Veterinary · Clinical · also Anaesthesia, Veterinary Anesthesia
Safe sedation and anaesthesia across species: premedication, local and regional blocks, injectable and inhalant anaesthesia, monitoring, emergencies and pain management.
In the exams: BCSE anaesthesia 20-23 items; ECFVG / NEB CPE anaesthesia section (about 4 h, pass/fail); AVE Anaesthesia OSCE; EAEVE Day One competences
Veterinary anaesthesiology is the discipline of making an animal unaware of, and unresponsive to, a painful procedure and then returning it safely to normal function. Analgesia is the narrower task of preventing or relieving pain, awake or anaesthetised. The two are taught together because almost every anaesthetic decision is also an analgesic one: the premedication that calms a dog also sets its pain control for the next six hours, and the local block that lets a cow stand for a flank laparotomy is itself the anaesthetic.
The subject is unusually species-bound. A cow is roughly ten times more sensitive to xylazine than a horse, a horse must be kept normotensive or it may not stand up again, a cat cannot glucuronidate paracetamol, a pig can develop malignant hyperthermia under a volatile agent, and a bird breathes through air sacs rather than a diaphragm-driven lung. A safe anaesthetist therefore learns general principles (the balance of hypnosis, analgesia and muscle relaxation; monitoring; the management of hypotension, hypoventilation and hypoxaemia) and then learns how each species bends them.
Worldwide the subject is examined in three ways. Knowledge papers such as the ICAR AIEEA (PG), Nepal's NLEV, Indian state veterinary officer papers and China's national practising-veterinarian exam ask recall: nerve blocks and their landmarks, drug classes and antagonists, stages of anaesthesia, and breathing systems. North American and Australasian licensing exams (BCSE, NAVLE, AVE) ask clinical vignettes: choose the protocol for this patient, interpret this capnogram, what to do now that the blood pressure has fallen. Practical exams (the ECFVG and NEB Clinical Proficiency Examination anaesthesia section, the AVE anaesthesia OSCE, the RCVS SME OSCE and the EAEVE Day One competences) require a candidate to plan, induce, monitor and recover a real patient and record it on an anaesthetic chart.
Drug doses in this manual are few and are given only where they are standard textbook values. Doses, licensing, and withdrawal periods for food-producing animals differ by country and product. Every dose below is followed by the reminder to check the label and the national formulary, and that reminder is meant literally.
Anaesthetic risk is judged before any drug is drawn up. The history asks about previous anaesthetics, current medication (for example NSAIDs, corticosteroids, anticonvulsants, cardiac drugs), exercise tolerance, coughing, vomiting, and when the animal last ate. The physical examination concentrates on the cardiovascular and respiratory systems: heart rate and rhythm, murmurs, pulse quality, mucous membrane colour and capillary refill time, respiratory pattern and auscultation. Body weight is measured, not guessed, and body condition is scored, because obese animals are dosed nearer lean weight for many drugs. Minimum laboratory work depends on age and illness; packed cell volume, total protein, blood glucose and urea or creatinine are a common minimum in a sick or older animal.
The American Society of Anesthesiologists (ASA) physical status scale is used across species. ASA I is a normal healthy patient; ASA II has mild systemic disease; ASA III has severe systemic disease; ASA IV has severe systemic disease that is a constant threat to life; ASA V is moribund and not expected to survive without the operation. The suffix E marks an emergency. The ASA grade describes the patient, not the procedure, but higher grades are consistently associated with higher peri-anaesthetic mortality in large practice-based studies of dogs, cats and horses.
Fasting reduces the risk of vomiting and aspiration in monogastric animals and of regurgitation and ruminal tympany in ruminants. Recommended times vary between guidelines and have shortened for dogs and cats in recent years; neonates and very small patients are fasted only briefly because of hypoglycaemia. Rabbits and guinea pigs cannot vomit and are not fasted in the usual sense, and water is withheld for far shorter periods than food in all species.
Premedication is drug treatment given before induction. Its aims are to calm the animal and make handling safe, to reduce the dose of induction and maintenance agents (and so their dose-dependent cardiorespiratory depression), to provide analgesia before the painful stimulus, to smooth induction and recovery, and in some cases to block unwanted autonomic reflexes. Neuroleptanalgesia is the combination of a tranquilliser or sedative with an opioid; the two act synergistically, so each can be given at a lower dose.
Anticholinergics (atropine and glycopyrrolate) block muscarinic receptors. They prevent or treat vagally mediated bradycardia and reduce salivary and bronchial secretions. Glycopyrrolate is a quaternary ammonium compound, so it crosses the blood-brain barrier and placenta poorly and has a slower onset and longer action than atropine. Routine anticholinergic use has declined because the drugs cause tachycardia, increase myocardial oxygen demand and can reduce gut motility. In horses they can precipitate ileus and colic. In ruminants they do not stop saliva production but make it more viscous and harder to clear, so they are not routine. Many rabbits carry serum atropinesterase, so glycopyrrolate is preferred in that species.
Phenothiazines, of which acepromazine is the veterinary standard, block dopamine receptors centrally and alpha-1 adrenoceptors peripherally. They give dose-dependent tranquillisation, antiemetic and antiarrhythmic effects, but no analgesia, cannot be reversed and cause vasodilation and hypotension; hypovolaemic patients should not receive them. Stallions and geldings may develop penile protrusion, and prolonged paraphimosis or priapism is a recognised risk. Dogs with the ABCB1 (formerly MDR1) gene mutation, common in collies and related herding breeds, show deeper and longer sedation with acepromazine and some opioids. Azaperone is a butyrophenone used mainly in pigs.
Benzodiazepines (diazepam, midazolam) act at the GABA-A receptor. They produce anxiolysis and muscle relaxation with minimal cardiovascular effect, and they are anticonvulsant. In healthy young dogs and cats they sedate poorly and can cause excitement, so they are most useful in the sick, the very old and the very young, or as co-induction agents. Diazepam is formulated in propylene glycol, which is painful intramuscularly and irritant to veins; midazolam is water-soluble at the formulated pH. Flumazenil antagonises both.
Alpha-2 adrenoceptor agonists (xylazine, detomidine, romifidine, medetomidine, dexmedetomidine) give reliable sedation, analgesia and muscle relaxation. Peripheral alpha-2 activation causes vasoconstriction and an early rise in blood pressure with reflex bradycardia, sometimes with second-degree atrioventricular block; central effects then lower sympathetic tone. Cardiac output falls markedly. Other effects include vomiting (especially in cats given xylazine), hyperglycaemia from reduced insulin release, diuresis, reduced gut motility, and in late-pregnant cattle increased uterine tone with xylazine. In sheep, alpha-2 agonists can cause marked hypoxaemia with pulmonary oedema. Selectivity for alpha-2 over alpha-1 receptors rises from xylazine (about 160:1) through detomidine and romifidine to medetomidine (about 1620:1). Atipamezole, yohimbine and tolazoline are antagonists; atipamezole is the most selective.
Local anaesthetics block voltage-gated sodium channels from the inside of the axon, preventing depolarisation and conduction. They are weak bases; the un-ionised fraction crosses the nerve membrane, and the ionised form binds the channel. In inflamed, acidic tissue a larger fraction is ionised outside the nerve, so blocks work less well in infected sites. Small, myelinated fibres and pain and temperature fibres are blocked earlier than large motor fibres. Chemically they are amides (lidocaine, mepivacaine, bupivacaine, ropivacaine), metabolised in the liver, or esters (procaine, tetracaine), hydrolysed by plasma esterases.
Lipid solubility determines potency, protein binding determines duration and pKa determines speed of onset. Lidocaine has a fast onset and intermediate duration; bupivacaine is slower in onset, much longer acting and more cardiotoxic. Bupivacaine must never be given intravenously. Adding adrenaline (epinephrine), commonly at 1:200,000 (5 micrograms per mL), causes local vasoconstriction, slows absorption and prolongs the block, but should not be used on end-arterial sites such as the tail, ears, digits or penis, or in wound edges where it may impair healing.
Systemic toxicity follows accidental intravascular injection or an excessive total dose. Central nervous signs (sedation, muscle twitching, convulsions) usually precede cardiovascular signs (bradycardia, hypotension, arrhythmias, arrest). Cats and small ruminants are more sensitive than dogs and cattle. Textbooks commonly quote a lidocaine ceiling in the region of 8 to 10 mg/kg in dogs and cattle and lower in cats, sheep and goats, where figures of about 6 mg/kg or less are often advised — confirm against the product label and your national formulary. The sensible working rule is to calculate the total dose before the first injection, dilute for small patients, and aspirate before every injection. Treatment is supportive: stop injecting, secure the airway, oxygenate, control seizures with a benzodiazepine and support circulation; intravenous lipid emulsion is used for severe toxicity, especially from bupivacaine.
Dehorning or disbudding is one of the commonest painful procedures in livestock, and local anaesthesia for it is a legal requirement in several countries and a welfare expectation in most. The horn and the skin around its base in cattle are supplied mainly by the cornual nerve, which arises from the zygomaticotemporal branch of the lacrimal nerve, part of the ophthalmic division of the trigeminal nerve. The nerve runs from the orbit up along the lateral edge of the frontal bone (the temporal line or ridge) towards the horn base, covered only by skin and a thin layer of the frontalis muscle.
The block is placed on the upper third of the temporal ridge, roughly halfway between the lateral canthus of the eye and the base of the horn. The needle is inserted just below the ridge, to a shallow depth of about a centimetre, and several millilitres of 2 percent lidocaine are deposited after aspiration; textbook volumes are about 5 to 10 mL for an adult — confirm against the product label and your national formulary. Analgesia develops within about ten to fifteen minutes and is tested by pricking the skin around the horn base before starting. In adult cattle with large horns, branches of the dorsal cervical nerves supply the caudal part of the horn base, so a ring block of the skin around the horn base is added. Failure of the block is usually due to depositing the drug too deep, beneath the ridge, or to missing a variant nerve.
Pain from dehorning and disbudding outlasts lidocaine. Current welfare guidance recommends adding a non-steroidal anti-inflammatory drug, licensed for the species in the country concerned, and sedation (often with an alpha-2 agonist) for handling calves. Disbudding is less painful and invasive than dehorning an animal with an established horn, and is preferred where horns must be removed.
The goat differs in two ways. First, each horn is supplied by two nerves: the cornual branch of the lacrimal nerve (via its zygomaticotemporal branch, as in cattle) and the cornual branch of the infratrochlear nerve. Both must be blocked. The lacrimal branch is blocked caudal to the root of the supraorbital process, and the infratrochlear branch at the dorsomedial margin of the orbit; many operators add a partial ring block. Second, kids are small and very sensitive to local anaesthetic toxicity. Four injection sites on a 3 to 5 kg kid can easily exceed a safe total, so the drug is diluted (for example 2 percent lidocaine diluted to 1 percent or less with sterile saline) and the total dose is calculated in advance. Disbudding irons applied too long to the thin skull of kids can cause thermal injury to the brain; this is an operator error, not an anaesthetic one, but it is examined together with the block.
Standing flank laparotomy (for rumenotomy, caesarean section, abomasal displacement correction or exploration) is routinely done in cattle under regional anaesthesia, avoiding the risks of general anaesthesia in ruminants. The skin, muscles and peritoneum of the flank are supplied by the ventral and dorsal branches of the last thoracic spinal nerve (T13) and the first and second lumbar spinal nerves (L1 and L2). Some authors also block L3 for incisions extending far caudally, accepting a risk of weakness in the ipsilateral pelvic limb if the femoral contribution is affected.
Paravertebral anaesthesia blocks these spinal nerves near where they leave the vertebral canal. Because each nerve emerges through the intervertebral foramen behind the vertebra of the same number and then runs caudolaterally, T13 is found near the cranial edge of the transverse process of L1, L1 near the cranial edge of L2, and L2 near the cranial edge of L3. This offset is a favourite examination point. Alternatives include the inverted L block, in which local anaesthetic is infiltrated along a line caudal to the last rib and ventral to the transverse processes, and a line block along the incision itself. These field blocks are technically easier but use larger volumes, do not relax deep muscle as well, and may affect wound healing if drug is placed in the incision.
The proximal technique, associated with Farquharson and Hall and sometimes called the Cambridge technique, deposits drug close to the intervertebral foramina, where the dorsal and ventral branches are still together. The operator locates the transverse processes, inserts a long needle through the skin near the cranial edge of the relevant process, walks it off the edge and advances it through the intertransverse ligament; a loss of resistance is felt. Drug is deposited ventral to the ligament for the ventral branch and then, while withdrawing, above the ligament for the dorsal branch. Textbook volumes for an adult cow are roughly 10 to 15 mL of 2 percent lidocaine below the ligament and a smaller volume, about 5 mL, above it at each site — confirm against the product label and your national formulary.
Signs of a successful proximal block are a rise in skin temperature from sympathetic blockade and vasodilation, loss of sensation over the flank, and scoliosis of the spine with the convexity towards the blocked side, because the epaxial muscles on that side are paralysed. Advantages are a small total drug volume, wide and uniform analgesia of skin, muscle and peritoneum, and good relaxation of the abdominal wall. Disadvantages are technical difficulty in fat or heavily muscled animals, the scoliosis itself (which can make closing the incision harder), and a small risk of penetrating a major vessel, particularly the aorta on the left or the caudal vena cava on the right.
The distal technique, associated with Magda and Cakala and sometimes called the Cornell technique, blocks the dorsal and ventral branches of the same nerves further out, near the tips of the transverse processes of L1, L2 and L4. At each site the needle is directed ventral to the tip of the process to reach the ventral branch and dorsal to it to reach the dorsal branch, with a fan-shaped infiltration because the nerve position is less predictable. Larger volumes are used than in the proximal technique.
The distal block uses an ordinary needle, carries little risk of puncturing a major vessel, and produces minimal scoliosis and no pelvic-limb weakness. Its weaknesses are the larger volume and more variable effect, especially where the transverse processes are hard to palpate or when the nerve course varies. In both techniques, the total lidocaine dose for the whole procedure, including any extra infiltration, must be tallied against the ceiling for the species. The same principles apply in sheep and goats, which are smaller and more sensitive to lidocaine, and in camelids.
Epidural anaesthesia is the injection of drug into the epidural space, outside the dura mater, where it acts on spinal nerve roots as they leave the canal and, for opioids and alpha-2 agonists, diffuses to receptors in the dorsal horn. Spinal (subarachnoid or intrathecal) anaesthesia places the drug in the cerebrospinal fluid and needs much smaller doses. The spread of an epidural depends mainly on the volume injected, and also on the site, the position of the animal and the size of the epidural space, which is reduced by obesity and pregnancy.
A caudal (low) epidural in a standing large animal is designed to block the sacral and coccygeal nerves, giving anaesthesia of the tail, anus, perineum, vulva, vagina and bladder without affecting the pelvic limbs. A cranial (high) epidural uses a larger volume to spread forward to the lumbar nerves; it can provide anaesthesia for the flank or hindquarters but causes pelvic-limb paralysis and recumbency, and it is used in small ruminants and pigs more readily than in adult cattle or horses. Sympathetic blockade from a large local anaesthetic epidural can cause hypotension, so hypovolaemic animals are poor candidates.
Contraindications common to all species are coagulopathy, infection or dermatitis over the site, uncorrected hypovolaemia, and anatomical abnormality of the site such as pelvic fractures. Complications include hypotension, pelvic-limb weakness, urinary retention (especially with opioids), pruritus, and, rarely, infection or haematoma.
In cattle the injection is made at the sacrococcygeal space or, more commonly, the first intercoccygeal space (Co1 to Co2). The space is found by moving the tail up and down in a pump-handle fashion and feeling the first moveable joint behind the sacrum. After clipping and skin preparation, a needle is inserted in the midline at about a right angle to the skin or slightly cranially. Correct placement is confirmed by the hanging-drop technique, in which a drop of fluid in the hub is drawn in by the negative pressure of the epidural space, or by lack of resistance to injection. In an adult cow a standard volume is about 5 to 6 mL of 2 percent lidocaine — confirm against the product label and your national formulary. Loss of tail tone is the first sign of effect. Caudal epidural is used for dystocia (it abolishes straining), rectal and vaginal prolapse, perineal surgery and tail amputation. Xylazine, alone or with lidocaine, gives longer epidural analgesia but some of it is absorbed and produces systemic sedation and bradycardia.
In the horse the site is also Co1 to Co2. The epidural space is deeper, and the operator must avoid a volume that causes pelvic-limb ataxia, because a horse that loses hind-limb control while standing may panic and fall. For this reason alpha-2 agonists or opioids, alone or mixed with a small volume of local anaesthetic, are used to give perineal analgesia with less motor block.
In dogs, cats and pigs the epidural is usually given at the lumbosacral space (L7 to S1), located by palpating the wings of the ilium and the dorsal spinous processes. In the dog the spinal cord ends at about the sixth or seventh lumbar vertebra, but the dural sac extends further caudally, so a lumbosacral needle may enter the subarachnoid space. In the cat the cord and dural sac extend further caudally still, so subarachnoid puncture is more likely. If cerebrospinal fluid appears, the needle is withdrawn into the epidural space or a reduced dose is given, because the full epidural dose given intrathecally spreads much further. Blood in the hub means a venous sinus has been entered and the needle should be repositioned.
Epidural morphine is widely used in dogs for pelvic-limb and caudal abdominal surgery; the textbook dose of preservative-free morphine is about 0.1 mg/kg, giving analgesia for many hours without motor block — confirm against the product label and your national formulary. Local anaesthetics such as lidocaine or bupivacaine add motor and sensory block. In pigs the lumbosacral epidural is used for castration, caesarean section and hind-limb procedures, often with the pig restrained in sternal or lateral recumbency.
Propofol is an alkylphenol in a lipid emulsion. It acts at the GABA-A receptor, gives rapid, smooth induction and rapid recovery with little accumulation in dogs, and has no analgesic effect. Its main adverse effects are dose-dependent apnoea and hypotension from vasodilation, so it is given slowly to effect. Cats conjugate phenols poorly; repeated daily propofol anaesthesia in cats has been associated with Heinz-body formation and slower recovery. The lipid emulsion supports bacterial growth, so opened vials without preservative are discarded within the time on the label.
Alfaxalone is a neuroactive steroid solubilised in a cyclodextrin. It also acts at GABA-A, causes less vasodilation than propofol at equivalent doses, and can be given intramuscularly in cats and small dogs (though in large volumes). Recovery can be rough if the animal is disturbed. Thiopental, an ultrashort-acting thiobarbiturate, is now unavailable in many countries but remains in textbooks: it is strongly alkaline and causes tissue necrosis if injected perivascularly (treated by diluting the site with saline and lidocaine); recovery depends on redistribution to muscle and fat, so lean sighthounds recover slowly; and repeated doses accumulate.
Ketamine is a dissociative agent and NMDA-receptor antagonist. It gives analgesia and a cataleptic state with open eyes, preserved laryngeal and pharyngeal reflexes (which are not protective) and stimulated sympathetic tone, so blood pressure and heart rate are usually maintained in patients whose sympathetic reserve is intact. Alone it causes muscle rigidity and can cause seizure-like activity, so it is always combined with a benzodiazepine or an alpha-2 agonist. It increases salivation. Cats excrete it largely unchanged in urine. Tiletamine with zolazepam is a fixed combination of a dissociative and a benzodiazepine. Etomidate gives almost no cardiovascular depression and is chosen for patients with severe cardiac disease; it transiently suppresses adrenocortical steroid synthesis and its propylene glycol vehicle can cause haemolysis and pain on injection.
In horses, general anaesthesia is almost always induced after profound alpha-2 sedation, with ketamine combined with a benzodiazepine (diazepam or midazolam) or with guaifenesin. Guaifenesin is a centrally acting muscle relaxant that acts at internuncial neurons of the spinal cord and brainstem; it relaxes skeletal muscle but has minimal effect on the diaphragm, and at high doses causes haemolysis and thrombophlebitis. Total intravenous anaesthesia (TIVA) for short field procedures in horses often uses an infusion of guaifenesin, ketamine and an alpha-2 agonist, known as triple drip. Duration is limited, usually to about an hour, because the drugs accumulate and recovery quality falls.
In cattle and small ruminants, xylazine with ketamine, or guaifenesin with ketamine, is used for short procedures, remembering the far lower xylazine doses needed in ruminants. In pigs, intravenous access is difficult (the auricular veins are used), so intramuscular combinations such as azaperone or an alpha-2 agonist with ketamine, or tiletamine with zolazepam, are common. Partial intravenous anaesthesia (PIVA) combines a reduced inhalant concentration with infusions of opioids, lidocaine, ketamine or alpha-2 agonists to lower the inhalant requirement.
Infusions are given as a dose per kilogram per unit time: micrograms per kilogram per minute (common for ketamine and dexmedetomidine) or per hour (common for fentanyl, lidocaine and methadone). The working steps are fixed: multiply dose rate by body weight to get amount per unit time, convert to per hour if needed, and divide by the concentration to get millilitres per hour. For example, fentanyl at 5 micrograms per kilogram per hour in a 20 kg dog is 100 micrograms per hour; fentanyl at 50 micrograms per mL gives 2 mL per hour — confirm against the product label and your national formulary. The figures here illustrate arithmetic; the dose itself must be taken from the label and formulary. Most calculation errors are unit slips between milligrams and micrograms or between per minute and per hour, and a tenfold error is the most dangerous. A second person checking every infusion calculation is a standard safety step.
Inhalant anaesthetics are delivered to the alveoli, taken up into blood and carried to the brain. Speed of induction and recovery depends mainly on solubility in blood, expressed as the blood:gas partition coefficient. A low coefficient means little of the agent dissolves in blood, alveolar and brain partial pressures rise quickly, and depth can be changed quickly. Approximate values are desflurane 0.42, nitrous oxide 0.47, sevoflurane 0.68, isoflurane 1.46 and halothane 2.54, so desflurane and sevoflurane are the fastest and halothane the slowest of the agents in current or recent use.
Potency is expressed as the minimum alveolar concentration (MAC): the alveolar concentration that prevents purposeful movement in response to a supramaximal noxious stimulus in 50 percent of animals. Potency correlates with lipid solubility (the oil:gas partition coefficient). MAC is roughly similar across mammals for a given agent but not identical: textbook values for isoflurane are about 1.3 percent in dogs and horses and about 1.6 percent in cats, and for sevoflurane about 2.1 to 2.4 percent in dogs and about 2.6 percent in cats. Surgical anaesthesia typically needs about 1.2 to 1.5 times MAC. MAC is reduced by premedicants, opioids, alpha-2 agonists, hypothermia, old age, pregnancy and severe hypotension, and increased by hyperthermia and in young animals. The MAC of nitrous oxide in animals is well above 100 percent, so it can only be an adjunct.
All the volatile agents cause dose-dependent respiratory depression, vasodilation and hypotension; isoflurane and sevoflurane preserve cardiac output better than halothane. Halothane sensitises the myocardium to catecholamine-induced arrhythmias and has been associated with hepatotoxicity. Sevoflurane can react with strong-base carbon dioxide absorbents to form compound A; its clinical importance in animals is uncertain. Desiccated absorbents can generate carbon monoxide with desflurane. Nitrous oxide diffuses into closed gas spaces faster than nitrogen leaves them, so it is contraindicated in pneumothorax, gastric dilatation-volvulus, intestinal obstruction and ruminal tympany; when it is stopped, its rapid outflow can dilute alveolar oxygen (diffusion hypoxia), prevented by giving 100 percent oxygen for several minutes.
The anaesthetic machine takes oxygen (and sometimes nitrous oxide or air) from cylinders or a pipeline, reduces its pressure, meters it through flowmeters and passes it through a vaporiser. Modern precision vaporisers are agent-specific, sit outside the breathing circuit, and compensate for temperature and flow so that the dial setting approximates the output concentration. Desflurane, which boils near room temperature, needs a heated, pressurised vaporiser. Filling a vaporiser with the wrong agent gives an unpredictable output. Oxygen-failure alarms and scavenging are standard safety features; waste anaesthetic gases are removed by active or passive scavenging to protect staff, and exposure limits are set by national occupational-health rules. A pre-use machine check is done before every list: the oxygen supply and reserve cylinder are checked, the flowmeters move freely, the vaporiser is filled and seated, the absorbent is not exhausted, the breathing system is assembled correctly, and the circuit is pressure-tested for leaks with the adjustable pressure-limiting (pop-off) valve closed, remembering to open it again before connecting a patient. A closed pop-off valve left in place is a recognised cause of barotrauma and death.
Rebreathing (circle) systems pass exhaled gas through a carbon dioxide absorbent (soda lime or similar, which changes colour when exhausted) and return it to the patient through one-way valves. They conserve heat, moisture and anaesthetic agent and allow low fresh gas flows, but they add resistance and dead space and change concentration slowly at low flows. They are generally used for patients above roughly 5 to 10 kg; the cut-off quoted varies by textbook and equipment.
Non-rebreathing systems rely on a high fresh gas flow to wash carbon dioxide out, so they have no absorbent and low resistance and are used for small patients. They are classified by the Mapleson scheme. The Magill (Mapleson A) and its coaxial form the Lack are efficient in spontaneous breathing, needing a flow about equal to minute volume. The Bain is a coaxial Mapleson D; the Ayre's T-piece with the Jackson-Rees modification is Mapleson F; both need flows of roughly two to three times minute volume. Minute volume in dogs and cats is commonly estimated at about 200 mL/kg/min, which gives the textbook fresh gas flow for a Bain or T-piece of about 400 to 600 mL/kg/min; some texts quote lower flows, so check the system's instructions. Rebreathing of carbon dioxide on the capnograph (a baseline that does not return to zero) means the flow is too low, the absorbent is exhausted or a valve is stuck.
Guedel's classical stages, described for ether, still frame the teaching of depth. Stage I is voluntary excitement and early analgesia; stage II is involuntary excitement, with struggling, breath-holding and exaggerated reflexes; stage III is surgical anaesthesia, divided into planes 1 to 4 of increasing depth; stage IV is overdose, with respiratory and cardiovascular collapse. Modern drug combinations blur the stages, so depth is judged by combining several signs.
In dogs and cats at a light surgical plane, the eye rotates ventromedially and the palpebral reflex is reduced; at a deep plane the eye returns to a central position, the pupil dilates and the palpebral and corneal reflexes are lost. Jaw tone relaxes progressively. The corneal reflex is the last to go and its loss suggests excessive depth. In horses, nystagmus suggests a light plane (though ketamine also produces it), and a brisk palpebral reflex, tearing and a rising respiratory rate suggest lightening. In cattle the eyeball rotates ventrally at light and medium planes and returns to a central position as depth increases. Ketamine keeps the eyes central and reflexes brisk, which misleads the inexperienced.
Autonomic responses to surgical stimulation (a rise in heart rate, blood pressure or respiratory rate) indicate inadequate depth or analgesia. Before deepening the inhalant, the anaesthetist should consider whether more analgesia, rather than more hypnosis, is what the patient needs.
The minimum monitoring standard of every veterinary anaesthesia body is continuous attention by a trained person and a written record at regular intervals, commonly every five minutes. Heart rate and rhythm are checked by auscultation, oesophageal stethoscope or electrocardiogram. Pulse quality and mucous membrane colour and capillary refill time give a rough guide to perfusion.
Arterial blood pressure is the most important cardiovascular variable in the anaesthetised patient. A mean arterial pressure (MAP) of at least 60 mmHg is the usual target in small animals to maintain renal and cerebral perfusion; in horses a MAP of 70 mmHg or higher is targeted because hypotension is associated with post-anaesthetic myopathy. MAP is estimated as diastolic pressure plus one third of the pulse pressure. Direct measurement uses an arterial catheter (the dorsal pedal artery in dogs; the facial, transverse facial or metatarsal arteries in horses; the auricular artery in ruminants). Indirect methods are Doppler ultrasonography, which gives systolic pressure in dogs, and oscillometry. The cuff width should be about 40 percent of the limb circumference in dogs; a cuff that is too narrow over-reads and one too wide under-reads.
Pulse oximetry measures the saturation of haemoglobin with oxygen (SpO2). Values of 95 percent or more are normal; 90 percent corresponds roughly to an arterial oxygen tension (PaO2) of 60 mmHg, the conventional threshold of hypoxaemia. Capnography measures end-tidal carbon dioxide (EtCO2), which approximates arterial carbon dioxide tension (PaCO2) and so reports ventilation: normal is about 35 to 45 mmHg. A gradual rise indicates hypoventilation; a sudden fall to zero indicates disconnection, extubation, oesophageal intubation or cardiac arrest; a baseline above zero indicates rebreathing. Arterial blood gas analysis gives PaO2, PaCO2 and pH directly; a patient on 100 percent oxygen with healthy lungs should have a PaO2 near five times the inspired percentage, about 500 mmHg.
Hypothermia is the commonest complication of anaesthesia in small animals. It slows drug metabolism, reduces MAC, delays recovery, impairs coagulation and immunity, and causes shivering that increases oxygen demand. Warm-air blankets, circulating warm-water pads, insulated surfaces, warmed fluids and minimising clipping and skin preparation reduce heat loss; electric heat pads without a thermostat cause burns.
Intraoperative crystalloid rates have been lowered in recent guidelines; the 2013 AAHA/AAFP fluid therapy guidelines suggested starting at about 5 mL/kg/h in dogs and 3 mL/kg/h in cats and adjusting to the patient — confirm against the product label and your national formulary. Urine output of about 1 to 2 mL/kg/h indicates adequate renal perfusion.
Recovery is part of anaesthesia; in large studies of dogs and cats, a large share of anaesthetic deaths occur in the first hours after the end of the procedure. Monitoring continues until the animal can maintain its own airway, is normothermic and is comfortable. Brachycephalic dogs are extubated late, when they can swallow and lift the head. Horses are recovered in a padded box, sometimes with head and tail ropes, and the quality of recovery is scored.
Hypotension (MAP below 60 mmHg in small animals) is treated by finding the cause. The first step is usually to reduce the inhalant concentration, supplementing analgesia with an opioid or local block if needed. Hypovolaemia is corrected with a crystalloid or colloid bolus; bradycardia is treated with an anticholinergic unless it is a reflex response to alpha-2 induced vasoconstriction; poor contractility is supported with a positive inotrope such as dobutamine; and vasodilation may need a vasopressor such as noradrenaline, phenylephrine or vasopressin. Dopamine and ephedrine have mixed effects and are also used.
Hypoventilation means PaCO2 or EtCO2 above about 45 to 50 mmHg. It is expected with most anaesthetic drugs and is worsened by obesity, abdominal distension and dorsal recumbency. Moderate hypercapnia is tolerated, but severe hypercapnia causes acidosis and arrhythmias and is treated by intermittent positive pressure ventilation (IPPV), manual or mechanical. Typical settings in dogs are a tidal volume around 10 to 15 mL/kg with a peak inspiratory pressure that avoids barotrauma.
Hypoxaemia (PaO2 below 60 mmHg, SpO2 below 90 percent) can result from low inspired oxygen, hypoventilation, ventilation-perfusion mismatch, shunt or diffusion impairment. Checks begin with the machine and airway (oxygen supply, disconnection, kinked or displaced tube, endobronchial intubation) and move to the patient. Horses in dorsal or lateral recumbency develop large areas of atelectasis in dependent lung and ventilation-perfusion mismatch, so hypoxaemia is common in them even on high inspired oxygen.
The Reassessment Campaign on Veterinary Resuscitation (RECOVER), first published in 2012 and updated since, set the evidence-based standard for dogs and cats. Basic life support comes first: chest compressions at 100 to 120 per minute, compressing about one third to one half of the chest width, in two-minute cycles without interruption, with the animal in lateral recumbency (dorsal for barrel-chested dogs, where compression is over the sternum), and ventilation through an endotracheal tube at about 10 breaths per minute. Compressors rotate each cycle.
Advanced life support includes monitoring with electrocardiogram and capnography (EtCO2 above about 15 to 20 mmHg suggests effective compressions and a sudden rise suggests return of spontaneous circulation), vascular access and drugs. RECOVER recommends low-dose adrenaline (epinephrine) at 0.01 mg/kg intravenously every other basic life support cycle, and atropine at 0.04 mg/kg for arrest associated with high vagal tone — confirm against the product label and your national formulary. Ventricular fibrillation and pulseless ventricular tachycardia are treated by electrical defibrillation. Reversal agents for any opioid, benzodiazepine or alpha-2 agonist given should be administered, and the volatile agent turned off. A common calculation slip is confusing adrenaline 1 mg/mL (1:1000) with the far weaker 1:10,000 preparation.
Malignant hyperthermia is a genetic disorder of the skeletal muscle ryanodine receptor (RYR1), well known in pigs as porcine stress syndrome and reported rarely in dogs, horses and other species. Volatile agents (and in some reports suxamethonium) trigger uncontrolled calcium release, causing muscle rigidity, a rapid rise in EtCO2, tachycardia, hyperthermia, hyperkalaemia and death. Treatment is to stop the volatile agent, change to a clean circuit, cool the animal, correct acidosis and hyperkalaemia and give dantrolene.
In ruminants, regurgitation of rumen content and ruminal tympany are the main dangers; they are managed by fasting, a cuffed endotracheal tube placed quickly, positioning the head with the poll raised and the mouth sloping downward so saliva and fluid drain away, and passing a stomach tube if bloat develops. In horses, post-anaesthetic myopathy (associated with hypotension, heavy muscle mass and long procedures) and peripheral neuropathy (for example radial or facial nerve paralysis from compression) are prevented by good padding and positioning, maintaining blood pressure and keeping procedures short. Cats are prone to laryngospasm at intubation, prevented by topical lidocaine on the larynx. Cats whose mouths are held wide open with spring-loaded gags have developed post-anaesthetic blindness, attributed to compromised maxillary artery flow. Brachycephalic dogs obstruct at induction and recovery. Cats with urethral obstruction may be hyperkalaemic, with bradycardia and arrhythmias, and are stabilised before anaesthesia.
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Nociception, the neural process of encoding a noxious stimulus, has four steps: transduction (conversion of the stimulus to electrical activity at nociceptors), transmission (along A-delta and C fibres to the dorsal horn and up the spinal tracts), modulation (amplification or inhibition in the dorsal horn and by descending pathways) and perception (the conscious experience in the cortex). Anaesthetised animals have nociception but not perception.
Tissue injury releases mediators (prostaglandins, bradykinin, histamine, substance P) that lower nociceptor thresholds: this is peripheral sensitisation. Repeated C-fibre input to the dorsal horn activates NMDA receptors and produces wind-up and central sensitisation, in which pain is amplified and spreads, and normally innocuous touch becomes painful (allodynia) or painful stimuli become more painful (hyperalgesia). Analgesics given before and throughout the injury and continued afterwards reduce sensitisation; this is preventive analgesia. Each step of the pathway is a target: NSAIDs and local anaesthetics act at transduction and transmission, opioids and alpha-2 agonists at modulation in the dorsal horn and elsewhere, and ketamine at NMDA receptors that sustain central sensitisation.
Animals cannot report pain, so it is inferred from behaviour and physiology. Heart rate, respiratory rate and blood pressure are unreliable on their own because fear, stress and drugs also change them. Simple scales include the simple descriptive scale, the numerical rating scale and the visual analogue scale; they depend heavily on the observer. Composite scales combine several validated behaviours and give intervention thresholds.
The Glasgow Composite Measure Pain Scale short form (CMPS-SF) for acute pain in dogs scores posture, vocalisation, attention to the wound, mobility, response to touch, demeanour and activity. The maximum is 24, or 20 when mobility cannot be assessed; the suggested threshold for analgesic intervention is 6 of 24 or 5 of 20. The Glasgow feline composite scale has a maximum of 20 with an intervention threshold of 5. The UNESP-Botucatu multidimensional composite pain scale was validated for postoperative pain in cats, and the Colorado State University acute pain scales are widely used in practice. The Feline Grimace Scale scores five facial action units (ear position, orbital tightening, muzzle tension, whisker position and head position) from 0 to 2 each, total 10; a score of 4 or more suggests rescue analgesia is needed. Chronic pain, mostly osteoarthritis, is assessed with owner questionnaires such as the Canine Brief Pain Inventory, the Helsinki Chronic Pain Index, the Liverpool Osteoarthritis in Dogs index and the Feline Musculoskeletal Pain Index.
In horses, the Composite Pain Scale and facial-expression scales such as the Horse Grimace Scale and the Equine Utrecht University Scale for Facial Assessment of Pain are used for acute and postoperative pain; colic pain is also assessed with specific scales. Grimace scales were first developed for laboratory mice and then extended to rats, rabbits, sheep, piglets and other species. In cattle, sheep and pigs, the UNESP-Botucatu family includes scales for postoperative pain in cattle and sheep, and behaviour such as reduced feed intake, weight shifting, lameness scoring, tail flicking and head position after disbudding are used in research and on farm. Whatever scale is used, it should be validated in that species for that type of pain, applied by trained staff at set intervals, and linked to an action plan: a score above threshold leads to analgesia and re-scoring. Scoring is also repeated after each analgesic dose, so that the scale records response to treatment and not just the presence of pain.
Multimodal analgesia combines drugs acting at different points on the pain pathway so that each can be given at a lower dose with fewer side effects. Opioids are the foundation for moderate to severe acute pain. Full mu agonists (morphine, methadone, hydromorphone, fentanyl, pethidine) give the greatest analgesia. Methadone is also an NMDA antagonist and rarely causes vomiting; morphine and hydromorphone commonly cause vomiting when given before surgery. Fentanyl is short-acting and is given by infusion. Buprenorphine is a partial mu agonist with slow onset, long duration, high receptor affinity (which makes it hard to displace by other opioids or naloxone) and a ceiling to its effect; in cats it is well absorbed through the oral mucosa. Butorphanol is a kappa agonist and mu antagonist; it is a good sedative and antitussive but a short-acting analgesic with limited effect on somatic pain. Naloxone is a pure antagonist.
Opioid adverse effects include respiratory depression (clinically modest in healthy dogs and cats, more important with other depressants or intracranial disease), bradycardia, panting, nausea, reduced gut motility, urinary retention and excitement in cats and horses at high doses; hyperthermia has been reported in cats given hydromorphone. In horses, opioids can cause increased locomotor activity and reduced gut motility and are usually combined with alpha-2 agonists. Opioid use in food-producing animals is restricted in many countries, and some opioids are controlled drugs whose storage and records are regulated.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX), reducing prostaglandin synthesis. Drugs more selective for COX-2 aim to spare the protective COX-1 functions in gastric mucosa, kidney and platelets. Adverse effects are gastrointestinal ulceration, renal injury (especially with hypotension or hypovolaemia) and, for some drugs, reduced platelet function and hepatotoxicity. They should not be combined with corticosteroids or other NSAIDs and should be withheld from dehydrated, hypotensive or renal patients until those problems are corrected. Cats have limited glucuronidation capacity, so NSAID duration is restricted to licensed regimens, and paracetamol (acetaminophen) is toxic to cats, causing methaemoglobinaemia and Heinz-body anaemia. Grapiprant is a prostaglandin EP4 receptor antagonist rather than a COX inhibitor. Monoclonal antibodies against nerve growth factor are now used for osteoarthritis pain in dogs and cats.
In food animals, only certain NSAIDs are licensed and withdrawal periods apply; the list differs by country. Phenylbutazone is prohibited in food-producing animals in the EU, and in the United States its use in female dairy cattle 20 months of age or older is prohibited.
Adjuncts include ketamine at subanaesthetic infusion doses (NMDA antagonism), lidocaine infusion in dogs and horses (analgesic and prokinetic in horses; used cautiously or avoided in cats because of cardiovascular depression), alpha-2 agonists at low doses, gabapentin and amantadine for chronic or neuropathic pain, and tramadol, whose active metabolite is formed more reliably in cats than dogs. Local and regional anaesthesia is the most effective way to block nociception completely and should be part of every protocol where a block is feasible, from dental nerve blocks and testicular blocks in dogs and cats to limb blocks and wound catheters.
A typical protocol for a healthy dog or cat is premedication with a sedative (an alpha-2 agonist or acepromazine) plus an opioid; intravenous catheter; induction with propofol or alfaxalone to effect, sometimes with a benzodiazepine co-induction; intubation and maintenance with isoflurane or sevoflurane in oxygen; local blocks; an NSAID when the patient is normovolaemic and has no contraindication; and pain scoring in recovery. Cats are intubated gently after topical lidocaine to the larynx, with an uncuffed or carefully inflated cuffed tube, because tracheal tears occur after over-inflated cuffs or when the patient is turned without disconnecting the circuit.
Brachycephalic dogs (with stenotic nares, elongated soft palate and everted laryngeal saccules) are preoxygenated, induced quickly with the intubation equipment ready, and extubated as late as possible. Sighthounds recover slowly from thiobarbiturates. Neonatal and paediatric patients have limited glycogen stores, immature hepatic metabolism and high oxygen demand, so they are fasted briefly, kept warm and given glucose-containing fluids if needed. Geriatric patients have reduced organ reserve and need lower doses.
Standing sedation with an alpha-2 agonist, often with butorphanol, is used for many procedures. General anaesthesia carries a higher mortality in horses than in dogs and cats; the Confidential Enquiry into Perioperative Equine Fatalities reported a death rate of about 0.9 percent for procedures other than colic surgery and a considerably higher rate when emergency colic cases were included. Induction follows deep alpha-2 sedation with ketamine and a benzodiazepine or guaifenesin; maintenance is with an inhalant in a large-animal circle or with TIVA. Horses are positioned on thick padding with the lower forelimb pulled forward in lateral recumbency to protect the radial nerve, the head supported to protect the facial nerve, and mean arterial pressure kept at 70 mmHg or above, often with a dobutamine infusion. Recovery is the most dangerous phase, because the horse tries to stand before it is coordinated; alpha-2 agonist sedation in recovery, a quiet padded box, and assisted recovery with ropes are used.
Cattle are best managed standing with sedation and local or regional anaesthesia wherever possible. If general anaesthesia is needed, food is withheld (often 12 to 24 hours in calves and longer in adults, with shorter water restriction; recommendations vary), an endotracheal tube is placed by palpation or laryngoscopy, the head is positioned for drainage and the rumen is decompressed if needed. Xylazine is used at about one tenth of the equine dose. Small ruminants are prone to hypoxaemia with alpha-2 agonists, sensitive to lidocaine and, in sheep, easily stressed by handling. Food-animal drug use is limited by licensing and withdrawal periods, so drug choice must account for when the animal or its milk will enter the food chain.
Pigs have few accessible superficial veins (the ear veins are used), a long narrow larynx with a pharyngeal diverticulum that makes intubation difficult, a tendency to hyperthermia, and in susceptible lines malignant hyperthermia. Intramuscular sedation with azaperone or an alpha-2 agonist, combined with ketamine or tiletamine-zolazepam, is usual, followed by injectable or inhalant maintenance. Castration of piglets is increasingly required to be done with anaesthesia and analgesia; national rules differ widely.
Birds have air sacs and no diaphragm; ventilation depends on movement of the keel and ribs, so restraint that restricts the keel can suffocate them. Complete tracheal rings mean that cuffed tubes are avoided or inflated with great care. Isoflurane or sevoflurane by mask is the usual induction, apnoea is common and IPPV is often needed, and body heat is lost rapidly. Rabbits breath-hold when exposed to the smell of volatile agents, which can cause hypoxaemia and bradycardia, so injectable premedication and induction are often used; they are hard to intubate because of a long, narrow oropharynx, and supraglottic airway devices are an option. They are not fasted, and post-operative ileus is prevented with analgesia and early feeding. Reptiles have a temperature-dependent metabolism, so they must be kept within their preferred temperature range, and they can breath-hold and shunt blood away from the lungs, making induction with inhalants slow; injectable induction is usual and IPPV during recovery helps to eliminate the inhalant.
In clinics you will be asked to take a pre-anaesthetic history, assign an ASA grade, calculate doses and volumes for premedication and induction, check the anaesthetic machine for leaks, choose a breathing system and fresh gas flow for the patient's weight, and fill in the anaesthetic record every five minutes. On large animals you will place a caudal epidural in a cow, locate the cornual nerve for disbudding and learn the landmarks for proximal and distal paravertebral blocks. Learn the nerve-block sites, the antagonist for every sedative, what a normal capnogram looks like and the thresholds for hypotension and hypoxaemia until they are automatic, because each is asked in almost every exam and each is used in the first week of practice.
Five years into practice you anaesthetise several animals a day, often with one nurse. Your decisions are protocol choices: which premedication for an anxious brachycephalic, whether an older cat with renal disease should have an NSAID, how to anaesthetise a hypovolaemic dog with a pyometra, and how to keep a calf comfortable after disbudding within the drug licensing of your country. You write pain-scoring into the hospital routine, use local blocks for dental extractions and castrations, run infusions with checked calculations, and respond to hypotension and apnoea without panic. You also review your own complications and your practice's anaesthetic deaths.
With twenty-five years of work you set the anaesthetic standards of a hospital, a herd-health practice or a state veterinary service. You write standard operating procedures for machine checks, monitoring and emergency drugs; decide which drugs the practice stocks and how controlled drugs are recorded; train nurses, paraveterinarians and new graduates; and take responsibility for welfare-driven changes such as analgesia for castration and disbudding. You handle the difficult cases: the colic horse with endotoxaemia, the camelid, the cow needing general anaesthesia, the brachycephalic in respiratory crisis. You audit mortality and near-misses and change practice when the data require it.
A researcher with a PhD and long experience works on questions the textbooks leave open: validating pain scales in species that lack them, pharmacokinetics of analgesics in food animals so that withdrawal periods can be set, mechanisms of equine post-anaesthetic myopathy and hypoxaemia, safer field anaesthesia for livestock and wildlife, and the ethics and economics of analgesia on farms. Such a person designs randomised, blinded clinical trials with appropriate power, advises regulators on drug licensing and welfare law, sits on specialist college examination boards and writes the guidelines, such as those for fluid therapy, pain management and resuscitation, that practitioners then follow.
This manual gives the principles and the standard textbook facts. It does not give a full dose table for any species: the few doses included are standard values and must be checked against the product label and the national formulary, and drug availability, licensing, controlled-drug law and food-animal withdrawal periods differ by country and are not listed. It does not yet cover neuromuscular blocking agents and their monitoring in detail, one-lung ventilation, anaesthesia for specific diseases (cardiac, hepatic, renal, endocrine, intracranial) beyond brief notes, detailed limb and dental nerve-block techniques in dogs, cats and horses, ultrasound-guided regional anaesthesia, camelid, wildlife and zoo-animal immobilisation (including potent opioids such as etorphine), fish and amphibian anaesthesia, euthanasia methods, or the law on anaesthesia for castration and disbudding country by country. MAC values and partition coefficients are approximate textbook figures and differ slightly between sources.
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 calculation questions are for arithmetic practice — confirm against the product label and your national formulary.
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