Anaesthetics - Introduction to anaesthesia 2 Flashcards
What are the main differences between general and local anaesthesia?
General anaesthesia prevents pain generated peripherally being interpreted as pain by the CNS. It does NOT stop transmission of pain from the source.
Local and regional anaesthetics prevents the transmission of painful stimuli reaching the CNS (via the thalamus).
How are local anaesthetics classified?
Local anaesthetics are weak bases. They are divided into 2 groups depending on the linkage between an aromatic ring, and an amine group (which all agents have). This linkage is either an amide or an ester.
Ester - e.g. cocaine, procaine, amethocaine
- allergic reactions are common*
- metabolized by plasma and liver cholinesterase
Amides (more common) - e.g. bupivacaine, lidocaine
- allergic reactions are rare
- metabolized by the liver
- allergic reaction occurs because metabolism results in the production of para-amino-benzoate
What is the mechanism of action of local anaesthetics?
LAs act by reversible inhibition of action potential propagation in all excitable tissues. They block voltage gated sodium channels on nerve cell membranes and prevent sodium influx and action potential propagation.
Only the uncharged or lipophilic form of the drug can cross the plasma membrane*. Once inside, the pH of the axon is more acidic which promotes ionization (i.e. the LA is now charged). This is the active component that blocks the Na channel. The higher the frequency of sodium channel opening the more susceptible the nerve is to blockade (use dependence) - sensory nerve fibres are blocked before motor nerves.
- physiological pH (7.4) promotes dissociation of the charged LA agent that is injected into H+ ions and an uncharged molecule
What determines the speed of onset of local anaesthetics?
This is related to the amount of drug in the unionized form that can cross the cell membrane. This depends on its pKa (pH at which 50% of the drug is in the ionized form).
For example, lidocaine (pKa 7.9) has a quicker speed of onset than bupivacaine (pKa 8.1) because more lidocaine is unionized at physiological pH and hence can cross the cell membrane.
Additives effect the speed of onset. For example, bicarbonate raises extracellular pH and thus increases the unionized fraction of the drug which can then cross the cell membrane.
What prolongs the duration of action of LAs?
Protein bound LAs have a longer duration of action. Ester LAs (e.g. cocaine) may have prolonged duration of action when plasma cholinesterase is reduced, for example in pregnancy, liver disease or when the enzyme is atypical or absent (e.g. pseudocholinesterase deficiency).
Why are vasoconstrictors added to LAs? Does this affect their maximum safe dose?
Vasoconstrictors (e.g. adrenaline, or felypressin) prolongs the duration of action of LAs by reducing systemic absorption. These aim to keep the LA concentrated at the site of administration to prolong its action, reduce toxicity and maybe to enhance block quality.
When SOME LAs are used with a vasoconstrictor their maximum safe dose increases - e.g. lidocaine is normally 3mg/kg, with adrenaline this goes up to 7mg/kg. Others (e.g. bupivacaine) remain unchanged.
When should LAs with a vasoconstrictor never be used?
They should never be used in areas with a terminal arterial blood supply where necrosis can occur - e.g. penis or digits.
How do hyperbaric solutions affect LA spread?
Hyperbaric solutions (e.g. by the addition of dextrose) effect the spread of LA when they are injected into the CSF. Dextrose is denser than CSF, and when combined in solution causes the LA to sink to the most dependent part - i.e. to the left or right if the patient is lying on their side or to the caudal area if sitting upright.
What causes toxicity of LAs?
This occurs as a result of membrane stabilisation of other excitable tissues (e.g. CNS, heart). Toxicity can be due to excessive dose of drug being given or due to a smaller dose being administered via the wrong route (e.g. IV).
What are the features of LA toxicity?
These are concentration (dose dependent):
- circumoral tingling
- feeling of impending doom
- dysrhythmias
- CVS collapse
- LOC
- convulsions
- cardiac arrest
How should LA toxicity be treated?
Treatment is supportive, including airway maintenance/ intubation if needed, IV fluids, and vasopressors (e.g. adrenaline) and control of seizures with benzodiazepines, thiopentol or propofol. If cardiac arrest occurs then CPR is performed.
IV lipid emulsion Intralipid 20% 1.5mL/kg is now recommended for LA toxicity/ cardiovascular collapse. But recovery can take over an hour so CPR may be prolonged.
What determines the rate of systemic absorption of LAs?
This depends on the site of administration: mucous membranes > intercostals > major nerve block > infiltration.
What is associated with prilocaine?
Prilocaine metabolism produces toludine, which reduces Hb to metHb. Excess prilocaine can therefore cause methaemoglobinaemia. It is treated with methylene blue.
What is the maximum safe dose of bupivicaine, lignocaine and prilocaine?
Bupivicaine = 2mg/kg Lignocaine = 3mg/kg Prilocaine = 6mg/kg
Bupivicaine has a lower CVS collapse: convulsion meaning that if it is injected intravenously it is particularly dangerous.
How can LAs be administered?
1) Topical application - EMLA ( = Eutetic mixture of local anaesthetics) - this is an emulsion of equal amounts of the base forms of prilocaine and lidocaine. Each drug lowers the melting point of the other. It takes about 45 mins to work though; lignocaine spray
2) Infiltration - e.g. cannulae, sutures
- Field block = larger injection of LA for inguinal hernias
- Wound infiltration - usually with adrenaline, watch total dose
At what level is spinal anaesthesia administered? How is it performed?
Usually L3-4 (because the cord has terminated by this level) and is administered using a 25-27g needle.
The anaesthetic is injected directly into the CSF with the needle having passed through all the dural layers. Small volumes of bupivocaine are often used, and there is a very rapid effect.
Unlike an epidural, a total block is usually achieved with motor and sensory loss.
Opioids such as fentanyl can also be given.
How is an epidural anaesthetic given?
A Tuohy needle is used to pierce through the ligaments of the spine to access the epidural “space” (this is a potential space). An LOR (loss of resistance technique) is used whereby saline is slowly forced through the needle until it can be injected into the space.
A catheter is then inserted and large volumes can be administered into the extradural space. It can be given in the thoracic, lumbar or sacral regions (esp. children) but should not produce a motor block.
- Both spinal and epidural are examples of regional anaesthesia
What are nerve blocks?
These are another example of regional anaesthesia. LA is injected close to a nerve which can run within a sheath alongside arteries and veins. It is important to avoid injecting anaesthetic into these.
If injecting for the brachial or sacral plexuses then up to 30mls of fluid may be required.
Single nerves (e.g. femoral) or multiple nerves (e.g. brachial plexus) can be blocked.
How is a Biers block performed and when is it used?
(Intravenous regional anaesthesia). A BP cuff is applied to the upper arm after placement of a cannula in the hand. After exsanguination of the limb by either elevation or the use of a compression bandage the BP cuff (or double torniquet) is inflated to 100mmHg above systolic BP.
Prilocaine is the preferred drug and is injected IV. It is unable to spread beyond the cuff and thus acts within a confined area. It provides good anaesthesia for distal limb procedures (e.g. fracture manipulation).
The cuff must be let down after 20 mins to allow the LA to spread into the adjacent tissues in order to prevent toxic plasma levels of LA following systemic absorption.
What is regional anaesthesia?
This involves the injection of a local anaesthetic and sometimes other drugs (e.g. opioids) targeted at specific nerves or nerve plexus to numb the area that the nerve innervates, including the spinal cord and its nerve roots.
What are the indications for nerve block?
Sole form of anaesthesia during an operation
Combined with general anaesthesia or sedation
Postoperative anaesthesia
Chronic pain conditions
What is a central (or neuraxial) blockade?
Central blockade is the introduction of drugs into the CSF within the subarachnoid space (spinal blockade) or the surrounding epidural space (epidural blockade). Anaesthesia is provided for surgery below the level of the umbilicus (T10).
What are the advantages of a central blockade?
Avoidance of GA in at risk patients - e.g. severe respiratory disease, difficult intubation, diabetic, myopathies, pregnant, malignant hyperthermia
Good post operative analgesia
Avoids sedation/ N&V, e.g. by morphine
Reduction in pulmonary embolism due to sympathetic blockade
Reduced blood loss
Reduced stress response to surgery
What are the side effects of central blockade?
Hypotension (sympathetic block)
N&V (hypotension, opiates)
Lower limb motor block
Post dural puncture headache (more likely with a large needle, non pencil point tip, inadvertent Tuohy needle puncture of the dura, young age)
High block can affect upper limb power and respiration (C3-5)
Loss of consciousness (total spinal)
Nerve damage (rare)
