Alison Bennell1, Kate Loomes2, and Marie Rippingale3 1 Philip Leverhulme Equine Hospital, University of Liverpool, Wirral, UK 2 Rainbow Equine Hospital, Malton, UK 3 Bottle Green Training Ltd, Derby, UK Anaesthesia is defined as: ‘the loss of sensation in a part or the whole body by controlled, reversible suppression of the central nervous system’. Anaesthesia and analgesia are essential for modern‐day veterinary practice, ensuring patient welfare, providing chemical restraint or immobility, and ensuring that required legal responsibilities are met. Equine anaesthesia is challenging and rewarding however, morbidity and mortality rates still remain high when compared to many other domesticated species [3]. Anaesthesia can be provided or facilitated in equine patients in a variety of ways which include: GA: a state of controlled unconsciousness caused by reversible suppression of the central nervous system (CNS) Epidural (extradural) anaesthesia: a drug is injected into the extradural space of the spinal canal (this is the space outside the dura mater, which is the outermost layer of the meninges). This is different from a spinal injection, where the injection is performed into the subarachnoid space (this is the space inside of the arachnoid mater, which is the middle layer of the meninges and contains the cerebrospinal fluid which bathes the spinal cord). Spinal injections are performed very uncommonly in horses. For further information, see Chapter 12. Noteworthy points about epidural anaesthesia are: Local anaesthesia: reversible block of neural transmission (sensory and/or motor function). Many methods to administer local anaesthetics are available: Other points to consider are as follows: Dissociative anaesthesia: a type of anaesthesia characterised by catalepsy, catatonia, analgesia and amnesia. The drug interferes with the transmission of sensory information into the cerebral cortex. Ketamine is the main dissociative drug used in equine anaesthesia. As horses are a prey species with a strong fight or flight response, it can be dangerous for them and personnel when trying to perform certain procedures, even if those procedures are non‐painful. Sedative agents can be used, and these decrease the response to external stimuli to allow a range of procedures to be undertaken safely, from diagnostic imaging to invasive surgeries, when adequate pain relief is also administered. It is worth always remembering that sedated horses are not always entirely predictable or safe, and they can still move suddenly and quickly, with minimal warning, and this can cause injury to personnel, the patients and damage to equipment. Common sedative drugs used in horses for standing sedation include the phenothiazine acepromazine, alpha‐2 adrenoceptor agonists and opioids. Additional analgesic drugs and the administration of local anaesthetics are also required to desensitise areas for surgery and ensure that pain is abolished or minimised. For short procedures, horses are often sedated with a single bolus of sedation, a one‐off IV injection, for example, which will allow sufficient time for the procedure to be completed. For longer procedures, additional boluses, or ‘top‐up doses’, usually a smaller dose than the initial one, may be required. This will inevitably cause peaks and troughs in the level of sedation, when the horse will be most deeply sedated shortly after drug administration, and as the sedative drugs ‘wears off’ (via drug redistribution, metabolism and excretion discussed later), the horse becomes more lightly sedated. Another method to maintain a steadier plane of sedation for longer procedures is to administer drugs as a constant rate infusion (CRI) via an ongoing IV drip or by fluid pump, or syringe driver, to continually administer low doses of drug to the patient, to avoid periods of excessively deep or light sedation. Various routes of administration exist for sedation and anaesthetic agents. These include: Different routes of administration will cause variability in the rate of drug uptake and the amount of drug delivered to target tissues. Many complex factors will influence drug availability, such as concentration at the site of administration, local blood flow, drug pKa, drug molecule size, pH of the surrounding fluid and surface area of the absorptive site. IV administration of drugs means the whole dose is administered directly into the circulation immediately, so it is often the route of choice for many drugs (see Chapter 9 for further information). The altered CNS function is the cornerstone of anaesthesia, and anaesthetic agents reduce consciousness and perception. Drugs can do this in two ways: For drugs to reach their target organ, they must first gain entry to the systemic circulation, where they will then be delivered around the body. As the main desired effect of most anaesthetic agents is action within the CNS, these drugs must first traverse the blood–brain barrier, which is present along the microvasculature of the CNS and presents a diffusion barrier which impedes the influx of many compounds from blood to the brain. The respiratory system functions to supply oxygen to the body and eliminate the waste produced as carbon dioxide. Oxygen is needed for cellular respiration, the process of energy production through metabolic reactions which takes place in cells. Energy from nutrients and oxygen combine to make adenosine triphosphate (ATP), which is used on a cellular level as an energy source. Water and carbon dioxide are the waste products made during aerobic metabolism. The critical oxygen tension is the level that is required for metabolic consumption to prevent tissue hypoxia. When oxygen levels in the body fall below a certain level, such as during intense exercise, the body also relies on anaerobic metabolism to produce energy from carbohydrates. This process requires different cellular processes and produces lactic acid as a waste product. Oxygen is therefore vital to life, and respiratory function, including gas exchange in the alveoli, must continually occur to provide oxygen to the body. Some anaesthetic agents can be delivered to the respiratory system, and are inhaled to get into the bloodstream. These volatile anaesthetic agents are vital as a method of maintaining GA. In terms of respiratory function, anaesthesia depresses the ventilatory response to hypercapnia, has effects on pulmonary gas exchange, can change bronchial muscle tone (bronchoconstrict or bronchodilate) and in combination with a large animal being placed in lateral or dorsal recumbency, will reduce functional residual capacity and can cause significant hypercapnia and hypoxaemia. As Guedel documented in the early 1900s, with increasing anaesthetic depth, cardiorespiratory function decreases [4]. One of the aims of anaesthesia is to maintain the functions of the autonomic nervous system, in a state of relative normality, but many anaesthetic drugs have profound effects on cardiovascular and respiratory function. Anaesthesia can affect cardiac output, heart rate, systemic vascular resistance (vasodilation or vasoconstriction), myocardial contractility and cardiac conduction. There are three components of the Nervous System: Anaesthetic drugs have wide‐ranging effects, not only the effects aimed at the CNS. The ANS regulates involuntary physiological processes such as heart rate, respiration, blood pressure, digestion, reproduction and this will also be affected by many of the anaesthetic drugs used. Generally, anaesthetic agents used for induction of anaesthesia and anaesthetic maintenance will depress these systems, especially at higher doses. When performing any anaesthetic, it is worth remembering the common complications associated with anaesthesia and depression of homeostatic mechanisms, particularly the three H’s which are defined as: Anaesthesia can also affect other organs, with the liver and kidneys also being worthy of consideration. Both these organs require significant blood flow to maintain normal function, so changes in blood pressure can affect their function greatly, especially renal function. Conversely, renal and hepatic functions are also vital for the metabolism and excretion of many of the drugs used, and any dysfunction can cause an accumulation of drugs, which can be problematic for a smooth and swift recovery. Pain is defined by the International Association for the Study of Pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’ [5]. Recognition and treatment of pain are pivotal to optimise the welfare of our patients, particularly in the peri‐operative period. The pain pathway is complex and acute pain, which can be beneficial to protect against further injury, and it occurs when there is tissue damage in the body. Persistent pain, on the contrary, is deleterious to health and can result in distress. Nociceptors (pain receptors) are located in many tissues such as skin, muscle, joints, periosteum and other soft tissues. Tissue damage can be physical (pressure, ischaemia), thermal (hot, cold) or chemical (when pain‐producing/inflammatory substances are released around nerve fibres). Once nociceptors receive input in peripheral tissues, the signal is then converted into an electrical signal (transduction), which is then transmitted along nerves to the spinal cord (transmission). Modulation of this information occurs at various sites within the CNS, and this step is responsible for hypoalgesia (reduced sensation when it is protective, e.g. allowing an animal to run away from a predator) but is also involved in the development of persistent pain states, including hyperalgesia (abnormally heightened sensitivity to pain) and allodynia (pain due to a stimulus that does not normally provoke pain). This information is finally passed to higher centres, and pain is perceived at a conscious level (see Figure 10.1). Figure 10.1 Simplified pain pathway. Source: Adapted from Wiley. Many drugs exert their effect on part of the pain pathway, to alter the signals produced and aim to decrease the level of pain perceived by the animal. It is important to remember that in an animal under GA, although pain cannot be perceived by the unconscious brain, the rest of the pain pathway is still ‘in action’, so when that animal recovers, pain is then perceived and can be distressing. This emphasises the need for adequate pain control in all patients. Pain scoring systems have gained popularity over the past few years [2] and are a useful tool to help improve pain recognition, especially in horses, who as a prey species, do not always demonstrate pain behaviours in the same way other companion species do. See Chapter 14 for more information on pain scoring. Analgesics can work on several different parts of the pain pathway, including nociceptors, the spinal pathways and the brain (Figure 10.2). Figure 10.2 Action of different analgesics at different parts of the pain pathway. Source: Dr Alison Bennell. Local anaesthetics prevent nociceptor activation and stop pain at sites of signal transmission. Non‐steroidal anti‐inflammatory drugs (NSAIDs) reduce nociceptor stimulation, by reducing inflammatory mediators. Many agents act at the modulation stage, impacting transmission to the brain. These include N‐methyl‐D‐aspartate (NMDA) antagonists, opioids, alpha‐2 agonists and gabapentin [6]. Pre‐emptive analgesia is a concept where antinociceptive/analgesic drugs/techniques are administered prior to the painful stimulus/surgery. The aim is to prevent ‘wind up’, which is the sensitisation of the nervous system to further stimuli that can amplify pain. Persistent pain is well‐recognised and problematic to treat, and the aim of timely and effective analgesia is to minimise the risk of animals developing chronic pain states. Multimodal analgesia is the use of two or more pharmacological classes of analgesic drugs, to target different receptors/areas of the pain pathway to lead to improved efficacy of analgesia, while minimising side‐effects of individual drugs. NSAIDs, opioids and alpha‐2 agonists are commonly used, alongside drugs such as ketamine [7]. Recovery from anaesthesia is dependent on many factors, and is determined by the speed of drug redistribution and clearance. Initial recovery from the effect of drugs can be seen when the drug is removed from the circulation and redistributed to other body tissues, including lean muscle and fat. The drug is then eliminated from the body, via excretion, metabolism or both. Emergence from volatile anaesthesia is dependent upon pulmonary elimination of the inhalational agent, which is determined by alveolar ventilation, pulmonary blood flow, the solubility of the volatile agent and the duration of administration. Volatile agents undergo minimal metabolism, and metabolism occurs in the liver and kidneys. Injectable agents need to be cleared from the systemic circulation, and their redistribution and elimination will be influenced by their drug properties (protein binding and lipid solubility), patient pathophysiological states (obesity, pregnancy, age), perfusion to organs responsible for metabolism and excretion and the functional status of clearance organs (metabolism may be delayed in patients with hepatic dysfunction). The term balanced anaesthesia is a term given to a drug protocol addressing the needs of the patient throughout the perianaesthetic period. The use of several different classes of drug give rise to a multimodal approach, reaping the benefits of multiple drugs, while aiming to reduce the likelihood of negative side effects of each drug, as smaller doses can be used for each. GA consists of a triad of: The ideal anaesthetic agent produces all three of the above, with no side effects, but this is almost impossible to achieve without causing undesirable adverse effects. This means instead, multiple drugs with specific actions are often used, to provide effective and safe anaesthesia, while aiming to minimise the risk of unwanted side effects. Premedication, the pre‐operative administration of drugs to decrease patient stress levels and improve ease of patient handling, can also decrease the requirements for other anaesthetic agents and provide analgesia, depending on the agent(s) used. A range of medications are commonly used, including phenothiazines (acepromazine), alpha‐2 agonists, opioids and NSAIDs. As a result, the entire peri‐anaesthetic period from induction through to recovery should be smoother. Usually, after premedication, horses are moderately to profoundly sedated before anaesthesia is induced. GA can be maintained via two main techniques: Volatile agents are the mainstay of anaesthetic maintenance during hospital anaesthesia, and are administered by inhalation via a breathing system. A carrier gas is a gas which passes through the vaporiser to deliver an inhalational anaesthetic agent to the patient. Oxygen is an indispensable carrier gas, as it is required for vital metabolic processes to keep the patient alive. Additive carrier gases included medical air, nitrous oxide and even gases such as xenon, although they were seldom used outside research settings due to expense. TIVA is the mainstay of field anaesthesia, as minimal equipment is needed and procedures are usually of short duration, which makes them well suited to anaesthesia being maintained with injectable agents. Several agents are available for TIVA, either alone or in combination, with ketamine, alpha‐2 agonists and guaiphenesin (GGE – a muscle relaxant), which are commonly used. When TIVA is undertaken, premedication and induction are often the same or very similar to that used with volatile maintenance. GA is then maintained with ‘top up’ doses, which means giving pre‐calculated doses of an anaesthetic drug, usually ketamine, every 10–15 minutes. This aims to achieve a suitable plasma level of the drug to maintain anaesthesia. Alpha‐2 agonists can also be administered with some top‐up doses of ketamine to help maintain sedation and smooth anaesthesia. Anaesthesia can also be maintained with an IV infusion of drugs, usually ketamine, GGE and alpha‐2 adrenoceptor agonists, a mixture commonly referred to as a ‘triple drip’. This is then administered, by a giving set, to maintain a sufficient depth of anaesthesia. The choice between methods of TIVA is largely down to personal preference, familiarity with each protocol, drugs available and length of procedure. For example, a short field anaesthetic (20 minutes) would probably lead to the wastage of a ‘triple drip’ solution after it has been made and the expense associated with said wastage. However, for longer anaesthetics, it may be more straightforward to use an infusion as it will maintain a steadier plasma level of agents and ideally a smoother plane of anaesthesia, with fewer peaks and troughs, which are associated with repeated boluses. An overview of IV verses inhalational maintenance can be found in Table 10.1. Moderate muscle relaxation is commonly achieved using various drugs in a standard anaesthetic protocol when adequate anaesthetic depth is achieved, but to enhance the degree of muscle relaxation due to anaesthetic drugs, excessive doses of these agents would need to be given. Additional muscle relaxation may be required for certain types of surgical procedures, such as ophthalmic procedures where the eye needs to be immobile and central or some orthopaedic and soft tissue procedures. Neuromuscular blocking agents (NMBAs), also known as relaxants or paralytic agents, are unique agents which cause relaxation of skeletal muscle by interfering with normal neuromuscular transmission. They do not provide analgesia, sedation or anaesthesia. Examples include atracurium and rocuronium. Table 10.1 IV versus inhalational maintenance overview. Source: Dr Alison Bennell. In 1937, Guedel described a well‐defined system pertaining to assessment of anaesthetic depth [4], with the anaesthetic agent, ether, after premedication with morphine and atropine. Stage 1: Analgesia and amnesia. From induction of GA to loss of consciousness. Stage 2: Delirium and unconsciousness. From loss of consciousness to onset of automatic breathing. Stage 3: Surgical anaesthesia. From automatic respiration to respiratory paralysis Stage 4: From apnoea (stoppage of breathing) to death. Anaesthetic overdose‐caused medullary paralysis. This system allows a basic understanding of the continuum of depth of anaesthesia, from consciousness to overdose and potential death. The introduction of newer drugs, and the use of balanced anaesthetic techniques, make the description seem rather basic, but still a useful reference to allow understanding of the consequences of using increasing dosages of an anaesthetic agent. Before a general anaesthetic is administered to a patient, pre‐anaesthetic checks and patient preparation need to be undertaken, including placing an IV catheter for further drug administration. Following this, the process of GA can be divided up into four phases: Depth of anaesthesia is a commonly used term to describe the level of CNS and autonomic depression caused by administration of anaesthetic agents. As the dose of anaesthetic agent administered increases, the depth of anaesthesia increases and level of CNS depression also increases. Monitoring CNS function by assessing reflexes, such as palpebral reflexes and anal tone, allow the anaesthetist to titrate the anaesthetic agents to the lowest possible level, while maintaining an adequate depth of anaesthesia to ensure patient welfare. There is a fine line between achieving a plane of anaesthesia required to perform procedures, and overdose, with associated adverse outcomes. Table 10.2 provides a summary of methods used to subjectively assess anaesthetic depth. Calculations are an essential everyday component of anaesthesia, from calculating drug dosages and fluid rates to calculating how much oxygen the patient needs while under anaesthesia. Calculations can be intimidating, but with practice, confidence soon follows. Table 10.2 Summary of methods used to subjectively assess anaesthetic depth. Source: Dr Alison Bennell. a Nystagmus is also present during ketamine induction and maintenance (TIVA). Palpebral reflexes are best performed in horses by gently stroking the eyelashes. Corneal reflexes are not checked due to risk of damaging the corneal surface. Calculators are helpful whenever drug calculations are required. However, if the numbers do not seem correct, calculations should be double‐checked to ensure accuracy. Calculation errors can have problematic outcomes, ranging from situations such as a mild overdose to potentially fatal overdose or significant safety issues for personnel. Gross error checks aim to minimise the potential for errors to be made. There are several ways to reduce possible errors, and these include: This calculation is needed when using non‐rebreathing breathing systems and is useful to know when considering positive pressure ventilation settings. Minute volume = tidal volume (ml) × respiratory rate (breaths per minute) The average tidal volume for a horse is 10–15 ml/kg. Respiratory rate is between 6 and 8 breaths/minute. Minute volume for a horse is approximately: 10 × 6 = 60 ml/kg bodyweight. In equine anaesthesia, rebreathing systems, such as a large animal circle, are the mainstay of administering oxygen and volatile anaesthetic agents. Occasionally, in smaller animals, or foals, a small animal circle or non‐rebreathing system may be used. Rebreathing systems require lower oxygen flow rates due to the removal of exhaled CO2 via soda lime in the circle, whereas non‐rebreathing circuits rely on a higher fresh gas flow (FGF) to remove the CO2 (and expired gases) from the circuit and into the scavenging. Using non‐rebreathing systems in horses would be impossible due to the high oxygen flow rates needed. When the patient is first placed on a rebreathing system, an initial higher FGF is used for two reasons: After the initial high FGF for approximately five minutes, the FGF can be reduced to maintenance rates as the patient only requires enough oxygen to meet the metabolic demand. Metabolic oxygen demand is 4–10 ml/kg. When the lower end of this rate is used, a leak‐proof breathing system must be used, and any losses from the circuit are added on (a side‐stream capnograph will draw approximately 200 ml/min into the monitor). Higher FGF will be needed when vaporiser settings are changed, or if just oxygen is to be administered to the patient, as this will speed up the change of volatile concentration in the breathing system. Another note to remember, only applicable to miniature horses and foals, is that flowmeters are poorly calibrated at <1 l/min, so it is wise to use this as a minimum, even if the FGF is calculated as <1 l/min. Converting units: 1000 mg = 1 g, so 1000 mcg = 1 mg, so % to mg/ml: A percentage solution is defined as the weight of the solute (in grams) per 100 ml volume of drug (also known as weight divided by volume or w/v). For example, a 2% lidocaine injection is made up of 2 g of lidocaine dissolved in 100 ml of carrier solution. and 50% glucose contains 50 g of glucose in 100 ml of carrier solution. To calculate a dose of medication: Dose (mg/kg) × patient bodyweight (kgs), then divide by drug concentration (mg/ml). For further information on calculating drug doses, see Chapter 9. IV infusions make it possible to administer medications at a low rate, continually. They are commonly used for drugs such as sedatives and analgesics and can be very useful, as they eliminate the peaks and troughs associated with intermittent dosing. There are two ways to administer IV infusions – either via a syringe driver/pump or in a small volume of IV fluids with a standard giving set. Infusion doses may be in mg/kg/minute, mg/kg/hour or mcg/kg/minute. It is often easier to work in mg/kg/hour, so it is worthwhile to calculate this first. Then take the dose (in mg/kg/hour) and multiply it by patient weight (in kg). Then, divide this by the drug concentration (in mg/ml) to get the infusion rate in ml/hour. When administering infusions via fluids and a giving set, a sensible drip rate needs to be calculated, so often a small volume of fluid is used (e.g. 500 ml/hour). To calculate the volume of the drug to add to a small volume of fluids: e.g. if 500 ml is to last 60 minutes, and a giving set is 20 drops/ml Many infusions, particularly of sedative drugs, need to be titrated to effect, but sensible starting doses are available in many texts [9]. An effective anaesthetic protocol often contains a number of different classes of drugs. As mentioned previously, the use of several different classes of drugs gives rise to a multimodal approach, where the benefits of using multiple drugs are reaped against a reduced likelihood of negative side effects occurring, as smaller doses of each drug can be used. The main properties of commonly used sedative and anaesthetic drugs are summarised in Table 10.3. It is the role of the veterinary surgeon (vet) in charge of the anaesthetic to prescribe the medication required. The administration of these medications may be delegated to a registered veterinary nurse (RVN). If ‘top up’ doses of medication are required, these should be prescribed by the vet. Top up doses can be prescribed by the vet and discussed with the RVN prior to the start of the procedure. See The British Equine Veterinary Association (BEVA) Schedule 3 guidelines for further information (details in the ‘Further reading’ section the end of this chapter). Effective sedation can be achieved with several drugs, delivered by various routes. The vet will give consideration to the horse’s temperament and the likely level of sedation required when deciding what drug and dose to choose. The external environment is a hugely important factor in achieving successful sedation, so a calm, quiet environment is optimal, with minimal interruptions. It is also worth remembering individual response to sedatives can be extremely variable. It is often easier to give more drugs if the desired effect is not achieved, as an over‐sedated horse can be a challenge to deal with. Table 10.3 Summary of the main properties of commonly used sedative and anaesthetic drugs. Source: Dr Alison Bennell. Acepromazine, a phenothiazine, exerts its mental calming effect by its actions of dopamine‐antagonism and subsequent depression of the reticular activating system of the CNS. It can be administered orally, or via the IV or the IM route. The sedation caused by acepromazine is mild, and can be unpredictable, especially when given to horses who are very stimulated or ‘wound‐up’. Acepromazine causes hypotension, so it should be avoided in horses where there is pre‐existing hypotension/hypovolaemia, for example, sick colics or patients who have suffered a significant haemorrhage. It is also contraindicated on the data sheet in breeding stallions due to the risk of priapism/paraphimosis, but as with many theoretical contraindications, it can be used after gaining informed consent from the owner if it is felt the potential benefits outweigh the potential risks of its use. The onset of action of mental calming is slow, around 30–45 minutes and it lasts for approximately 4–6 hours, but can last longer with higher doses. Acepromazine is often used in combination with other drugs, or as an initial premedicant, as it will not cause profound sedation when given alone. It provides no analgesia. Acepromazine undergoes hepatic metabolism and renal excretion. Alpha‐2 agonists are the mainstay of equine sedation. They provide predictable and dose‐dependent sedation and also have analgesic and muscle relaxant properties. Alpha‐2 adrenoceptors are found in the CNS and periphery giving rise to the clinical effects seen. Xylazine, romifidine and detomidine are licensed in the United Kingdom. All are licensed to be given by the IV route and detomidine is also licensed for IM and transmucosal administration, which is particularly useful in fractious or poorly handled horses. Xylazine has the quickest onset of action, about 2–3 minutes, compared to 5 minutes for romifidine and detomidine when given IV. Xylazine also has the shortest duration of action, about 20 minutes. Detomidine has a duration of action of around 40–60 minutes, and romifidine has around 60 minutes. After alpha‐2 agonist administration, vasoconstriction and a transient increase in blood pressure causes reflex bradycardia. Vascular tone then relaxes and blood pressure returns to near normal. Respiratory effects are largely unimportant as although animals may show a slight decrease in respiratory rate, tidal volume may increase. The muscle relaxation caused by alpha‐2 agonists in horses leads to ataxia, with romifidine generally causing the least ataxia when effective doses of alpha‐2 agonists are used. Other important side effects of alpha‐2 agonist administration include diuresis, sweating and decreased gastrointestinal motility. Alpha‐2 agonists undergo hepatic metabolism and renal excretion. Opioids are often used in sedative protocols, but are discussed in detail in the analgesia section. Benzodiazepines are discussed later as they are used as sedative drugs in foals but not in adult horses. Ketamine and thiopental are induction agents that can be used for induction of anaesthesia in horses in the United Kingdom. These drugs are often used alongside co‐induction agents, such as benzodiazepines and GGE, used for their muscle relaxant properties. Ketamine is a dissociative anaesthetic agent and is an NMDA antagonist. It is the most commonly used induction agent in horses. Dissociative anaesthesia is characterised by catalepsy, and is accompanied by nystagmus. Due to the effect of ketamine on receptors, it is also an excellent analgesic, providing analgesia at sub‐anaesthetic doses, although this only lasts for a short period of time. Horses need to be adequately sedated with alpha‐2 agonists prior to induction of anaesthesia with ketamine, or excitation can occur, which can be dangerous for both the patient and any personnel involved. In healthy animals, ketamine causes indirect stimulation of the cardiovascular system (via the sympathetic nervous system), but in unhealthy animals, myocardial depression can be seen. Respiration and respiratory reflexes are maintained after ketamine administration, with horses often demonstrating an apneustic breathing pattern (deep inspiration and inspiratory pauses). Another effect of ketamine is that muscle hypertonus is seen at/immediately after induction. Co‐administration of benzodiazepines helps to offset the muscle rigidity, smoothing the process of induction and inducing recumbency. This makes placing a mouth gag and subsequent tracheal intubation easier. This effect also facilitates the hoisting and transportation of horses into the theatre. Ketamine has a relatively short onset of action, of approximately 60–90 seconds and duration of action is 10–20 minutes. Ketamine is rapidly redistributed to tissues from the CNS, so recovery can be rapid. It undergoes hepatic metabolism and renal excretion, and when prolonged infusions are used, the production of an active metabolite, norketamine, can accumulate and cause poor‐quality recoveries. For this reason, TIVA protocols with ketamine are kept under 60 minutes duration. Thiopentone is an ultra‐short‐acting barbiturate, and a GABAA agonist, which is still used in equine anaesthesia. It can be used as an IV induction agent, and is also useful when unexpected movement/a light plane of anaesthesia is encountered as it is quick acting and will deepen anaesthetic depth promptly. It has an onset of action of around 20–30 seconds and a duration of action of 10–20 minutes. Thiopentone causes a good level of muscle relaxation, and although ideally used after alpha‐2 agonist premedication, it can be used without prior sedative administration, to induce GA. Thiopentone is an extremely alkaline medication (pH 10.5), and if injected perivascularly, it can cause significant irritation and tissue sloughing, so a patent IV catheter must always be used for administration. Thiopentone will cause a reduction in myocardial contractility, can cause mild vasodilation and mild respiratory depression. Thiopentone is redistributed to tissues, and this can be limited in animals with low body fat and neonates, which can cause slower recoveries. It has no analgesic properties. Thiopentone undergoes hepatic metabolism and renal excretion. Due to slow metabolism, and its propensity to redistribute to fat, recovery can become prolonged when multiple doses or infusions are used, so it is not suitable for TIVA maintenance. There is no current UK‐licensed thiopentone for veterinary use, although there are veterinary‐licensed products available to import. Benzodiazepines are often used for co‐induction of GA as they are centrally‐acting muscle relaxants, useful in offsetting the muscle hypertonus caused by ketamine. Midazolam and diazepam are most commonly used; Midazolam is currently licensed for co‐induction of anaesthesia in the United Kingdom. Benzodiazepines also cause sedation in some species, but they are not administered as sedative agents to horses as the muscle weakness they cause produces panic, which is difficult to manage safely. They can be used in neonates, however, as they tend to lie down voluntarily after administration. Benzodiazepines have few side effects, with minimal cardiovascular or respiratory depression at clinically useful doses. They have no analgesic effects. Benzodiazepines undergo hepatic metabolism and renal excretion. GGE is another centrally acting muscle relaxant, acting on spinal cord and brainstem pathways to reduce postural muscle tone. It is commercially available as a 10% solution, which can be used for co‐induction of anaesthesia, or as part of a TIVA protocol. GGE must be administered via the IV route and is combined with anaesthetic drugs as it provides minimal sedation and no analgesia. GGE can also be a vascular irritant, so care must be taken when administering, and it is advisable to flush IV catheters well before removing them after GGE has been used, to ensure no traces are drawn through the perivascular tissues. GGE undergoes hepatic metabolism and renal excretion. Propofol and alfaxalone are anaesthetic induction agents licensed in small animal species. Although they can be used off‐license in horses, ketamine is the mainstay of equine induction agents. The volumes required of propofol and alfaxalone make them more suited to miniature horses and foals, when they can be used via the cascade. See Chapter 9 for further information regarding the cascade. In the United Kingdom, isoflurane is licensed for use in horses and is the mainstay of inhalational maintenance, but sevoflurane and desflurane can be used, when justified via the cascade. The exact mechanisms of action of volatile anaesthetic agents still remain elusive, although this is likely due to receptor‐based mechanisms. Inhalational anaesthetic agents are administered, carried in oxygen, into the respiratory tract, where they passively diffuse via the lungs into the bloodstream. Both respiratory and physical factors will determine the speed of uptake, and the amount of drug taken into the bloodstream. Once dissolved in the blood, the inhalational agent is then distributed to the organs, including the target organ, the brain, where they have to cross the blood–brain barrier to be effective. Anaesthetic potency is described by a concept known as minimum alveolar concentration (MAC). MAC describes the amount of anaesthetic agents where 50% of the sample population does not respond to noxious stimuli (e.g. skin incision) with purposeful movement. This gives a guide as to how much anaesthetic agent is required to achieve a level of anaesthetic depth where surgery can be humanely performed. MAC is inversely related to potency; therefore, a high MAC relates to an agent with a low potency. MAC values vary depending on the source; however, MAC values for commonly used inhalation agents are as follows: Volatile agents cause vasodilation and myocardial depression, leading to dose‐dependent hypotension. They are also respiratory depressants, especially in horses, so dose‐dependent hypoventilation is seen [10]. Volatile agents possess no analgesic properties. Nitrous oxide, a colourless gas which is an NMDA‐antagonist, is well recognised for its analgesic properties when inhaled. Other volatile anaesthetic agents work through different receptors and channels, so they work synergistically to cause a volatile‐sparing effect. Nitrous oxide has low anaesthetic potency, meaning a concentration of over 100% is required to achieve MAC anaesthesia, which is clearly impossible to achieve at atmospheric pressure. However, the physiochemical properties mean its use alongside volatile anaesthetic agents can speed up the onset of inhalational agents due to its ‘second gas effect’. This means as nitrous oxide diffuses rapidly across the alveolus, it concentrates the remaining alveolar gases (volatile agent, oxygen), which increases the driving pressure of volatile agent into the bloodstream. Another sequelae of nitrous oxide’s physiochemical properties is its propensity to diffuse into gas‐filled spaces. This can be particularly problematic in horses, due to the considerable amounts of gas found in a normal gastrointestinal tract, and in abnormal ones, such as commonly found in horses with colic. Diffusion hypoxia occurs when delivery of nitrous oxide ends and the direction of diffusion reverses (from blood into the alveolar space); this means that alveolar oxygen may be diluted, and therefore the animal requires pure oxygen (100%) rather than room air (20%) for at least 3 minutes after termination of nitrous oxide delivery to prevent hypoxia. Nitrous oxide has significant global warming potential and is a significant contributor to the greenhouse effect in the United Kingdom, as well as having ozone‐depleting potential. The negative environmental impact is a major reason for a recent decline in use. Nitrous oxide has also been implicated in reduced fertility and negatively impacts pregnancies in female theatre workers, so it is regulated under the Control of Substances Hazardous to Health (COSHH) regulations in the United Kingdom. As mentioned previously, oxygen is an indispensable carrier gas. Additive carrier gases include medical air, and even gases such as xenon, although they are seldom used outside research settings due to expense. Opioids, one of the oldest forms of analgesia, exert their effects by binding to opioid receptors, which are largely found in the CNS, but also peripherally in areas such as joints. Different classes of opioids are used in veterinary medicine, based on the subset of opioid receptors on which they exert their effects. Pure mu‐agonists, such as methadone, pethidine and morphine are efficacious analgesics. Partial mu‐agonists such as buprenorphine are also useful analgesics. Mu‐antagonists/kappa agonists, such as butorphanol, provide little analgesia, but are often combined with alpha‐2 agonists to aid sedation. When selecting an appropriate opioid, several factors need to be considered: legalities/licensing/the cascade, the level of analgesia desired, the drug onset and duration of action, route of administration and potential side effects. Cost and availability are also practical factors worth consideration. Opioids can be administered via several routes with IV (not pethidine), IM, intra‐articular and extradural routes all well described in the literature. At clinically used doses, cardiovascular side effects are minimal, as are respiratory effects. Opioids can cause a reduction in propulsive gastrointestinal motility and ileus, particularly with repeated dosing. Many texts discuss the possibility of opioid‐induced excitation, although this is seldom seen clinically for various reasons [11]. Painful animals are far less likely to experience opioid‐induced excitation, and in non‐painful animals the administration of sedation, such as alpha‐2 agonists, prior to opioid administration will also decrease the likelihood of this side effect. NSAIDs are the most commonly prescribed class of drugs used to treat pain in horses. Their mode of action is to block specific enzymes, cyclooxygenase or COX, which is a vital part of the arachidonic acid pathway leading to the production of prostaglandins, which are involved in inflammation. Many licensed NSAIDs are available in the United Kingdom, including phenylbutazone, flunixin, meloxicam, suxibuzone and firocoxib, to name a few. NSAIDs have recognised negative side effects, including gastrointestinal injury (gastric ulceration and right dorsal colitis) and renal injury. Gastrointestinal side effects are usually seen when high doses are used, when NSAIDs are used for long periods of time, or in foals. The choice of NSAID needs to take into consideration licensing (e.g. phenylbutazone is not to be administered to food‐producing horses), cost, route of administration, availability and palatability. NSAIDs are commonly used due to their relatively cheap cost, ease of owner administration and relatively good safety profile, particularly in healthy animals. Local anaesthetics are true analgesics as they block the transmission part of the pain pathway, so no action potential is produced in nociceptive fibres when nociceptors are stimulated. Local anaesthetics exert their actions by blocking voltage‐gated sodium channels. Many different local anaesthetics exist, with procaine, lidocaine and mepivacaine being licensed in horses, although bupivacaine is commonly used due to its longer duration of action (Table 10.4). Local anaesthetics can be used in many ways, including topical application, splash blocks, local infiltration, peripheral nerve blocks, intrathecal administration, epidural injection and IV infusion. Local anaesthetics can cause local tissue irritation and when used in high doses, can cause toxicity. This is most likely seen when IV infusion is used, or when supramaximal doses are used for local infiltration. Toxicity is seen in the CNS, and at higher doses cardiotoxicity is also seen. The use of paracetamol in the veterinary world has gained momentum over the past few years, but its analgesic mechanisms are not completely understood, and its metabolism is complex. It is largely believed that paracetamol exerts its actions via an active metabolite, AM404, which acts on vanilloid and cannabinoid receptors in the CNS. Although no equine‐licensed product is available, and there is limited literature available on its use in the horse, it can be a useful additional drug when dealing with painful equine patients. Table 10.4 Main properties of commonly used local anaesthetics. Source: Dr Alison Bennell. Gabapentin produces its analgesic actions through ion channel effects, and can be useful in persistent pain states. It can cause sedation/mental calming and ataxia. As has been discussed previously, alpha‐2 agonists [12] and ketamine also have analgesic actions. Neuromuscular blocking agents (NMBAs) are agents which paralyse skeletal muscle movement, including respiratory muscles and ocular muscles, by blocking the movement of neurotransmitters at neuromuscular junctions. They do not provide any analgesia or anaesthesia, so they must always be used in combination with anaesthetic and analgesic drugs, or the patient will be awake and aware, but unable to move. NMBAs are not commonly used in equine anaesthesia, but are indicated in some types of surgery, such as ophthalmic procedures where the eye needs to be in a central position. Horses who have had NMBAs administered will require mechanical ventilation. The effectiveness of neuromuscular blockade requires monitoring with a peripheral nerve stimulator. Some subjective components of monitoring anaesthetic depth, such as eye position, nystagmus and reflexes, are abolished when NMBAs have been administered. NMBAs are classified into depolarising and non‐depolarising agents, according to their mechanism of action: Monitoring neuromuscular function is important when NMBAs are used as it allows the assessment of the effectiveness of blockade and if repeat dosing with the NMBA is required. It will also reduce the incidence of complications associated with residual blockade in recovery, allowing the anaesthetist to decide if the block has worn off, or needs to be antagonised or reversed to ensure it is safe to attempt to recover the patient. There are several techniques used to monitor neuromuscular function, all based on the fact that NMBAs stop transmission at the neuromuscular junction and therefore muscle function. A peripheral nerve stimulator, placed with an electrode over an accessible peripheral nerve, will evoke a response in the corresponding muscle. This can then be quantified and monitored throughout the anaesthetic to monitor the effectiveness of blockade. Because NMBAs block skeletal muscle function, it is vital to ensure normal muscle function is restored prior to recovery and tracheal extubation. Ideally, the length of time the NMBA agent is active for should be matched to the specific drug chosen. However, there are times when the residual blockade is still present at the end of the procedure. In the case of non‐depolarising NMBAs, as they are competitive agonists, reversal of the drug is possible by increasing the amount of acetylcholine at the neuromuscular junction. This can be achieved by using drugs such as neostigmine or edrophonium, although commonly seen side effects include bradycardia and bronchospasm. Sugammadex, a reversal agent, is also available, which encapsulates some NMBAs, such as rocuronium, rendering it ineffective. An anaesthetic machine comprises several components (Figure 10.3). The design and arrangement of the machine and its components may influence the individual appearance of the anaesthetic machine. However, the overall functional aim of the anaesthetic machine is a common one: to deliver oxygen and inhalational anaesthetic agents to the patient in a controlled manner and to remove exhaled gases. The main components of a large animal anaesthetic machine include: Figure 10.3 Example of a large animal anaesthetic machine with a large animal circle breathing system and mechanical ventilator. Source: Dr Kate Loomes. Cylinders are made of thin‐walled seamless molybdenum steel, in which gases and vapours are stored under high pressure [13]. Compressed gas cylinders can be used to store and supply medical gases. They have several features which facilitate their safe use (Figure 10.4). Smaller size cylinders, such as size E, may be mounted on the anaesthetic machine for use in small animal patients. If cylinders are machine‐mounted, they must be clamped onto the machine by a yoke arrangement and secured tightly using a wing nut [14]. Larger cylinders, such as size J, are commonly used in large animal anaesthesia. Large‐size cylinders are not usually machine‐mounted due to their size and weight. Larger cylinders are usually stored in a location that is easy to access for delivery and safe for storage. Cylinders may be used individually or linked together to form a manifold. Cylinders forming a manifold may be divided into two groups, to allow a swift changeover from one supply to the other when one manifold is exhausted. The number of cylinders on the manifold depends on the expected demand [13]. Cylinders should be housed in a well‐ventilated room, built using fire‐proof material and located away from the main buildings of the hospital [13]. The cylinder housing should provide shelter from the extremes of temperature associated with hot and cold weather. Cylinders should not be stored near flammable materials such as oil or grease or near any source of heat [13]. The manifold room should not be used as a general cylinder store, and empty cylinders should be removed to avoid confusion [13]. Figure 10.4 Compressed gas cylinders have several features which facilitate their safe use. Source: Dr Kate Loomes. Copper alloy pipes are used to form a conduit for gas from a central supply point to regions of the hospital where medical gases are required. The gas outlets or sockets are colour and shape coded to accept the matching Schrader probes [13] (Figure 10.5). Flexible colour‐coded pipelines are used to connect the anaesthetic machine to the gas outlets [13]. The gas outlets or sockets may be wall or ceiling mounted. The probe for each gas supply has a protruding indexing collar with a unique diameter, which fits the Schrader socket assembly for the same gas only [15]. If the connection is faulty, or the wrong hose is connected to the wall Schrader valve, the hose will disconnect from the wall when pulled during the ‘tug test’ [16]. Pressure regulators are unique for each gas and are required to be fitted to all cylinders. They provide a constant low pressure suitable for delivery to the anaesthetic machine from the variable high‐pressure cylinders. The pressure delivered from a cylinder is far too high to be used safely with apparatus where a sudden surge of pressure may accidentally be delivered to the patient [14]. Pressure regulators protect the components of the anaesthetic machine against pressure surges [13]. They ensure that a constant flow rate is maintained from a cylinder irrespective of the cylinder contents [14]. Figure 10.5 The Schrader probes and gas outlets or sockets for an individual gas have a unique shape and colour to avoid errors in connection. Source: Dr Kate Loomes. The CGO delivers gas from the flowmeter and vaporiser to the anaesthetic breathing system [17]. There is usually one CGO per machine. Machines must have no more than one CGO unless there is an integral circle breathing system; in this case, the gas flow may be switched between this and the CGO [14]. The CGO may be fixed or swivelled through 90° (Cardiff Swivel) and should be robust enough to withstand the attachment of heavy equipment [14]. The swivel design of the CGO reduces the risk of disconnection or kinked tubing when either the patient or the anaesthetic machine is moved. The CGO is a standard size (22 mm male/15 mm female) allowing for connection of breathing apparatus [18]. Flowmeters are variable orifice, fixed‐pressure devices [16] which control the fresh gas flow (FGF). The FGF is the gas which enters the breathing system from the common gas outlet on the anaesthetic machine. The gas contains oxygen and an inhalational anaesthetic agent if the gas has passed through a vaporiser. Flowmeters accurately control the flow of gas through the anaesthetic machine [14]. One flowmeter is provided on the anaesthetic machine for each gas and are individually calibrated [13]. The flowmeter tubes are a specific length and diameter for each gas. The control knob is colour‐coded for each gas and is a safety feature. The tubes have an anti‐static coating on both surfaces, preventing the bobbin from sticking [15]. The tube is leak‐proofed at the top and bottom by ‘O’ rings, neoprene sockets or washers [14]. The bobbin will rise as gas flows increase and stop where gravity equals the pressure of upwards gas flow [16]. The bobbin is visible throughout the length of the tube [15]. The bobbin may have a white dot to allow observation that the bobbin is freely spinning and not lodged in the tube. The reading is taken from the top of the bobbin or if a ball is used (Figure 10.6), then the reading is usually taken from the midpoint of the ball [13]. To minimise risk of hypoxic gas mixtures being delivered to the patient, some machines will mechanically link flow‐control valves to ensure that a minimal ratio of oxygen to other gases is provided [18]. Figure 10.6 An oxygen flowmeter. Source: Dr Kate Loomes. The control knob opens a needle valve which allows gas to flow in and enter the tapered tube. The gas flowing up the tube holds the bobbin in a floating position. The higher the flow rate, the higher the bobbin position [13]. The bobbin floats and rotates inside the sight tube, without touching the sides, giving an accurate measurement of the gas flow [14]. Many inhalational agents are liquids under normal storage conditions and need to be in a vapour form before they can be administered to a patient [19]. A vaporiser adds a controlled amount of inhalational agent, after changing it from liquid to vapour, to the fresh gas flow [13]. Vaporisers can be classified according to their location ‘inside’ or ‘outside’ the breathing system: Figure 10.7 Example of a plenum vaporiser. Source: Dr Kate Loomes. The breathing system conducts oxygen and anaesthetic gases from the common gas outlet to the patient and removes exhaled gases from the patient [17]. In the equine hospital setting, a large animal circle breathing system is most commonly used for the delivery of inhalational anaesthetic agents and oxygen to maintain GA. Circle breathing systems use one‐way valves to unidirectionally route gases through the carbon dioxide absorbent material and back to the horse [17]. The optimal functioning of one‐way valves is crucial to prevent rebreathing of exhaled gases. The Waters’ to‐and‐fro system is valveless and gases are exhaled through the carbon dioxide absorbent into a rebreathing bag and drawn back through the absorbent during inhalation [17]. Advantages and disadvantages of the circle breathing system and the Waters’ to‐and‐fro system are presented in Tables 10.5 and 10.6. Table 10.5 Advantages and disadvantages of the circle breathing system. Source: Dr Kate Loomes. Various carbon‐dioxide absorbent materials are available. Soda lime can be used to absorb exhaled carbon dioxide when a circular breathing system is used. Carbon dioxide is absorbed by chemical reactions [17]. Soda lime granules are placed in an appropriately sized canister for the size of patient and the circle breathing system in use. Soda lime consists of 94% calcium hydroxide and 5% sodium hydroxide with a small amount (<0.1%) of potassium hydroxide [13]. Exhaled gases pass through the soda lime granules in the canister allowing carbon dioxide absorption to take place. An exothermic reaction occurs and water and heat are produced. The warmed and humified gas then joins the fresh gas flow to be delivered to the patient [13]. Soda lime granules undergo a pH change in response to carbon dioxide absorption, which allows the use of indicator dyes to show when the absorption capacity is exhausted [22]. The colour change is specific to each brand of soda lime and should be verified before use to avoid confusion. 1 kg of soda lime on average can absorb 250 l of carbon dioxide [22]. A canister containing 5 kg of absorbent material typically remains active for a period of 6–8 hours of GA (assuming a 450 kg horse and 5 l/min oxygen flow rate) [17]. However, the duration that carbon dioxide absorbent material is effective before it must be changed varies with the size of the horse, the individual CO2 production (metabolic rate) of the horse, the fresh gas flow and the size and location of the canister [17]. The best method of monitoring when to change carbon dioxide absorbent material is to monitor inspired gas for CO2 using a capnograph [17]. Table 10.6 Advantages and disadvantages of the to‐and‐fro system. Source: Dr Kate Loomes. The terminology used for the bag depends on the breathing system in which it is used [21]: The reservoir or rebreathing bag is the rubber bag that is situated in the breathing system. It allows the accumulation of gas during exhalation and creates a ‘reservoir’ of gas for inhalation. Patient breathing can be visualised as the reservoir/rebreathing bag deflates and inflates in time with the patient’s respiratory pattern. The reservoir/rebreathing bag should be of such a size that the capacity to which it may be easily distended must exceed the patient’s tidal volume [23] (tidal volume (VT) = 10–15 ml/kg bodyweight). The reservoir/rebreathing bag needs to be at least 2–6 times the patient’s tidal volume. The maximum volume of the bag should be 5–10 times the tidal volume [17]. The APL valve allows the escape of exhaled and surplus gases from a breathing system but does not allow entry of the outside air [22]. The pressure required to open the valve is low to minimise resistance to expiration [22]. The valve can be manually opened and closed. The ‘open’ or ‘closed’ position of the APL valve can be adjusted, which determines when the ‘escape’ pressure is reached. Ideal characteristics of an oxygen alarm include: The Ritchie Whistle was introduced in the 1960s, and forms the basis for most modern oxygen failure devices [14]. The Ritchie Whistle uses the failing oxygen supply for power and requires no other power supply [14]. The alarm is powered by an oxygen supply at a pressure of 420 kPa. When the oxygen pressure drops, the pathway of oxygen through the valve changes causing a whistle sound. This whistling sounds continuous until oxygen pressure falls to 40.5 kPa. When oxygen pressure falls to 200 kPa, the valve cuts off the supply of anaesthetic gases to the patient and allows the patient to inspire room air [14]. An emergency oxygen flush is located upstream from the back bar and flowmeters. The oxygen delivered is at high pressure and does not pass through the vaporiser [16]. It directs a high‐pressure flow of oxygen directly to the common gas outlet from the source, either pipeline or cylinder, bypassing all intermediate meters and vaporisers [15]. Barotrauma may result from accidental deployment of the emergency oxygen flush, particularly in smaller patients. Use of the emergency oxygen flush is contraindicated when a patient is connected to the machine because oxygen will be delivered at flows of 30–40 l/min and at a pressure of 400 kPa thereby putting the patient’s airways at severe risk of barotrauma. Use of the emergency oxygen flush should be restricted to the flushing of breathing systems when not connected to a patient [18]. To prevent accidental activation, the emergency oxygen flush button is usually placed in a recessed setting and will deactivate as soon as the finger activating the switch is removed [15]. The COSHH regulations sets out the legal requirements for protecting the health of people in the workplace from hazardous substances: anaesthetic gases and volatile agents are covered by COSHH. The regulations apply to people who are exposed to anaesthetic gases and volatile agents during the course of their work [24]. In order to estimate exposure in the operating theatre, the following items should be considered [24]: To ensure that the methods in place to reduce workplace exposure to anaesthetic gases are effective, regular personal exposure limits should be measured. Personal exposure levels can be measured by taking time‐weighted air samples in the breathing zone of those potentially most exposed (usually the anaesthetist). Personal diffusive sampling techniques are suitable for measuring exposure to anaesthetic agents, and the diffusive samplers are small and easily attached to clothing [24]. Minimising exposure to waste anaesthetic gases involves maintenance of equipment, training of personnel and regular routine exposure monitoring [13]. Routine leak testing of equipment should be carried out, and active scavenging should be available in locations where inhalational agents are used. Effective ventilation in operating theatres can help to control infection and also help to control exposure to anaesthetic gases. Air movement should ensure that any leakage of the anaesthetic agent is diluted and removed from the theatre environment [24]. In the United Kingdom, current recommended maximum accepted concentrations over an 8‐hour time period are: 50 particles per million (ppm) for isoflurane. Methods to reduce theatre pollution of waste anaesthetic gases include: A scavenging system is capable of collecting waste gases from the breathing system and discarding them safely [13]. They consist of several components: a collecting system, a transfer system, a receiving system and a disposal system [25]. Passive scavenging is now not recommended, but both types of systems are described to highlight the differences between systems [25]. Figure 10.8 Barnsley receiver air‐brake. Source: Marie Rippingale. Anaesthetic breathing systems function to deliver oxygen and an inhalational anaesthetic agent to the patient and remove carbon dioxide. Breathing systems can also be used to deliver controlled mechanical ventilation (CMV) to the patient. Figure 10.9 Diagram of a large animal circle breathing system showing the component parts labelled: fresh gas flow inlet (F), vaporiser (V), inspiratory (I) and expiratory (E) limbs, Y‐piece (Y), one‐way valves (O), carbon‐dioxide absorbent canister (C), rebreathing bag (B) and an adjustable pressure limiting (APL) valve. Source: Dr Kate Loomes. Anaesthetic breathing systems are broadly classified into rebreathing and non‐rebreathing systems. Equine anaesthetic breathing systems are the most commonly rebreathing systems. The two main types of rebreathing systems include the circle and the to‐and‐fro system. The circle breathing system is a very popular choice of equine anaesthetic breathing system. The circle breathing system consists of a fresh gas flow inlet, inspiratory and expiratory limbs, Y‐piece, one‐way valves, a carbon‐dioxide absorbent canister, a rebreathing bag and an APL valve. Circle systems come in different sizes: large circles (Figure 10.9) and small circles (Figure 10.10). Figure 10.10 Diagram of a small animal circle breathing system the component parts labelled: fresh gas flow inlet, inspiratory and expiratory limbs, Y‐piece, one‐way valves, carbon‐dioxide absorbent canister, rebreathing bag and an adjustable pressure limiting (APL) valve. Source: Dr Kate Loomes. Figure 10.11 Example of the Waters’ to‐and‐fro rebreathing system with the following parts labelled: connector to the patient’s endotracheal tube, fresh gas supply, adjustable pressure limiting (APL) valve, carbon dioxide absorbent canister and rebreathing bag. Source: Dr Catriona Mackenzie. Non‐rebreathing systems are mainly used in small animal anaesthesia but can be used in foals. Their use is limited to foals <25 kg bodyweight. Non‐rebreathing systems rely on fresh gas flow to maintain a one‐way flow of gases and avoid rebreathing of exhaled carbon dioxide. They do not contain carbon dioxide absorbent canisters or one‐way valves. There are several types of non‐rebreathing systems available, which are named according to Mapleson’s classifications (Tables 10.7 and 10.8). The advantages and disadvantages of non‐rebreathing systems are displayed in Table 10.9. Controlled mechanical ventilation (CMV) is routinely used in equine anaesthesia, with many different options available to facilitate the delivery of mechanical breaths [26]. In anaesthetised horses, the dose‐dependent respiratory depression produced by isoflurane [27] and the effect of recumbency may necessitate CMV to improve pulmonary function [28]. The ventilators available for use in horses may vary in design and appearance. However, they are all based on the same physical principle: the application of an inspiratory flow of gas to inflate the lungs, thereby overcoming the forces that resist thoracic expansion and the flow itself [26]. Techniques to provide ventilatory support in horses exclusively use positive pressure to expand the lungs [29]. The provision of CMV may also be referred to as intermittent positive pressure ventilation (IPPV). While CMV is a common technique employed in equine anaesthesia, there can be negative effects. During ‘normal’ spontaneous respiration, intra‐thoracic pressure is sub‐atmospheric, which favours venous return to the heart. When CMV is employed, intra‐thoracic pressure becomes positive, which reduces venous return to the heart and therefore has a negative cardiovascular effect. This effect may be particularly noticeable in hypovolaemic horses. The advantages and disadvantages of implementing CMV in healthy adult horses are displayed in Table 10.10. Table 10.7 Mapleson D (Ayre’s T‐piece and the Bain system). Source: Dr Kate Loomes. Images used with kind permission from Dr Victoria Phillips. Table 10.8 Mapleson A (Lack and Magill system). Source: Dr Kate Loomes. Images used with kind permission from Dr Victoria Phillips and Marie Rippingale. Table 10.9 The advantages and disadvantages of non‐rebreathing systems. Source: Dr Kate Loomes. Table 10.10 The advantages and disadvantages of implementing controlled mechanical ventilation in healthy adult horses. Source: Dr Kate Loomes. There are three main types of ventilators: direct blowers, bellow‐squeezers and piston‐driven ventilators [26]. Ventilator settings can be adjusted to deliver CMV, which is tailored to each horse. The variables that can be adjusted differ between ventilators. In the volume‐controlled mode, the adjustable variable is tidal volume, whereas in the pressure‐controlled mode, it is peak inspiratory pressure [29]. Other adjustable variables may include respiratory frequency (Rf), inspiratory flow rate and time, inspiratory to expiratory ratio (I : E ratio), and expiratory time [29]. The ventilator can be set to deliver a certain volume or peak inspiratory pressure at a pre‐set frequency independent of the patient’s spontaneous efforts [30]. It is important to recognise that changes in the compliance of the thoracic compartment will influence ventilator performance differently [29]. Large animal ventilators display airway pressure, but they do not measure effective tidal volume. A rough visual estimation of the tidal volume can be made using graduations on concertina‐type bellows [29]. The following formulas explain how the variables can be adjusted to tailor CMV: As a general rule, these are recommended settings for delivering CMV to an adult horse: Tidal volume = 10–15 ml/kg Respiratory frequency = 6–8 breaths per minute Peak inspiratory pressure = 20–30 cmH 2 O [29] I:E ratio 1 : 2 to 1 : 3 [33] Ventilator settings can be tailored to target arterial carbon dioxide tension (PaCO2) values of 45–60 mmHg [33]. If blood gas analysis is not available, ventilation tailored to achieve an end‐tidal carbon dioxide tension (ETCO2) of 35–45 mmHg should maintain the PaCO2 within a normal range. However, blood gas analysis is preferable to ensure that normal PaCO2 values are achieved, particularly in compromised horses [34]. CMV has significant effects on the cardiorespiratory systems and also has negative cardiovascular effects, including hypotension. A ventilator‐induced reduction in venous return may occur and is consistent with a cyclical depression in systolic arterial pressure synchronised with the ventilator cycle. This variation between pressure waves is known as pulse pressure variation and is more pronounced during CMV in hypovolaemic horses. CMV may have an unpredictable effect on arterial oxygen tension (PaO2). CMV is usually effective in correcting hypoventilation and hypercapnia. However, it is important not to cause hypocapnia. Endotracheal intubation during inhalation anaesthesia is routine in veterinary medicine. Endotracheal intubation: Endotracheal intubation is usually performed blind in horses. If assistance is required, endoscopic guidance can be used to visualise the larynx during endotracheal intubation in difficult cases. *Note: During endo/nasotracheal intubation, spontaneous respiration should be present. Horses do not typically show a period of apnoea after the induction of GA, which may be experienced in small animals where the agents used for anaesthetic induction are different. *Note: the relatively smaller airway produced by nasotracheal intubation increases the resistance to breathing. The nasal tube should be exchanged for an ETT if increased airway resistance compromises adequate ventilation or causes respiratory distress [35]. An appropriately sized ETT helps to prevent leakage of air, minimises laryngeal and/or tracheal injury and limits airway resistance [37]. Increased airway resistance can occur through the use of narrow ETT [32]. Airway resistance decreases as the ETT diameter increases. Endotracheal intubation can decrease work of breathing by bypassing the upper airway [38]. However, using an ETT with too narrow internal diameters results in an increase in resistance and work of breathing [38]. Using too large an ETT and/or excessive force to place the ETT should be avoided and this can cause tracheal/laryngeal damage [35]. Intubation using a 30 mm internal diameter ETT in an average‐sized horse (500 kg) has been documented to have a high rate of tracheal injury [36]. Selection of an appropriate ETT size develops with experience. A 20–25 mm internal diameter tube is suitable for most adult horses. Ultrasound measurements of the trachea have been used in humans to predict ETT size [39]. Further studies are needed to develop a technique to accurately measure the tracheal size in horses [37]. Correct placement of the ETT can be confirmed by the presence of airflow consistent with expiration. Horses should breathe spontaneously after induction of GA and ETT placement, so there should be no need to compress the chest to check for ETT patency. Apnoea after induction of GA and/or ETT intubation may be a cause for concern, and the reason for apnoea should be investigated immediately. Once the ETT is attached to an anaesthetic breathing system, correct ETT placement can be confirmed by visualising movement of the rebreathing bag synchronous with the horse’s inspiratory and expiratory respiratory pattern. Correct ETT placement can also be verified using capnography. If a capnograph trace of relatively normal appearance is present after connection of the breathing system to the ETT, then tracheal intubation can be confirmed. A leak around the cuff may be diagnosed using the capnograph trace. The rectangular shape of the capnograph trace will not be present as CO2 escapes around the cuff and is therefore not sampled at the Y‐piece. It is important to confirm correct ETT placement prior to connection of the ETT to the breathing system when CMV is used. This is because there is potential for gastric distension and rupture if the ETT is incorrectly placed (into the oesophagus) and CMV delivers positive pressure ventilation to the stomach via the oesophagus. The cuff on the tube should be inflated in order to prevent air leakage around the ETT, thereby avoiding room contamination with anaesthetic gas [37]. The cuff on the ETT should be inflated in order to prevent pulmonary aspiration of fluids such as gastric contents, blood or surgical lavage fluids [35]. The cuff should be inflated until no leak is discernible, and the cuff pressure should be checked using a pressure gauge to minimise tracheal epithelial damage [40]. To manually check for escape of air around the cuff, place a hand or stethoscope on the horse’s neck in the region of the cuff during a forced inspiration. If vibration is detected as air escapes around the ETT, it is likely that a leak is present [41]. The cuff is inflated with air to seal the airway when the lung is pressurised to 20–25 cmH2O. This is accomplished by connecting the patient end of the ETT to the Y‐piece of the breathing system and squeezing the rebreathing bag or compressing the ventilator bellows to develop pressure within the breathing system of 20–25 cmH2O. A leak may be present if: Reported complications of tracheal intubation in the horse include laryngeal haematomas on the epiglottis and arytenoids, swollen tongue, pharyngeal perforation, epiglottic trauma and retroversion, laryngeal mucosal damage, laryngeal paralysis/paresis [35]. Injury to the larynx and/or trachea associated with endotracheal intubation, may be caused by: Defects or weakness in the cuff can lead to asymmetric inflation and may result in cuff herniation and obstruction of the lumen of the ETT [43]. Nasotracheal intubation can cause haemorrhage in the ventral or middle meatus, with the potential for airway obstruction by blood clots as well as aspiration [40]. ETTS should be regularly inspected for signs of wear or damage. Particular attention should be paid to the cuff. Check cuff integrity prior to using an ETT on every occasion. ETTs and nasotracheal tubes (NTTs) should be cleaned as soon as possible after extubation. ETTs and NTTs for horses are expensive and not disposable [36]. Clean all tubes thoroughly inside and out. The presence of organic material impedes chemical disinfection. After being cleaned or gross contamination, tracheal tubes can be soaked in an appropriate disinfectant solution to further reduce the chance of nosocomial infection [36]. Ensure thorough rinsing of the tracheal tubes prior to storage/use. Chemical injury to the airway can be caused by residual disinfectant on the ETT or NTT. Silicone is the only material that can withstand steam autoclaving. Manufacturer recommendations for temperature and contact time should be followed [36]. Store ETTs and NTTs carefully and ensure that they are not in contact with anything. Custom‐made racks can be used to hang ETTs and NTTs. It is useful to store ETTs and NTTs in size order to facilitate rapid selection of a particular size. The performance of pre‐anaesthetic safety checks are a crucial part of pre‐anaesthetic preparation. Prior to use, ETTs and NTTs must be checked for patency and closely inspected for signs of damage. The integrity of the cuff must be verified before use on every occasion. A note should made in the patient’s anaesthetic record that the anaesthetic machine check has been performed, that appropriate monitoring is in place and functional, and that the integrity, patency and safety of the whole breathing system has been assured [18]. This verification of machine checks may be incorporated into the surgical safety checklist and performed for each patient. When TIVA is used, there must be a continuous IV infusion of anaesthetic agent or agents; interruption may result in awareness [18]. In equine anaesthesia, awareness may result in sudden movement, which can be dangerous to the horse and to personnel. Anaesthetists using TIVA must be familiar with the drugs, the technique and all equipment and disposables being used [18]. If an infusion pump is used, its function and calibration must be checked before use. Infusion lines must be correctly placed in infusion pumps and free of obstruction or points of compression. Infusion lines must be patent and primed with a solution ready for use. The drugs required for the procedure and consumables should be readily available. During TIVA sites of IV infusions should be visible so that they may be monitored for disconnection, leaks or infusion into subcutaneous tissues [18]. A responsible person or persons should be appointed to organise repair and servicing of anaesthetic equipment. Faulty equipment including the nature of the fault may be recorded in a log book or reported directly to the responsible person. Where there are multiple pieces of the same type of equipment such as infusion pumps; each individual infusion pump should be identifiable so that recurring faults affecting a single piece of equipment can be identified. Each hospital must ensure that all machines are fully serviced at the regular intervals designated by the manufacturer and that a service record is maintained [18]. As it is possible for errors to occur when reassembling an anaesthetic machine, it is essential to confirm that the machine is correctly configured for use after each service. Anaesthetists should be aware of the options available in the event of mains power failure. A backup generator should be available, and backup batteries for monitors should be available and charged. Alternative methods of ventilating a patient (for example, a rebreathing bag) should be available in the event of mechanical ventilator failure. The Association of Veterinary Anaesthetists (AVA) recommends that a dedicated anaesthetist should be available to monitor each case. The dedicated anaesthetist should be a qualified member of veterinary staff who has received anaesthesia training [46]. Basic ‘hands‐on’ monitoring of anaesthesia requires no equipment and is a core skill for every anaesthetist. Basic monitoring techniques that require no equipment, including ocular and mucous membrane assessment and pulse palpation, are recommended for every general anaesthetic procedure [47]. As technology advances, many more electronic monitoring options have become available [47]. Electronic monitoring equipment should not replace the ‘hands‐on’ approach to monitoring but may be used to complement it. An understanding of the function and limitations of monitoring equipment is crucial to enable its effective use and correct interpretation. For each case, a minimum panel of electronic monitoring, including capnography, pulse oximetry, electrocardiography (ECG) and blood pressure monitoring devices has been recommended [48]. It is recognised that anaesthesia in horses is performed in a variety of places with different facilities and using various drug combinations [47]. Table 10.12 provides a summary of electronic monitoring devices used in equine practice. Anaesthetic monitoring is covered in more detail in Section 10.5. Table 10.11 The correct steps to follow to carry out an anaesthetic machine safety checks. Source: Dr Kate Loomes. The preliminary results of The Confidential Enquiry into Perioperative Equine Fatalities 4 (CEPEF 4) study suggested that horses still carry a high risk of mortality associated with GA [3]. The total mortality from perioperative complications was found to be 1%. This is still high compared to mortality rates reported for cats and dogs. However, the preliminary data from CEPEF 4 suggested that the current mortality rate for horses is lower than 20 years ago [3]. Even though risks seem to be getting lower, consideration must be given to the fact that equine patients still carry a high risk for GA. Vets and RVNs involved with equine anaesthesia must do everything possible to reduce risk in elective and emergency patients. Table 10.12 Summary of electronic monitoring devices used in equine practice. Source: Dr Kate Loomes. Once the history has been taken, and a physical examination has been carried out (see Chapter 12), the patient should be assigned to one of the ASA physical status classes [67]. Allocation of an ASA score can help the anaesthetist to decide whether anaesthesia can proceed or whether further investigations and/or stabilisation are required first [67]. The basic ASA descriptors are given below; however, a recent veterinary version has been devised. Please see the further reading for more information. ASA physical status classes [67]: E. An ‘E’ should be added to any class to identify the patient as an emergency (where a delay in treatment will significantly increase the threat to life or limb). If pre‐operative support or stabilisation is required, this may include [68]: The patient should be monitored carefully; all treatments and observations should be recorded. If the patient is deemed fit for anaesthesia, pre‐anaesthetic preparations can proceed. It is beyond the scope of this section to discuss every specific risk and management protocol for high‐risk patients. However, the most important considerations are summarised below. Readers are directed to the texts in the reference list for further information. Horses with colic are often considered to be one of the most high risk patients to anaesthetise. The results of CEPEF 4 suggest that mortality for horses undergoing colic surgery is around 3.4%, which is high when compared to non‐colic patients at 0.6% [3]. The positive news is that fatal outcomes for colic, and non‐colic patients are less frequent than 20 years ago when the previous CEPEF study was conducted [3]. The reason colic patients are such a high risk to anaesthetise is that they often present with a wide range of physiological states, which can vary depending on the type of obstruction present. There are two types of gastrointestinal tract (GIT) obstructions: non‐strangulating and strangulating [68]. With non‐strangulating obstructions, secretions tend to accumulate in the gut lumen, leading to extracellular fluid loss, which promotes the development of hypovolaemia [68]. Bacterial fermentation of gut contents may cause a build‐up of gas. This, along with the accumulation of fluid in the gut lumen, leads to distension of the gut, and this causes pain. Distension and displacement of the gut can also put traction on the mesentery causing further pain [68]. The stretch caused to the gut wall compromises its perfusion, and it becomes ischemic, hypoxic and oedematous, compromising perfusion further. This system of events leads to the mucosa becoming ‘leaky’ and endotoxaemia and systemic inflammatory response syndrome (SIRS) occurs, which serves to complicate the initial hypovolemia further [68]. With strangulating lesions, the mucosal barrier becomes compromised more quickly, and this allows bacteria and toxins to enter the bloodstream [68]. In this case, endotoxaemia and hypovolaemia co‐exist from the start. Ischaemic bowel becomes necrotic, and peritonitis can develop as a result of this, which adds to pain levels. Hypovolaemia is initially characterised by tachycardia and weak peripheral pulses. Later on, cold, pale extremities and tachypnoea will develop. Tachypnoea helps to produce a respiratory alkalosis to compensate for the metabolic acidosis that commonly occurs. Eventually, the animal reaches a point where it can no longer compensate, and the periphery demands more perfusion. Significant vasodilation occurs, which then causes a drop in blood pressure. This loads the blood with acidic metabolites and causes the patient to deteriorate rapidly [68]. An endotoxaemic patient will present with a dull and depressed demeanour. Disseminated intravascular coagulation (DIC) may be present, and this develops secondary to the primary disease. DIC is characterised by the activation of the coagulation cascade. The disease process is dynamic with early thrombosis being followed by perfuse bleeding. Haemorrhagic diathesis (a tendency to bleed easily) is often seen, which manifests as petechiae (pinpoint spots) on mucous membranes. Congested mucous membranes and a prolonged capillary refill time may also be observed. A quick but thorough examination is required. Human safety should be a primary consideration when dealing with painful colic patients. Handlers should wear sufficient personal protective equipment (PPE) such as a hard hat, gloves and steel toe‐capped boots. The need for sedation and or analgesia should be assessed quickly. Any medication required should be prescribed by the case vet. Following this, the RVN can administer the medication. Once it is safe to do so, the following procedures can commence [68]: It is beyond the scope of this section to discuss all considerations for anaesthesia in colic patients; however, the most important considerations are summarised below. Readers are directed to the texts in the reference list for further information. Colic cases will require close monitoring and ongoing support in the first few days following surgery. Analgesia and fluid therapy are paramount to a successful recovery [68]. Acid–base and electrolyte imbalances may require attention. The patient will also require nutritional support and intensive nursing care. See Chapter 13 for further information. Horses with limb fractures pose a significant risk when presented for GA. The most significant concerns relate to guiding the horse safely into recumbency, and then successfully recovering it from recumbency to a standing position without further catastrophic injury occurring. Good analgesia will be required as these patients are often painful and agitated [68]. Slings can be used for assisted induction to safely lower the horse into recumbency. Not all horses will tolerate being put in a sling, so the temperament of the patient should be considered before this is attempted. Rope recovery should be considered for these patients to facilitate a safe transition from recumbency to standing following the anaesthetic. Neonatal foals carry specific considerations for GA. An accurate weight is essential for these patients to ensure correct drug dosing. In the first two weeks of life, cardiac output is largely dependent upon heart rate as the ventricles are less compliant. For this reason, alpha‐2 agonists should be avoided where possible, as they cause a marked reduction in heart rate and cardiac output [68]. Midazolam or diazepam may be used to provide sedation and encourage recumbency. Pulmonary hypertension should be avoided, especially in the first week of life, as a transitional circulation exists at this time. The foetal ductus arteriosus and foramen ovale are only functionally closed. Marked pulmonary hypertension can cause these structures to re‐open, creating a shift back to a foetal circulation that leads to a vicious cycle of worsening hypoxaemia [68]. Causes of pulmonary hypertension include hypovolemia, hypothermia, hypoxaemia, acidosis and pain [68]. An appropriate anaesthetic breathing circuit should be selected for example a non‐rebreathing circuit for very small foals, or a small circle for larger foals [68]. Neonatal foals are prone to hypothermia due to their large surface area to volume ratio. Heat should be conserved as much as possible, and the following should be considered [68]: Neonates are prone to hypoglycaemia as the neonatal liver has a limited ability to store glycogen and therefore has a poorly developed ability for glucogenesis. In neonatal foals, there is a high metabolic rate, which leads to a high demand for glucose [67]. For this reason, foals are rarely starved before GA. Neonatal foals are prone to gastric ulceration, and gastroprotectants should be considered in high‐risk patients. Stringent monitoring should be carried out during the anaesthetic (see Section 10.5 for details). The foal should be kept warm and dry in recovery. Oxygen administration can continue until the foal is in sternal recumbency. Foals that are 100–150 kg can be assisted to stand [69]. Once the foal is steady on its feet, it should be reunited with the dam as quickly as possible and allowed to feed. Healthy older foals can be considered more like mature horses. Alpha‐2 agonists can be used for sedation. Premedication may still result in recumbency, which can make the induction process smoother and safer for all involved [68]. Geriatric patients may have significant age‐related co‐morbidities which require consideration for anaesthetic management [69]. PPID also known as equine Cushing’s disease (ECD) (see Chapter 13 for further information) may be a consideration in a geriatric horse. Hyperglycaemia associated with PPID may cause abnormalities leading to alternations in body fluid and electrolyte imbalances. Therefore, the hydration and electrolyte status of the patient should be checked before GA, where possible [69]. PPID can cause muscle wasting and weakness in geriatric patients; therefore, careful positioning and padding should be considered under GA to reduce the chances of post‐anaesthetic myopathy (PAM) or post‐anaesthetic neuropathy (PAN) developing [69]. Some horses with PPID can develop chronic hypercortisolism, and this can lead to osteoporosis. This is a consideration for patients during recovery as the risk of developing complicating pathological fractures could be higher [69]. Assisted recovery could be used to help to address this risk. Musculoskeletal disease and lameness, specifically osteoarthritis, represent the second most frequent reason for referral and a major reason for euthanasia in geriatric horses [70]. As stated above, careful positioning and padding should be used along with rope‐assisted recovery in these cases. Multimodal analgesia should also be considered to ensure adequate comfort levels in these patients [69]. Equine asthma is the most prevalent respiratory disease seen in geriatric horses [70]. The primary anaesthetic concerns associated with equine asthma are bronchoconstriction and hypoxaemia. If a horse is presented for an elective procedure with poorly controlled asthma, the procedure should be postponed until the condition is under control [71]. In urgent or emergency cases, pre‐anaesthetic optimisation can be achieved with short‐term dose escalation of medications such as bronchodilators and steroids. Administration of inhaled salbutamol just prior to anaesthesia could be considered, which has been shown to improve oxygenation in anaesthetised horses [71]. Subsequent administration of salbutamol at the end of anaesthesia may help to reduce hypoxaemia during recovery [71]. Cardiac murmurs are detected in more than 20% of horses aged 15 years or older [69]. Geriatric horses should have a full pre‐anaesthetic clinical examination to help to identify any murmurs or arrhythmias before anaesthesia is induced. If abnormalities are detected, and it has been deemed safe to continue with the anaesthetic, particular attention should be paid to maintaining fluid balance and blood pressure. Stringent monitoring of the cardiovascular system should occur, as detailed in Section 10.5. Obesity is a growing problem in equine populations and is a serious health concern. Obesity asserts negative effects on the cardiovascular system; therefore, an important first step when considering an anaesthetic in an obese equine patient is to identify any cardiac or cardiovascular abnormalities if they exist [69]. A thorough clinical examination should be carried out. In addition, indirect blood pressure monitoring could be used to identify hypertension, and an ECG could be used to assist in identifying cardiac dysrhythmias [69]. Both ventilation and oxygenation are affected by obesity. Hypoxaemia and hypoventilation in obese equine patients could be addressed using the following strategies [69]: The risk of an obese the patient developing a PAM must be considered. Adequate padding and careful positioning must be carried out. The anaesthetic time should be kept to an absolute minimum. Blood pressure should be monitored throughout the procedure, and hypotension should be prevented with the use of IV fluids and dobutamine if necessary. If the proposed procedure is an elective one, the patient could be sent away to follow a weight loss management program and come back for the surgery when appropriate weight loss has been achieved. A parturient mare presented for a caesarean section will have similar needs to those of any acute case. There are two additional considerations one being the effect of the gravid uterus on the mare and the other being the effect of anaesthetic drugs on the foal [72]. Risk factors include exhaustion and marginal dehydration in the mare. Anaesthetic drugs should be considered carefully, and barbiturates should be avoided. The major risk for caesarean sections in mares is the compression of the vena cava when the mare is placed in dorsal recumbency [72]. Serious or fatal hypotension can occur if the mare is placed symmetrically in dorsal recumbency. For this reason, recommendations are to tilt the mare off midline as much as possible (Figure 10.12) and monitor for hypotension with direct blood pressure monitoring [72]. Caution should be taken not to overload the dependent gluteal muscle when tilting the patient, as this could contribute to the risk of developing a post anaesthetic myopathy. A separate team with equipment and medication should be prepared to perform resuscitation on the foal. Figure 10.12 A mare undergoing a caesarean section should be tilted off midline as much as possible to reduce the pressure from the gravid uterus on the vena cava [6]. Source: Rosina Lillywhite. The acute trauma case will often present as distressed and painful. If the horse has been injured during an athletic endeavour, it may also be restless and excitable, which can make these patients dangerous to handle. Personnel should wear PPE when handling these horses. Sedatives and analgesics should be considered in the first instance. Other risk factors for these patients are dehydration, blood loss and hypovolaemia. If the horse has lost a substantial amount of blood, the circulating volume should be restored prior to anaesthesia. The exception to this is if anaesthesia is required to stem the source of bleeding [72]. If hypovolemia is suspected, phenothiazines should be avoided as the resulting hypotension may cause the horse to lose consciousness. Colloids such as gelofusine or plasma may be given to help to restore circulating volume. Isotonic crystalloids should also be given to address dehydration. If a large amount of blood has been lost, a blood transfusion should be considered. Hypertonic saline may also be administered if circulatory collapse is suspected. This must always be followed up with isotonic crystalloids [68]. The vet in charge of the case will prescribe the fluids required for the stabilisation protocol. The RVN can then administer these fluids as directed. The patient should be monitored constantly throughout this procedure. Once the patient has been stabilised, anaesthesia can commence. Before anaesthesia is induced, the patient should be carefully assessed and prepared. Patient preparation is covered in detail in Chapter 12. Induction is a potentially dangerous time for the patient, and any veterinary personnel involved. PPE should be worn, and induction protocols should be adhered to. As discussed in Section 10.2, anaesthesia is most commonly induced in horses using IV agents. It is important that the patient has been adequately pre‐medicated before induction is attempted. Premedication is the administration of an appropriate medication prior to anaesthesia to facilitate induction, maintenance and recovery. Premedication often involves using many different types of medication together to give a balanced overall effect. This is known as multi‐modal anaesthesia. Medications used for premedication include phenothiazines, alpha‐2 agonists, NSAIDs and opioids. These medications and their uses are discussed in Section 10.2. Antibiotics may need to be administered prior to anaesthesia. The vet in charge of the anaesthetic and the surgeon should discuss and agree on the antibiotics required prior to surgery, and these should be given pre‐operatively. Antibiotic protocols should be in place and based on the BEVA ‘Protect ME’ campaign, aimed at promoting responsible antimicrobial use and any emerging evidence‐based practice. See Chapter 6 for more information. The RVN should liaise closely with the case vet to develop an anaesthetic protocol that is appropriate for each individual patient. Once the has prescribed the required medication, the RVN can calculate drug doses and administer the medication for the premed. The RVN must have all equipment and medication prepared before induction takes place. This also involves checking and preparing ETTs, as described in Section 10.3. In a practice setting, horses are usually induced in a padded induction box (see Chapter 11 for further information). The patient must be sedated with an alpha‐2 agonist prior to induction. To optimise sedation, alpha‐2 agonists are often combined with an opioid. This sedative must be given enough time to take effect and will work much better if given in a quiet, calm environment. Once the patient is deemed ready, anaesthesia can be induced by the anaesthetist. Induction agents used in horses are discussed in Section 10.2. The most common medications used are ketamine and midazolam or diazepam. During induction, the RVN should assist the anaesthetist with patient restraint and positioning. There are different methods for trying to control anaesthetic induction for equine patients. Figure 10.13 Swing door induction. Source: Rosina Lillywhite. There are advantages and disadvantages to each induction method. The RVN should discuss the most appropriate method to use with the anaesthetist, considering the facilities and trained personnel available, as well as the temperament of the patient. Following induction, monitoring of vital signs should begin as soon as possible [68]. The patient will be intubated as described in Section 10.3 (Figure 10.14). As this is happening, the horses’ hooves will be covered (Figure 10.15), hobbles will be applied, and the patient will be attached to the hoist in readiness to be transported into the operating theatre. Health and safety must be considered at all times during this process, and appropriate PPE worn by personnel. In some practices, the horse is attached to the anaesthetic circuit in the induction box before being transported into the theatre. In other practices, the horse is attached to the anaesthetic circuit once it has been transported into the theatre. In either situation, the anaesthetic circuit should be set up ready, having been leak tested previously. Once the patient is deemed ready by the anaesthetist, it can be transported into the theatre on the hoist and carefully positioned ready for the surgical procedure. Anaesthetic monitoring equipment should be set up ready so it can be attached at the earliest possible moment. For more information regarding monitoring equipment, see Section 10.5. Figure 10.14 A horse being intubated. Source: Rosina Lillywhite. Figure 10.15 Horses hooves are covered before they are attached to the hoist. Source: Rosina Lillywhite. During equine anaesthesia, the anaesthetist aims to balance the preservation of normal equine physiology while providing an adequate plane of anaesthesia and analgesia to enable the procedure to be performed. To achieve this, the following must be considered: All basic monitoring techniques that require no equipment, such as ocular and mucous membrane assessment and pulse palpation, are recommended for every general anaesthetic procedure [47]. Guedel [74] described the stages and planes of anaesthesia in humans after the administration of ether. Guedel’s classification of anaesthetic depth remains in use today [74] (see Section 10.1 for further details). The maintenance of an adequate plane of anaesthesia is very important in horses due to the potential for injury to personnel and/or the patient in the event of movement. Furthermore, an inappropriately deep plane of anaesthesia may significantly compromise physiological function. Monitoring reflexes and patient characteristics using a ‘hand‐on’ approach is a crucial and fundamental skill for the equine anaesthetist in both field and hospital settings [47]. Anaesthetic depth as determined by eye position, ocular reflexes, presence of nystagmus and muscle or anal tone helps the anaesthetist avoid too light or too deep a plane of anaesthesia [75]. The palpebral reflex is triggered by stroking the cilia [47]. Care must be taken not to test this reflex repeatedly as it will fatigue [47]. Contact with the corneal surface should be avoided, as this will produce a false result and may cause corneal injury. A very rapid blink or spontaneous blinking may indicate a light plane of anaesthesia. The palpebral reflex is progressively depressed as anaesthetic drug effects intensify [66]. In most horses under inhalational agent anaesthesia, the palpebral reflex should always be present. An absent palpebral reflex may indicate a deep plane of anaesthesia. However, since the palpebral response can be significantly depressed by inhalational agents, in some horses, it may become absent during surgical levels of inhalational agent anaesthesia [66]. After induction of GA with ketamine, an active palpebral reflex is maintained during the transition from injectable to inhalational agent anaesthesia [66]. During TIVA, the palpebral reflex is often more brisk during a surgical plane of anaesthesia, particularly when agents such as ketamine are used. Touching the cornea may cause corneal injury, so routine evaluation of the corneal reflex is not recommended [47]. Touching the cornea should always provoke a blink response. The absence of a corneal reflex with any anaesthetic drug protocol should raise concern of an anaesthetic overdose [66]. Nystagmus describes a repetitive, rhythmic and involuntary oscillation or movement of the eyeball. The rate of nystagmus is variable. During volatile agent anaesthesia, nystagmus can indicate an inadequate or light plane of anaesthesia. The development of a brisk palpebral reflex and the appearance of nystagmus are associated with the lightening of anaesthesia, and the eye may also rotate dorsocaudally [53]. TIVA involving the administration of ketamine, causes the eye to be either centrally placed or directed slightly rostroventral, the palpebral reflex is brisk and small amplitude nystagmus is often present [53]. A reduction in anal contraction on stimulation is associated with increasing anaesthetic plane [66]. Palpation of the neck muscles is a useful way to assess muscle relaxation and depth of anaesthesia. Increased tension or tightening of the muscles in the neck and shoulders may indicate a light plane of anaesthesia [66]. Palpation of limb muscle tone is a useful method to assess anaesthetic depth. Muscle tone should be relaxed, and the distal limb should be easily moved with no resistance to manual flexion/extension. A response to surgery or ‘lightening of the plane of anaesthesia’ is usually signalled by an increased tone or slow movement of the forelimbs [76]. Shivering and increased muscle tension (particularly in the neck and legs) are often useful indicators of an inadequate plane of anaesthesia for surgical stimulus, although impending conscious or unconscious movement remains challenging to predict [47]. During inhalational agent anaesthesia, swallowing may indicate a light or inadequate plane of anaesthesia. TIVA may not be appropriate for airway surgery, as swallowing can occur throughout surgery [76]. During TIVA, horses may appear lightly anaesthetised, often with a brisk palpebral reflex, occasional nystagmus, swallowing, and lacrimation, good muscle tone, and yet little response to surgery [76]. Most anaesthetic and sedative agents have effects on the cardiovascular system. Therefore, during sedation and GA, it is important to monitor the cardiovascular system. Injectable and inhalant anaesthetic drugs used in horses may decrease cardiac output and reduce arterial blood pressure [77]. The detrimental effects that anaesthetic agents may have on cardiovascular function necessitate that anaesthetic drugs are titrated to effect. During GA, it is important to monitor the cardiovascular system continuously and assess the effects of anaesthetic drugs on cardiovascular function. An appropriate level of anaesthesia needs to be maintained while minimising the negative effects of the drugs on the cardiorespiratory system. A rapid and effective method of making a subjective assessment of cardiac output is by palpating a peripheral pulse. Heart rate can be counted, and the strength of the pulse can be estimated as subjective [82]. The normal heart rate for anaesthetised horses is 30–45 beats per minute [83]. The pulse rate should match the heart rate. Gentle pressure on a peripheral artery using a finger enables palpation of the expansion of the artery as pressure builds. The rise in pressure (pulse pressure) equates to the systolic pressure minus the diastolic pressure [82]. A strong pulse indicates a large stroke volume, and a weak pulse indicates a low stroke volume [82]. Subjective indication of peripheral tissue perfusion. Normal mucous membrane colour is pink in most horses. Pale pink or greyish mucous membranes may indicate poor perfusion due to either reduced CO or vasoconstriction, which is common after alpha‐2 agonist administration [56]. Congested or bright red mucous membranes can be secondary to vasodilation. This is occasionally seen with hypercapnia but, more commonly, in cases of septic shock [47]. Mucous membrane colour should not be relied upon for assessment of oxygenation status and rather, used as a prompt for further investigation [47]. CRT offers a subjective indication of peripheral perfusion. In healthy horses, CRT is less than 2 seconds. Slow or sluggish capillary refill times (>2 seconds) and pale pink or greyish colouration may indicate poor perfusion [56]. Electronic monitoring methods should not replace the anaesthetist’s ‘hand‐on’ core skills in monitoring anaesthesia but should complement them. During equine anaesthesia, cardiovascular monitoring usually consists of an ECG and IBP measurement [84]. Supporting MAP is important in the prevention of severe complications, such as myopathies [84]. An ECG is used to monitor heart rate and rhythm. A surface ECG records the electrical activity of depolarisation and repolarisation of myocardial tissue, using electrodes placed at the skin [57]. While the consistent placement of the electrodes may aid in producing a familiar trace, any orientation of pairs of electrodes will produce a waveform if they span the heart [56]. The ECG trace represents events in the cardiac cycle (Figure 10.16): The base‐apex lead is the most common lead system used for ECG analysis in horses [59]. Electrical impulses which spread across the heart muscle can be detected and amplified at the skin surface using electrodes [47, 55]. A minimum of three electrode contact points with crocodile clips or adhesive gel electrodes can be configured in a ‘base–apex orientation’ [55]: Figure 10.16 Example of an electrocardiograph: showing the P‐wave, QRS complex and T‐wave. Source: Dr Kate Loomes. The normal HR for anaesthetised horses is 30–45 beats per minute [83]. The normal HR for anaesthetised foals maybe 35–60 beats per minute, as their resting heart rate is 100 beats per minute at birth [83, 86]. In horses, heart rate may not vary significantly with anaesthetic depth or surgical stimulation. Heart rate is not a reliable indicator of appropriate anaesthetic depth in horses. Bradycardia <25 beats per minute and may occur in response to increased vagal tone or the administration of agents such as alpha‐2 agonists or dobutamine [87]. Tachycardia >50 beats per minute [20] and may be associated with sympathetic stimulation, pain, hypoxaemia, dobutamine administration or tourniquet use [87, 88]. An ECG enables further investigation of rhythm disturbances, for example, second‐degree (AV) block (Figure 10.17), atrial premature contractions, ventricular premature contractions and atrial fibrillation (Figure 10.18). Figure 10.17 Second‐degree AV block. This is a regularly irregular rhythm where the heart misses a beat in a regular rhythm. It is the most common intraoperative rhythm disturbance seen. Second‐degree AV blocks rarely require treatment and usually resolve spontaneously. See Chapter 13 for further information. Source: Dr Mark Bowen. Figure 10.18 Atrial fibrillation. This is an irregularly irregular rhythm which occasionally develops during anaesthesia. The atria contract randomly causing an irregular and sometimes extreme tachycardia. Treatment may not be required if blood pressure remains normal. If treatment is required, electrolyte infusion, reduction of the volatile agent and dobutamine can be initiated depending on the circumstances [73]. A horse found to be in atrial fibrillation prior to GA should be treated and converted prior to anaesthesia [73]. See Chapter 13 for further information. Source: Dr Mark Bowen. ABP is a marker of circulatory status and is the product of CO and SVR [59]. Blood flow rather than blood pressure is the driving force for tissue perfusion. However, while the direct measurement of flow is currently impractical, blood pressure is used as an estimate of flow [59]. ABP can be measured using direct (invasive) or indirect (non‐invasive) methods. ABP measured directly or invasively (IBP) is considered the gold standard ABP measurement technique [58]. The technique requires an intra‐arterial catheter connected to a transducer via a non‐compliant fluid‐filled extension set [59] (Figure 10.19). The lateral dorsal metatarsal artery, the transverse facial artery and the facial artery are most commonly used for arterial catheterisation [59] (Figure 10.20). The fluid extension set should be visually inspected for air bubbles, kinks, fluid leaks, obstructions, or clots, which can lead to damping the system response and erroneous ABP measurements [59]. Measurement of arterial pressure using a peripheral arterial catheter is commonly practised in equine anaesthesia because hypotension has adverse consequences in horses, and the arterial catheter facilitates sampling for blood‐gas analysis [89]. Direct ABP monitoring provides a continuous display of pressure waveforms and values for systolic arterial pressure (SAP), mean arterial pressure (MAP) and diastolic arterial pressure (DAP) [59]. (Figure 10.21). Catheterisation of a peripheral artery is required in order to measure arterial blood pressure directly. Figure 10.19 A catheter placed in a peripheral artery is used to measure arterial blood pressure directly during GA in horses. Source: Dr Kate Loomes. Figure 10.20 Arterial trace generated from catheterisation of the dorsal metatarsal artery in a horse in lateral recumbency. Source: Dr Kate Loomes. Arterial catheterisation must be performed using an aseptic technique and requires skill and practice to perform effectively. Potential complications of arterial catheterisation include: Saline‐filled, heparinised, non‐distensible tubing is used to connect the arterial catheter to an electrical transducer, which is connected to a monitor. Pressure wave changes within the transducer transmit electrical signals for interpretation and display on the patient‐side monitor [58]. The electrical transducer is placed at the level of the heart. The measurement and display of systolic, diastolic and mean arterial blood pressure values and the arterial pressure waveform provide important information regarding cardiovascular function and status [83]. Equine anaesthetists normally aim to maintain MAP above 70 mmHg [81]. Since intra‐compartmental pressure in the dependent muscles of adult horses, on an adequately padded surface, reaches values of 30–40 mmHg [90] and a vascular transmural pressure needs to be greater than 30 mmHg for adequate microcirculation [91], a MAP >70 mmHg should support adequate tissue perfusion in healthy horses. Normal DAP in healthy adult anaesthetised horses is >45 mmHg. Low DAP (<45 mmHg) may indicate relative (due to vasodilation) or absolute (due to haemorrhage or dehydration) hypovolaema [87]. Figure 10.21 Arterial trace generated from catheterisation of the mandibular branch of the facial artery. Features of the arterial waveform reflect the distension and behaviour of the vasculature. Source: Dr Kate Loomes. Hypotension is usually defined as MAP <70 mmHg [92]. Causes may include: When hypotension occurs, contributing factors such as decreases in circulating volume (for example, blood loss), cardiac output or systemic vascular resistance should be considered [81]. Hypotension is commonly corrected with dobutamine during GA. Hypertension occurs when MAP > 100 mmHg. Causes may include: Both severe hypotension and hypertension should be prevented to avoid the negative effect of abnormal tissue perfusion [60]. NIBP or indirect methods of measuring blood pressure include manometric measurements (Korotkoff sounds) as well as oscillometric and Doppler methods [59]. Oscillometric NIBP devices utilise a peripherally placed arterial bladder cuff to record pressure wave oscillations induced by blood flow turbulence during vascular release. The monitor measures MAP at maximal oscillation amplitude and then uses proprietary algorithms to calculate SAP and DAP [58]. Cuff placement sites include: In situations where IBP measurement is not possible, oscillometric NIBP measurement may be used, but the limitations of the technique should be considered. Poor agreement between NIBP measured by an oscillometric device and IBP has been reported in horses [58, 93]. Devices that measure ABP non‐invasively are routinely used in human and small domestic animal patients; however, inaccuracy and poor reliability compared with IBP mean they remain underused in horses [58]. CVP is an estimate of preload and right ventricular filling pressure (right atrial pressure) and is an approximation of the ratio of blood volume to blood volume or vessel capacity [59]. Complex techniques and trained personnel are required to measure CVP; therefore, measurement of CVP is usually reserved for experimental procedures or specialist centres. There is evidence that jugular venous pressure has an adequate correlation with CVP in healthy, euvolemic, laterally recumbent anaesthetized adult horses [61]. One study showed that while jugular venous pressure cannot replace CVP measurement, but it may be used clinically to estimate CVP [61]. The measurement of CO can be used to indicate tissue perfusion and to assess the effects of drugs on circulation [77]. Techniques described for the measurement of CO include: Measurement of CO requires specific equipment and trained personnel and is usually reserved for experimental procedures or specialist centres. Respiration should be observed carefully. Visualising the rate and degree of chest wall or rebreathing bag movement is a basic but important method of assessing respiratory rate and pattern. Tidal volume (VT) may be roughly estimated by observing the degree of collapse of the rebreathing bag when using inhalational agent anaesthesia [83]. More sophisticated mechanical ventilators may have the facility to measure tidal volume using spirometry. Thoracic auscultation may be difficult in the recumbent horse due to positioning and extraneous background noise [83]. Capnometry is the measurement of carbon dioxide (CO2) in a sample of gas [94]. Capnography provides information relating to ventilation, gas exchange and metabolism. During anaesthesia, end‐tidal CO2 partial pressure (ETCO2) from the gases in the breathing circuit are sampled close to the patient [47]. Capnography is the continuous monitoring of the concentration or partial pressure of CO2 in respiratory gases [94]. Capnography produces a continuous waveform of CO2 partial pressure [47] (Figure 10.22). The characteristic shape of the capnograph corresponds to events in the respiratory cycle (Figure 10.23). Infra‐red spectroscopy is used to measure the CO2 content of gas [94]. A beam of infrared light is passed across the gas sample and directed to a sensor. The presence of CO2 in the gas leads to a reduction in the amount of light which is transmitted to the sensor and a change in the circuit voltage [94]. This information is interpreted by the monitor, and a real‐time continuous waveform is produced. Figure 10.22 Carbon dioxide in expired gas is represented in a graphical form, with time on the X‐axis and expired partial pressure of CO2 on the Y‐axis: the result is a capnography trace or waveform. Source: Dr Kate Loomes. Figure 10.23 The capnograph trace has a characteristic shape which corresponds to the different parts of the respiratory cycle. Phase I (inspiratory baseline) represents inspiration and therefore, no CO2 is detected. Phase II (expiratory upstroke) represents expiration of both dead space gas and alveoli gas from the respiratory bronchioles and alveoli. Phase III (alveolar plateau) represents expiration of alveolar gases. At the end of phase III, the maximal value of CO2 measured is equivalent to the ETCO2. Phase IV (expiratory downstroke) represents the beginning of the next breath, with the CO2 content returning rapidly to zero. The continuous waveform allows a visual breath‐by‐breath assessment of a patient’s airway and ventilation, with the contour of the waveform giving considerably more information than the ETCO2 value alone [94]. Source: Dr Kate Loomes and Rosina Lillywhite. A sudden drop in ETCO2 may be a result of extubation, equipment failure, for example, a leak from the ETT cuff, massive pulmonary embolism or cardiopulmonary arrest [96] (Figure 10.24). Stepwise reductions in ETCO2 (Figure 10.25) may be indicative of falling CO and is a cause for concern. Capnography can provide evidence that the circulatory system is capable of CO2 transport as a fall in cardiac output results in a reduction in ETCO2 when ventilation is constant [47]. Increased ETCO2 (>60 mmHg) (hypercapnia) may indicate hypoventilation due to anaesthetic agent‐associated respiratory depression caused by CNS depression and respiratory muscle weakness [63]. Increased ETCO2 may be seen in states of malignant hyperthermia, fever or sepsis [96]. There may be cardiovascular benefits of mild hypoventilation, with some studies advocating maintaining PaCO2 between 50–70 mmHg [33] or below 70–75 mmHg [97]. Note this reference is to PaCO2 and not ETCO2. Measurement of arterial carbon dioxide tension (PaCO2) requires blood gas analysis. The difference between ETCO2 and PaCO2 can be used to estimate how effectively CO2 is being transferred from the blood to the alveoli before being exhaled. Increased ETCO2–PaCO2 difference (>20 mmHg) indicates increased alveolar dead space ventilation, incomplete alveolar emptying, ventilation‐perfusion mismatch or a leak in the sampling system [83]. ETCO2–PaCO2 difference tends to increase with increased anaesthetic time and is affected by body position and mode of ventilation. ETCO2 gives a relatively poor indication of PaCO2 in both healthy and compromised horses, especially during CMV [98]. For this reason, it is important to use blood gas analysis to provide an accurate PaCO2. Capnography monitoring is key when performing CPCR, as the return of the waveform highlights the return of spontaneous circulation, indicating that the procedure has been successful [50]. Figure 10.24 Decreased ETCO2 and a loss of the normal capnograph shape may be seen when there is a leak around the endotracheal tube cuff. Source: Dr Kate Loomes. Figure 10.25 Stepwise reductions in ETCO2 may be indicative of falling cardiac output and is a cause for concern. Source: Dr Kate Loomes. Pulse oximetry displays heart rate and estimates the percentage of arterial blood haemoglobin which is saturated with oxygen (SpO2) [83] (Figure 10.26). It indicates the presence of pulsatile flow to tissues and displays the pulse rate [47, 54] and a beat‐to‐beat value for arterial haemoglobin saturation (SpO2) [52]. It can detect hypoxaemia without the need to measure arterial blood gas [52]. Pulse oximetry is non‐invasive and offers immediate and continuous measurements of SpO2 [47, 59]. The portable nature of the pulse oximeter makes it useful for field anaesthesia [47]. A pulse oximeter uses two light‐emitting diodes and a photodetector. Red and infrared light is transmitted through superficial tissue such as the tongue. A photodetector measures the relative absorption of light by arterial blood in the tissue. Pulse oximeters estimate SpO2 by evaluating the relative absorption of light of two different frequencies, red (660 nm) and infrared (940 nm), by oxyhaemoglobin and the reduced form of Hb (deoxyhaemoglobin) [99]. Figure 10.26 Pulse oximetry provides a digital and audible display of pulse rate [59]. Source: Dr Kate Loomes. Normal SpO2 during GA in an adult horse receiving 100% oxygen is >95%. Oxygen is routinely used in veterinary anaesthesia as the sole carrier gas and therefore patients are commonly exposed to nearly 100% oxygen [100]. Hypoxaemia (SpO2 < 95%) may be due to an inadequate oxygen supply, respiratory obstruction, ETT obstruction, ventilation‐perfusion mismatch. Ventilation‐perfusion inequality is the most common reason for the development of hypoxaemia in horses. Poor signal quality is the major reason for inaccuracy of pulse oximeters [98]. Inaccuracies may arise due to ambient light, movement and vasoconstriction. Inaccuracy of a pulse oximeter to obtain the exact correct heart rate correlates with the inaccuracy of SpO2 readings [98]. Pulse oximetry and arterial blood analysis complement one another. Continuous monitoring of SpO2 via oximetry can be coupled with intermittent arterial blood gas analysis as required [59]. The shape of the sensor, thickness of tissue placed within the sensor, presence of pigment and hair and movement of the patient can be responsible for the pulse oximeter failing to measure arterial oxygen saturation [53]. The pulse rate displayed on the oximeter must correspond to the rate obtained by palpation or ECG before the measurement can be assumed to be accurate. During GA, when 100% oxygen is being delivered: normal SpO2 > 95%. Hypoxaemia (SpO2 < 95%) mainly occurs due to ventilation‐perfusion inequality but may also be caused by hypoventilation [54]. Arterial blood gas analysis provides information relating to oxygenation, ventilation and acid–base balance [66]. Venous blood analysis provides information relating to assess ventilation and acid–base balance [63]. It is indicated in horses undergoing colic surgery or under GA with other causes of critical illness. Samples must be drawn anaerobically for accurate analysis of oxygenation parameters. Blood is introduced into a blood gas analyser, which contains a series of electrodes that measure pH, oxygen tension (PO2) and carbon dioxide tension (PCO2). The other information provided by the analyser is calculated from these measured parameters. Machines used to measure blood gas values may also offer the facility to measure electrolytes (sodium, calcium, glucose and potassium), PCV, haemoglobin, lactate, urea and creatinine. Arterial blood samples can be drawn from a peripheral arterial catheter placed for IBP measurement. If needle puncture is used, the site for arterial puncture should be prepared with an antiseptic. Clipping or shaving the hair may facilitate visualisation or palpation of the artery [59]. The blood should be collected in a syringe coated with heparin and kept anaerobic and on ice [59]. Blood gas analysis is not continuous, so its use is limited by the number of samples taken and the time taken to obtain the results. Samples should be collected as needed, most commonly every 30–60 minutes or more frequently if the horse’s condition requires it [63]. Blood gas analysers use small electrodes which measure pH, arterial and venous tension of carbon dioxide (PaCO2, PvCO2) and oxygen (PaO2, PvO2). During GA in an adult horse, normal PaCO2 is 40–60 mmHg and normal PaO2 is 100–500 mmHg [83]. Increased PaCO2 (>65–70 mmHg) (hypercapnia) indicates hypoventilation, which may be due to anaesthetic agent‐associated respiratory depression or inadequate mechanical ventilation. Decreased PaCO2 (<40 mmHg) (hypocapnia) indicates hyperventilation, which may be due to pain, excitement, light plane of anaesthesia or over‐zealous use of mechanical ventilation. Severe hyperventilation resulting in hypocapnia may cause respiratory alkalosis and a reduction in cerebral blood flow [59]. Hypoxemia is defined as a state of reduced oxygen tension in arterial blood (PaO2 < 60 mmHg) that can lead to reduced oxygen levels in the tissues (hypoxia) [63]. PaO2 values <80 mmHg indicate hypoxemia and correlate with an SaO2 < 95% [59]. Values below 60 mmHg (SaO2 of approximately 90%) indicate severe hypoxemia [59]. Rapid desaturation of haemoglobin occurs below this level [98]. During clinical large animal anaesthesia, the use of spirometry to monitor ventilation is not routine because of the lack of a reliable and practical method adapted to large animals [101]. Purpose‐made equipment does exist allowing the routine use of spirometry in horses in some centres. Spirometry measures tidal volume (VT), minute ventilation (MV), dynamic compliance and resistance. Spirometry allowed continuous measurement of tidal and minute volume on a breath‐to‐breath basis and quick detection of any changes [101]. The information measured using spirometry can be used to create a pressure‐volume (PV) loop, which provides information about compliance and a flow‐volume (FV) loop, which determines the resistance [63]. Spirometers may use a pitot tube‐based flow sensor with an integrated respiratory gas sample port and a dedicated host monitor. The pressure difference generated is converted to flow and volume. The flow sensor is placed between the ETT and the breathing circuit [101]. Temperature monitoring is important in all equine patients peri‐operatively but particularly important in foals. All horses are susceptible to heat loss due to the vasodilatory effects of sedative and anaesthetic agents, which promote heat loss to the periphery. Perioperative hypothermia may be associated with an increased incidence of surgical‐wound infection, weakness and ataxia during recovery [53]. Foals are particularly susceptible to hypothermia, owing to a large body surface area to mass ratio, minimal fat stores, depressed thermoregulatory centres in the brain and poor vasomotor tone [75]. Adverse effects of hypothermia include decreased anaesthetic requirements, prolonged recovery, bradycardia and hypotension unresponsive to catecholamine administration [75]. Methods to prevent and treat hypothermia should be instituted immediately at or before the onset of anaesthesia in foals [75]. Blankets, limb wraps and/or forced air warmers may be used to maintain normothermia depending on requirements and the ambient theatre temperature. Oxygen analysers are incorporated into most anaesthesia monitors. Oxygen analysis can be performed in inhaled and exhaled gases and usually takes the form of a paramagnetic cell [102]. Volatile agent analysis can be carried out by some monitors. End‐tidal and fractional‐inspired volatile agent concentrations are displayed as a percentage. Oxygen cylinders should be checked before use to ensure that they contain enough oxygen for the anticipated anaesthetic duration. Spare cylinders should always be available and clearly labelled. A spare vaporiser should be available in case of equipment failure. Breathing systems and ETTs must be checked for leaks or imperfections prior to use. Leak testing is an important part of the pre‐anaesthetic machine check and should be carried out prior to use in every patient. If a surgical procedure is anticipated to cause significant blood loss, the horse should be cross‐matched before surgery to identify an appropriate blood donor or donor [87]. The blood volume of a horse is approximately 8% of its body weight (kg) [103]. Therefore, a 500‐kg horse normally has about 40–50 l of blood [87]. Blood loss of less than 15% (<12 ml/kg) of total blood volume is often insignificant and may not be clinically detected [104]. It can often be fully compensated by physiological mechanisms and generally does not require fluid or blood‐product therapy [105]. More severe haemorrhage, >25% of blood volume (>20 ml/kg), often requires crystalloid or blood product replacement. Acute blood loss of greater than 30% (>24 ml/kg) may result in haemorrhagic shock requiring resuscitation treatments [106, 107]. Blood loss of greater than 40% is characterised by marked clinical abnormalities, severe shock and imminent death [104]. Haemorrhage may also be classified as: The accurate quantification of blood loss can be difficult in the anaesthetised horse [107]. In cases of acute haemorrhage, changes in heart rate, respiratory rate, capillary refill time, and anxiety level are appreciated after approximately 15–20% of total blood volume is lost [104]. However, during GA, additional factors such as pre‐haemorrhage arterial blood pressure and heart rate, surgical stimulation, body position, anaesthesia duration and administration of agents to support blood pressure may affect the physiological response to haemorrhage. Methods used to quantify blood loss include: Urine output is an indicator of renal blood flow [59]. It may be used as an indirect marker of end‐organ perfusion and fluid balance [59]. During GA, IV fluid therapy and the administration of drugs, including alpha‐2 adrenoreceptor agonists may influence urine output [47]. Urine‐specific gravity provides useful information in differentiating pre‐renal azotaemia from renal failure [59]. Adult horses vary in terms of urine‐specific gravity; however, dehydration should also result in concentrated urine, whereas renal failure yields isosthenuria [59, 110]. Urinalysis, with cytologic evaluation of sediment, complements the monitoring of renal function [59]. One goal of routine IV fluid administration during inhalation anaesthesia is to maintain sufficient vascular volume and venous return to the heart despite anaesthetic‐related vasodilation [87]. In the event of a haemorrhage, the administration of IV fluids and blood products should be tailored to the severity of the blood loss and the individual patient’s physiological response. Aim to support cardiac output and blood flow to vital organs and try to stop the bleeding [108]. If the haemorrhage can be controlled (for example, the vessel can be ligated), then initial efforts to resuscitate the horse should focus on increasing perfusion pressure and blood flow to organs as quickly as possible with crystalloids or colloids while assessing the need for whole blood transfusion [108]. IV fluids are needed to restore intravascular volume in cases of haemorrhagic shock. Unfortunately, these fluids can also dilute platelets and clotting factors and negatively affect clot formation [103]. The approach to fluid resuscitation requires consideration of the severity of the haemorrhage and the volume of blood lost together with the physiological response shown by the horse. Crystalloids can be defined based on their tonicity, use and/or electrolyte composition. Most crystalloids are isotonic, meaning that they have similar tonicity to fluid within the body, both intra‐ and extra‐cellularly [111]. A variety of crystalloid fluids are available, but few are available in volumes large enough for the practical administration of horses. Most practices stock a single type of fluid. In general, it is a replacement fluid, as these are available in large sizes, are most commonly used, and can be given rapidly to patients in need of resuscitation [111]. Hartmann’s solution or lactated ringers solution is commonly stocked by equine practices as a replacement fluid. These fluids have a composition that is similar to extracellular fluid but are not exactly the same. Therefore, given the electrochemical makeup of these fluids, maintaining patients on this type of fluids, beyond the initial replacement period, inevitably results in sodium loading and inadequate replacement of other electrolytes [111]. One of the most common reasons for fluid administration is the resuscitation of a critically ill patient with insufficient preload due to hypovolemic, distributive, or obstructive shock. These patients require rapid, significant intravascular volume expansion [111]. Rapid intravascular volume expansion is best achieved by administering fluids directly into the vascular space [111]. In order to achieve rapid administration of large volumes of fluid: a large (10–14) gauge catheter, wide‐bore administration set, and the ability to suspend the fluids from a sufficient height above the horse are required [112]. Balanced crystalloid solutions such as Hartmann’s solution can be used in relatively large volumes to improve circulating volume; however, the effect is relatively short‐lived (20–30 minutes). After acute controlled haemorrhage, perfusion pressure and blood flow can be quickly improved by rapid (over 20–30 minutes) IV infusion of high volume (10 ml/kg) crystalloid solution (Hartmann’s solution) [108]. The current approach is typically to administer a 10–20 ml/kg bolus of crystalloid followed by a reassessment of indicators of perfusion (e.g. heart rate, capillary refill time, pulse quality, extremity temperature, systemic lactate, urination, blood pressure) and intravascular volume (jugular fill) [113]. An additional infusion of 10–20 ml/kg may be needed to replace the blood volume lost from severe haemorrhage (>30% blood volume) [108]. Large‐volume crystalloid replacement that allows the HCT to fall to an extremely low concentration could theoretically have a negative effect on microcirculatory flow by decreasing blood viscosity [114]. Available as a 7.2% solution with a high sodium content and a tonicity almost nine times that of plasma. Hypertonic saline has the potential of increasing both blood volume and blood pressure with low‐volume administration due to the rapid shifts of the fluid between the cellular and interstitial spaces into the intravascular compartment following administration [108]. Administration of hypertonic solution results in significant and rapid fluid shifts into the intravascular space, initially from the other extracellular compartments (i.e. interstitial space) and will continue from the intracellular space [111]. After acute controlled haemorrhage, perfusion pressure and blood flow can be quickly improved by IV infusion of low volume (1–4 ml/kg) IV infusion of hypertonic saline. Hypertonic saline as a resuscitation fluid in haemorrhagic shock has been shown to have an immediate and favourable hemodynamic effect, decrease secondary inflammation via attenuating the leukocyte‐activated endothelial damage, decrease the incidence of organ failure, and improve survival in some animal models of haemorrhagic shock [115]. In a model of induced haemorrhagic shock, administration of hypertonic saline resulted in rapid plasma volume expansion and urine output, along with sustained elevations in numerous cardiovascular parameters, including cardiac output, stroke volume, MAP and contractility [106]. Be aware that hypertonic solutions draw fluid from the interstitial space into the vascular space, therefore effectively depleting the interstitial space. Balanced isotonic crystalloid fluids (Hartmann’s solution) can be used to replenish the interstitial space. For a sustained effect and to avoid ill effects of intracellular dehydration, hypertonic saline administration should be followed by larger quantities of IV isotonic replacement crystalloids [111]. Avoid the use of hypertonic solutions in foals due to the high sodium content. Despite such a rapid initial expansion, this effect is relatively short‐lived, due to the redistribution of electrolytes and water across the vessel wall as expected with all IV crystalloid administration [111]. As a result of these fluid shifts, the effective expansion of circulating volume is in the order of 3.5 times the administered volume [113]. Colloid administration generally has two goals: improving colloid oncotic pressure (COP) or inducing more rapid and sustained volume expansion than crystalloids during fluid resuscitation of critically ill patients [116]. Combining hypertonic saline and a synthetic colloid as an initial low‐infusion volume treatment may be superior to hypertonic saline alone [117]. Although some synthetic colloids have been shown to be associated with acute kidney injury in people receiving resuscitation therapy, this undesirable effect in horses has not been reported [108]. Large volumes >10–20 ml/kg of colloids may impede coagulation. Statistically significant changes in coagulation testing. It should be recognised that most changes were mild, with values often remaining in the normal range and unlikely to be clinically significant [116]. Additional work is needed to evaluate these effects in clinical patients, particularly those more likely to be at risk for pre‐existing thrombocytopenia, thrombocytopathies or coagulopathy [111], such as horses suffering from the effects of haemorrhage. Similar to a hypertonic saline infusion, colloid treatment may increase plasma volume 4 times compared to a similar volume treatment with a balanced isotonic crystalloid. Natural colloids such as whole blood or plasma are often administered for a particular purpose in certain cases – such as replenishing red cells, plasma proteins and coagulation factors in the case of whole blood or for anti‐endotoxic or coagulation benefits in the case of plasma [111]. If the horse has lost >30% blood volume and is suffering from haemorrhagic shock, it is likely that a whole blood transfusion will be needed as re‐establishment of normal perfusion alone may not enable adequate oxygen delivery [108]. After the initial crystalloid treatments, whole blood transfusion should be strongly considered if clinical signs are not improving, HCT decreases to <18%, heart and respiratory rates remain above normal, blood lactate is not decreasing, or pulmonary venous oxygen tension remains <30 mmHg. These findings suggest the need for haemoglobin replacement [108]. Blood transfusion is a life‐saving treatment for horses with acute haemorrhage [104]. Blood transfusions improve oxygen delivery to the tissues via increased blood volume and haemoglobin concentration [104]. Indications for blood transfusion may not be clear cut and an individual patient approach is warranted. The following factors may be indications for blood transfusion in cases of acute haemorrhage:
10
Anaesthesia and Analgesia
Glossary
10.1 The Principles of Anaesthesia
Introduction
Types of Anaesthesia and Analgesia
Sedative Drugs
The Physiology of GA
The Effect of Anaesthetics on the Respiratory and Cardiovascular Systems
Effect of Anaesthetic Agents on the Autonomic Nervous System
Effect of Anaesthetic Agents on the Hepatic and Renal Systems
Pain
Pre‐emptive Analgesia
Multimodal Analgesia
Recovery from Anaesthesia
Balanced Anaesthesia
Triad of Anaesthesia
Objectives of Premedication
Methods Used for Maintaining GA
Inhalational/Volatile Anaesthetic
Carrier Gases
Total Intravenous Anaesthesia (TIVA)
Top‐up Doses
Infusion Maintenance
Neuromuscular Blockade
IV – bolus administration or infusion
Inhalational administration
Minimal equipment needed, so less initial outlay of cost
Expensive/specialist equipment required for delivery
Elimination depends on organ function
Can change depth of anaesthesia quickly
Upper limit to duration of anaesthesia, without causing drug accumulation and adversely affecting recovery
Can maintain anaesthesia for a longer time period
Generally quicker recoveries (but accumulation of drugs and poorer quality recoveries if GA > 60 minutes)
May have slower recoveries
Reduced stress response
Risk of exposure to waste anaesthetic gases
Better cardiovascular function
Easier to deliver oxygen as trachea is always intubated
Stages and Levels of Anaesthesia
CNS Function
Phases of Anaesthesia
Anaesthetic Depth
Anaesthetic Calculations
Indicator
Plane of anaesthetic depth
Light
Adequate
Deep
Eye position
Rapid nystagmusa
Wandering
Central, dilated pupils
Palpebral reflex
Brisk
Slow
Absent
Corneal reflex
Present
Present
Present, may be slow
Lacrimation
Tear overflow
Some
None
Anal tone
Present
Present
Absent
Spontaneous movement/increase in muscle tone
Present
Absent
Absent
Respiratory rate/pattern
Can all vary and are influenced by drug protocol and physiological state of animal
Blood pressure
Heart rate
Use of Calculators
Gross Error Checks
Calculation of Minute Volume and Tidal Volume
Fresh Gas Flow Rates
Calculation Formulae
Drug Dosages
Infusions
Using a Pump/Syringe Driver
10.2 Anaesthetic Drugs
Sedatives
Achieving Effective Sedation
Drug class
Clinical effect
Mechanism of action
Side effects
Phenothiazines
Mental calming: mild–moderate
Dopamine antagonist
Hypotension
No analgesia
Alpha‐2 agonists
Sedation: dose‐dependent, can be profound
Analgesia
Some muscle relaxation
Alpha‐2 adrenoceptor agonist in CNS (sedation) and periphery. Analgesic effects due to actions at both sites
Vascular tone changes and bradycardia (reduced CO)
Diuresis
Sweating
Opioids
Analgesia
Opioid receptors in CNS. Action at receptor will depend on drug (agonist/antagonist)
Can reduce gastrointestinal motility
Can increase locomotor activity
Benzodiazepines
Muscle relaxation
Used for co‐induction with ketamine
y‐Aminobutyric acid type A (GABAA) agonist
No analgesia
Cause ataxia so not used for sedation in adult horses. Used commonly for sedation in neonatal foals
Volatile agents
Anaesthetic maintenance
Unknown
Hypotension
Hypoventilation
Ketamine
Anaesthetic induction
Analgesia
NMDA antagonist
Dissociative anaesthetic
Can cause excitation
Sympathomimetic effects
Thiopental
(ultra‐short acting barbiturate)
Anaesthetic induction
Also useful peri‐operatively if unexpected movement to deepen plane of anaesthesia quickly
GABAA agonist
No analgesia
Irritant if injected perivascularly/extravascularly
Can cause prolonged/ataxic recovery, especially if repeated doses used
Phenothiazines (Acepromazine)
Alpha‐2 Adrenoceptor Agonists
Opioids
Benzodiazepines
Injectable Induction Agents
Ketamine
Thiopentone/Thiopental
Benzodiazepines
Guaiphenesin/Glyceryl Guaiacolate Ether (GGE)
Other Induction Agents
Inhalation Anaesthetics
Volatile Agents
Carrier Gases
Nitrous Oxide
Analgesics
Opioid Analgesics
NSAIDs
Local Anaesthetics
Other Agents with Analgesic Properties
Paracetamol
Drug
Onset of action
Duration of action
Notes
Procaine
5–10 minutes
45–60 minutes
Licensed preparation includes adrenaline
Lidocaine
Fewer than 120 seconds
Up to 2 hours without adrenaline, up to 3 hours with adrenaline
Licensed preparation includes adrenaline
Mepivacaine
30–120 seconds
2–3 hours
Most commonly used for nerve blocks for lameness investigation
Bupivacaine
5–10 minutes
4–8 hours
Unlicensed
Gabapentin
Others
Neuromuscular Blocking Agents
10.3 Anaesthetic Equipment
Function and Maintenance of the Anaesthetic Machine
Components of the Large Animal Anaesthetic Machine
Gas Supply
Cylinders
Cylinder Safety
Piped Gases
Pressure Regulators or Pressure Reducing Valves
Common Gas Outlet (CGO)
Flowmeter (Rotameter)
Flowmeter Mechanism of Action
Vaporiser
Inside the Breathing System
Outside the Breathing System
Vaporiser Safety Features
Care and Maintenance
The Anaesthetic Breathing System
Advantages
Disadvantages
Low fresh gas flows can be used resulting in greater economy
Increased resistance created by the carbon dioxide absorbent canister and one‐way valves
Dead space remains constant [15]
Long inspiratory and expiratory limbs can create equipment dead space particularly in smaller horses
Inspired gas is warmed and moistened
The Y‐piece may be heavy which creates drag on the endotracheal tube
Low flow systems result in less environmental pollution
Anaesthetic agent concentration may be slow to change if low fresh gas flows are used
Mechanical ventilation can be easily used with a circle breathing system
The equipment can be expensive to buy and can be complicated to repair
Temperature is relatively uniform throughout the system [15]
Equipment is not easily transported
Minimum chance of inhaling alkaline dust from the absorbent material [15]
Carbon Dioxide Absorbent and Canister
Advantages
Disadvantages
Simple to use
The horizontal position of the carbon dioxide absorbent canister can lead to ‘channelling’ of gases which reduces carbon dioxide absorption efficiency
Portable
The carbon dioxide absorbent becomes exhausted on the surface closest to the patient first and then as anaesthesia progresses, this area of exhausted absorbent extends which results in increased equipment dead space over time [20]
Easy to assemble/dissemble
The close proximity of the canister to the patient connector also creates some drag on the endotracheal tube as the canister can be quite heavy
Straightforward to clean
The close positioning of the canister to the patient connector can lead to inhalation of irritant dust from the carbon dioxide absorbent [20]
Relatively rapid change in anaesthetic concentration for a given fresh gas flow [15]
The close positioning of the canister to the patient connector can lead to heat being produced near to the endotracheal tube attachment [15]
Rebreathing/Reservoir Bag
Adjustable Pressure Limiting (APL) Valve or Pressure Relief Valve
Oxygen Supply Failure Alarm
Ritchie Whistle
Emergency Oxygen Flush
Scavenging
Monitoring Exposure Levels of Anaesthetic Gases
Minimising Anaesthetic Gas Exposure
Scavenging Systems
Passive Scavenging
Active Scavenging
Absorption Systems (Activated Charcoal)
Anaesthetic Breathing Systems
Useful Terminology
Rebreathing Systems
Circle System
Pathway of Gas Around a Circle Breathing System
Non‐rebreathing Systems
Controlled Mechanical Ventilation
Breathing system
Ayre’s T piece
Bain
Fresh gas flow (ml/kg/minute)
500–600
200–400
Maximum bodyweight (kg)
10
15–20
Use with controlled mechanical ventilation?
Yes
Yes
Image
Breathing system
Magill
Lack
Fresh gas flow (ml/kg/minute)
160–200
160–200
Maximum bodyweight (kg)
25–30
25–30
Use with controlled mechanical ventilation?
No
No
Image
Advantages
Disadvantages
Low resistance to breathing. No carbon dioxide absorbent canister or one‐way valves in the system
High fresh gas flows are required which makes use uneconomical for patients >25 kg bodyweight
Changing delivered anaesthetic agent concentration is rapid
High fresh gas flows can lead to increased expense and environmental pollution
Cheaper to purchase compared to rebreathing systems
Narrow inspiratory and expiratory limbs may cause increased resistance to breathing in larger foals
Inspired gas can be cold and dry which can lead to hypothermia in small foals
Advantages
Disadvantages
CMV results in a reduction in the work of breathing [30]
CMV results in negative cardiovascular effects including a reduction in venous return and cardiac output [30]
CMV can effectively treat hypoventilation
CMV may have the potential to cause lung injury
CMV may be used to reduce atelectasis by using techniques such as continuous positive airway pressure (CPAP) and positive end‐expiratory pressure (PEEP) [31]
CMV may cause increases in proinflammatory cytokines, which have been associated with inflammatory lung diseases [22]
CMV can be used with techniques such as a recruitment manoeuvre (RM) to re‐inflate collapsed alveoli [31]
The provision of CMV requires expensive equipment which must be maintained
Ventilator Types
Direct Blower – Demand Valve
Bellow Squeezer – Bellows in a Box
Piston Driven – Tafonius®
Ventilator Settings
Monitoring the Effect of Controlled Mechanical Ventilation
Endotracheal Tubes
Intubation Procedure: How to Intubate a Horse
Endotracheal Intubation [35]
Nasotracheal Intubation [35]
Types of ETT
Silicone
Red Rubber
Tube Selection
Checking for Patency
Cuff Inflation
Complications Associated with ETTs
ETT Obstruction
Nasotracheal Tubes
Cuff‐related Complications
Maintenance of Endotracheal Tubes
Cleaning, Sterilisation and Storage
Safety Checks
Endotracheal Tubes
Anaesthetic Machine Check
Checking Equipment Used for TIVA
Equipment Fault Reporting
Servicing of Equipment
Emergency Power Supply
Anaesthetic Monitoring Equipment
Ensure all flow control valves and vaporisers are turned off
Oxygen/Medical Air Supply
For individual cylinder supply: Check that each cylinder is secured in place. Open each cylinder in turn and check the pressure, label each cylinder ‘full’ or ‘in‐use’ accordingly. Replace any cylinders that are empty
For pipeline gases: Open the cylinders or the manifold as applicable. Check that the contents of the cylinders are adequate for the intended anaesthetic duration. Label cylinders ‘full’ or ‘in‐use’ accordingly and replace any empty cylinders
Check the connection between the gas pipelines and the supply ports using the ‘tug test’ [19]
Oxygen Flowmeter
Slowly turn the oxygen flowmeter control valve on and then back off again. Watch the bobbin as you do so; the function should be smooth with the bobbin rising as you open the valve and then falling back to zero as you close the valve. The bobbin should be spinning and free of resistance. Repeat with the other gases
Vaporiser
Check that the vaporiser is securely fastened to the back bar and that the locking mechanism is fully engaged [19]. Check that the vaporiser is full of agents but not overfilled and that the filling port is tightly closed [9]. Turn the percentage control dial all the way on and then off again. The function should be smooth
Oxygen Supply Failure Alarm
Turn the oxygen flow meter control valve on and then disconnect the oxygen supply. The oxygen supply failure alarm should be audible and continuous until supply is restored
Soda Lime
Check canister contents (colour change and indicated level of use) [19]
Scavenging
Passive scavenging: Check the connection of the scavenging tubing to the adjustable APL valve. Check the length of the scavenging tubing from the anaesthetic machine connection to the external exit point and ensure that the tubing is not obstructed at any point and that there are no signs of wear or damage
Active scavenging: Turn on the scavenging and ensure that the float inside the Barnsley receiver or similar receiving device is elevated and spinning
Mechanical Ventilator
Ensure that the tubing associated with the ventilator is correctly configured. Check that pressures/volumes/times are appropriately set for the size of the patient. Check that alarms are functioning if present. Prepare an alternative method of ventilation in the event of ventilator malfunction
Leak Test for a Circle Breathing System
For a circle breathing system and reservoir bag:
Plug the patient’s end of the breathing system, close the APL valve and turn on the fresh gas flow to inflate the reservoir bag. Inflate bag to a set pressure or so that it is moderately distended. Turn off the fresh gas flow and observe for any loss of pressure or volume within the system
After performing the leak test, ALWAYS remember to re‐open the APL valve
Using the two‐bag test: Attach the patient end of the breathing system to a reservoir bag or ‘test‐lung’. Set the fresh gas flow to 5 l/min and ventilate manually. Check that the whole breathing system is patent, and the unidirectional valves are moving. Check the function of the APL valve by squeezing both bags [19]
For a circle breathing system and mechanical ventilator:
Using the two‐bag test: Attach the patient end of the breathing system to a reservoir bag or ‘test‐lung’. It may be useful to place the ‘test lung’ in a box or bin to simulate the thorax. Turn on the ventilator and check that the ventilator cycles correctly according to pre‐set pressures and/or volumes
Monitors
Check monitors are working and configured correctly. Check alarm limits and volumes [19]
10.4 Anaesthetic Risks and Induction
Anaesthetic Risks
Monitoring equipment
When to use
Reason for use
How to use
Comments
Capnography
Capnography should be employed during the GA of all intubated patients
Capnography measures the amount of carbon dioxide (CO2) that is expired (end tidal CO2 (ETCO2) [50] and inspired (fractional inspired CO2 (FiCO2) in one breath
CO2 absorbs infra‐red light. A sensor detects how much infrared light is absorbed and this is directly comparable to the level of CO2 expired in one breath [51]. The CO2 tension during the respiratory cycle is displayed as a number and also as a trace, or capnograph. Capnography may use mainstream or side stream analysers. Side stream analysers are the common type in practice
Capnography provides an insight into ventilation, anaesthetic depth, cardiac output as well as any equipment malfunction [50]. It can be used to diagnose rebreathing, airway obstruction or leaks in the breathing system or anaesthetic machine [50]
Pulse oximetry
Pulse oximetry can be employed in all patients under GA
Pulse oximetry provides a non‐invasive, continuous and inexpensive method to assess the cardiovascular and respiratory functions of horses under anaesthesia [52]
Pulse oximetry uses red and infra‐red light to detect the saturation of haemoglobin with oxygen (SpO2). The principles of measurement are based on the different light absorption spectra of oxyhaemoglobin and deoxyhaemoglobin, and the detection of a pulsatile signal [53, 54]
Limitations include interference due to light, movement, poor perfusion and the absence of a commercially available pulse oximeter calibrated for horse blood [53]
Electrocardiography (ECG)
ECG can be used to identify abnormal cardiac rhythm before or during anaesthesia [53]
Electrical activity in the heart is detected by skin electrodes and can be transformed into a characteristic trace, the morphology of which corresponds to events in the cardiac cycle
Conduction of electrical activity in the heart follows a fairly fixed pathway: from the sinus node, across the atrial myocardium, through the atrioventricular node, His bundle, bundle branches, and Purkinje system to the ventricular myocardium [55]. This electrical activity generates a characteristic ECG waveform which can be used to assess heart rate and rhythm. Recognition of the normal P‐QRS‐T morphology is required in order to accurately assess an ECG recording and the timing intervals [55]
Good electrical contact is required between the clips and the skin, and this can be facilitated using alcohol or electrode gel [53]
Arterial blood pressure measurement (ABP)
ABP should be measured in all horses under GA
ABP measurement provides important information relating to the cardiovascular system [58]. ABP monitoring is particularly important in haemodynamically compromised horses, for example, those undergoing colic surgery
There are two ways to measure ABP:
Direct (invasive) arterial blood pressure (IBP) measurement: In horses, IBP is considered the gold standard ABP measurement technique [59]
Indirect or non‐invasive blood pressure (NIBP) measurement: Inaccuracy and poor reliability of NIBP devices compared with IBP mean they remain underused in horses [60]. NIBP measurement may be useful in foals, where placement of an arterial catheter may be more challenging
In situations where IBP monitoring is not available/viable, then NIBP measurement can be performed however, this is not as accurate in adult horses compared to foals
Central Venous Pressure (CVP)
CVP is not routinely monitored in horses but may be measured for experimental reasons
CVP provides information relating to blood volume and cardiac preload. It may be used in states of hypo and hypervolaemia and used to assess the response to treatment
Measuring CVP is complex and includes placing an IV catheter through the jugular vein into the right atrium and observing the characteristic pressure waveforms and values on an oscilloscope or IBP monitor.
This technique is invasive, challenging and requires trained personnel. The technique itself and the catheter can cause arrhythmia, infection and trauma [61].
Blood gas analysis
Arterial blood gas analysis is useful in all horses undergoing GA to assess adequacy of ventilation and acid base balance [62]
Blood gas analysis provides information about respiratory and cardiovascular function and metabolic status [53, 63, 64]. The level of accuracy and the information gained cannot be replaced by any non‐invasive method [65, 66] such as pulse oximetry or capnography
Arterial blood samples are usually drawn from a pre‐placed peripheral arterial catheter used for direct blood pressure measurement. Peripheral catheters used for this purpose are most commonly placed in the facial, transverse facial or metatarsal artery. Venous blood samples are usually drawn from the jugular vein
Blood gas analysis is limited by the number of samples taken and the time needed to obtain the results; therefore, the samples are collected as needed, most often at intervals of 30 or 60 minutes but more frequently if the patient’s condition requires it
Thermometers
Monitoring body temperature is important during GA, and particularly important in foals
Maintenance of normothermia is required to preserve normal physiological function [66]. GA inhibits vasoconstriction which allows generalised redistribution of body heat. A decrease in body temperature occurs as heat is lost to the environment [53]
The end of the thermometer should be lubricated. The lubricated end of the thermometer should be inserted about 2 inches into the rectum and held against the rectal wall to avoid faecal material, which may cause an inaccurate reading. Once the thermometer alarm sounds, the thermometer should be carefully removed, the reading noted, and the thermometer should be turned off and cleaned
Rectal temperature should be monitored at 15 minutes intervals during inhalational anaesthesia [53]
American Society of Anaesthesiologists (ASA) Anaesthetic Risk Score
Risks for Specific Patients
Colic Patients
Non‐strangulating GIT Obstructions
Strangulating GIT Obstructions
Clinical Signs
Clinical Examination and Preparation
Considerations for Anaesthesia
Post‐operative Care
Limb Fractures
Neonates (<4 Weeks)
Older Foals (>4 Weeks)
Geriatric Patients
Pituitary Pars Intermedia Dysfunction (PPID)
Musculoskeletal Considerations
Respiratory Considerations
Cardiovascular Considerations
Obesity
Caesarean Section
Trauma
Anaesthetic Induction
Premedication
The Induction Process
10.5 Monitoring Techniques for Anaesthetised Equine Patients
Introduction
Anaesthetic Monitoring Observations
Level of Consciousness
Reflexes and Observations Indicative of Anaesthetic Depth
Ocular Reflexes and Movement
Palpebral Reflex
Corneal Reflex
Nystagmus
Anal Reflex
Muscle Tone
Neck
Limbs
Swallowing
Reflexes and Patient Observations During TIVA
Anaesthetic Monitoring Observations of the Cardiovascular System
Useful Terminology
Manual Palpation of Pulse Rate and Quality
Mucous Membrane Colour
Capillary Refill Time (CRT)
Monitoring the Cardiorespiratory Systems with Equipment
ECG
Arterial Blood Pressure (ABP) Measurement
Invasive Arterial Blood Pressure (IBP) Monitoring
Non‐invasive Blood Pressure (NIBP) Monitoring
Central Venous Pressure (CVP)
CO Monitoring
Anaesthetic Monitoring Observations of the Respiratory System
Useful Terminology
Anaesthetic Monitoring of the Respiratory System with Equipment
Capnography
Pulse Oximetry
Arterial Blood Gas Analysis
Spirometry
Temperature
Equipment Observations
Care Requirements of an Anaesthetised Equine Patient
Blood Loss
Changes in Physiological Parameters in Response to Haemorrhage
Urine Output
Treatment of Haemorrhage
Crystalloids
Isotonic Fluids
Hypertonic Saline
Colloids
Natural Colloids
Blood Products
Blood
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