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17. Local Anaesthetics (R Verbeek) Part I Anaesthesia Refresher Course – 2018 17 University of Cape Town Local Anaesthetics Dr Renier Verbeek Private Practice Honorary lecturer- University of Cape Town Cocaine is the only naturally occurring local anaesthetic, found in the Andes, West Indies and Java and was introduced to Europe in the 1800’s. In 1860, cocaine was extracted from the leaves of the Erythroxylon coca bush. Interestingly, Sigmund Freud used cocaine on some of his patients, but became addicted through self-experimenting. Halsted was the first person to use cocaine for nerve blocks, in 1885, but also became addicted through self-experimentation. Procaine was the first synthetic local anaesthetic in 1904. Procaine was only available as a powder and had to be dissolved before injected. It also had a short duration of action. Amethocaine was released in 1930. These agents were esters and, despite a risk of allergic reactions, were widely used. During the 1940’s one third of all surgeries (in Sweden) were performed under local and regional anaesthesia, with toxicity posing a major risk when well perfused tissues were injected. Surgeons had to be vigilant for spasms and convulsions (that were treated with barbiturates). Lignocaine was synthesized in Stockholm by Nils Löfgren in 1943, he gave the compound to his self-experimenting assistant, Bengt Lundqvist, to try. It was used during the latter stages of the Second World War. Lignocaine is an amide and had a low risk of allergic reactions. This was followed by mepivacaine (1957), prilocaine (1960), bupivacaine (1963), ropivacaine(1997) and levobupivacaine (2000). Physiology Neurones have a resting potential value of approximately -70 mV. The resting potential is determined by the concentrations of the ions on both sides of the cell membrane and the ion transport proteins. Sodium influx is necessary for the depolarization of nerve cell membranes and propagation of impulses. The axons of neurones are wrapped by myelin and separated in segments, these intervals are known as nodes of Ranvier. It is produced by Schwann cells exclusively in the peripheral nervous system, and by oligodendrocytes exclusively in the central nervous system. The myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node. Local Anaesthetics Dr R Verbeek Formulation Local anaesthetics are formulated as the hydrochloride salt to render them water soluble. Multidose vials often contain preservatives, but carry the risk of producing arachnoiditis when injected in the spine. Single-dose ampoules without additives (apart from glucose at 80 mg/ml used in ‘heavy’ bupivacaine) are suitable for subarachnoid administration. Most local anaesthetics are racemic mixtures except levobupivacaine and ropivacaine, where the s- enantiomer is used, which is less toxic, more potent and longer acting. Liposomal Bupivacaine (Exparel) is a longer acting form of Bupivacaine, where the bupivacaine is delivered via a multivesicular liposomal system. Mechanism Local anaesthetic action is dependent on intracellular blockade of the voltage gated Na+ channels. Unionised lipid-soluble drug passes through the phospholipid membrane where it is ionised. In its ionised form it binds to the Na+ channel, preventing it from leaving the inactive state. The degree of blockade in vitro is proportional to the frequency of depolarization, local anaesthetic bind to ‘open’ Na+ rather than inactivated channels. ‘Membrane expansion’ offers an additional mechanism of action. Unionised drug dissolves into the phospholipid membrane and may cause swelling of the Na+ channel/lipoprotein matrix, resulting in its inactivation. Local anaesthetics are weak bases and exist predominantly in the ionised form at physiological pH, as their pKa exceeds 7.4. They fall into one of two chemical groupings, amino esters or amino amides, which describes the linkage between the aromatic lipophilic group and the hydrophilic group Ester = Hydroxyl group (-OH) replaced by an alkyl (-O) group) Esters Amide = Hydroxyl group (-OH) replaced by an amine group or ammonia Amides All local anaesthetic agents are weak bases, they exist in two forms: ionised (BH+) and unionised (B). The pKa of local anaesthetics determines the pH at which both forms exist in equal amounts. As the pH of tissues differs from the pKa of specific drugs, more of the drug exists in either the ionised or unionised form. This is expressed in the Henderson-Hasselbalch equation: pKa – pH = log [BH+] / [B] where [B] is the concentration of unionised and [BH+] the concentration of ionised drug. Lignocaine has a pKa of 7.9, a high fraction is present in the unionised form and, therefore, has a fast onset of action. Bupivacaine, with a higher pKa of 8.1, has a greater fraction present in the ionised form, which is unable to penetrate the phospholipid membrane, resulting in a slower onset of action. 17 - 2 Local Anaesthetics Dr R Verbeek (*Any local anaesthetic containing 2 i’s is an amide) Potency Potency is correlated to lipid solubility in vitro, but less so in vivo. Factors such as vasodilator properties and tissue perfusion, determine the amount of local anaesthetic that is available at the nerve. The duration of action is determined by its protein binding. Local anaesthetics with limited protein binding have a short duration of action and those with more extensive protein binding have a longer duration of action. The intrinsic vasodilator activity varies between drugs and influences potency and duration of action. Vasodilatation occurs via direct relaxation of arteriolar smooth muscle fibres. In general, local anaesthetics cause vasodilatation at low concentration (prilocaine>lignocaine>bupivacaine>ropivacaine) and vasoconstriction at higher concentrations. Cocaine has vasoconstrictor actions by inhibiting neuronal uptake of catecholamines (uptake 1) and inhibiting monoamine oxidase (MAO). Local anaesthetics are generally ineffective when used in inflamed tissue, due to a more acidic environment. The acidic environment reduces the unionised fraction of drug available to diffuse into and block the nerve. There may also be increased local vascularity, which increases removal of drug from the site. Pharmacokinetics Absorption The absorption of local anaesthetics into the systemic circulation varies depending on the site of injection. This will be influenced by the characteristics of the agent used and presence of added vasoconstrictor. If local anaesthetic is injected intravascular, very high systemic levels will result and potentially cause central nervous system or cardiovascular toxicity. Distribution The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. Ester local anaesthetics are minimally bound, while amides are more extensively bound in the 17 - 3 Local Anaesthetics Dr R Verbeek plasma. Alpha–acid glycoprotein binds local anaesthetic with high affinity, although albumin binds a greater quantity due to its relative abundance. When protein binding is decreased, the free fraction of drug is increased. The degree of protein binding will affect the amount of placental transfer. Bupivacaine is more highly bound than lidocaine, so less crosses the placenta. If the foetus becomes acidotic, there will be an increase in the ionised fraction and local anaesthetic will accumulate in the foetus (ion trapping). Ester local anaesthetics do not cross the placenta in significant amounts due to their rapid metabolism. Metabolism and excretion Amides are metabolised hepatically by amidases. Amidase metabolism is much slower than plasma hydrolysis and so amides are more prone to accumulation when administered by continuous infusion. Reduced hepatic blood flow or hepatic dysfunction can decrease amide metabolism. Esters (except cocaine) are metabolized by pseudocholinesterases to inactive compounds and have a short half-life. Para-aminobenzoate is one of the main metabolites and has been associated with hypersensitivity reactions. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal. Local anaesthetic toxicity Local anaesthetics may be toxic if sufficient amounts are absorbed into the systemic circulation. Bupivacaine appears to be the most dangerous, although all can be harmful. The incidence of Local Anaesthetic Systemic Toxicity (LAST) has decreased significantly in the last 30 years due to increased awareness of toxicity. Central Nervous System Local anaesthetics penetrate the CNS rapidly and have a bi-phasic effect. Inhibitory interneurons are blocked first with initial excitatory phenomena, resulting in circumoral tingling, visual disturbance, tremors and dizziness. This is followed by convulsions. Finally, all central neurones are depressed, leading to apnoea and coma. Cardiac Local anaesthetic drugs block cardiac Na+ channels and decrease the maximum rate of increase of phase 0 of the cardiac action potential. They also have direct myocardial depressant properties. Lignocaine is used as an antiarrhythmic to treat ventricular arrhythmias. Bupivacaine has a prolonged binding to Na channels and therefore may lead to re-entrant arrhythmias and ventricular fibrillation. In addition, tachycardia may enhance frequency-dependent blockade by bupivacaine, which adds to its cardiac toxicity. Ca++ and K+ channels are also affected. (*CNS toxic signs and symptoms occur at a lower serum levels than cardiac toxic levels and give a degree of advance warning as
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