Learning Outcomes Flashcards
define frailty
“susceptibility state that leads to a person being more likely to lose function in the face of a given environmental challenge”
the triad of anaesthesia
the triad: analgesia, opiates and general anaesthetic agents feeding into “analgesia(removal of unpleasant stimulus), hypnosis, relaxation(muscle relaxation).”
biochemistry of general anaesthetic agents
interfere with neuronal ion channels by hyperpolarising them to reduce action potentials. Either inhalation to dissolve via membranes or I.V and bind to GABA receptors to open chloride channels.
physiology of general anaesthetic
Cerebral function lost from top down starting with complex processes, with reflexes relatively spared. IV rapid unconsciousness but rapid recovery. Blood level is very high but falls, muscle picks up the drug slowly but the effect is large because of the relative mass of skeletal muscle, fatty tissue picks up drug even more slowly but stores it due to solubility.
depolarising physiology of muscle relaxants
Depolarising (NMBS) depolarise motor end plate, render post-junctional membrane refractory to further stimulus.
physiology of non-depolarising muscle relaxants
Neuromuscular block non depolarising physiology competitive block of nicotinic acetylcholine which prevents the opening of sodium channels
central effects of general anaesthesia
depresses CV centre by reducing sympathetic outflow, ionotropic effect on the heart particularly on the cardiac output, reduced vasoconstrictor tone leading to vasodilation.
direct effects of general anaesthesia
: negative inotropic, vasodilation and venodilation decreased venous return and cardiac output.
respiratory effects of general anaesthesia
depressant reduces hypoxic and hyperbaric drive, decreased tidal volume, paralyse cilia and decrease Function respiratory capacity.
local anaesthetics physiology
sodium channel blockers, prevent propagation of action potential. LA molecules must pass into axon to block sodium channel from within, must be un-ionised to cross membranes
limiting factor of local anaesthetic
toxicity, absorption > rate of metabolism = high plasma levels
effects of local anaesthetic
Retain awareness, lack of global effects and proportional to anaesthetised area. All effects of RA are due to sympathectomy due to LA blockage of mixed spinal nerves.
spinal injection of local anaesthetic is in
the subarachnoid
epidural injections of local anaesthetic is in
extradural
how does one monitor consciousness during anaesthesia
loss of verbal contact, visually with movement, respiratory pattern and processed EEG.
monitoring
respiratory parameters, ECG, NIBP, FiO2, ETCO2, Agent monitoring, temperature, urine output, NMJ, arterial monitoring,
triple airway manoeuvre
Head tilt/chin lift/ jaw thrust.
potential of airway maintenances during anaesthesia
face mask triple airway manoeuvre oropharyngeal airway laryngeal mask airway endotracheal intubation
oropharyngeal airway guidance
only tolerated in unconscious patient, may cause vomiting or laryngospasm
laryngeal mask airway guidance
cuffed tube mask, maintain airway but doesn’t protect. I-gel, easy insertion.
endotracheal intubation guidance
placement of cuffed tube in trachea: - protects from aspiration, artificial ventilation, prevents risk of blood contamination, strict control of blood gas
how to counteract the toxicity of anaesthesia
used alongside vasoconstrictors to reduce blood flow to reduce absorption
toxicity risk factors for anaesthesia
Toxicity depends on dose used, rate of absorption, patient weight and drug.
signs of anaesthetic toxicity
twitching, tinnitus, drowsiness, convulsion, coma and CV arrest
laryngospasm is
forced reflex adduction of vocal cords, may result in complete obstruction. Maye be caused by excitation phase on anaesthesia.