Intro Flashcards
Difference between anaesthesia and sleep?
When patients are anaesthetised they are not asleep but they are unconscious. Patients who are asleep can move, respond to main, swallow (prevents pharyngeal secretions) and maintain there own airway. Anaesthetised patients do not. Importantly, they cannot respond to pain (although may develop a tacchycardia or move slightly if under light anaesthesia) and cannot maintain there own airway. Neither are anaesthetised patients hypnotised.
3 Components of GA?
1) Need to provide sleep (!), hypnosis or a state of unawareness 2) Need to prevent movement (muscular relaxation) which could interfere with surgery 3) Need to obtund painful stimuli (analgesia)* *Pain is a conscious sensation (requires both a sensory input and emotion) so strictly speaking anaesthetised patients do not feel pain because they are unconscious. But they can still respond to noxious stimuli so analgesia is given to prevent this.
What is balanced anaesthesia?
Achieving the components of anaesthesia can either be done using: i) Large dose of IV or inhalational anaesthetic, or ii) A combination of drugs ( = an anaesthetic at a much lower dose + analgesia +/- muscle relaxant) - this is balanced anaesthesia
What are the adv/disadv of single agent anaesthesia?
- simple: only one agent and therefore one delivery system required - respiratory and cardiac depression: due to large doses of agents required to produce muscle relaxation - death: most likely due to profound cardio-respiratory depression - can be used for short procedures - e.g. #wrist resetting
What are the different types of anaesthesia?
i) local, ii) regional or iii) general. i) Local - topical (e.g. emla cream), or infiltration (e.g. subcutaneous injection for dental procedures) ii) Regional - peripheral nerve block, epidural, spinal or intravenous regional (Bayer’s block) iii) General - single agent anaesthesia or balanced anaesthesia, both of which can be given by inhalation or total intravenous anaesthesia (TIVA)* *The important thing to remember about GA is that it can be induced by intravenous or inhalational agents, it can be maintained by intravenous or inhalational agents, they can be combined with other drugs as part of a balanced anaesthesia and with the patient breathing spontaneously or with ventilatory support
Local v general?
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 LA 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
MOA of LA?
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 speed of onset of LA?
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