Anaesthesia - principles and pharmacology

Question 1

what is the triad of anasthesia?

Answer 1

analgesia, hypnosis, relaxation

Question 2

name iv anaesthesia agents and their functions?

Answer 2

thiopentone or propofol - cause rapid onset of unconciousness (1arm-brain circulation time) with a rapid recovery (due to dissapearance from circulations and redistribution metabolism)

Question 3

describe the levels of conc of iv anaesthesia over time

Answer 3

Initially the blood level is very high but falls initially as the drug moves into highly perfused tissues. Muscle picks up the drug more slowly but the effect is large because of the relative mass of skeletal muscle in the body. Fatty tissue picks up drug even more slowly but can store large amounts due to the high fat solubility of these drugs..

Question 4

How do general anaesthetic agents work?

Answer 4

all let cl into neurones to hyperpolarise the neurones so they are less likely to fire. Inhalational agents dissolve in membranes (Direct physical effect), iv agents use allosteric binding i.e. gaba - open cl channels. Cerebral function is lost.

Question 5

inhalationsal anaesthetics

Answer 5

halogenated hydrocarbons, cross alveolar bm easily, arterial conc equates closely to alveolar partial pressure. Inhalational anaesthetic agents are all halogenated hydrocarbons and are taken up and almost exclusively excreted via the lungs. At induction the patient is given a relatively high concentration of the agent to breath. The gas then moves down the concentration gradient in to the patients blood and finally brain to achieve a high enough partial pressure there to produce unconsciousness. Arterial concentration equates closely to alveolar partial pressure

Question 6

what is MAC?

Answer 6

minimum alveolar conc. It is a measure of potency. A lower number = higher potency. MAC is the concept of the concentration of the drug required in the alveoli which is required to produce anaesthesia with any particular agent. Therefore a low MAC value means an agent is potent. E.g. Halothane (MAC = 0.8%) is more potent than Desflurane (MAC = 6%) because it takes a lesser concentration of the agent to produce the same effect.

Question 7

what is the phyhsiological effect of general anaesthesia?

Answer 7

Depress cardiovascular centre - Reduce sympathetic outflow, Negative inotropic/chronotropic effect on heart, Reduced vasoconstrictor tone = vasodilation
Direct: Negatively inotropic, Vasodilation – decreased peripheral resistance, Venodilation – decreased venous return and cardiac output
Respiratory - All anaesthetic agents are respiratory depressants: Reduce hypoxic and hypercarbic drive, Decreased tidal volume and increased rate, Paralyse cilia, Decreased FRC:, Lower lung volumes, VQ mismatch.

Question 8

how do muscle relaxants work?

Answer 8

They indiscriminately paralyse skeletal muscle therefore including respiratory and airway muscles, Systemic muscle relaxation must be accompanied by unconsciousness because being paralysed and awake is very unpleasant

Question 9

when are muscle relaxants used?

Answer 9

ventilation and intubation, for immobility, body cavity surgery.

Question 10

what are the problems with muscle relaxants?

Answer 10

incomplete reversal, apnoea

Question 11

how do NMB’s (neuromuscular blocking agents)?

Answer 11

Competitive block of nicotine acetylcholine (Ach) receptors at NMJ – prevent the opening of Na+ channels
Reversal: Ach overcomes the block, Anticholinesterase reversal agents stop the removal of Ach from the synapse.
Creates a myasthenic-like state – reducing the number of available receptors.

Question 12

how to depolarising NMB’s work?

Answer 12

Depolarise motor end plate, Renders post-junctional membrane refractory to further stimulus
Suxamethonium – very fast and short acting makes it valuable for emergency control of the airway

Question 13

How does local anaesthesia work physiologically?

Answer 13

Sodium channel blockers, Prevent propagation of action potential, LAs are pharmacologically filthy – they act indiscriminately on a huge range of tissues because all excitable membranes in the body contain sodium channels. Limiting factor in use is toxicity, Toxicity comes from a high plasma level of LA. Absorption > rate of metabolism = high plasma levels

Question 14

what does toxicity depend on?

Answer 14

Dose, rate of absorption, weight, drug used (bupivacaine > lignocaine > prilocaine) some LAs produce more toxic effects for the same plasma levels

Question 15

sx of local anaesthetic toxicity?

Answer 15

Circumoral and lingual numbness and tingling, Light-headedness, Tinntius, visual disturbances, Muscular twitching, Drowsiness, Cardiovascular depression, Convulsions, Coma, Cardiorespiratory arrest.

Question 16

How does regional anaesthesia work in regard to the patients experience?

Answer 16

Retain awareness, Derangement of CVS physiology - proportional to size of anaesthetised area, Relative sparing of respiratory function, Blocks which affect greater area of the body produce greater physiological impact – from local anaesthesia to epidural and spinal

Question 17

what are indications for spinal and epidural anaesthesia?

Answer 17

Avoidance of general anaesthesia, Severe respiratory disease due to less respiratory physiological impact, Avoid airway problems, Allergies/reactions to GA agents

Question 18

what are contraindications for spinal and epidural anaesthesia?

Answer 18

Patient refusal, Fixed cardiac output – aortic/mitral stenosis, Infection, Bleeding diasthesis/anticoagulation, Technical difficulties, Spinal problems/neurology.

Question 19

how does spinal anaesthesia work?

Answer 19

subarachnoid injection, rapid onset, complete block, usually all modalities, 2-3hr duration, cannot be extended.

Question 20

how does Epidural anaesthesia work?

Answer 20

Injection is extradural, Onset is slow = 30-45 mins, Segmental block, Good analgesia with motor sparing, Duration = 3-4 hours, extandable.