Inhaled Anesthetics Flashcards
Toxicity of sevoflurane?
Compound A - more likely with low FGF, inc [sev] inc canister temp, dec water content, inc freshness of absorbent (compound A causes nephrotoxicity in rats - not exactly proven in humans but can see some transient effects on the kidneys)
Which volatile anesthetics and conditions produce CO2?
Des > Isf > Sevoflurane dry absorbents high temp in absorbents high [des] Baralyme > soda lime
Value of MAC awake
O.3
Eg MAC of Iso is 1. 1 x 0.3 = 0.3
what properties of an anesthetic make it quick on and off
dec blood/gas solubility
MOA of inhaled anesthetics
act at ion channels in CNS and PNS to potentiate inhibitory pathways (GABA, glycine) and inhibit excitatory pathways (NMDA)
relationship b/w lipid solubility and potency
inc lipid solubility will increase potency (remember the brain and spinal cord are largely lipid so the inhaled agent that is lipid soluble will quickly get to the brain and spinal cord)
what is MAC pertaining to inhaled anesthetics
the % of alveolar concentration at which 50% of patients will not move to surgical incision
MAC % of Sevo
about 2
MAC % of Des
6
MAC % of Iso
1
what is MAC aware?
about 0.6 (vs awake is 0.3)
relationship b/w potency and MAC %
higher the potency, the lower the MAC%
what types of conditions decrease MAC %
pregnancy, acute alcohol, hypothermia
what types of conditions increase MAC %
chronic alcohol, acute meth, hyperthermia, hypernatremia. nb thyroid dz will not affect MAC
what is typical BIS range desired during anesthesia
40-60 (most say < 50)
how does MAC % relate to partial pressures
multiply MAC% by atm mmHG to find out what partial pressure is.
e.g. for Iso Mac is 1.2% x 760 mmHg = 9 mmHg is MAC
why is des heated and pressurized?
has a high vapor pressure. (heating would normally inc vp but with des it’s pressurized which would promote cooling/condensation so it has to be heated. net effect is still that the heating + pressure lowers the vapor pressure so we can deliver set amounts to the pt)
why does the anesthesia machine need to pump some fresh gas flow around the vaporizer?
b/c the vp of all the inhaled agents at room temperature is higher than the MAC % that we want to deliver to pts (eg Sevo vp is 157 mmHg which is 21 % of atm pressure. MAC of sevo is only ~ 2% so we need to divert a lot of fresh gas around the vapor so we only deliver 2% vs 21% to the pt)
which inhaled agent has the lowest blood/gas solubility (aka which is fastest on and off agent)
Desflurane
anesthetic agent where correlates with the rate of onset of anesthetic state
rate of rise of partial pressure of agent in the alveolus (NOT blood) correlates with rate of onset of anesthetic state
how can i increase the alveolar partial pressure of an inhaled agent faster (3-4)
inc alveolar ventilation
inc inspired concentration
second gas effect
system
how to increase the rate at which inhaled anesthetics are eliminated
inc cardiac outpot
inc solubility in blood
inc v/q mismatch
lave a-v partial pressure differencse
how is anesthitic eliminated/metabolized
- most expired via lungs unchanged
- small bit metabolized via P-450 (most metab is SEVO)
most irritating inhaled agent to the aw
desflurane (may activate sympathetics)
most potent inhaled agents
Iso > sevo > des
1% 2% 6%
what can happen if you quickly increase Des or Iso concentrations
cardiovascular stimulation (may be less in neonate and geris)
effect of volatile anesthetics on CV system
- negative inotropy (dec strength of mm contraction) ↓ CO
- HR: des> iso >sevo may inc HR BUT w/concurrent opioids there’s little effect
- iso, sevo, des ↓ SVR by arterial vasodilation (via B stimulation) and ↓ CO (no expected compensation from normal svr to co relationship) so ↓ BP
if pt has LQTS how will you proceed with inhaled anesthetic
inhaled agents (esp SEVO) can prolong QT so can still use on these pts but smart to treat with bblockers
effect of volatile anesthetics on resp system
- all gases ↑ RR & ↓ TV overall ↓ min vent; depresses hypoxic drive
- all gases ↓ hypoxic drive/↑ apneic threshold (blunt response to hi CO2 and low O2)
- Iso > Sevo is a bronchodilator (may irritate upper airways) and ↓ HPV
- PVR: volatile gases ↓ but N2O ↑
effect of inhaled agents on CNS (CBF, ICP, CMRO2)
- all gases dilate cerebral blood vessels -> inc CBF -> inc ICP (predominate effect when > 0.5 MAC) (iso least potent) n.b. hypocapnia can counteract ↑ICP)
- all gases put pt to sleep so ↓ CMRO2 (predominate effect when < 0.5 MAC
- depress/slowed EEG: anesth induction inc freq and amplitude of EEG waveforms. At 1 MAC EEG slows. Burst suppression (isoelectric) w/sevo or iso @ 2 MAC)
- all agents inc latency and dec amplitude of evoked potentials at > 1 MAC
how do volatile anesthetics affect NMB
potentiate effects of both sux and non-depolarizing as they relax skeletal mm
which agents trigger MH
inhaled anesthetics and sux can both do it
5 things to dx MH
1) inc ETCO2
2) tachycardia
3) mm rigidity
4) temp inc
5) respiratory acidosis
which agent is most irritating to aw; least?
desflurane
sevo is least
how NO affects CV
stimulates release of endogenous catechols; depresses heart contractility, inc pulm vasc resistance
how NO affects resp
inc rrr, dec tv, inhibits hypoxic drive
how NO affects CNS
inc CBF, inc ICP - don’t use in neuro cases
NM effects of NO
no relaxation; no MH trigger, may inc PONV
what caution must be taken with NO and closed spaces
NO will diffuse into them increasing pressure
name and explain 3 factors which affect uptake of anesthetic gases
1) solubility (determined by blood-gas coeff…less solb is faster b/c it takes less time to “fill up the tank” before levels equilibrate with the brain)
2) CO - ↑ CO -> more blood thru lungs -> more anesthetic removed from the gas phase therefore lower alveolar partial pressure of gas (FA) and slower build up (affects more soluble gases the most)
3) partial pressure difference of gas b/w alveoli and pulmonary vein: more difference encourages gas to go into blood. (V-Q mismatch: inc FA, dec FI; L to R cardiac shunt w/normal tissue perfusion doesn’t affect anesthetic uptake; R to L cardiac shunt: bypassing of blood past the lungs = slower rate of inc in art concentration & slower induction of anesthesia
effect of volatile anesthetic on renal fxn
- all gases ↓ RBF (via inc renal vasc resistance), ↓ GFR, ↓ UOP
- Sevo -> Compound A (occurs @ low fgf rates; nephrotoxic in rats) so use FGF 2L/min
effect of volatile anesthetics on hepatic fxn
- all gases ↓ hepatic blood flow
- cytochrome P450 produces trifluoroacetylated protein antigens (moreso w/Iso)
effect of volatile anesthetic on hematologic and immune system
- N2O oxidizes B12 so inhibits enzymes requiring B12 (methionine synthetase (myelin) and thymidylate synthetase (DNA)) bone marrow depression (megaloblastic anemia) and neurologic deficiencies (PN)
what is significant about 1.3 MAC
stops movement in 95% of pts and typically allows intubation (ED95)
significance of 1.5 MAC
“MAC BAR” - block adrenergic response (nb. opioids and N20 dec MAC BAR)
when is MAC highest?
3-6 mos old
which factors inc MAC?
- amphetamines
- ephedrine (more catechols)
- age < 6 mos
- hyperthermia
- hyperthyroid
- hyperNa
- red hair (FALSE!!!!)
which factors dec MAC?
- opioid, benzo, propofol, ketamine, a2-agonist, iv LA
- acute ETOH abuse
- inc age > 1 yr
- pregnancy
- hypothermia
- hypoTN
- hypoxemia
- anemia
- metabolic acidosis
- sepsis
- lithium
- verpamil
what are the max trace concentrations that NIOSH allows in the OR?
- halogenated agent alone = 2 ppm
- if combined w/nitrous = 0.5 ppm
- high exposure (>10 to the third ppm) inc risk of abortion and dec fertility
