Regarding pretreatment agents given prior to RSI, which ONE of the following statements is TRUE?
Answer: A: Laryngoscopy and intubation stimulate reflex responses to protect the airway, such as gagging and coughing. Other reflex responses include sympathetic stimulation in adults that can cause significant increases in heart rate, blood pressure and intracranial pressure and parasympathetically mediated bronchospasm. Parasympathetic stimulation usually dominates in young children and can cause profound bradycardia. Pretreatment agents are commonly used prior to rapid sequence intubation in an attempt to attenuate these adverse physiological responses. Lignocaine has been recommended in patients with raised intracranial pressure (ICP) and bronchospasm due to its potential ability to reduce bronchospasm and blunt increases in intracranial pressure. However, there is no high-quality evidence to demonstrate its effectiveness. Additionally, there are also no studies to demonstrate that pretreatment with lignocaine improves outcome in patients undergoing RSI.
Pretreatment with atropine does not consistently prevent bradycardia in children and is now only recommended for symptomatic bradycardia and not as a routine agent. Some practitioners still prefer to use it, especially in infants, as they are more likely to develop bradycardia. Traditionally, preadministration of a defasciculating dose (one tenth of a non-depolarising muscle relaxant) has been recommended to prevent fasciculations and muscle pains associated with suxamethonium. However, there is no evidence to support its use, and pretreatment with a non-depolarising agent is no longer recommended.
Fentanyl is an ultra short-acting opioid that may be used in patients with elevated ICP or cardiovascular disease that may be exacerbated by sudden elevations in blood pressure. Adverse reaction such as chest wall rigidity and respiratory depression are minimised when fentanyl is given over 30–60 seconds. Chest rigidity and the subsequent inability to ventilate a patient is an uncommon adverse effect of fentanyl, and is generally associated with administration of large doses and if fentanyl is given rapidly. The exact mechanism by which fentanyl induces muscle rigidity is still unknown. Suxamethonium and naloxone, an opiod recepter antagonist, might be useful in reversing chest rigidity.
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Regarding the use of propofol as an induction agent during RSI, which ONE of the following is TRUE?
Answer: D: Propofol is presented as a white emulsion of soya bean oil and egg lecithin and should be avoided in patients with allergies to egg or soya. Saying that, most egg allergies involve a reaction to egg white (egg albumin), whereas egg lecithin is extracted from egg yolk. Hypotension is due to myocardial suppression and vasodilatation. Propofol does not cause histamine release. Hypotension is more pronounced in the elderly and patients with hypovolaemia. One of propofol’s advantages is its antiemetic property. Propofol formulations can support the growth of bacteria, so good sterile technique must be used in preparation and handling. Administration should be completed within 6 hours of opening the ampule.
Regarding the use of suxamethonium as a paralytic agent in RSI, which ONE of the following is TRUE?
Answer: C: Suxamethonium is the paralytic agent of choice for RSI in the ED due to its rapid onset (45–60 seconds) and short duration of action (3–5 minutes). It is not without any side effects and may be contraindicated in certain populations in the ED, especially those patients at risk of a life-threatening hyperkalaemic response. A clinically significant hyperkalaemic response can occur ≥5 days after a burn, denervation or crush injury due to acetylcholine receptor upregulation at the neuromuscular junction with resultant exaggerated hyperkalaemic response. Similarly, patients with pre-existing myopathies, myasthenia gravis and pre-existing hyperkalaemia are also at risk and suxamethonium should be avoided in this population.
Fasciculations and muscle pains are common and the use of 1.5 mg/kg of suxamethonium is associated with less fasciculation and myalgia than occur with 1 mg/kg. A dose of 1.5–2 mg/kg is now recommended in adults as it provides excellent intubation conditions and do not increase the risk to the patient, whereas inadequate doses can leave the patient inadequately paralysed and difficult to intubate. Neonates and infants require a slightly higher dose of suxamethonium (2 mg/kg intravenously) owing to their higher volume of distribution. Muscle fasciculation may contribute to an increase in intracranial pressure but this is not clinically significant. The benefit associated with optimal intubation conditions far exceeds this theoretical risk.
Suxamethonium can be negative chronotropic with resultant bradycardia following administration, especially in children. This may be due to direct cardiac muscarinic stimulation as well as stimulation of autonomic ganglia by suxamethonium. It is, however, difficult to separate the effects of suxamethonium on the heart from the effects induced by the autonomic responses to laryngoscopy and intubation. Sinus bradycardia is treated with atropine, if necessary, but is often self-limiting. Some paediatric practitioners recommend pretreatment with atropine for children younger than 1 year old, but there is no evidence for benefit.
Regarding the use of lignocaine as a local anaesthetic agent, which ONE of the following is TRUE?
Answer: D: Lignocaine is an amide-type anaesthetic agent. When lignocaine is administered by direct infiltration, the onset of action is within seconds and lasts 20–60 minutes. When administered as a nerve block, onset occurs in 4–6 minutes and the effective duration is longer, usually 75 minutes. It may remain effective for up to 120 minutes.
The maximum safe dose of lignocaine without adrenaline is 3 to 5 mg/kg and should not exceed 300 mg at a single injection. More volume can be added safely every 30 minutes if needed. The addition of adrenaline to lignocaine causes vasoconstriction and subsequently less systemic absorption. Not only does the resulting vasoconstriction prolong the anaesthetic effect for 2–6 hours, but it also increases the safe dose to 5–7 mg/kg.
Anaesthetic solutions contain uncharged and charged forms. It is the uncharged form that crosses tissue and nerve barriers. Once the uncharged drug is through a barrier, it re-equilibrates into uncharged and charged forms in a proportion dependent on the prevailing pH. The charged form is responsible for the actual neuronal blockade. The speed of onset of any local anaesthetic agent is directly related to how quickly that agent, after injection, can diffuse through tissues to the nerve and through the nerve membrane. The concentration of the uncharged form is increased in a more alkaline environment (raised pH) and therefore a more rapid onset of action can be expected. An alkaline environment can be achieved by adding 1 mL of sodium bicarbonate 8.4% to 10 mL of lignocaine without compromising the quality of anaesthesia. Not only does the addition of a sodium bicarbonate solution to local anaesthetics shorten the onset of action but it also reduces the pain of injection.
Which ONE of the following is TRUE regarding the use of bupivacaine as a local anaesthetic agent?
Answer: B: Like lignocaine, bupivacaine is an amide-type local anaesthetic agent. The onset of action is slightly slower than that of lignocaine, but the duration of anesthesia is 4–8 times longer.
The reported safe dose of bupivacaine in adults is approximately 1.5 mg/kg without adrenaline and 3 mg/kg with adrenaline. The dose can be repeated every 3 hours, not exceeding a total of more than 400 mg in a 24-hour period. Bupivacaine is not recommended in children younger than 12 years of age.
All local anaesthetics can cause rapid and profound cardiovascular depression. Bupivacaine is a more potent cardiodepressant than lignocaine and has arrythmogenic potential as well. The ratio of the dosage required for irreversible cardiovascular collapse (CC) and the dosage that will produce CNS toxicity (CNS), that is the CC/CNS ratio, is lower for bupivacaine than for lignocaine. Furthermore, cardiac 244 CHAPTER 12 Emergency Anaesthes ia and Pain Mana gement resuscitation is more difficult after bupivacaineinduced cardiovascular collapse, and acidosis and hypoxia markedly potentiate the cardiotoxicity.
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