Anaesthesia Flashcards
(30 cards)
What are the stages of anaesthesia? In general, what types of anaesthetic agents are used at each stage?
- Premedication (hypnotics, benzodiazepines)
- Induction (IV or inhalational for children/needle phobics)
- Intra-operative analgesia (opioid)
- Muscle paralysis (opioids; facilitates intubation/ventilation/stillness)
- Maintenance (IV or inhalational)
- Reversal of muscle paralysis and recovery (post-op analgesia e.g. opioids, NSAIDs, paracetamol; anti-emetics for post-op N&V)
Give some examples of inhalational anaesthetic agents. How are these administered?
Principal agent mixed with oxygen, air, and nitrous oxide (reduces dose of anaesthetic required to reduce ADRs)
Vaporiser is used (alter % of inspired gas which contains the volatile substance)
- nitrous oxide (N2O)
- ether
- chloroform
- xenon
- Cl and F containing compounds
Why do relatively large concentration of inhalational anaesthetics need to be administered?
Weakly interacts with ligand binding site (easily reversed)
Give some examples of intravenous anaesthetic agents and their respective onset times.
- propofol (rapid) = rapidly reaches CNS, highly protein-bound, highly lipophilic (rapidly redistributes in the CNS)
- barbiturates (rapid)
- ketamine (slower)
What are the different degrees of anaesthesia known as? How is breathing, muscle tone, and eye movement affected in each stage?
Guedel’s signs
- Analgesia and consciousness
- normal muscle tone
- slight eye movement - Excitement (delirium can occur)
- unconscious
- erratic breathing
- normal-markedly increased muscle tone
- moderate eye movement - Surgical anaesthesia
- increasing depth until breathing weak
- slightly relaxed muscle tone
- no eye movement - Respiratory paralysis (& death)
- flaccid muscle tone
- no eye movement
What are the different components of anaesthesia?
ANALGESIA
HYPNOSIS (loss of consciousness)
AMNESIA
Depression of spinal reflexes
Muscle relaxation (insensibility and immobility)
How is the potency of volatile anaesthetics measured?
Minimum Alveolar Concentration (MAC) = concentration of anaesthetic at alveoli at 1atm at which 50% of subjects fail to move to surgical stimulus
Higher MAC, higher % of volatile required to produce anaesthesia (reduced potency)
Relates to lipid solubility of drug
note: at equilibrium [anaesthetic]alveoli = [anaesthetic]spinal cord
note: MACawake = [anaesthetic]alveoli as patient is waking up
note: MAC-BAR = autonomic response, including CVS collapse
What are the factors affecting induction and recovery from volatile anaesthetic agents?
Blood:gas = volume of gas in litres that can dissolve in 1l of blood
- low value indicates fast induction and recovery
- high value means the anaesthetic enters the blood more readily
Oil:gas = determines potency and slow accumulation due to partition into fat (lipid-soluble drugs form reservoir in fat which redistribute during the recovery phase)
Give some examples of factors that affect the minimum alveolar concentration of anaesthetic agents.
Age (MAC is higher in infants and lower in elderly)
Hyperthermia increases MAC, hypothermia decreases MAC
Pregnancy increases MAC
Alcoholism increases MAC
Central stimulants (e.g. amphetamine) increase MAC
Other anaesthetics and sedatives decrease MAC
Opioids decrease MAC
note: MAC for individual agents is reduced when combined when nitrous oxide, fentanyl, etc.
At what minimum alveolar concentration range is surgical anaesthesia usually required?
1.2-1.5
Increased lipid solubility increases potency of anaesthetic? CHECK
CHECK
What are some receptors which volatile anaesthetics bind to?
GABA-A receptors
NMDA receptors (glutamate)
+ glycine Cl- channels have increased sensitivity when anaesthetics bind (reduces excitability —> inhibits transmission in brain and spinal cord —> reduced response to noxious stimuli)
Which volatile anaesthetic agents bind to GABA-A receptors? What is the mechanism of action? What effect does this have?
Majority of anaesthetic agents except xenon, nitrous oxide, and ketamine
INCREASE sensitivity to GABA (+ increased potency and efficacy via allosteric modulation)
Increase Cl- conductance —> hyperpolarisation —> inhibitory post-synaptic potential —> reduced CNS activity
- anxiolysis
- sedation
- anaesthesia
Which volatile anaesthetic agents bind to NMDA receptors? What is the mechanism of action? What effect does this have?
Xenon, nitrous oxide, ketamine
Inhibit NMDA receptors (+ reduced efficacy via allosteric modulation)
Increased Ca2+ influx —> depolarisation —> excitatory post-synaptic potential —> increased CNS activity
Which parts of the nervous systems are affected by volatile anaesthetics?
Reticular formation (hindbrain, midbrain, thalamus): - depressed ---> reduced connectivity between brain regions ---> reduced arousal
Hippocampus:
- depressed —> reduced memory
Brainstem:
- depressed —> resp. and CVS depression
Spinal cord:
- depressed dorsal horn —> analgesia
- depressed motor neuronal activity
note: some volatile anaesthetics inhibit neuronal nAChR —> reduced excitability of Na+ currents —> analgesia and amnesia
Contrast the action of intravenous and volatile anaesthetics on receptors and areas of the nervous system.
Same except IV ketamine does not affect NMDA receptors
How is the potency of intravenous anaesthetics described?
Plasma concentration required to achieve a specific end-point
e.g. loss of eyelash reflex, bispectral index (measure of cortical activity)
Give some examples of local/regional anaesthetics and when they are indicated.
e.g. lidocaine, procaine
Indications:
- dentistry
- obstetrics
- regional surgery (patient awake)
- post-op wound pain
- chronic pain management
What is the general chemical structure of local/regional anaesthetics?
Aromatic ring - ester or amide link - amine
What are some of the pharmacokinetics of local anaesthetics?
Lipid solubility (greater lipid solubility, the greater potency)
Lower dissociation constant —> faster onset (does not dissociate away from site as quickly)
Higher protein binding —> longer duration of action
Ester link present is broken in blood (short-acting)
Amide link present means it will be longer-acting
What is the mechanism of action of local anaesthetics?
Block voltage-gated sodium channels
Use-dependent block (increased firing of channel —> increased block)
Block small myelinated afferent nerves preferentially (block sympathetic fibres of nociceptive nerves first)
note: give adrenaline to cause vasoconstriction and keep the local anaesthetic in the area (increase duration of action)
Give some examples of ADRs associated with anaesthetic agents.
General anaesthetics:
- post-op N&V (opioids)
- hypotension (reduced CNS activity)
- post-op cognitive dysfunction (long term: hrs-days)
- chest infection (reduced mobility of chest during anaesthesia)
Local anaesthesia:
- anaesthetic enters circulation —> cardiovascular toxicity
In general, what are the different types of anaesthesia?
General = unconsciousness and absence of sensation
- inhalational (volatile)
- intravenous
Regional = larger regions of body but remain conscious
e.g. spinal/epidural
Local = defined peripheral nerve block
Dissociative = inhibits transmission of impulses between higher and lower centres of the brain
- e.g. ketamine
- indicated for elderly and children for short procedures (less susceptible to post-op hallucinogenic effects)
Conscious sedation = use of small amounts of anaesthetic/benzodiazepines to produce a “sleep-like” state
- maintains verbal contact but feel more comfortable
- e.g. dental treatment, minor surgery
What areas of the brain are responsible for the major actions of anaesthetics?
RETICULAR FORMATION = connections between hindbrain, midbrain, and thalamus depressed —> reduced arousal
THALAMUS = transmits/modifies sensory information
HIPPOCAMPUS = depressed —> amnesia
BRAINSTEM = depressed —> CVS depression and resp. depression
SPINAL CORD = dorsal horn depression —> analgesia
