deck_2484437 Flashcards
enflurane class
halogenated methyl ethyl ether- isomer of isoflorane
enflurane MOA
unsure exact MOA but Myer overton theory is widely accepted
enflurane PK
sweet mild; elimated by exhalation. metabolized but the liver 2-5%.
enflurane SE
increase CBF/ICP; decreases CMRO2; increases csf secretion and resistance to csf outflow; Sz possible bc reg changes; decreases bp svr co; increase HR; bronchodilation ; decreases mucocilliary fx; decreases RBF, GFR, UOP, HBF; sensitizes heart to Epi=increase likelihood of dysthrythmias. respiratory depression
enflourane CI
renal dysfunction, sz, mh. potentiates NMB
enflurane dose
vp= 175; bg1.8; MAc 1.68
Halothane class
halogenated alkane derivative with bromide substitution
halothane MOa
uncertain- myer overtion theory widel accepted
Halothane PK
nonflammable, sweet, thymol preservative, eliminated by exhalation. metabolized 15-20% in the liver
halothane SE
increases CBF/ICp, decreases CMRO2. direct myocardial depressant, decrease SA/AV node transmission, sensitizes heart to EPI; decreases BP and CO. no change with SVR; no change or decreased HR; CA dilator; Bronchodilation; can cause halothane hepatitis from response to trifluroacetic acid; decreased rbf, gFR, uo. decrease hepatic BF
halothane Cl
liver disorder, CCB, BB, TCA/MAoi’s, MH, AS. no kidney disease/ neuro/pheochromocytoma. aminophylline cause ventricular dysthrythmias, hypovolemia; impares metabolism of fentanyl, phenytoin, verapamil; potentiated by NMB.
halothane dose
VP=244; BG 2.4; MAC 0.74
propofol class
nonbarbituate induction agent 26 di isoprophenol
propofol MOA
discourages GABA from disassociating from the GABA A receptor, prolonging action and increasing conductance of CL= hyperplarizes the cell and decreases neuronal transmission; inhibits glutamate at NMDA receptor
propofol PK
lipid soluble; VD= 2.5-4.5L/KG; onset 30 seconts; quickly redistributed in 2-8 min; E1/2 1hr; conjugated in the liver to glucuronide and sulfate by cytochrome P-450 to produce water soluble compounds which are excreted by the kidneys; extrahepatic metabolism or extra renal elimination is suggested; lungs play role in extrahepatic metabolism and are responsible for uptake and first pass elimination
propofol SE
decrease CBF/ICP/CMRO2/CPP/IOP/eeg bursts. apnea- decreased response to CO2/hypoxia, broncholdialation/pulmonary vasoconstriction reflex intact, , myoclonus, hiccups, decreases BP 25-45%, SV/CO/SVR. HR= myocardial depression, antiemetic, antipuretic, amnestic >30mcg/kg/min
propofol CI
hypotension/hypovolemia/soy/egg yoke allergy. decrease dose in elderly, increase dose in <2yr old; crosses placenta. does not potentiate MR
propofol dose
induciotn 1-2.5mg/kg; sedation 25-100mcg/kg/min; main 100-300mcg/kg/min
Desflurane class
florinated methyl ethyl ether; structure sim to iso but a F exchanged for Cl
Desflurane MOA
myer overton theory most widely accepted
DesfluranePK
have to use a Tec 6 vacorizor bc VP so high; fast on fast off because of BG coefficient; eliminated by exhalation. oxidative hepatic metabolism <0.02% by p450- low risk for halothane hepatitis,
Desflurane SE
increase CBF/ICP, decreased CMRO2/CPP; transient SNS activity proceeds a decreased BP/SVR/Co increased HR~; doesn’t dilate CA; myocardial contractility depressant, boncholdialtion; decreases RBF/GFR/UOP. decreases HBF- transient increase in LFTs; aW irritant- can causes cough/laryngospasm/increased secretions; dose related respiratory depression= increase RR and decreased TV, • Reduces hypoxic pulmonary vasoconstriction at doses >1 MAC increasing the risk of hypoxia during one lung ventilation ; high rate of emergence delirium esp in pecs; PONV
Desflurane CI
potentiates NMB; MH, Peds, CAD and myocardial ischemia- bc of the increased Cardiac demand with HR
Desflurane dose
VP 664; BG 0.42; MAC 6%
