Week 1: Basics and assessment Flashcards
Basics to Anesthesia Set UP
SOAP: Suction, Airway, Pharm
Suction (in SOAP)
Make sure suction is on and accessible
Oxygen (SOAP)
Have oxygen setup and ambubag
Check gas machine
Airway (SOAP)
-ETT w/ or w/o stylet
-LMA
-Oral airway
-Esophageal stethoscope or temp probe
-Oral Airway
Pharm (SOAP)
Meds LABLED:
-Strength
-Date and time
-Initials
MS MAIDS (OR setup)
Machine
Suction
Monitor
Airway equipment
IV poles
Drugs
Special equipment
MS MAID
(Machine)
Machine check and backup supplies (Ambu!)
MS MAIDS
(Suction)
Suction is on and working, at head of bead for easy access
MS MAIDS
(Monitor)
Have all monitors for appropriate case
-BP
-Tele
-O2
-ETCO2
MS MAIDS
(airway equipment)
Tubes, blades, various airways:
-ETT w/ or w/o stylet
-Oral airway
-LMA
MS MAIDS
(Drugs)
table top and case specific drugs ready
labeled if drawn up
MS MAIDS
(Special equipment)
Two drape clips, bair hugger, fluid warmer, OG tube, IV pumps, swa ganz/CVP monitor, shoulder roll, pillows
Anesthesia Stages
- Pre- induction
- induction
- Maintenance
- Emergence
Induction stage, must
Ensure adequate oxygenation and airexchange with bag valve mask
Maintenance stage
Sustain surgical anesthesia
Emergence Stage
Discontinuation of anesthesia–>return to consciousness and protective physiologic reflexes are regained
reversals for muscle relaxants are given
Depth of Anesthesia
Degree to which CNS is depressed
Useful parameter for individualizing anesthesia
Stage 1 depth of anesthesia
Analgesia - amnesia and reduced awareness
Pt progresses to drowsy, poor coordination
VS and pupils UNCHANGED
Stage II depth of anesthesia
Increased SNS activity = Excitement - delirium and possibly combative behavior
Larygospasm can occur
Pupils are dilated
Stage III anesthesia depth
Adequately anesthetized for procedure
eventual loss of spontaneous movement
Eyelid reflex disappears
gag reflex is obtunded
Stage IV anesthesia depth
Medullary paralysis
Too much, overdose, arrest
Pain is
Conscious perception of noxious stimuli
NOT absence of movement
Prys-Roberts theory
Anesthesia is a state which patient does not perceive or recall noxious stimuli
Modern thoughts on anesthesia depths
Drug-induced non response to stimulation
CALIBRATED
against strength of surgical stimulus and diffiiculty of suppressing the response
Depth depends on what is happing in procedure
(i.e. Toe bunion vs open heart surgery)
Theory of General Anesthesia
Loss of response and perception of all external stimuli
Where in CNS to anesthetics work?
Spinal chord to inhibit movement
Hippocampus and amygdala to cause amnesia
Most relevant site of anesthetic action
Synapse
Basic anesthetic MOA
Presynaptic inhibition of neurotransmitter release –> enhancement of inhibitory neurotransmitter effects–>inhibition of excitatory neurotransmitter effect
Anesthetics modulate:
Ligand-gated ion channels
Ligand-gated ion channel mediate
fast excitatory and inhibitory neurotransmission
3 Ligand activated ion channels in anesthetics and basic ligand function
5-HT3
Glycine
Nicotonic
Ligand channel activation inhibits fast excitatory synaptic transmission and/or facilitates fast inhibitory synaptic transmission
Anesthetics and Glycine
Anesthetics increase affinity of receptor for glycine (potentiate glycine activated currents)
possibly contributes to action of volatile and some parenteral anesthetics
5HT3 channels are affected by
Volatiles but NOT propofol
possible responsible for PONV
Nicotinic receptors and anesthesia
Inhibited
may contribute to amnesia
Why are ligand gated ion channels a logical target for anesthetics?
Selective effects on these channels could either
INHIBIT fast excitatory synaptic transmission and/or FACILITATE fast inhibitory synaptic transmission
Most important inhibitory neurotransmitter in CNS
GABA
GABA
inhibitory neurotransmitter
GABA receptor location
abundantly in CNS
GABA nuerotranmitter type
ligand gated Cl - channel
GABAa and anesthetics
Potentiated by many anesthetics
Probably target molecular target of anesthetics
Glutamate
Major excitatory neurotransmitter in CNS
Glutamate -activated ion channels
nonselective, involved in fast excitatory synaptic transmission