• Pressure in room is POSITIVE
– Air flow is from ceiling to floor: air inlet near
ceiling and exhaust near floor
• Minimum of 20 air exchanges/hr with a
minimum of 4 which must be fresh
• 1977 NIOSH
– 25 ppm for N2O
– 2 ppm for halogenated agents
– 0.5 ppm for halogenated agents with N2O
• 3. Gowns of the surgical team are
considered sterile in front from chest to
level of sterile field. Sleeves are
considered sterile from 2 inches above the
elbow to the cuff
• 8. Items of doubtful sterility must be
considered unsterile
• Agonists: capable of eliciting full agonist (morphine-like)
effects
• Partial agonist: Has a dose effect ceiling lower than
max. effect produced by a full agonist
• Agonist-antagonists: Act as partial agonist at one
receptor and antagonist at another receptor (nubain)
• Antagonists: bind to a receptor and produce no effects
(narcan)
• Nitro, atropine, naloxone, glucagon & benadryl? may
treat biliary spasm benadryl is believed to prevent the
histamine release that causes spasm
• Mu (μ):
– Mu-1:
• Supraspinal (brain) analgesia
• Euphoria
• Miosis
• Urinary retention
– Mu-2:
• Respiratory depression (primarily responsible)
• Spinal and supraspinal analgesia
• Physical dependence
• Constipation
• bradycardia
• Kappa (κ):
– Spinal analgesia
– Sedation
– Dysphoria ( the bad high)
• Delta (δ):
– Spinal (mostly), supraspinal analgesia
– Some respiratory depression
Narcan competative
• Naloxone: (narcan)
– Most frequently used antagonist in anesthesia.
– Great affinity for the Mu receptors and is a competitive
antagonist
– Can reverse unconsciousness from narcotic overdose
– Reverses resp. depression: give in 20-40 mcq increments
• Will reverse resp depression (mu-2) but can maintain analgesia
• Peaks in 1-2 min and lasts 30-45 min
• Narcan cont’d…..
• Abrupt reversal can cause excessive SNS stimulation
– Arrythmias, ^HR, ^BP, n/v, and pulmonary edema
• Mix: 1 ampule (0.4 mg) with 9 cc’s of NS. Give 1 cc at a
time
• Butorphanol: (stadol)
–
–
–
–
–
–
Produces analgesia and resp. depression similar to 10 mg of MSO4
Causes more sedation than nalbuphine
Incidence of dysphoria is low
Does not increase intrabiliary pressure
Can be used to treat post op shivering
Dose: 0.5-3 mg IV
• Nalbuphine: (nubain)
– MSO4 like analgesia
– May cause some sedation but not as much as stadol
– Given IV will reverse the resp depressant effects of narcotics but
sustain analgesic effects
–
–
–
–
Also used to antagonize itching from epidural and intrathecal MSO4
May be given IV or IM
Dosage: 5-10 mg
Can cause withdrawal symptoms in pt’s addicted to opioids
REmi
•
•
•
•
Similar potency of fentanyl
Extremely rapid onset, clearance and recovery
E ½ time: 15-30 min.
Dosage:
– 1mcq/kg IV over 60-90 sec. then 0.25-1 mcq/kg OR
0.05-2 mcq/kg/min
• Metabolized by non-specific plasma and tissue
esterases
• Once infusion is stopped no more analgesic
effects!!!
Alfi the fast weak geek
• 1/5 – 1/10 as potent as fentanyl
• Intra-op dosage:
– 10-100 mcq/kg
• More rapid onset but shorter duration of
action than fentanyl and sufenta
• E ½ time: 1 ½ hrs
Su-fent (super fentanyl)
• 7-10x’s more potent than fentanyl
• Dosage:
– Intra-op: 0.2-0.8 mcq/kg
– CT surg: 10-30 mcq/kg
• E ½ time:
– 2 ½ - 3 1/2 hrs
fentanyl
• Structurally related to meperidine
• 100 x’s more potent than morphine
• E ½ time: 3-6 hrs
• Dosage:
– Intra-op: 2-10 mcq/kg
– CT surg: 30-50 mcq/kg
– Post-op: 0.5-1.5 mcq/kg
• 1cc= 50 mcq’s
• Minimal CV depressant effects
– May decrease HR
• Can cause chest wall rigidity
•
meperidine
The 1st completely synthetic opioid
–
–
•
Dosage:
–
–
•
Incr. HR
Some histamine release (less than MSO4)
Used to decr. Shivering post-op
–
•
0.5-1 mg/kg IM
0.2-0.5 mg/kg IV
Structural similarities to atropine
–
•
•
1/10th the potency of MSO4
E ½ time: 3-5 hrs
Mechanism unclear thought possibly due to stimulation of kappa receptors, decr. Shivering threshold and
alpha-2 receptor agonist
Breaks down into normeperidine
–
–
Also excreted by the kidneys
Neurotoxic in high concentrations
–
•
Do NOT give to pt’s on MAOI’s (nardil) (Parnate) (Marplan) (Emsam)
–
Causes a severe excitatory state
•
•
•
•
Incr. HR, BP, temp
Delerium, seizures
Possible death
Breaks down into normeperidine
–
–
Also excreted by the kidneys
Neurotoxic in high concentrations
–
•
Myoclonus and seizures
Myoclonus and seizures
Do NOT give to pt’s on MAOI’s (nardil) (Parnate) (Marplan) (Emsam)
–
Causes a severe excitatory state
•
•
•
Incr. HR, BP, temp
Delerium, seizures
Possible death
Morphine
•
•
The prototype opioid agonist to which all others are compared (E ½ time=
1.5-3 hrs)
Dosage:
– Intra-op: 0.1-1 mg/kg IV
– Post-op: .05-0.2 mg/kg IM
.03-0.15 mg/kg IV
• Major feature is histamine release
– Causes decr. BP, incr. HR and flushing
– Slowing administration helps decr. histamine release
•
Broken down into active metabolites
– Morphine 3-glucuronide & morphine 6-glucuronide
• 6-glucuronide is a more potent and longer acting agonist than morphine
•
Metabolism
– Biotransformed by the liver
– Excreted by the kidneys
• Problem therefore with renal failure patients
NMB
• Some surgeries (thyroid, breast, facial) may
necessitate that you not use relaxants
• These receptors have 5 subunits
–2 alpha, 1 beta, 1 gamma, and 1
delta
• Only the 2 alpha subunits are capable of
binding ACh
• ACh is rapidly metabolized (hydrolyzed) by
the enzyme acetylcholinesterase (true
cholinesterase)
•
•
•
•
•
•
sux
NOT metabolized by acetylcholinesterase therefore concentration in
synaptic cleft high for longer period
Rapid onset: 30-60 sec
Short duration: 3-10 min
Dose: 1-1.5 mg/kg IV
4-5 mg/kg IM in children
Upon entering circulation metabolized by
psuedocholinesterase(Plasma Cholinesterase) into
succinylmonocholine
Decreased amount of plasma cholinesterase =prolonged blocks
– Causes:
• Severe liver disease
• Use of certain drugs: anticholinesterases are found in insecticides, drugs to
treat myasthenia gravis and some chemo drugs
• SE: Myoglobinuria
• ^ IOP, ICP and IGP
• Trismus Lock Jaw
• Trigger agent for MH 1:15,000 peds 1:50,000 adults
blocks
Phase I
• Depolarizer
• fasiculations
Phase II
• Due to ionic and conformational changes
that accompany a prolonged membrane
depolarization
• Atypical plasma cholinesterase:
– Have a gene which causes atypical plasma cholinesterase
• Unable to hydrolyze the ester bonds in drugs like suxx and mivacurium
• Dibucaine test watch esmolol and adenosine
– Dibucaine is a local anesthetic that will inhibit normal plasma
cholinesterase activity by ~80%
• The % of inhibition of pseudocholinesterase activity is termed the
dibucaine number
– 80% of activity (normal) your dibucaine # is 80
– 40-60:
• Only inhibited 40-60 %. heterozygous (one normal and one abnormal)
atypical enzyme
• prolonged block of 30-60 (20-40) minutes from suxx
– If dibucaine # is 20:
• Only inhibited 20% of activity. You have homozygous atypical genes
MH treatment
•
•
•
•
•
•
•
•
Terminate all agents
Call for HELP
Hyperventilate 100%O2
Cool
Bicarb (1-2mEq/kg)
Diurese
CV support (no Ca channel blockers)
DANTROLENE: 2.5 mg/kg IV q 5 min. until termination
of episode….up to max. dose of 10 mg/kg (inhibits Ca ion
release from the sarcoplasmic reticulum)
– will be given after initial control for up to 24-72 hrs at 1mg/kg
doses q 6 hrs to prevent reoccurance
Non depols
• Compete with Ach to occupy receptors
• Unlike suxx, do not mimic Ach and open
channels
• They block them so no depolarization occurs
• 2 chemical classifications:
• Benzylisoquinolines
• Steroid Derivatives
– Pancuronium
– Vecuronium
– pipecuronium
• Tend to be vagolytic
–
–
–
–
d-tubo
Atracurium
Mivacurium
Cisatricurium
• Tend to release
histamine
Long acting : PDPDMG
• Pancuronium: (pavulon)
– Dose: intub.= .08-.12 mg/kg
–
maint.= .01 mg/kg
– Excretion primarily renal (up to 40%)
• Can stimulate the SNS and block vagus therefore may see ^ HR
– Caution??
• Doxacurium:
– Dose: intub.= .05 mg/kg (onset 4-6 min.)
–
maint.= .005 mg/kg
• Pipercuronium:
– Dose: Intub.= .06-0.1 mg/kg IV
• DTc: d-tubocurarine
– Not used for NMB, but for pre-tx with suxx to prevent fasciculations
– 3mg IV 3-5 min. before suxx
• Causes
• Metocurine
• Gallamine
histamine release
Intermediate acting: VACR
•
Vecuronium: (norcuron):
–
–
–
–
–
•
Dose: intub.= .08-.12 mg/kg
maint.= .01 mg/kg
infusion= 1-2 mcq/kg/min
Onset: 3 min
Primarily biliary excretion; secondary renal excretion (25%)
Atracurium: (tracrium)
–
–
–
–
Dose: intub.= 0.5 mg/kg over 30-60 sec
maint. = 0.1 mg/kg
infusion= 5-10 mcq/kg/min
Hoffman elimination:
•
Undergoes spont. Non-enzymatic degradation
•
•
Secondary is by non specific tissue esterases
good for renal pt’s
–
–
Laudanosine: product of metabolism
–
SE: histamine
•
•
CNS stimulant
Cisatracurium: Nimbex
–
Stereoisomer of atracurium
–
–
–
Dose: intub.= 0.1-0.15 mg/kg
infusion= 1-2 mcq/kg/min
Hoffman elimination
•
•
•
Normal temp and pH
Slower onset less histamine
Laudanosine but less than atracurium
Rocuronium: (zemuron)
–
–
–
Unique in that onset is very rapid ~30-90 sec
Can be used as an alternative to suxx
Dose: intub.= .6 mg/kg
–
–
low side effect profile
Under goes little metabolism and is largely excreted unchanged in the bile and somewhat excreted in urine
Rapid sequence= 1.2 mg/kg (will make onset more rapid and longer duration)
• Short acting
– Mivacurium (mivacron)
• Duration 12-20 minutes
• Dose: intub.= .15-.2 mg/kg
infusion= 4-10 mcq/kg/mi
• Metabolism is via hydrolysis by plasma
cholinesterase
– So… if atypical plasma cholinesterase prolonged block
• Histamine release, push more slowly to decr.
• Spont. Recovery from block is rapid and need for
reversal is controversial
reversal
• Reversal of blockade depends on:
– Gradual diffusion, redistribution, metabolism, and excretion
– Administration of reversal agents…….
• Cholinesterase inhibitors/ anticholinesterases
– Primary use of this class of drug is to reverse non-depolarizing muscle
blockade
– Inhibit the enzyme that breaks down Ach
– “indirectly” increase the amount of Ach available to compete with the
nondepolarizing agent which will therefore reestablish neuromuscular
transmission
• Increase in Ach affects more than the nicotinic receptors on skeletal
muscle
– Can act at cholinergic receptors anywhere in the body:
• CV: brady M2
• Resp: bronchospasm M3
• GI: n/v M1and M3
(No Go) (PoGo)(end all)(physo)
Anticholinesterase
Dose
Neostigmine 0.037-0.07
mg/kg
pyridostigmin 0.15-0.35
e
mg/kg
edrophonium 0.5-1
mg/kg
Physostigmin 0.01-0.03
e
mg/kg
Anticholinergic
Dose per mg of
anticholinesteras
e
Glycopyrolate
Glycopyrolate
Atropine
0.2 mg
0.05 mg
0.014 mg
Not
NA
recommen
ded
Anticholinergic syndrome
• Develops in response to high doses of atropine
and scopolamine
• S/S
– CNS:
• Restlessness, shivering, mania, hallucinations, delirium,
drowsiness, agitation, disorientation
– Peripheral:
• Blurred vision, dry mouth, tachydcardia, dry flushed skin,
hypotension, rash on face, neck and upper chest
• Tx: Physostigmine 15-60 mcq’s/kg IV
– Non-ionized, (tertiary
– Lipid soluble
ammonium)
Cholinergic syndrome (cholinergic
crisis)too much acetylcholine
• Excessive use of cholinesterase inhibitors or organic
insecticides
– Excessive acetylcholine peripherally and or centrally
• S/S
– Miosis, salivation, bronchoconstriction, bradycardia, abd.
Cramping
– Weakness
– CNS: dysphoria, confusion, seizures, coma
• Tx:Atropine 35-70 mcq’s/kg
• Pralidoxime 15 mg/kg IV every 20 min
– Reactivates acetylcholinesterase
• Diazepam (benzos)
– As needed for seizures
Special notes
• Physostigmine:
– A “tertiary amine” which makes it more lipid
soluble therefore the only cholinesterase
inhibitor to cross the BBB
• Used to treat central anticholinergic toxicity
• Not used to reverse Neuromuscular blockade
• Too much anticholinesterase can cause
weakness and blockade due to excessive
amount of Ach in neuromuscular junction
• Anticholinesterase drugs will prolong the
block of succinylcholine