Tips for Anaesthesia Attachments

During your anaesthetic attachment take the opportunity to:

• discuss the pharmacology of the drugs used in anaesthesia for:

induction of anaesthesia;

maintenance of anaesthesia;

analgesia;

achieving neuromuscular blockade in different circumstances;

prevention and treatment of nausea and vomiting;

local anaesthesia;

• discuss the different fluids used in the perioperative period:

crystalloids;

colloids;

blood and its components;

• discuss the indications and limitations of the different fluids available;
  
• develop plans for postoperative fluid management after different types of surgical procedures.

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Anaesthetists have to be familiar with a wide range of drugs – those directly associated with anaesthesia, and also medications that may impact upon anaesthesia. Furthermore, unlike in most other branches of medicine, drugs associated with anaesthesia are almost always given parenterally, either intravenously or via inhalation, usually produce profound physiological changes, and often have serious undesirable actions in addition to their intended effects. As well as drugs, many patients will also require intravenous fluids, blood, and blood products during anaesthesia, surgery, and postoperatively.

Premedication

Intravenous Anaesthetic Drugs

This group of drugs is most commonly used to induce anaesthesia. After intravenous (IV) injection, these drugs are carried in the bloodstream into the cerebral circulation. As they are very lipid soluble, they quickly cross the blood-brain barrier, resulting in loss of consciousness. Subsequently the drug is rapidly redistributed to other tissues (initially the muscles and then fat), and so the plasma and brain concentrations fall and the patient recovers consciousness. A single bolus of these drugs has a rapid onset, short duration of action with rapid recovery. Despite this, complete elimination of some drugs, usually by hepatic metabolism, takes much longer and repeated doses may lead to accumulation and delayed recovery. This is seen typically with thiopental and currently the only exception to this is propofol (see below). All these drugs cause depression of the cardiovascular and respiratory systems. The dose required to induce anaesthesia is significantly reduced in those patients who are elderly, frail, hypovolaemic or have compromise of their cardiovascular system. A synopsis of the drugs commonly used is given in Table 3.1.

Table 3.1 Intravenous drugs used for the induction of anaesthesia and their effects

Inhaled Anaesthetic Drugs

Although these drugs can be used to induce anaesthesia, they are most commonly used to maintain anaesthesia. Apart from nitrous oxide (N₂O), they are halogenated hydrocarbons. They all have relatively low boiling points, so they evaporate easily at ambient temperature and hence are often referred to as vapours. A controlled amount of the vapour that is produced is added to the fresh gas flow (oxygen and air or nitrous oxide) and breathed by the patient. Once in the lungs the vapour diffuses into the pulmonary capillary blood and is distributed via the systemic circulation to the brain and other tissues. The depth of anaesthesia produced is directly related to the partial pressure that the vapour exerts in the brain, and this is closely related to the partial pressure in the alveoli. The rate at which the alveolar partial pressure can be changed determines the rate of change in the brain and hence the speed of, induction, change in depth, and recovery from anaesthesia. Even the most rapid induction using these drugs takes several minutes to achieve the same depth of anaesthesia that is achieved within seconds of giving an IV anaesthetic drug. The inspired concentration of all of these compounds is expressed as the percentage by volume. All the inhalational anaesthetics cause dose-dependent depression of the cardiovascular and respiratory systems. A synopsis of the currently used drugs used is given in Table 3.2.

Table 3.2 Inhalational anaesthetic drugs and their effects

There are two concepts that will help in understanding the use of inhalational anaesthetics: solubility and minimum alveolar concentration (MAC).

Solubility

The rate of change of depth of anaesthesia is determined by how quickly the alveolar, and hence brain, partial pressure of anaesthetic can be altered. One of the main factors governing alveolar partial pressure for a given inhalational anaesthetic is its solubility in blood. One that is relatively soluble in blood (for example, isoflurane) will dissolve readily in the plasma and not exert a very high partial pressure. Consequently, a relatively large amount of the anaesthetic has to diffuse from the alveoli before the partial pressure in the blood and the brain begins to rise. Conversely, if an agent is insoluble in blood (for example, desflurane), only a small amount has to diffuse from the alveoli into the blood to cause a rise blood and brain partial pressure and therefore an increase in depth of anaesthesia can be achieved more quickly. Reducing the depth or recovery from anaesthesia follows similar principles in reverse; a greater amount of a soluble agent will have to be excreted for the brain, blood and alveolar partial pressure to fall, which takes proportionately longer.

Other factors that determine the speed at which the alveolar concentration rises include:

• A high inspired concentration, limited clinically by the degree of irritation caused by the vapour.
  
• Alveolar ventilation. This is most pronounced for drugs with a high solubility. As large amounts are removed from the alveoli, increasing ventilation ensures more rapid replacement.
  
• Cardiac output: If high, this results in a greater pulmonary blood flow, increasing uptake and thereby lowering the alveolar partial pressure. If low, the converse occurs and the alveolar concentration rises more rapidly.

Minimum Alveolar Concentration

To compare the potencies and side effects of the inhalational anaesthetics the concept of minimum alveolar concentration (MAC) is used. Minimum alveolar concentration is the concentration required to prevent movement following a surgical stimulus in 50% of subjects. At 1 MAC, or multiples thereof, the anaesthetic effect of different drugs will be the same and a comparison of the side-effects can be made. Compounds with a low potency (such as desflurane) will have a high MAC; those with a high potency (such as isoflurane) will have a low MAC.

The effects of inhalational anaesthetics are additive, therefore two values for MAC are often quoted – the value in oxygen (Table 3.2) and the value when given with a stated percentage of nitrous oxide (which has its own MAC), which will clearly be less. The value of MAC is also affected by a number of other patient factors (Table 3.3).

Table 3.3 Factors affecting the minimum alveolar concentration (MAC) of inhalational anaesthetic drugs

Nitrous Oxide

Nitrous oxide (N₂O) is a colourless, sweet-smelling, non-irritant vapour with moderate analgesic properties but low anaesthetic potency (MAC 105%). The maximum safe inspired concentration that can be administered without the risk of causing hypoxia is approximately 70%, therefore unconsciousness or anaesthesia sufficient to allow surgery is rarely achieved. Consequently, it is usually given in conjunction with one of the other vapours. Nitrous oxide is available in cylinders premixed with oxygen as a 50:50 mixture called ‘Entonox’, which is used as an analgesic in obstetrics and by the emergency services.

Systemic effects

• Cardiovascular depression, worse in patients with pre-existing cardiac disease.
  
• Slight increase in the respiratory rate and a decrease in the tidal volume. It decreases the ventilatory response to hypercarbia and hypoxia.
  
• Cerebral vasodilatation, increasing intracranial pressure (ICP).
  
• Diffuses into air-filled cavities more rapidly than nitrogen can escape, causing either a rise in pressure (for example, in the middle ear) or an increase in volume (for example, within the gut or an air embolus).
  
• May cause bone-marrow suppression by inhibiting the production of factors necessary for the synthesis of DNA. The length of exposure necessary may be as short as a few hours, and recovery usually occurs within 1 week.
  
• At the end of anaesthesia, nitrous oxide rapidly diffuses into the alveoli reducing the partial pressure of oxygen and can result in hypoxia (diffusion hypoxia) if the patient is breathing air. This can be overcome by increasing the inspired oxygen concentration during recovery from anaesthesia.

Total Intravenous Anaesthesia

Neuromuscular Blocking Drugs

Suxamethonium has no direct effect on the cardiovascular, respiratory, or central nervous systems. Bradycardia secondary to vagal stimulation is common after very large or repeated doses, and can be avoided by pretreatment with atropine. Suxamethonium has a number of important side effects (Table 3.4).

Table 3.4 Important side effects of suxamethonium

• Malignant hyperpyrexia in susceptible patients

• Increased intraocular pressure which may cause loss of vitreous in penetrating eye injuries

• Muscular pain around the limb girdles, most common 24 h after administration in young adults

• Histamine release: usually localized but may cause an anaphylactic reaction

• Prolonged apnoea in patients with pseudocholinesterase deficiency (see below)

• A predictable rise in serum potassium by 0.5–0.7 mmol/L in all patients

• A massive rise in serum potassium may provoke arrhythmias in patients with:

burns, maximal 3 weeks to 3 months after the burn

denervation injury, e.g. spinal cord trauma, maximal after 1 week

muscle dystrophies, e.g. Duchenne’s

crush injury

Pseudocholinesterase deficiency

A variety of genes have been identified that are involved in plasma cholinesterase production, some of which lead to altered metabolism of suxamethonium. The most significant genotypes are:

• normal homozygotes: sufficient enzyme activity to hydrolyse suxamethonium in 4–6 min (950 per 1000 population);
  
• atypical heterozygotes: slightly reduced enzyme activity levels; suxamethonium lasts 10–20 min (50 per 1000);
  
• atypical homozygotes: marked deficiency of active enzyme; members of this group remain apnoeic for up to 2 hours after being given suxamethonium (<1 per 1000).

Treatment of a patient found to have severe deficiency of pseudocholinesterase is with maintenance of anaesthesia or sedation and ventilatory support until spontaneous recovery occurs. The patient should subsequently be warned and given a card that carries details and, because of its inherited nature, the remainder of the family should be investigated.

Non-Depolarizing Neuromuscular Blocking Drugs

These drugs compete with acetylcholine and block its access to the postsynaptic receptor sites on the muscle but do not cause depolarization. (They may also block presynaptic receptors responsible for facilitating the release of acetylcholine.) The time to maximum effect, that is when relaxation is adequate to allow tracheal intubation, is relatively slow compared with suxamethonium, generally 1.5–3 min. A synopsis of the drugs used is given in Table 3.5.

Table 3.5 Non depolarizing neuromuscular blocking drugs

They are used in two ways:

• following suxamethonium to maintain muscle relaxation during surgery;
  
• to facilitate tracheal intubation in non-urgent situations.

Related posts:

Anaesthetic Assessment and Preparation for Surgery Local and Regional Anaesthesia The Practice of General Anaesthesia Special Circumstances Anaesthetic Equipment and Monitoring Post-Anaesthesia Care

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