneuver on induction: \201 rm backward pressure (aim for force of 10N \211\210 1kg) on cricoid cartilage occluding esophagus may stop gastric re \202 ux to the larynx. 36,37 \200 Give induction agent (eg propofol) then immediately give muscle relax ant (eg suxamethonium). 38 Wait 60sec for muscle relaxant to work. The trachea is then intu bated, and the cuff of the ET tube in \202 ated. RSI: a quick overview \200 NGT and IV access \200 Pre-oxygenate \200 IV induction \200 Fast muscle relaxant \200 Cricoid pressure \200 ET intubation. Once the ET tube is positioned and cuff in \202 ated, cri- coid pressure may be released, and a volatile agent added to maintain anesthesia. Give a longer-acting muscle relaxant (ie non-depo- larizing) when suxamethonium wears off . Maintaining anesthesia (see BOX \200\230Gauging depth of anesthesia \200\231, p631) 1 Volatile agent added to N2O/O2 mixture as before. Either spontaneously breathing or venti lation, with or without opiates. If the patient is venti- lated, muscle relaxants are gener ally used. 2 IV infusion anesthesia, eg propofol opiates. Maintenance dose, p620. 3 High-dose opiat es with mechanical ventilation. \200\207NB: There is a consider- able risk of awareness wi th this, and it is only used in exceptional circum- stances. Whatever the technique, the dose and concentration of each drug is adjusted according to th e level of anesthesia achieved vs the desired level (determined by monitoring vital signs \200\224eg HR, BP, signs of sympathetic stimulation, p631). End of anesthesia Change inspir ed gasses to 100% oxygen only, then: \200 Discontinue any infusions of anesthetic drugs. \200 After ascertaining that some spontaneous reversal has occurred (use a peripheral ner ve stimulator), reverse any residual muscle paralysis with ne- ostigmine ( 2.5mg in adults) + an anticholinergic to prevent muscarinic side eff ects ( \200\201HR, salivation), eg atr opine/glycopyrronium. \200 Once spontaneously breathing, inspect mouth and oropharynx und er direct vision. Remove ET tube then administer oxygen by facemask. If no problems, transfer to recovery, but be prepared to reassess at any time. 627 Intubation technique Preparation is the key. Assess the neck pre-op. Pre- diction of diffi cult intubation may be possible with assessment of the Mallampati classi \201 cation (how much of the soft palate is obscured on looking into the open mouth), thyromental and sterno mental dis- tances. 39 Know your PLAN A (e.g tracheal tube); PLAN B (ILMA/LMA \200\224both below); PLAN C (bag-mask ventilation/wake pt if able) and PLAN D (needle/surgical crycothyr oidectomy) before you start. 40 ET tube sizes: (mm internal diameter, ID): Diffi cult intubation: \200 Obese \200 Short neck \200 Receding chin/mandible \200 Protruding teeth. Adult ID: \200 = 8.5mm, \200 = 7.5mm Children ID = [age in years/4] + 4.0mm Neonate ID = 3 \200\2233.5mm Length (oral) = [age of child/2] + 12.5cm Length (nasal) = [age of child/ 2] + 14.5cm a i s e h t s e a n A NB: Broselow tape-measures are said to be more accurate. Lubricate the tube, and check that its cuff and the laryngoscope work. \200 Position the patient with neck \202 exed and head extended using a pillow ( \200\230sniffi ng the morning air \200\231). Hold the laryngoscope in the left hand; open the mouth with the right. \200 Slide the lar yngoscope blade down the right side of the tongue into the val- lecula (area between tongue and epiglottis), guarding the lip and teeth with the \201 ngers of your right hand. \200 Lift the laryngoscope blade upwards and away from yourself. \200\207Do not le- ver o n the teeth or you may damage them. Lift the epiglottis from view: the cords should become visible. When they are, insert the tube with your right hand (anatomy \200\224p 567). Once the cuff of the ET tube is beyond the cords, remove the laryngoscope; ask the assistant to in \202 ate the cuff to prevent air leak. Attach to the circuit. Gently in \202 ate lungs. Watch the chest move. Do both sides move equally? Is the abdomen moving and not the chest? Auscultate both sides of chest. Is air entry equal? Fix the tube with a tie. \200 Con \201 rm correct placement with capnography (detects CO2, p628). \200\207Remember: if in do ubt, take it out. It is safer to re-intubate than to risk leaving a tube in the esophagus. Tubes may slip down a main bronchus (usu- ally right). If so, withdraw until both sides of the chest move equally and air entry is equal (so avoiding collapse in the unventilated lun g, or pneumo- thorax on the overventilated side). If you are having problems intubating: \200\207Adequate oxygenation is top priority: \200 Get senior help \200 Employ the loca l or national failed intubation guidelines \200 Do not repeat the dose of suxam- ethonium : allow the relaxant to wear off whilst maintaining oxygenation \200 Consider a LMA (belo w). Laryngeal mask airway (LMA) is used in 50% of elective UK surgery, and in cardiac arres ts where a skilled intubator is not present. It consists of a tube with a cuff designed to sit over the larynx. A cuff takes 30mL of air (depends on size). It is more effi cient tha n masks. Advantages are that no laryngoscope is needed (no damage to teeth or cord stimulat ion), and ease of insertion. Lubri- cate the cuff , and slide over the palate so the device sits over the larynx. Learn the method on a mannequin; practice with an anesthetist. It is available in a range of sizes from 1.0 to 5.0. It is safe and eff ective. 41 Specialized L MAs can as- sist with diffi cult intubation (eg an Intubating Laryngeal Mask Airway, ILMA), 42 and may allow air and \202 uid to be aspirated from the stomach (eg Proseal ). 43 If unable to intubate? Employ failed intubation guidelines. 40 Monitoring during anesthesia AAGBI (17) The continuous presence of the anesthetist is by fa r the most important monitor. Clinical monitoring of the patient supplemented by (not subst ituted by) a range of monitors of the patient and the anesthetic delivery apparatus is mand atory. The process begins prior to induction of anesthesia and contin- ues throughout. \200\207A warm, pink, and well-perfused patient is the aim. Sweat- ing and lacrimation inva riably indicate something is wrong: Respiration: Rate, depth. BP: Intra-arterial in long/tr icky cases (also allows ABG analysis). T : Particularly important in infants, as the large surface area to body mass may lead to hypothermia. A warm environment, warming blankets, a nd warm IV \202 uids, are important in long cases. Pulse oximetry: Computes HR and arteri al O2 saturation. ECG: Reveals rate, arrhythmias, and ischaemia. CVP: Helps diff er- entiat e hypovolaemia from \200\201cardiac function. Insert when large blood loss is anticipated, or in unstable patients. Capnography is essential: a low end-tidal CO2 warns of a displace d ET tube, emboli, and more. Inspired oxygen concen- tration and end-tidal volatile agent c oncentration should also be monitored. Also monitor urine output, neuromuscular status, and ventilator pressures. Alarms should be set to appropriate levels prior to the case. 628 \200 a i s e h t s e a n A Some complications of anesthesia \200\207The commonest respiratory complication is airway obstruction from loss of muscle tone in the soft palate ( \200\230swallowing the tongue \200\231). \200 Anaphylaxis See p237 and OHCM p780. \200 Aspiration See p624. Atelectasis and pneumonia Atelectasis is best seen on CT (not CXR). It starts within minutes of induct ion, and is partly caused by using 100% O2. \201\227: Good pain relief aids coughing. Arra nge physiotherapy + antibiotics (OHCM p161). Awareness This is most distressing for patient s. Paralysis makes its diagnosis diffi cult; the BIS monitor (p631) may \200\201incidence. Prevalence: Much less than 1% even in emergency/obstetric anesthesia (here doses are minim ized, to avoid shock). It is still rarer in other contexts (eg 0.2%). See p631 for assessme nt. Bronchospasm If intubated, check tube position (carina stimulation may be the cause: wi thdraw tube slightly). Check for pneumothorax. Ventilate with 100% O2. Increase concentrati on of volatile agent if he is \200\230light \200\231 \200\224most volatiles (especially se vo \202 urane) are good bronchodilators. Salbutamol aminophylline 250mg IV. MgSO4 2g IV may help Give hydrocortisone 100mg IV. \200 Laryngospasm The cords are \201 rmly shut. Treat with 100% oxygen. Deepen anesthesia \200\224attempt to ventilate. It may be necessary to paralyze and intubate. \200 Malignant hyperthermia: Rare, autosomal dominant, life-thr eatening con- dition triggered by exposure to suxamethonium or volatile anesthetics. Sus- p ect when there is unexpected \200\200oxygen consumption, hypercapnia and tachy- cardia. Ra pid temperature rise (>2oC/h) may be a late sign. Treatment: Stop trigger agents (install a clean breathing circuit); \200 Get help. Hyperventilate with 100% O2; maintain anesthesi a with IV agent (eg propofol); abandon surgery; muscle relaxant with non-depolarizing muscl e relaxant. Give dantrolene 2.5mg/ kg IV as initial bolus, then 1mg/kg as needed to a maxim um of 10mg/kg. Check for and treat hyperkalaemia, arrhythmias; acidosis; myoglobinaemia (ma nnitol/ furosemide/sodium bicarbonate/renal replacement therapy); coagulopathy; raised crea tinine kinase. Take to ICU; counsel family, refer for follow up. 44 Suxamethonium apnoea Ab normal cholinesterase leads to prolonged re- ceptor inactivity. Ventilate until relaxant ef f ect has worn off . Shivering hypothermia May be treated by radiant heat/warming blanke ts. Shivering can be treated with clonidine, pethidine, tramadol or nefopam4 0.2. Be aware that shivering increases O2 consumption 5-fold. 629 Autonomic learning \200 Dilation (mydriasis) Sympathetic Parasympathetic Constriction (meiosis) Eye III Tear gland Superior cervical ganglion VII Increased secretions Decreased secretions IX Airways Vagus (X) T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3 S4 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3 S4 Increased rate and contrachility a i s e h t s e a n A Heart Decreased rate and contractility Vasomotor sudomotor piloerection Skin Liver Pro-expenditure Spleen Stomach Reduced mobility Pancreas Renin release Kidney Duodenum Adrenal Catechol- amine release Pro-storage and increased motility Ilium Colon Relaxes Contracts Sphincter relaxation Rectum Ureter Sphincter and detrusor contraction Ejaculation Uterine relaxation Erection Female Male Bladder Fig 1. The autonomic nervous system may be primitive, but it is anything but simple. Many o f the drugs used in anesthesia (eg atropine, \200 -blockers) have an eff ect on this syste m, and at more than one place at once. This means that it is useful to remind your- self of exactly where each arm of the autonomic nervous system spreads its tendrils, and how it me diates eff ects: Sympathetic Site Pre-ganglionic Neurotransmitter Receptor type All Adrenal gland1 Sweat glands All other ACh NAChR ACh NAChR Post-ganglionic ACh2 MAChR2 NA NAR Parasympathetic Site Pre-ganglionic Post-ganglionic Key: ACh = acetylcholine, NAChR = nicot inic acetylcholine receptor, MAChR = muscarinic acetylcholine receptor; NA = noradrenaline; NAR = noradrenaline receptor 1 The sympathetic \201 bres that innervate the adrenal glan d are pre-ganglionic 2 This is the main oddity: sweat glands have MAChRS in the sympathetic system NB: there are a number of other (co-)transmitters in the autonomic system (such as ATP to adeno- sine receptors). The gut also has a large independent neuronal network. If on ly we could let our minds learn with the same autonomy that it has to control the function of individual organs and homeostasis. Perhaps it is best that we are able to switch off our higher functions from time to time, leav- ing the autonomic nervous system to its usual bu siness! Neurotransmitter Receptor type All All ACh NAChR ACh MAChR Sedation De \201 nition Sedation is a range of depressed conscious levels from relief of a nxiety (minimal sedation) to general anesthesia (see BOX). 630 \200 Doctors in many specialties may be required to administer sedation. \200\207The doctor giv ing moderate or deeper sedation must not also be responsible for performing any procedure ( such as manipulation of a dislocated joint). Her sole responsibility is to ensure that the sedation is adequate, and to monitor the patient \200\231s airway, breathing, and circulati on. Sedation is not a short cut to avoid formal anesthesia, and it does not excuse the pati ent from an appro- priate work-up or reasonable fasting ( \200\207risking aspiration of gas tric contents, p624). Monitoring is mandatory, and must include at least pulse oximetry, HR and BP. 45 It is easy for sedation to become general anesthesia, with its at- tendant risk s (see p628). The loss of the \200\230eyelash re \202 ex \200\231 (gentle stroking of the upper eyelashes to produce blinking) is a good guide to the onset of general anesthesia. In the elderly, \200\201cognition after GA may persist for months; 46 regional anaes- thes ia may decrease it, 47 it is unclear if sedation can obviate it \200\224although it seems r eduction in duration of anesthesia may limit risk. 48 Agents \200 Midazolam: Initial adul t dose 2mg IV over 1min (1mg if elderly). Further 0.5 \200\2231mg IV as needed after 2min. Usual range 3.5 \200\2237.5mg (elderly max 3.5mg). SE: psychomotor function \200\201. 49 \200 Propofol: Widely used for sedation, see p620. Rapid acting anesthetic \200\224but may lead to hypotension and apnoea. In many circumstances (eg manipula- tion of large joint; p ainful dressing changes) a narcotic analgesic may be used too (eg morphine in 1 \200\2232mg aliquots IV, or shorter-acting opioids such as fentanyl) as propofol doesn t have analgesi c properties. a i s e h t s e a n A Ketamine may be administered. This is a dissociative anesthetic agent which can be used as an induction agent (1.5 \200\2232mg/kg), or for procedural se- dation ( 1mg/kg). It produce s deep analgesia with super \201 cial sleep without loss of airway re \202 exes or hypote nsion. Side-eff ects include nausea, vomiting, emergency delirium and hallucinations. Ketam ine and propofol can be com- bined in a single syringe to produce a sedative agent with les s hypotensive eff ects than propofol alone, and less nausea/emergence problems than keta- m ine. 50,51 This is sometimes referred to as a ketofol sedation. \200\207Remember the need for oxygen and equipment to support ventilation as well as appropriate monitoring when unde rtaking any form of sedation. Recovery from anesthesia \200 Oxygen supplementation via facemask: as much and for as lon g as necessary to counteract hypoxia due to diff usion hypoxia, respiratory depression, or ventilation/perfusion mismatch.1 Monitor pulse and BP; keep the patient warm. \200 Look for hypoventilation (?inadequate r eversal \200\224check with nerve stimula- tor; narcosis \200\224reverse opiates with naloxo ne \200\224cautiously to minimize pain; check for airway obstruction). Ensure adequate anal gesia. Return the patient to the ward when you are satis \201 ed with his cardiovascu- lar and respiratory status and pain relief. Give clear instructions on post-operative \202 uid regimens, blood transfusions, oxygen therapy, pain relief, and physiotherapy. Post-operative nausea and vomiting (PONV, p617) is partly preventable by a 5-HT3 receptor a ntagonist, eg granisetron or dexamethasone. 52 Metoclopra- mide is less eff ective. 53,54 1 For a short duration (<5min) while very soluble nitrous oxide is diff using out of the ci rculation into the alveoli, the concentration of O2 in alveolar gas will be falling (diff u sion hypoxia).55 631 Level of sedation Minimal sedation (anxiolysis): is a drug-induced state where the patient is still able to r espond to speech. Cognitive function and coordination are impaired but airway, breathing an d cardiovascular systems are unaff ected. Moderate sedation (conscious sedation): is drug-i nduced reduction of consciousness during which the patient is able to make a purposeful re- sponse to voice or light touch. Response to pain only indicates deeper seda- tion. At this level of sedation no airway adjuncts are required, breathing and cardiovascular function s hould be adequate. Deep sedation: drug-induced reduction in consciousness to a point where the patient cannot be easily roused but does respond purposefully to pain- ful stimuli (wit hdrawal is not purposeful). At this level airway intervention may be required (jaw thrust/ chin lift). Spontaneous ventilation may become inadequate. General anesthesia: drug-induced loss of consciousness during which patients are not able to be roused, even with repeated painful stimulation. Airway typically requires intervention, spontaneous ventilation is fre quently inadequate and cardiovascular function may be impaired. a i s e h t s e a n A