Anaesthesia And Pain Flashcards
Pain receptors are
Nociceptors
Pain is
Subjective, unpleasant sensory and emotional experience and is a protective mechanism. Memory of pain can help avoid future harmful events
Chronic pain
Lasts more than 6 months, exaggerated afferent pain impulses or permanent sensitised dorsal horn or a poor descending pathway
Pain reaches the brain by
Stimulus providing detecting by nociceptors, generation of an action potential and receptors reach the spinal cord via the dorsal root which synapses with the dorsal horn and ascends to the brain via thalamus and somatosensory cortex
4 phases of GA
Induction - inducing unconsciousness
Maintenance - homeostasis and anaesthesia
Emergence - unconscious - concious
Recovery
Analgesia is
Suppression of physiological responses to painful stimuli
Anaesthesia is
Administration of meds that block feeling of pain / deep state of unconsciousness. Relieve pain and support physiological functions during a procedure
Local anaesthetic
Induces absence of pain locally by injecting around a nerve / trunk to provide anaesthesia in the peripheral nervous system, inhibits excitation conduction process
GA strives to achieve 4 A’s
Lack of awareness,
Amnesia,
Analgesia and
Akinesia
Pre meds
Benzodiazepines - hypnotics /sedatives to relieve anxiety
Analgesics - morphine/panadol/NSAIDS
Anticholinergics - reduce saliva control/bradycardia/ antiemetic to reduce pop nausea
Antis - reduce wound infection
GABA is
An inhibitory neurotransmitter widely distributed in the CNS.
Neuronal activation - GABA released to synapse and acts on post synaptic GABA receptors
Thiopentone - mimics GABA - depresses excitatory neurotransmission
Propofol
Acts on specific GABAa receptor to shorten channel opening times at nicotine’s ACh receptors - rapid induction
Ketamine
Glutamate receptor antagonist, interacts with Nictotinic ACh receptors and voltage gated CA channels
Inhalation agents
Face mask - alveolar capillary membrane- circulation.
Binds to lipid layer of cell membranes to cause small expansion/swelling to distort ion channels - inhibiting excitatory brain and spinal cord activity
Volatile agent examples
Desflurane
Isoflurane
Sevoflurane
N20
All are triggers of malignant hyperthermia
There is no antidote to
Inhaled agents
Pain impulses at nociceptors are transmitted to the CNS via
myelinated delta fibres in response to mechanical and thermal pain
unmyelinated C fibres (slow pathway) in response to chemical, slow burning
Neurotransmitters involved with pain are
Substance P - activates ascending pathway to brain
and
Glutamate - neurotransmitter on dorsal horn, causes permeability changes to allow ca entry to dorsal horn = increased excitability.
Opioids receptor inhibits at the afferent pain fibre synapse
Descending analgesic pathway
inhibits pain transmission, endogneous opioids are released which inhibit substance p release and block the pain impulses to the brain
Opioids found throughout the CNS and perpiheral tissues
inhibit afferent pathway,
activate descending pathway and
inhibit excitation of sensory nerve terminals.
Gate control theory of pain
proposes how pain is reduced by activating a nonpainful sensation by the alpha delta smaller sensory nerve, decreasing pain in the dorsal horn. E.g rubbing a painful area
Gate control theory of pain
proposes how pain is reduced by activating a nonpainful sensation by the alpha delta smaller sensory nerve, decreasing pain in the dorsal horn. E.g rubbing a painful area
Pain management by multimodal approach
Mild pain - Non opioid, paracetomol, NSAID
Mod Pain - Weak opioid & non-opioid
Severe pain - strong opioid
Inhalation (volatile) agents used for induction are…
Desflurane, Isoflurane, Sevoflurane,
- act on alveolar-capillary membrane to enter systemic, crosses BBB (lipophillic) to distort ion channels and inhibit excitatory activity in CNS
