Volatiles Flashcards
Desflurane
Desflurane
class: florinated methyl ethyl ether, volatile anesthetic.
MOA: Unknown,
meyer-overton theory has been largely abandoned, now believed that volatiles work on certain channels and either inhibit the stimulators or stimulate the inhibitors. some channels they may work on: voltage gated sodium channels, 2 pore potassium channels at the TREK and TASK channel, inotropic or metabotropic channels.
Pk:
MAC: 6%
BG: 0.42
VP: 669
It requires a tec 6 vaporizer r/t to how high its vapor pressure it, metabolized <0.1% by the liver to triflouroacetic acid.
Largely eliminated by exhalation.
highest risk of carbon monoxide formation with degraded co2 absorber.
SE:
CNS: increase ICP, increase cerebral blood flow, decrease cerebral metabolic oxygen rate. Potentiate the effects of NMB.
Direct myocardial depressants but does have increase SNS stim with initial overpressurization. So it will transiently increase HR, BP, and the r/f myocardial ischemia. Then will decrease BP, SVR, HR remains elevated, CO is maintained.
Will activate K-ATP channels in vessels and myocardium, hyperpolarize membranes, and may protect heart from ishemic events.
Resp: increase RR, decrease TV, decrease MV, very pugnent odor, should not be used in children or ashamtics.
N/V common. Will decrase renal blood flow, gfr, urine output, and also DECREASE HEPATIC blood flow, may have transient increase inLFTs.
C/I:
Hx or family hx of malignant hyperthermia
inhalational induction in kids r/t laryngospasm
ashtmatics
Isoflurane
Isoflurane
class: HALOGENATED methyl ethyl ether.
MOA: unknown, Meyer-Overton theory largely abandoned at this point. Believed that volatiles act on target proteins and either inhibit the stimulators or stimulate the inhibitors. some target proteins they may act on inlcude:
Voltage gated Na sodiums
2 pore potassium channels, specifically at TREK and TASK channels
metabotropic and inotropic channels.
Pk:
MAC = 1.2
BG: 1.4
VP: 240
Metabolized 0.2 to 2% in liver,
largely eliminated via exhalation to trifluroacetic acid.
SE:
Increased cerebral blood flow, ICP, decreased cerebral metabolic oxygen demand at or above 1 MAC, does ENHANCE CSF REABSORPTION
produces muscle relaxation,
SILENT EEG at 2 MAC
Myocardial depressant - decreases BP, SVR, mild increase HR, no change to CO
Coronary artery vasodilator - risk for coronary steal syndrome.
Increase RR, decreaes TV, bronchodilator.
Decreases RBF, decreases GFR, decreaes UOP, MAINTAINS HBF.
C/I:
Peds - r/t pungent odor, r/f laryngospasm
Hx or family hx of MH
caution in CAD or neuro anesthesia - consider 1/2 MAC
caution with over pressuring r/t increase HR and B
can react with CO2 scrubber to form carboxyhgb in pt
N2O
N2O:
class: inorganic gas with a double bond between two nitrogen atoms, volatile anesthetic.
MOA: Unknown.
Meyer-Overton theory abandoned, now believed that volatiles work at certain ion channels to inhibit the stimulators or stimulate the inhibitor. Some ion channels they may work on:
voltage gated sodium channels
two pore potassium channels at TREK or TASK channels
inotropic or metabotropic channels.
NMDA channels to block glutamate.
Pk:
MAC: 105
BG: 0.46
VP: 39,000
SE:
Increase ICP, increase cerebral blood flow, and INCREASE CMRO2
N2O is a direct myocardial depressant but also increases SNS outflow so there is overall minimal increase in HR, SVR, BP, CO.
INCREASE PULMONARY VASCULAR RESISTANCE.
Increase respiratory rate, decrease tidal volume,
DIFFUSION HYPOXIA WITH D/C
DECREASES HEPATIC BLOOD FLOW.
decreases GFR, RBF, UOP.
Nausea/vomiting common -
inhibits B12 dependent enzymes responsible for myelin formation and DNA synthesis.
c/I:
PTX, air embolism, tympanic membrane surgery, eye surgery, abdominal surgery, pULMONARY HTN. Caution in CAD or with epinephrine use - increase r/f dysrthmias
Sevoflurane
Sevoflurane
Class: florinated methyl ethyl isopropyl ether , volatile anesthetic
MOA:
MOA unknown, meyer-overton theory largely abandoned at this point. Now believed that volatiles work on certain channels, either stimulate the inhibitors or inhibit the stimulators.
some channels they may work at are the
voltage gated sodium channels
the 2 pore potassium channels at the TREK and TASK channels
the inotropic or metabotropic channel
Pk:
MAC: 2
BG: 0.69
VP: 160
Eliminated mostly by exhalation
metabolized 2-5% by liver, produces no triflouroacetic acid r/t to its isopropyl structure.
3.5% is excereted as inorganic flouride ions in urine.
SE:
Increased ICP, increased cerebral blood flow, decrease cerebral metabolic oxygen rate at 1 MAC or above.
Preferred in neuro anesthesia because it has the relateively smallest increase in ICP and CPP is decreased.
Muscle relaxation, potentiantes effects of neuromusclar blocking drugs.
Seizures
High rate of emergency delierum in children.
CV - dose dependent myocardial depression. Decrease in SVR, BP, no increase in HR when greater than 2 MAC, CO may decrease more than with other agents.
No SNS activation with over pressuring!
Activates K-ATP channels in myocardium and vessels that hyperpolarize membranes and may protect heart against ishcemic events.
RR - increase RR, decrease TV. Decrease minutevolume.
Sweet odor, least irritating compared to other agents so most prefered in asthma and in chidlren.
Bronchodilatoin.
Reduce hypoxic pulmonary constriction at greater than 1 MAC.
GI/GU - does cause N/V
decrease RBF, decrease UOP, MAINTAINS hepatic blood flow.
Theoretical risk for nephrotoxicity r/t compound A, to compensate for compound A, we administer sevo with a FGF of at least 2L/min
C/I:
hx or family hx of malignant hyperhermia
severe renal diseae
