Veterinary · Para-clinical · also MSVE VPT-321
Drugs acting on the central nervous system: sedatives, tranquillisers, alpha-2 agonists, general and local anaesthetics, opioids, anticonvulsants and muscle relaxants.
In the exams: ICAR AICE-JRF core group 07; ICAR AIEEA-PG 13 (Pharmacology & Toxicology); BCSE anaesthesia 20-23 items
Veterinary neuropharmacology is the study of drugs that act on the central and peripheral nervous system: sedatives and tranquillisers, alpha-2 adrenergic agonists, injectable and inhalant general anaesthetics, local anaesthetics, opioid and other analgesics, anticonvulsants and muscle relaxants, with the principles that tie them together and the drugs used to end life humanely. It is the pharmacology behind every sedation, anaesthetic, nerve block and seizure emergency a veterinarian manages.
The drugs are powerful and their margins narrow. Most drug-related harm in anaesthesia comes from known species differences and simple errors: the equine concentration of xylazine given to a cow, a tenfold infusion mistake, bromide started in a cat. This manual is written to prevent those errors by explaining mechanism first, then the effects that follow from it, then species differences.
Worldwide, the subject is taught in the second and third years of veterinary degrees (in India as VPT-321 under the Minimum Standards of Veterinary Education) and overlaps with anaesthesia in surgery courses. It is examined in Indian postgraduate and PhD entrance papers, in state veterinary officer recruitment, and in licensing examinations such as the NAVLE and BCSE in North America, the RCVS Statutory Membership Examination, the Australasian Veterinary Examination, and national licensing examinations in the Philippines, Nepal and China. Recall questions test mechanisms, antagonists and adverse effects; clinical questions test drug choice for a species and a patient; numerical questions test dose volumes, infusion rates and MAC reasoning.
Doses: only one standard textbook dose is given, and it is labelled. Authorised drugs, doses, controlled drug schedules and food-animal withdrawal periods differ by country and product, so every dose must be checked against the product label and your national formulary.
Almost every drug in this subject works by making inhibition in the central nervous system (CNS) stronger or excitation weaker. The main inhibitory transmitter in the brain is gamma-aminobutyric acid (GABA). Its GABA-A receptor is a ligand-gated chloride channel: when it opens, chloride enters, the neurone hyperpolarises and is less likely to fire. Benzodiazepines, barbiturates, propofol, alfaxalone and etomidate all act at GABA-A, but at different sites. Benzodiazepines increase how often the channel opens when GABA is present; barbiturates increase how long it stays open and, at high concentration, open it directly. That difference is why barbiturates can kill by overdose and benzodiazepines alone rarely do. In the spinal cord the main inhibitory transmitter is glycine; strychnine blocks glycine receptors, which is why strychnine poisoning causes extensor rigidity and convulsions on stimulation.
The main excitatory transmitter is glutamate. Its N-methyl-D-aspartate (NMDA) receptor is an ion channel blocked by magnesium at rest; ketamine and tiletamine block it from inside the channel. NMDA activity in the dorsal horn of the spinal cord drives central sensitisation ('wind-up'), the amplification of pain after tissue injury, so NMDA antagonists are useful analgesic adjuncts even at doses that do not anaesthetise.
The monoamines matter too. Dopamine D2 receptor blockade explains the calming and antiemetic effects of phenothiazines and butyrophenones. Noradrenaline released from the locus coeruleus maintains arousal; alpha-2 adrenergic agonists switch it off. Serotonin (5-HT) pathways modulate mood and descending pain inhibition, which is why tramadol, which also blocks serotonin and noradrenaline reuptake, has effects beyond its opioid metabolite. Endogenous opioid peptides (endorphins, enkephalins, dynorphins) act at mu, kappa and delta receptors, which are G-protein-coupled receptors that close calcium channels and open potassium channels, reducing transmitter release and neuronal firing.
The blood-brain barrier is formed by capillary endothelial cells joined by tight junctions. Small, lipid-soluble, un-ionised molecules cross it readily; ionised and protein-bound fractions cross poorly. That is why lipid-soluble induction agents act within one arm-brain circulation time and why quaternary ammonium compounds such as glycopyrrolate and neostigmine have little central action. P-glycoprotein, the efflux pump coded by the ABCB1 (MDR1) gene, pumps many drugs back out of the brain. Dogs of herding breeds that carry the ABCB1 deletion lack a working pump and show exaggerated CNS depression with some drugs, including acepromazine and butorphanol, as well as the better-known ivermectin toxicity.
The duration of a single intravenous dose of a highly lipid-soluble drug is usually set not by metabolism but by redistribution: the drug moves from brain (high blood flow) into muscle and then fat, so the patient wakes while most of the dose is still in the body. Repeated doses or infusions fill these peripheral stores and recovery then depends on elimination, which is the basis of the 'context-sensitive half-time' of infusions.
CNS depressants can be arranged on a continuum. With increasing dose a drug may give anxiolysis, sedation (drowsiness, still rousable), hypnosis (sleep), general anaesthesia (unconsciousness with loss of response to painful stimuli), and finally medullary depression and death. Tranquillisers (such as the phenothiazines) calm without producing sleep even at high doses and cannot produce anaesthesia on their own; hypnotics and general anaesthetics can. Neuroleptanalgesia is the combination of a tranquilliser with an opioid.
General anaesthesia is a reversible, drug-induced loss of consciousness in which the patient neither perceives nor recalls noxious stimulation. Its components are unconsciousness, analgesia (strictly, antinociception), muscle relaxation and suppression of harmful autonomic reflexes. No single drug gives all four ideally, which is the logic of balanced anaesthesia.
The classical stages were described for ether in unpremedicated people (Guedel) and are still taught. Stage I is from the start of administration to loss of consciousness. Stage II is involuntary excitement: struggling, breath-holding, vocalising and irregular breathing; it is dangerous and a good induction passes through it quickly. Stage III is surgical anaesthesia, divided into planes of increasing depth, with progressive loss of reflexes and of intercostal muscle activity. Stage IV is medullary paralysis: respiratory arrest followed by circulatory collapse.
In practice depth is judged from several signs together. In dogs and cats at a surgical plane with inhalants, the eyeball rotates ventromedially, the palpebral reflex is weak or absent, jaw tone is relaxed and heart rate and breathing do not rise with surgical stimulation. When the eye returns to a central position with a dilated pupil and absent reflexes the patient is dangerously deep. Horses keep a palpebral reflex and can show slow nystagmus at a light plane. Ketamine is the exception to eye rules: the eyes stay central and open, and palpebral and corneal reflexes persist even at adequate depth. No one reflex is reliable across species and drugs, which is why monitoring blood pressure, end-tidal carbon dioxide and pulse oximetry is standard.
Anticholinergics block muscarinic receptors. Atropine is a tertiary amine that crosses the blood-brain barrier and placenta; glycopyrrolate is quaternary, crosses neither to a useful degree, lasts longer and causes less tachycardia. They are used to treat bradycardia of vagal origin, for example during ocular surgery (oculocardiac reflex) or after opioids, and to reduce salivary and bronchial secretion. Routine use is no longer taught for every patient, because tachycardia raises myocardial oxygen demand. In ruminants anticholinergics do not stop salivation but make saliva more viscous and harder to clear, and they can reduce gut motility. In horses they can cause ileus and colic, so they are used only for a specific indication. Some rabbits have serum atropinesterase, so atropine may be short-acting in them and glycopyrrolate is preferred.
Sympathomimetics support circulation under anaesthesia. Dobutamine is a mainly beta-1 agonist used as an infusion to raise cardiac output and arterial pressure in anaesthetised horses. Adrenaline is the vasopressor of cardiopulmonary resuscitation. Doxapram stimulates breathing through carotid body chemoreceptors and the medulla; its effect is short, it raises oxygen consumption, and ventilatory support is better where available, but it is still used, for example, in some neonatal resuscitation protocols.
Acepromazine is the phenothiazine used most in veterinary practice; chlorpromazine and promazine are older relatives. Phenothiazines block dopamine D2 receptors, which gives calming and an antiemetic effect at the chemoreceptor trigger zone, and they also block alpha-1 adrenergic, histamine H1 and muscarinic receptors. Alpha-1 blockade causes vasodilation and dose-dependent hypotension; this is the most important clinical adverse effect, so acepromazine is avoided in hypovolaemic, shocked or severely dehydrated patients. It also lowers packed cell volume, because the spleen relaxes and stores red cells, which matters in anaemic patients and when interpreting a blood sample taken after sedation. Phenothiazines cause hypothermia by vasodilation and by resetting thermoregulation.
The effect is tranquillisation, not hypnosis and not analgesia: a tranquillised animal can still be roused and can still bite or kick when stimulated. Increasing the dose lengthens the effect more than it deepens it. There is no specific antagonist. Acepromazine reduces the dose of induction and maintenance agents needed and smooths recovery. It has anti-arrhythmic action against catecholamine-induced arrhythmias.
Species and breed points are examined often. In male horses, especially stallions, phenothiazines can cause penile prolapse and, rarely, persistent priapism with paralysis of the retractor penis muscle, so many clinicians avoid them in breeding stallions. Boxers are said to be prone to vasovagal collapse, and ABCB1-deficient dogs have prolonged and deeper sedation. The old teaching that acepromazine lowers the seizure threshold and must never be given to epileptic dogs is now questioned by retrospective studies; many texts still advise caution.
Butyrophenones (azaperone, droperidol, haloperidol) are also D2 antagonists. Azaperone is authorised in pigs in many countries for sedation and to reduce fighting when pigs are mixed; it causes less hypotension than acepromazine at usual doses.
Diazepam and midazolam are the benzodiazepines used most; zolazepam is used only in a fixed combination with tiletamine. They bind a site on the GABA-A receptor (between alpha and gamma subunits) and increase the frequency of chloride channel opening in the presence of GABA. Effects are anxiolysis, sedation, anticonvulsant action and centrally mediated muscle relaxation, with minimal cardiovascular and respiratory depression. That safety makes them valuable in sick, old and cardiac patients and as co-induction agents that reduce the propofol or alfaxalone dose. They are the first-line drugs for status epilepticus.
In healthy young dogs, cats and horses given a benzodiazepine alone, the result is often not sedation but disinhibition: excitement, ataxia and agitation. They are therefore usually combined with an opioid, ketamine or an alpha-2 agonist. In horses, benzodiazepines cause muscle weakness and ataxia, so they are given after or with a sedative or at induction, not to a standing horse on their own. Benzodiazepines give reliable sedation in small ruminants and in birds and small mammals.
Formulation matters. Diazepam is insoluble in water and is dissolved in propylene glycol, which is painful by intramuscular injection and absorbed unpredictably, and which can cause thrombophlebitis and, rarely, haemolysis and hypotension if given rapidly intravenously. Diazepam also binds to plastic, so it should not be left in plastic syringes or infusion bags for long. Midazolam is water-soluble at acidic pH in the vial and becomes lipid-soluble at body pH, so it is suitable for intramuscular and intranasal use. Oral diazepam in cats has been associated with idiosyncratic acute hepatic necrosis.
Flumazenil is a competitive antagonist at the benzodiazepine site. Its half-life is shorter than that of diazepam, so sedation can return.
Barbiturates at low doses sedate, but their narrow margin means they are now used mainly as anticonvulsants (phenobarbital) and for euthanasia (pentobarbital). Chloral hydrate was historically used in horses and cattle as a sedative-hypnotic; it is converted to trichloroethanol, is very irritant perivascularly, and has been replaced by safer drugs.
Alpha-2 adrenergic agonists are the most powerful sedatives in veterinary use and have their own chapter. Opioids add sedation, especially in dogs, and are combined with tranquillisers or alpha-2 agonists in neuroleptanalgesia.
For situational anxiety and fear before veterinary visits, oral gabapentin (an alpha-2-delta calcium channel ligand) and trazodone (a serotonin antagonist and reuptake inhibitor) are widely used in cats and dogs. Some human oral solutions of gabapentin contain xylitol, which is toxic to dogs, so only suitable formulations should be dispensed. Evidence and authorisation for these uses differ by country; they are part of low-stress handling, not a replacement for it.
Xylazine, detomidine, romifidine, medetomidine and dexmedetomidine stimulate alpha-2 adrenergic receptors. These G-protein-coupled receptors sit before the synapse on noradrenergic neurones, where they reduce noradrenaline release, and on neurones of the locus coeruleus and dorsal horn. The result is sedation, analgesia (spinal and supraspinal) and muscle relaxation, all dose-dependent. Medetomidine is a racemic mixture; dexmedetomidine is its active enantiomer, so it is given at about half the mass dose of medetomidine for the same effect. The drugs differ in alpha-2:alpha-1 selectivity (xylazine is the least selective, medetomidine and dexmedetomidine the most) and in duration (romifidine and detomidine longer than xylazine in horses).
The cardiovascular effects are characteristic and examined everywhere. Stimulation of peripheral vascular alpha-2B receptors causes vasoconstriction and a rise in blood pressure; the baroreceptor reflex then slows the heart, giving marked bradycardia and often second-degree atrioventricular block. Later, central sympatholytic action lowers pressure towards or below baseline. Cardiac output falls substantially. Mucous membranes may look pale or bluish because of vasoconstriction, so pulse oximetry can be unreliable. Giving an anticholinergic to treat the bradycardia is controversial because it raises heart rate against a high afterload and increases cardiac work.
Other effects: reduced insulin release causing transient hyperglycaemia; diuresis (reduced antidiuretic hormone action and hyperglycaemia); vomiting, frequent in cats after xylazine and also seen in dogs; reduced gastrointestinal motility; hypothermia; and, in ruminants, ruminal atony with risk of tympany. Xylazine increases uterine tone and intrauterine pressure in cattle, so it is used cautiously in late pregnancy. In sheep, alpha-2 agonists can cause hypoxaemia through pulmonary interstitial oedema, varying with breed and drug. A sedated horse can still kick accurately when touched on the hindquarters, so sedation is not a guarantee of safety.
Species differ greatly. Ruminants, especially cattle, are much more sensitive to xylazine than horses; cattle need roughly one tenth of the horse dose. Confusing the equine product (commonly 100 mg/mL) with the small-animal product (commonly 20 mg/mL) is a classic, sometimes fatal, error, so the concentration on the vial must be read every time. Pigs are relatively resistant to alpha-2 agonists and are usually sedated with combinations. As one standard textbook value, xylazine in the horse is commonly given at 1.1 mg/kg intravenously for standing sedation — confirm against the product label and your national formulary.
Alpha-2 agonists combine well. With an opioid (butorphanol is the traditional partner in horses) they give deeper sedation and better analgesia; with ketamine they form the basis of short field anaesthesia in horses, cattle, small ruminants, dogs and cats. They reduce the dose of induction agent and the minimum alveolar concentration (MAC) of inhalants markedly. Constant rate infusions of dexmedetomidine, detomidine or romifidine are used during inhalant anaesthesia and for standing surgery.
The effects can be reversed with alpha-2 antagonists. Atipamezole is highly selective and is the usual choice in dogs and cats; in dogs it is given intramuscularly at five times the mass of medetomidine, which works out as the same volume when the products are 1 mg/mL medetomidine and 5 mg/mL atipamezole; for dexmedetomidine (0.5 mg/mL) the mass ratio is ten to one, again an equal volume. Yohimbine and tolazoline are less selective and are used more in ruminants and horses; tolazoline has been associated with adverse effects when overdosed. Reversal also removes the analgesia, so an alternative analgesic must be in place before an animal in pain is reversed.
In food animals, withdrawal periods for alpha-2 agonists and their antagonists vary by country and some uses are off-label; the national formulary rules.
Barbiturates are classified by duration. Thiopental is an ultra-short-acting thiobarbiturate: a single intravenous dose gives anaesthesia for minutes because it redistributes out of the brain. It is strongly alkaline, so perivascular injection causes tissue necrosis and slough; it can cause transient arrhythmias and apnoea, and repeated doses accumulate in fat. Sighthounds (greyhounds and related breeds) recover slowly because they have little body fat and metabolise thiobarbiturates more slowly. Thiopental is no longer available in several countries. Pentobarbital, a short-acting oxybarbiturate, was once the standard laboratory and small-animal anaesthetic but recovery is long and stormy and the margin is narrow; today its main veterinary use is euthanasia. Barbiturates cross the placenta and depress neonates.
Propofol (2,6-diisopropylphenol) acts at GABA-A. It is formulated as a lipid emulsion without, or in some products with, a preservative; preservative-free emulsion supports bacterial growth and must be discarded within the time on the label. Induction is smooth and recovery rapid because clearance is high and partly extrahepatic, including the lungs. The main adverse effects are dose- and rate-dependent apnoea and hypotension from vasodilation and reduced contractility. It provides no analgesia. Cats, which have limited glucuronidation capacity, develop Heinz bodies and slower recovery after propofol on consecutive days. It is used for induction and total intravenous anaesthesia (TIVA) in small animals.
Alfaxalone is a neuroactive steroid that also potentiates GABA-A. It is solubilised in a cyclodextrin, and its cardiovascular depression is modest at induction doses, though apnoea occurs. Because the solution is not irritant, it can be given intramuscularly, which is useful in cats and small exotic species, although the volume is large.
Etomidate, an imidazole, keeps heart rate, contractility and blood pressure almost unchanged, which makes it attractive for dogs with severe cardiac disease. It inhibits adrenal 11-beta-hydroxylase and so suppresses cortisol synthesis for hours after a single dose; its propylene glycol formulation can cause haemolysis and pain. It is given after premedication, since alone it causes myoclonus and retching.
Ketamine and tiletamine are phencyclidine derivatives that block NMDA receptors. They produce dissociative anaesthesia: a cataleptic state in which the eyes stay open, pharyngeal and laryngeal reflexes are partly kept, muscle tone increases and the patient seems disconnected from its surroundings. Somatic analgesia is good. Ketamine stimulates the sympathetic nervous system, raising heart rate and arterial pressure in healthy animals, although it has direct negative inotropic action that shows when catecholamine reserves are exhausted. Breathing may become apneustic (a pause at the end of inspiration). Salivation increases. Because muscle rigidity and occasional convulsions occur, ketamine is almost always combined with a benzodiazepine or an alpha-2 agonist.
Ketamine raises intraocular and intracranial pressure through its haemodynamic effects, so it is used cautiously in patients with penetrating eye injury or head trauma, although this teaching has been softened for ventilated patients. In cats a large part of ketamine is excreted unchanged or as the active metabolite norketamine in urine, so recovery is prolonged in cats with urethral obstruction or renal failure. In horses ketamine given without prior sedation causes excitement and must follow an alpha-2 agonist. At subanaesthetic doses given as an infusion, ketamine is an analgesic adjunct against central sensitisation.
Tiletamine is available only as a fixed 1:1 combination with the benzodiazepine zolazepam. It is used in cats, dogs, wildlife and zoo animals. The two components are cleared at different rates in different species: in dogs zolazepam is cleared first, which can give a rough recovery dominated by tiletamine; in cats tiletamine is cleared first.
No single injectable agent is ideal, so combinations are used. Neuroleptanalgesia combines a tranquilliser or sedative with an opioid; historical fixed combinations have been replaced by flexible mixtures such as acepromazine or dexmedetomidine with methadone or buprenorphine. Premedication with these reduces the induction dose and gives smoother recovery.
For horses in the field, a standard pattern is sedation with an alpha-2 agonist, induction with ketamine, often with a benzodiazepine or guaifenesin for muscle relaxation, and maintenance for a short procedure by top-ups or by an infusion. The traditional 'triple drip' infuses guaifenesin, ketamine and xylazine together to effect; duration should be limited because recovery quality falls and guaifenesin accumulates. Cattle and small ruminants are often anaesthetised with an alpha-2 agonist plus ketamine combination, or with ketamine plus a benzodiazepine, and should be positioned to reduce regurgitation and bloat.
Total intravenous anaesthesia (TIVA) is maintenance entirely by injectable drugs, for example a propofol or alfaxalone infusion with an opioid infusion. It avoids inhalant pollution and is useful where inhalant equipment is absent, during airway procedures and in patients prone to malignant hyperthermia. Infusion rates are calculated from mg/kg/h or micrograms/kg/min and the drug concentration; the calculation must be checked by a second person because tenfold errors are common.
Inhalant anaesthetics (isoflurane, sevoflurane, desflurane, the older halothane, and the gas nitrous oxide) are delivered to the alveoli, dissolve in blood and move to the brain. At equilibrium the partial pressure in brain equals that in alveoli, so alveolar concentration, measured as end-tidal concentration, is a good index of brain concentration.
The blood:gas partition coefficient is the ratio of concentrations in blood and gas at equilibrium. A low coefficient means the agent is poorly soluble in blood, so alveolar and brain partial pressures rise quickly: induction, change of depth and recovery are fast. The approximate textbook order from least to most soluble is desflurane (about 0.42) and nitrous oxide (about 0.47), then sevoflurane (about 0.68), isoflurane (about 1.4) and halothane (about 2.4); published values differ slightly between sources. The oil:gas partition coefficient reflects lipid solubility and correlates inversely with MAC: the more lipid-soluble the agent, the more potent it is (the Meyer-Overton correlation).
Other factors speed induction: a higher inspired concentration, higher fresh gas flow, greater alveolar ventilation and a lower cardiac output (less agent carried away from alveoli, so alveolar concentration rises faster; this is why shocked patients are induced quickly and easily overdosed). When nitrous oxide is given at a high concentration with a second agent, its rapid uptake concentrates the second agent in the alveoli (the second-gas effect). At the end of nitrous oxide anaesthesia the reverse happens: nitrous oxide floods into the alveoli and dilutes oxygen (diffusion hypoxia), so 100 per cent oxygen is given for several minutes. Nitrous oxide also diffuses into closed gas spaces faster than nitrogen leaves them, so it is avoided in gastric dilatation, colic, pneumothorax and in ruminants with a gas-filled rumen.
Elimination is almost entirely through the lungs. Metabolism is roughly 20 to 25 per cent for halothane, a few per cent for sevoflurane, about 0.2 per cent for isoflurane and less for desflurane.
The minimum alveolar concentration (MAC) is the alveolar concentration of an inhalant at one atmosphere that prevents gross purposeful movement in response to a supramaximal noxious stimulus in 50 per cent of subjects. It is the ED50 of inhalants and allows potency to be compared: the lower the MAC, the more potent the agent. Surgical anaesthesia usually needs about 1.2 to 1.5 times MAC; around 2 MAC, cardiovascular depression is severe with most agents. MAC values of the same agent are broadly similar across mammals but not identical; representative values for isoflurane in dogs are around 1.3 per cent and for sevoflurane around 2.3 per cent, but each reference gives its own figures. Nitrous oxide has a MAC of well over 100 per cent in dogs, cats and horses, so it cannot be used alone and contributes only a fraction of a MAC. MAC multiples of different agents are roughly additive.
MAC is reduced by premedicants and co-administered drugs (opioids, alpha-2 agonists, benzodiazepines, ketamine and lidocaine infusions), by hypothermia, increasing age, pregnancy, severe hypotension, severe hypoxaemia, hyponatraemia and acute alcohol intoxication in people. It is increased by hyperthermia, hypernatraemia and drugs that raise CNS catecholamines. It is largely unaffected by the duration of anaesthesia, sex, and by moderate changes in potassium or in carbon dioxide within the normal range.
Isoflurane is the most widely used veterinary inhalant: stable, cheap, little metabolised, causing dose-dependent vasodilation, hypotension and respiratory depression but little myocardial sensitisation. Sevoflurane is less pungent and less soluble, so mask and chamber induction and changes of depth are faster; it reacts with dry carbon dioxide absorbents to form compound A, nephrotoxic in rats, which has not been a practical problem in animals. Desflurane is the least soluble; it boils near room temperature and needs a heated, pressurised vaporiser, and its pungency makes it poor for mask induction. Halothane depresses the myocardium more, sensitises the heart to catecholamine-induced arrhythmias, is extensively metabolised and has been withdrawn from many markets. All the halogenated agents can trigger malignant hyperthermia in susceptible pigs (mutation in the ryanodine receptor RYR1, the same gene behind porcine stress syndrome), and occasionally in dogs and horses; treatment is stopping the trigger, cooling, and dantrolene.
Volatile agents are given from precision, agent-specific vaporisers outside the breathing circuit, compensated for flow and temperature. Each agent has its own saturated vapour pressure, so filling a vaporiser with the wrong agent gives the wrong concentration. Rebreathing (circle) systems with a carbon dioxide absorbent are used for larger patients and allow low fresh gas flows; non-rebreathing systems need fresh gas flows several times minute ventilation and are chosen for small patients; the weight cut-off varies between texts.
Waste anaesthetic gas is an occupational hazard; scavenging, leak testing, cuffed endotracheal tubes and avoiding mask and chamber maintenance reduce exposure.
Local anaesthetics block voltage-gated sodium channels in nerve membranes and so stop the generation and conduction of action potentials. A typical molecule has a lipophilic aromatic ring, an intermediate chain containing either an ester or an amide link, and an ionisable amine. Esters (procaine, tetracaine, benzocaine, chloroprocaine) are hydrolysed by plasma cholinesterase; a metabolite, para-aminobenzoic acid, is responsible for the occasional allergic reactions. Amides (lidocaine, mepivacaine, bupivacaine, ropivacaine) are metabolised in the liver, so liver disease and low hepatic blood flow prolong their action.
They are weak bases with a pKa of about 7.6 to 9, above tissue pH, so most of the drug is ionised in the body. The un-ionised base crosses the nerve membrane; inside, the ionised form binds the sodium channel from the cytoplasmic side. Block is use-dependent: rapidly firing nerves are blocked more readily. In inflamed or infected tissue the pH is low, so even less drug is un-ionised and the block is poor; this explains failure of infiltration around an abscess. A higher pKa means slower onset for the same reason.
Lipid solubility determines potency, protein binding determines duration and pKa determines onset. Lidocaine has a fast onset and intermediate duration; bupivacaine is more lipid-soluble, more protein-bound, slower in onset and longer-acting; mepivacaine is intermediate and widely used in equine diagnostic nerve blocks because it causes little tissue irritation. Small-diameter myelinated and unmyelinated fibres (B, A-delta and C fibres, carrying autonomic, sharp and dull pain signals) are blocked before large motor fibres, so pain and sympathetic tone go first and motor function last.
Adding adrenaline (commonly at 1:200,000, which is 5 micrograms per mL) causes vasoconstriction, slows absorption, prolongs the block and lowers peak plasma concentration. It is avoided where end arteries supply the tissue (ear tips, digits, tail, penis) and in intravenous regional anaesthesia.
Systemic toxicity follows accidental intravascular injection or absorption of too much drug. CNS signs come first, because the drug blocks inhibitory neurones before excitatory ones: sedation, muscle twitching, then convulsions, followed at higher concentrations by CNS depression. Cardiovascular toxicity (bradycardia, conduction block, hypotension, ventricular arrhythmias) follows. Bupivacaine is markedly more cardiotoxic than lidocaine because it dissociates slowly from cardiac sodium channels, so it must never be given intravenously and is not used for intravenous regional anaesthesia. Cats are more sensitive than dogs to local anaesthetic toxicity, and small patients are easily overdosed when dilute solutions are given by volume, so the total dose in mg/kg is always calculated before infiltration. Maximum safe totals quoted in texts vary by species, drug and whether adrenaline is added; use your formulary. Treatment of toxicity is supportive (oxygen, a benzodiazepine for seizures, circulatory support) and intravenous lipid emulsion for severe cardiotoxicity. Benzocaine sprays can cause methaemoglobinaemia.
Lidocaine given intravenously has uses of its own. It is a class Ib antiarrhythmic, the classic first choice for ventricular tachycardia in dogs. As a constant rate infusion it gives analgesia, reduces inhalant MAC and, in horses, is used for postoperative ileus and as part of balanced anaesthesia. Infusions are used cautiously in anaesthetised cats because of cardiovascular depression. Lidocaine infusions must be stopped some time before recovery in horses because they can cause ataxia.
Local and regional anaesthesia let much large-animal surgery be done standing, cheaply and without the risks of recumbency.
In cattle, the cornual nerve block, used for dehorning, blocks the cornual branch of the zygomaticotemporal nerve (from the ophthalmic division of the trigeminal) along the lateral ridge of the frontal bone between the lateral canthus and the horn base. Goats need both the cornual branch of the lacrimal nerve and the cornual branch of the infratrochlear nerve blocked, and are more easily overdosed because of their size. Flank surgery (laparotomy, caesarean section) uses an inverted L block, a line block, or paravertebral anaesthesia of the thirteenth thoracic and first and second lumbar spinal nerves (proximal or distal approaches). Caudal epidural anaesthesia, injected at the sacrococcygeal or first intercoccygeal space, desensitises the tail, perineum, anus, vulva and vagina for obstetric and perineal procedures; a volume large enough to reach the lumbar nerves causes hindlimb weakness and recumbency. The eye can be anaesthetised by the Peterson block or a retrobulbar (four-point) block, and eyelid akinesia is produced by the auriculopalpebral block. Intravenous regional anaesthesia (Bier block) of the bovine distal limb uses lidocaine without adrenaline injected into a superficial vein distal to a tourniquet; the tourniquet stays on for the procedure and is released slowly.
In horses, perineural and intra-articular blocks are the core of lameness diagnosis, starting distally and moving proximally; standing surgery combines sedation with local blocks. In dogs and cats, epidural anaesthesia at the lumbosacral space, dental nerve blocks (infraorbital, maxillary, mental, inferior alveolar), brachial plexus, femoral and sciatic blocks, and incisional or intraperitoneal lidocaine or bupivacaine are standard.
Opioids act at mu (MOP), kappa (KOP) and delta (DOP) receptors in the brain, spinal cord dorsal horn and periphery. Mu agonism gives the strongest analgesia and also respiratory depression, sedation or euphoria depending on species, nausea and vomiting, reduced gut motility, and miosis in dogs and people. Cats, horses and ruminants develop mydriasis instead. Kappa agonism gives analgesia, particularly visceral, and sedation with less respiratory depression, but can cause dysphoria.
Opioids are classified by what they do at the receptor. Full mu agonists (morphine, methadone, hydromorphone, pethidine, fentanyl and its relatives) have high efficacy and no practical ceiling to analgesia. Partial mu agonists (buprenorphine) have lower efficacy, so a ceiling to both analgesia and respiratory depression, but very high receptor affinity. Agonist-antagonists (butorphanol, nalbuphine) are kappa agonists and mu antagonists or weak partial agonists. Pure antagonists (naloxone, naltrexone) bind without activating; diprenorphine is the antagonist traditionally paired with etorphine in wildlife work. Because buprenorphine binds tightly, giving a full agonist shortly after it may work poorly, and naloxone reverses buprenorphine only partially and with high doses. Butorphanol given after a full agonist can reverse some of its effects, which is used deliberately to reduce respiratory depression while keeping some analgesia.
The order of potency relative to morphine is a common exam question: fentanyl is roughly 50 to 100 times as potent as morphine; ultrapotent opioids such as etorphine and carfentanil, used for capturing large wildlife, are thousands of times as potent and are dangerous to people, so operators keep the human antagonist ready and work in pairs. Potency is not efficacy: buprenorphine is more potent by mass than morphine but less efficacious.
Morphine is the reference opioid. It is metabolised by glucuronidation; cats, which have limited glucuronidation, form little morphine-6-glucuronide and may get less analgesia from it. Given intravenously quickly, morphine releases histamine and can cause hypotension. In dogs it often causes vomiting after intramuscular or subcutaneous injection, which is avoided when vomiting is dangerous (raised intracranial or intraocular pressure, oesophageal foreign body). Methadone is a full mu agonist that also blocks NMDA receptors and rarely causes vomiting. Pethidine (meperidine) is short-acting and given only intramuscularly, because intravenous injection releases histamine. Fentanyl is short-acting after a bolus and is used by infusion or in transdermal delivery; absorption from patches is variable. Remifentanil is hydrolysed by plasma and tissue esterases, so its offset is rapid and independent of liver and kidney function.
Butorphanol is a good sedative adjunct and antitussive, with short, ceilinged analgesia that is better for visceral than somatic pain. Buprenorphine lasts longer and, in cats, is well absorbed across the oral mucosa, because the alkaline mouth increases the un-ionised fraction of this weak base. Tramadol is a prodrug; its O-desmethyl metabolite is the mu agonist. Dogs form little of this metabolite, which may explain inconsistent analgesia in dogs, while cats form it.
Species responses to opioids differ. Dogs usually become sedated. Cats given high doses of full agonists can become excited ('morphine mania'), but at appropriate doses combined with sedatives they are well analgesed; mydriasis makes them sensitive to bright light. Horses given opioids alone can show increased locomotor activity, box walking and head pressing, and opioids reduce gut motility, raising concern about colic; they are therefore combined with an alpha-2 agonist. Ruminants tolerate opioids but evidence on analgesia in cattle is limited, and authorisation of opioids in food animals is restricted in many countries. Opioids reduce inhalant MAC and are part of almost all premedication protocols for painful procedures.
Naloxone reverses all opioid effects, including analgesia. Its duration is shorter than that of many opioids, so sedation or respiratory depression can return (renarcotisation), and the patient must be watched. Giving it to an animal in pain can cause sudden pain, agitation and sympathetic surge; titration is preferred. Naltrexone is longer-acting and has been used in wildlife.
Most opioids are controlled drugs. Storage in a locked cabinet, registers of receipt and use, destruction witnessed according to law, and prescription rules all vary by country; the practitioner must know the national schedule.
Pain is best treated by several mechanisms together (multimodal analgesia) and before the stimulus where possible (pre-emptive analgesia). Alongside opioids, the main tools are non-steroidal anti-inflammatory drugs (NSAIDs), alpha-2 agonists, local anaesthetics, and NMDA antagonists such as ketamine. NSAIDs inhibit cyclo-oxygenase (COX): COX-1 is expressed constitutively and supports gastric mucosa, platelets and renal blood flow; COX-2 is induced by inflammation, although it is also constitutive in kidney and brain. Drugs that prefer COX-2 (such as carprofen, meloxicam, and the coxibs firocoxib, robenacoxib and mavacoxib) aim to spare COX-1. Adverse effects are gastrointestinal ulceration, renal injury (worst when renal perfusion is low, as in anaesthetic hypotension or dehydration) and, rarely, idiosyncratic hepatotoxicity. NSAIDs are not combined with corticosteroids or another NSAID. Cats metabolise many NSAIDs slowly because of limited glucuronidation, so aspirin has a long half-life in cats, and paracetamol (acetaminophen), which dogs can tolerate at appropriate doses, is highly toxic to cats. Flunixin meglumine is widely used for visceral pain in horses and cattle. Phenylbutazone is prohibited in food animals in many jurisdictions. Grapiprant blocks the EP4 prostaglandin receptor rather than COX.
Validated pain scales (for example composite scales for dogs and cats, grimace scales for several species) turn observation into a score that guides when to give more analgesia.
A seizure is the clinical expression of excessive, hypersynchronous activity of cortical neurones. Epilepsy is a disease of recurrent unprovoked seizures; idiopathic epilepsy, presumed genetic, is common in dogs, particularly certain breeds, and less common in cats. Reactive seizures arise from metabolic or toxic causes (hypoglycaemia, hypocalcaemia, hepatic encephalopathy, lead, organophosphates, metaldehyde) and are treated by correcting the cause. Status epilepticus is a seizure lasting more than about five minutes, or repeated seizures without full recovery between them; it is an emergency because of hyperthermia, hypoxia and neuronal death. Cluster seizures are two or more within 24 hours.
Anticonvulsants act by enhancing GABA-mediated inhibition (phenobarbital, benzodiazepines, imepitoin), by blocking voltage-gated sodium channels (phenytoin, zonisamide in part), by blocking T-type calcium channels (zonisamide, ethosuximide), by binding the synaptic vesicle protein SV2A (levetiracetam), or by binding the alpha-2-delta subunit of voltage-gated calcium channels (gabapentin, pregabalin). Bromide works by crossing chloride channels and hyperpolarising neurones.
Starting maintenance treatment is usually recommended when there are repeated seizures within a short time, cluster seizures or status epilepticus, severe post-ictal signs, or a structural cause; guidelines from veterinary neurology consensus groups set out these criteria.
Phenobarbital is a long-acting barbiturate and a first-line maintenance drug in dogs and cats. It potentiates GABA-A. It is well absorbed orally, has a long half-life, reaching steady state after about five half-lives (commonly one to three weeks), and induces hepatic microsomal enzymes, including its own metabolism, so its half-life shortens over months and the dose may need adjustment. Induction also speeds the clearance of other drugs (for example levetiracetam, some corticosteroids) and alters thyroid hormone results. Adverse effects are sedation and ataxia early in treatment, polyuria, polydipsia and polyphagia, raised serum alkaline phosphatase (enzyme induction, not necessarily damage), and hepatotoxicity at high serum concentrations. Serum concentration is measured after steady state and when control changes. Primidone is metabolised to phenobarbital and phenylethylmalonamide and adds hepatotoxicity without clear benefit.
Potassium bromide (and sodium bromide) is excreted unchanged by the kidney, so it is useful where liver disease limits phenobarbital. Its half-life in dogs is long (about three to four weeks), so steady state takes months unless a loading regimen is used. Bromide and chloride compete for renal reabsorption: a high-salt diet or chloride-containing fluids increase bromide excretion and can cause breakthrough seizures, while a sudden change to a low-salt diet can cause toxicity (bromism: sedation, ataxia, hindlimb weakness). Bromide is associated with pancreatitis and gastric irritation. In cats bromide causes eosinophilic bronchitis-like lower airway disease in a proportion of patients, so it is generally avoided in cats.
Levetiracetam is cleared mainly by the kidney with little hepatic metabolism, has a wide safety margin and few adverse effects, and can be given intravenously; its short half-life in dogs requires frequent dosing or extended-release forms, and phenobarbital speeds its clearance. It is used as an add-on and in cluster seizures ('pulse' therapy). Imepitoin is a low-affinity partial agonist at the benzodiazepine site, authorised in some countries for idiopathic epilepsy in dogs; it is not intended for cluster seizures or status epilepticus. Zonisamide, a sulfonamide, is used as add-on therapy. Phenytoin is unsuitable in dogs (very rapid metabolism) and dangerous in cats (very slow metabolism).
Status epilepticus is treated immediately with a benzodiazepine: diazepam intravenously or rectally, or midazolam intravenously, intramuscularly or intranasally. If seizures continue, second-line options include intravenous levetiracetam and phenobarbital loading. Refractory status is treated with anaesthetic doses of propofol, a ketamine infusion (which acts on NMDA receptors that become more important as status continues and GABA-A receptors are internalised), or inhalant anaesthesia, with airway protection, oxygen, temperature control and correction of glucose and electrolytes.
In cats, phenobarbital and levetiracetam are the usual maintenance choices; bromide is avoided, and oral diazepam has caused fatal hepatic necrosis. In horses, seizures in foals (for example with neonatal encephalopathy) are controlled with a benzodiazepine or phenobarbital. In ruminants seizures are usually reactive (polioencephalomalacia, hypomagnesaemia, lead poisoning), so specific therapy (thiamine, magnesium, calcium disodium edetate) matters more than anticonvulsants; a sedative may still be needed to stop the seizure.
Centrally acting relaxants reduce skeletal muscle tone by depressing polysynaptic reflexes in the spinal cord and brainstem, without paralysing the neuromuscular junction. Guaifenesin (glyceryl guaiacolate) is the classic example in large animal anaesthesia. It relaxes muscles, including those of the larynx and pharynx, with minimal effect on the diaphragm at usual doses, so breathing continues; it has little analgesic or hypnotic effect of its own and is always combined with an anaesthetic such as ketamine. It is infused to effect from a dilute solution because concentrated solutions cause haemolysis and thrombophlebitis. Overdose causes apneustic breathing and muscle rigidity paradoxically. Methocarbamol is used orally or intravenously in dogs and cats for muscle spasm and tremors, for example in permethrin toxicity in cats, metaldehyde poisoning and tetanus. Benzodiazepines relax muscles through GABA-A receptors in the spinal cord.
Dantrolene acts directly on skeletal muscle by blocking the ryanodine receptor (RYR1) calcium release channel in the sarcoplasmic reticulum. It is the specific treatment for malignant hyperthermia and is used in horses with exertional rhabdomyolysis and for urethral striated-muscle spasm in dogs and cats.
Neuromuscular blocking agents (NMBAs) act at nicotinic acetylcholine receptors of the motor end plate. They produce paralysis without any sedation, unconsciousness or analgesia, so they are used only in anaesthetised patients under controlled ventilation. They are chosen to provide relaxation for intraocular surgery (a central, still eye), to facilitate ventilation, and to reduce inhalant requirement during some procedures. Giving them to a conscious animal, or using them as a method of restraint or euthanasia, is unacceptable.
Depolarising agents (succinylcholine, also called suxamethonium) are agonists: they open the receptor channel, causing fasciculation followed by a flaccid paralysis because the end plate stays depolarised (phase I block). Anticholinesterases potentiate, not reverse, this block. Succinylcholine is hydrolysed by plasma cholinesterase, so its action is prolonged in animals recently exposed to organophosphates. It can raise serum potassium and trigger malignant hyperthermia.
Non-depolarising agents are competitive antagonists. Atracurium is broken down by Hofmann elimination (spontaneous degradation dependent on pH and temperature) and ester hydrolysis, so its duration is little affected by liver or kidney disease; cisatracurium is a purer isomer that releases less histamine. Vecuronium and rocuronium are aminosteroids with intermediate duration. Pancuronium is long-acting and vagolytic, raising heart rate. Block is potentiated by inhalant anaesthetics, aminoglycoside antibiotics, magnesium, hypothermia, acidosis and hypokalaemia; it is exaggerated in myasthenia gravis.
Neuromuscular function is monitored with a peripheral nerve stimulator, typically on the peroneal or ulnar nerve in dogs. The train-of-four (TOF) delivers four supramaximal stimuli at 2 Hz; with a non-depolarising block the twitches fade (each is weaker than the last) and the ratio of the fourth to the first twitch indicates recovery. A depolarising phase I block shows reduced but equal twitches without fade.
Non-depolarising block is reversed by anticholinesterases (neostigmine or edrophonium), which raise acetylcholine at the junction so it can compete with the blocker. Because acetylcholine also rises at muscarinic sites, an anticholinergic (atropine or glycopyrrolate) is given with or before the anticholinesterase to prevent bradycardia, salivation and bronchospasm. Reversal is attempted only when some twitches have returned. Sugammadex is a modified cyclodextrin that encapsulates rocuronium and, less strongly, vecuronium, reversing even deep block without muscarinic effects; it does not work on atracurium or succinylcholine.
Euthanasia means ending an animal's life with minimal pain and distress. Guidelines from the World Organisation for Animal Health (WOAH), the American Veterinary Medical Association (AVMA) and national bodies judge methods by their ability to cause rapid unconsciousness followed by death, reliability, safety for people, irreversibility, compatibility with the species, age and circumstances, and the emotional effect on observers. This chapter covers agents by principle; approved agents, doses and legal controls differ by country and must be checked locally.
Methods act in three basic ways. The first is direct depression of the neurones needed for consciousness and life: barbiturates and inhalant anaesthetics in overdose produce unconsciousness, then apnoea and cardiac arrest. The second is hypoxia: this is acceptable only when unconsciousness comes first or the method itself causes rapid unconsciousness, which is why agents that paralyse without first causing unconsciousness (neuromuscular blockers, and potassium or magnesium salts given to a conscious animal) are unacceptable on their own. The third is physical disruption of brain activity (captive bolt, gunshot, electrical stunning), mainly for livestock, used with a follow-up method where required.
Pentobarbital given intravenously in overdose is the reference injectable agent for companion animals and horses: it rapidly causes unconsciousness, then deep anaesthesia, respiratory arrest and cardiac arrest. Where intravenous access is impossible, some guidelines accept intraperitoneal injection in small animals, which is slower. Intracardiac injection is acceptable only in an animal that is already unconscious or deeply anaesthetised. Potassium chloride or magnesium sulphate intravenously, and neuromuscular blocking agents, are acceptable only in an animal already under general anaesthesia. Sedation before euthanasia, for example with an alpha-2 agonist or a dissociative combination, reduces distress and makes intravenous injection safer.
Barbiturate residues persist in the carcass. Wildlife and pets that feed on carcasses of animals euthanased with pentobarbital (eagles and other scavengers, and dogs) can be poisoned, so these carcasses must be disposed of by burial at adequate depth, incineration or rendering according to local law, and never enter the food chain. For this reason, animals intended for the human food chain are slaughtered by approved stunning and bleeding methods, not by chemical euthanasia.
Inhaled agents are used for small animals, laboratory rodents and poultry: overdose of an inhalant anaesthetic, and carbon dioxide in some settings, with debate about aversion to high carbon dioxide concentrations. Fish and amphibians may be euthanased by overdose of an immersion anaesthetic such as tricaine methanesulfonate, followed by a physical method where recommended. Guidelines for each species set which agents are acceptable, acceptable with conditions, or unacceptable.
Death must be confirmed by several signs together: absence of heartbeat on auscultation over a period of time, absence of breathing, loss of corneal reflex, and fixed dilated pupils; rigor mortis is definitive but late.
Ruminants differ from other species in ways that shape every anaesthetic. Cattle, sheep and goats are more sensitive than horses to alpha-2 agonists, especially xylazine. Under sedation and general anaesthesia the rumen continues to ferment but stops contracting and eructation stops, so gas accumulates (tympany), which compresses the diaphragm and major vessels; regurgitation of ruminal content risks aspiration pneumonia. Preparation therefore includes withholding feed and water for a period appropriate to the species and procedure, intubation with a cuffed tube, positioning with the head lower and the poll raised so saliva drains, and passing a stomach tube where needed. Ruminants salivate profusely throughout anaesthesia; anticholinergics make saliva viscous and are not given for this purpose. Wherever possible, cattle surgery is done standing under sedation with local or regional anaesthesia. Drugs used in food animals must be authorised for that species or used under legal off-label rules with a set withdrawal period; many anaesthetic and analgesic drugs are not authorised in food animals in some countries, and phenylbutazone and some other drugs are prohibited.
Pigs are difficult to restrain and to cannulate (the auricular veins are used), are relatively resistant to alpha-2 agonists alone and are often sedated with azaperone or combinations given intramuscularly. Certain pig lines carry the RYR1 mutation that causes malignant hyperthermia when exposed to halogenated inhalants or succinylcholine, and porcine stress syndrome when stressed; dantrolene is the treatment.
Horses are large, flight animals and recovery from general anaesthesia is the most dangerous phase: fractures, myopathy and neuropathy occur during recovery, and published mortality for elective equine anaesthesia is higher than in dogs and cats. Standing procedures under sedation (alpha-2 agonist, often with an opioid) and local anaesthesia are preferred whenever possible. Ketamine must follow adequate alpha-2 sedation. Opioids alone can cause excitement and increased locomotor activity. Acepromazine can cause penile prolapse. Anticholinergics can cause ileus. Hypotension under inhalant anaesthesia is associated with postanaesthetic myopathy, so arterial pressure is monitored and supported, often with dobutamine.
NSAIDs such as flunixin meglumine and phenylbutazone are central in equine analgesia, but horses that may enter the food chain are subject to medicine records and prohibitions that vary by country (for example the equine passport system in Europe).
Cats have low activity of several UDP-glucuronosyltransferase enzymes. This explains slow clearance of aspirin and other NSAIDs, the toxicity of paracetamol, slower recovery and Heinz bodies after repeated propofol, and possibly poorer conversion of morphine to its active glucuronide. Cats vomit readily after xylazine and dexmedetomidine, develop mydriasis with opioids, excrete active ketamine in urine, and are more sensitive to local anaesthetic toxicity. They should not receive bromide or oral diazepam routinely, and phenytoin accumulates in them.
Dogs vary by breed. ABCB1 (MDR1)-deficient herding breeds need lower doses of acepromazine and butorphanol. Sighthounds recover slowly from thiobarbiturates. Brachycephalic breeds have airway obstruction, so they are pre-oxygenated, induced quickly and extubated late, when they can swallow and lift the head. Boxers are said to be sensitive to acepromazine.
Birds have air sacs and no diaphragm, so inhalant uptake and depth change rapidly and breath-holding is common; intermittent ventilation is often needed. Fish and amphibians are anaesthetised by immersion in buffered anaesthetic solutions.
Age matters in all species. Neonates have immature hepatic metabolism, lower plasma protein, a more permeable blood-brain barrier and a heart rate-dependent cardiac output, so drugs last longer and bradycardia is poorly tolerated. Geriatric patients need lower doses and have reduced MAC. Pregnant animals have reduced MAC and any drug that crosses the placenta, which includes most CNS drugs, can depress the fetus; in caesarean section, drugs with rapid clearance or that can be reversed are preferred.
A student must be able to explain why each premedicant, induction agent and analgesic is chosen, and to calculate a dose volume and an infusion rate without error. Before a practical anaesthesia rotation, learn the antagonist for each class, the cardiovascular effects of acepromazine and alpha-2 agonists, the order of blood:gas coefficients and what changes MAC, and the local anaesthetic totals for small patients. Practise reading vial concentrations aloud (the 20 and 100 mg/mL xylazine trap), converting percentages to mg/mL, and checking every calculation with a second person. Learn the cattle cornual, paravertebral and caudal epidural blocks on specimens before live animals.
In the first years of practice the daily decisions are: which sedation protocol suits this fractious cat or this old dog with a murmur; how to anaesthetise a brachycephalic dog; which analgesic plan to send home and whether an NSAID is safe with this kidney value; how to manage a dog in status epilepticus at night; how to sedate a cow for a flank caesarean or a horse for a laceration in the field. Build standard written protocols with calculated dose charts for your commonest species and weights, a reversal plan for every sedation, and a checklist that includes airway, access, monitoring and recovery. Audit your anaesthetic complications.
A senior clinician sets the practice's anaesthesia and analgesia policy: which drugs are stocked, how controlled drugs are stored and recorded, which monitoring is mandatory, how infusions are prepared and double-checked, and how staff are trained in emergency drugs and resuscitation. They handle the difficult cases: equine colic anaesthesia with hypotension, geriatric patients with several diseases, epileptic dogs not controlled on two drugs, and euthanasia decisions and disposal. They also track changes in national rules on food-animal drugs, withdrawal periods and phenylbutazone, and advise on waste gas exposure and the climate cost of inhalants.
Research-level work asks questions the textbooks leave open: species differences in receptor pharmacology and drug metabolism (feline glucuronidation, canine tramadol metabolism, bovine alpha-2 sensitivity), MAC-sparing interactions measured by proper crossover designs, population pharmacokinetics of infusions in horses and cattle, validated pain scales and their measurement properties, genetic markers for drug sensitivity such as ABCB1 and RYR1, and the evidence base for anticonvulsant selection in canine idiopathic epilepsy. Well-designed trials in veterinary anaesthesia are scarce; blinded, adequately powered studies and pharmacovigilance data are valuable contributions, as is work on analgesia in food animals where authorised options are few.
This manual gives one standard dose only (xylazine for standing sedation in the horse); all other doses, maximum local anaesthetic totals, infusion rates, serum anticonvulsant target ranges and withdrawal periods are left to the product label and national formulary because they vary by country, product and species. Specific MAC values are given only as representative and approximate. Detailed anaesthetic equipment (breathing-system selection by weight, ventilator settings), monitoring interpretation and cardiopulmonary resuscitation belong to veterinary anaesthesiology and are touched on only. Exotic, avian, aquatic, zoo and wildlife anaesthesia are summarised briefly. Controlled drug schedules and food-animal authorisations are named in principle but not tabulated by country. Evidence for newer drugs (grapiprant, imepitoin outside Europe, gabapentin and trazodone for anxiety) is still developing.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions. Doses in numerical questions are values stated in the question's own protocol for practising calculation, not dosing recommendations; confirm any dose against the product label and your national formulary.
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