Volatile Anesthetics

Question 1

Sevoflurane

Answer 1

Inhaled induction
Non-pungent (sweet) , prime circuit; 8%, 8L/min for approx 60sec
LOC 1min
NMBD

MAC 2.15%

Broncho-D
Can for CO In dedicated CO2 absorbent
Compound A in absorbent - nephrotoxic: fresh gas > 2L/min to prevent rebreathing

Question 2

Nitrous oxide

Answer 2

MAC 104%
Insoluble - rapid
No muscle relaxation
+/- PONV

NMDA antagonist- ?analgesic

Can expand w/in cuff - trach injury

Sympathomimetic
Minimizes dose-related decrease in SVR when combined to other IAs
CNS: cerebral vaso-d -> inc. CBF
Prolonged exposure- bone marrow suppression (methionine synthase inhibition), peripheral neuropathy

Question 3

Isoflurane

Answer 3

Highly pungent 
Second most potent (clinically used) 
MAC 1.2%  (at 2 silent EEG)
Neuro - preserves flow-metabolism coupling CMO2 to CBF 
Vaso-D; coronary steal

Question 4

Desflurane

Answer 4

Low potency, lowest blood:gass solubility
MAC 6.8%
Vapor P close to ATM = boil at sea lvl
Very pungent:
Can cause broncho/laryngospasm, coughing…
Also CO in dedicated CO2
Can cause sympathetic response

Question 5

General

Answer 5

MAP: decreased (except N2O) via decreased SVR
Diminished baroreceptor

HR:
Iso, sevo, des will increase HR (sympathetic)
MAC: iso > des > sevo

Des seems to have the better CV profile (not for CAD)

Prolonged QT, esp sevoflurane

Protective effect on heart - limiting area of ischemic injury, enhanced ischemic preconditioning via opening of mitochondrial ATP-sensitive K channels

Vent: increase RR, decrease Vt - although relative preservation of MV (dose dependent) the decreased Vt leads to increased dead space vent- PaCO2 increases proportionally with [anesthetic]. Also decreased response to CO2 and O2
Impairs hypoxic pulmonary vasco-c

CNS
CBF: N2O = increased
Cerebral vaso-d
ICP: increased at more than 1 MAC for all IAs

All will enhance NMB, esp roc + des